Evoked Potentials PDF

SECTION I Evoked Potentials CHAPTER...

SECTION I Evoked Potentials CHAPTER Thoru Yamada 1 Elizabeth Meng Peter Seaba Principles of Evoked Potentials INTRODUCTION when recorded from the scalp or the body surface. They are obscured by ongoing EEG activity or contaminated by EKG, The evoked potential (EP) is an electrical response of the EMG, or other biological and nonbiological electrical activities. nervous system to various sensory stimuli. Unlike the EEG that The averaging method allows extracting the response or signal shows the constantly and spontaneously changing electrical (which is time locked to the stimulus) from the noise (random activity of the brain, the EP is time locked to the onset of the electrical activity unrelated to the stimulus). This is accom- stimulation and consists of a series of waves characteristic to plished by collecting and summating each response to repeated each stimulus modality. For clinical testing, visual, auditory, and somatosensory stimuli are used. Some EPs, such as the driving response to photic stimulation or lambda waves in response to scanning eye movements, are readily identified in routine EEG. However, most EPs have a small or a low amplitude (3 SD). In patient B, OD had a normal P100 latency, but OS showed a significantly delayed P100. In subject C, the latencies of both eyes were within normal limits, but the amplitude was much smaller on OS than on OD. The amplitude difference was due to decreased visual acuity in OS (20/200) compared to that of OD (20/20). Yamada, Thoru, and Elizabeth Meng. Practical Guide for Clinical Neurophysiologic Testing : EP, LTM, IOM, PSG, and NCS, Wolters Kluwer Health, 2011. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/mccollege-ebooks/detail.action?docID=2031854. Created from mccollege-ebooks on 2023-03-31 22:11:36. Yamada_Chap02.indd 24 3/10/2011 12:16:50 PM  Chapter 2 Visual Evoked Potentials 25 In the case of low-amplitude VEP, especially in both eyes, it TABLE 2.1 VEP Normal Values may be necessary to examine the response at the anterior, pos- Absolute 25 min 50 min 100 min terior, or lateral electrodes because the maximum P100 ampli- tude may not necessarily be at the MO electrode. If, however, Mean 97.2 97.7 100.3 the amplitude in one eye is depressed greater than 50% to 75% SD 4.5 3.7 3.6 as compared to the other eye, this can be considered to be Upper limit 110.7 108.8 111.1 abnormal (see Fig. 2-11C). L-R Difference 25 min 50 min 100 min P100 amplitude also correlates with visual acuity, and any Mean (ms) 1.8 1.3 1.5 condition that impairs visual acuity will decrease the amplitude. SD 1.4 1.0 0.9 Therefore, VEP should be tested with the best corrected vision Upper limit 6.0 4.3 4.2 if the patient wears glasses. Technical factors such as poor fixa- tion, defocusing, nystagmus, or drowsiness can cause the ampli- The above values are in milliseconds. tude reduction. TOPOGRAPHIC ABNORMALITIES AMPLITUDE ABNORMALITIES A mild degree of amplitude asymmetry between left and right The amplitude varies considerably between subjects and also laterally placed electrodes (LO and RO) to full-field monocular between two eyes within one subject. Since amplitude as well as stimulation is not uncommon in normal subjects. However, if interocular amplitude ratios do not follow the normal the amplitude asymmetry is greater than 50% or there is a sig- (Gaussian) distribution, mean plus standard derivation cannot nificant difference in waveforms between LO and RO responses be used for abnormal criteria. The most reliable amplitude (Fig. 2-12), it is necessary to perform hemi- or partial-field stim- abnormality is the total absence of response or exceedingly low ulation to determine the significance of the asymmetry. For amplitude response in one eye or both eyes. In this case, the example, depressed LO response to both left and right mon- analysis time may be increased to 300 ms or greater to exclude ocular stimulation raises the possibility of a postchiasmal lesion the possibility that the P100 latency is extremely prolonged in the right hemisphere (due to paradoxical lateralization). In beyond the routine time scale of 200 to 300 ms. this case, the depressed or absent response to the left hemifield Copyright © 2011. Wolters Kluwer Health. All rights reserved. Figure 2-12. Examples of asymmetric VEPs between LO and RO electrodes to full-field left monocular stimulation. Note the depressed ampli- tude with a negative “bump” in the vicinity of P100 at RO in patient A. These features resemble half-field stimulation (see Fig. 2-9). In subject B, the amplitude was much depressed at LO compared to RO. These asymmetries suggest a possible visual field defect; the abnormality is at the left occipital lobe in patient A and right occipital lobe in patient B, suggesting a right and left visual field defect, respectively. Whether or not these asym- metric VEP features truly represent a visual field defect must be verified by half-field stimulation. Yamada, Thoru, and Elizabeth Meng. Practical Guide for Clinical Neurophysiologic Testing : EP, LTM, IOM, PSG, and NCS, Wolters Kluwer Health, 2011. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/mccollege-ebooks/detail.action?docID=2031854. Created from mccollege-ebooks on 2023-03-31 22:11:36. Yamada_Chap02.indd 25 3/10/2011 12:16:51 PM  26 Practical Guide for Clinical Neurophysiologic Testing stimulation confirms the abnormality. If the abnormality by Since VEP abnormalities tend to persist after the clinical hemifield stimulation is limited to one eye, this suggests a symptoms of optic neuritis disappear, abnormal VEP is useful prechiasmal dysfunction. to confirm a past history of optic neuritis. The VEP sensitivity is overall higher than MRI in detecting optic nerve lesions. This is especially true in asymptomatic patients who show MRI WAVEFORM ABNORMALITIES abnormalities only in 20%.34 Optic neuritis is a risk factor for The morphological deviation of the VEP waveform, such as MS because many patients with optic neuritis eventually loss of N75 or N145, should not be considered abnormal in develop MS.35 the presence of normal P100 latency and amplitude. The most confusing waveform is a double peaked or “W”-shaped P100. It MULTIPLE SCLEROSIS is difficult to determine if the first or second peak is P100 or if neither or both are P100. There are a few possibilities to Optic nerve demyelination, which runs parallel with a high account for a “W”-shaped P100. P100 is primarily generated by incidence of VEP abnormalities, is common in multiple the central visual field.29 If the patient has a central scotoma, sclerosis (MS) patients. VEP may be abnormal in MS patients the VEP may show a negative instead of a positive peak at the who have no present or past history of visual symptoms. The midline due to the removal of the central visual field input. abnormal VEP demonstrating a clinically “silent” optic nerve This would result in a “W”-formed P100 by partial contribu- lesion raises the diagnostic possibility of MS in patients who tion of positivity by surviving central vision and negativity by have no visual symptoms but who have signs of other CNS peripheral vision. In this case, laterally placed electrodes may lesions. The abnormal incidence in MS as a whole is about show a “true” P100. The bifid P100 may also occur when the 60%.17,33,34,36–38 When the MS diagnosis is classified as possible, upper visual field contributes negative activity that may be probable, or definite, the abnormal ratios are about 40%, shifted in latency relative to the P100 positivity. In this case, 60%, or 80% to 90%, respectively. If there is clinical evidence the lower half-field stimulation delineates a “true” P100. In of optic neuritis, the abnormal incidence is close to 90%.39 some cases, different check sizes solve the problem as shown in Even without clinical evidence of optic nerve involvement, Figure 2-8. One or two check sizes may show bifid P100, but half of the MS patients are expected to have abnormal VEPs. one additional check may show a well-defined single peak. In Conversely, it is extremely rare to find abnormal neuro-oph- this case, the peak that corresponds to the single-peaked P100 thalmological examinations when the VEP is normal.39 should be chosen as P100. Another possibility of a “W” wave- Although VEP abnormalities tend to remain following an form results from a contribution of N100 from the MF elec- acute episode of optic neuritis,40 in some patients (5% to 15%) trode which has a different latency from that of the occipital prolonged P100 latency may return to normal within months P100. In this case, P100 should be measured from MO with an to a few years.41,42 ear reference derivation. VEP abnormalities in MS patients are characterized by latency prolongation, by either absolute or interocular latency differ- ence (see Figs. 2-10 and 2-11). The amplitude and waveforms VEP AND CLINICAL CORRELATES are often well preserved. Significant prolongation of P100 latency with well-preserved amplitude in patients who have nor- VEP examines the integration of visual pathway including the mal or near-normal visual acuity strongly suggests a demyelinat- cornea, retina, optic nerve, optic tract, lateral geniculate ing process rather than axonal or compressed optic nerve body, optic radiation, and occipital cortex (see Fig. 2-1). An lesions. The abnormal incidence is higher with the use of smaller abnormal VEP may be found in lesions along any of these ana- check size (25′ or smaller), but the abnormality may be limited tomical structures. In general, the sensitivity is higher in to only a large check size (100′) in some patients (Fig. 2-13).26 lesions involving the optic nerve, especially when secondary Alternative stimulus methods such as hemifield stimulation42 to a demyelinating disease. Despite a high sensitivity of VEP or lower luminance stimuli43 reported an increased incidence Copyright © 2011. Wolters Kluwer Health. All rights reserved. abnormalities in optic neuritis and MS, the abnormalities are of abnormalities in MS patients. not etiologically specific. COMPRESSIVE OR AXONAL OPTIC OPTIC NEURITIS NERVE LESIONS Following pioneering work by Halliday et al.,2 a number of stud- Tumors compressing the optic nerve mainly affect the ampli- ies have agreed that the incidence of VEP abnormalities is close tude and waveform with relative preservation of latency to 90% in patients who have a history of optic neuritis.10,19,30–33 (see Fig. 2-11C). A latency prolongation of more than 20 ms The VEP abnormality is characterized by a prolonged P100 with well preserved amplitude, which is common in demyeli- latency. Since the abnormality is most commonly monocular, nating optic nerve lesions, is rare in compressive lesions. Unlike interocular latency difference is probably the most sensitive an abnormal VEP revealing clinically “silent” lesions in MS measure indicative of optic nerve dysfunction (see Fig. 2-11A,B). patients, an abnormal VEP due to a compressive lesion is usu- If both eyes are affected, degrees of P100 latency prolongation ally accompanied by visual symptoms such as decreased visual may be considerably different. Unlike axonal optic nerve acuity, optic atrophy, or visual field defects44 and/or abnormal pathology, the amplitude and waveform of P100 are often well ophthalmological defects. Papilledema due to increased intrac- preserved, which is characteristic for a demyelinating process. ranial pressure or pseudotumor cerebri usually does not pro- Complete absence of the VEP is rare except in patients with an duce an abnormal VEP until a severe degree of increased acute state or severely impaired vision. pressure occurs.45 Yamada, Thoru, and Elizabeth Meng. Practical Guide for Clinical Neurophysiologic Testing : EP, LTM, IOM, PSG, and NCS, Wolters Kluwer Health, 2011. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/mccollege-ebooks/detail.action?docID=2031854. Created from mccollege-ebooks on 2023-03-31 22:11:36. Yamada_Chap02.indd 26 3/10/2011 12:16:53 PM  Chapter 2 Visual Evoked Potentials 27 Figure 2-13. Two examples of abnormality limited to one check size observed in patients with multiple sclerosis. In patient A, the abnor- mality was limited to the smallest (25′) check size while in patient B, the abnormality was seen only with the largest (100′) check size. Vertical lines indicate upper limit of normal value for each check size. Ischemic optic neuropathy also affects the amplitude more groups rather than on individual findings. Using a sinusoidal than the latency. The latency may be prolonged but usually not grating stimulation, P100 latency in the normal group was 116 ± as dramatically as in MS.46 9 ms but in a group of Parkinson patients, it was 139 ± 22 ms.6 The results after treatment with dopamine varied, but one study found a reduced abnormality based on decreased interocular SPINOCEREBELLAR DEGENERATION latency differences.54 The responsible site for the abnormality is Abnormal VEP is found in about two thirds of patients with thought to be the inner plexiform layer of the retina which shows Friedreich’s ataxia.47–49 The abnormality is usually bilateral with decreased dopaminergic cells in Parkinson patients. fairly symmetric prolongation of P100 latency. The amplitude is usually preserved but may be more affected than in MS patients, TRANSVERSE MYELITIS Copyright © 2011. Wolters Kluwer Health. All rights reserved. especially in patients with severe visual impairments. VEP in acute transverse myelitis is usually normal. The inci- In contrast to the high incidence of VEP abnormalities in dence of abnormality increases in chronic progressive myelitis, Friedreich’s ataxia, other types of spinocerebellar degeneration ranging from 35%55 to 76%.56 The diagnosis of MS becomes usually have normal VEPs; they include hereditary spastic highly likely if abnormal VEP is found in patients with clinical paraplegia,50 hereditary cerebellar ataxia,48 hereditary spastic evidence of myelopathy. ataxia,51 and olivopontocerebellar atrophy.49,52 CHIASMAL LESION CHARCOT-MARIE-TOOTH DISEASE Pituitary tumor, craniopharyngioma, or tumor near the sella VEP is abnormal in some patients with this disease (7 of 17 patients turcica compressing the optic chiasm produces bitemporal hemi- in one study),53 although the patients usually do not have clinical anopsia (see Fig. 2-1). Based on paradoxical lateralization, the evidence of optic nerve involvement. The VEP abnormalities are monocular full-field stimulation may show an asymmetric response not related to the clinical severity of the disease. between the left and right occipital electrodes with a depressed response on the electrodes ipsilateral to the side of visual field defect. Monocular temporal half-field stimulation produces either PARKINSON’S DISEASE depressed response or no response in all electrodes. Due to con- VEP abnormalities reported in patients with Parkinson’s disease siderable variation of waveform distribution, however, VEPs are of are based on the statistical difference between normal and patient limited value in detecting a chiasmal lesion. Yamada, Thoru, and Elizabeth Meng. Practical Guide for Clinical Neurophysiologic Testing : EP, LTM, IOM, PSG, and NCS, Wolters Kluwer Health, 2011. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/mccollege-ebooks/detail.action?docID=2031854. Created from mccollege-ebooks on 2023-03-31 22:11:36. Yamada_Chap02.indd 27 3/10/2011 12:16:53 PM  28 Practical Guide for Clinical Neurophysiologic Testing RETROCHIASMAL LESION disturbance or malingering problem is suspected. However, it should be noted that if the patient is capable of defocusing In evaluation of postchiasmal lesions, VEP recorded from later- intentionally to avoid perceiving the stimulus or of converging ally placed electrodes (LO/RO or LT/RT; see Fig. 2-5) to partial- the eyes during the test, this could produce prolonged or absent field stimulation must be examined. Due to paradoxical lateral- P100. Some subjects can produce voluntary nystagmus during ization, a depressed left occipital response, for example, to both delivery of the stimulus. This may produce diminished P100 left and right monocular full-field stimulation suggests a lesion amplitude but with normal latency.72 in the right hemisphere associated with left homonymous hemi- anopsia. Since the asymmetric responses between LO and RO are relatively common in normal subjects, presumably due to ELECTRORETINOGRAM anatomical variations of occipital cortex, this alone is not a reli- able finding to predict postchiasmal lesions. The findings, even Concomitant recording of electroretinogram (ERG) with VEP with the use of half-field stimulation may not always be accu- can aid in differentiating if a VEP abnormality is reflected by a rate.57,58 In a study of 50 patients with homonymous field defects retinal disease or dysfunction of the central visual pathway. The confirmed by perimetry, 79% showed VEP abnormalities.59 ERG to flash stimulation is generated by cells in the outer and In order to circumvent the technical difficulty of half-field stim- inner nuclear layer of the retina (F-ERG) and the ERG to pattern ulation, sequential stimulation presenting left and right half-field stimulation is generated by the ganglion cells in the inner nuclear stimulation alternately may yield more reliable results.60,61 layer (P-ERG).73 Both F- and P-ERGs consist of an initial negative a-wave, and subsequent positive b-wave. Both a- and b-waves are ALBINISM larger in amplitude and shorter in latency in F-ERG than in P-ERG. Both F- and P-ERGs require the use of corneal lens electrodes and This is an interesting condition in which about 20% of nasal half pupil dilation for quantitative analysis. The ERG (either flash or field from each eye projects to the contralateral visual cortex, in pattern) recorded by surface electrodes placed near the perior- contrast to the normal in whom nasal half field projects to the bital skin referenced to a distant site (such as the mastoid) can be ipsilateral hemisphere (see Fig. 2-1). Therefore, the inputs from used only as a screening examination. The ERG recorded with the temporal and some of the nasal visual fields from each eye corneal electrodes is required to verify suspected abnormality reach the contralateral occipital cortex. Full-field monocular noted by ERG recorded with surface periorbital electrodes. stimulation thus shows a similar VEP asymmetry as elicited by P-ERG is best recorded with a large field (>9 degrees) and the half-field stimulation.62 with check sizes of 30′ to 60′.74 P-ERG consists of initial negative with latency of about 30 ms (N30) followed by relatively large HUNTINGTON’S CHOREA positive (P50) and broad negative waves (N95). The characteristic VEP feature of Huntington’s chorea is low P100 amplitude but with normal latency.63,64 The low-amplitude STEADY STATE VEP VEP may be seen in asymptomatic offsprings or high-risk sub- jects. Interestingly, the low-voltage EEG and somatosensory Increasing stimulus rates above 6 Hz, either by pattern reversal or evoked potentials are also characteristic features for Hunting- strobe flash stimulation, produces rhythmic trains of waves of the ton’s chorea.63,65 same frequency as the stimulus rates. This is similar to the photic driving response seen in routine EEG recording. Because the CORTICAL BLINDNESS responses are extracted by averaging, a more detailed analysis is possible by this steady-state VEP, as compared to the photic driving VEP results in patients with cortical blindness have been incon- response seen in routine EEG testing. The response amplitudes sistent. In a patient with lesions at Brodmann’s area 17 (primar- become progressively smaller as the stimulus rate increases. ily visual cortex) but sparing area 18 and 19 (association cortex), The steady-state VEP is assessed by phase lag and amplitude Copyright © 2011. Wolters Kluwer Health. All rights reserved. transient and steady-state VEPs were found to be normal.66 at various stimulus rates. The time difference between each peak However, VEP was found to be abnormal when high-frequency of the VEP and stimulus is expressed by a phase lag, which spatial grating was used.67 The results of VEP using flash stimula- changes depending on the stimulus rates. The amplitude tion have also been inconsistent.68–70 Since some patients with decreases progressively with the faster stimulus rates, and even- cortical blindness may have normal VEPs, differentiating tually disappears. Generally, the highest frequency to flash stim- between functional (factitious, hysterical, or malingering) and uli at which the response can be recognized (critical frequency) organic visual loss may be difficult. In general, however, the pres- is about 60 to 70 Hz. Although steady-state VEPs have been ence of well-formed normal VEP in patients complaining of a investigated in patients with MS and optic neuritis,75,76 or occipi- severe degree of visual loss, for example, visual acuity of less than tal infarction or tumor with visual field defects,77–79 it has not 20/120, strongly suggests a functional visual disturbance.71 been popularized as a routine visual function test. This is because of interindividual variability of amplitude and difficulty in estab- FUNCTIONAL BLINDNESS, HYSTERIA lishing strict criteria for determining the presence or absence of OR MALINGERING the steady-state VEP at different frequencies. However, if there is greater than 10 Hz difference in critical frequency between two The presence of well-defined normal VEP is incompatible with eyes in the same subject, it is reasonable to conclude that the eye moderate-to-severe visual disturbance. In this case, a functional with the lower critical frequency is abnormal. Yamada, Thoru, and Elizabeth Meng. Practical Guide for Clinical Neurophysiologic Testing : EP, LTM, IOM, PSG, and NCS, Wolters Kluwer Health, 2011. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/mccollege-ebooks/detail.action?docID=2031854. Created from mccollege-ebooks on 2023-03-31 22:11:36. Yamada_Chap02.indd 28 3/10/2011 12:16:54 PM  Chapter 2 Visual Evoked Potentials 29 REFERENCES 1. Kooi KA, Guvener AM, Bagchi BK. Visual evoked responses in lesions of the higher optic pathways. Neurology 1965;15:841–854. 2. Halliday AM, McDonald WI, Mushin J. Delayed visual evoked responses in optic neuritis. Lancet 1972;I:982–985. 3. Lowitzsch K, Rudolph HD, Trincker D, et al. Flash and pattern-reversal visual evoked responses in retrobulbar neuritis and controls: a comparison of conventional and TV stim- ulation techniques. In: Lechner H, Aranibar A, eds. Electroencephalography and Clinical Neurophysiology. Amsterdam, The Netherlands: Excerpta Medica, 1980:451–463. 4. 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LED or FVEP can also be used patient with multiple sclerosis. Neurology 1985;35:1461–1465. for patients who have severe refractive errors. Assessment relies 27. Barrett G, Blumhardt LD, Halliday AM, et al. A paradox in the lateralization of the visual only on the presence or absence of a response, not on latency, evoked response. Nature 1976;261:253–255. 28. Chain F, Lesevre N, Pinel JF, et al. Spatio-temporal study of visual evoked potentials in waveform, or amplitude measures. patient with homonymous hemianopia. In: Courjon J, Mauguiere F, Revol M, eds. Clinical Applications of Evoked Potentials in Neurology. New York, NY: Raven Press, 1982:453–457. 29. Blumhardt LD, Barrett G, Halliday AM, et al. The effect of experimental “scotomata” on OTHER STIMULUS DEVICES FOR VEP the ipsilateral and contralateral responses to pattern-reversal in one half-field. Electroen- cephalogr Clin Neurophysiol 1978;45:376–392. There are many other stimulus devices available. There are 30. Chiappa KH. 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Practical Guide for Clinical Neurophysiologic Testing : EP, LTM, IOM, PSG, and NCS, Wolters Kluwer Health, 2011. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/mccollege-ebooks/detail.action?docID=2031854. Created from mccollege-ebooks on 2023-03-31 22:11:36. Yamada_Chap02.indd 30 3/10/2011 12:16:55 PM  CHAPTER 3 Thoru Yamada Elizabeth Meng Brainstem Auditory Evoked Potentials and Auditory Evoked Potentials ANATOMY OF AUDITORY PATHWAY BRAINSTEM AUDITORY EVOKED IN BRAINSTEM POTENTIALS The brainstem auditory evoked potential (BAEP) deals with the The brainstem auditory evoked potential (BAEP) was the first auditory pathway within the brainstem. Sounds entering the ear clinical application to utilize the far-field potential. The far-field canal cause a vibration of the tympanic membrane of the exter- potential (FFP) was introduced by Jewett et al.1 who discovered nal ear. The sound waves are then amplified by a piston-like a series of wavelets (called “Jewett bumps” named after his pio- function of three ossicles (small bones consisting of the mal- neering work) following auditory stimulations. Unlike the con- leus, incus, and stapes) in the middle ear. This is received by the ventional evoked potentials or action potentials (APs) that are cochlea, where the mechanical vibration from the stapes bone best recorded from electrodes near the generator source, the is converted into pressure waves, stimulating the hair cells of BAEP is recorded from electrodes a distance from the genera- the organ of Corti. The organ of Corti serves as an auditory tor source, that is, the auditory pathway within the brainstem. frequency analyzer. The activation of hair cells sends the The potentials can be recorded from a wide area of scalp elec- impulses to the cochlear nerve. The cochlear nerve is a part of trodes as a result of a volume conduction spread through brain the VIII cranial nerve (auditory or vestibulocochlear nerve), tissue, CSF, skull, and scalp (Fig. 3-3). One can perceive the FFP which also includes the vestibular nerve (Fig. 3-1). The vestibu- as if the distant scalp electrode is examining the events occur- lar nerve receives impulses from the semicircular ducts that ring in the brainstem via a telescope. FFPs are generally of posi- respond to movements of the head. The vestibular system tive polarity and are considered to represent positive dipole relates to coordination in the eyes, neck, and body for mainte- fields that appear at a distance from the generator source. The nance of posture and movement of the head. negative field more commonly occurs near the generator The impulses from the cochlear nerve enter the brainstem source. Each wave of the BAEP (except for wave I) is generated Copyright © 2011. Wolters Kluwer Health. All rights reserved. at the upper medulla, close to the junction of the medulla and when the auditory impulse passes through a specific portion of the pons. It then reaches the anterior and posterior cochlear the auditory pathway within the brainstem. The generation nucleus (Fig. 3-2). After synaptic connection at the cochlear mechanisms of FFPs are better delineated later by somatosen- nuclei, the axons from these nuclei enter the superior olivary sory evoked potentials and will be discussed in more detail in nuclei. Some fibers stay on the same side, while others cross to Chapter 4 of this section. Wave I is not an FFP but a near-field the opposite side. After the olivary nuclei, fibers ascend the lat- potential, picked up by the ear reference electrode on the side eral lemniscus at the pons via the nuclei of the lateral lemnis- of stimulation, generated as a negative potential by the cochlear cus. The ascending fibers make a synaptic connection at the nerve before the entrance into the brainstem. inferior colliculus of the midbrain and the medial geniculate body. After the sensory relay station at the medial geniculate body, the final path reaches the primary auditory sensory cor- TECHNICAL PARAMETERS tex situated at the anterior-superior temporal gyrus (gyrus of Heschl, Brodmann’s area 41 and 42). It is important to recog- STIMULATION nize that the auditory nerves receive bilateral input; therefore, Stimulus Types a central lesion affecting only one side of the brain or brain- stem does not cause deafness. Deafness in one ear usually indi- The stimulus used for BAEP is a click delivered through an ear- cates a lesion at the cochlear nerve. phone. The click is a broad-band sound, delivering a wide range 31 Yamada, Thoru, and Elizabeth Meng. Practical Guide for Clinical Neurophysiologic Testing : EP, LTM, IOM, PSG, and NCS, Wolters Kluwer Health, 2011. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/mccollege-ebooks/detail.action?docID=2031854. Created from mccollege-ebooks on 2023-03-31 22:11:36. Yamada_Chap03.indd 31 3/8/2011 8:18:49 PM  32 Practical Guide for Clinical Neurophysiologic Testing Figure 3-1. Schematic model of the anatomy of the cochlear duct and the semicircular duct in relationship to cochlear nerve and vestibular nerve. The VIII cranial nerve (auditory and vestibulocochlear nerves) serves two separate functions. One is the auditory function via cochlear duct and cochlear nerve. The other is the balance/coordination function via semicircular duct and vestibular nerve. The ampullas of lateral, superior and posterior semicircular ducts serve as a vestibular function. The cochlear duct and spiral ganglion of cochlea serve as an auditory function. (From Snell RS. Clinical Neurophysiology for Medical Students, 5th ed. Baltimore, MD: Lippincott Williams & Wilkins, 2001, with permission.) of audio frequencies. These clicks are generated by 100-ms polarity that was used while collecting normative data. On some rectangular pulses. The sound pressure waves elicited by a occasions, alternating clicks may be used to reduce the stimulus monophasic square wave pulse consist of a single large wave fol- artifact or cochlear-microphonic responses (see Fig. 3-7). How- lowed by multiple wavelets lasting up to 2 ms (Fig. 3-4). These ever, it should be noted that the waveform and latency may be sound pressure waves activate the tympanic membrane. Click altered depending on which click polarity is used. stimuli that have a sudden onset are suitable for eliciting BAEP but not suitable for audiologic studies because they consist of Stimulus Intensity multiple frequencies. For testing a specific frequency sound, tones with a fixed frequency must be used. Since tone frequency, Stimulus intensity is expressed in decibels (dB), which is a loga- especially a low-frequency tone, requires a long duration, it may rithmic unit of sound intensity. There are four terms used in not be suitable for BAEP but may be used for medium or long quantifying sound intensity: sound pressure level (SPL), peak- latency auditory evoked potentials (AEP) or event related equivalent sound pressure level (peSPL), hearing level (HL), potentials (ERP) (see page 48 in this chapter, “Auditory P300 and sensation level (SL). The first two are pure physical mea- ERP”). Tone pips or bursts have symmetrical rising and falling sures of intensity. SPL is based on measuring an arbitrary zero phases, and the rise, fall, and plateau time can be electronically reference point set at 0.0002 dyne2/cm2 (20 micropascals). Copyright © 2011. Wolters Kluwer Health. All rights reserved.