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