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JOURNALOF THE

ASSOCIATION OFNEUROPHYSIOLOGICAL SCIENTISTS

Volume 6 Number 1 (2013)

ISSN 1757-8973

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JOURNAL OF THE ASSOCIATION OF NEUROPHYSIOLOGICAL SCIENTISTS (2013) 1 01

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Index

INDEXPage No.

Editor’s Foreword 3

Obituary — Lyn Davies 5

Stanton Memorial Prizewinner 6

Corrections 6

OSET Update Kelly St. Pier 8

Teaching Paper SomatoSensory Evoked Potentials ANS Evoked Potential writing group 9

Postgraduate Dissertation 32 Can the theta/alpha QEEG index be used to identify normal/abnormal EEGs in patients screened with 6-CIT for cognitive impairment? Michael Pridgeon

Unimed Prizewinner Undergraduate Dissertation 45 A comparison of the Pattern Reversal Visual Evoked Response obtained with

Cathode Ray Tube (CRT) technology to that obtained with a Liquid Crystal Display (LCD). Donna Formby

Regional Report 55 An overview of neurophysiological services in Northern Ireland Lezlie Huntley

Audit Thesafetyandefficacyofhyperventilation 59

during routine EEG: a national survey Lawrence, SJ, Kandler, RH, Kane, N, Grocott, L, Pang, C

Safety of video-telemetry units: a national survey Charlton G, Lai M, Kandler RH, 64 Ponnusamy A, Bland JP, Pang C

Professional Affairs Chartered Scientist Award Kelly St. Pier 74 What Csci means to me Dr Sharon Ann Holgate 76

ANS Meeting and Reports ANSScientificmeetingApril2013 Programme 77 Abstracts 79 Meeting report Amy Hopper and Hollie Grainger 82

Journal Review The Neurodiagnostic Journal Susan Brenan 85

Charity News Illona Sempers 88

Notice Board The ANS Council 2013-2014 92

Future Meetings 95 Dissertation Report Form 96 Revised Brief Guide for Authors 97 Revised Guidelines for Preparing a Paper for JANS 98

JOURNAL OFTHE ASSOCIATION OF NEUROPHYSIOLOGICAL SCIENTISTS



JOURNAL OF THE ASSOCIATION OF NEUROPHYSIOLOGICAL SCIENTISTS (2013) 102

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COUNCIL OFFICERS Hon. Chair: Peter Bill email: [email protected] Hon. Vice Chair: Miss Kelly St. Pier email: [email protected] Hon. Secretary: Joanne Horrocks email: [email protected] Hon. Treasurer: Ms Mary Boland email: [email protected]

INDIVIDUAL MEMBERSHIPMembership of the Association is open to all those engaged in clinical neurophysiological practice. Application forms should be obtained from the Membership Secretary. Annual subscriptions are payable on the 1st of March and the current rates are: Full Member £55; Associate Member £55; Commercial Member £55; Student Member £15; Airmail Surcharge – Printed Copy £20. There is an initial registration/re-registration fee of £15. No fees should be sent until the Membership Secretary has allocated the appropriate grade of membership.

Membership Secretary: Joanne Horrocks

Clinical Neurophysiology Department,York District Hospital

Wigginton RoadYork

YO31 8HEemail: [email protected].

SUBSCRIPTIONSAnnual subscriptions for institutions, libraries and departments, are due on 1st March. The current rate is £55 (including P&P), for one copy of the journal, three issues p.a. Payment should be made to “A.N.S.” - in £

Sterling only - and sent to the address below: ANS Business Administrator: Mrs Lindsey Sevier-White

c/o EBS, City Wharf Davidson Road,

Lichfield, Staffs WS14 9DZ email: [email protected]

JOURNAL OF THE ASSOCIATION OF NEUROPHYSIOLOGICAL SCIENTISTS (JANS)

J. Assn. Neurophysiol. Sci. ISSN number: 1757-8973

Former title: The Journal of Electrophysiological Technology (JET)

J. Electrophysiol. Technol. Former ISSN number: 0307-5095

Published by ANS

Managing Editor: Mrs Sara Callen

7 Albert Terrace, Buckhurst Hill Essex, IG9 6DU

email: [email protected] or [email protected]

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below. For current pricing, please contact ANS Business Administrator: Mrs Lindsey Sevier-White, c/o EBS, City Wharf, Davidson Road,

Lichfield,StaffsWS149DZ.email:[email protected]

Copy deadline for future editions are: Vol. 6 No.1 - 30 September 2013 Vol. 7 No. 1 30th January 2014

There will be a surcharge for late payments, and also for any changes made to the advertisements after the originals have been

submitted for printing.

THE ASSOCIATION OF NEUROPHYSIOLOGICAL SCIENTISTS (ANS)

Formerly known as The Electrophysiological Technologists’ Association (EPTA) WEB SITE: www.ansuk.org

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© ANS 2013. The Journal of the Association of Neurophysiological Scientists (JANS) is published by the Association of Neurophysiological Scientists (ANS). The photocopying of individual articles for private study or research is permitted by ANS. Single or multiple copying of any item, by any means, or electronic storage or transmission, for any other purpose, without the prior permission of the Managing Editor, on behalf of ANS, is in breach of Copyright Law.

ANS Council, the Editorial Board and the Editor do not take responsibility for, or validate, comments or opinions expressed by individual authors, or advertisers, in this journal, including equipment, its usage or procedures in current practice.

INDEX OF ADVERTISERS Nihon Kohden Front inside cover Optima Medical Pages 4, 7, 44 Micromed Page 73 Digitimer Page 84 Unimed Back inside cover

Index/ ANS Information



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Editor’s Foreword

EDITOR’S FOREWORD

Welcome to the first of two issues of JANS Volume 6 planned for 2013; I intend to produce 3 issues for next year, 2014, providing there is a steady flow of material for publication.

The rather indifferent spring weather has meant that keeping my nose to the editorial grindstone hasn’t been too onerous – temptation to get outside, do the gardening, or just explore the local area has been minimal. I am sure we have all found the grey days disappointing, and a bit of a drain, so I am hoping this issue will provide stimulation for the little grey cells.

In sombre mood, there is an obituary for Dr Lyn Davies, written by Dr John Stradling (first published in the ARTP Newsletter). Many of us will have had the pleasure of working with Lyn, when he was involved with Nervus EEG systems in the early 1990s. Lyn put all his engineering expertise and energy into solving the many teething problems of matching sophisticated video-EEG software to hardware that was not yet up to its demands. His patience and resourcefulness were legendary. I remember him fondly, and was shocked and saddened to hear of his death.

A significant part of this issue is the second of the ANS Education Committee’s Evoked Potential teaching papers - this time on Somatosensory EPs, substantially the work of Peter Walsh and Fiona Cave. I am impressed by the thoroughness of their work, especially in context of their full time jobs and other professional commitments. It’s an inspiration to us all. I look forward to the next instalment – which I guess will be Visual EPs. Take note: involvement in such projects is a great way to support CPD, and a published paper is a great piece of evidence!

No less important, however, are two final degree dissertation papers. In the first Michael Pridgeon describes his MSc project, an innovative idea which shows real potential for the use of quantitative EEG (QEEG) in the identification of subtle changes in theta/alpha index in people with cognitive decline and dementia. As the population ages, and a greater number suffer with age-related decline, early identification becomes central to timely diagnosis and appropriate treatment. Donna Formby has been awarded the Unimed prize for her final year BSc dissertation, which she presented at the ANS Scientific meeting in September 2012. She compared Pattern Visual Evoked Responses to stimulation from (CRT) cathode ray tube and LED (liquid crystal display) monitors, finding important evidence responses to LED stimulation are delayed relative to those elicited by a CRT screen. This research is relevant to all departments who upgrade from CRT to LED monitors.

Lezlie Huntley has responded to my request for an overview of Neurophysiology in Northern Ireland (NI). She is the ANS Council NI representative, and I thought it would be helpful for us to know a bit more about the set up there, which differs to mainland UK (which also has differences between the three countries – I am hopeful that similar overviews might be forthcoming from representatives in each country).

We all recognise the importance of audit, and the need to improve practice and raise standards nationally. Therefore the two audit reports, on the safety of hyperventilation during routine EEG, and the safety of video-telemetry units, are timely. These are, again, the result of a great deal of hard work ‘behind the scenes’ which benefits us all.

Reading through the Journal review, I came across a new word (to me, at least) – privademic – and wondered what it meant. I found this definition on-line: “...the safe and effective practice of academic medicine within a community setting...” – not sure if it will catch on here in the UK! I have always found the Neurodiagnostic Journal a worthwhile addition to the neurophysiology department’s library, and am grateful for Susan Brennan’s regular reviews.

Please note the updated ANS Council members list on page 2, followed by Future meetings page. I have updated the Brief Guide to Authors, to reflect current on-line/electronic practice, and will update and re-publish Guidelines for Preparing a paper for Publication in the next issue of JANS.

Sara CallenManaging Editor

[email protected]@hotmail.com





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OBITUARY

Lyn Davies 1951 – 2013

Lyn Davies, founder of Stowood Scientific Instruments, died after a short illness on May 30th 2013. Many of you will remember Lyn as an extraordinary one-off in the sleep world. He was truly someone who made a difference to those around him and beyond. Born in 1951 in Morriston, near Swansea, he was educated at Amman Valley and Ystalyfera Grammar Schools. He went on to study engineering at University College Cardiff, graduating with the best engineering degree in Wales in his year. It was during this time that he developed an interest in classic motorbikes and met Cathy his future wife. Following graduation, he worked on modelling ocular microtremor for a bioengineering PhD at Cardiff. His first jobs were working for the NHS in Nottingham and subsequently at the John Radcliffe Hospital in Oxford. From 1984 to 1992, working for Oxford Medical (part of the Oxford Instruments Group), he was the driving force developing their sleep monitoring systems. Prior to this the available systems had been rather embryonic, and the new devices were successfully used by many around the world. Indeed it was at this time that I first met Lyn, who was extremely helpful in getting the Oxford Sleep Unit’s monitoring capability off the ground. Oxford Instruments then made an unwise choice, deciding there was no future in sleep monitoring equipment, and Lyn decided to go it alone, setting up Stowood Scientific Instruments (SSI) in his garage in 1992. With help from several previous collaborators, in particular Hugh Goodwin and Paul Gladding, SSI developed several products for the sleep world that were designed to do exactly what was required. Lyn always paid close attention to the needs of clinicians and technicians to ensure that the equipment SSI developed met their needs; an ethos that his SSI colleagues are keen to continue. Despite the competition from giants in the industry, Lyn’s company prospered (in a now enlarged and modernised ‘garage’!); one of the main reasons SSI is and will continue to be successful was Lyn’s intelligence, personality and personal approach, a legacy he leaves behind. He was kind and generous, always willing to stop, talk, help and problem solve, both in and out of work. Many will remember his wry sense of humour and leg-pulling expertise. Away from work, apart from classic motorbike restoration, Lyn developed a passion for singing and was a key member of the Oxford Welsh Male Voice Choir, developing a wonderful and moving solo voice, which in recent years featured in many concerts around the country. Many in the ARTP will remember his passionate rendering of Why Why Why Delilah at the karaoke contest during their annual conference dinner a couple of years ago - it brought the house down. It was characteristic of Lyn that when he knew the end was near he wanted to have a party he could enjoy, to which he could invite as many friends as possible, and say goodbye. Thus a week before his death, 175 friends and family assembled in a marquee in his garden. They shared in a program of readings and musical performances, selected by Lyn, and all organised with lightning speed by the family. The program included both moving and humorous performances by his Welsh choir and their musical director. His death leaves a void in many peoples’ lives, but in particular those of his wife Cathy and two sons, Gwilym and Pierre.

Because of his long support for the ARTP, they wish to commemorate Lyn’s contributions with an annual prize at their conference in January. Anyone wishing to contribute to this memorial prize, could they please send any donations (payee ARTP) to:- ARTP (Lyn Davies Award), c/o EBS, City Wharf, Davidson Road, Lichfield,Staffs,WS149DZ

John StradlingARTP – Association for Respiratory Technology and Physiology

Photographed sourced from Stowood Instruments Limited website: http://stowood.co.uk/About.html



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THE WILLIAM STANTON MEMORIAL PRIZEWINNER

2011–2 – Wilma Gerrie

Wilma Gerrie was awarded the William Stanton Memorial Prize for 2011-2-12, for her paper: West Syndrome – An Overview and Interesting Case Studies (JANS 2011.Vol 4(2);82-95). Wilma explains: “The paper was written following interesting cases I studied in depth for the excellent MSc module in Paediatric Neurophysiology 2008/9 provided by Westminster College, which sadly is no longer available. I wrote the paper as an opportunity to present at OSET in Germany, where it was well received, and I had a great experience. Following this, I was persuaded to adapt it for publication in JANS by Nikki Broomfield, who was the Editor at the time. In addition, I have also presented the talk to local Grand Rounds, in Royal Aberdeen Children’s Hospital, to the Scottish Neurophysiology Group and to the Scottish Epilepsy Group. I would recommend any clinical physiologist to study and present as this has been very rewarding.”

Wilma was surprised and delighted to receive the award at the spring ANS Scientific Meeting and AGM, in Crewe (April 2013). As she wrote: “I had a great time at the meeting seeing old friends and making new ones. The talks were all very interesting too. It was so good to be able to attend and be presented with my award amongst the other award winners, and I am sorry you (i.e. your Editor) weren’t there to see it all.”

Wilma sent the photograph above, taken by her husband, of her proudly holding her certificate. She added: “I am going to get a nice keepsake with the award money. Many thanks again for your nomination. It has been a real highlight in my career. Best wishes, Wilma.”

I hope Wilma’s pleasure and encouraging words will inspire more Neurophysiological Scientists to submit papers to JANS – remember, you too might be a prize winner!

Stanton Memorial Prize

CORRECTIONSPlease note that the e-mail for Susan Brennan, Journal Review editor/Reviewer was wrong in the last issue of JANS. Her work e-mail is: [email protected]

Apologies to our esteemed ANS administrator – Mrs Lindsey Sevier White, who is not a Ms or a Miss (for contact details, see page 2)!

EXAMINATION RESULTS 2012Part 1: June 2012 Electroencephalography (EEG)Apologies, also, to Amy Hopper, whose name was missing from the list of successful Part 1 students in the previous issue of JANS. Well done Amy! And to all our hard working trainees.





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INTERNATIONAL NEWS – OSET UPDATE

Following on from last successful OSET congress, held in Bielefeld, Germany, 2011, I am happy to announce the next congress will be held in Turku, Finland, 8-12th June 2015 http://congress.utu.fi/oset2015/. Turku, at this time of the year, has approximately 20 hours of sunshine and is surrounded by thousands of islands; a beautiful archipelago. The Association of Biomedical Laboratory Scientists in Finland and The Finnish Society of Clinical Neurophysiologic Nurses are working collaboratively to deliver the Congress program. All ANS members are encouraged to view the new OSET website: www.oset.org, where more information on OSET and the 2015 congress can be found. ANS members are encouraged to attend and, maybe, even offer to present at the congress. It is always a stimulating program, an enjoyable social event and a great opportunity to network with our international colleagues. Current member countries are: Australia, Canada,Denmark,Finland,France,Germany, Ireland, Italy,Netherlands,Norway,NewZealand,Sweden,Switzerland, UK, and USA.

There have been changes in the OSET Presidency: the current President is Ms Angela Borbelj, from Canberra, Australia, a change from the Immediate Past President, Karen Wilson, UK.

The new updated website has an e-Learning portal, which provides access to member societies, for sharing newsletters and other items of importance.

Just a reminder to all ANS members: the purpose of OSET is for all member countries to strive to promote education and the attainment of the highest level of knowledge and understanding in the field of Electrophysiological Technology. With this in mind, ANS has recently suggested an OSET project on Standards of International Clinical Practice, and this is currently being investigated and will build on previous work relating to standards of training and education.

Kelly St. PierANS OSET Representative

[email protected]

International News



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TEACHING PAPER

SOMATOSENSORY EVOKED POTENTIALS

ANS Evoked Potential Writing Group

IntroductionEven when recording directly from the cortical surface, responses that are less than a few microvolts in

amplitude are difficult to distinguish from background (non-event related) potentials without specialised equipment and techniques.

In the mid 1940s, Dawson found an exaggerated EEG response after brief electrical shocks were delivered to the peripheral nerves in a patient with myoclonic epilepsy. Dawson superimposed photographic traces of responses, so that the nonrelated potentials could be suppressed and visualisation of the time locked response could be resolved. Subsequently, he invented an electromechanical device that was able to store and ‘average’ the responses after each stimulus (Dawson, 1946; Dawson, 1947).

With this new method, attention shifted away from the middle (40-100msec) and long (>100msec) latency cortical responses after sensory stimulation, and when spinal evoked potentials were recorded in humans, from electrodes placed in the subarachnoid space (Magladery et al., 1951), it enabled detailed studies in patients with neurological disease. When advances in transistor technology and physiological amplifiers became more readily available in the 1970s, faster and more reliable resolution of the high frequency, far field and sub cortical somatosensory evoked potentials (SEPs) enabled noninvasive surface recordings of the spinal potentials to be recorded (Cracco, 1973).

Since then the understanding of the neurophysiological generators of the short latency SEPs from the spine and scalp have been advanced by others (Ertekin, 1976a, 1976b; Desmedt and Huy 1984; Lee and Seyal, 1998), and their application in neurological disease has been widely used (Cruccu et al., 2008; Kraft et al 1998; Walsh et al., 2005).

When used clinically, it is important to understand the anatomy of the system under investigation and to record SEPs from the peripheral nerves being stimulated, and from the spine, and from the scalp, so that the anatomic site of the lesion causing disruption of the action potential propagation can be accurately determined and correlated to the patient’s clinical symptoms.

This review will cover the anatomy and physiology of the medial lemniscal somatosensory pathways, describe current recording techniques, the neural generators of the SEPs of the median and posterior tibial nerves, and will briefly discuss their clinical utility.

Anatomy and PhysiologyAscending tracts carry impulses from pain, thermal, tactile, muscle and joint receptors to the brain. Some

of this information will reach the conscious level within the cerebral cortex, whilst other information is processed at a subconscious level in other centres, such as the cerebellum. The somatosensory system consists of two major systems: the spinothalamic tract which subserves thermoreception, visceropception and nociception, while the dorsal column-lemniscal system subserves mechanoreception and proprioception (Figure 1 overleaf).

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Figure 1

Sensory cortex

Medulla Nucleus gracilis Nucleus cuneatus

Internal arcuate fibres

Cervical cord

Lumbar cord

Medial lemnicsal fibres

VPL Thalamus

Leg area

Arm area

Lower limb afferent

Upper limb afferent

Fasciculus gracilis

Fasciculus cuneatus

The central pathways of the medial-lemniscal dorsal columns

The peripheral terminals of the first order neurones are Meissner’s corpuscular nerve endings in the dermis of the skin and, along with other skin surface touch receptors (Pacinian corpuscles, Merkel cells, Ruffini endings) and proprioceptive muscle spindles. They send the nerve action potentials from the periphery into the spinal cord via the dorsal root of a spinal root. The primary afferent nerve fibres, which project into the dorsal column-lemniscalsystem,arethelargediameterandmyelinatedfibres(groupsIandII,orAαandAβ),whichconduct with velocities of 30-80m/s, and have their cell bodies lying within the dorsal root ganglion. Within the spinal cord the central process gives off collateral branches that make synaptic connections ipsilaterally and contralaterally in deeper laminae of the spinal cord grey matter, and these mediate various spinal reflexes and intersegmental co-ordination. The main fibre travels up the ipsilateral spinal cord in the dorsal column and, at each successive spinal level, fibres entering the posterior columns add on laterally to those already present. Those fibres that join the cord from the sacral, lumbar and lower thoracic roots form the fasciculus gracilis and

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are close to the mid-line in a somatotopic representation; the fibres from the upper thoracic and cervical are more laterally situated and form the fasciculus cuneatus.

The dorsal column fibres ascend without interruption to the dorsal column nuclei in the lower brainstem, whereupon they synapse with the second order neurones in the medulla oblongata, which are located in the nucleus gracilis and nucleus cuneatus. The axons of these second neurones cross the midline as internal arcuate fibres and ascend rostrally through the medulla, pons, and midbrain as the medial lemniscus fibres to the thalamus.

Third order neurones have their cell bodies within the ventroposterior thalamus, and these fibres ascend through the posterior limb of the internal capsule to the primary somatosensory cortex (SI) in the post central gyrus of the parietal lobe. The mechanoreceptive inputs terminate within Brodmann areas 3b and 1.

The standard SEP techniques described later only assess the function of the dorsal column-lemniscal system. Although the presence of an SEP abnormality provides good evidence for an impairment of the somatosensory system, normal SEP findings cannot exclude a selective impairment of the spinothalamic system.

Recording techniquesFilter settings

The various components of the SEP are made up of both low and high frequencies, and the optimisation of these various waveforms can be determined by the choice of filter setting used. A high pass filter set at less than 3Hz and a low pass filter set at over 2000Hz are optimal to record all SEP components without distortion. Since the filter settings for recording SEPs will affect the latency and the morphology of the waveforms, it is necessary to ensure that clinical testing is performed with the same filter settings that were used to acquire normative data.

When recording potentials from the spinal cord, or when using a non-cephalic reference to record sub-cortical potentials, the use of a higher low frequency setting, of 10-30Hz, will reduce the electrocardiographic (especially T-wave) contamination, but this may come at the cost of increasing the amount of stimulus artefact. The high filter should be set to approximately 3000Hz (Desmedt et al., 1974; ACNS, 2006). For the low frequency and high frequency filters the roll-off of the analog filter should not exceed 12 and 24dB/octave respectively (IFCN, 2009).

Analysis timeFor short-latency SEPs, the major components for clinical analysis following upper and lower limb

stimulation typically occur before 50msec and 100msec respectively. However, it may be necessary to increase the time-base if the major potentials from the cortex are delayed or thought to be absent.

Number of averagesThe signal-to-noise ratio of the various SEP components being recorded will determine the number of trials

required to be averaged for the waveforms to be accurately interpreted. For the peripheral Erb’s point, popliteal fossa potentials and the major cortical potentials, 500 trials are usually sufficient. For the, typically lower amplitude, spinal and sub-cortical potentials it may be necessary to average 1000-2000 trials. Each set of recordings should be replicated and superimposed and, when the recordings are of lower amplitude or have high levels of noise in them, then more than two replications may be necessary. The amplitude values of each of the measured components should ideally be within 20% of each other, and the latency values should not vary by more than 0.25msec of each other (0.5msec for the initial major scalp positivity after lower limb stimulation).

StimulationFor upper limb recordings, the median nerve is typically selected, although the ulnar and radial nerves may

also be stimulated separately. The anode of the stimulator is placed at the wrist crease and the cathode is placed 2-3cm proximally, over the course of the median nerve between the tendons of the palmaris longus and flexor carpi radialis muscles. The posterior tibial nerve is typically selected for lower limb recordings, although the common peroneal and sural nerves may also be tested separately. The cathode of the stimulator is placed over the posterior tibial nerve, midway between the medial border of the Achilles tendon and the posterior border of the medial malleolus, with the anode located 3cm distally.

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For interpretation in standard clinical testing, an adequately tolerated muscle twitch is usually sufficient to produce the requisite waveforms, and this can usually be achieved with stimulus intensities set at motor plus sensory threshold for mixed nerves (Lesser et al., 1979), and 2-3 times the sensory threshold for cutaneous nerves (Sadatoshi et al., 1984; Shiga et al., 2001). For the median nerve, constant abduction of the thumb should be maintained throughout the time of recording, and for the posterior tibial nerve a 1-2cm plantar flexion of the toes should be maintained. The exact location of the posterior tibial nerve can be determined by finding the position that requires the lowest intensity to produce a radiating paraesthesia towards the toes, and increasing until a twitch, which includes flexion of the medial and lateral group of toes, is produced (Miura et al., 2003). Approximately the same stimulus intensity should be able to be achieved on both sides, and any obvious discrepancy could be due to positioning of the stimulator or clinical disease.

Stimulus duration and rateEither a constant voltage or constant current stimulator is used to deliver monophasic rectangular pulses,

with a pulse width of 0.1-0.5msec, with 0.2msec being used typically. The stimulus rate is a compromise, between presenting the stimulus at a fast enough rate to limit the exposure time of the patient to the stimulus and limiting the attenuation of the recorded potentials’ amplitude caused by rapid rates of delivery. For routine clinical recordings a rate of 2-3Hz for lower limb stimulation (Tinazzi et al., 1996a) can produce better defined cortical and spinal potentials (Chiappa, 1990), whilst for upper limb stimulation, rates of around 5Hz (Figure 2) can be used (Delberghe et al., 1990; Fujji et al., 1994). Stimulus frequencies that are exact harmonics of 50Hz (e.g. 2.5 and 5Hz) should be avoided, as these can time-lock 50Hz mains interference to the average.

Figure 2

The percentage amplitude of the EP (y-axis) reduces as the stimulus frequency (x-axis) increases. The advantageous increase in speed of data collection and disadvantageous loss of EP amplitude is maximised at

around 5Hz (From Nuwer and Dawson, 1984).

Ground electrodeThe ground electrode should be placed on the stimulated limb, between the stimulation site and the recording

electrodes, to minimise the electrical artefact produced by stimulation. A flexible metal strip, covered with saline-soaked cloth, wrapped around the limb, or large disposable stick-on electrode close to the stimulus site, can be used.

Median nerve stimulationFollowing stimulation of the median nerve at the wrist, a series of sequential potentials from the peripheral

nerve and the medial lemniscal somatosensory pathways can be recorded, by utilising a combination of near field and far field recording channels (Figure 3, on following page).

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Erb’s point potentialAfter stimulation of the median nerve at the wrist, the afferent volley is recorded as a near field potential

over the proximal brachial plexus, as a triphasic positive-negative-positive waveform - generated mainly by sensory fibres - over the supraclavicular fossa. An electrode placed at the posterior border of the clavicular head of the sternocleidomastoid muscle (which can be seen when the patient is asked to bend their head against resistance), and 2-3 cm above the clavicle, will record the Erb’s point potential. The subsequent components of the median nerve SEP are commonly measured relative to the negative (N9) peak of this potential, and the presence of this potential confirms adequate stimulation of the peripheral nerve.

Figure 3

Normal SEPs after median nerve stimulation (time base is 5msec/div and the vertical scale is 0.5uV/div).

The active electrode, ipsilateral to the site of stimulation, is designated EPi (ANCS, 2006; IFCN, 1999), and the reference electrode can be either the contralateral Erb’s point electrode site (designated EPc), or on the scalp (i.e. Fz). However, when a scalp electrode is used as the reference, an inverted image of the far field potential will be recorded simultaneously on this channel. A positive far-field potential can also be recorded over the scalp (Emerson and Pedley, 1984; Emerson et al., 1984), reflecting an afferent volley as it passes through the plexus. The latency of the N9 Erb’s point negativity is measured to its peak on the Epi-EPc channel. The amplitude of the N9 is measured on the Epi-EPc channel, from the peak of the N9 to that of the succeeding positive deflections.

Cervical potentialThe postsynaptic activity in the cervical cord can be recorded with the active electrode placed over the

posterior neck (Lueders et al., 1983; Emerson et al., 1984). The N13 is the negative end of the stationary (nonpropagated) dipole arising from grey matter interneurones; the potential becomes attenuated when recording from electrodes placed circumferentially around the lateral aspect of the neck, before becoming positive over the anterior region of the neck, as the synchronous positive, P13, end of the dipole (Figure 4, overleaf).

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Figure 4

The posterior aspect of the neck records the negative pole of the segmental horizontal dipole whilst the anterior aspect of the neck records the positive pole of the dipole

The N11 potential is recorded on the ascending slope of the N13 potential, and its onset latency increases from the lower to higher cervical levels when using a noncephalic reference, suggesting that it is generated by ascending action potential volleys within the dorsal columns. The N13 signal has its maximum amplitude over the mid-lower cervical region (Cv7/6/5) and, unlike the N11 potential, its latency does not change when the active electrode is placed at higher levels of the cervical region (Mauguiere, 2000).

The seventh cervical spinal process is the most prominent process at the base of the neck when the head is placed onto the chest, and the fifth spinous process (Cv5) can be palpated by counting two processes superior to the seventh.

The contralateral Erb’s point can be used as a reference to record the cervical response. However, accurate identification and measurement of the amplitude is made by using an electrode placed over the anterior aspect of the neck in the mid-line (designated AC) over the supraglottal region. When recording the cervical potential with a reference electrode placed on the scalp (i.e. Fz), the near-field potential generated in the spinal cord becomes combined with the more rostrally generated far-field potentials recorded at, or above, the foramen magnum, which can be seen when using a scalp –noncephalic recording montage (Figure 5, on following page). This single composite waveform cannot therefore distinguish the temporally coincident signals that arise from these two quiet distinct neural structures.

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Figure 5

The top trace (Cv5-Fz) shows the composite of the inverted far-field channel (Fz-EPc) and the cervical potential recorded in isolation (Cv5-EPc, middle channel). There is a latency shift of the cervical N13 to the maximal negativity on the Cv5-Fz channel that actually reflects the brainstem P14 potential. The optimal cervical channel (bottom trace) takes advantage of the out-of-phase anterior (AC-EPC) and posterior (Cv5-EPc) cervical dipole.

The choice of recording channel and, in particular, the reference site for the cervical potentials becomes an important issue, when the signals being recorded can be affected differentially by different neurological lesions (Figure 6, overleaf). It is recommended that the ‘true‘ N13 cervical signal be recorded separately, using a Cv5-AC bipolar channel, and the later brainstem (P13/P14/N18) potentials be recorded using a scalp-noncephalic referential derivation (Mauguiere and Restuccia, 1991).

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Figure 6

Selective loss of the cervical N13 potential due to a subsequent far field potential in a patient with cervical syringomyelia (time base 5msec/div, vertical scale 2uv/div).

The latency of the N13 is measured on the Cv-Ac channel. The amplitude of the N13 in normal subjects does not show a Gaussian distribution (Restuccia et al., 1992), so the best way to evaluate the amplitude is to calculate the ratio of the N9-P9 dorsal root potential to the proceeding N13 (Figure 7). The N13-to-N9 amplitude in normal subjects is usually >1.1. When the number of responding dorsal horn neurons becomes reduced, or there is temporal dispersal of the afferent dorsal volley, the N13 potential becomes reduced in amplitude.

Figure 7

The amplitude ratio of the N13 to the N9 potential should be >1.1

Far field potentialsA scalp-noncephalic recording channel (for instance Cc or Ci referenced to EPc) can be used to record the

supraspinal-subcortical responses, which are generated predominately at the cervico-medullary junction. In the scalp-non-cephalic channel recordings, 3 or 4 stationary positivities are consistently observed before the major N20 potential is recorded on the scalp channel. These potentials have a wide distribution across the scalp, with mediofrontal predominance. In normal adults these potentials peak with mean latencies of 9, 11, 13 and 14ms respectively and are, therefore, labelled as P9, P11, P13 and P14 (Figure 8, on following page).

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Figure 8

Far-field potentials recorded from a scalp to non-cephalic montage.

The P9 potential is picked up at the neck, as well as on the scalp, and reflects the afferent volley in the trunks of the brachial plexus within the axilla and supra clavicular fossa, and is recorded just before the arrival of the afferent volley at Erb’s point. The onset latency of the P9 can be altered, by changes in the positioning of the shoulder, and probably reflects a ‘junctional potential’, generated as the volley crosses the boundary between the arm and the trunk (Yamada et al., 1985; Desmedt, 1983).

The P11 potential reflects the ascending volley of the fibres in dorsal columns at cervical level. Its onset begins in synchrony with the N11 potential at cervical Cv6 level, which is close to the dorsal root entry zone of the median nerve as it enters the cervical cord. The P11 potential is recordable in about 80% of normal controls, and the clinical significance of its absence cannot be relied upon. However, when it is present, and the later scalp components are abnormal, it can be used as an indicator that the dorsal columns are functioning and that the lesion is located in the medulla oblongata or at the cervico-medullary junction.

The P13 and 14 potentials are consistently recorded in normal subjects, although there is individual variation as to which of these predominate. In some subjects the P14 is seen on the ascending phase of the P13 and, in others, the P13 and P14 can be hard to differentiate, although the P14 always peaks later than the cervical N13 potential and this can aid identification. The P14 potential is maximal from the frontal region of the scalp, and the identification of this particular potential can be optimised by recording with a scalp-earlobe (Fz-Ac) montage. The P14 potential arises from the lower brainstem, close to the cervico-medullary junction, after the synaptic relay in the nucleus cuneatus (Ibanez et al., 1989).

After the P13/P14 potential, a long-lasting negative shift, called the N18, can be seen on the scalp (Figure 9, overleaf). This potential can only be identified when using a non-cephalic reference montage from the parietal regions ipsilateral to stimulation, where there is no or minimal interference with cortical potentials (i.e. Ci-EPc). Studies in patients with lesions in the pons or rostral medulla suggest that the N18 has brainstem origin, situated below the thalamus and above the foramen magnum, with a major contribution coming from the cuneate nucleus. It has been proposed that the N18 corresponds to ‘primary afferent depolarisation’, lasting tens of milliseconds, produced by inhibitory cuneate interneurons that synapse on presynaptic dorsal column fibres (Sonoo, 2000).

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Figure 9

The N18 potential is seen in this scalp to non-cephalic reference Montage, and is attenuated at higher low frequency filter settings.

Cortical potential N20When recording from the scalp, the earliest major potential from the parietal cortex contralateral to the side

of stimulation is the N20 potential. The scalp electrodes are placed over the parietal region, 2cm behind the locations of the 10-20 international system electrodes C3 and C4, and are designated Cc and Ci when they are contralateral and ipsilateral to the side of stimulation respectively. Alternatively, the electrodes can be positioned more posteriorly (ASCN, 2006), halfway between C3 or C4 and P3 or P4, and designated CPc and CPi. The reference can be placed at Fz or at Fpz’ (that is mid-way between Fpz and Fz), to cancel out the widespread far-field (P14 and N18) potentials.

The rising limb of the N20 waveform is generated by a single dipole. This is oriented at a right angle within Brodmann area 3b, in the posterior bank of the central sulcus (Allison et al., 1980; Desmedt et al., 1987). The subsequent positivity arises from a separate radial dipole in the adjacent Brodmann area 1 of the primary sensory cortex, and has virtually no negative counterpart recordable from the scalp (Deiber et al., 1986). This positivity is labelled as either P22, or P25, and depends on the low frequency filter being used to record the potential.

The latency of N20 is measured to the point of maximal negativity that precedes the sharp drop-off into the P25 trough. The amplitude of this cortical potential is measured from the N20 to the following positive trough. Deflections can be seen on the descending slope of this potential making exact determination difficult, but a transverse scalp montage (CPc-CPi) can be used to record the N20 in isolation, as this removes other pre-central and post-central contralateral scalp potentials from being injected onto the amplifier (Desmedt et al., 1981).

Posterior tibial nerve stimulationThe potentials recorded after stimulation of the posterior tibial nerve are similar to those recorded from the

median nerve, with similar generators for the spinal and far-field potentials. The lower limb cortical potentials, however, can show considerable individual variation, which reflects the different orientations of the primary somatosensory cortex for the foot and hand (Figure 10, on following page).

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Figure 10

Normal SEPs after posterior tibial nerve stimulation (time base 10msec/div vertical scale 0.5uV/div)

Popliteal Fossa potentialThe peripheral compound nerve action potential (CMAP) after posterior tibial nerve stimulation can be

recorded 2-4cm above the popliteal crease, mid-way between the tendon of the biceps femoris laterally and the combined tendons of the semimembranosus and semitendinosus muscles medially (these tendons can be brought out by getting the patient to bend the knee against resistance). This active electrode is designated PF, and the reference electrode can either be placed over the medial femoral condyle on the medial surface of the knee (IFCN, 1999) or 2-3cm above the active electrode (ASCN, 2006).

The near field afferent volley generates the popliteal fossa potential, and the latency of this is measured at the maximal negative deflection in the PF-ref channel. The amplitude is measured from the negative peak to the succeeding positive trough.

Lumbar potential (N22)Over the lumbar enlargement of the spinal cord a postsynaptically generated negative potential, analogous to

the cervical N13, can be recorded, with a simultaneous positivity, the P22, recorded over the anterior abdominal wall (Emerson, 1988). The latency of this negative potential does not alter with varying electrode positions along the lower thoracic and upper lumbar spine (Seyal and Gabor, 1985), although the amplitude, which is maximal 5-15cm above the L4 spinous process, rapidly declines rostrally and caudally (Figure 11, overlaf).

The L4 spinous process can be estimated from a line connecting the posterior inferior iliac crests, and from this level the L1/T12 spinous process can then be located by counting up the corresponding spinal processes. The spinal processes can be made to stand out more by asking the subject to bend forward and then the processes can be palpated. This region is optimal for the recording of the segmental dorsal horn response, designated N22. A reference electrode placed over the supra-umbilical region (Um) takes advantage of the out-of-phase N22/P22 stationary dipole, and can increase the signal-to-noise ratio, as both of these electrode sites detect the T-wave of the ECG, which can contaminate the recording when using the alternate iliac crest (Ic), contralateral to the site of stimulation, as a reference. Using a reference electrode placed 2-3cm above the lumbar active electrode, along the course of the spinal cord, will cancel out the majority of N22 signal that overlies the dorsal root entry zone for the spinal segments that carry the posterior tibial nerve fibres, and so should be avoided.

The latency to N22 can be measured at the time of the greatest negative activity at L1/T12 electrodes, and the amplitude is measured from N22 to the succeeding positive peak.

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Figure 11

Sequential recordings along the lumbar axis. The referential montage (left side) shows the N22 potential at a consistent latency 5-15cm above the L4 line, with maximal and nearly equal amplitude being demonstrated on the bipolar montage (right side) 5-10cm above the L4 line.

Far field potential (P30)The ascending volley of the spinal somatosensory pathways reaches the cervical level with a latency of

about 27msec. but, due to the temporal dispersion of these afferent impulses, no consistent potential can be recorded with a surface electrode placed over the cervical region. Confusion arises when an electrode placed over the posterior neck referenced to a mid-frontal electrode is used, as this produces the N30 potential. However, as it is known that there is no segmental response located at the cervical cord level after lower limb stimulation, the neck can be considered to be virtually inactive. Therefore, in fact the frontal scalp electrode is the active electrode. The actual potential being recorded is likely to have the same origin as the median nerve P14 potential, at cervico-medullary level. When the potential is recorded from the scalp, a mid-frontal electrode position is optimal because, if the site is too posterior, the waveform can be contaminated by subsequent cortical potentials and the P30 becomes combined with the P40 post-central potential. In patients with spinal cord lesions, the latency of this potential can be used to calculate the spinal cord conduction time, and the most practical reference site is the cervical vertebrae (Tinnazi et al., 1995; Tinazzi et al., 1996)

Cortical potential P40Unlike the potentials from the median nerve, the voltage field generated in the cortex after stimulation of

the posterior tibial nerve typically extends to involve both hemispheres. This is because the primary sensory cortex for the foot is on the mesial aspect of the contralateral hemisphere, within the longitudinal fissure. There is known to be intra-limb and intra-individual variability (Lesser et al., 1987) that can make the resultant scalp topography complex.

To record the earliest major positivity on the scalp, the P40, the active recording electrode can be positioned at Cz’, 2cm behind Cz (IFCN, 1999), or more posteriorly, midway between Cz and Pz, at CPz (ACNS, 2006). The reference electrode is typically placed over the frontal region, and this montage can usually record the P40 in most normal subjects.

When the dipole is vertically oriented, and the maximal positivity is towards the vertex, then a longitudinal (Cz’-Fz) montage is sufficient to record the P40 potential, because the post-central electrode records the positive end of the dipole in relative isolation. However, if the dipole is deeper within the fissure, then it may be orientated horizontally, and the subsequent P40 may be absent, or may be attenuated in amplitude (Figure 12, on following page). This is because the mid-line (Cz’) electrode records the positive and the negative ends of the dipole simultaneously in equal amounts. When recording an additional transverse (Ci-Cc) recording channel it may be possible to identify the P40 because the electrode ipsilateral to the side of stimulation will

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record the positive end of the dipole, whilst the electrode contralateral to the side of stimulation will record the negative end of the dipole. In a study of 100 patients (P Walsh personal communication) the P40 was present in the longitudinal and transverse montage in 83%, the potentials were absent in both montages in 7% due to underlying pathological conditions (i.e. spinal tumours, cerebral tumours and peripheral neuropathy). The cortical potential was present in the longitudinal but not the transverse montage in 7% and was present in the transverse but not the longitudinal montage in 3%, indicating that the additional transverse montage may be beneficial in a small sub-set of patients when the cortical is unexpectedly absent. This ‘paradoxical lateralisation’ (Cruse et al 1982, Lesser et al 1987) is not observed when the proximal leg is stimulated (Yamada et al 1996) as the cortical representation is more lateral.

Figure 12

The top picture shows the dipole oriented towards the posterior aspect of the head, and the positivity is picked up preferentially with an electrode positioned between Cz and Pz.

The middle pictures shows an array of transverse electrodes positioned posteriorly. The dipole is orientated horizontally, the positivity is maximal on the same side as the stimulation and the negative is maximal on the contralateral side. This ‘paradoxical lateralisation’ is identified with a transverse (Ci-Cc) montage, because a longitudinal montage (Cz’-Fz) would not detect any positivity at the vertex.

The bottom picture illustrates the utility of the transverse montage in the same patient. After left leg stimulation, the P40 potential is present on both montages. After right leg stimulation the P40 potential is not recorded, and may be interpreted as either being delayed or absent. However, the transverse montage shows a normal potential.

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The latency of the P40 is measurable in any of the scalp channels of the two montages described above (Cz-Fz or Ci-Cc), although the latency on the transverse montage may be 1-2msec shorter. The amplitude of the cortical peak is measured either from the major positivity, P40 to the subsequent negativity or from the baseline.

InterpretationAll of the SEP components are directly influenced by arm and leg length and temperature, and so the

absolute latencies of these potentials should not be used solely as a criterion of abnormality.

Following median nerve stimulation, each of the obligate components of the SEP (N9, N13, P14, N18 and N20) should be identified. An absence of any of these obligate waveforms, which cannot be explained by technical factors, may be interpreted as either dysfunction of the corresponding generator or failure of that structure to receive the ascending input. A prolongation of the interpeak latencies and interside interpeak latencies beyond 2.5 or 3 standard deviations greater than the control population should be interpreted as abnormal, in consideration of the neurological problem under investigation. It is important that each department assess their own normative data before applying clinical interpretation to the results.

The plexus-cord conduction time is calculated by subtracting N9 and N13 latencies, and corresponds to the conduction through the proximal plexus and roots up to the dorsal horn of the cervical cord. The conduction time from the proximal plexus, through the roots and spinal cord, up to the cervico-medullary junction, can be calculated by subtracting the N9 and P14 latencies. The central conduction time can be calculated from the N13-N20 interval, whilst the intracranial conduction time can be calculated from the P14-N20 interval.

After lower limb stimulation, the obligate components of the posterior tibial nerve SEP (PF, N22, P30 and P40) should be identified. The central conduction time is calculated by subtracting N22 and P40 latencies, and reflects the entire extent of the central sensory pathway from the lumbar spinal cord to primary sensory cortex. Evaluation of the N22 to P30 and P30 to P40 latencies gives conduction between the spinal cord and brainstem, and brainstem and cortex.

The interpeak latencies are measured LP, P37 and P37, approximating the conduction time between the lumbar spinal cord and primary sensory cortex. Some laboratories evaluate N22-P30 and P30-P40 interpeak latencies, approximating the conduction time between lumbar spinal cord and brainstem, and brainstem and cortex.

The central interpeak latency is measured as the difference between the N22 and P40 latencies. This corresponds to the central conduction time (CCT) in the entire extent of the central sensory pathway from lumbro-sacral cord level to primary somatosensory cortex. The spinal CCT is measured by the N22-P30 interpeak interval, and the P30-P39 interval measures the intracranial conduction time from lower brainstem to cortex.

Clinical utilityComa

When the neurological examination is limited, or compromised, in patients who are unconscious, or receiving neurosuppressive medication and/or are pharamacologically paralysed, then bilateral median SEPs can be used to provide prognostic information in those patients suffering severe cerebral injury that results in coma.

The cerebral cortex is more vulnerable to the effects of anoxia than brainstem structures and meaningful physiological function is compromised 5 minutes after normothermic ischaemic anoxia. If the brainstem has become damaged by an anoxic insult, it is likely that the cortex has suffered an even worse insult. However, it is common for patients to suffer sufficient oxygen deficiency so as to damage or destroy the cortex while maintaining some or all brainstem function (Wijdicks et al., 2010). The early cortical peak of the SEP parallels the increasing level of encephalopathy, but will remain present even at levels of sedation that produce an isoelectric EEG, making SEPs a ‘global’ index of brain function in the absence of a relevant lesion (Amantini et al., 2008).

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In patients with severe cerebral injury resulting in coma from anoxia, bilateral absence of the N20 potential more than 12 hours after the onset of coma has always been associated with permanent vegetative state or death (Crucco et al., 2008). Although some case reports describe favourable outcome after bilateral loss of the SEP in coma, the causes were conditions other than anoxia, and most of them were children (Schwartz et al., 1999; Wohlrab et al., 2001). Most studies agree that there is a specificity of virtually 100% for the absence of the N20 potential predicting poor outcome. The presence of these waveforms does not, however, mean that the patient will recover consciousness, as sensitivity is low (55-67%). It is important to use a non-cephalic reference to record the P14 wave in these suspected cases, as this will act as a caudal landmark for sub-cortical conduction. An increase in central conduction time (defined, in this instance, as the P14-N20 interpeak latency), without distortion of the N20 potential, usually indicates a reversible dysfunction, and a mildly abnormal SEP does not allow a prognostic conclusion to be drawn.

In the case of traumatic or vascular brain injury, the presence of the cortical N20 (even if it is mildly altered in latency), but with evidence of intact subcortical function, is a favourable pattern for good recovery and awakening in 80-90% of patients. Even if the cortical potentials are absent, it has been reported that 15% of these patients may recover, probably due to focal midbrain dysfunction caused by oedema.

Therefore, the SEPs are a powerful tool to give a bad (but not a good) prognosis in coma following anoxic brain damage, and are excellent in providing a good (but not a bad) prognosis in coma following head trauma.

Multiple sclerosisThe main effect of central demyelination is to increase the time dispersion of impulses in the dorsal columns,

medial lemniscus, and thalamocortical fibres, and subsequently slow down the conduction time. SEPs were the first evoked responses to be tested in patients with MS (Namerow, 1968) and, although the role of SEPs has largely been supplanted by MRI, these evoked potentials can still play a role in the assessment of the sensory nervous system, as they are abnormal in approximately 50% of MS patients without current sensory signs or symptoms, and they can be used to quantify the clinical dysfunction caused by the demyelinating lesion (Leocani et al., 2000; Comi et al., 1999).

Lower limb SEPs are most likely to be abnormal, as these assess the conduction along the longest myelinated nerve of any of the evoked potentials. A prolonged central conduction time, or absence of the P40 component, are the most common findings in patients with MS, followed by delayed or absent P14 and N20 potentials to median nerve stimulation. A reduced or absent cervical response is a frequent finding in MS when using neck to Fz recording montage after median nerve stimulation. However, this would suggest that the demyelination is at the root entry zone, and causing dispersion of the post synaptic dorsal horn response. When recording with a cervical to non-cephalic montage, a reduced N13 spinal potential is an infrequent finding and, in most instances, it is the reduced P14, which has been injected as a negativity in the frontal montage, that is the cause of this reduced cervical response. In more than 90% of MS patients with abnormal SEPs the P9/P14 amplitude ratio was reduced (Garcia-Larrea et al., 1988; Yamada et al., 1986) and, in patients with an absent P14 and/or N20 response, there is a significant correlation with upper limb impairment (Viviana et al., 2008).

In a group of patients suffering various forms of MS, the lower SEPs (Table 1, overleaf) were found to be more frequently abnormal than upper limb SEPs (Leocani et al., 2006).

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Table 1

Primary Progressive MS

Secondary Progressive MS

Relapsing –Remitting MS

All MS

SEP UL 69.2 60.7 44.2 53.6

SEP LL 100 92.9 69.8 82.1

% abnormalities of the SEPs in different types of MS

As the patient’s symptoms may be unilateral or bilateral, and may only involve one limb, the detection of abnormal SEPs is maximal when all four limbs are tested, with the diagnostic yield increasing by nearly 10% when the upper limb is tested, even after the tibial SEPs are found to be normal.

Patients with suspected MS are 2.4 to 3.9 times as likely to develop clinically definite MS when SEPs are abnormal, in comparison to those patients in whom the SEPs are normal (Hume and Waxman, 1988; Matthews et al., 1982). Whilst it is possible to diagnose MS in its early stage, the individual patient’s disability progression is unpredictable, because of the different pathological mechanisms underlying MS, combining inflammation and neurodegeneration, demyelination, and axonal damage with the variable clinical course between different patients and within individuals at varying phases of the disease (Lublin and Reingold, 1996; Lucchinetti et al., 2000). As the disease progresses, it would be expected that pathological changes, such as conduction block, increased temporal dispersion and axonal degeneration, would significantly alter the latency, amplitude and morphology of the evoked response. Therefore, the parametric measures of these absolute values prevent the subsequent use of these evoked responses to document disease progression in longitudinal studies, due to their ceiling effect. However, converting the data to non-parametric measures can overcome this problem (Figure 13, on following page) and, by using an ordinal 4-point abnormality score (0=normal, 1= increased latency with normal amplitude, 2=decrease in amplitude, 3=absence of a major potential), evoked potentials may be used as an electronic surrogate to assess symptom severity (O’Connor et al., 1998). The left and right upper and lower SEP abnormality score is the sum of these scores (from 0 to 12), and also shows that lower limbs are more readily affected than upper limbs in the various MS types (Table 2).

Table 2

Primary Progressive MS

Secondary Progressive MS

Relapsing –Remitting MS

All MS

SEP UL 2.1 1.7 1.9 1.8SEP LL 5.2 2.5 4.1 3.4

Global scores of SEPs in different types of MS

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Figure 13

Global SEP scores: Top left. Normal SEPs (grade 0); Top right. Prolonged cortical latencies of normal amplitude (grade 1); Bottom left. Prolonged cortical latencies with a reduced amplitude (grade 2); Bottom right. Absent

cortical potential.

The Expanded Disability Status Score (EDSS) is a conventional protocol to assess the neurological condition of patients with MS (Kurtzke, 1983), but clinical assessment on its own is unable to predict the clinical course of the patient’s disease. It has been shown that there is a marked correlation between the severity of evoked potential abnormality at baseline with subsequent disease progression, in particular the correlation between SEP abnormalities and EDSS changes are high. In those patients who had SEPs performed within two years of disease onset (Kallmann et al., 2006), an abnormal SEP was able to predict an EDSS >3.5 at 5 years, with a significant odds ratio of 7.5 (p<0.001), probably because of the close relationship between spinal cord function and increasing disability scores (Leocani et al., 2006).

The early detection of patients at high risk of disease progression versus those at low risk is important (Schlaeger et al., 2012), particularly when the most cost effective treatments need to be administered appropriately and, in particular, now that disease modifying strategies are available (Rice et al., 2010).

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Myoclonus and epilepsyThe main physiological classification categories for myoclonus are cortical, cortical-subcortical, subcortical-

supraspinal, spinal and peripheral. It is important to determine the site of the generation of the myoclonus, to establish the appropriate diagnosis (Shibasaki and Hallett, 2005). Most patients with cortical myoclonus show extremely enhanced cortical SEPs, and the size of the SEP is generally correlated with the intensity of the myoclonic activity. Both the N1-P2 and P2-N2 components of the cortical responses may be of increased amplitude, whilst the N20 potential that corresponds to the N1 may be normal, suggesting sensory input into the cortex is normal (Kakigi and Shibasaki, 1987).

Although there is no definitive criterion, the N1-P1-N2 complex of the median nerve SEP is usually between 1-5uV, and it was never recorded larger than 7uV in normal volunteers or patients without myoclonus (Obesso et al., 1986). It can, therefore, be accepted that 10uV represents the threshold above which cortical responses may be considered enlarged, the so-called giant SEP (Cassim and Houdayer, 2006).

Cortical myoclonus can be further classified into spontaneous, cortical reflex myoclonus and epilepsia partialis continua. Myoclonic jerks that are of cortical origin are predominantly stimulus sensitive, and are seen in patients with progressive myoclonic epilepsy (PME) and other disorders, including Lance-Adam syndrome (post-anoxic myoclonus), juvenile myoclonic epilepsy (JME) and in the late stages of Creutzfeldt-Jacob disease (CJD). All are due to a hyperexcitable sensorimotor cortex, and it is also known that patients with dementia, and patients with cortical atrophy, may also show enhanced potentials (Shibasaki and Hallett, 2005).

In patients with focal cortical lesions with focal motor seizures, but who do not have somatosensory stimulated myoclonus, giant SEPs are often recorded and, in children who are neurologically normal, extreme SEPs, evoked after single tactile stimulation, may herald the possible occurrence of partial motor seizures (De Marco and Tassinari, 1981).

In a single case report (Schorl, 2007), a comatose patient, who had suffered a head injury, showed enlarged SEPs, along with repetitive pseudoperiodic complexes, which were interpreted as non-convulsive status epilepticus. Treatment with Clonazepam resolved the EEG pattern and the SEP amplitude returned to normal values. It was hypothesised that cortical disinhibition was the likely explanation for both the status epilepticus and the giant SEPs, as enlarged SEPs are an unexpected finding in traumatic brain injury, and there were no signs of metabolic encephalopathy to explain the EEG complexes. This raises the possibility that continuous SEP monitoring of the enlarged cortical waveform may be an adjunct for monitoring in patients on ITU who may be prone to bouts of status.

StrokeSEPs are not commonly used for evaluation of stroke but, if performed, will show a delayed, attenuated, or

even absent cortical potential following stimulation of the limbs of the affected side (La Joie, 1982). Occlusion of the middle cerebral artery, which produces a lesion of the motor-sensory cortical region, is more likely to produce abnormal SEPs than a lesion elsewhere in the brain. It was found that analysis of various posterior tibial SEP cortical potential parameters, such as P40 latency, amplitude, and amplitude ratio between the affected and healthy side, was able to significantly increase prognostic capability when incorporated with motor scores (Tzventanov et al., 2003).

The N20 potential had a lower amplitude ratio in patients who had recently suffered a stroke, in comparison to normal controls, and the latency was significantly prolonged, and the latency increase was able to differentiate lacunar from large-vessel stroke (Al-Rawi et al., 2009).

Spinal Cord InjurySpinal cord transection will abolish the potentials generated above the lesion. However, most lesions are

incomplete, and the resultant SEP finding may be variable, and could be normal, delayed, reduced in amplitude or lost, depending on the severity of the lesion. Some patients may have undetectable scalp potentials, despite preservation of some cord function, and in the early stages an absent SEP does not reliably distinguish between a complete from an incomplete lesion (Sedgwick, 1980). When the lesion affects the pathways serving position sense, then the SEPs are more likely to be altered; a preserved response, or its early return after injury, indicates a better prognosis (Rowed, 1978). The timing of the examination after the injury will obviously determine the findings, but SEPs may have a prognostic role following acute spinal cord injury (Li et al., 1990).

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Tethered Cord SyndromePosterior tibial SEPs have been shown to be a sensitive indicator of neurological impairment in children

and young adults with tethered cord syndrome (Yamada, 1983). Abnormalities of the lumbar spine N22, delayed P40 or reduced cortical P40-N45 amplitudes, and/or delays in central conduction time have all been reported (Roy, 1986). There is a correlation between the severity of the SEP responses and the severity of both the clinical and the intraoperative findings. A change between the preoperative-SEPs versus the postoperative-SEPs correlates with the functional outcome after de-tethering.

Peripheral NeuropathySince the early history of SEPs, it has been demonstrated that, in those patients in whom a peripheral SNAP

could not be recorded directly from the nerve, stimulation of the afferent nerve at a proximal and distal site would enable the time difference between the latencies of the resultant N20 potentials to be used to calculate the conduction velocity in severe neuropathies (Desmedt et al., 1966). SEPs have been used to evaluate a range of peripheral nerves disorders, including diabetic and hereditary neuropathies, infectious and toxic neuropathies and inflammatory polyradiculopathies. (Olney et al., 1990 ; Moglia et al., 1991 ; Aramideh et al., 1992; Bartholomietal.,1991;Ziegleretal.,1993).Typically, theperipheralpotentials showprolongedabsolutelatencies, with subsequently prolonged spinal and cortical potential latencies, but with preserved inter peak latencies. In Guillain-Barré syndrome, the plexus conduction may be affected preferentially, and SEPs can be used to support the diagnosis in the acute stage, when the results of more conventional neurophysiological tests are still inconclusive (Vajsar et al., 1992).

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Al-Rawi, M.A., Hamdan, F.B., Abdul-Muttalib, A.K. (2009) Somatosensory Evoked Potentials as a Predictor for Functional Recovery of the Upper Limb in Patients with Stroke. Journal of Stroke and Cerebrovascular Diseases. 18:262–268

Amantini, A., Amadori, A., Fossi, A. (2008) Evoked potentials in the ICU Eur J Anaesthisiol. 25:196-202

American Clinical Neurophysiology Society. (2006) Guideline 9D: Guidelines on Short-Latency Somatosensory Evoked Potentials. J Clin Neurophysiol. 23:168-179

Aramideh, M., Hoogendijk, J.E., Aalfs, C.M., Posthumus Meyjes, F.E., De Visser, M., Ongerboer de Visser, B.W. (1992) Somatosensory evoked potentials, sensory nerve potentials and sensory nerve conduction in hereditary motor and sensory neuropathy type I. J Neurol. 239:277-283

Bartholomi, L., Leili, S., Negrin, P.(1991) Somatosensory evoked potentials in diabetes type I. Electromyogr Clin Neurophysiol. 31:43-46

Cassim, G., Houdayer, E. (2006) Neurophysiology of myoclonus. Neurophysiologie Clin. 36:281-291.

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POSTGRADUATE DISSERTATION MSc CLINICAL PHYSIOLOGY FINAL YEAR PROJECT

CAN THE THETA/ALPHA QEEG INDEX BE USED TO IDENTIFY NORMAL/ABNORMAL EEGS IN PATIENTS SCREENED WITH 6CIT FOR

COGNITIVE IMPAIRMENT?M. Pridgeon, Advanced Clinical PhysiologistDr P. Cresswell, Lead Clinical Physiologist

Dept. Neurophysiology, Walton Centre NHS Foundation Trust LiverpoolAddress for contact: [email protected]

AbstractThe aim of the study was to determine if quantitative EEG using the theta/alpha index could be used to

identify abnormal slow wave changes on the EEG associated with cognitive impairment, when compared to visual analysis. Non-specific slow wave changes on the EEG (electroencephalograph) have been associated with cognitive impairment and dementia. The diagnostic utility of the EEG in dementia and cognitive impairment remains unclear, and still not considered a routine test in the diagnosis of dementia.

Key Words: Quantitative EEG, electroencephalography, theta / alpha index, power spectra, 6-CIT, dementia, cognitive impairment

IntroductionCognitive impairment:

There appears to be a lack of consensus in the literature on classification of cognitive impairment. Numerous classification systems have been developed that are biased towards identifying individuals at high risk of progressing to dementia. Matthews et al. (2007) summarised this by stating that cognitive impairment represents an intermediate phase between normal cognitive function and pathological brain aging.

Dementia:Dementia is defined in the literature as a global cognitive impairment, a decline from previous level of

functioning, associated with behavioural and psychiatric symptoms, and is characterised by a progressive decline in memory, reasoning and communication skills. The World Health Organisation (WHO) (1993) consider memory decline, particularly memory involved in learning and recall, to be the most important symptom in diagnosing dementia. They classify dementia in terms of mild, moderate, and severe memory and cognitive function impairment. According to the WHO (ibid) dementia is specified as having a minimum duration of six months, to prevent misdiagnosis with behavioural syndromes or trauma.

Individuals who are not severe enough to meet the criteria set for dementia are considered to have mild cognitive impairment (Matthews et al., 2007; Blossom et al., 2008). There is currently no agreed standardised or uniform classification system for mild cognitive impairment, which results in inconsistency and variability of diagnosis. Patients with mild cognitive impairment may progress to dementia, may continue to have mild cognitive impairment without further decline or improve (Figure 1).

Figure 1

Normal Non pathological MCI Pathological MCI Dementia

Classification of mild Cognitive impairment (MCI), Blossom et al. (2008). Death can occur at any stage, left arrow head indicates improvement or recovery; establishing where each stage ends and begins is problematic

and subjective.

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Conversion rates per year, from mild cognitive impairment to dementia, vary in the literature. Blossom et al. (2008) quote 7.3% in the community and 15% of clinical based samples; Visser (2006) quotes 10%; Jelic & Kowalski (2009) quote 12-15%; Rossini et al. (2006) quote 6-40%; Peterson et al. (1999) quote 10-12%, and Jiang (2005a) quotes 1-25%.

Due to recent investigations into conversion rates of mild cognitive impairment this group of patients is becoming of interest for treatment trials, prediction studies and intervention trials for Alzheimer’s disease and dementia.

Quantitative EEG (QEEG):Quantitative EEG (QEEG) is an objective mathematical transformation of EEG activity using discrete Fast

Fourier Transformation (FFT). The EEG is transformed into spectral power frequency components and organised into specific frequency bands (Shenal et al., 2001). Spectral power combines frequency and amplitude together,toproducetheoverallenergyofawaveformwithinaparticularfrequencyband(µV2/Hz).Zietschetal. (2007) state that spectral power reflects the direct function of underlying pyramidal cells. Klimesch (1999) adds that spectral power is directly related to the number of neurons that discharge synchronously.

Klimesch(1999)andZietschetal.(2007)arguethatalphaspectralpowerhasbeenshowntobepositivelycorrelated to cognitive performance and brain maturity. However there is a lack of evidence as to the relationship with other frequency spectral power and cognitive function. Spectral power indices compare the percentage of absolute power values of two specific frequency bands. A range of different indices have been proposed within the literature with varying success. Forstl et al. (1996) concluded that the theta/alpha index was the most useful when investigating cognitive impairment, and represents a possible early indicator for dementia.

The 6-CIT Kingshill version 2000 is a short questionnaire, consisting of 6 questions, that take 3-4 minutes to perform, and aims to identify individuals with cognitive impairment associated with dementia. Brooke & Bullock (1999) validated this questionnaire against the MMSE and concluded that the 6-item test, in comparison to MMSE, was a faster, simpler test for the assessment of cognitive impairment associated with dementia, with higher sensitivity and specificity than the MMSE, most marked in the mild dementia group.

Aims The main aim of this study was to determine if the theta/alpha index QEEG parameter could be used to

identify abnormal slow wave activity associated with cognitive impairment in patients assessed with 6-CIT, when compared to traditional visual interpretation.

1. To explore inter-rater variability of qualitative visual interpretation of the EEG2. To compare the theta/alpha index to visually analysed EEG findings and 6-CIT score.

Primary research question: How does the theta/alpha index compare to visual interpretation for the identification of abnormal slow wave activity in patients assessed with 6-CIT?

Subsidiary questions: • Can the theta/alpha index be compared to 6-CIT?• Do the theta/alpha index scores depend on the 6-CIT score?• Can the theta/alpha index be used to predict cognitive impairment?

MethodRetrospective patients were selected from the adult EEG service at the Walton Centre Foundation Trust,

from January 2008 to January 2010. Prior to selection patients were sorted into two groups, based on 6-CIT score and screened using an inclusion/exclusion criteria - see Table 1. A 6-CIT cut-off value of 8 was used to sort patients into the two groups; patients who had not had a 6CIT assessment were excluded from the study.

• Normal 6CIT score 0-7 – No significant cognitive impairment• Abnormal 6CIT score 8-28 – Significant cognitive impairment

Fifty patients were randomly selected from the two groups and combined and randomised.




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Table 1

Inclusion ExclusionAdult patients aged between 20-90 years Patients with sleep disordersEEG undertaken between 2008-2010 at the Walton Centre NHS Foundation Trust

Patients with brain tumour

Patients referred into the service with cognitive decline, confusion or memory problems

Patients with a history of stroke or TIA

Patients received standard clinical EEG protocol with 6CIT assessment

Patients with traumatic brain injury

Male and female patients included Patients with learning difficultiesPatients with known dementiaChildren/NeonatesPatients with a history of illicit drug or alcohol abusePatients with known depression, affective or psychiatric disordersPatients on medication known to elicit slow wave changes on the EEG

Inclusion/exclusion criteria used to screen patients prior to sampling

All patients included in the study received the standard clinical EEG recording protocol used at the Walton Centre Foundation Trust. A 3-minute epoch of EEG was selected from the beginning of each patient’s EEG recording (baseline) and contained a period of eye closure. The samples were free from eye movement artefact, blink artefact and muscle artefact. Samples were not taken from periods of hyperventilation, intermittent photic stimulation or sleep. Samples contaminated by drowsiness were excluded; drowsiness was indentified using lateral eye movements. Each sample was converted to a European data format (EDF), a universal format used for the exchange and storage of multi-channel digital physiological data.

Each 3-minute EEG sample, in turn, was scored by two individuals, who were blinded to the project. The first rater was a Consultant Clinical Neurophysiologist, and the second rater was a senior Clinical Scientist with a PhD in sleep Neurophysiology who has over ten years experience reporting EEG recordings. All 100 patient samples were reviewed, and were classified as either “normal” or “abnormal” with respect to the amount of slow wave activity in each sample, in relation to age, using their own clinical judgement and reporting experience - modelling our current practice for clinical EEG interpretation.

Each 3-minute EDF EEG sample was exported to the Neuroguide deluxe quantitative EEG analysis software, installed on a regular computer. Each sample was transformed into spectral EEG data, using a dynamic Fast Fourier Transformation (FFT), and displayed as absolute power plotted against spectral frequency. The theta/alpha index was then calculated for each patient using the Neuroguide program. This index shows the difference between the percentage of theta and alpha absolute power in each patient’s QEEG spectrum.

Results:Visual EEG analysis and theta/alpha index

• Number of observed agreements: 91 (91% of the observations)• Number of agreements expected by chance: 49.8 ( 49.76% of the observations) • Kappa statistic = 0.821 • Standard error of kappa statistic = 0.056

According to Levin, Paik & Fleiss (2003), inter-rater agreement with a kappa statistic of 0.821 is considered to be ‘very good’ with 91% of observations in agreement.




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The EEG samples were sorted into two groups based on agreement:• Normal: 46 patient EEG samples• Abnormal: 45 patient EEG samples• Borderline (poor agreement): 9 patient EEG samples

Samples from the borderline group were excluded from statistical analysis of theta/alpha index scores sorted with visual analysis. Theta/alpha index scores were checked for normality prior to statistical analysis using a Kolmogorov-Smirnov test. Data sets that were found not to be normally distributed were transformed using log10 and then retested.

The mean theta/alpha index scores for the normal and abnormal groups were compared using transformed data sets with a two sample t-test.

• Hypothesis: The mean theta/alpha index in the normal group is different from the mean theta/alpha index in the abnormal group

• Null hypothesis: The mean theta/alpha index in the normal group is the same as the mean theta/alpha index in the abnormal group

Null hypothesis rejected when P value <0.05 with a 95% confidence interval for difference• T-value = -11.03• P-value = 0.000

The calculated P-value (0.000) was less than 0.05, rejecting the Null hypothesis, indicating that there was a significant difference between the mean theta/alpha index scores in the two groups. In the normal group the mean and median theta/alpha index scores were <1.0 compared to the abnormal group where the scores were >1.0.

Sex differences:• Hypothesis: Mean male theta/alpha index is different from mean female theta/alpha index• Null hypothesis: Mean male theta/alpha index is the same as mean female theta/alpha index

Null hypothesis rejected when P value <0.05 with a 95% confidence interval for difference.

1. Normal groupThe male to female sex ratio in the normal group was equal; the calculated P-value (0.894) for the normal

group was greater than 0.05. Therefore the null hypothesis was accepted, suggesting that there were no significant differences between male and female theta/alpha index scores.

2. Abnormal groupThe male to female sex ratio in the abnormal group was equal; the calculated P-value (0.258) for the

abnormal group was greater than 0.05. Therefore the null hypothesis was accepted, indicating that there were no significant differences between male and female theta/alpha index scores.

Age trends:1. Normal group

• Correlation coefficient (r) = 0.066 • P-value = 0.663

Correlation coefficient values that lie between -0.3 and +0.3 show little or no correlation. Therefore a value of 0.066 indicated that there was no correlation between the theta/alpha index. A P-value of 0.663 was calculated, and was greater than 0.05, accepting the null hypothesis that no significant differences existed between the theta/alpha index scores and age.

2. Abnormal group• Correlation coefficient (r) = 0.311• P-value = 0.038

Correlation coefficient values that lie between +0.3 and +0.7 show weak positive correlation; the abnormal group calculated a correlation coefficient of +0.311, indicating borderline weak positive correlation between




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theta/alpha index and age. A P-value of 0.038 was calculated, and was less than 0.05, rejecting the null hypothesis, and indicating that the weak positive correlation observed was significant with age.

Graph 1

Do theta / alpha index scores depend on 6-CIT scores in predicting cognitive function?A scatter plot for 6-CIT score plotted against theta/alpha index score in 100 patients suspected of cognitive

impairment

Linear regression: Regression equation:• Theta/alpha index = 0.669 + 0.0933 6-CIT• Intercept = 0.669• R2 = 20.6%• Confidence intervals of 95%• Analysis of variance; F= 25.39, P-value = 0.000

Linear regression results for the intercept and slope, when 6-CIT was plotted against theta/alpha index in 100 patients suspected of cognitive impairment. A weak positive association was seen between 6-CIT and theta/alpha index. Both the intercept and slope of the graph had P-values less than 0.05, indicating that the slope and intercept were significantly different from zero, and that the weak positive relationship observed was significant. Using the regression calculation a theta/alpha index cut-off score was calculated when a 6-CIT cut off value of 8 was used.

• Theta/alpha index = 0.669 + 0.0933 6-CIT score of 8• Theta/alpha index cut off value = 1.44

The R2 value for the graph was 20.6%, and related to the amount of variation explained by regression. This result suggests that approximately 20.6% of the variation seen in the theta/alpha index score could be explained by the 6-CIT score, resulting in a weak relationship between the two variables. The remaining 79.4% of variation was attributed to other confounding factors or inherent variability. An analysis of variance was




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undertaken to compare the variation explained by the line of best fit to the theta/alpha index predicted values and assumed a normal distribution. A P-value of <0.05 was calculated, indicating that the variation from the line of best fit was significantly different from zero, as indicated by the R2 value.

Inter-rater agreement between visual analysis and QEEG analysis using theta/alpha index cut off value:Using the calculated theta/alpha index cut-off value, patient samples were reclassified and the inter-rater

agreement between visual analysis and QEEG analysis were compared, using a Cohen’s Kappa statistical analysis of the two methods.

• Number of observed agreements: 83 (91.21% of the observations)• Number of agreements expected by chance: 45.5 (50.05 % of the observations) • Kappa statistic = 0.824• Standard error of kappa statistic = 0.059

Very good inter-rater agreement was found between visual and QEEG methods, with 91.2% of observations in agreement. In addition, 5 patients, excluded as borderline candidates from the visual analysis method, were reclassified as normal and 4 patients as abnormal.

A two-sample t-test was used to compare the transformed mean theta/alpha index values in the two normal groups (visual analysis versus QEEG analysis):

• T-value = -0.28• P-value = 0.783

The calculated P-value (0.783) was greater than 0.05; suggesting that no significant differences existed between the visual and QEEG methods for classifying patients as normal with regards to the amount of slow wave activity.

A Mann-Whitney U-test was used to compare the median theta/alpha index values for the two abnormal groups (visual analysis versus QEEG analysis). A P-value of 0.495 greater than 0.05 was calculated, suggesting that no significant differences existed between the visual and QEEG methods for classifying patients as abnormal with regards to the amount of slow wave activity.

DiscussionThe results from this study were similar to Gawel et al. (2007), who sorted patients suspected of subcortical

dementia into two groups, normal and abnormal, with respect to the amount of slow wave activity in relation to age, using two individuals’ own clinical judgement and reporting experience. The mean theta/alpha index scores (transformed log10) for the two groups were significantly different. This comparison indicates that, in my study, the normal group was dominated by a greater percentage of alpha absolute power in the frequency spectrum and the abnormal group had a greater percentage of theta absolute power in the frequency spectrum, agreeing with Gawel et al. (ibid.). The mean frequency for absolute power observed in the normal group was 9.0 Hz, and was distributed in two distinct alpha spectral patterns: a single alpha peak and a double alpha peak. In contrast, the mean frequency for absolute power observed in the abnormal group was 5.8 Hz, indicating theta dominant absolute power spectra.

Sex differences:Both normal and abnormal groups showed no significant difference between male and female theta/alpha

index scores. There is a large body of evidence in the literature that supports the hypothesis that there are no significant differences between QEEG measures in male and female subjects. The majority of these studies examine patients with dementia (Coben et al., 1985; Claus et al., 1998; Jeong, 2004; Jiang, 2005b; Babiloni et al., 2006; Gawel et al., 2007; Van-der-Hiele et al., 2007, and Babiloni et al., 2010).

Age trends:Theta/alpha index scores for the normal group were correlated to age; no correlation was found. Using the

model proposed by Wu & Liu (1995), the effects of age in the normal group can be explained. Wu & Liu (ibid.) discussed the idea that, in normal healthy adult subjects, aging affects the alpha absolute frequency band by causing a decrease in alpha absolute power. They also report increases in theta absolute power. Giaquinto & Nolfe (1986) add that slowing of the alpha frequency band in the elderly is minimal. They concluded that the




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alpha rhythm under goes a deceleration of 0.5 Hz in the human lifespan, and that only 10% of elderly normal age-matched subjects show increased theta activity. Therefore changes due to age in the normal group are expected to be minimal. In the normal group 72% of patients had alpha frequency dominant absolute power spectra.

In the abnormal group, only 9% of patients had alpha absolute power dominant spectra, and 27% of patients had a single theta peak, with a smaller alpha peak spectral pattern. Wu & Liu (1995) consider this pattern to be associated with age in normal subjects. This would suggest that a proportion of patients with slow wave changes on the EEG due to aging were wrongly classified as abnormal in this study, due to interpreter bias.

The P-value for the correlation between theta/alpha index and aging was less than 0.05, indicating that the weak positive association observed for age was significant. Klimesch (1999) reviewed the literature and found thatavarietyofstudiesreportedthatsubject’s≥50yearsshowedgeneralslowingoftheEEGto≤7Hz.Hestates that an age-related decrease in alpha activity is often masked by an age-related increase in theta activity, and may explain the weak positive association seen in my abnormal group. The theta/alpha index would also be sensitive to this change.

Age was found to be a factor contributing to the variability seen in abnormal theta/alpha index scores, showing a significant weak positive correlation. Thatcher et al. (2003) state that age is a common factor contributing to variability in QEEG studies, and recommend comparing raw QEEG values to a normative database using z-scores. They argue that this technique improves interpretability of QEEG parameters, by comparing raw QEEG values against a normal age-matched reference curve, removing age-related bias. They explain that the calculated z-score allows raw scores to be compared to normal controls. A mean z-score of zero would indicate that the mean QEEG values were comparable to age-matched normal individuals; mean z-scores greater than zero would indicate that mean QEEG values were greater than age-matched normal individuals, and mean z-scores less than zero would indicate that the mean QEEG values were less than age-matched normal individuals. Thatcher et al. (ibid.) recommend using the dynamic lifespan eyes open and eyes closed reference normative database in all QEEG studies. This database is included on the neuroguide software package. Due to the large amount of variability seen in this study, I intend to incorporate z-score analysis into any future QEEG investigation.

Do theta/alpha index scores depend on 6-CIT scores in predicting cognitive function?Linear regression found a weak positive association between 6-CIT and theta/alpha index, with a R2 value

for the graph of 20.6%. This weak relationship supports earlier reports of increased theta absolute power and decreased alpha absolute power with worsening neuropsychological test performance in patients with dementia (Bennys et al., 2001; Gawel et al., 2007; Van-der-Hiele et al., 2007), and support the hypothesis that a shift to a dominant theta absolute power can be considered as an indirect measure of increased cognitive impairment. Gawel et al. (2007) reported a much higher R2 value of 60% in subcortical dementia patients. The results from my study showed greater variability between predicted values and the line of best fit than Gawel et al. (ibid.). The reason for this is that they used patients known to have dementia. My patient group were suspected to have cognitive impairment, and were biased by possible mild forms of depression and daytime sleepiness that were hard to control for when using retrospective data, and were not excluded from the study; this weakened the relationship seen. Age was also seen to be a contributing factor that weakened the relationship further.

Visual analysis of EEG versus QEEG analysis using the theta/alpha index:I used the calculated theta/alpha index cut-off value (1.44) to sort all 100 patients theta/alpha index scores

into either normal (<1.44) or abnormal (>1.44). An inter-rater agreement of 91.21% was found between the two methods, indicating a very good strength of agreement. I was also able to classify the borderline patients that visual analysis failed to classify, removing subjective bias from clinical interpretation. I compared the two “normal” groups and the two “abnormal groups” (visual analysis and QEEG analysis) together, and found no significant differences. The results suggest that the theta/alpha index can be used to identify abnormal slow wave activity on an EEG, when compared to traditional visual methods. No authors in the literature have compared visual EEG analysis to QEEG analysis using theta/alpha index in this way.




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Future workTo validate my findings, a prospective study is required, with patients sorted into distinct defined groups:

patients with suspected mild cognitive impairment, patients with dementia, and patients suspected not to have mild cognitive impairment or depression but presenting with memory problems (neurological controls). Furthermore, a prospective study would allow the screening of depression and sleepiness in each patient prior to their EEG, reducing bias and variability.

Van-der-Hiele et al. (2007) concluded that longitudinal prospective studies, aimed at predicting longitudinal cognitive decline in dementia, are required, due to insufficient evidence in the literature; the theta/alpha index was included in their suggested battery of QEEG parameters. Despite this, to date, there are still few longitudinal studies available. In addition, the sensitivity and specificity of the theta/alpha index as a diagnostic test for dementia or cognitive impairment is poorly understood. Bennys et al. (2001) are the only authors who have, so far, investigated the diagnostic value, sensitivity and specificity of the theta/alpha index in Alzheimer’s disease. Therefore, future work should include a longitudinal component, following patients in each group over a standardised period of time, to gain an understanding of longitudinal cognitive decline in dementia and mild cognitive impairment, and the effect this has on the theta/alpha index. The 6-CIT is a validated method of predicting cognitive function. Future work should include sensitivity and specificity of the theta/alpha index in the three patient groups, analysed using a Receiver Operator Characteristic Curve (ROC analysis).

ConclusionThe results from the study suggest that the theta/alpha index a QEEG parameter can be used to identify

abnormal slow wave activity on the EEG when compared to traditional visual analysis. Good inter-rater agreement was found between traditional visual EEG analysis and QEEG analysis using the theta/alpha index. Theta/alpha index scores were used to assess EEG samples that were discordant between interpreters, removing interpreter subjective bias on whether slow wave activity on the EEG was normal or abnormal. Due to interpreter subjective bias, visual EEG analysis appears to be less precise than the theta/alpha index at identifying abnormal slow wave activity on the EEG.

Theta/alpha index scores were correlated with mental impairment and abnormal 6-CIT results, consistent with findings reported in the literature. The significant weak positive relationship is not as strong as reported in the literature for patients with dementia and, therefore, should not replace 6-CIT as a measure of cognitive impairment.

The early detection of subjects with mild cognitive impairment who are at high risk of progressing to Alzheimer’sdiseaseiscrucialforcurrentavailabletreatmentstrategies(Zhengetal.,2007).Theresultsfromthis current study suggest that the theta alpha index might prove useful in the early detection of mild cognitive impairment when used in conjunction with 6-CIT.

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UNDERGRADUATE DISSERTATION

Awarded UniMed prize 2013

A COMPARISON OF THE PATTERN REVERSAL VISUAL EVOKED RESPONSE OBTAINED WITH CATHODE RAY TUBE (CRT) TECHNOLOGY TO THAT OBTAINED

WITH A LIQUID CRYSTAL DISPLAY (LCD)

Donna Formby, York Hospitale-mail: [email protected]

AbstractThe Pattern Reversal Visual Evoked Potential (PRVEP) P100 can vary in both latency and amplitude with

alteration of visual stimulus parameters. Liquid Crystal Display (LCD) technology is currently replacing traditional Cathode Ray Tube (CRT) monitors used to present the pattern stimulus in Neurophysiological testing. A study was performed to compare the PRVEP P100 components obtained with an LCD monitor to those obtained with more traditional CRT monitors, in order to assess whether the newer LCDs provide a comparable response. Two groups were tested in a cross over study, and included 50 non symptomatic eyes and 9 eyes with demyelinating visual pathology. Monocular full field PRVEPs were obtained, using a 16x12 black and white checkerboard reversing at 2Hz. The luminance and contrast of the monitors were closely matched. Both the P100 latency and amplitude were recorded. The results showed that the LCD produced P100 components of significantly longer latencies (at 95% confidence interval; Wilcoxen p<0.001) and higher amplitudes than the CRT (at 95% confidence interval; Wilcoxen p<0.001) in non symptomatic participants. In those with anterior pathway demyelinating pathology there was no significant difference in the P100 latencies obtained with both monitors (at 95% confidence interval; t-test p-0.057). The results could reflect the differences in magnocellular visual pathway activation by LCDs, as a result of motion blur. Demyelinating pathology may preferentially affect the magnocellular mechanisms, eliminating this variable between the monitors.

Key Words: PRVEP, LCD, CRT, P100.

Introduction

Visual Evoked PotentialsVisual evoked potentials (VEPs) are the cortical responses to foveal stimulation of the visual pathway. In a

clinical setting, visual stimuli can include near white light flash, which produces a cortical response to a change in luminance. The preferred method of visual stimulation, however, is to use a checkerboard pattern, first used to describe human VEPs in 1965 by Spehlmann (Halliday, 1982). Pattern stimuli can be presented as ‘onset’, ‘offset’ or reversal. With pattern reversal, the black and white checkerboard stimulates the visual pathway, using change in direction of contrast and with sharp contours. This gives rise to a positive cortical potential, recordable with scalp electrodes over the occipital lobe, having a latency of around 100m/s (P100).

Visual ProcessingProcessing of the pattern stimuli begins in the retina, with ganglion cells that extend to the lateral geniculate

nucleus (LGN) of the thalamus. It has been suggested by Kaplan et al. (1987) that the LGN modifies the information received from the retina before relaying it to the primary visual cortex, which is interested in large changes in visual stimulus, and its structure is adapted to function. Ocular dominance columns of the visual cortex deal with binocular vision and depth perception (Sherwood, 2012), whereas orientation columns deal with perception of form and movement. Differentiation of edges, borders, orientation and motion is further achieved with two parallel pathways, described by Mishkin et al. (1983), - the magnocellular pathway (M pathway) and the parvocellular pathway (P pathway) - each of which deliver information to the primary visual cortex (Figure 1, overleaf).

Undergraduate Dissertation



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Figure 1

The M pathway extends through the V1 and V2 levels of the striate, through to the middle temporal area (MT/V5), ending in the posterior parietal cortex, and is termed the dorsal pathway. The P pathway also extends throught the V1 and V2 layers, projecting to V4, reaching the inferior temporal cortex. This is termed the Ventral pathway.

Sourced from: http://camelot.mssm.edu/~ygyu/constructingvisualimage.html

According to Kaplan and Shapley (1986), the magnocellular (dorsal) pathway is more sensitive to low luminance contrast (as little as 2%), but also has high sensitivity to temporal frequency and can convey motion and depth. The parvocellular (ventral) pathway does not respond to contrasts lower than 10% and has a high sensitivity to spatial frequency, and is concerned with interpreting edges and borders to produce image form and contours. This pathway is also associated with colour vision, as Tobimatsu et al. (2006) observed, the p cells in the LGN are responsive to changes in wavelength.

There is believed to be a difference in pathway stimulation between pattern onset and offset presentation and pattern reversal. Di Russo (2005) argues that the motion-sensitive area of the visual cortex (V5) is activated by pattern-reversal stimuli because the reversal of the light and dark checks produces a perception of movement of the checks ‘streaming’ across the screen. In a previous study (Di Russo et al., 2001), activation of V5 was not found for pattern-onset stimuli that were not associated with a perception of motion.

Factors affecting the PRVEPPattern check size:

One study, by Nakamura et al. (2000), showed that latencies of the P100 increased with smaller check sizes. Results of a study, by Spekreijse et al. (1973), also supports this view and, additionally, has shown that very large checks also elicit longer P100 latencies.

Pattern Reversal Rate:Reversal rate of the pattern stimulus or transition time has been shown to affect the VEP response. Halliday

(1982) found the latency of the P100 was increased by 15ms using a longer transition time of 35ms, compared to a 10ms pattern reversal. Heckenlively et al. (2006), however, note that temporal frequency should not exceed 2 reversals per second, as the transient evoked potential is then lost and the steady state potential arises.

Pattern luminance:Mean luminance has an effect on pattern reversal VERs, with P100 latencies increasing with reduced

luminance. According to Burkard (2007), the latency of the P100 increases by 10-15 milliseconds per log unit of decreased retinal luminance.




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Pattern contrast:Halliday (1982) writes that changes in the VEP with contrast tend to saturate at levels of contrast over 40%.

Small changes in contrast above this threshold, therefore, have little impact on the VEP.

Gender:PRVEP latencies are generally shorter in females than males (Halliday 1982, Stockard et al. 1979). Stockard

et al. (1979) attribute differences in the P100 to higher deep body temperature in women.

Age:Halliday’s analysis of the literature (Halliday, 1982) showed that those under 15 years of age, and over 65,

showed significantly longer P100 latencies. This is postulated to be due to gradual maturation of the visual pathway throughout childhood, and the degeneration that occurs within the nervous system in older age.

Acuity:Poor visual acuity, as a result of accommodation or pathology, can affect the PRVEP. Misra et al. (2006)

state that a visual acuity of 6/36 or below does not produce a well formed PRVEP. Compliance may also affect the VEP, with near point focusing giving rise to pupil constriction, convergence and near accommodation. Tan et al. (1984) found that this was the most successful method of voluntarily altering the PRVEP waveform.

Technology and the PRVEPAs discussed previously, the PRVEP is hugely dependant on stimulus parameters. The image production

from the CRT and LCD differs greatly and, with current transitions being made in neurophysiology departments from CRT technology to LCD, it is important to see if the change in technology has an impact on the stimulus parameters and therefore the electrophysiological responses.

Only a few studies have compared VEP responses obtained with both LCD and CRT monitors. Husain et al. (2009) assessed the PRVEP using a CRT monitor and three LCD monitors of differing response times. The response time refers to the time it takes for a pixel to change from one value to another and back. They found that the P100 latency was shortest for the CRT monitor in all cases. However, the response time of the LCD was a significant factor, as longer response times produced longer P100 latencies. The shortest response time of 2ms produced a P100 latency 8 milliseconds longer than that of the CRT. This study, however, only included 6 subjects. A further study by Nagy et al. (2011) compared the PRVEP responses with CRT and LCD monitors at various contrast levels and spatial frequencies. They found a significant difference in the latency times between the monitors at all contrasts and spatial frequencies, although the contrast value in itself did not appear to have a significant effect. The LCD always produced the longest latency response, at an average of 9ms longer, which concurs with the previous study.

Figure 2

An electron beam is fired at a screen made up of blue, green and red phosphor dots. A magnetic deflection coil acts on it to produce a raster scanning motion across the CRT screen. The motion energy of the electron beam is converted to visible light when it hits this screen, producing a colour image. The deflection of the electron beam by the magnetic deflection coil determines the image output.

CRT image constructionSourced from : http://www.jegsworks.com/Lessons/lesson5/crt.gif



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Figure 3

A liquid crystal matrix lies between a horizontal and vertical polarizing filter. Light passes through the first filter producing vertically polarized light. The polarized light then passes through the liquid crystal cells. Depending on the electrical signal provided to the crystal, it will twist to a different alignment to rotate the polarized light to allow it to pass through the vertical polarizing filter.

LCD image constructionSourced from: http://es.wikipedia.org/wiki/Archivo:LCD_subpixel_(en).png

Aims and Objectives of this studyWith the purchase of new VEP equipment in the department, including a new LCD monitor for presentation

of the visual stimulus, the aim of the study was to find out if the P100 component of the PRVEP from the new LCD monitor significantly differed from that obtained with the old CRT monitor. Using the new normative data for the LCD monitor a new normal range could then be established. For additional information a symptomatic patient group was also included in the study, to assess whether visual pathology had an effect on any differences between the responses obtained with LCD and CRT.

Method Two departmental monitors were compared. The cathode ray tube monitor was a 17” ViewSonic GS773

model (VCDTS21583-2). The liquid crystal display was a 22” LG model (W2261VP) with a 2ms response time. The pattern stimuli for both monitors were calibrated using the methods and calculations in the ISCEV guidelines for calibration of stimulus and recording parameters (Brigell et al., 2003). A large check (3°) was used to take luminance measurements for the purpose of calculating central and peripheral mean luminance. Central mean luminance of the CRT was 64.1cd/m2. For the LCD monitor, central mean luminance was calculated to 63.6cd/m2. Contrast for the CRT was 97.8%, whereas the contrast of the LCD was 99%.

The stimulus used during data collection was a full field 16 x 12 black and white checkerboard pattern, with checks subtending to the eye at a visual angle of 1.2 degrees (+- 0.1 degree). A viewing aspect ratio of 4:3 was used and the reversal rate for stimulus presentation was set to 2Hz on both monitors.

12 Symptomatic participants were identified from incoming referrals for PRVEP. 25 non symptomatic participants were recruited from neighbouring departments in York hospital. Non symptomatic participants were required to answer a few general health questions to make sure they were suitable for this group. Table 1 (on following page) shows the inclusion and exclusion criteria for both the symptomatic and non symptomatic participants.



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Table 1

Inclusion Exclusion

Non

Sym

ptom

atic

Age 18-60 years Outside of 18-60 age bracket

Those with refractive errors whose vision is able to be corrected (i.e. by glasses, lenses).

History of or current visual pathology to include:

-Optic neuritis-Optic atrophy-Macular degeneration

Those that suffer with migraine not experiencing symptoms at the time of testing.

Other health problems to include:-MS-Polyneuropathy-Cancer

Male or Female

Age 18-60 years Outside of 18-60 age bracket

Sym

ptom

atic

Those with a relevant referral for Pattern VEP. Inadequate clinical history with no suggestion of central or peripheral nervous system dysfunction.

Those patients deemed able to comply and can give consent.

Those patients who are unable to comply and need flash VEP.

Those with refractive errors whose vision has been corrected (i.e. by glasses, lenses)

Those with Visual acuity of more than 6/36.

Male or Female

Inclusion & Exclusion criteria for study Participants

Those outside the 18-60 years age bracket were not asked to participate, as previous studies have concluded that the effect of luminance and contrast change of the pattern reversal stimulus varies with age. Limiting the inclusion age bracket also ensured that there were no maturational differences, and a normal range for an adult population could be established. Each subject had their visual acuity measured monocularly, at 6 metres, with corrective lenses, if worn. Each participant viewed both monitors. The order the monitors were viewed was randomly assigned. A monocular full field PRVEP were then obtained with128 sweeps averaged during a single run. Three runs were taken to ensure the acquired PRVEP was reproducible. The latency and amplitude of the P100 component were recorded for each run, and the process repeated with the other eye. The subject was given 10 minutes to relax between viewing each monitor so that fatigue did not affect results.

Results50 non symptomatic eyes were tested from 25 participants, with no exclusions. Only 9 eyes were included

of the 24 eyes tested in the symptomatic group, due to insufficient evidence of visual pathology in the excluded 15. All of the symptomatic eyes included had an abnormal PRVEP with conduction delay.




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Non-Symptomatic GroupResults for measurement of P100 latency

CRT LCD

Mean Latency (ms) 103 107

Min Latency (ms) 98 98

Max Latency (ms) 111 115

Standard deviation from the mean 3.518 3.995

Normal Range (ms) n/a 99-115

Using the Wilcoxen paired rank test, the data provided statistically significant evidence at 95% confidence interval, that the median P100 latency from the LCD significantly differs from the median P100 latency from theCRT(Z=-5.858,p<0.001)(Table2).ThemeanofthepositiverankswheretheLCDP100latenciesweregreater than the CRT was 26.30, while the mean of the negative ranks (CRT latencies being greater than the LCD) was 4.75. This suggests that LCD monitors significantly increase the latency of the P100 component in the non symptomatic population. The positive or negative differences between the two monitors can be seen in the graph below (fig. 4).

Figure 4

The blue bars represent positive differences or ranks (LCD>CRT), the white bars representing the negative ranks (CRT>LCD).

Results for measurement of P100 AmplitudesA Wilcoxen paired rank test was used, and the data provided statistically significant evidence at 95%

confidence interval, that the median P100 amplitude from the LCD significantly differs from the median P100 amplitudefromtheCRT(Z=-3.584,p<0.001),withtheLCDproducinggreateramplitudesthantheCRT.

Symptomatic GroupResults for measurement of P100 latency

As the latencies from both monitors were normally distributed, a paired samples T-test was used to analyse the data. The results indicated that with a 95% confidence interval there was not a significant difference between the P100 latencies obtained using the LCD compared to the CRT, giving t -2.224, p-0.057 (2-tailed).




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Results for measurement of P100 amplitudePaired t-test results indicated that with a 95% confidence interval there was a significant difference between

the P100 amplitudes obtained using the LCD compared to the CRT, giving t(8) = t -3.000, p 0.017 (2-tailed), with the LCD producing greater amplitudes.

Discussion and ConclusionsThe project has shown that, in a normal healthy population, presenting a reversing checkerboard stimulus

using an LCD monitor produces significant differences in PRVEP P100 components, compared to a CRT monitor. The LCD monitor increases the latency and amplitude of the P100, therefore a new normal range is required when updating or substituting CRT VEP systems.

Both monitors had comparable field and viewing angles, both stimulating within the central 1.5° of the

fovea. The luminance and contrast were measured from a still large check stimulus, both having near 100% contrast ratios; well above the 40% saturation levels discussed in the literature. Small changes in contrast should, therefore, not have impacted on results but, however, may explain why the LCD produced larger amplitude responses, as the contrast ratio was higher for this monitor.

The differences in the P100 components, therefore, may be better explained by the differences in image formation of the two monitors. Lee (2005) states that one of these differences is the length of time each pixel is illuminated in each refresh cycle. In an LCD each pixel is addressed once per frame and luminance of the pixel stays constant during that frame. The time the pixel is illuminated is, therefore, significantly longer than in the CRT.

Tourancheou et al. (2007) elaborate that with this ‘hold type’ display method, the light intensity is maintained on the screen for the duration of the frame, whereas, on a CRT display, the light intensity is a pulse, which fades over the frame duration. When tracking a moving object on LCD, for a given frame, the picture is sustained on the screen, while the eyes anticipate movement. The edges of the object are displaced on the retina, resulting in a motion blur. Increase in resolution of the screen results in augmentation of the defect.

Pan et al. (2005) state that this ‘hold type’ motion blur is a physiological phenomenon, and occurs in human eyes rather than on the screen of the LCD. However, in addition the LCD has a ‘slow response’ motion blur, which does physically occur on the LCD screen. The response or reaction time is the time required for a pixel to change state from light blocking to light transmitting or vice versa. In reality the transition of an LCD pixel from one display value to another is not instantaneous and, in some LCDs, can take longer than one frame (see Figure 5, overleaf). More recent technology has considerably lowered LCD response times, to around 2ms. However, the CRT still responds in less than 1ms.

The LCD, therefore, may affect V5 contribution to the pattern reversal VEP. As discussed, the perception of movement is thought to contribute the PRVEP response. Motion is also detected by the magnocellular pathway. If clear perception of movement is reduced due to ‘hold’ type motion blur of the LCD, then the faster conducting magnocellular pathway may not be invoked, which may then give rise to longer latencies.

If there is a reduction in magnocellular processing, due to reduced m-cell stimulation in the retina with LCDs, then it would be likely that a reduction in amplitude of the responses would also be seen. However, if total retinal illuminance is higher in LCDs - due to pixel ‘hold’ - then more photoreceptors may be stimulated in the fovea, in turn stimulating more p- cells, which are located more densely in the fovea than m-cells. This may at least compensate for the reduction in m-cell activation, or give rise to greater amplitude responses in some individuals.




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Figure 5

CRT and LCD luminance vs. time curvesSourced from: Kaltwasser et al. 2009.

Symptomatic group

The results for the symptomatic group differ from those of the non symptomatic group, as P100 latencies were not significantly different using LCD compared to CRT. This suggests that pathology may desensitise the visual pathway to any differences between the two monitors and the way they present the pattern stimulus. The symptomatic eyes used for analysis were all considered to have a demyelinating pathology of the anterior visual pathway due to optic neuritis or MS. One explanation for the disease process causing the observed results is that there may be selective dysfunction of the magnocellular system with anterior pathway demyelinating pathologies (Tassinari et al. 1999).

If the differences between the two monitors are attributed to the difference between their stimulation of the m-pathway, and if this pathway is affected due to pathology, then the differences of the two monitors should not be demonstrated. Pathology would be expected to affect the p-pathway to a certain extent and, overall, all responses would be delayed. The limitations of this theory are that there are contradictions in the literature, that state parvocellular mechanisms are the most affected by anterior pathway demyelination (Miller et al., 2005).

The m-pathway is more sensitive at high temporal frequencies, to which I have theoretically attributed the faster transition times of the CRT. The p-pathway is more sensitive at lower temporal frequencies, which, it is argued are evoked more by the LCD. A further theory to explain the symptomatic group results is found in a study by Caruana et al. (2000), who state that the difference in temporal response between the two pathways may be confounded by demyelination, as it acts as a low pass filter. All high-frequency responses would therefore be attenuated, independently of fibre type, producing similar responses between monitors.




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REFERENCES

Brigell, M., Bach, M., Barber, C., Moskowitz, A., Robson, J. (2003) Guidelines for calibration of stimulus and recording parameters used in clinical electrophysiology of vision’. Documenta Ophthalmologica 107:185-193.

Burkard R, F., Don, M., Eggermont, J.J. (2007) Auditory evoked potentials: basic principles and clinical application. Lippincott, Williams and Wilkins, USA.

Caruana, P. A., Davies, M. B., Weatherby, S. J. M., Williams, R., Haq, N., Foster, D. H., Hawkins, C. P., (2000) Correlation of MRI lesions with visual psychophysical deficit in secondary progressive multiple sclerosis. Brain, 123:1471-1480

Di Russo, F., Pitzalis, S., Spitoni, G., Aprile, T., Patria, F., Spinelli, D., Hillyard, S. A., (2005) Identification of the neural sources of the pattern-reversal VEP. NeuroImage, 24:874-886.

Di Russo, F., Martınez, A., Sereno, M. I., Pitzalis, S., Hillyard, S. A., (2001) The cortical sources of the early components of the visual evoked potential. Hum. Brain Mapp.15:95– 111. Halliday, A. M., (1982) Evoked Potentials in Clinical Testing, Churchill Livingstone. pp1-121.

Heckenlively, J. R., Arden, G. B., (2006) Principles and practice of clinical electrophysiology of vision, 2nd edition. Massachusetts Institute of Technology. pp220-221

Husain, A. M., Hayes, S., Young, M., Dharmen, S., (2009) Visual evoked potentials with CRT and LCD monitors: When newer is not better. Neurology, 72(2):162-164.

Kaplan, E., Purpura, K., Shapley, R. M., (1987) Contrast affects the transmission of visual information through the mammalian lateral geniculate nucleus. J. Physiol, 391:267-288.

Kaplan, E., Shapley, R. M., (1986) The primate retina contains two types of ganglion cells, with high and low contrast sensitivity. Proc. Nail. Acad. Sci. USA, 83:2755-2757.

Kaltwasser C, Horn F.K, Kremers J, Juenemann A, (2009) A comparison of the suitability of cathode ray tube (CRT) and Liquid crystal display (LCD) monitors as visual stimulators in mfERG diagnostics. Doc. Opthalmol. 118(3):179-189.

Lee, H. C., (2005) Introduction to Color Imaging Science. Cambridge University Press. p535.

Miller, N. R., Newman N. J., (2005) Walsh and Hoyt’s Clinical Neuro-Ophthalmology: Volume three, 6th edition. Lippincott, Williams & Wilkins. USA. p3430.

Mishkin, M., Ungerleider, L. G., Macko, K. A., (1983) Object vision and spatial vision: two cortical pathways. Trends in Neuroscience, 6:414-417.

Misra, U. K., Kalita, J., (2006) Clinical Neurophysiology, 2nd edition, Elsevier, India. p421

Nagy, B. V., Gemesi, S., Heller, D., Magyar, A., Farkas. A., Abraham, G., Varsanyi, B., (2011). Comparison of pattern VEP results acquired using CRT and TFT stimulators in the clinical practice. Doc Ophthalmol, 122:157-162.

Nakamura, M., Kakigi, R., Okusa, T., Hoshiyama, M., Watanabe, K., (2000) Effects of check size on pattern reversal visual evoked magnetic field and potential. Brain Research; 872(1-2):77-86.

Pan, H., Feng, X. F., Daly, S., (2005) LCD motion blur modelling and analysis. International Conference on Image Processing, 2005.




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Sherwood, L., (2012) Human Physiology: from cells to systems. 8th edition. Thomson Brooks/Cole. p209Spekreijse,H.,Van derTweel, L.H., Zuidema,T., (1973)Contrast evoked responses inman.Vision Res; 13:1577.

Spekreijse, H., Van der Tweel, L.H., Zuidema, T., (1973) Contrast evoked responses in man. Vision Res; 13:1577.

Stockard, J. J., Hughes, J. F., Sharbrough, F.W., (1979) Visually evoked potentials to electronic pattern reversal: latency variations with gender, age and technical factors. American Journal of EEG Technology, 19:171-204.

Tan, C.T., Murray, N. M. F., Sawyers, D., Leonard, T. J. K, (1984) Deliberate alteration of the visual evoked potential. Journal of Neurology, Neurosurgery, and Psychiatry, 47:518-523

Tassinari, G., Marzi, C. A., Lee, B. B., Di Lollo, V., Campara, D., (1999) A possible selective impairment of magnocellular function in compression of the anterior visual pathways. Experimental brain research, 127(4):391-401.

Tobimatsu, S., Celesia, G. G., (2006) Studies of human visual pathophysiology with evoked potentials. Clinical Neurophysiology; 117(7):1414-1433.

Tourancheau, S., Le Callet, P., Barba, D., (2007) Impact of the Resolution on the difference of perceptual video quality between CRT and LCD. International Conference on Image Processing. 3:441-444.




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REGIONAL REPORT

AN OVERVIEW OF NEUROPHYSIOLOGICAL SERVICES IN NORTHERN IRELAND

Lezlie Huntley, Craigavon Area Hospital;[email protected]

The island of Ireland is divided between the Republic of Ireland, which covers just under five-sixths of the island as a whole, and Northern Ireland, a part of the United Kingdom, which covers the remainder and is located in the north-east of the island. The total population of Ireland is approximately 6.4 million. There are 4.6 million inhabitants in the Republic and just over 1.82 million in Northern Ireland (NISRA, Northern Ireland Statistics & Research Agency, May 2013).

There are a total of 31 hospitals, governed by five Health and Social Care Trusts, IN Northern Ireland, each providing a variety of services across all of its six Counties; Antrim, Londonderry, Fermanagh, Tyrone, Armagh and Down. Of these 31 hospital sites, only 6 have specialist Clinical Neurophysiology Departments; four of which are located in the Belfast Trust, one in the Southern Trust and the other in the Western Trust (as of December 2012).

Regional Report



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Province-wide, we have a total of 21 Clinical Physiologists in Neurophysiology (around a third are part-time), six of whom have just taken up permanent posts within the Belfast Trust this month. The majority of staff (16) are employed throughout the Belfast Trust, 4 by the Southern Trust, and a single member of staff at present in the newly opened Department at Altnagelvin Area Hospital, situated in the Western Health and Social Care Trust. Our two Consultant Clinical Neurophysiologists, who are both based in the Royal Victoria Hospital, Belfast, also provide a satellite service to the rest of the region, reporting on all investigations carried out, with the exception of those performed at the Royal Belfast Hospital for Sick Children.

In N.I we hold one annual ANS meeting which usually takes place each year on a Saturday, traditionally in the autumn. A different department takes charge of the organisation and content of the meeting each successive year. Apart from general subjects of interest such as Training & Education, ANS news, Treasurers report etc. we always incorporate a scientific programme into the day.

Belfast Health & Social Care TrustThis is the largest of the five trusts, accepting referrals from 21 of the 31 hospitals around Northern Ireland.

• Royal Victoria Hospital (RVH) – treats over 80,000 people as inpatients and 350,000 people as outpatients every year, providing local services to the people of Belfast and a large number of regional specialist services to people from across Northern Ireland. These specialist services include Cardiac Surgery, Critical Care, and the Regional Trauma Centre.

The RVH delivers an extensive Neurophysiological service, exclusively to adult in-patients and out-patients. It provides a regional service for Intra-Operative Monitoring, Long Term Video-EEG monitoring, Magnetic Stimulation, Peripheral Neurophysiology (NCS & EMG) and Eye Movement recordings. In addition, the department offers routine, sleep deprived, provocative and portable EEGs, as well as all modalities of Evoked Potentials, on both upper and lower limbs.

• Mater Hospital – The Mater Infirmorum is an acute hospital providing services, including acute in-patient, A&E, Day procedures, Mental Illness and Maternity care to North Belfast and the surrounding areas.

This site offers routine and sleep deprived EEG investigations to both adult and paediatric patients. It is the regional Sleep Centre for Northern Ireland, and also receives the largest number of Psychiatric referrals. Furthermore, the department also carries out Multiple Sleep Latency Testing, Maintenance of Wakefulness, at-home ambulatory EEG and occasionally assist during ECT (Electro-Convulsive Therapy). The Mater hospital is responsible for providing a peripatetic service to the Northern Trust.

• Belfast City Hospital – is a 900-bed modern university teaching hospital, providing local acute services and key regional specialties, including renal medicine and transplantation, as well as a comprehensive range of cancer services. Similarly to the Mater hospital, the City’s Neurophysiology Department performs all modalities of EEG investigations on both adult and paediatric patients, including Multiple Sleep Latency testing. In addition, they also offer Evoked Potentials and Peripheral Neurophysiology.

• Royal Belfast Hospital for Sick Children – is the only hospital in Northern Ireland dedicated specifically to the care of children. It has 107 beds, and provides general hospital care for children living in Belfast, as well as providing most of the paediatric regional specialities for children throughout Northern Ireland. The specialist services provided in the Children’s hospital include: • Paediatric Intensive Care Unit • Neonatal Surgery • Children’s Haematology/ Oncology • Cardiology• Burns and Plastics • Trauma and Orthopaedics • Neurology/Neurosurgery • Nephrology

Regional Report



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• Respiratory Paediatrics • Cystic Fibrosis• Infectious diseases • Children’s Emergency department.

This two staffed Neurophysiology Department offers a regional Paediatric service, obtaining either sleep deprived or drug induced sleep recordings on all their in-patients and out-patients. Long term ambulatory monitoring & video telemetry are also available. These EEGs are routinely reported on by the resident Paediatric Neurology Consultants.

Southern Health & Social Care Trust• Craigavon Area Hospital – provides a wide range of acute inpatient and outpatient services.

Historically, CAH has been responsible for all Neurophysiology referrals received from the remaining hospitals throughout the Southern & Western Trusts, offering routine, provocative, portable, ambulatory, sleep deprived/drug induced sleep and prolonged video EEGs on a wide patient spectrum, with Psychiatric, Neurology and Paediatric patients making up the largest components of referrals to this centre. As well as EEG, this site also offers MSLTs, Pattern Reversal & Flash VEPs, upper & lower limb SSEPs and, on rare occasions, BAEPs.

Western Health & Social Care Trust• Altnagelvin Area Hospital – is an acute hospital, which offers a range of services, including a 24-hour

Accident and Emergency Department, and is one of Northern Ireland’s five designated cancer units. It has 481 inpatient beds and 48 day case beds.

Funding became available in December 2012 to open the first Neurophysiology Department in the Western Health & Social Care Trust. Although operating at present with a single member of staff, the department is already providing an EEG service for adult in-patients and out-patients, predominantly referred via the Consultant Neurologists. It is hopeful that this service will expand in the near future, in terms of both workforce and range of investigations available to patients in the Western Trust.

Training & EducationIn 1997 the University of Ulster’s Jordanstown campus launched a four-year, full-time BSc Hons. in Clinical

Physiology. The first semester of Year 1 gave the students a foundation in modules such as anatomy and physiology, skills for clinical physiology, and knowledge and skills for professional practice, before subsequently progressing along their chosen specialist pathway in Year 2 - e.g. Respiratory, Cardiology or Neurophysiology. Year 3 was comprised of a full year placement, although there were also brief periods of clinical placement during years 1, 2 and 4, some of which obviously involved placement during the summer months.

Clinical placement experience is an absolute requirement for Clinical Physiology, and for Registration with

the professional body, in this case ANS. The availability of clinical placements was dependant upon arrangements with the individual Clinical Neurophysiology Departments in the various Hospital Trusts and, due to the increasing demand for Neurophysiological services without a correlating accumulation in our workforce, it proved difficult to facilitate more than 1-2 students per academic year.

However, this arrangement remained very successful for 15yrs, with around 17 students graduating with a BSc Hons degree in Clinical Physiology (Neurophysiology), plus attaining their professional body qualifications, initially ECNE Part 1 and in more recent years ECNE Part 2. The BSc Hons. Clinical Physiology programme also met the accreditation requirements for provisional registration with the voluntary Registration Council for Clinical Physiology (RCCP). Of these 17 graduates, 13 have successfully secured employment, 10 in the North, and 3 in the Republic of Ireland/other parts of the UK, with the remainder following alternative career pathways.

Unfortunately, in June 2012 after the subsequent graduation of our final year BSc Hons. students, it was deemed no longer viable to continue to offer Neurophysiology as an option at the University of Ulster. This raises significant concerns, not only regarding the training and recruitment of future Neurophysiology students

Regional Report



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here in Northern Ireland but, additionally, in terms of workforce planning, given the fact that about a third of our current employees will be due for retirement in less than ten years.

However, the same does not apply to some of the other Clinical Physiology specialities, namely Cardiology and Respiratory, who have already developed PTP and STP programmes, in line with the new UK healthcare structure of Modernising Scientific Careers. Consequently, until the time comes when we can collectively develop, promote, and are in a position to offer an adequate Neurophysiology programme, Cardiology and Respiratory will remain the only Clinical Physiology options available to students who wish to avail themselves of Clinical Physiology degrees in Northern Ireland.

Contact detailsAltnagelvin Area HospitalGlenshane RoadLondonderryBT47 6SBTel: 02871 345171

Belfast City Hospital51 Lisburn RoadBelfastBT9 7ABTel: 02890 638457

Craigavon Area Hospital68 Lurgan RoadPortadownBT63 5QQTel: 02838 612194

Mater Hospital45-51 Crumlin RoadBelfastBT14 6ABTel: 02890 638693

Royal Belfast Hospital for Sick Children274 Grosvenor RoadBelfastBT12 6BATel: 02890 240503

Royal Victoria Hospital274 Grosvenor RoadBelfastBT12 6BATel: 02890 240503

Regional Report

COULD YOU BE A JANS REVIEWER?

Share knowledge and expertise with your fellow professionals!

I’m wondering if someone out there would be willing to do a review of the newsletter for JANS. If so please let me know... (see contact e-mails below).

There are most certainly other newsletters and journals of interest to the JANS readership, and we’d really appreciate reviews, as a ‘one off’ or on a regular basis. Also, there are always new books coming onto the scene – you may have bought one, read it, and thought ‘This is really good, every department should have one’. Tell us about it! Or, maybe, you’ve thought a book might be relevant, but hesitate to buy it. If you let us know, we can ask the publisher for a review copy, which would be sent to you, for you to read and review (and keep!).

Sara Callen, Hon. JANS Editor, e-mail: [email protected] Hudson, Book Review Editor, e-mail: [email protected]@nhs.ukSusan Brennan, Journal Editor, e-mail: [email protected]



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AUDIT REPORT

THE SAFETY AND EFFICACY OF HYPERVENTILATION DURING ROUTINE EEG: A NATIONAL SURVEY

Lawrence, S.J1, Kandler, R.H.1, Kane, N.2, Grocott, L.3 and Pang, C.4 1The Department of Clinical Neurophysiology, Royal Hallamshire Hospital, Sheffield; 2The Grey Walter

Department of Clinical Neurophysiology, Frenchay Hospital, Bristol; 3The Clinical Neurophysiology Department, University Hospital of North Staffordshire. 4The Department of Clinical Neurophysiology,

University Hospital of Coventry and Warwickshire.

IntroductionHyperventilation has been routinely used as an activation procedure in EEG since its seizure-precipitating

effect was discovered by Berger in 1934 (Blume, 2006) It is thought to enhance pre-existing abnormalities and induce abnormal findings in an otherwise normal EEG (Niedermeyer and Lopes Da Silva, 2005), and is widely used in Clinical Neurophysiology centres across the country. However, as no national guidelines are currently available, it is likely that practice differs amongst departments. The aim of the study was to survey departments to obtain information on current practice, particularly with regard to safety issues. The findings from the survey, taken together with the results from a parallel prospective service evaluation, will be used to reach a consensus to establish national standards and guidelines for hyperventilation.

Methodology63 forms were sent out to Clinical Neurophysiology departments across the United Kingdom and Ireland

containing questions regarding the safety of hyperventilation (Appendix 1). 56 forms were completed and returned, representing a response rate of 89%. The collated data was entered onto an Access database for analysis.

Results1. Do you use published guidelines for the safety of hyperventilation?

45 centres did not use guidelines and 11 centres reported that they did use guidelines. However, on review, only 7 of these guidelines were relevant to safety, and only one contained an evidence based reference (Table 1, overleaf).

2. Do you use a local protocol for the safety of hyperventilation?6 centres did not use a protocol and 50 centres did use a protocol. However, 3 of these were not provided

for review as they were under revision at the time of the survey. Out of the 47 available protocols, the following safety considerations were mentioned: contraindications in 78%, age restrictions in 70%, consent issues in 58%, possible side effects in 22% and reasons to terminate the procedure in 18%.

Contraindications: The most frequent contraindications to hyperventilation mentioned were cerebrovascular, cardiovascular and respiratory disease. Other suggested contraindications included hypertension, pregnancy, findings on the present EEG/ECG, Moya Moya disease, Sickle Cell Anaemia, compliance/consent issues, or issues relating to drivers licences or pre-existing medical conditions (Figure 1, overleaf).



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Table 1

Guideline ReferencedNICE 2004. 2006 NoIncreasing the yield of EEG (Mendez, O. et al., 2006, Journal of Clinical Neurophysiology)

No

Electroencephalography; Basic Principles, Clinical Applications and Related Fields (Niedermeyer, E. et al., 1981)

Yes

Paediatric Neurophysiology: Special Techniques and Applications (Binnie, C. et al., 2003. Clinical Neurophysiology, Volume 2: EEG)

No

Fundamentals of EEG Technology: Basic Concepts and Methods (Fay, S. et al., 1983)

No

Awake and Sleep EEG Activation Procedures and Artefacts (Crespel, A. et al 2005. Atlas of Encephalography: Volume 1: EEG)

No

Minimum Technical Requirements for Performing Clinical Electroencephalography. (ACSN Guideline One, 2006)

No

Published Guidelines Used for the Safety of Hyperventilation

Figure 1

Contraindications to hyperventilation

Cerebro

vascular disease

Cardiovascular d

isease

Respirato

ry d isease

Hypertension

Pregnancy

Findings on EEG/E

CG

Moya Moya

Sick le Cel l

Compl iance/consent i

ssuesOth

er

Contraindications

Num

ber o

f cen

tres

50

45

40

35

30

25

20

15

10

5

0

Contraindications mentioned in the departmental protocols

Age Restrictions: 19 centres stated that only patients below the age of 65 years should carry out the hyperventilation procedure.

10 gave an upper age limit of 60 years old, 2 of 70 years and 1of 50 years. 13 centres stated that hyperventilation should be performed on all age groups and 2 centres did not mention an age limit.



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Consent Issues: 30 centres mentioned the necessity for consent to hyperventilation and 17 did not.

Possible Side Effects: The protocols documented the following possible side effects from hyperventilation: sensory symptoms

(tingling, numbness, pins and needles) from 10 centres, dizziness/light-headedness from 8, decrease in temperature/shivering from 3 and tetany from 3. Other possible side effects mentioned included excessive yawning, epigastric symptoms or stiffness (1 centre each).

Reasons to Terminate:

The most frequently mentioned reason for terminating hyperventilation was if the patient was unable to continue (10 centres). Other reasons involved seizures or auras (9), clear cut epileptiform activity or focal slowing (6), ECG abnormality (3) or obvious breathing difficulty (1).

3. Have you performed a local or regional audit on this topic?7 centres had performed an audit on hyperventilation and 49 centres had not. Of the 7 audits, only 2 were

related to safety/efficacy issues and both investigated the usefulness of hyperventilation in different age groups.

4. Can you remember any adverse events that occurred during hyperventilation, regardless of how long ago they occurred?

50 centres could not remember an adverse event during hyperventilation. 6 recalled an adverse event, but 5 of these were expected outcomes from hyperventilation, such as epileptic seizures or the inability to stop hyperventilating. One report was considered to be a true adverse event, where hyperventilation in a young boy induced bradycardia followed by a 10-second period of asystole.

ConclusionVery few departments (20%) use published guidelines for the safety of hyperventilation and of these only

one contained an evidence based reference (Klass, and Daly, 1979). Most departments have safety protocols (84%), focusing on areas such as age limitations, contraindications and consent issues. Where age limitations are mentioned, a limit of 65 years is the one most commonly enforced. The most frequent contraindications to hyperventilation mentioned in protocols are cerebrovascular, cardiovascular and respiratory disease. Only one memory from the vast experience across the departments over the years was truly adverse. In conclusion, therefore, hyperventilation appears to be a safe procedure. However, an evidence base is essential prior to standardisations being agreed. In order to collect the data, the National Audit Group carried out a large prospective service evaluation study to assess the safety of hyperventilation in the United Kingdom. The results of this study will allow national standards and guidelines for hyperventilation to be produced, with a view to using them to audit clinical practice in the future.

AcknowledgementsWe are grateful to the other members of the national audit planning group who assisted with preparing and

piloting the project paperwork, namely: Jeff Holman and Ming Lai. The Association of Neurophysiological Scientists and British Society for Clinical Neurophysiology supported the project and provided funding for data input. We thank the staff of all the Neurophysiology centres involved in this audit (Appendix 2).

REFERENCES

Blume, W.T., 2006. Hyperventilation, More Than Just Hot Air. Epilepsy Curr. 6(3):76-77

Niedermeyer, E., Lopes Da Silva, F. 2005. Electroencephalography; Basic Principles, Clinical Applications and Related Fields. 5th edition; Lippincott, Williams and Wilkins

Klass, D.W, Daly, D.D, (1979) Appendix, in Current Practice of Clinical EEGs. Eds. D.W. Klass and D.D. Daly. pp491-492. New York, Raven Press



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Audit

Appendix 1: National Audit Form

HV AU

DIT

FORM A: Please complete once only for each department

Postcode of Centre(Please complete)

I. GUIDELINES

1. Do you use published guidelines for safety of Hyperventilation? Yes/No

2. If so please give reference

3. Do you use a local protocol for safety of Hyperventilation? Yes/No

4. If so please attach copy Attached/not applicable

5.Have you performed a local or regional audit on this topic? Yes/No

6. If so please provide a summary and main recommendations.

7. Can you remember any adverse events that occurred duringHyperventilation regardless of how long ago they may have occurred?

Yes/No

8. If so, please give details and has there been a change in clinical practice as a result?



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Audit

Appendix 2: The Neurophysiology centres participating in this audit

Aberdeen Royal InfirmaryQueen Elizabeth Hospital, BirminghamBirmingham City HospitalBirmingham Children’s HospitalPoole HospitalFrenchay Hospital, BristolRoyal Belfast Hospital for Sick ChildrenRoyal Victoria Hospital, BelfastAddenbrooke’s Hospital, CambridgeUniversity Hospital of Wales, CardiffKent and Canterbury HospitalUniversity Hospital Coventry and WarwickshireNinewells Hospital, DundeeWestern General Hospital EdinburghRoyal Hospital for Sick Children, Edinburgh Royal Devon and Exeter HospitalNorth Devon District Hospital, BarnstapleForth Valley Royal Hospital, LarbertGlasgow Royal InfirmarySouthern General Hospital, GlasgowRoyal Surrey County Hospital, GuildfordCounty Hospital, HerefordIpswich Hospital Raigmore Hospital, InvernessSt Peter’s Hospital, ChertseyLeicester Royal InfirmaryThe Betsi Cadwaladr University Hospital, Clwyd Leeds General InfirmarySt Mary’s Hospital, ManchesterManchester Royal Infirmary

Salford Royal HospitalNorth Manchester General HospitalNorthampton General HospitalNorfolk and Norwich University HospitalUniversity College Hospital, LondonThe Scottish Epilepsy CentreThe Queen Elizabeth Hospital, Kings Lynn Derriford Hospital, PlymouthQueen’s Alexandra Hospital, PortsmouthRoyal Preston HospitalHurstwood Park Neurological Centre, Haywoods HeathRoyal Hallamshire Hospital, Sheffield King’s College Hospital, LondonThe National Society for Epilepsy, Chalfont CentreSt Helier Hospital, SurreyUniversity Hospital, SouthamptonSunderland Royal HospitalStafford General Hospital University Hospital of North Staffordshire, Stoke-on-TrentSt George’s Healthcare Trust, LondonMusgrove Park Hospital, TauntonThe James Cook University Hospital, MiddlesbroughNational Hospital for Neurology and Neurosurgery, LondonWorcestershire Royal HospitalThe Royal Wolverhampton HospitalYork NHS Trust



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AUDIT REPORT

SAFETY OF VIDEO-TELEMETRY UNITS: A NATIONAL SURVEYCharlton, G.1, Lai, M.1, Kandler, R.H.2, Ponnusamy, A.2, Bland, J.P.3, Pang, C.4

1 Department of Clinical Neurophysiology, Royal Victoria Infirmary, Newcastle, UK; 2 Department of Clinical Neurophysiology, Royal Hallamshire Hospital, Sheffield, UK; 3 Department of Clinical Neurophysiology, Kent and Canterbury Hospital, Canterbury, UK; 4 Department of Clinical Neurophysiology, University Hospital Coventry and Warwickshire, Coventry, UK.

IntroductionVideo-telemetry (VT) is a procedure which allows capturing and reviewing of a paroxysmal clinical event,

such as an epileptic seizure, by the simultaneous recording of video with the electrical activity of the brain (EEG).

The uses of videotelemetry are:1. Diagnostic: the nature of a clinical event - for example focal or generalised epileptic seizure, non-

epileptic attack with a psychological or psychiatric cause, and REM sleep behaviour disorder - is determined.

2. Classification of an underlying seizure disorder. This is important because primary generalised seizures and focal onset seizures have very different management.

3. Surgical evaluation: localization of the seizure onset in the planning of surgical treatment for epilepsy.

Increasingly there is a requirement for VT to confirm whether the patient is experiencing epileptic or non-epileptic seizures, as the treatment is very different. If this cannot be ascertained by a routine EEG or day case VT EEG, then a prolonged VT over several days and nights is requested.

Epilepsy is a diagnosis that has huge medical and social implications for a person. A diagnosis of epilepsy will mean loss of a driving licence 1 (and often employment), as well as committing a person to prolonged treatment with potentially toxic medications. It is essential that the diagnosis is accurate. The most common causes for “seizures” misdiagnosed as epilepsy are psychogenic non-epileptic attacks and cardiac arrhythmias. These patients are treated unnecessarily with antiepileptic drugs and fail to receive appropriate treatment for their condition, sometimes with fatal consequences. Video telemetry enables the diagnosis of epilepsy to be confirmed or refuted, and is an essential tool.

In-patient Video Telemetry units are increasing in number across the UK. It is important to record the patient’s habitual seizures if the investigation is to give a definitive diagnosis. During seizures patients are at risk of complications, including injury and sudden unexpected death in epilepsy (SUDEP). 2-6 This becomes an important safety issue as, commonly, the seizures are deliberately being provoked by medication withdrawal.

The study was divided into 3 parts, each with the following aims:

PART AI – Guidelines • to survey departments throughout the UK, to obtain information on current practice, in particular with

regard to guidelines and protocols usedto survey the occurrence of past adverse events during seizuresPART AII – Unit Infrastructure

• To evaluate the size of units and the level of nursing coverPART B (survey period November & December 2011)

• To evaluate the timeliness of nursing attendance, and adverse incidents occurring during seizures, with the level and type of supervision, and make recommendations for appropriate patient surveillance in VT units

This report will only concentrate on PART AI with some reference made to PART A II.

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Methodology63 forms were sent out to Clinical Neurophysiology departments across the United Kingdom and Ireland,

containing questions regarding the safety of video-telemetry (Appendix 1- survey questionnaire). Not all departments have a VT unit, and replies were received from 31 departments, with 27 used for the survey, 4 being excluded for incomplete data. This represents a response rate of 49% of all units, but over 80% of those with a VT service.

Results1. Do you use published guidelines for safety of VT?

21 departments did not use published guidelines, with 6 departments reporting that they did. These 6 centres reported using one or more of 11 published guidelines as reference (Table 1). However, on review, only 4 of the guidelines related to safety, and 4 departments refer to them, each department citing a different reference. None of the referenced guidelines state how to monitor adequately, with no minimum guidelines/recommendations.

Table 1

Reference Concern Safety

No. Centres that use

BPNA Spring 2001 – VT Safety Audit Yes 1

Labiner, D.M., Bagic A.I. et al. (2010) Essential Services, personnel, facilities in specialised epilepsy centres-Revised 2010 guidelines. Epilepsia, 51(11):2322-2333

Yes 1

Noe, K.H.and Drazkowski, J.F. (2009) Mayo Clinical Proc, 84 (6):495-500

Yes 1

Association of Advancement of Medical Instrumentation 1993 (Equipment safety)

Yes 1

Guideline 12 – Guidelines for Long Term Monitoring for Epilepsy (2008) Journal of Clinical Neurophysiology, 25(3):170-180

No 1

Tatum, W.O.(2001) – Long Term EEG Monitoring, Journal of Clinical Neurophysiology, 18 (5):442-455

No 1

NICE Guidelines 2004 – Guidelines on diagnosis and management of epilepsy in adults and children (guideline G20)

No 2

ILAE commission report: Recommendations regarding the requirements and applications for long term monitoring in epilepsy. Epilepsia 2007; 48:379-384

No 1

E1467-94 Standard for transfer of digital neurophysiological data between independent computer systems (American Soc. For Testing & Materials)

No 1

US DNP Guidelines 1985 Unknown 1

American Academy of Neurology 1989 Unknown 1

Published guidelines used for the safety of VT

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2. Do you use a local protocol for the safety of VT?7 departments did not use a local protocol, with 20 reporting that they did. 15 departments included their

protocols for review, and all state that some safety measures are in place, e.g. cot sides used, ECG monitored, Venflon in situ (Table 2).

Table 2

Safety measures in place No. Centres (Total 27)

Cot sides policy (either to use or not) 20

Record ECG (part of form A II) • ECG visible to ward staff

2717

Leads tied together/attached to patient 4

Drug reduction policy • No reduction of drugs with long half life (phenytoin/phenobarbitone)• No drug reduction for pregnancy• Not reduced if >1 tonic clonic seizure/month• Drugs to be reinstated for 24 hours prior to discharge• Venflon in situ for rapid drug administration if required for seizure

or status

10

Importance of being in camera view stressed 6

Close supervision of patient 4

Measure oxygen saturation 2

No bathing/showering policy 4

Falls/trips risk assessment policy 3

Patient alarms 2

Alteration to environment 2

Patient safety notices provided 2

Electronic tagging of patients (if patient is at risk of post ictal confusion & wandering)

1

Safety measures used by departments taken from protocols

3. Have you performed a local or regional audit on this topic?9 departments reported having performed an audit on VT, whilst 18 had not. Of the 9 audits, only 5 related

to safety, with the other 4 relating to evaluation of the VT service.Recommendations arising as a result of these safety audits varied, with the following examples recorded:• replacing standard floor vinyl with protective cushioned vinyl • adding padding to cot sides• monitoring of ECG and/or using a pulse oximeter to monitor oxygen saturation levels• change doors to en-suites to sliding doors• increase the levels of nursing cover on the ward dependent on the number of VT patients being

monitored / or at known busy periods e.g. meal times• introduction of 1:1 nursing supervision• documenting if patient refuses to use cot sides

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4. Can you remember any adverse events that occurred during video telemetry regardless of how long ago they occurred?

From the 27 respondents, only 2 departments did not report any adverse events, with the remaining 25(92.6%) reporting an adverse event of some description. In total the 25 departments collectively reported 59 adverse events. These varied in nature and severity, e.g. from seizures occurring off camera to SUDEP, with the vast majority being due to falls from standing/chair or bed during seizures. Of the 59 reported events, 6 were potentially life-threatening and 3 actually involved the patient dying whilst connected to VT (Table 3, and Figure 1 [overleaf]).

Table 3

Adverse events remembered (Total no. 59) No. Times reported (x/59)

No. Centres reporting

Falls from standing/chair/bed 21 15

Injuries sustained in seizures 3 3

Damage to equipment 2 1

Assault of VT patient by another patient 1 1

Equipment/Staff failure 5 3

Unattended/ missed seizures 8 7

Seizure off camera (patient behind door) 1 1

Post ictal psychosis 3 3

Problems with drugs (AEDs re-instated later/sooner than appropriate/delay in venflon insertion)

3 3

Status Epilepticus 1 1

Problems with cot sides 3 * *1 near choking

3

Compromised respiration 1 1

Asystole during seizures 2 2

Cardiac Arrest (following seizure) 1 1

SUDEP 3 2

Wires wrapped around patient in sleep 1 1

Adverse events remembered

5. Has there been a change in clinical practice as a result?23 of the 25 departments report some kind of change to their clinical practice in response to adverse events

occurring, whilst 2 departments did not report any changes to their practice. Changes in practice varied, with examples such as recording Oxygen Saturation levels, monitoring of ECG, and staff training mentioned. The most common change to practice was the introduction of a cot sides policy - most departments introducing a ‘cot sides up’ policy, although there was one department which introduced ‘no cot sides to be used’, but to lower the bed instead (Table 4, overleaf).

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Figure 1

Safety measures used by departments taken from protocols

Table 4

Changes in practice as a result of adverse events No. Departments

Record Oxygen saturations 1

Staff training in place • Patient alarm• Seizure recognition• Interaction with patient during seizure

3

Cot sides to be raised 7

Cannulation of all patients for drug reduction 1

24hr hospital stay following drug re-introduction 2

Cardiac monitoring of all patients 1

Dedicated staff/carer 4

Using sliding doors for en-suite 1

Risk assess each patient for falls

Attach leads to patient 1

Cot sides not used-lower bed 1

Low impact flooring 1

No sharp edges on furniture 1

Increase in staffing level 2

No changes 2

Changes in practice as a result of adverse events and local audit.

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Very few departments use published guidelines for the safety of VT, and of the published guidelines used, less than half of them relate to safety issues. The majority of departments do use a local protocol. However, implicit practice appears to exist, in that not all steps are written down, and there is no uniform standard between departments; e.g. ECG – only 22% of departments state recording ECG in protocol, but 100% actually do. Whilst most departments can remember an adverse event happening, only a fifth of departments have carried out a VT audit related to safety of the service. The majority of adverse events were due to falls/injuries sustained during a seizure, but there were also 9 reported events, which were life-threatening, with 3 deaths occurring. Of the remaining 6 life-threatening events, 3 were cardiac in origin.

RecommendationsThere is a dearth of information in the published literature, and from department protocols regarding

requirements for patient safety on videotelemetry units. Guidance on appropriate staffing of VT units is particularly lacking. This survey confirms the need for a national audit to address this issue. It also highlights that displaying ECG on all VT patients, so that it is visible to staff monitoring the patient on the ward, is an easy improvement to make for patient safety.

AcknowledgementsWe are grateful to the other members of the national audit planning group who assisted with preparing and

piloting the project paperwork, namely: Jeff Holman and Nick Kane. The Association of Neurophysiological Scientists and British Society for Clinical Neurophysiology supported the project. We thank the staff of all the Neurophysiology centres involved in this audit (Appendix 2).

REFERENCES1. Epilepsy Society, Driving and epilepsyhttp://www.epilepsysociety.org.uk/AboutEpilepsy/Livingwithepilepsy/Drivingandtravel/Drivingandtransport

2. Bateman, L., Spitz, M., Seyal, M. (2009) Ictal hypoventilation contributes to cardiac arrhythmia and SUDEP: Report on two deaths in video-EEG-monitored patients. Epilepsia, 51(5):916–920

3. Tomson, T., Nashef, L., Ryvlin, P., (2008) Sudden unexpected death in epilepsy: current knowledge and future directions. Lancet Neurology, 7:1021 – 31

4. Noe, K., Drazkowski, J.F. (2009) Safety of Long-term Video-Electroencephalographic Monitoring for Evaluation of Epilepsy. Mayo Clin Proc, 84(6):495-500

5. Dobesberger, J., Walser, G., Unterberger, I., Seppi, K., Kuchukhide, G., Larch, J., Bauer, G., Bodner, T., Falkenstetter, T., Ortler, M., Luef, G., Trinka, E. (2011) Video-EEG monitoring: Safety and adverse events in 507 consecutive patients. Epilepsia, 52(3): 443–452

6. Shafer, P., Buelow, J., Ficker, D., Pugh, M., Kanner, A., Levisohn, P. (2011) Risk of adverse events on epilepsy monitoring units: A survey of epilepsy professionals. Epilepsy and Behaviour, 20:502–505

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Appendix 1: National Audit Form

Questionnaires - Forms AI and AIIQuestionnaires - Forms AI and AII

FORM A: Please complete Parts I and II once only for each department

Postcode of Centre(Please complete)

I. GUIDELINES

1. Do you use published guidelines for safety of video telemetry? Yes/No

2. If so please give reference

3. Do you use a local protocol for safety of video telemetry? Yes/No

4. If so please attach copy Attached/not applicable

5.Have you performed a local or regional audit on this topic? Yes/No

6. If so please provide a summary and main recommendations.

7. Can you remember any adverse events that occurred during video-telemetry regardless of how long ago they may have occurred?

Yes/No

8. If so, please give details and has there been a change in clinical practice as a result?

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II. UNIT INFRASTRUCTURE

9. How many video-telemetry beds do you have?

10. How many video-telemetry beds are in single occupancy cubicles?

11. How many video-telemetry beds are in multiple occupancy bays?

12. Do you have a dedicated unit for videotelemetry distinct from the general neurology or neurosurgery ward?If “Yes” please go to question 17If “No” please go to question 13

Yes/No

13. How many beds are there on the ward in total?

14. What is the minimum number of nurses*on the ward during the day?

15. What is the minimum number of nurses on the ward during the night?

16. Do your telemetry beds have nurses: (Please tick one option)

If '2' please go to question 19

1. Dedicated to the VT bedsor2. Looking after the patients on VT as part of general nursing duties

17. If nurses are dedicated to telemetry or if it is a dedicated VT unit, how many nurses at any one time monitor the patient(s) during the day?

18. If nurses are dedicated to telemetry or if it is a dedicated VT unit, how many nurses at any one time monitor the patient(s) during the night?

19. Is the VT bed in direct view from the nurses’ station? Yes/No

20. How do the nurses monitor the patients? Please tick all that apply

TV or computer monitor at a nurses station

Nurses sitting outside the patient’s room

Nurses sitting within the patient’s room

Alarms

Other e.g. via relatives, carers

21. Is ECG monitored for all patients undergoing VT? Yes/No

22. Can the nurses monitoring the patient easily see the ECG? Yes/No

23. Is there a cot-side policy? Yes/No

24. If so what is it?

25. Overall do you find the intensity of nursing care appropriate? Yes/No

*For the purposes of the questionnaire, the term 'nurses' includes unqualified healthcare assistants, support workers etc

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Appendix 2: Participating Centres

Aberdeen Royal InfirmaryAddenbrookes Hospital, CambridgeBirmingham Children’s HospitalDerriford Hospital, PlymouthEvalina Children’s Hospital, LondonFrenchay Hospital, BristolHurstwood Park Neurosciences Centre, Haywards HeathJames Cook University Hospital, MiddlesbroughKent and Canterbury HospitalKing’s College Hospital, LondonLeeds General InfirmaryLeicester Royal InfirmaryManchester Children’s HospitalNational Hospital for Neurology and Neurosurgery, LondonNational Society for Epilepsy, Chalfont Centre

Ninewells Hospital, DundeePoole HospitalQueen Elizabeth Hospital, BirminghamRoyal Belfast Hospital for Sick ChildrenRoyal Devon and Exeter HospitalRoyal Hallamshire Hospital, SheffieldRoyal Hospital for Sick Children, Edinburgh Royal Victoria Infirmary, NewcastleSalford Royal NHS Foundation TrustSouthampton General HospitalSouthern General Hospital, GlasgowSt George’s Hospital, LondonSt Thomas’s Hospital, LondonThe University Hospital of Wales, CardiffWestern General Hospital, EdinburghYork NHS Trust

ANS UniMed Prize Application Form

Unimed, who have generously sponsored this award for several years, have increased the prize money this year, to £500, which makes it an even greater incentive for graduates to present their final year projects at an ANS Scientific meeting or Conference, and also to publish in JANS.

Presentations should be of 30 minutes duration (including time for questions). The format for publication in JANS is on page 94 – the revised Brief Guide for Authors – and the JANS Editor is very happy to help with the process of tailoring the dissertation for publication. Once the article is accepted for publication the prize money will be sent to the winner.

ANS will pay travel expenses, for attendance at the meeting where the presentation is given, plus day delegate rate for the day of the presentation. Any other associated meeting expenses must be self funded.

Application will be considered by a panel formed of ANS Council members. Applicants will be notified of the outcome, via e-mail. The panel’s decision is final.

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PROFESSIONAL AFFAIRS

CHARTERED SCIENTIST AWARD

ANS opened their new Chartered Scientist (CSci) register in June 1012, after succeeding in their application to become a licence body through the Science Council. Currently, there are 9 registered ANS CSci members and a number of applications going through the validation process.

So why would you want to be a Chartered Scientist?CSci represents a single chartered mark for all scientists, recognising equally high levels of professionalism

and competence across science disciplines at Masters (M) level. CSci also recognises equivalence with Clinical Scientist colleagues, but it is not a pre-requisite to have obtained a taught masters degree in order to apply. Anyone applying for CSci must be able to demonstrate that they are working at this higher level, which will be advantageous for the current workforce in the context of the introduction of the new STP (M-level).

To qualify for the Chartered Scientist designation, applicants must possess a combination of high-level scientific knowledge and experience. This can be demonstrated in 2 ways: Route 1 is typically demonstrated by an accredited Masters qualification, together with four years of post graduation-level experience sufficient to meet the CSci competencies. Having a masters qualification is not mandatory for Route 2 and, where a candidate does not hold an accredited masters degree, they may still show equivalence of M-Level learning through:

• academic qualifications (including those at Diploma (D) Level),• accredited prior learning,• portfolios, and• assessed scientific and technical reports (including published peer-reviewed papers)

Chartered Scientist is set at the same high level as other chartered titles, such as Chartered Mathematician and Chartered Engineer, with the exemplifying educational standard being at M-Level. Currently there are around 15,000 Chartered Scientists, working across a vast array of settings and across all scientific and related sectors (in contrast to ~400 clinical physiologists with ANS membership). CSci is well established within Life Sciences (e.g. Biomedical Scientists) and senior grade bio-medical scientists are frequently required to demonstrate that they practise, and maintain practice (through the CPD process), at the highest level.

Five overarching competency statements illustrate the professional skills and attributes Chartered Scientists are expected to demonstrate through a combination of their knowledge and experience:

1. Deal with complex scientific issues, both systematically and creatively, make sound judgements in the absence of complete data and communicate their conclusions clearly to specialist and non-specialist audiences.

2. Exercise self-direction and originality in solving problems, and exercise substantial personal autonomy in planning and implementing tasks at a professional level.

3. Continue to advance their knowledge, understanding and competence to a high level, and demonstrate a commitment to CPD.

4. Demonstrate an understanding and commitment to Health and Safety and environmental issues related to employment.

5. Comply with the relevant Codes of ConductCSci status has many benefits and not just to the individual:

Professional affairs



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To the individual• by giving you wider recognition outside of your specific discipline or sector• by demonstrating your commitment to professionalism and continuing high levels of competence and

development• by reflecting the likely breadth of your career across science

To the employer• by giving assurance of the competence and professionalism of your employees• by providing your employees with a platform for networking across disciplines and sectors, by showing

your customers or competitors that your staff are practicing at the highest level

To the profession• by benchmarking all professional scientists at the same high level, no matter which discipline or sector

they work in• by ensuring that all chartered scientists must be participating in cpd to continue to hold the award• by encouraging networking and bringing together multidisciplinary teams of professional scientists

To the public• by creating a single badge of professionalism that the public can recognise across the science professions

and beyond• by maintaining and increasing the public’s trust in scientists through professional standards, codes of

conduct and mandatory revalidation

Applicants are expected to demonstrate a minimum of two years’ prior CPD activity in order to register as Chartered Scientists, and must continue to participate in, and record CPD throughout their working lives in order to retain the award. Any ANS member holding RCCP registration will, currently, be keeping an up-to-date portfolio, and so the concept of the CSci CPD process will be familiar.

For anyone interested in applying for CSci, please contact Kelly St. Pier, by either email: [email protected], or telephone: 0207 405 9200, extn. 1466.

Further information can be found on the ANS website with a link to the application forms or alternatively go directly to www.clinphys.force9.co.uk/m-level.

Kelly St. Pier, RCCP, CSci. [email protected]




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PROFESSIONAL AFFAIRS

WHAT CSci MEANS TO ME

Dr Sharon Ann Holgate, Freelance science writer and broadcaster

[email protected]

My work covers many different fields and genres, including so far: writing an undergraduate physics textbook, co-authoring a children’s popular science book, writing brochures and careers leaflets for science institutions, presenting science programmes on BBC Radio 4, and magazine and newspaper journalism. As every facet of my work requires a slightly different skills set which must be constantly updated, Continuing Professional Development is a must. I find the structure of the CPD scheme I follow for CSci incredibly helpful when deciding what training will be most beneficial for me. I also feel a sense of perspective and achievement from the reflection and planning aspect of the CPD, although my yearly ‘Action Plan’ sometimes goes out of the window if I suddenly need to acquire new knowledge for a particular contract! You can feel quite isolated working as a freelancer, so I find additional benefit on a more personal level from having a mentor to discuss my progress with.

I first applied for CSci status when the Institute of Physics informed their members about the scheme, and my licensing body is now the Institute of Physics and Engineering in Medicine. Whilst I am no longer active in a lab, I am constantly applying analytical skills learned during my degrees to my current work, and many of the new skills I have since been acquiring – such as learning new languages - would be transferable to other science-based jobs. Having CSci status reinforces a sense of continuity between the research I carried out for my doctorate and communicating science, and makes me feel part of a wider scientific community. The CPD required to maintain CSci is equally important to me, as it is a constant reminder that - however experienced any of us may feel - we can always learn something new.

Photographer: Stuart Robinson; Text and photo copyright: Sharon Ann Holgate




22670 8 July 2013 10:31 AM Proof 522670 8 July 2013 10:31 AM Proof 1

ANS SPRING SCIENTIFIC MEETING AND AGM

12-13 April 2013, at Crewe Hall, Crewe, Cheshire

Hosted by University Hospital of North Staffordshire

PROGRAMMEFriday 12th April

12:00 Registration and Exhibition

Session One

12:55 Welcome Lesley Grocott – Chair Service Manager/ Lead Scientist Clinical Neurophysiology, UHNS

13:00 Multiple Sclerosis, Mimics and updates on treatments Dr A Al-Araji Consultant Neurologist, UHNS

13:40 Paediatric Epilepsies Dr Singh Consultant Paediatrician, UHNS

14:20 Epilepsy and Memory Dr Andy Hawkins Consultant Clinical Neuropsyc Queen Elizabeth Hospital, Birmingham

15:00 Refreshments and Exhibition

Session Two

Jacqueline Handley - Chair15:30 Principles of Neurosurgery and Epilepsy Mr Ramesh Chelvarajah Consultant Neurosurgeon, UHB

16:00 Orthopaedic Surgery Mr N Ahmed Consultant Orthopaedic Surgeon, UHNS

16:30 Intra-operative monitoring during spinal surgery Jim Oluwole Consultant Scientist, UHNS

17:00 Close

ANS Meeting Agenda





Saturday 13th April

9:00 Registration

Session One

9:25 Welcome Janet Catterall - Chair

9:30 “Hanging in the Balance” Samantha Taylor Associate Neurophysiological Scientist, UHNS

10:00 The effect of mood and anxiety on the perception of pain in routine carpel tunnel screening Jennifer Warner Associate Neurophysiological Scientist, UHNS

10:30 Neonatal EEG “Across the pond” Laura Partridge Chief Neurophysiological Scientist, UHNS

11:00 Refreshments and Exhibitions

11.30 AGM

12:30 Lunch and Exhibitions

Session Two

Hilary Collinge - Chair

13:30 Performing a 5 minute Neurological Examination Dr J Partridge Consultant Neurologist, UHNS

14:00 How to manage a dizzy patient Dr S Ellis Consultant Neurologist, UHNS

14:30 ANS/BSCN National Audit Update April 2013 Lesley Grocott Service Manager/ Lead Scientist, UHNS

15:00 Not the brain perhaps? Dr A Holton Consultant Neurophysiologist, UHNS

15:30 Close

ANS Meeting Agenda



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ABSTRACTS

MULTIPLE SCLEROSIS - MIMICS AND UPDATES ON TREATMENTSDr Adnan Al-Araji, Neurology Department, UHNS Trust; [email protected]

Multiple sclerosis (MS) is one of the relatively common neurological conditions in neuroscience clinics. It is a leading cause of neurological disability in young adults. In this presentation a few cases will be presented to highlight the pattern of the clinical presentation and discuss conditions that might mimic these patterns of presentations.

This presentation will include review and updates on the natural history of MS, in addition to highlights on the treatments of MS relapses and the various disease-modifying therapies used in the modern treatment of MS.

PRINCIPLES OF EPILEPSY SURGERYMr Ramesh Chelvarajah, Queen Elizabeth Hospital Birmingham; [email protected]

Epilepsy surgery comes into consideration when pharmacoresistance is established. This very specialised and highly complex field of neurosurgery draws on five core principles:

• Establishing Concordance• Seizure Onset Localisation• Deciding on Curative or Palliative Surgery• DefiningtheEpileptogenicZone• Safeguarding Eloquent Function

This lecture will use examples of patients managed in the Birmingham Tertiary Epilepsy Service’s surgery programme, to illustrate these principles and the issues encountered when making investigation and treatment choices along the patient pathway. Refractory Epilepsy is very difficult to manage with anti-epileptic medication, but rewarding results can be achieved with appropriately designed surgery.

INTRA-OPERATIVE NEUROPHYSIOLOGICAL MONITORING DURING SPINAL SURGERY

James Oluwole, University Hospital of North Staffordshire; [email protected]

Starting from an assumed viewpoint of those about to embark on Intra-Operative Neurophysiological Monitoring (IONM) without a Consultant Neurophysiologist in theatre, I will briefly highlight some of the recent experiences from the Clinical Physiologist lead IONM service at the University Hospital of North Staffordshire, Stoke-on-Trent, UK.

My apologies to any experienced IONM practitioners in the audience if this talk is too simplistic and devoid of technical details, but I hope that they, and especially those about to partake in neuromonitoring for the first time, will find this talk useful and inspiring. I also hope this presentation will provide a platform for further discussion and, perhaps, areas of development for more experienced IONM centres.

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‘HANGING IN THE BALANCE’Samantha Taylor, University Hospital of North Staffordshire

[email protected]

Post-hypoxic myoclonus (PHM) refers to a rare movement disorder which is a consequence of a cardiopulmonary arrest and the associated ischaemic brain injury. There are two types; Chronic and Acute Post-hypoxic myoclonus. Acute PHM usually occurs within 24 hours of the ischaemic injury taking place, with the patient in a comatose state exhibiting severe, generalised myoclonus which is often difficult to control and associated with a poor outcome.

Chronic PHM, also known as Lance-Adams Syndrome, typically occurs after 48 hours - or up to a few weeks - after the hypoxia. This is characterised by the patient developing action myoclonus, predominantly involving the limbs, after waking from a coma but, unlike acute PHM, is associated with a good prognosis. The pathophysiology of the condition is poorly understood, in part due to the variation and diversity of its origin (cortical or subcortical), the time of onset, and the severity of the symptoms.

This case study aims to provide an insightful introduction to a rare condition, using an unusual aetiology to illustrate Lance-Adams syndrome.

THE EFFECTS OF MOOD AND ANXIETY ON PERCEPTION OF PAIN DURING ROUTINE NERVE CONDUCTION STUDIES

Jennifer Warner, University Hospital of North Staffordshire; [email protected]

This research was carried out in partial fulfilment of a BSc in Clinical Physiology. Since the introduction of the gate control theory, in 1965, it has become widely accepted that pain is not simply a physiological phenomenon, but a psychological one too. Consequently, there is now an abundance of experimental evidence that supports the notion that psychological factors can modulate the relationship between physical pathology and pain. Therefore, the key purpose of this research was to investigate whether or not there is a significant relationship between patient’s mood, level of anxiety and perception of pain during a routine nerve conduction study.

Participants were asked to complete questionnaires, to assess their level of anxiety and mood prior to nerve conduction studies. A routine carpal tunnel screen, according to the department protocol at the University Hospital of North Staffordshire, was then carried out and the level of stimulation used for each participant was recorded. Following the carpal tunnel screen, patients were asked to complete the McGill’s pain questionnaire, to measure their perception of the pain experienced.

It is hypothesised that higher levels of anxiety and lower mood will be significantly correlated with higher levels of perceived pain. To investigate this hypothesis statistical analysis will be performed. The results will be presented and discussed.

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NEONATAL EEG ACROSS THE PONDLaura Partridge, University Hospital of North Staffordshire; [email protected]

The neonatal EEG is an area which can evoke anxiety for the clinical physiologist, particularly for those of us who work predominantly with adults. Interpreting the EEG must take account of the complex development at this stage of life and, at times, it is difficult to separate the normal from the abnormal! I found the remedy was to enter the world of paediatrics, by working full-time in a children’s hospital. As I’d always wanted to travel, I went further afield - to Canada.

I intend to present a brief review of neurophysiology services provided by British Columbia Children’s Hospital, plus an overview of the normal and abnormal neonatal EEG.

ANS/BSCN NATIONAL AUDIT UPDATE APRIL 2013Lesley Grocott, University Hospital of North Staffordshire; [email protected]

The professional bodies, the Association of Neurophysiological Scientists (ANS) and the British Society of Clinical Neurophysiologists (BSCN) recognised the need of their members for the development of national guidelines in a number of areas of our clinical practice.

National audits were undertaken by the national audit group, which comprises of members from the two professional bodies. There was wide participation in three areas:

1. The Safety and Value of Hyperventilation during EEG2. Carpal Tunnel Syndrome Screening - Audit of Standards3. Patient Safety During Video Telemetry, to Investigate Paroxysmal Events

The results of these audits, together with the basis for suggested national guidelines, were presented in London in October 2012.

The presentation at the spring Scientific Meeting 2013 will be a summary of the above audit findings and proposed guidelines, together with an update on progress made so far.

Ideas for future audit topics, which have already been put forward, will be shared, and the floor invited to put forward any further comments or ideas.

“NOT THE BRAIN, PERHAPS?”Dr Andrew Holton, University Hospital of North Staffordshire

Applying EEG electrodes is often an opportunity to review the clinical history. In the physiological measurement that then follows, electrical recording is routinely from heart as well as over the scalp. It is worth reflecting on this technical work, packaging EEG with history and ECG.

As originally intended, co-recorded ECG identifies artefact on EEG, but is that all it is good for? Doubts sometimes arise, at least from the limited history available, whether what prompted being sent for EEG had been truly epileptic (e.g. rather than pre-syncope or convulsive syncope). Should EEG emerge as uninformative, one might worry whether symptoms could have arisen, not from epilepsy, but from interrupted cerebrovascular perfusion. Since our ECG is not reported, nor added to the patient’s case-notes, it usually remains privy to the EEG department. Is this ethical? What are the abnormalities to take note of? Is a non-expert looking at ECG a nuisance, or a potential safety net?

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MEETING REPORT


12-13 April 2013

The ANS 2013 AGM and Spring Scientific meeting was hosted by staff from the University Hospital of North Staffordshire (UHNS) and was located at the idyllic setting of Crewe Hall. The meeting was opened on the Friday by Lesley Grocott (Neurophysiology Service Manager, UHNS), who gave a brief history of Crewe Hall and the nearby surrounding area of Stoke. Crewe Hall is one of the finest Jacobean houses in Cheshire and is a listed Grade I building. It was built in 1615-1636 for Sir Randolph Crewe, was one of the country’s largest houses in the 17th century, and was said to have ‘brought London into Cheshire’.

The first lecture was delivered by Dr Al-Araji (Consultant Neurologist, UHNS), and was about multiple sclerosis (MS), and other disorders which can mimic the disease. He used individual case studies to emphasise the point that the symptoms of MS can easily be diagnosed as other illnesses. He also mentioned that MRI and VEPs are two of the best diagnostic tests for MS, and that less weight is now placed on the use of SSEPs and BAEPs. The current treatment for the condition, and future medications, were discussed towards the end of the talk.

Dr Al-Araji was then followed by Dr Singh (Consultant Paediatrician, UHNS), who talked about paediatric epilepsies. Dr Singh described the ‘Fits, Faints and Funny Turns’ clinic run in Manchester, and emphasised the point that the clinical history is very important, as a specific diagnosis leads to a more successful outcome. He also stated that the EEG is a widely abused investigation, and should not be used inappropriately to exclude and rule out a diagnosis of epilepsy. He concluded that paediatric epilepsy is becoming less common due to more accurate diagnosis and better healthcare in the early stages of life.

The lecture before the afternoon break was given by Dr Andy Hawkins (Consultant Clinical Neuropsychologist, Birmingham), on the topic of epilepsy and memory. He discussed his role and involvement within a multi-disciplinary team, particularly working with patients with severe epilepsy who may be undergoing epilepsy surgery.

Following an afternoon break, Mr Ahmed (Consultant Orthopaedic Surgeon, UHNS) gave an interesting presentation about orthopaedic surgery. He described the different types of spinal deformities, the different surgeries performed and the differing types of rods which can be used. Jim Oluwole (Consultant Scientist, UHNS) followed this with a related talk on the clinical physiologist’s role in spinal surgery. He discussed spinal cord monitoring, using interesting case examples, and emphasising the importance of team work between the surgeon, and the anaesthetist and the physiologist. To finish the day Mr Ramesh Chelvarajah (Consultant Neurosurgeon, UHB) gave a lecture on the principles of neurosurgery in relation to epilepsy. He described the type of patient who would be a candidate for epilepsy surgery, and the different types of surgery which can be performed.

The evening arrangements centred on a masquerade ball in the main part of Crewe Hall. Everyone looked elegant, and this was quite fitting, as the building was very grand, and can only be described as a scene from Hogwarts in Harry Potter. During the evening Evadne Cookman and Anne Burge were presented with flowers for their involvement and work for ANS and RCCP. Following the meal there was much drinking and dancing into the early hours of the night.

The second day was opened and chaired by Janet Catterall, UHNS, who introduced Samantha Taylor

(Associate Clinical Physiologist, UHNS), the first speaker of the session, who gave a very good talk about Adam-Lance Syndrome, chronic post-hypoxic myoclonus, which she based an interesting case study of a patient she had seen a few times. Jennifer Warner (Associate Clinical Physiologist, UHNS) then presented an innovative study showing the effect on patients’ mood and anxiety due to their perception of pain in routine carpal tunnel screening. She found that the higher the level of anxiety from the patient, the more painful they found the test. She also found, in the majority of cases, that the test was not as painful as most patients had

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anticipated. She finished by saying we should look at ways to make the patient feel less anxious. Maybe we all need fish bowls in the clinic rooms?!

Laura Partridge (Chief Neurophysiological Scientist, UHNS) talked about her experience of working at the British Columbia Children’s Hospital in Vancouver. It was very interesting to hear about the different protocols and practices used there. One particular different approach to running the service is the fact they document in the notes if the clinical physiologist does not agree with the consultant report!

The annual ANS AGM followed refreshments. A number of awards were presented including Part I (Portfolio Prize shared by Hollie Morris, Nicola Pilsbury and Rebecca Sinfield; Practical prize, Samantha Taylor) and Part II (Portfolio prize, Hollie Grainger; Practical prize, Adam Pearson) examination awards. Wilma Gerrie was presented the William Stanton Memorial Prize, for her paper on West Syndrome; Jayne Fotheringham was awarded ANS Fellow membership grade, in recognition for her work - especially in education, and Karene Taylor was presented with a gift on retiring from Council as membership secretary, after many, many years. Finally, ANS members who have recently achieved Chartered Scientist status were also congratulated on their achievement and presented with their certificates.

The afternoon session commenced with a lecture from Dr Partridge (Consultant Neurologist, UHNS) who made some valuable points about incorporating a shortened 5-minute neurological examination into our history taking, as and when required. Dr Ellis (Consultant Neurologist, UHNS) gave a talk about ‘the dizzy patient’. He mentioned the many differential diagnosis for dizziness, and how to manage the patient when they are experiencing these symptoms.

Lesley Grocott then discussed the recent ANS/BCSN national audits, which included recent national studies regarding carpal tunnel screening, the use of hyperventilation and video telemetry. Some really interesting points regarding the three audits were highlighted, and it was clear that a lot of hard work and dedication had been put into this by the people involved. Clinical physiologists are encouraged to view the full findings on the ANS website (and published here in this issue of JANS, Ed.).

The afternoon finished with a presentation from Dr Holton (Consultant Neurophysiologist, UHNS), who addressed the need for us to remember that it is not always the brain that causes patients’ episodes. He talked about how we should also observe the ECG, and comment in the EEG report if it suggests an abnormality.

Finally, I am sure that those who attended the meeting would agree that the whole weekend was a great success, being full of very interesting talks and recent research. It also gave members an opportunity to talk to the manufacturers about new and upcoming equipment during breaks and at lunch, all of whom were very helpful in answering questions and demonstrating the equipment. The meeting was held in such a beautiful location, and many thanks go to the staff at UHNS for organising such a wonderful event. I am sure everyone is looking forward to the next ANS meeting, in September 2013, in Wales.

Amy Hopper and Hollie Grainger Diana, Princess of Wales Hospital, Grimsby

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JOURNAL REVIEW

THE NEURODIAGNOSTIC JOURNAL

(The Official Journal of ASET — The Neurodiagnostic Society)

Volume 52, No. 4 December 2012

In Memoriam: Peter J. Seaba. Neurodiagn J. Vol.52(4): 309-311Four contributors have paid their respects to Peter Seaba, electrical engineer, with reminiscences of his life

both within the EEG laboratory and as a family man. He was an obvious expert in the engineering side of EEGs and was always ready to embrace new technology, coping well with the advent of the digital age and computing into the field of neurophysiology. He was also a well respected lecturer, able to impart his knowledge at all levels.

Intraoperative Neurophysiological Monitoring of Somatosensory Evoked Potentials during Hip Arthroscopy Surgery. Ochs, B. C., Herzka, A., Yaylalai, I. Neurodiagn J. Vol.52 (4):312-319

During hip arthroscopy surgery, complications are rare but, if the leg is stretched too far or for too long, some nerve damage can occur. Somatosensory evoked potential (SSEP) recordings of the posterior tibial nerve, stimulating at the ankle and recording over the scalp from the sensory cortex, are a reliable and reproducible means of detecting changes that could lead to possible damage. The recordist can then alert the surgeon and rectifying measures taken. The procedure is explained, and results from 31 patients analysed in this paper. The encouraging results suggest that this technique is a viable use of SSEPs, but the authors also suggest that further work is necessary to fully validate the concept.

Preventing Lower Cranial Nerve Injuries during Fourth Ventricle Tumour Resection by Utilizing Intraoperative Neurophysiological Monitoring. Jahangiri, F.R., Minhas, M., Jane Jr, J. Neurodiagn J. Vol. 52 (4):320-332

Resection of tumours within or near the brain stem was, for many years, considered impossible, with so many nerves, and sensory and motor pathways at risk during an operation. However, with the advent of neuroimaging techniques, the impossible has become a reality, and including the use of multimodality intraoperative neurophysiological monitoring, such as Somatosensory evoked potentials (SSEPs), Transcranial motor evoked potentials (TCeMEP’s), brainstem auditory evoked potentials (BAERs) and brainstem mapping (BSM), damage to nerves can be detected and, hopefully, post operative neurological deficit kept to a minimum. Two paediatric case studies are described and illustrated in some detail, and show clearly how the monitoring played a significant role in guiding the surgeon and preventing damage to the cranial nerves and the brainstem.

Technical Tips: Performing EEGs and Polysomnograms on Children with Neurodevelopmental DisabilitiesPaasch, V., Hoosier, T.M., Accardo, J., Ewen, J.B., Slifer, K. J. Neurodiagn J. Vol. 52 (4): 333-348

This paper is written by the staff of an EEG recording laboratory who regularly work with children with Neurodevelopmental disabilities (NDD), and have given us the benefit of their expertise. Their starting point is a useful overview of the types of disabilities that we might expect to encounter in referrals for EEG/Polysomnogram recordings. They then move on to suggest the type of information worth gathering from the family/carers of the children before the child actually comes to the department. The skills that we, as the recordist, actually need in order to be successful with these children is also discussed.

The largest section of the paper is given over to a discussion of the types of behaviour that the child might exhibit and the behaviour strategies that we might need to employ in order to obtain a successful outcome – some very useful hints and tips are included here! The final section deals with the actual EEG findings that we might expect to see, and also suggests how to be prepared to deal with possible medical emergencies that may arise from dealing with these cases.

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In summarising, the authors stress that every child is different, and it is always best to be ready with a flexible, improvisational approach to dealing with children with NDD. They also recommend gaining experience from other well qualified staff in units where these cases are more commonly seen.

ASET — The Neurodiagnostic Society 53rd Annual Conference Neurodiagn J. Vol. 52 (4): 349-368

The proceedings of the Society are separated, as in previous years, into Platform and Poster presentations. Some have already appeared in the Journal and been reviewed or will appear in future issues and be reviewed; lists of both follow:

PLATFORM PRESENTATIONS:• Applying Evidence Based Organisational Development Techniques for Neurophysiology Departmental

Improvements• Multiple Hippocampal Transections for Seizure Control without Interfering with Memory Function. A

Pilot Study at University Hospitals Case Medical Centre• Clinical Use of Oral Appliance Therapy in the Treatment of Sleep Disordered Breathing• Microvascular Decompression for Hemifacial Spasm and the Lateral Spread Response: A Case Study• The Importance of Cardiac Monitoring in the Epilepsy Monitoring Unit: A Case presentation of Ictal

Asystole• The Technologist’s Role in Improving Safety in the EMU• Multi-site Neuro-telemetry Model• Creative Marketing Ideas for Neurodiagnostics in Challenging Economic Times• A Tribute to Dr. Niedermeyer• Ellen Grass Lecture: Extraordinary Biorhythms• How do Hospitals Choose an IOM Service?• MEG in the Evaluation of Post-Resection Seizure Recurrence• The ASET Government Advocacy Committee: A Vital Resource for Neurodiagnostic Professionals• Developments in Credentialing• Kathleen Mears Memorial Lecture: Patient Safety Recommendations• An Update: What Doctors Expect from their Technical Staff• EEG Changes and Dialysis: What Does the Evidence Show?• Relevance of the Neurodiagnostic ‘‘Specialist’’ in Today’s Job Market• Where Are We Going with Therapeutic Hypothermia?• Mapping of Broca’s Area and the Primary Motor Cortex for Laryngeal Muscles Under General

Anaesthesia – A Review of 4 Cases

POSTERS:• Lessons Learned from Loss of Motor Evoked Potentials during Craniotomy for Aneurysm Clipping: A

Technologist’s Perspective• Stopping Progression in Its Tracks: A Timeline that Traces the Steps of Rasmussen Encephalitis in a

4-year-old Patient from Onset to Post-Operative Care in Less than 30 Days• Aicardi Syndrome: A Case Review• Intraoperative Neuromonitoring and Anaesthetic Fade with Total Intravenous Anaesthesia (TIVA): A

Preliminary Review of the Completed Study• Intraoperative Monitoring during Surgical Treatment for Moyamoya Disease: A Case Presentation• Verification of Accurate Placement and Labelling of 10-10 Scalp Electrodes and Intracranial Grid/Strip

Electrodes Using Documentation Tools• A 31-year Old patient with Drug Overdose: EEG and SSEP Studies• PRES Syndrome and the Benefits of Neurotelemetry: A Case Study• Foramen Ovale Electrodes Discover the Hidden Truth• Capital Equipment Purchases: How Does a Privademic Medical Centre Decide?• Response of Interictal Epileptiform Discharges to Hypoglycaemia• EEG and VEP Changes in Levels of Awareness (Awake, Sedation, Intubation)• The Value of Continuous EEG Monitoring with Remote Review in a Case of Viral Encephalopathy• A Comparison of Disc Electrode Application Methods

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• TCeMEPs – Retrospective Perspective of Optimal Paradigm: Is There Such a Thing?Waveform Window #23Nonconvulsive Status EpilepticusNeurodiagn J. Vol.52 (4):369-373

The condition of Nonconvulsive Status Epilepticus is becoming increasingly more common, and can be difficult to diagnose. This brief article recommends the use of continuous EEG (cEEG) recording in an ICU setting as a means of aiding diagnosis. There is also an emphasis on the training of not only the technologists, but also the medical personnel who may be caring for the patients, in recognising certain EEG patterns that may need immediate attention or treatment. Some illustrations of the type of recording pattern that might be encountered are provided.

Media ReviewNeurodiagn J. Vol 52(4):376-377The John Hopkins Atlas of Digital EEG: An Interactive Training Guide: Second Edition edited by Krauss, G. L., Fisher, R. S and Kaplan, P.W.The John Hopkins University Press, Baltimore Maryland, 2011, Price $110, pp438

The reviewers of this resource (book and DVD combined) recommend it as a concise guide, with the DVD alone worth the cost. The book has clear EEG examples, well labelled and large enough to be of real use, with a clear 2-chapter introduction aimed at new professionals to the field, and a further 7 chapters which build on this foundation.

The DVD is an interactive resource of EEG examples and includes colour videos of seizures with accompanying EEG traces - a really useful teaching exercise. A self test of 40 questions is also provided. This Atlas gets a clear thumbs-up, and is recommended for any Neurology department.

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CHARITY NEWS

MULTIPLE SCLEROSIS SOCIETY

MS care lottery revealed by groundbreaking MS Society research

Published 26 April 2013

Alarming numbers of people with MS in the UK are facing a lottery when it comes to accessing the care and support they need to manage their condition.

“A lottery of treatment and care: MS services across the UK”, is published today to mark the start of MS Week. It uncovers major disparities across the UK in access to MS medicines, social care support, employment support, and health professionals for people with MS.

Researchers found:• 6 out of 10 eligible people with MS are not taking a disease modifying drug for their condition• Just two in 100 people with MS use one of two licensed symptom management treatments • If you have MS, and live in Northern Ireland, you are twice as likely to be taking a DMT (Disease

Modifying Therapy) than if you live in Wales.• Half of those who are struggling financially and are in need of social care support are unable to access

it. By contrast, nine out of 10 of people who are financially comfortable and need social care are able to access it

• Access to MS nurses, neurologists, powered wheelchairs and support to make home adaptations is often based on where you live, not your clinical needs

The findings are based on a survey we issued last year asking people with MS what services they needed and to what extent those needs had been met over the previous 12 months. More than 10,500 adults responded – the largest ever survey of people with MS in the UK.

Stop the MS LotteryTo coincide with the report, we’re launching the “Stop the MS lottery campaign”, calling for everyone with

MS to have fair access to the treatments and services they need, when they need them, wherever they live in the UK. We want every person with MS to have a personalised treatment, care and support plan, with two comprehensive reviews each year.

Nick Rijke, Director for Policy & Research at the MS Society, said: “Our survey findings worryingly suggest that the likelihood of someone receiving a life changing treatment or service is often based on luck – like where they live or how helpful their healthcare professional is – rather than their genuine clinical need.”

“When it comes to MS drug prescription rates, the UK ranks 25th out of 27 European countries; given the relative wealth of the UK this is simply unacceptable.”

EPILEPSY SOCIETY

Brain implant device to predict seizures

Published 2 May 2013

Epilepsy Society’s medical director, Professor Ley Sander, says a new device, which uses the brain’s electrical activity to tell patients if their risk of a seizure is high, moderate or low, is ‘a very interesting approach and shows that it is possible to predict seizures reliably.’

He cautions, “The technology is, however, still very invasive and will not have practical use in the short term, apart from in specialist centres and for people with frequent seizures.”

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Professor Sander was commenting on a small study published in the Lancet today (1 May) which showed a small brain implant device has accurately predicted epilepsy seizures in some patients.

Improved quality of lifeThe study was led by Professor Mark Cook, chair of medicine at the University of Melbourne and director

of neurology at St Vincent’s Hospital. He said: “Knowing when a seizure might happen could dramatically improve the quality of life and independence of people with epilepsy.”

Professor Cook and his team, with Professors Terry O’Brien and Sam Berkovic, worked with researchers at Seattle-based company, NeuroVista, which developed a device which could be implanted between the skull and brain surface to monitor long-term electrical signals in the brain (EEG data).

They worked together to develop a second device implanted under the chest, which transmitted from electrodes recorded in the brain to a hand-held device, providing a series of lights warning patients of the high (red), moderate (white), or low (blue) likelihood of having a seizure in the hours ahead.

Uncontrolled seizuresThe two-year study included 15 people with epilepsy aged between 20 and 62 years, who experienced

between two and 12 seizures per month and had not had their seizures controlled with existing treatments.

For the first month of the trial, the system was set purely to record EEG data, which allowed Professor Cook and his team to construct individual algorithms of seizure prediction for each patient.

The system correctly predicted seizures with a high warning 65 percent of the time, and worked to a level better than 50 percent in 11 of the 15 patients. Eight of the 11 patients had their seizures accurately predicted between 56 and 100 percent of the time.

Uncontrolled epilepsy“One to two percent of the population have chronic epilepsy, and up to 10 percent of people will have a

seizure at some point in their lives, so it’s very common. It’s debilitating because it affects young people predominantly, and it affects them often across their entire lifespan.” Professor Cook said.

“The problem is that people with epilepsy are, for the most part, otherwise extremely well. So their activities are limited entirely by this condition, which might affect only a few minutes of every year of their life, and yet have catastrophic consequences like falls, burns and drowning.”

Professor Cook hopes to replicate the findings of the study in larger clinical trials, and is optimistic the technology will lead to improved management strategies for epilepsy in the future. Collaborators on the study included the Royal Melbourne Hospital and Austin Health, Australia.

MENINGITIS TRUST

Viral Meningitis Week is coming

Published 29 April 2013

The Meningitis Trust’s first Viral Meningitis Week is taking place between 6 and 10 May, and aims to dispel misconceptions among health professionals and the general public that the disease is always ‘mild’ and highlight the long-term difficulties sufferers can face.

It is estimated there are around 5,000 cases of viral meningitis each year in the UK, and the week coincides with the start of the peak season for viral meningitis, with the majority of cases happening during the warmer months.

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We are asking our supporters to use the week, entitled “Take it Seriously”, to deliver a letter to their local GP’s surgery calling for better understanding, treatment and after-care of those who contract the disease. Our recent survey showed that 97% of viral meningitis victims who responded are left with debilitating after-effects including exhaustion, headaches, memory loss, depression, anxiety and hearing difficulties. Of those who took part in the survey, over 40% did not receive any information on the disease and only one in three was offered a follow up hospital appointment. We are using the findings to help further improve the support we provide, and to educate health professionals and the public and empower victims.

“Our survey showed the true impact of viral meningitis, prompting us to take more action on behalf of all sufferers and their families” said Sue Davie, Chief Executive of the Meningitis Trust and Meningitis UK. “Because viral meningitis is rarely life-threatening, many sufferers feel that their illness is taken less seriously than bacterial meningitis. But over half of those who took part in our survey said the disease had caused them difficulty at work or in education, and many felt that family, friends, health professionals or employers did not understand its full impact. We want our awareness week to hammer home the message that viral meningitis is not always the mild illness it is usually portrayed as.”

MND ASSOCIATION

Stem cell discovery gives insight into motor neurone disease

Published April 2013

A discovery, using stem cells from a person living with motor neurone disease, could help researchers learn more about the causes of MND. Funded by the Motor Neurone Disease Association and led by the University of Edinburgh, the study provides fresh insight into the mechanisms involved in the disease.

The study used a patient’s skin cells to create motor neurons - nerve cells that control muscle activity - and the cells that support them, called astrocytes. Researchers studied these two types of cells in the laboratory. They found that a faulty protein linked to motor neurone disease, which is called TDP-43, caused the astrocytes to die. Although TDP-43 mistakes are a rare cause of MND, scientists are especially interested in the gene because, in the vast majority of cases of MND, TDP-43 protein forms pathological clumps inside motor neurons.

This study shows for the first time that abnormal TDP-43 protein causes death of astrocytes. The researchers, however, found that the damaged astrocytes were not directly toxic to motor neurons. Better understanding the role of astrocytes could help to inform research into treatments for MND.

Professor Siddharthan Chandran, of the University of Edinburgh, said: “Motor neurone disease is a devastating and ultimately fatal condition, for which there is no cure or effective treatment. It is not just a question of looking solely at motor neurones, but also the cells that surround them, to understand why motor neurones die. Our aim is to find ways to slow down progression of this devastating disease and ultimately develop a cure.”

These findings, published in the journal Proceedings of the National Academy of Sciences, are significant, as they show that different mechanisms are at work in different types of MND.

The research, led by the University of Edinburgh’s Euan MacDonald Centre for Motor Neurone Research, was carried out in collaboration with King’s College, London; Columbia University in New York; the University of California, and the Gladstone Institutes in San Francisco.

Dr Steve Finkbeiner, Associate Director of Neurological Research at the Gladstone Institutes, said: “We were delighted to be part of this international team, which brought together critical tools, innovative technologies and complementary expertise to do something that no single group could. We are hopeful that the creation of human models of ALS* will deepen our understanding of the disease in ways that will help us ultimately find relevant therapies for patients.”

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Reference: Serio et al. (2013) Astrocyte pathology and the absence of non-cell autonomy in an induced pluripotent

stem cell model of TDP-43 proteinopathy. PNAS 2013

*ALS, also known as amyotrophic lateral sclerosis, is the most common form of MND and the name given to the disease in America.

ALZHEIMER’S SOCIETYAlzheimer’s Society to train all CQC staff in dementia awareness

Published 2 May 2013

Staff at the body responsible for standards of care in care homes and hospitals will, for the first time, be trained in dementia awareness. A new partnership between Alzheimer’s Society and the Care Quality Commission (CQC), the regulator of health and care services in England, will see experts from the charity train all of the regulator’s staff to spot the signs and symptoms of the condition.

80 per cent of people in care homes have either dementia or severe memory problems, whilst a quarter of hospital beds are occupied by someone with the condition. The training will be delivered to over 2,000 staff – from inspectors to support staff such as policymakers — in sessions this spring. The training will cover what dementia is, give an insight into the experience of living with the condition, and explore issues around communicating with people with dementia. Ensuring that all CQC staff have a baseline understanding of dementia aims to put those who inspect care homes and hospitals in a better position to assess the quality of care for those with the condition.

Jeremy Hughes, Chief Executive at Alzheimer’s Society said: “The CQC has a vital role to play in ensuring that people with dementia receive the best care, whatever environment they live in. As the people who are responsible for care standards, it’s crucial that all CQC staff are aware of the particular needs of people with dementia. There are 800,000 people with dementia in the UK. We know that they too often go into hospital when it’s not the best option, stay too long, and that those in care homes are not always enjoying a good quality of life. We can’t go on like this. It’s encouraging to see the CQC bring in our experts to work with their staff in order to improve the lives of people with the condition.”

David Behan, Chief Executive of the Care Quality Commission said: “It is important that CQC staff are able to recognise high quality care for people with dementia. This new partnership with the Alzheimer’s Society means staff will be supported and developed to do this, by the leading expert organisation.”

Complied by Ilona Sempers, Charity Liaison Officer, Queens Medical Centre, Nottingham

For further information about any of the charities please contact:THE MULTIPLE SCLEROSIS SOCIETY

MS Helpline Tel: 0808 800 8000MS Email [email protected] Website www.mssociety.org.ukk

THE MND ASSOCIATIONMND Helpline Tel: 08457 626262MND Email [email protected] Website www.mndassociation.org.uk

MENINGITIS TRUSTMeningitis Helpline Tel: 0808 80 10 388Meningitis Email [email protected] Website www.meningitis-trust.org

ALZHEIMER’S SOCIETYHelpline Tel: 0300 222 11 22Email [email protected] www.alzheimers.org.uk

EPILEPSY SOCIETYES Helpline Tel: 01494 601 400ES Website www.epilepsysociety.org.uk

Updated May 2013

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THE ANS COUNCIL 2013-2014

ab*/ Hon. President Nigel Hudson Clinical Neurophysiology Department Derriford Hospital Derriford Road Plymouth PL6 8DH Tel.01752 792329 Fax.01752 792328 e-mail: [email protected]

ab/ Hon. Chair Peter Bill Neurophysiology Department Birmingham Children’s Hospital NHS

Foundation Trust Steelhouse Lane Birmingham B4 6NH Tel:0121 333 9264 Fax:0121 333 9261 e:mail: [email protected]

ab#* Hon Vice Chair OSET CSci lead Rep RCCP Rep Kelly St. Pier Videotelemetry Department Koala Ward Level 5, Morgan Stanley Clinical Building, Great Ormond Street Hospital, London WC1N 3JH Tel: 020 7405 9200 ext 1466 Fax: 020 7829 8627 e-mail: [email protected]

ab* Hon. Secretary Archivist

Joanne Horrocks Clinical Neurophysiology Department York District Hospital Wigginton Road York YO31 8HE Tel: 01904 725663 Fax: 01904 726373 e-mail: [email protected]

ab* Hon. Treasurer Mary Boland Department of Clinical Neurophysiology 3rd Floor Central

250 Euston Road London NW1 2PG

Tel: 020 7380 9046 Fax: 020 7380 9002 e-mail: [email protected]

b/ Chair of Education Peter Walsh Clinical Neurophysiology Frenchay Hospital Bristol BS16 1LE Tel: 0117 340 3645 Fax: 0117 3406797 e-mail: [email protected]

b/* Chair of National Examination Board Ann Harvey Department of Clinical Neurology (NO39) Ipswich Hospital NHS Trust Heath Road Ipswich IP4 5PD Tel: 01473 704922 Fax. 01473 704004 e-mail: [email protected]

b Professional Affairs Advisor Simon Veal Neurophysiology Department Queen Alexandra Hospital Portsmouth PO6 3LY Tel: 023 92286659 Fax: 023 92286683 e-mail: [email protected]

b * Membership Secretary Joanne Horrocks Clinical Neurophysiology Department York District Hospital Wigginton Road York YO31 8HE Tel: 01904 725663 Fax: 01904 726373 e-mail: [email protected]

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b JANS Editor Sara Callen 7 Albert Terrace Buckhurst Hill Essex, IG9 6DU Tel. 020 8926 8437 Mobile: 07774 404983 Email : [email protected] and [email protected]

b Newsletter Editor Naomi Thornton Clinical Neurophysiology Department Sandringham Building Level 1 Leicester Royal Infirmary NHS Trust Leicester LE1 5WW Tel. 0116 2585621/2585722 Fax. 0116 2585724 e-mail: [email protected] or [email protected]

c Newsletter Distributor Jane Glover Clinical Neurophysiology Department Sandringham Building Level 1 Leicester Royal Infirmary Leicester LE1 5WW Tel. 0116 2585621/2585722 Fax: 0116 2585724 e-mail: [email protected] and [email protected]

/ Administrator Meetings organiser Lindsey Sevier –White

Executive Business Support (EBS) ANS Business Administrator City Wharf, Davidson Road Lichfield Staffordshire WS149DZ Tel: 0845 519 4045 Fax: 0121 355 2420 email: [email protected] and [email protected]

/ Careers Advisor NPDAG rep Richard Pottinger Barts & The Royal London NHS Trust Department of Neurophysiology St. Bartholomew’s Hospital London EC1A 7BE Tel: 020 7601 8183 Fax: 020 7601 7875 e-mail:[email protected]

Irish Delegate Lezlie Huntley Neurophysiology Department Craigavon Area Hospital 68, Lurgan Road Portadown, Craigavon BT63 5QQ Tel: (direct line): 02838612346 Email:[email protected]

Website Manager Martyn Thompson Calderdale Royal Hospital Halifax HX3 0PW Tel: 01422 222976 Fax: 01422 223972 e-mail: [email protected] or [email protected]

Clinical Governance Stuart Lodwick Clinical Neurophysiology Salford Royal Foundation Trust Stott Lane Eccles N6 8HD Tel: 0161 206 4617 e-mail: [email protected]

c National Audit rep Catherine Pang University Hospitals Coventry And

Warwickshire NHS Trust Clifford Bridge Road Coventry West Midlands CV2 2DX email: [email protected]

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/ School of HCS board rep Elected 2012 Rachel Hutchings Clinical Neurophysiology Nottingham University Hospitals NHS Trust QMC campus Derby Road Nottingham NG7 2UH Tel: 0115 924 9924 ext 64859 e mail: [email protected]

Elected 2012 Laura Lea-Thomas Videotelemetry Department, Koala ward, Floor 5 Morgan Stanley Clinical Building, Great Ormond Street Hospital, LONDON WC1N 3JH Tel: 020 7405 9200 ext 5154 Fax: 020 7829 8627 e-mail:[email protected]

Elected 2013 Adrian Tearle Norfolk and Norwich University Hospital Colney Lane Norwich NR4 7UY Tel: 01603 287149 Fax: 01603 287307 e-mail:[email protected]

Notice Board

a Executive Council Memberb Ex-Officio Memberc Co-opted Member/ Education Sub-Committee* CSci representatives# OSET Representative




FUTURE MEETINGS

June 21st 2013 Epilepsy in Children 2013; 10th national neuroscience conference, America Square Conference Centre, London

June 23rd-27th 2013 ILAE 30th ICE, Montreal, Canada http://www.epilepsycongress.org

July 4th-5th 2013 BSCN & SNCLF Joint Meeting: Horizons in Clinical Neurophysiology, Oxford http//www.bscn.org.uk

July 10th-13th 2013 20th International Meeting on Advanced Spine Techniques (IMAST), Vancouver, BC, Canada http://www.srs.org/Imast/2013/

September 5th-7th 2013 ILAE British Chapter Annual Meeting, Glasgow http://www.ilae-ukconf.org.uk

September 6th 2013 N Spine 2013: Spine Course for Neurophysiologists, Nottingham. http://www.nspine.co.uk

September 9th-11th 2013 9th International Paediatric EMG Course Downing College, Cambridge

September 20th-21st 2013 ANS Scientific Meeting, Cardiff

October 4th 2013 BSCN Scientific Meeting and AGM, London

October 17th-19th 2013 British Sleep Society, 25th Anniversary Scientific Meeting, Edinburgh

November 11th -13th 2013 Third ISIN Educational Course, Cape Town, South Africa November 14th-16th 2013 International Conference on Intra-operative Neurophysiology,

Cape Town, South Africa

November 18th-22nd 2013 Introduction to EEG and Paediatric EEG, Birmingham Children’s Hospital

December 6th-10th 2013 67th American Epilepsy Society Meeting, Washington DC, USA

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DISSERTATION REPORT FORM

Students and graduates are invited to submit an abstract (300 words) or report with references (1000 words) on the work undertaken for their dissertations. The article should provide a brief account of the study, with an introduction, the methods used, the results, discussion, summary, and key words. Students should follow the ‘Brief Guide for Authors’ published at the end of each JANS.

Alternatively, full papers, based on the original work, can be submitted and should be no more than 3000 words in length, plus references, and figures should be included, where available. This original academic work is worthy of publication and other students or colleagues may wish to build on this in the future. If this work is not published, and the subject is pursued by others, the original author may not get the deserved recognition.

DISSERTATION REPORT

TITLE:

Introduction:

Methods:

Results:

Discussion:

Summary:

Key Words:

Name and address of author – Please print clearly:

Mr/Mrs/Ms/Miss . . . . . . . . . . . . . . . . First name . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Address . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Town/City . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Postcode . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Telephone (daytime) . . . . . . . . . . . . . . . . . . . . . . . . . . . . Fax . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

e-mail . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

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A BRIEF GUIDE FOR AUTHORS

JANS will accept, subject to independent review, a variety of articles, including original research, case studies, reviews, audits, historical articles, technical notes and correspondence in the field of electrophysiology and its clinical applications. Notices about relevant meetings and training courses are also accepted. The format for original work should be arranged with an Introduction, Methods, Results and concluded with a Discussion, to ensure uniformity with all other scientific communications. Key Words should also be included, in compliance with international electronic abstracting database services.

The text should be typed with single spacing in MS Word (ideally in Times New Roman font) and submitted via e-mail to the Editor (address below). Avoid complicated layouts, multiple layers of indenting, and boldface or italic headings. The files should not be locked, as the editor will need to adapt the text to the house style of JANS. Tables, figures and any illustrations should be also submitted as separate files, and must be of publishable quality.

The title page should give a short running title, an abstract not exceeding 300 words, and the key words used in the main body of the paper. The full name(s), title(s), work address (es) of the authors should be included, with the email address of the author to whom correspondence should be addressed. Numerical data should use S.I. units. Where abbreviations are used (such as AED, SUDEP, OSET, RCCP), the full term should be included at least once within the text. References in the text should be cited by author(s) name(s), and the year. If there are more than two authors, then only the first surname of the group is required, followed by “et al”. More than one publication for an author in a year is distinguished by a, b, etc. after the date.

The reference list should be typed in alphabetical order, with all authors listed in full for each reference, and using the style laid out below. This reference style is based on the widely used Harvard system. Titles of journals should be abbreviated, in conformity with the World List of Scientific Periodicals. For examples of citations, see previous issues of JANS, or ask the advice of your librarian.

Where case studies are to be published, WRITTEN PERMISSION from the patient (or relative, if appropriate) must be enclosed with the submission. Written approval from the local ethics committee must be enclosed with other clinical studies and trials.

For further information on preparing a paper for publication, please refer to the Guidelines (updated version following pages). The Editor is very happy to work with authors to prepare papers for publication.

Example of reference: Shaw, J.C. (2001) Historical Review: In the Footsteps of Beck. J. Electrophysiol. Technol. 27: 124-126.

All material should be sent to The Managing Editor: Sara Callen

e-mail: [email protected] or [email protected]

This issue was prepared for printing May 2013

Printed and distributed by: Jones and Palmer Limited. 92-95 Carver Street, Birmingham B1 3AR. Tel: 0121 236 9007. www.jonesandpalmer.co.uk

Environmental information: The paper used for the printing of this journal is produced from wood from sustainable forests and is Elemental Chlorine Free (ECF).

Guidelines



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GUIDELINES FOR PREPARING A PAPER FOR SUBMISSION TO JT

Who is your target audience? Within Clinical Neurophysiology, the majority of ANS members are qualified Neurophysiological

Scientists practicing within the UK. We also have student members, medical members, clinical scientists, engineers and commercial company staff. We have members abroad, who look to JANS as one source of information to help keep them up to date, as well as institutional members – hospital medical libraries and university libraries. Student members may be a minority, but you need to bear in mind that they (as well as other health care professionals, browsing hospital and university library shelves) may read your article, and need to grasp the essence of your paper.

What are you wishing to convey?Is it an original piece of work, (including case studies) contributing to the existing “body of knowledge”

within the literature (journals, text-books and web-sites) on your chosen subject? Or, is it a teaching article? In which case is it for new students, at PTP or STP levels, or for qualified, experienced practitioners? It would be useful to indicate which.

Or, is it a literature review? If so, what is its purpose? How does it contribute to the existing literature? Have you done a thorough search, so that the most pertinent articles are used and referenced? Have you checked on the original sources of your topic and referenced them? whether from journals, books or on-line resources. Have you checked on the latest work, publications and protocols, and referenced them?

Have you checked through the past JANS, JET/Proc.EPTA journals for articles on your topic, and referenced them, if appropriate? There are currently 2 published indexes of old journals:

Cumulative Index 1950 – 1974 Proc.EPTA Vol. 21 No. 4 Dec (1974) pages 243-262

Cumulative Index 1975 – 1988 JET Vol. 14 No. 5 (1988) pages 231-345 If you are unable to locate any particular articles (from any journal) in your local library, all publications

are held in the British Library, including Proc.EPTAs, JETs and JANS. Your hospital librarian should be able to obtain copies for you (although it could take a few weeks, as they may have to be retrieved from archives). Also, you, or your department, may be charged a fee.

Have you checked the Brief Guide for Authors, at the back of the latest JANS?Submissions for a formal publication need to be structured and presented in the way the journal specifies.

All journals have their own ‘house’ style and individual requirements. If you have already published an article in a different journal, it is quite likely that the required presentation differs slightly from JANS. Original papers will be sent out for peer review, before submission for publication. House style currently utilises Times New Roman font.

Have you got a structure for your paper?Most scientific papers need an introduction and, sometimes, an historical background may be pertinent or

of interest. This should be followed by the methods you have used for your study, and then your results. At this point you may like to bring in the work of others, discuss what they have done, who has done what, and where and when these studies were undertaken. It may be of interest to compare results and debate any variables, differences in methods etc. It is useful for our readers if you bring the paper to a conclusion, if that is possible, even if the study throws up more, or new, questions! NB: THE WORK OF OTHER PEOPLE SHOULD ALWAYS BE CAREFULLY AND THOROUGHLY REFERENCED to avoid breach of copyright and plagiarism.

Guidelines



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Have you presented your REFERENCES and / or BIBLIOGRAPHY in an appropriate format? For all references you need to include the full list of authors’ names* (surnames and initials), the title of the

work, the year of publication and pages, PLUS: – if the reference is from a journal, you need to include the abbreviated name of the journal, the volume

number (the issue number) and the page numbers, OR: – if the reference is from a book, you need to include the edition number (if this is not the first edition),

the publisher and the place of publication.

(NB * Main/first author with ‘et al’ for multiple author teams is NOT an acceptable entry in the reference list, and should only be used for the reference within the text of the article.)

Examples of references:

Journal reference (from JET):Smith, S. (1999) Message from the Honorary President. J. Electrophysiol. Technol. 25 (3):154.

Journal reference, multiple authors:Sackett, D.L., Rosenberg, W.M.C., Gray, J.A.M., Hughes, R.B. and Richardson, W.S. (1996) Evidence Based Medicine: What It Is and What It Isn’t. Brit. Med. J. 312:71-72.

Textbook reference:Chiappa, K.H. (1990) Evoked Potentials in Clinical Medicine. 2nd Edition. Raven Press, New York: 75-83.

Textbook reference, multiple volumes:Gibbs, F.A. and Gibbs, E.L. (1951) Atlas of Electroencephalography. Vol. I: Methodology and Controls. Addison-Wesley, Reading, Massachusetts: 125-132.

Textbook reference, the author of a chapter/appendix:Wisman, T. (1982) ‘Extended Testing of EEG Machines.’ In: Binnie, C.D., Rowan, A.J. and Gutter, T.H. A Manual of Electroencephalographic Technology. Cambridge University Press, Cambridge: 334-337.

Edited textbook/journal supplement:Deuschl, G. and Eisen, A. (Editors), (1999) Recommendations for the Practice of Clinical Neurophysiology: Guidelines of the International Federation of Clinical Neurophysiology. 2nd Edition. Elsevier, Amsterdam. /Electroenceph. Clin. Neurophysiol. Suppl.52.

Historical reference:Brazier, M.A.B. (1968) The Electrical Activity of the Nervous System. 3rd Edition. Pitman Medical, London: 269.

Caton, R. (1875) The Electric Currents of the Brain. Brit. Med. J. ii: 278. In: Brazier, M.A.B. The Electrical Activity of the Nervous System. 3rd Edition. Pitman Medical, London: 269.

Reference of an organisation/committee report (with no named author):American EEG Society (1994) Guideline Nine: Guidelines on Evoked Potentials. J. Clin. Neurophysiol. 11:40-73.

Electronic reference:Trend Micro Weekly Virus Report (2002)* http://www.antivirus.com/trendsetter/virus_report/ [accessed 11th May 2002]** (NB * = year of publication; ** = date website accessed)

References in recent editions of JANS, and other medical journals, will also act as a guide.

Guidelines



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Is this your first submission for publication?If so, you may feel quite daunted by the prospect! Don’t despair. We’ve all had to learn how to present our

papers. It would be useful to read through some articles in recent editions of JANS, to get a feel for how they’ve been constructed and presented for publication. The first time you prepare an article for publication is quite a challenge. It is an opportunity for personal development, a new learning curve etc… don’t worry if it comes back for modification or correction, that’s all part of the process. Even old hands/experienced authors often have to do corrections.

Are you hoping to use this publication as part of your work for a dissertation?You will need to check with your university supervisor and make sure that you comply with the local

regulations, which vary between institutions. Management strategies, including financial and human resource management, health and safety, training processes and audits are all potential topics for research, as well as clinical subjects and case studies.

CHECKLIST FOR PUBLICATION

Have you:

• Followed A Brief Guide for Authors in the latest edition of JANS? • Formatted your paper according to the Guidelines?

• Followed a structure, to include an introduction, method, results, discussion and conclusion? • Double-checked your reference list, for matching entries within the body of your text?

• Checked your grammar, spelling and word flow? If in doubt, you could ask a senior colleague for a second opinion. The Editor is also very happy to work with you on drafts, to make the process easier.

• Checked your content, to suit the JANS audience?

• Obtained appropriate, written ‘permissions’ from patients, ethics committees and other publications, as appropriate, and enclosed them with your paper?

Guidelines updated by Sara CallenHon. Editor JANS – May 2013

Guidelines



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JOURNALOF THE

ASSOCIATION OFNEUROPHYSIOLOGICAL SCIENTISTS (JANS)


CONTENTS (in brief)

JO

UR

NA

L OF T

HE

ASSO

CIAT

ION

OF N

EU

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PHY

SIOL

OG

ICA

L SCIE

NT

ISTS

Volume 6 N

umber 1 (2013)

Page No.Editor’s Foreward 3

Obituary — Lyn Davies 5

Stanton Memorial Prizewinner 6

Corrections 6

OSET Update Kelly St. Pier 8

Teaching Paper SomatoSensory Evoked Potentials ANS Evoked Potential writing group 9

Postgraduate Dissertation 32 Can the theta/alpha QEEG index be used to identify normal/abnormal EEGs in patients screened with 6-CIT for cognitive impairment? Michael Pridgeon

Unimed Prizewinner Undergraduate Dissertation 45 A comparison of the Pattern Reversal Visual Evoked Response obtained with

Cathode Ray Tube (CRT) technology to that obtained with a Liquid Crystal Display (LCD). Donna Formby

Regional Report 55 An overview of neurophysiological services in Northern Ireland Lezlie Huntley

Audit Thesafetyandefficacyofhyperventilation 59

during routine EEG: a national survey Lawrence, SJ, Kandler, RH, Kane, N, Grocott, L,Pang, C

Safety of video-telemetry units: a national survey Charlton G, Lai M, Kandler RH, 64 Ponnusamy A, Bland JP, Pang C

Professional Affairs Chartered Scientist Award Kelly St. Pier 74 What Csci means to me Dr Sharon Ann Holgate 76

ANS Meeting and Reports 77 ANSScientificmeetingApril2013

Journal Review The Neurodiagnostic Journal Susan Brenan 85

Charity News Illona Sempers 88

Notice Board The ANS Council 2013-2014 92 Future Meetings 95


JOURNAL OF THE ASSOCIATION OF NEUROPHYSIOLOGICAL SCIENTISTS videotelemetry... · unimed prizewinner undergraduate ... journal of the association of neurophysiological scientists ...

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