EDX: Evoked potentilas
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EDX: Evoked potentilas

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SSEP

SSEP
SEP
VEP
ABR
MS

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EDX: Evoked potentilas EDX: Evoked potentilas Presentation Transcript

  • God protect us Electrodiagnosis text review Presented by: S.Sadeqi MD , PM&R res. SBUMC Jan-feb 2013 Sadeqi.shahram@gmail.com
  • Dumitru Chap.9 Delisa Chap.4 kimura
  • Historical aspects Anatomical basis Nomenclature Instrument Waveform Technique VEP ABR Clinical usage
  • oRichard caton o1875 oVEP oEEG oABR  1891 Avraging  Beck Time locked  ABR Evoked
  • Dorsal column Lemniscal sys Dorsal root gangilia
  • Gracillis Cuneatus
  • Medial lemniscus VPL
  • •Thalamocortical fibers •SS cortex Spinomedullothalamic Nucleos Z VPL
  • homunculus
  • nomenclature AES standarde electrode site waveform morphologic nomenclature instrumentation parameters recording practices interpretive qualifications reference data collection
  • Cephalic VS noncephalic montage
  • 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 can be applied
  • Four standard landmarks are required to locate all positions necessary for SEP purposes
  • Cz C3 and C4 C3' and C4‘ FpZ Fz FpZ'
  • Upper Limb Stimulation Erb’s point (EP1/EP2) 2-3 cm superior to the clavicle and just lateral to the clavicular head of the sternocleidomastoid muscle The Erb's point electrode defined as E-l is ipsilateral to the stimulated limb
  • Cervical Spinous Process C2S C5S C7S REF:FPZ
  • Montage for upper limb SEP Ch1: scalp electrode (C3' or C4') Ch2: C3' or C4‘ Ch3: CS5 or C2S (C7S) Ch4: ipsilateral EP midfrontal region FpZ‘ contralateral EP scalp's FpZ‘ contralateral EP
  • Lower Limb Stimulation Popliteal Fossa  EI electrode located over the tibial nerve approximately 4 cm proximal 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 surface of the knee.
  • Thoracolumbar Spinous Processes L3S or L4S E2: 4cm rostral or on controlateral Iliac crest  Calculate the interval between PF and L3S, yielding the conduction time 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.
  • 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 be used for both left and right lower limb stimulations •It is important to recognize that the lumbosacral spine potentials may 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.
  • Scalp for lower limb SEP 2 cm posterior to the vertex of the skull (CZ) utilizing the 10-20 system and is called CZ‘ The same E-2 , FpZ', as that used for upper limb
  • 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
  • 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 :/
  • 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.
  • SEP WAVEFORMS Polarity Peak nomenclature  AES N20/N30 Peak latency Inter peak latency
  • Peak latency A recommended practice is to always perform two separate trials of 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
  • Final solution
  • Inter peak latency impulse's time of propagation between recording sites central conduction time EP and PF are the markers of peripheral nerve function
  • Amplitude measurment side-to side amplitude differences of 50% or more are considered indicative of a possible abnormality.  It must be recognized, however, that normal persons can have considerable side-to-side amplitude differences, approaching 80% or more Base to peak VS peak to peak  maxima of consecutive SEP peaks of opposite polarity  mixing apples and oranges
  • 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
  • SEP INSTRUMENTATION
  • ELECTRODES Silver Gold Tin Platinum stainless steel  stainless steel  Platinum  mixed with another metal
  • 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 Ω .  Short period 1-2 hr  Longer than 2hr
  • 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 Ω can easily be achieved with surface electrodes. Needle electrodes usually have impedances greater than 3000 Ω and can even reach 10,000-13,000 Ω Ω  risk of infection  Discomfort  higher electrical noise  ease of pulling out
  • 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 to Creutzfeldt disease or other possible slow virus disorders should be safely and immediately discarded.
  • 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.
  • STIMULATING ELECTRODES stimulus pulse of 200--300 µS Duration Sensory threshold is defined as the current intensity when 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
  • Suboptimal stimulus delivery delayed arrival smaller amplitude Unexpected morphology A good judge of an adequate stimulus for mixed nerve studies is observing an adequate muscle twitch
  • 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
  • 60 HZ signal resonance
  • Resonance! :
  • Notch filter
  • 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.
  • 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 filter Amplifier ringing Myogenic synchronous movements
  • FACTORS AFFECTING THE SEP
  • PATIENT COOPERATION PATIENT HEIGHT AGE GENDER TEMPERATURE MEDICATION SLEEP
  • Height When considering central conduction times for median nerve excitation, 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
  • Age Cortical SEP Amp : U shaped curve Spinal SEP: infant> the others Unlike age-related amplitude effects, the correlation between 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
  • 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
  • gender prolongation of potential latencies in men The central conduction time appears to bear no relationship to the gender of the subjec sex
  • Enviro. Temp. Surface temperature of the upper limb at or proximal to the site of nerve stimulation should be maintained at 32°C or more, while the lower limb should be approximately 30°C or higher  Central core temperature is subject to less fluctuation with respect to emotional or environmental conditions omeasuring latencies in patients with fevers (38.0-39.7°C) and again 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.
  • 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 halogenated hydrocarbon 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.
  • These effects are countered by employing a balanced anesthesia technique that uses a strong narcotic in addition to a muscle relaxant plus a weak anesthetic like nitrous oxide or low concentrations of isoflurane.
  • sleeeeeeee p In general, sleep tends to reduce the amplitude and increase the latencies of recorded SEPs
  • Far field and near filed potentials
  • Kimura’s rail road
  • Size changes producing farfield potentials.
  • SEP waveform neural-generators
  • 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).
  • 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.
  • Good correlation was obtained between the clinical examination and abnormal SEPs, implying that the SEP directly correlated to both the dorsal column pathway and the modalities of vibration and proprioception.
  • Upper limb SEP EP: N9/10 Plexus  it is absent in patients with lesions of the brachial plexus but present in patients with cervical root avulsions •Motor fibers are involved, too!
  • Upper limb SEP C2s, C5s, C7s  N11:  dorsal root E.zone  DCV  The refractory period of this waveform is short Hypothermia studies demonstrate an increase of the waveform's amplitude similar to that found in peripheral nerves
  • Upper limb SEP N13: Stationary pot.  relatively long refractory period, suggesting the involvement of synaptic transmission cervical cord's dorsal gray matter
  • Upper limb SEP N13a: 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
  • Upper limb SEP N14: Medial lemniscus  N13 and N14 peaks likely represent generators below and above the foramen magnum.
  • Upper limb SEP
  • Upper limb SEP Scalp: N19/20 N18: thalamus Various lesions in patients with thalamic pathology support the view that the l8-ms negative peak is associated with the thalamus or its projections to the cerebral cortex.
  • Lower limb SEP PF N7-10
  • Lower limb SEP Third Lumbar Vertebra N17-21 A short refractory period suggests that synaptic relays are not associated with the propagation of this wavefront from the lower limb to the thoracic aspects of the spinal cord. cauda equina
  • Lower limb SEP Twelfth Thoracic Vertebra N22 Long refractory period: 6-10 ms Synaptic transmission dorsal 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
  • Lower limb SEP Farfield satationary P. On T12 level at N22
  • Lower limb SEP Second Cervical Potential N29 Stationary potentials oA rather long refractory period is noted for this cervical potentiaI nucleus gracilis
  • Lower limb SEP Scalp P37/N45 The amplitude of the cortical waveform is slightly larger over the ipsilateral scalp postcentral gyrus area of the cortex
  • Lower limb SEP
  • Contravercy! neural generators Variability of latencies and amplitudes reference data Appropriate applications
  • SEP Techniques
  • 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 category Surronding muscles and inviromental noise Only scalp recording be performed  segmental stimulation results in more easily obtainable and somewhat larger responses than dermatomal SEPs, as more nerve fibers are excited.
  • Mixed nerve SEP median nerve 1- Erb point: N10 2- C2S, C5S, C7S : N13 3- Scalp: N20  Analysis time : 50 ms  Between 300 – 1000 Av.
  • 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 + 0.78 for men for women  N19 = 0.095H + 0.049A + 1.19 for men  N19 = 0.085H + 0.043A + 2.72 for women
  • Mixed nerve SEP ulnar nerve Identical recording sites are used for the ulnar nerve as those for the median nerve.  smaller response than median N. .
  • Alternate recordings  Between humeral epicondyles  Ulnar groove or olecranon
  • Segmental sensory SEP  sensory threshold : 3-4 A *2.5-3.5 = 6-12 A  no muscle twich  difficult recording over erb and spine Central amplification
  • Upper limb segmental SSEP 1. Median: first 3 digit 2. Ulnar: 5th digit 3. SRN : 2cm proximal to radial styloid 4. LAC: 2cm lat. To BB tendon, 2 FB below anticubital crease: injury to MC nerve or C5 root
  • LOWER LIMB SEPs 1- mixed nerve 2- segmental SSEP 3- dermatomal SSEP lower limb dermatomal and segmental studies are somewhat easier to perform than upper limb segmental SEPs because lower limb cortical waveforms are usually larger.
  • 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
  • N22 = 0.174(H) + 0.076A - 9.2525 N22 = 0.1619H + 0.0694A - 7.5235 for men for women P37 (40) = 0.199H + 0.0852A + 3.8025 for 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 - 0.2076 for M for W
  • Alternaive recordings When stimulation on PF Recording from sciatic N. E1: on sciatic notch E2: greater trochanter Fpz’ spinal cord conduction time bilateral tibila nerve st. Be needed  C7s-
  • LOWER LIMB SEGMENTAL SOMATOSENSORY EVOKED POTENTIALS  Sural : between lat. Malleolus and achilles SPN: between the middle and lateral thirds of this imaginary Line 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
  • The clinical utility of both segmental and dermatomal studies is unclear :| and the relative value of either compared with the other is also unknown :|
  • DERMATOMAL SOMATOSENSORY EVOKED POTENTIALS The techniques to record dermatomal SEPs are relatively straightforward.  Considerable latency (up to 8-9 ms) and amplitude (80%) side to side differences can occur in normal persons
  • L5 dermatomal SEP omedial aspect of the first metatarsophalangeal joint oon the dorsum of the foot between the first and second digit oon the dorsum of the foot surrounding the first metatarsophalangeal joint Stimulation:  pulse duration of 200 µs 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
  • Recording: as other lower limb SSEP E1 on CZ’ E2 on Fpz’ 100 ms (sweep of 10 ms/div) combined with 500 to 1000 averages P40 = 8.3 + 22.4 (Height) + 0.086 (Age) ± 2.7 ms
  • S1 Dermatomal SEP lateral margin of the foot at the fifth metatarsophalangeal joint P(40) = 8.6 + 24.0 (Height) + 0.038 (Age) 2.9 ms
  • one obvious limitation of the dermatomal response Only one recording site No peripheral recording site Either peripheral or central pathology in Abnolrmal SSEP
  • Miscellaneous SEP techniques
  • 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 Erection oEjaculation
  •  Stimulation: on the shaft of penis cathode proximal 200 µs 2-3 times folded sensory threshold 5 Hz Recording Scalp: CZ’ refrenced to FpZ’ Spine: L1s : usually in M, rarely in W
  • Clinical use  Anal sphincter manometric abnormality W/O structural defect Impotence or orgasmic or gynecologic disturbbances Scaral plexus continuty Sacral level radiculopthies Metabolic Dis. Affecting bowel/bladder or sexual function Unexplained 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
  • 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.
  • Normal values  biphasic: pos- neg Pos: 37-45ms (P1 peak ) Neg: 48-60 ms (N1 peak ) Peak to peak : 1.25-5 µV for men Women are usually smaller  The P1 (onset ) latency for the PN-SEP is generally 6-10 ms longer than that from the peroneal nerve response from knee level stimulation.
  • Trigeminal Nerve SEP sensory receptors trigeminal (semilunar, gasserian) ganglion dorsal trigeminothalamic tract both ipsilaterally and contralaterally to the (VPL) postcentral gyrus
  • Stimulation: cathode is in contact with the angle of the mouth anode is rested on the lower lip pulse of 200 µs ,2-3 times sensory threshold ,2-3 Hz stimulus artifact
  • 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
  • Medial/lateral Plantar And Calcaneal Nerves  the medial and lateral plantar responses should be obtained in all normal persons, the calcaneal nerve response may be absent because of too much impedance on the heel.
  • Clinical uses of evoked potentials Coma Evaluation Traumatic myelopathic evaluation Intraoperative Monitoring Sleep Disorders Brain death CVA MS
  • Coma Evaluation  GSC  Brain stem reflexes creatine kinase BB band levels in the cerebrospinal fluid (CSF-CK)
  • median SEPs have the strongest evidence to suggest their utility in predicting outcome after coma. 1.5 times the motor threshold is used. The strongest indicator of a poor prognosis is a bilateral absence of the short-latency cortical response with median nerve stimulation. Absence of a response is often defined as potentials less 0.5 µV .
  • $$$$$ Live or died $$$$$  A: normal healthy person  B: went to glory!  C: absolutely wana live
  • 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
  • SensitivityVS Specificity  Avoiding falsely predicting nonawakening  correctly predicting nonawakening Fatality 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 to median-nerve stimulation have a very poor prognosis for awakening
  • Traumatic myelopathic evaluation Chance to return:  clinically incomplete lesions  Early partial return during first 48 hrs preservation of even partial sensory function alone often has been 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
  • Distinction between motor and SSEP passages!  Complete/incomplete chronic/acute SEP could not be obtained in about 15% of clinically incomplete patients, 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 a significant role in the prognosis of recovery following SCl.
  • 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.
  • Intraoperative Monitoring: Spine Surgery SC malfunction rate: 1% in instrumentation 10% pedicle screw removal of the rods within 6 hours usually resolves the problem
  • SSEP/ESG The SEP is usually of larger amplitude than the ESG and theoretically 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
  • What is the criteria?! All peaks of the SEP or the MEP response disappear entirely or become markedly 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 inputs Houston! Houston! We’ve hade a problem here!
  • 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 blood flow and perfusion have resulted in SEP reappearance without postoperative neurologic deficits.
  • Intraoperative Monitoring: Carotid Endarterectomy  cerebral ischemia secondary to carotid clamping  detecting early cerebral ischemia  identifying patients in whom a bypass shunt is required
  • 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 100g per min: electrical activity is normal  in the range,approximately, of 16 mL to 18 mL per 100g per min : the SEP latency begins to lengthen, and changes start occurring in the EEG  At about 10 mL per 100g per min, both electrical indices are essentially flat
  • VEP & ABR
  • Visual evoked potentials
  • VEP Retinal photo receptors optic nerve Chiasma optic optic tract Lateral geniculate body optic radiaion primary visual cortex 17 Secondry 18 – 19
  • VEP
  • VEP Recording: Oz O1 and O2 Refrenced to Cz Gr on Fz  corrective devices must been put on No midriatic along 12hr Room darkened Monitor contrast at max. Availble Cervical spine relaxed
  • VEP Patterned St. : checkerboard Unpat. St. : flushing  eliminates the flash-stimulus problem  reduces certain acuity and astigmatism variables  gives more easily standardized responses
  • VEP Flash 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
  • VEP The VEP amplitude normally is inversely proportional to check size Distance: 70 -100 cm Pattern reversing: 2 Hz Check size: 2.91 mm First both eyes together, then separateley
  • VEP N 75 : 65-90 P 100 : 88-114 N 140 : up to 151  The P100 latencies shorten during the first year of life, 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.
  • VEP Hemifield stimulation is used to evaluate a unilateral postchiasmal to occipital cortex lesion
  • VEP Paradox  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 observed because the larger potential in this example, recorded over the left occipital (i.e., O1) lobe from left hemifield stimulation
  • VEP Conditions that affect central retinal or macular function can cause 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 VEP until the macula is involved central retinal artery occlusion may not produce any VEP abnormality 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.
  • VEP Cortical blindness usually abolishes the VEP differentiating conversion symptoms from organic lesions MS and other demyelinating diseases giving latency prolongations 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 or hemifield stimulation
  • 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 auditory processing deficits  evaluating cochlear damage from noise exposure  when tinnitus is part of the presenting report
  • 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
  • ABR Recording: Active: Cz Ref to ipsilateral earlobe (A) or mastoid bone (M) Gr is contralateral ref. ! Otoscopic exam before test Test 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 than condensation when all other recording parameters are the
  • ABR auditory 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.
  • ABR The I-III interpeak latency difference: lesions in the peripheral auditory mechanism, auditory nerve or lower pons level lesions The I-V interpeak latency difference Lesion in brainstem, thalamocortical tract when the I-III interpeak latency is normal Diffuse involvement both in the I-III and III-V : MS and other demyelinating processes
  • ABR ABR use in adults unexplained central hearing losses on auditory tests differential diagnosis of sudden-onset unilateral deafness or severe 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
  • ABR ABR 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
  • Evoked potentias in MS
  • Evoked potentias in MS VEP  The VEP abnormalities are related most often 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 of optic nerve dysfunction 3. Relative amplitude diminution: total amplitude less than 3 µV 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
  • Evoked potentias in MS Chronologic relation between MS and VEP when the pattern shift VEP was normal, there was never an abnormality 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
  • Evoked potentias in MS ABR Abnormal in  30% of possible MS  41% of probable MS  67% of definite MS patients 1) 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
  • Evoked potentias in MS 1. Peak latency prolongation 2. Prolongation of interpotential latency 3. Diminution of amplitude 4. Absence of component peaks 5. Change in the morphology various combination of abnormalities
  • Evoked potentias in MS Abnormal SEP 58% for all clinical MS classifications 77 in definite MS 67% in probable MS 49% in possible MS Abnormal evoked potentials in MS: 40% in SSEP 37% in VEP 25% in ABR
  • Evoked potentias in MS Motor cortex electrical or magnetic stimulation cord-to-axilla conduction to be normal in both groups whereas central conduction ( cortex-to-cord or cord-to-cord conduction) was markedly slowed in MS patients
  • Evoked potentias in MS MRI In brainstem lesions, the ABR is more sensitive than MRI in optic neuritis secondary to MS, the MRI usually has been normal, whereas pattern shift VEPs are abnormal in approximately 95% of patients
  • Bradley: Neurology in Clinical Practice, 5th ed Table 58-9 Comparison of Sensitivity of Laboratory Testing in Multiple Sclerosis VER BAER SSEP OCB MRI 80-85% 50-65% 65-80% 85-90% 90-97%
  • Brain Death
  • Methods for monitoring EP recording intracranial pressure measurement serial EEG recording cerebral blood flow measurement apnea testing ultrasound techniques
  • EEG findings do not correlate well with the diagnosis of brain death essentially a test of cortical function In brain death, the ABR typically has no identifiable waves, or only isolated unilateral or bilateral wave I can be recorded. Only rarely is wave II present.
  • cases of hypoxic brain injury Absence of a cortical SEP with preservation of the ABR loss of cortical function preservation of brainstem function proceeding to a chronic vegetative state ABR 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
  • . . . this is the End.
  • Dedicated to: Best regards