1. God protect usElectrodiagnosis text reviewPresented by: S.Sadeqi MD , PM&R res. SBUMC Jan-feb 2013Sadeqi.shahram@gmail.com

2. Dumitru Chap.9 Delisa Chap.4 kimura 3. Historical aspects Anatomical basis Nomenclature InstrumentWaveform Technique VEP ABR Clinical usage 4. oRichard caton o1875 oVEP oEEG oABR 1891Avraging BeckTime locked ABREvoked 5. Dorsal column Lemniscal sys Dorsal root gangilia 6. Gracillis Cuneatus 7. Medial lemniscus VPL 8. Thalamocortical fibers SS cortexSpinomedullothalamic Nucleos ZVPL 9. homunculus 10. nomenclature AESstandarde electrode site waveform morphologic nomenclature instrumentation parameters recording practices interpretive qualifications reference data collection 11. Cephalic VS noncephalic montage 12. Scalp l0-20 International System (I) electrode sites are located on the scalp by using measurements based on a percentage of the skull's size with respect to standard landmarks (usually 10 or 20%) and not absolute distances (2) the entire skull is represented in the system (3) Electrode sites are labeled according to assumed cortical structures over which the electrodes are placed. After 6 months of age a full electrode complement usually canbe applied 13. Four standard landmarks are required to locate allpositions necessary for SEP purposes 14. Cz C3 and C4C3' and C4 FpZ Fz FpZ' 15. Upper Limb Stimulation Erbs point (EP1/EP2)2-3 cm superior to the clavicle and just lateral to the clavicular head of the sternocleidomastoid muscleThe Erb's point electrode defined asE-l is ipsilateral to the stimulated limb 16. Cervical Spinous Process C2S C5S C7S REF:FPZ 17. Montage for upper limb SEP Ch1: scalp electrode (C3' or C4') Ch2: C3' or C4 Ch3: CS5 or C2S (C7S) Ch4: ipsilateral EPmidfrontal region FpZ contralateral EP scalp's FpZ contralateral EP 18. Lower Limb Stimulation Popliteal Fossa EI electrode located over the tibial nerve approximately 4 cmproximal to the popliteal crease midway between the tendons of the semimembranous/semitendinous muscles medially and the tendon of biceps femoris laterally PF The E-2 electrode is usually placed on the medial surfaceof the knee. 19. Thoracolumbar Spinous Processes L3S or L4S E2: 4cm rostral or on controlateral Iliac crest Calculate the interval between PF and L3S, yielding the conductiontime from the knee to the cauda equina region It may be clinically relevant to obtain this potentia] in patients suspected of having peripheral nerve lesions. 20. T12S or L1S E2: placed 4 cm rostral to this location or CL iliac crest It is important to note that both of these spinal electrodes can beused for both left and right lower limb stimulationsIt is important to recognize that the lumbosacral spine potentialsmay normally be unobtainable in older or obese persons, and at times in healthy young individuals; hence absence of the response should not be considered abnormal. 21. Scalp for lower limb SEP 2 cm posterior to the vertex of the skull (CZ) utilizingthe 10-20 system and is called CZ The same E-2 , FpZ', as that used for upper limb 22. Montage for lower limb SEP CH1: CZ' referenced to FpZ CH2: TI2S or LIS referenced to the electrode 4cm superior to this location or the iliac crest CH3: L3S or L4S referenced to the electrode placed 4 cm rostral to this location or the iliac crest CH4: PF to medial knee 23. Montage for 2 channel set Upper limb: CH1: (C3' or C4') refrenced to EP CH2: C2S (C5S or C7S) referenced to FpZ'Lower limb: Para spinalis noise :/ 24. Another possibility may be to forego the PF and one of the spine sites, e.g., L3S. If the spinal potential is normal, PF is of questionable value. Of course, if there is an abnormality in the spinous process electrode chosen, it is then necessary to explore the possibility of a peripheral nerve versus plexus lesion. In this case, the needle electromyographic examination is the procedure of choice in delineating the lesion and not the SEP. 25. SEP WAVEFORMS Polarity Peak nomenclature AES N20/N30 Peak latency Inter peak latency 26. Peak latency A recommended practice is to always perform two separate trialsof each response to ensure reproducibility. averaged trace obtained in the absence of a stimulus alternate the polarity of the stimulator during data collection Rotating the anode about the cathode 27. Final solution 28. Inter peak latencyimpulse's time of propagation between recording sites central conduction time EP and PF are the markers of peripheral nerve function 29. Amplitude measurment side-to side amplitude differences of 50% or more areconsidered indicative of a possible abnormality. It must be recognized, however, that normal persons can have considerable side-to-side amplitude differences, approaching 80% or moreBase to peak VS peak to peak maxima of consecutive SEP peaks of opposite polarity mixing apples and oranges 30. WAVEFORM MORPHOLOGY the shape of SEP waveforms is not heavily weighed in the criteria to decide if a particular waveform should be described as abnormal 31. SEP INSTRUMENTATION 32. ELECTRODES Silver Gold Tin Platinumstainless steel stainless steel Platinum mixed with another metal 33. Skin preparation It is generally accepted that abrasion is considered sufficient when the impedance measured across two such electrode preparation sites is between 1000 and 5000 ohms . Short period 1-2 hr Longer than 2hr 34. So which one is better? Needle or surface? needle electrodes can have higher impedances than surface electrodes.Once the skin is abraded sufficiently, an impedance of 2000 can easily be achieved with surface electrodes. Needle electrodes usually have impedances greater than 3000 and can even reach 10,000-13,000 risk of infection Discomfort higher electrical noise ease of pulling out 35. Concerns regarding contamination with the HIV and the hepatitis virus are similar for both needle and surface electrodes.Any electrode, surface or needle, potentially exposed toCreutzfeldt disease or other possible slow virus disorders should be safely and immediately discarded. 36. In the only study to compare scalp recorded SEPs utilizing surface and needle electrodes, no statistically significant difference was detected between waveform latency and amplitude.. . . So; use needle electrodes only on the scalp and place surface cup electrodes at all other recording locations. 37. STIMULATING ELECTRODES stimulus pulse of 200--300 S Duration Sensory threshold is defined as the current intensitywhen the patient first describes a sensation resulting from the stimulating pulse. Raising' the current intensity to 2.5-3.5 times this value, given patient tolerance, should suffice in producing a clearly defined sensory SEP. A moderately vigorous twitch 38. Suboptimal stimulus delivery delayed arrival smaller amplitude Unexpected morphologyA good judge of an adequate stimulus for mixed nervestudies is observing an adequate muscle twitch 39. Analysis time: UL: 50 ms 20 HZ 5 HZ 5.1 LL: 100 ms 10 HZ 2-3 Hz 2.8 In both upper and lower limb investigations, the rate of stimulation should not be an integral of 60 Hz so as to minimize recording this common environmental noise 40. 60 HZ signal resonance 41. Resonance! : 42. Notch filter 43. Averaging To improve S/N ratio To have good signal analysis , in theory the time sampling rate must be at least twice the highest frequency of the EP signal that is to be recorded. 44. Be ware of events that are not directly triggered by stimulus, but repaeted or time locked signals: Line current noise Regular brain wave rhythm Stimuls induced filterAmplifier ringing Myogenic synchronous movements 45. FACTORS AFFECTING THE SEP 46. PATIENT COOPERATION PATIENT HEIGHT AGE GENDERTEMPERATURE MEDICATION SLEEP 47. Height When considering central conduction times for median nerveexcitation, N13 to N20 inter-peak latency, there appears to be little correlation with arm length or height The lumbar N20 to cortical P37 (P40 as designated by some authors) inter-peak latency (central conduction time) for tibial nerve stimulation, however, is correlated with an individual's height 48. Age Cortical SEP Amp : U shaped curve Spinal SEP: infant> the others Unlike age-related amplitude effects, the correlationbetween age and conduction time (conduction velocity) is less clear. peripheral nervous system initially demonstrates slow conduction velocities until about 4 or 5 years of age, at which time adult values are achieved Adult SEP conduction values are usually achieved between 5 and 8 years of age 49. A final consensus regarding the effects of aging on central conduction is not yet at hand, but there appears to be a small central conduction velocity declinein persons over 60 years of age.0.3 ms/yr 50. gender prolongation of potential latencies in menThe central conduction time appears to bear norelationship to the gender of the subjec sex 51. Enviro. Temp. Surface temperature of the upper limb at or proximal to the siteof nerve stimulation should be maintained at 32C or more, while the lower limb should be approximately 30C or higher Central core temperature is subject to less fluctuation withrespect to emotional or environmental conditions omeasuring latencies in patients with fevers (38.0-39.7C) andagain following fever resolution. oNo significant latency changes were noted in these patients Over 42 c: no obtainable SEP Below 29: amp dec. And pro L. 52. Medication Phenobarbital : no effect Phenytoin: Latency prolonged. AMP fix CMZ and pirimidone: no effect Diazepam: no effect, hypnotic effect, dec. Muscle artifact the volatile agents in high concentrations such as the halogenatedhydrocarbon inhalation agents (halothane, enflurane, and isoflurane) produce an increase in cortical potential latencies in addition to a reduction in cortical potential amplitudes and central conduction time us prolonged. 53. These effects are countered by employing a balancedanesthesia technique that uses a strong narcotic in addition to a muscle relaxant plus a weak anesthetic like nitrous oxide or low concentrations of isoflurane. 54. sleeeeeeeepIn general, sleep tends to reduce the amplitude andincrease the latencies of recorded SEPs 55. Far field and near filed potentials 56. Kimuras rail road 57. Size changes producing farfield potentials. 58. SEP waveform neural-generators 59. Spinal pathway In patients with multiple sclerosis presenting with alterations in vibration and proprioception, namerow found that these individuals had abnormalities of their SEPs in proportion to the clinical loss of these particular clinical modalities (proprioception and vibration). 60. in persons with clinical evidence of thalamic pathology, the SEPs were clearly abnormal, whereas those patients with brain stem lesions not involving the lemniscal fibers had normal SEPs.dorsal columns impulses generating the SEP. 61. Good correlation was obtained between the clinicalexamination and abnormal SEPs, implying that the SEP directly correlated to both the dorsal column pathway and the modalities of vibration and proprioception. 62. Upper limb SEP EP: N9/10 Plexus it is absent in patients with lesions of the brachial plexus but presentin patients with cervical root avulsionsMotor fibers are involved, too! 63. Upper limb SEP C2s, C5s, C7s N11: dorsal root E.zone DCV The refractory period of this waveform is shortHypothermia studies demonstrate an increase of the waveform'samplitude similar to that found in peripheral nerves 64. Upper limb SEPN13: Stationary pot. relatively long refractory period, suggesting the involvement ofsynaptic transmissioncervical cord's dorsal gray matter 65. Upper limb SEPN13a: dorsal gray of the cervical cord N13b: cuneatus N. hypothermia reduces the amplitude of this waveform, suggesting that synaptic transmission is involved in its production 66. Upper limb SEPN14: Medial lemniscus N13 and N14 peaks likely represent generators below and above the foramen magnum. 67. Upper limb SEP 68. Upper limb SEPScalp: N19/20 N18: thalamus Various lesions in patients with thalamic pathology support theview that the l8-ms negative peak is associated with the thalamus or its projections to the cerebral cortex. 69. Lower limb SEPPF N7-10 70. Lower limb SEP Third Lumbar Vertebra N17-21 A short refractory period suggests that synaptic relays are notassociated with the propagation of this wavefront from the lower limb to the thoracic aspects of the spinal cord.cauda equina 71. Lower limb SEP Twelfth Thoracic Vertebra N22Long refractory period: 6-10 ms Synaptic transmissiondorsal gray's interneuronal population of cells associated with the root entry zone of the tibial nerve's compartment fibers in the caudal portion of the spinal cord 72. Lower limb SEP Farfield satationary P. On T12 level at N22 73. Lower limb SEP Second Cervical Potential N29 Stationary potentialsoA rather long refractory period is noted for this cervicalpotentiaInucleus gracilis 74. Lower limb SEP Scalp P37/N45The amplitude of the cortical waveform is slightly largerover the ipsilateral scalppostcentral gyrus area of the cortex 75. Lower limb SEP 76. Contravercy! neural generators Variability of latencies and amplitudes reference data Appropriate applications 77. SEP Techniques 78. 1- Stimulating of mixed peripheral nerve and recoding from spine and scalp 2- Stimulating a pure sensory nerve (Segmental SEP) * 3- Dermatomal SEP, not involving nerve trunk ** Beacuse of very low Amp.Response in the 2nd and 3rd categorySurronding muscles and inviromental noise Only scalp recording be performed segmental stimulation results in more easily obtainable and somewhatlarger responses than dermatomal SEPs, as more nerve fibers are excited. 79. Mixed nerve SEP median nerve1- Erb point: N10 2- C2S, C5S, C7S : N13 3- Scalp: N20 Analysis time : 50 ms Between 300 1000 Av. 80. Central conduction time (N 13-N20 latency) demonstrating a mean conduction time of 5.6 ms EP = 0.086H + 0.038A - 5.88 for men EP =0.054H + 0.03A - 0.59 for women N13 = 0.099H + 0.045A - 4.98 N13 = O.064H + 0.035A + 0.78for men for women N19 = 0.095H + 0.049A + 1.19for men N19 = 0.085H + 0.043A + 2.72 for women 81. Mixed nerve SEP ulnar nerve Identical recording sites are used for the ulnar nerve asthose for the median nerve. smaller response than median N. . 82. Alternate recordings Between humeral epicondyles Ulnar groove or olecranon 83. Segmental sensory SEP sensory threshold : 3-4 A *2.5-3.5 = 6-12 A no muscle twich difficult recording over erb and spineCentral amplification 84. Upper limb segmental SSEP1. Median: first 3 digit 2. Ulnar: 5th digit 3. SRN : 2cm proximal to radial styloid4. LAC: 2cm lat. To BB tendon, 2 FB below anticubital crease:injury to MC nerve or C5 root 85. LOWER LIMB SEPs 1- mixed nerve 2- segmental SSEP 3- dermatomal SSEP lower limb dermatomal and segmental studies are somewhateasier to perform than upper limb segmental SEPs because lower limb cortical waveforms are usually larger. 86. Tibial Nerve mixed SSEP Stimulation on : 1- medial malleolus 2- PF Recording sites ; 1- PF: as the marker for peripheral nerve function 2- L3s/L4s: quada equina 3- T12/L1: most quadal portion of the cord N22 4- Scalp P37 87. N22 = 0.174(H) + 0.076A - 9.2525 N22 = 0.1619H + 0.0694A - 7.5235for men for womenP37 (40) = 0.199H + 0.0852A + 3.8025for M P37 (40) = 0.2222H + 0.5995A + 1.1210 for W N22/P37 = 0.944H + 0.0233A - 0.2730 N22/P37 = 0.0943H + 0.0425A - 0.2076for M for W 88. Alternaive recordings When stimulation on PFRecording from sciatic N. E1: on sciatic notch E2: greater trochanter Fpz spinal cord conduction time bilateral tibila nerve st. Be needed C7s- 89. LOWER LIMB SEGMENTAL SOMATOSENSORY EVOKED POTENTIALS Sural : between lat. Malleolus and achilles SPN: between the middle and lateral thirds of this imaginaryLine Connecting the medial and lateral malleoli Saphenous: 1 FB anterior to med. Malleolous A second site of stimulation is in the groove formed by the medial aspect of the tibia and the medial gastrocnemius. lateral femoral cut. N. : 12 cm distal to ASIS 90. The clinical utility of both segmental and dermatomal studies isunclear :| and the relative value of either compared with the other is also unknown :| 91. DERMATOMAL SOMATOSENSORY EVOKED POTENTIALSThe techniques to record dermatomal SEPs are relativelystraightforward. Considerable latency (up to 8-9 ms) and amplitude (80%)side to side differences can occur in normal persons 92. L5 dermatomal SEP omedial aspect of the first metatarsophalangeal joint oon the dorsum of the foot between the first and second digitoon the dorsum of the foot surrounding the first metatarsophalangeal jointStimulation: pulse duration of 200 s cathode should be located at either the level of the first metatarsophalangeal joint along its medial aspect rate less than 5 Hz 2 and 3 times the or in the sensory threshold web space between the first and second digit in the foot 93. Recording: as other lower limb SSEP E1 on CZ E2 on Fpz 100 ms (sweep of 10 ms/div) combined with 500 to 1000 averagesP40 = 8.3 + 22.4 (Height) + 0.086 (Age) 2.7 ms 94. S1 Dermatomal SEP lateral margin of the foot at the fifth metatarsophalangeal jointP(40) = 8.6 + 24.0 (Height) + 0.038 (Age)2.9 ms 95. one obvious limitation of the dermatomal response Only one recording site No peripheral recording site Either peripheral or central pathology in Abnolrmal SSEP 96. Miscellaneous SEP techniques 97. PUDENDAL NERVE SEP S2,3,4 SNS: T12 and upper lumbars * PNS: S2-4 : Ant. Spinal nerve root : hypogastric plexus Sensory afferent : dorsalis penis/clitoris Motor: anal sphincter oUrinary Control oBowel Control oSexaul Responsiviness oPenile ErectionoEjaculation 98. Stimulation: on the shaft of penis cathode proximal 200 s 2-3 times folded sensory threshold 5 HzRecordingScalp: CZ refrenced to FpZ Spine: L1s : usually in M, rarely in W 99. Clinical use Anal sphincter manometric abnormality W/O structural defectImpotence or orgasmic or gynecologic disturbbances Scaral plexus continuty Sacral level radiculopthies Metabolic Dis. Affecting bowel/bladder or sexual functionUnexplained perineal numbness or pian CNS cause of anorectal dysfunction: MS,QE,SCI,ALS Probable PN injury in pt. With Hx of pelvic surgery Neuromyopathic/myopathic process affecting continence 100. more common etiologies of recurrent/chronic traction (partial) injuries to the pudendal or perineal nerve distal motor branches (which innervate the perineum and anus) are Prolapse 2. dyschezia 3. Multiparity 4. forceps delivery 5. increased duration of the second stage of labor 6. a third-degree perineal tear 7. high-birth-weight children 8. prior pelvic surgery 9. chronic straining from constipation 10. the aging process. 1. 101. Normal values biphasic: pos-neg Pos: 37-45ms (P1 peak ) Neg: 48-60 ms (N1 peak )Peak to peak : 1.25-5 V for men Women are usually smaller The P1 (onset ) latency for the PN-SEP is generally 6-10 mslonger than that from the peroneal nerve response from knee level stimulation. 102. Trigeminal Nerve SEP sensory receptors trigeminal (semilunar, gasserian) ganglion dorsal trigeminothalamic tract both ipsilaterally and contralaterally to the (VPL) postcentral gyrus 103. Stimulation: cathode is in contact with the angle of the mouth anode is rested on the lower lip pulse of 200 s ,2-3 times sensory threshold ,2-3 Hz stimulus artifact 104. Recording: Only one channel, scalp triphasic with an initial negative deflection C5' for left and C6' for right trigeminal nerve stimulation 2 cm posterior to the line bisecting the ears and 10% of the total coronal distance superior to the tragus region 105. Medial/lateral Plantar And Calcaneal Nerves the medial and lateral plantar responses should be obtained in allnormal persons, the calcaneal nerve response may be absent because of too much impedance on the heel. 106. Clinical uses of evoked potentials Coma Evaluation Traumatic myelopathic evaluation Intraoperative Monitoring Sleep DisordersBrain death CVA MS 107. Coma Evaluation GSC Brain stem reflexes creatine kinase BB band levels in the cerebrospinal fluid(CSF-CK) 108. median SEPs have the strongest evidence to suggest their utilityin predicting outcome after coma. 1.5 times the motor threshold is used.The strongest indicator of a poor prognosis is a bilateralabsence of the short-latency cortical response with median nerve stimulation.Absence of a response is often defined as potentials less 0.5 V . 109. $$$$$ Live or died $$$$$ A: normal healthy person B: went to glory! C: absolutely wana live 110. Absolute peak latency, interpeak latency, and amplitude of the short-latency cortical responses have not been shown to have a strong prognostic significance.Pitfalls: Peripheral nerve, cervical spine, and brain stem 111. SensitivityVS Specificity Avoiding falsely predicting nonawakening correctly predicting nonawakeningFatality rate in BACR among below main categories: Hypoxic-Ischemic Coma (Adults): 100% died or PVS Coma Due to Intracranial Bleed (Adults): 99% Traumatic Coma (Adults) : 95% adults in coma due to nontraumatic causes with BACRs tomedian-nerve stimulation have a very poor prognosis for awakening 112. Traumatic myelopathic evaluation Chance to return: clinically incomplete lesions Early partial return during first 48 hrspreservation of even partial sensory function alone often hasbeen followed by return of voluntary motion fairly good correlation between the SEP and motor function return early return of the SEP was usually, though not always, a harbinger of motor recovery 113. Distinction between motorand SSEP passages! Complete/incomplete chronic/acute SEP could not be obtained in about 15% of clinically incompletepatients, yet these patients did just as well as other clinically incomplete patients in whom the SEP was present there is no strong evidence to suggest that SEPs can play asignificant role in the prognosis of recovery following SCl. 114. It would appear, then, in the awake, cooperative patient, as opposed to the unconscious one, a routine SEP study does not substitute for a thorough clinical examination, which still appears to be the best prognostic indicator. 115. Intraoperative Monitoring: Spine Surgery SC malfunction rate: 1% in instrumentation 10% pedicle screwremoval of the rods within 6 hours usually resolves the problem 116. SSEP/ESG The SEP is usually of larger amplitude than the ESG andtheoretically requires less averaging. The SEP, however, has a much greater sensitivity than the ESG to anesthetic agents, producing a dose-related amplitude decrease and latency prolongation 117. What is the criteria?! All peaks of the SEP or the MEP response disappear entirely or becomemarkedly smaller (less than 50%), or significant latency prolongation (greater than 5.5 msec) number of repeat trials over the next 5 or more minutes Checking with the anesthesiologist observed changes are not due to cranial volume conduction changes Checking the stimulating circuit and recording inputsHouston! Houston! Weve hade a problem here! 118. Intra operative monitoring: Aortic/Cardiac surgery Risk of paraplegia: from 0.5 % in COA to 15% in TAA changes in SSEP after 3 of cord ischemia total loss of all peaks after about 9 Maneuvers designed to increase both distal spinal cord bloodflow and perfusion have resulted in SEP reappearance without postoperative neurologic deficits. 119. Intraoperative Monitoring: Carotid Endarterectomy cerebral ischemia secondary to carotid clamping detecting early cerebral ischemia identifying patients in whom a bypass shunt is required 120. The pathophysiologic process is the inability of the brain to maintain appropriate electrical capabilities as it becomes ischemic regional cerebral blood flow greater than about 20 mL per 100gper min: electrical activity is normal in the range,approximately, of 16 mL to 18 mL per 100g permin : the SEP latency begins to lengthen, and changes start occurring in the EEG At about 10 mL per 100g per min, both electrical indices areessentially flat 121. VEP & ABR 122. Visual evoked potentials 123. VEPRetinal photo receptors optic nerve Chiasma optic optic tract Lateral geniculate body optic radiaionprimary visual cortex 17 Secondry 18 19 124. VEP 125. VEPRecording: Oz O1 and O2 Refrenced to Cz Gr on Fz corrective devices must been put on No midriatic along 12hrRoom darkened Monitor contrast at max. Availble Cervical spine relaxed 126. VEPPatterned St. : checkerboardUnpat. St. : flushing eliminates the flash-stimulus problem reduces certain acuity and astigmatism variables gives more easily standardized responses 127. VEPFlash or Goggle stimulators can be used on children with patients who are not able to maintain steady focusing owing to behavioral or neuromuscular difficulties during operations sedated or unconscious patients visual acuity precludes shorter distance or larger check patterned stimulus testing 128. VEPThe VEP amplitude normally is inversely proportional to check sizeDistance: 70 -100 cm Pattern reversing: 2 Hz Check size: 2.91 mm First both eyes together, then separateley 129. VEPN 75 : 65-90 P 100 : 88-114N 140 : up to 151 The P100 latencies shorten during the first year oflife, reaching a plateau by 6 or 7 years of age, and then increase gradually with age after 60 years. Women tend to have slightly shorter latencies. 130. VEP Hemifield stimulation is used to evaluate a unilateral postchiasmal to occipital cortex lesion 131. VEPParadox unilateral CVA on Lt. Occiput cortex Lt. Hemifield St. Large VEP on Lt and NL on Rt Rt. Hemifield St. Small VEP on Rt. And tiny on Lt.The paradoxical response is observedbecause the larger potential in this example, recorded over the left occipital (i.e., O1) lobe from left hemifield stimulation 132. VEP Conditions that affect central retinal or macular function cancause alterations in the VEP amplitude or waveform, rather than latency, and require that a small check pattern be used Peripheral retinal diseases will not significantly alter the VEPuntil the macula is involved central retinal artery occlusion may not produce any VEPabnormality ischemic or compressive optic neuropathies can cause waveform and amplitude abnormalities that are out of proportion to the latenvy delay Papilledema, in the absence of secondary ischemic atrophy, may not give any VEP abnormalities. 133. VEP Cortical blindness usually abolishes the VEPdifferentiating conversion symptoms from organic lesions MS and other demyelinating diseases giving latencyprolongations up to the 250-msec range Toxic or nutritional amblyopias, which are considered demyelinating, usually are not associated with significant VEP alteration. Chiasmal lesions generally alter the VEP bilaterally Postchiasmal focal lesions are best defined with partial orhemifield stimulation 134. Oto-acoustic emission cochlear outer hair cells' vigorous motility superior screening of early hearing problems in infants for early detection of hearing loss from ototoxic drugs part of an assessment battery for children with auditoryprocessing deficits evaluating cochlear damage from noise exposure when tinnitus is part of the presenting report 135. Auditory brainstem response the smallest of the EP responses amplitude usually is no more than 600 nanovolts o organ of Corti o spiral ganglion o auditory or cochlear nerve o cochlear nuclei # 3 o lateral lemniscus o superior olivary complex o Medial geniculate body (4 ) o auditory cortex 41 136. ABRRecording: Active: Cz Ref to ipsilateral earlobe (A) or mastoid bone (M) Gr is contralateral ref. ! Otoscopic exam before testTest room sould be free of noise or distraction Basic hearing treshold Opp. Ear masked with white noise Click! Rarefaction/condansation Rarefaction generally produces a shorter latency peak thancondensation when all other recording parameters are the 137. ABRauditory nerve II. cochlear nucleus at the pontomedullary junction III. superior olivary complex in the caudal pons IV. lateral lemniscus in the pons V. inferior colliculus in the midbrain VI. medial geniculate body of the thalamus VII.auditory radiations of the thalamocortical tract I. 138. ABRThe I-III interpeak latency difference: lesions in the peripheral auditory mechanism, auditory nerve or lower pons level lesionsThe I-V interpeak latency difference Lesion in brainstem, thalamocortical tract when the I-III interpeak latency is normalDiffuse involvement both in the I-III and III-V : MS and other demyelinating processes 139. ABRABR use in adults unexplained central hearing losses on auditory tests differential diagnosis of sudden-onset unilateral deafness orsevere hearing loss detecting multiple sclerosis (MS), other demyelinating processes, and acoustic neuromas during cranial intraoperative monitoring (IOM) monitoring brainstem function during barbiturate coma brain death confirmition 140. ABRABR in children infants and newborns to detect the early hearing loss considered in infants of 6 months of age or less who are suspected of hearing loss, and in children up to 2 years of age who appear to have hearing or behavioral problems prognostic considerations following hypoxic encephalopathies 141. Evoked potentias in MS 142. Evoked potentias in MSVEP The VEP abnormalities are related mostoften to optic neuritis one usually affected more than the other 1. Prolonged P100 latency : greater than 10 to 30 msec 2. Interocular latency differences: the most sensitive indicator ofoptic nerve dysfunction 3. Relative amplitude diminution: total amplitude less than 3 V suspicious side-to-side amplitude difference greater than 50% abnormal 4. Dispersion or change in duration of the P100 potential 5. Other waveform morphology changes 143. Evoked potentias in MSChronologic relation between MS and VEP when the pattern shift VEP was normal, there was never anabnormality found on clinical examination. Even when the pattern shift VEP was abnormal, various clinical examinations remained normal when optic neuritis was clearly present, more than 95% of patients had VEP abnormalities 144. Evoked potentias in MSABR Abnormal in 30% of possible MS 41% of probable MS 67% of definite MS patients1) Absence of waves, especially peak V (III) 2) Marked diminution of amplitude of the waves 3) Increased interpeak latency differences :III-V IPL more frequently involved than the I-III 4) Reversal of I/V amplitude ratio 145. Evoked potentias in MS1. Peak latency prolongation 2. Prolongation of interpotential latency3. Diminution of amplitude 4. Absence of component peaks 5. Change in the morphologyvarious combination of abnormalities 146. Evoked potentias in MSAbnormal SEP 58% for all clinical MS classifications 77 in definite MS 67% in probable MS 49% in possible MSAbnormal evoked potentials in MS: 40% in SSEP 37% in VEP 25% in ABR 147. Evoked potentias in MSMotor cortex electrical or magnetic stimulationcord-to-axilla conduction to be normal in both groups whereas central conduction ( cortex-to-cord or cord-to-cordconduction) was markedly slowed in MS patients 148. Evoked potentias in MSMRIIn brainstem lesions, the ABR is more sensitive than MRI in optic neuritis secondary to MS, the MRI usually has beennormal, whereas pattern shift VEPs are abnormal in approximately 95% of patients 149. Bradley: Neurology in Clinical Practice, 5th ed Table 58-9Comparison of Sensitivity of Laboratory Testing in Multiple Sclerosis VER BAER SSEP OCB MRI 80-85% 50-65% 65-80% 85-90% 90-97% 150. Brain Death 151. Methods for monitoring EP recording intracranial pressure measurement serial EEG recording cerebral blood flow measurement apnea testing ultrasound techniques 152. EEG findings do not correlate well with the diagnosis of brain death essentially a test of cortical functionIn brain death, the ABR typically has no identifiable waves, or only isolated unilateral or bilateral wave Ican be recorded. Only rarely is wave II present. 153. cases of hypoxic brain injury Absence of a cortical SEP with preservation of the ABRloss of cortical function preservation of brainstem function proceeding to a chronic vegetative stateABR recordings in decerebration and bulbar syndromes considerable instability increase in the wave I latency and the interpeak latencies Increase in central conduction time marked peak III and V amplitude reductions 154. . . . this is the End. 155. Dedicated to:Best regards