Phase 2a David Gregg David Stewart-Watson The Peer Teaching Society is not liable for false or misleading information…

Phase 2a

David GreggDavid Stewart-Watson

The Peer Teaching Society is not liable for false or misleading information…

Two questions to ask in neurology:1.Where is the lesion?2.What is the pathology?

Weakness can be due to any location along the nervous pathway – what possible locations are there?


Muscle•Cushing’s syndrome, thyroid disease, hyperparathyroidism, influenza, myositis, dermatomyositis, sarcoidosis, sarcoma

Neuromuscular Junction•Myasthenia gravis, Lambert-Eaton myasthenic syndrome, Clostridium botulinum infection

Peripheral Nerves (mono, multiplex, poly)•Carpal tunnel syndrome, trauma•PAN, SLE, RA, herpes zoster, HIV, sarcoid, DM, amyloid (multiplex)•Guillian-Barre syndrome, PAN, SLE, RA, CIDP, DM, renal failure, amyloid, Vitamin B1/6/12 deficiency

Spinal nerve root•Infection, prolapsed disc, spinal stenosis, spondylosis, tumour, vertebral fracture dislocation

Anterior horn cell•Motor neruone disease, polio

Spinal cord•OA, HIV, TB, MS, sarcoid, RA, Paget’s, trauma, prolapsed disc, tumour, subacute degeneration of the spinal cord, MND

Cerebral hemispheres•MS, Stroke, TIA Meningitis, encephalitis, HIV, malaria, TB, sarcoid, SLE, Wilson’s disease, tumour,


Possible Sites

1. Myasthenia gravis2. Carpal tunnel3. Guillian-Barre syndrome4. Spinal nerve root lesion5. Motor neurone disease6. Spinal cord compression (+ cauda equina)7. MS8. Stroke (+TIA)


PathophysiologyIn normal muscle, the amount of Ach released with each AP decreases with repetitive activity, thus the magnitude of each end-plate potential falls. In MG, anti-Ach antibodies have taken out Ach receptors. This means that the decreased amount of Ach released becomes insufficient to cause sufficient end-plate potential to trigger a muscular contraction.

Anti-MUSK antibodies are seen in a subsection of patients.

The thymus is hyperplastic in half of MG patients, and a thymoma is present in 15%. If someone has MG look for a thymoma, and if someone has a big thymus check for MG!


Myasthenia Gravis

Clinical Features•Painless, fatiguable muscle weakness – particularly proximal limbs, extra-ocular, bulbar and facial muscles•Wasting can be seen after many years•Respiratory difficulties can be prominent especially during a myasthenic crisis•Average 20-40 years at presentation •More women than men•Associated with hyperthyroidism, RA, SLE•Other signs and symptoms include ptosis, diplopia, voice weakening with continuous speaking and dysphagia


Myasthenia Gravis

Investigations•Serum anti-AChR; serum anti-MUSK•Electromyography (used to confirm diagnosis)•Tensilon (edrophonium) test (rarely done nowadays – risk of cardiac arrest!)•Mediastinal MR for thymoma

Course and Management•Fluctuates in severity, protracted, lifelong•Exacerbations are unpredictable, can be brought on by infections and aminoglycoside use•Emergency ventilation may be required


Myasthenia Gravis

Treatment1.Oral anticholinesterases

– Pyridostigmine is widely used, dose is determined by response– Prolongs Ach action by inhibiting cholinesterase– These help the weakness but do not alter the course of disease

1.Immunosuppressants– Used in those non-responsive to above/who relapse– Steroids are often used, azathioprine/mycophenylate are also used

2.Thymectomy– Useful in those with positive AchR antibodies, even if no thymoma. Anti-MUSK cases do less well. If a

thymoma is present, then it is also necessary

3.Plasmapharesis/IV Ig– Useful during exacerbations


Myasthenia Gravis

PathophysiologyDue to median nerve compression in the limited space of the carpal tunnel. It is not typically associated with any disease. It can be seen in hypothyroidism, DM, obesity, RA, acromegaly, amyloid and renal dialysis

Clinical Features•Patient wakes with numbness, tingling and pain in a median nerve distribution.•The pain radiates to the forearm•The fingers feel swollen but usually aren’t•Wasting of the abductor pollicis brevis develops with sensory loss in the palm and radial 3 ½ fingers•Tinel’s or Phalen’s sign may be positive


Carpal Tunnel Syndrome

Treatment1.Splinting

– Holds wrist in dorsiflexion overnight. If this relives symptoms, it is diagnostic. It can produce full recovery if used for several weeks

2.Corticosteroid injection– Helps in 70% of cases, but may recur

3.Nerve conduction studies + surgical decompression– Persistent symptoms or nerve damage requires referral for nerve conduction studies– A prolonged latency across the carpal tunnel demonstrates CTS and surgical

decompression is needed

– Weight loss helps in obese patients– CTS in pregnancy usually disappears post-partum– Other mononeuropathies occur with similar tingling and weakness distal to site of

compression (ulnar, radial, lateral cutaneous nerve of the thigh and common peroneal)


Carpal Tunnel Syndrome

• Many causes• Symptoms are easy to predict• Learn what the cranial nerves do, the lesions

at each nerve result in a deficit of that e.g• CN1 – Anosmia• CN6 – Failure of eye abduction


Cranial Nerve Lesion

• Occurs in DM, vasculitis, sarcoidosis, amyloidosis, malignancy and HIV

• Clinical picture of multiple mononeuropathies occurring sequentially or simultaneously

• Mononeuropathies are confirmed using nerve conduction

• Appropriate investigation into underlying cause (BM, inflammatory markers, serum ACE)


Mononeuritis Multiplex

Clinical Features•Commonest acute polyneuropathy•Usually demyelinating, though can cause axonal damage•Pt complains of weakness in distal limb muscles and/or distal numbness•Progresses proximally over days to weeks•Areflexia is invariable; autonomic features can occur•Follows 1-3 weeks after an infection (usually trivial)•C.jejuni and CMV are well-recognised causes of severe GBS; the organisms induce Ab responses against peripheral nerves. Similarity between epitopes on the nerves and microorganisms is thought to be the mechanism•In 20% respiratory and facial muscles become weak, sometimes to total paralysis


Guillian-Barre Syndrome

Diagnosis•Made clinically; confirmed by nerve conduction studies•These studies show conduction slowing, prolonged motor latency and/or conduction block

Course and Management•Monitoring of vital capacity and blood gases to recognise emerging respiratory muscle weakness – prolonged ventilatory support may be necessary•IV Ig reduces duration and severity of paralysis (screen for IgA deficiency due to potential for anaphylaxis)•Recovery begins within 6 weeks from outset•15% are left disabled or die


Guillian-Barre syndrome

Diabetic neuropathySeveral varieties1.Symetrical sensory – starts distally, loss of vibration, pain and temperature sensation in the feet, ‘glove and stocking’2.Diffuse painful – burning/crawling pain in the feet, shin and anterior thighs, typically worse at night3.Autonomic neuropathy – postural hypotension, GI symptoms, bladder problems, ED

Does not typically involve the motor systems at all

More common in T2DM due to long-term hyperglycaemia prior to diagnosis. Good management can largely prevent the above in T1DM.


Other Polyneuropathies

Toxic NeuropathiesCauses include alcohol, prescribed drugs, lead, plastic industry by-products, arsenic and glue sniffing

Vitamin NeuropathiesThiamine deficiency causes a polyneuropathy combined with cardiac failure. It also lead to Wernicke-Korsakoff psychosis. The commonest cause is alcohol abuse. Prophylactic thiamine is given to prevent Korsakoff’s

Vitamin B12 deficiency leads to sub-acute degeneration of the spinal cord. Sensory loss, numbness and tingling and loss of reflexes distally are the usual presenting features. Pt will be anaemic. This is an irreversible consquence.


Other Polyneuropathies

Produce a variable picture that needs nerve conduction studies to fully understand

Only one of any relevance to Phase 2 is a Pancoast tumour – an apical bronchial carcinoma which compresses the brachial plexus with consequent small muscle wasting, weakness and/or pain in the hand/arms


Plexus Lesions

• Also called radiculopathies• Due to mechanical compression of a nerve as it leaves the spinal cord• Commonest locations are C6+7 and L5+S1• Causes include:

– Osteophytic growth– Disc degeneration and lateral protrusion– Vertebral collapse – osteoporosis, infection (TB)– Tumour growth

• Clinical features are: pain, sensory disturbance, loss of reflexes, tingling and numbness that occurs in a dermatomal/myotomal distribution

• Treatment is rest and analgesia. If symptoms persist, then surgical decompression may be appropriate

• MRI is required if considering for surgery; other investigations may be indicated by history e.g. in a Pt with one of the 5 Bs that go to bone


Spinal Root Lesions

Clinical FeaturesFour broad patterns – usually merge as MND progresses.1.Amyotrophic lateral sclerosis (ALS)

– Progressive spasticity, weakness and wasting with added lower motor neurone signs and fasciculation

– Also called Lou Gehrig’s disease

2.Progressive muscular atrophy– Wasting begins in the small muscles of the hand. Fasciculation is common. Cramps may

occur

3.Progressive bulbar and pseudobulbar palsy– Bulbar describes LMN signs from the 9th, 10th and 12th CN lesions i.e. wasted fibrilating

tongue; pseudobulbar palsy describes UMN lesions of the same i.e. spastic weak palate– Presents as dysarthria, dysphagai, regurgitation and choking on fluids– Eye movements are unaffected

4.Primary lateral sclerosis – tetraparesis, pseudobulbar palsy


Motor Neurone Disease

Diagnosis•Largely clinical•Denervation (seen in all forms except primary lateral sclerosis) can be confirmed by EMG•Potential mimics include subacute degeneration of the spinal cord, syringomyelia, motor neuropathy and bulbar myasthenia gravis.

Course and Management•Survival of more than 3 years is unusual; death is often from bronchopneumonia•Symptomatic management and support (e.g ventialtion, gastrostomy) helps prolong survival•Accurate prognosis is difficult – think of Stephen Hawking!


MND

Pathophysiology•Caused my multiple demyelinating plaques due to T-cell mediated response•These heal poorly causing relapsing and remitting symptoms•Prolonged demyelination causes axonal loss and clinically progressive symptoms

Epidemiology•Commoner in Northern latitudes - ?Vit D•Migrants take risk with them; 2nd generation acquires risk of where they settled•Commoner in women


Multiple Sclerosis (MS)

Clinical Features•Presentation is usually monosymptomatic – unilateral optic neuritis, leg weakness, numbness/tingling in the limbs or brainstem/cerebellar signs•In the long term, almost any neurological sign can become part of MS due to the pathophysiology•Uthoff’s sign is the worsening of MS when exposed to heat i.e. bath•Lermitte’s sign is the ‘barber chair sign’; electrical sensation down neck and into the limbs when flexing the neck

Diagnosis•‘Dr Who disease’•2 separate lesions required disseminated in time and space


MS

CourseThree major courses1.Relapsing and remitting (80%)2.Primary progressive (20%) – from presentation there is a gradual decrease in neurological function3.Secondary progressive – R&R turning into primary progressive

There are cases of fulminant MS, where a massive demyelinating episode causes critical illness and death over the course of days


MS

Management•Non-pharmaceutical – education, PT/OT, MS nurse involvement, social services involvement, minimise disability•MS Pts with stress-free happy lives get less attacks

•Active pharmaceutical treatment include– Methylpredinisolone IV, other oral – for acute relapses, use sparingly– Interferons – prevents relapses in R&R MS– Natalizumab – reduces relapses in R&R– Other treatments are being considered, many patients are willing to into research trials– Once the disease is secondary progressive, clinical trials are the sole option


MS

AnatomyThe spinal cord runs from the medulla oblongata (C1) to the conus medulllaris (L1).

Clinical Feature•Wasted intercostal muscles, sensory loss, root pain (sensory level)•Loss of contralateral pain and temperature sensation (spinothalamic tracts decussate at cord)•Ipsilateral UMN signs•Diminished proprioception and light touch

•Depending on exactly where the cord is being compressed, all the above can be bilateral i.e. total obliteration


Spinal Cord Compression

Causes•Primary tumour – glioma, ependymoma, meningioma, neurofibroma•Metastases – the five Bs•Vertebral body destruction – osteomyelitis, osteoporosis•Trauma•Degenerative prolapse•Abscess

Management1.Spinal MRI ASAP2.Biopsy/exploration to determine nature of mass may be necessary3.Consider bloods to rule out pathologies (e.g. PSA)4.CXR useful for excluding lung primaries and TB lesions5.If malignant, give IV dexamethasone. 6.Surgery is the definitive cure; may not always be possible7.Malignancy needs an oncological input


Spinal Cord Compression

• Due to a central disc protrusion, which can be acute or chronic• Causes a syndrome of

– Bilateral flaccid paralysis – Areflexia– Sacral numbness– Retention of urine– Incontinence of urine and stool– Erectile dysfunction

– Back pain • Requires urgent MRI and surgical decompression

IF someone with back pain develops urinary retention, sacral numbness or incontinence, this is an emergency!


Cauda Equina Syndrome

PathologyA sudden event in which disturbance of CNS function occurs due to vascular disease.

This can be ischaemic (the majority) or haemorrhagic (the worst).

Ischaemic causes include arterial stenosis due to atherosclerosis, arterial occlusion due to emboli, arterial dissection, SLE, antiphosphoplip, thrombophilc states, and infections (TB, HIV)

Haemorrhagic causes include AVM, amyloid angiopathy, tumours, venous thrombosis, aneurysm and hypercoaguable states


Stroke

Risk Factors•Age – 5x more likely over 75 than 55-64•Hypertension – 7x more likely over 160/95 than 120/80•Smoking – 2x more likely•Diabetes – 2x more likely•Ischaemic Heart Disease – 3x more likely•Atrial Fibrilation – 5x more likely – use CHA2DS2-VASC•Previous TIA – 5x more likely


Stroke

Stroke SyndromesStrokes to different parts of the brain give characteristic clinical patterns. Here are some:1.Partial Anterior Circulatory Stroke (PACS)

– Higher dysfunction or partial unilateral motor/sensory defect– The addition of homonymous hemianopia to one of the above

2.Total Anterior Cicrulatory Stroke (TACS– All of higher dysfunction, partial motor/sensory defect and homonymous hemianopia

3.Posterior Occiptal Circulatory Stroke (POCS)– Any of: cranial nerve palsy, bilateral motor/sensory defect, eye movement problems,

cerebellar dysfunction– Isolated homonymous hemianopia

4.Lacunar Stroke (LACS)– 5 classic LAC sub-syndromes – pure motor stroke/hemiparesis, ataxic hemiparesis,

dysarhtria/clumsy hand, pure sensory stroke, mixed sensorimotor


Stroke

Investigations - Imaging1.CT to exclude haemorrhage2.MRI for diagnosis3.Carotid dopplers to investigate stenosis

If MRI demonstrates a stroke and dopplers show stenosis, then order CT angiogram for confirmation of stenosis.

If CT angio shows stenosis, refer to vascular MDT for stenting/endarterectomy

If MRI demonstrates a stroke but dopplers show no stenosis, order a 72 hour tape and an echocardiogram


Stroke

Investigations – Bloods1.Calcium – exclude hyper/hypocalcaemia2.U+E – exclude hyponatraemia3.LFTs – exclude mimics (i.e. acute liver failure)4.FBC – exclude polycythaemia, thrombocytopenia, anaemia5.Creatinine – exclude renal problems6.TFTS 7.Cholesterol - risk factor for stroke8.Clotting screen – exclude coagulopathy and check suitability for anti-clotting agents9.BM – exclude hypoglycaemia


Stroke

Second Line InvestigationsIf 1st line bloods and dopplers have not pinpointed a cause, consider:•Thrombophilia screen – Factor V Leiden, SLE, antiphospholipid•Blood cultures – thinking of infective endocarditis or TB•HIV test•Syphilis serology – not as usual, if appropriate from history•Homocysteine – always think of if Pt has a weird vascular presentation•Lactate•Cardiac enzymes•Haemophilia/Von Willlebrand screen (haemorrhagic only) – especially if non-HTN, non-aneurysmal and under 60. If +ve family history for any of the above revealed in basic history, go for the test in the first line.


Stroke

Management in Hospital - General1.Admit to stroke unit2.Treat BP if >220/120 (>185/115 if haemorrhagic)3.Oxygen if sats <92%4.Monitor BMS as hyperglycaemia results in poorer outcomes5.Arrange SALT assessment if any suspicion of dangerous swallow6.PT/OT input7.Prevent DVTs – keep hydrated, LMWH if immobilised >2 weeks, compression stocking8.Look out for psych problems – depression is common in old people9.Start on a statin, especially if cholesterol is high


Stroke

Management in Hospital – Ischaemic1.Thrombolysis if within 4.5 hours (NICE guidelines) – possible change due to evidence from IST-3 trial. Lots of contraindications2.Be aware haemorrhagic transformation is a risk – especially with thrombolysis3.Start antiplatelet drugs once CT was excluded haemorrhage. Aspirin is usually given for 2 weeks.4.If patient has AF or stroke was cardioembolic, oral anticoagulation is given after 2 weeks. Typically, this is warfarin


Stroke

Management in Hospital – Haemorrhagic1.Stop anticoagulants and antiplatelets2.Correct coagulation problems3.If hydrocephalus develops due to mass effect and midline shift, refer to neurosurgery for decompression/shunting.

NB: This can occur in ischaemic stroke due to oedema around infarct


Stroke

What are the modifiable vascular risk factors?

Risk Factor Action Infarction risk Haemorrhagic risk

Hypertension Treat and monitor Major Major

Smoking Stop Major Moderate

Sedentary lifestyle More activity Moderate -

High alcohol Moderate intake Moderate -

High cholesterol Statins, change diet Moderate -

AF Anticoagulate Moderate Slight

Obesity Weight reduction Probable Probable

Diabetes Good control Probable -

Severe carotid stenosis

Surgery Major risk -

Sleep apnoea Treat Moderate -


Stroke

Secondary Stroke Prevention1.Post TIA – dipyrimadole + aspirin2.Post-ischaemic stroke – clopidogrel dipyrimadole+aspirin

If intolerant to any of the above, give either dipyrimadole or aspirin in isolation

If prescribing aspirin, a PPI should be given as well.

Control BP to a target of 130/80


Stroke

• Cause sudden neurological deficit, onset is over seconds and lasts less than >24 hours

• Can be separated into anterior (carotid circulation) and posterior (vertebrobasilar circulation)

• Investigations should be tailored towards looking for future causes of stroke

• Follow the same investigations you would for a stroke • Important mimic include mass lesions (spot on CT), focal epilepsy (picked

up in history), migraines (headaches rare in TIA) and Bell’s palsy (look for forehead sparing)

• Treat any underlying conditions and reduce risk factors – 30% for TIAs become a stroke in 5 years, 15% become MIs


Transient Ischaemic Attack

ABCD2 ScoreAge >60 – score one

Blood pressure systolic >140/diastolic>90 – score one

Clinical features Speech impairment – score oneUnilateral weakness – score two

NB: Use highest, don’t addDuration <60 minutes – score one

>60 minutes – score two

Diabetes Present – score one

The higher the score, the higher the risk of stroke in the next 90 days – a score of >4 is good justification for admission. Less than that should still be followed up in the community


TIA

An 82 year old female patient wakes up with weakness in the entire right side of her body

A 56 year old patient with badly controlled diabetes has developed numbness, pins and needles in his feet over the last 6 months

A 36 year old male patient presents with increasing unsteadiness which started two days ago. Two years ago he had blurred vision in his left eye which improved considerably within a few weeks, but left him with some minor deficit. Eight years ago he had a 3 week episode of numbness in his left arm.


Exam Qs

A 72 year old man with uncontrolled blood sugar has presented with ulcers in his right foot & bilateral loss of sensation below knee

A 77 year old lady with 15 year history of hypertension is brought to A&E. She is unable to speak & cannot move her right arm & leg.

A 17 year old boy comes to the clinic with his mother. He complains of recurrent transient episodes of tingling & weakness in his left leg. You also notice his mother has swollen MCP joints & ulnar deviation in both hands.


Exam Qs

A 66 year old woman presents with fatigue, breathlessness & paraesthesia in all limbs. Examination reveals pallor, loss of position sense & impaired vibration sense.

A 40 year old man with pulmonary tuberculosis is in the second month of treatment with isoniazid, rifampicin & pyrazinamide. He complains of a burning sensation in his hands & feet. There is impaired sensation to pin prick & light touch.

A 67 year old overweight Asian woman presents with painful feet. Direct questioning revealed that she has had nocturia for the last 3 months.


Exam Qs

A 50 year old man develops sudden onset of weakness, numbness & paraesthesiae on the left side of his body. His symptoms faded gradually before disappearing 12 hours later.

A 30 year old lady presented with pain in the left eye; numbness & weakness of her right leg. 2 months earlier she had an episode of double vision in the left eye

A 40 year old lady with pain & tingling in the left hand, worse at night time when she had to get out of bed to shake the hand for relief.

A 25 year old pregnant lady with increasing muscle weakness. She also complains of double vision & drooping eye lids.


Exam Qs


Neuro-pharmacology


Case 1


Causes of Epilepsy


Types of Epilepsy Primary Generalised Epilepsy Location Related Epilepsy

20% of patients with epilepsy 80% of patients with epilepsy

Onset in childhood/teenage years Can be any age, traditionally older patients

Brain is structurally normal abnormality is in ion channels and neurotransmitters

Structural abnormality of grey matter

Examples: Childhood absence epilepsy, Juvenile myoclonic epilepsy

Example: Temporal sclerosis, Mass lesions

• Generalized Tonic-Clonic Seizure – Sodium Valproate– Levetiracetam

• Location Related Epilepsy– Carbamazepine – Lamotrigine

• Myoclonic Epilepsy– Sodium Valproate– Levetiracetam


Management

• Combined seizure(s) for 30 mins• General measure

– ABC, IV access and infusions

• Early Status– IV lorazepam, repeated after 10 mins if needed

• Established Status – Phenytoin infusion

• Refractory Status– Anesthesia


Status Epilepticus

Fits Faints

Tongue biting and incontinent Posture

Post-ictal period Prodrome

Colour change Precipitant

Stereotyped behaviours


Faints Vs Fits


Case 2


Parkinson’s Disease

• No known cause • Can be drug induced • Clinical Feature

– Bradykinesia– Tremor– Rigidity


Parkinson’s Disease

• Autosomal Dominant Neurodegenerative disease• Due to CAG trinucleotide repeat • Classical Triad

– Physical – Cognitive – Psychiatric

• Management – No Disease modifying treatment – Symptomatic management BDZ, dopamine blocking

drugs, anti-psychotics The Peer Teaching Society is not liable for false or misleading information…

Huntington’s Disease


Case 3

• Pathogenesis – Aura spreading wave of cortical depolarization and

depression – Pain due to activation of the trigeminovascular system and

sensitization

• Pain sensing structures in the Brain – Dura – Arteries (meningeal and cerebral) – Venous Sinuses – CN 5,7,9 and 10 + the Cervical nerves


Migraine

• Headache lasting 4 hours - 3 days (untreated)• At least one of:

– Unilateral– Throbbing – Moderate to severe intensity – Motion sensitivity

• At least one of:– Nausea/vomiting – Photophobia/phonophobia – Normal examination/no other obvious cause


Migraine – Diagnostic Criteria

• Treatment of attacks – Analgesics Aspirin , Paracetamol, Naproxen – Triptans sumatriptan

• Migraine prophylaxis – Anti-epileptics EG valproate– B-Blockers slow release propanolol – Tricyclics – Botulinum toxins repeated injections into scalp


Migraine - Management

• Unknown aetiology but depression is a frequent co-morbidity• Often attributed to cervical spondylosis, refractive errors,

hypertension • Clinical Features

– Mild-moderate pain – Bilateral – Features tight band, pressure behind eyes, bursting sensation

• Management – Simple analgesia – Physical ice packs, massage


Tension Headaches

• Rare condition that usually affect males 20-40 yo• Features

– Unilateral, retro-orbital pain – Autonomic activation (inc. transient Horner's syndrome) – Clusters typically last 1-2 years

• Management – Only effective management is S/C sumatriptan– Prophylaxis lithium, verapamil


Cluster Headaches


Case 4

• Aetiology – Berry aneurysms (can be associated with PKD)– AVM– Trauma/no vascular abnormalities

• Pathogeneses– 15% immediately fatal – Distal vasospasm Infarction

• Risk factors– Hypertension– Smoking

– Excess alcohol


Subarachnoid Hemorrhage


Subarachnoid hemorrhage

• Features– Thunder-clap headache – Increase ICP– Signs of meningism

• Investigation– CT– LP– angiography


Subarachnoid Hemorrhage • Management

– Bed rest – Calcium channel antagonists

• Complications – Obstructive Hydrocephalus

• Aetiology – Compression of the trigeminal nerve by a microaneurysm – In younger pt MS

• Clinical features – Knife like pain spreading from V3, usually unilateral– Episodes happen multiple times a day, with innoxious

triggers – Relapse with remission

• Management – Carbamazepine– Surgical – microvascular decompression


Trigeminal Neuralgia

• Granulomatous Inflammation of the temporal arteries

• Clinically – Scalp pain, jaw and tongue claudication – Very rare in under 50s

• Diagnosis – Raise ESR (>50)– Temporal artery biopsy

• Management – Prednisolone 60mg


Giant cell arteritis


Case 5

• Bacterial – Neisseria

Meningitides – Streptococcus

pneumoniae – Staphylococcus

aureus – TB – Leptospirosis in

older patients or occupation exposure


Meningitis – Organisms • Viral

– Most cases are viral – HIV – Enterovirus

• Fungal – Candida albicans – Cryptococcus

• Meningitic triad Headache + Neck stiffness + Photophobia

• Fever• Bacterial intense malaise, fever, petechial rash• Viral less severe and self-limiting


Meningitis - Clinical features

• Cefotaxamine (IV)• Benzylpenicillin (IM) – for meningococcal disease • LP – Shows pus, increase polymorphs, decrease

glucose• Prophylaxis

– Vaccine – Chemoprophylaxis – Rifampicin


Management

• 90% viral– Mumps– Rabies– HSV 1/2 – Often never identified

• Clinical feature – Decrease consciousness– Confusion/personality change– Seizures– Headache + fever


Encephalitis

• Investigation – MRI inflammation and swelling – EEG– LP increase lymphocytes, PCR to detect virus

• Management – If EBV acyclovir – Supportive


Encephalitis


Herpes Zoster (shingles)

• Reactivation of varicella zoster virus in Dorsal Root ganglia – Due to decrease Immunity

• Clinical features– Dermatomal – Cranial nerve only sensory, particularly 5 and 7 – Post-herpic neuralgia

• Management – Acyclovir


Herpes Zoster (shingles)


Case 6

• Direct effect • Raised ICP• Seizures • Investigation

– CT/MRI– Look for Primary CXR, CT, PET– Biopsy


Clinical Features


Secondary Brain tumours

• Arise from: Bronchus Breast Stomach Prostate Thyroid Kidney

• 50% of all brain cancers

• Malignant tumour of neuroepithelia

• Astrocytoma • Oligodendromas


Glioma

• Usually slow growing and not malignant

• From arachnoid


Meningioma

• From Schwann cells • Affect vestibulocochlear

nerve, can affect facial nerve is large


Acoustic Neuroma

• Dexamethasone decreases oedema• Antiepileptics prevents seizures • Surgery complete excision or de-bulking • Radiotherapy • Intra-thecal chemotherapy


Management

• From direct or hematological spread• Causative organisms

– S. Aureus; S. Pyogenes; anaerobes; gram –ve

• Features – Fever– Focal neurology– Seizure

• Treatment– Cefotaxime + flucloxacillin + metronidazole


Brain Abscesses


Brain Abscesses


Intra-cranial Haematomas • After head injury – briefly knocked out

then normal before deteriorating • Features – decrease consciousness,

fixed, dilated pupil; focal neurology • Treat with craniotomy

• After head injury – often trivial• Associated with old age and alcoholism • Feature headache, drowsiness, confusion• Advances to focal signs and decrease

consciousness• Management – drainage by burr hole

• a. Two other causes of seizures • b. Two types of generalised seizures• c. Two drugs for generalised seizures • c. Two things to inform him of driving


Exam Questions – Epilepsy

• a. How long do you wait for LP and why? • b. Why take 3 samples of LP • c. What pathological structure causes SAH? • d. Circle of Willis anatomy • e. Why headaches pre-SAH


Exam Questions – SAH

• 53 yo F presents with headache, fever, photophobia. O/E nuchal rigidity. Lumbar puncture demonstrates gram +ve cocci. Which organism?

• a. N meningitidis • b. Listeria monocytogenes • c. E coli • d. Strep pneumoniae • e. Strep agalactiae


Exam Questions – meningitis

• a. How long do you wait for LP and why? • b. Why take 3 samples of LP • c. What pathological structure causes SAH? • d. Circle of Willis anatomy • e. Why headaches pre-SAH


Exam Questions – SAH

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