Introduction to EEG, EMG- NCV Jose Paciano Reyes, MD, FPNA ASMPH
Dec 31, 2015
Introduction to EEG, EMG-NCVJose Paciano Reyes, MD, FPNAASMPH
ElectroEncephaloGraphy
What is EEG?Non-invasive recording of brain electrical activity from electrodes placed on the scalp
Uses of EEG in epilepsyEvaluation of suspected epilepsyPresence of electrographic seizure activity during a behavioral disturbance that could represent a seizure establishes the diagnosisMay detect interictal epileptiform activity
Classification of seizure disorderPetit mal: episodic generalized 3 Hz spike-and-wave activityComplex partial seizures: focal epileptiform discharges
Uses of EEG in epilepsyAssessment & prognosis of seizuresNormal EEG implies a more favorable prognosis for seizure controlManagement of status epilepticusMonitor seizure activity in patients who have received neuromuscular blocking agent or on pentobarbital-induced coma
Diagnosis of non-convulsive status epilepticus or absence status epilepticus
Other uses of EEGDetection of structural brain lesionsDiagnosis of neurologic disorders Herpes simplex encephalitis repetitive slow wave complexes over temporal lobes Creutzfeldt-Jakob disease or SSEP periodic complexes in a patient with an acute dementing disorderEvaluation of altered consciousness
How does it work?Sum of excitatory postsynaptic potentials (EPSPs) & inhibitory postsynaptic potentials (IPSPs)EEG rhythm depends on thalamic pacemaker cells and the reticular activating formation
1/3 of the cortex can be seen by scalp electrodesAt least 6 cm2 of cortex must be involved to be detected by surface electrodes
Excitatory Synaptic Potentials &Spike Generation0mV-60-70ThresholdResting potentialEPSPEETime
Interaction of Excitatory & Inhibitory Synapses0mV-60-70ThresholdIPSPEETimeI
The main generators of the EEG are voltage gradients along dendrites in the upper cortical layers. This in turn causes a current flow in the conducting medium surrounding it. Several thousands of parallely oriented neighboring dendrites have to be active synchronously to produce a measurable signal.The summed activity within a small area of cortex can be described by a so-called dipole.
How is it done?10-20 System
How is it done?
How is it done?MontagesBipolarLocalizes potential by direction of pen deflection (phase reversal)Distorts shape and amplitude
ReferentialLocalizes potential by amplitude of pen deflectionPotentials at the reference electrode may appear in all channelsInterelectrode distance alters amplitude
How is it done?Activation proceduresHyperventilationNormal: generalized slowing (3 5 min)Elicits 75% of absence seizuresPhotic stimulationNormal: occipital driving at stimulus frequency or no responsePhotoconvulsive response
EEG abnormalitiesAmplitudeDecreased generalized activity (hypoxia, hypothermia)Decreased alpha (mild metabolic disturbances)Decreased focal activity (stroke, tumors)Increased beta (hyperthyroidism, benzodiazepines)FrequencyGeneralized asynchronous slow waves (anoxia)Focal slow wave(stroke, tumors, multiple sclerosis)
Epileptiform dischargeSpikesSharp waves
EEG and consciousness
EEG of an 8 year old girl with uremia and in coma
ElectroMyoGraphy, Nerve Conduction Studies
ANerve terminalAxonMuscleNa+CholineBAcCoA + CholineChATAChAchATP, PAchATP, PAChCa2+Nicotinic ReceptorsAchesteraseCholineAcetatePresynapticreceptors
Neuromuscular Junction
Neuromuscular Junction
What is EMG-NCV?Technique in the diagnosis of myopathic and neurogenic disordersAssessment of neuromuscular transmissionAssessment of peripheral nerve and root disorders (diffuse neuropathy, focal lesion, evaluate severity of nerve injury)An extension of the neurologic examination
Uses of Nerve Stimulation StudiesDetermine whether sensory symptoms are caused by a lesion proximal or distal to the dorsal root ganglionDetecting subclinical involvement of other perpipheral nervesDetermine site of a focal lesion and prognosis Distinguish between polyneuropaty and mononeuropathy multiplexFollow progression of peripheral nerve disordersIndicate predominant pathologic change demyelinating vs axonal neuropathies
Uses of ElectromyographyDetect disorders of the motor units and can indicate the site of the underlying lesion (anterior horn cell, spinal root, plexus, peripheral nerve)Recognition of neuromuscular disordersProvide a guide for prognosis
How is it done?Motor Nerve Conduction StudiesRecording the electrical response of a muscle to stimulation of its motor nerve at two or more points along its course.Compound muscle action potentialLatency, amplitude, nerve conduction velocity
How is it done?Sensory Nerve Conduction StudiesRecording the electrical response of a sensory nerve to stimulation at one or more points along its course.Sensory nerve action potentialLatency, amplitude, nerve conduction velocityOrthodromic, Antidromic
How is it done?MV or uV00msec1st latency2nd latency1st amplitude2nd amplitude
Nerve Conduction StudiesF-waveMeasure in any motor nerveSupramaximal stimulusAntidromic conduction, measure reflected impulseNo synapseTests entire length of motor nerveSlower than H-reflexVery early finding in GBSH-reflexNeurophysiologic counterpart of the ankle jerkSeen only calf muscles in adultsSubmaximal stimulusStimulate IA afferent sensory nerveInvolves a synapseRepresents nerve conduction velocity near cordFaster than F-waves
How is it done?Electromyography - Activity at RestInsertional ActivityCrisp burst of activity as needle entersIncrease with denervation or irritationDecreased when muscle is replace by fat or connective tissueFibrillation potentials positive sharp wavesMuscle fiber irritabilityFasciculation potentialsSpontaneous activity of motor units
How is it done?Electromyography - Activity During Voluntary Muscle ContractionMotor Unit PotentialsRecorded with minimal muscle contractionAmplitude (0.5 5.0 mV) decreased in myopathy and increased with reinervation and axonal sproutingDuration (5 14 msec) decreased in myopathy and increased with renervation Polyphasic in myopathy and renervation
How is it done?Electromyography - Activity During Voluntary Muscle Contraction
Interference PatternRecorded during maximal muscle contractionDecreased recruitment seen in neuropathic processIncreased recruitment seen in myopathic process
ElectromyographyEndplate activityNormal spontaneous finding near endplateOcean surf soundFibrillationsPositive sharp wavesNerve potentials
ElectromyographyPositive Sharp WavesMonophasic downward (positive) deflectionDull thuds, like rain on tin roofDuration: 4 20 msecAmplitude: 50 - 4000 mVIndicate denervation or myopathy
ElectromyographyFibrillationSpontaneous firing of single muscle fiberDiphasic with initial downward (positive) deflectionSounds like crisp ticsDuration: 0.5 3 msecAmplitude: 50 - 200 mVIndicate hypersensitivity of muscle to Ach or axonal injury or myopathy10% of normal muscles have areas of fibs
ElectromyographyFasciculationSpontaneous firing of single motor unit action potentialLarge deflectionsUsually occur with proximal lesions like those of the nerve root or anterior horn cellsOccur in 15% of normal population
ElectromyographyMyotonic PotentialsSpontaneous discharges that wax and wane in frequency and amplitudeDive bomber soundIndicate myotonic disorders and periodic paralysisResolve in true myotonia
ElectromyographyGiant MUAPsMUAP > 5 mV during active contractionIndicate renervation with axonal sprouting and chronic changes
ElectromyographyActiveSmall, short duration CMAPIncreased recruitmentDecreased interference pattern amplitudeFibrillationsPositive sharp wavesChronicDecreased CMAP amplitudeDecreased insertional activityNo fibrillations or postive sharp waves
Myopathic pattern
Axonal Degeneration vs. Segmental Demyelination: Electrophysiologic Features Axonal Degeneration Segmental DemyelinationMotor Nerve Conduction StudiesCMAP amplitudeDecreasedNormal (except with CB)Distal latencyNormalProlongedConduction velocityNormalSlowConduction blockAbsentPresentTemporal dispersionAbsentPresentF waveNormalProlonged or AbsentH reflexNormalProlonged or Absent
Axonal Degeneration vs. Segmental Demyelination: Electrophysiologic Features Axonal Degeneration Segmental DemyelinationSensory Nerve Conduction StudiesSNAP AmplitudeDecreasedNormalDistal latencyNormalProlongedConduction VelocityNormalSlowNeedle EMGSpontaneous ActivityFibrillationsPresentAbsentFasciculationsPresentAbsentVoluntary Motor Unit PotentialsRecruitmentDecreasedDecreasedMorphology Long duration/polyphasicNormal
NCV FACTSReinervation begins 1-3 weeks after injury, progress at 1 mm/day and EMG evidence is not seen for weeks or monthsAfter trauma, neuromuscular transmission fails before NCV changeSensory NCV preserved > motor NCV
NCV FACTSMotor nerves degenerate faster than sensory nervesSensory nerve NCV change little as nerve degeneratesLesions proximal to the dorsal root ganglion causes loss of sensation but normal NCVsTerm infant NCV is half of adult NCV
EMG FACTSEMG evidence of denervationMay not be present for up to 3 weeks post-injuryPositive sharp waves typically appear 8 days post-injuryFibs appear 14 days post-injury
Evoked Potentials
Evoked PotentialsSpinal or cerebral potentials evoked by noninvasive stimulation of specific afferent pathways Test functional integrity of the pathway but do not indicate nature of the lesionSmall responses thus responses to a number of stimuli are recorded and averaged (with a computer)
Types of evoked potentialsStimulus modalityVisual evoked potentials Auditory evoked potentialsSomatosensory evoked potentialsMotor evoked potentialsEP originCorticalSubcorticalBrainstemSpinalBrachial plexusCauda equinaSensory nerveRecording siteScalpNeckClavicularLumbosacral
Visual Evoked PotentialsMonoocular visual stimulation with checkerboard pattern used to elicit VEPRecorded from midoccipital region of the scalp
Visual Evoked PotentialsP100 responsePositive peak with latency of ~100 msPresence and latency noted
Brainstem Auditory Evoked ResponseMonoaural stimulation with repetitive clicks used to elicit responseRecorded at the vertex of the skull
Brainstem Auditory Evoked ResponseSeries of potentials recorded 10 ms after auditory stimulus represent sequential activation of structures in subcortical auditory pathway
Brainstem Auditory Evoked ResponsePresence, latency and interpeak intervals of first five positive potentials at vertex are noted
Brainstem Auditory Evoked ResponseWave I - acoustic nerveWave II - cochlear nucleusWave III - superior oliveWave IV - lateral lemniscusWave V - inferior colliculus
Brainstem Auditory Evoked ResponseMost waves are generated by more than one anatomical structure and each structure may contribute to more than one waveWave I III conduction through lower brainstem (medulla to pons)Wave III V conduction through upper brainstem (pons to midbrain)
SomatoSensory Evoked PotentialsElectrical stimulation of a peripheral nerve is used to elicit somatosensory potentials recorded in the scalp and spine
N9: brachial plexusN13: lower medullaN20: somatosensory cortex
Clinical uses of EPsDetection of lesions in mutiple sclerosis and other CNS disorders (neurosyphilis, AIDS, vitamin E or B12 deficiency)Assessment of prognosis after CNS trauma or hypoxiaIntraoperative monitoringEvaluation of visual or auditory acuity (specially in patients who cannot cooperate in behavioral testing due to age or mental incapacity)
Cortical SEPStudies done during intra-operative monitoring for carotid endarterectomy