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Human cortical potentials evoked by stimulation of the median nerve. II. Cytoarchitectonic areas generating long-latency activity.

1. The anatomic generators of human median nerve somatosensory evoked potentials (SEPs) in the 40 to 250-ms latency range were investigated in 54 patients by means of cortical-surface and transcortical recordings obtained during neurosurgery. 2. Contralateral stimulation evoked three groups of SEPs recorded from the hand representation area of sensorimotor cortex: P45-N80-P180, recorded anterior to the central sulcus (CS) and maximal on the precentral gyrus; N45-P80-N180, recorded posterior to the CS and maximal on the postcentral gyrus; and P50-N90-P190, recorded near and on either side of the CS. 3. P45-N80-P180 inverted in polarity to N45-P80-N180 across the CS but was similar in polarity from the cortical surface and white matter in transcortical recordings. These spatial distributions were similar to those of the short-latency P20-N30 and N20-P30 potentials described in the preceding paper, suggesting that these long-latency potentials are generated in area 3b of somatosensory cortex. 4. P50-N90-P190 was largest over the anterior one-half of somatosensory cortex and did not show polarity inversion across the CS. This spatial distribution was similar to that of the short-latency P25-N35 potentials described in the preceding paper and, together with our and Goldring et al. 1970; Stohr and Goldring 1969 transcortical recordings, suggest that these long-latency potentials are generated in area 1 of somatosensory cortex. 5. SEPs of apparently local origin were recorded from several regions of sensorimotor cortex to stimulation of the ipsilateral median nerve. Surface and transcortical recordings suggest that the ipsilateral potentials are generated not in area 3b, but rather in other regions of sensorimotor cortex perhaps including areas 4, 1, 2, and 7. This spatial distribution suggests that the ipsilateral potentials are generated by transcallosal input from the contralateral hemisphere. 6. Recordings from the periSylvian region were characterized by P100 and N100, recorded above and below the Sylvian sulcus (SS) respectively. This distribution suggests a tangential generator located in the upper wall of the SS in the second somatosensory area (SII). In addition, N125 and P200, recorded near and on either side of the SS, suggest a radial generator in a portion of SII located in surface cortex above the SS. 7. In comparison with the short-latency SEPs described in the preceding paper, the long-latency potentials were more variable and were more affected by intraoperative conditions.

Cerebral Cortex↗

Thalamocortical interactions in the somatosensory system: interpretations of latency and cross-correlation analyses.

1. Isolated extracellular neuronal responses to cutaneous stimulation were simultaneously recorded from corresponding peripheral representations in the ventrobasal nucleus and primary somatosensory cortex of intact, halothane-anesthetized rats. Thalamic and cortical neurons representing hairy skin on the forelimb were activated by hair movements produced by a series of 50 or 100 discrete air jets. A corresponding set of neurons representing the glabrous pads of the hind paw were activated by a similar number of punctate mechanical displacements. 2. Cortical electrode penetrations were histologically reconstructed, and 118 neurons in the glabrous skin representation exhibited cutaneous responses that were categorized into supragranular, granular, or infragranular groups according to their laminar position. Minimum latencies of cortical neurons responding to glabrous skin displacement were analyzed, and significant differences were found in the distribution of minimum latencies for the different cortical layers. Mean values for minimum latencies in the infragranular and granular layers were 15.8 and 16.3 ms, respectively, whereas supragranular neurons were characterized by minimum latencies having a mean of 20 ms. The differences between these groups suggests that stimulus-induced afferent activity reaches infragranular and granular layers before contacting supragranular neurons. Average latencies were also calculated on responses occurring during the 1st 20 trials, but the cortical distributions of these values overlapped considerably, and differences between the laminar groups were not statistically significant. 3. In several recording sites, two cortical neurons were recorded simultaneously, and the response latencies of these matched pairs were often substantially different despite the similarity in laminar position. This result indicates that laminar location is not the only determinant of response latency and that serially organized circuits are distributed within, as well as between, cortical layers. 4. From a sample of 302 neurons exhibiting cutaneous responses within histologically identified regions of thalamus or cortex, a set of 143 pairs of neurons recorded simultaneously from both regions was available for cross-correlation analysis. Significant thalamocortical interactions were found in 38 neurons pairs. Analysis of these significant interactions revealed that thalamocortical connection strength, as measured by neuronal efficacy, was two to four times larger for neuron pairs having the cortical cell in granular layer IV than for neuron pairs having an extragranular layer cortical neuron. There was no difference in thalamocortical connection strength between neuron pairs containing supra- or infragranular cortical neurons. 5. Summed peristimulus time histograms revealed stimulus-locked inhibition of spontaneous activity in 4% (8/195) or cortical and 18% (20/107) of thalamic neurons.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Somatosensory cortical efferent neurons of the awake rabbit: latencies to activation via supra--and subthreshold receptive fields.

1. Latencies to peripheral sensory stimulation were examined in four classes of antidromically identified efferent neurons in the primary somatosensory cortex (S1) of awake rabbits. Both suprathreshold responses (action potentials) and subthreshold responses were examined. Subthreshold responses were examined by monitoring the thresholds of efferent neurons to juxtasomal current pulses (JSCPs) delivered through the recording microelectrode (usually 1-3 microA). Through the use of this method, excitatory postsynaptic potentials (EPSPs) and inhibitory postsynaptic potentials (IPSPs) were manifested as decreases and increases in threshold, respectively. Efferent populations examined included callosal (CC) neurons, ipsilateral corticocortical (C-IC) neurons, and descending corticofugal neurons of layer 5 (CF-5) and layer 6 (CF-6). Very brief air puffs (rise and fall times 0.6 ms) were delivered to the receptor periphery via a high-speed solenoid valve. 2. Whereas all CF-5 neurons had demonstrable suprathreshold excitatory and/or inhibitory responses to peripheral stimulation, most CC, C-IC, and CF-6 neurons did not. CC and CF-6 neurons that yielded no suprathreshold response to the stimulus had lower axonal conduction velocities than those that did respond (P < 0.0001 in both cases). However, subthreshold receptive fields could be demonstrated in many of the otherwise unresponsive CC (81%), C-IC (88%), and CF-6 (43%) neurons. The subthreshold responses usually consisted of an initial excitatory component (a decrease in the threshold to the JSCP) and a subsequent long-duration (> 80 ms) inhibitory component. A few neurons (1 CC, 1 C-IC, and 5 CF-6) showed an initial short latency inhibitory response in the absence of any excitatory component. 3. Some CC and C-IC neurons yielded supra- and/or subthreshold responses to peripheral stimulation at latencies of 6.1-7 ms. All such neurons were found at intermediate cortical depths (thought to correspond to deep layer 2-3 through layer 5). It is argued that such latencies are indicative of monosynaptic activation via thalamic afferents. Very superficial CC and C-IC neurons, and all CF-6 neurons responded to latencies of > 7 ms. All CF-5 neurons responded to latencies of > 8 ms, although many were found at the same depth as the deeper CC and C-IC neurons that responded at monosynaptic latencies. These results indicate that cortical cell type as well as laminar position are important factors that determine the sequence of intracortical neuronal activation after peripheral sensory stimulation.

Action Potentials↗

Role of herpes simplex virus thymidine kinase expression in viral pathogenesis and latency.

Herpes simplex virus (HSV) thymidine kinase (TK) expression and the HSV TK gene have been evaluated in studies of gene control, as well as in animal and human studies of viral pathogenesis, including HSV latency. In investigations of the biological role of HSV TK, enzyme expression was noted to be important for HSV infection of nonreplicating cells in culture; and, in experimental animal studies, HSV TK was shown to be important for in vivo latent infection of sensory ganglion neurons. Latency in these studies was determined by the ability of HSV to reactivate from sensory ganglion explants. In recent studies, investigators sought to determine whether the role HSV TK expression plays in latency is primarily in the establishment and maintenance of latency or in the reactivation process. Following infection of experimental animals with HSV TK-deficient mutants, the presence of HSV in ganglia was detected in complementation, rescue, and molecular biological studies. Results suggest that HSV TK expression may be important for HSV reactivation from latency. This was supported by in situ hybridization investigations. In the latter studies, HSV latency associated transcript (LAT) was present in ganglion neurons, although reactivation of HSV from such ganglia was defective. LAT-expressing, reactivation-defective infections established by TK mutants of HSV are considered examples of incomplete latency. From the present review, it appears that HSV TK expression, particularly TK expression of HSV-1, is important for the reactivation of latent HSV infection of sensory ganglion neurons, probably because of limited neuronal TK expression and absent replication capacity of these cells.

Animals↗

P300 latency in geriatric depression.

OBJECTIVE: The purpose of this study was to determine if P300 latency is prolonged in geriatric depression and if longer P300 latency and deficits in initiation and errors of perseveration in depressed elderly patients are related to risk factors for vascular disease. METHOD: Geriatric patients with unipolar depression (N = 43) and elderly comparison subjects (N = 24) were assessed for depressive symptoms, cognitive functions, risk factors for vascular disease, and P300 latency. RESULTS: Depressed elderly patients had longer P300 latency than normal elderly subjects. In the depressed patients, P300 latency was related to deficits in initiation and errors in perseveration. Risk factors for vascular disease were associated not only with P300 latency but also with deficits in initiation and errors in perseveration. CONCLUSIONS: Functional impairment of the cortico-striato-pallido-thalamo-cortical pathways from vascular disease, implicated in late-life depressive disorders, may explain not only deficits in initiation and errors in perseveration but also longer P300 latency in depressed elderly patients. These results are preliminary and need further examination with brain imaging and more sensitive neuropsychological measures.

Aged↗

Effect of click rate on the latency of auditory brain stem responses in humans.

Auditory brain stem responses are the far-field reflections of electrical activity originating in the auditory pathway in its course from the cochlea to cortex that can be recorded from scalp electrodes using computer averaging techniques. There are seven components in the initial 10 msec following a click signal which have been shown to have an orderly change in latency as a function of signal intensity. The results of this study show that click repetition rate can also significantly affect the response latency measure. Responses were measured in six normal hearing subjects at click rates of 10, 30, 50 and 100/sec and af four intensity levels (30, 40, 50, and 60 dB sensation level). The mean latency shift of component V was approximately 0.5 msec when the responses at 10 and 100/sec were compared. This is equivalent to a 15-20 dB decrease in signal intensity at the 10/sec click rate. An analysis of the time of occurrence of this shift using brief click trains at 100/sec showed the shift in latency to be complete by the fifth click. The latency shift was similar at the four signal levels tested. The latency shift was similar at the four signal levels tested. The latency shift of component V appeared to be a monaural and therefore a potentially peripheral process. The results are interpreted as an objective measure of adaptation in the human auditory system with implications for the measurement in disorders of hearing.

Acoustic Stimulation↗

The role of the facial nerve latency test in the prognosis of Bell's palsy.

Eighty patients with idiopathic facial nerve palsy were evaluated by the facial nerve latency test. Depending on the latency time, the patients were classified into the following four groups: group A patients had normal latency times (3.25 msec); group B patients had slightly extended latency times (4 to 7 msec) and a mean of 5.6 msec; group C patients had extended latency times (10 to 14 msec) and a mean of 10.2 msec; and group D patients displayed complete disappearance of evoked compound muscle action potential (no responses). Under the same therapeutic regimen, it was determined that, when the latency time was normal or close to normal, the functional recovery of the nerve was complete or almost complete, and the recovery time was short. When the latency time was extended or there was no response, the functional recovery of the nerve was either incomplete or absent.

Adolescent↗

Utility of P300 auditory event related potential latency in detecting cognitive dysfunction in growth hormone (GH) deficient patients with Sheehan's syndrome and effects of GH replacement therapy.

OBJECTIVE: Impaired cognitive function has been demonstrated in adults with growth hormone (GH) deficiency (GHD) by using different neuropsychological tests. Despite several studies, present knowledge about the impact of GHD and GH replacement therapy (GHRT) on cognitive function is limited. P300 event-related potential (ERP) application is a well-established neurophysiological approach in the assessment of cognitive functions including the updating of working memory content and the speed of stimulus evaluation. GHD is a well-known feature of Sheehan's syndrome and cognitive changes due to GHD and the effects of GHRT remain to be clarified. The present study was designed to investigate the effects of GHD and 6 months of GHRT on cognitive function in patients with Sheehan's syndrome by using P300 latency. DESIGN AND METHODS: The study comprised 14 patients with Sheehan's syndrome (mean age, 49.5+/-7.8 years) and 10 age-, education- and sex-matched healthy controls. With hormone replacement therapy, basal hormone levels other than GH were stable before enrollment and throughout the GHRT. The diagnosis of GH deficiency was established by insulin-tolerance test (ITT), and mean peak level of GH in response to insulin hypoglycemia was 0.77+/-0.35 mIU/l. Treatment with GH was started at a dose of 0.45 IU (0.15 mg)/day in month 1, was increased to 0.9 IU (0.30 mg)/day in month 2 and was maintained at 2 IU (0.66 mg)/day. Initially baseline auditory ERPs in patients and controls were recorded at frontal (Fz), central (Cz), and parietal (P3 and P4) electrode sites. In the patient group, ERPs were re-evaluated after 6 months of GH replacement therapy. During each session P300 amplitude and latency were measured. RESULTS: Mean serum insulin-like growth factor-I (IGF-I) concentration in the patient group before GHRT was 23+/-13 ng/ml. After 6 months of GH therapy mean IGF-I significantly increased to an acceptable level, 234+/-71 ng/ml (P<0.05). The mean latencies (at all electrode sites) of the patients before GHRT were found to be significantly prolonged when compared with those of normal controls (P<0.05). After 6 months of GHRT mean P300 latencies (at all electrode sites) were decreased significantly when compared with latencies before treatment (P<0.05). CONCLUSIONS: The present study, using P300 ERP latencies, therefore suggests an impairment of cognitive abilities due to severe GHD in patients with Sheehan's syndrome and an improvement of cognitive function after 6 months of physiological GHRT. Moreover, this was a novel application of P300 ERP latencies in cognitive function detection in patients with GHD. Further studies with different patient groups need to be done to assess the clinical use of this electrophysiological method in the diagnosis of cognitive dysfunction due to GHD.

Acoustic Stimulation↗

Auditory generalization gradients for response latency in the monkey.

Two monkeys were trained to press and hold a response key in the presence of a light and to release it at the onset of a pure tone. Initially, all responses with latencies shorter than 1 sec were reinforced without regard to the frequency of the pure tone, and the intensity of the pure tone that resulted in equal latencies at each frequency was determined. The second stage of the experiment consisted of discrimination training, during which releases to one pure-tone frequency (positive stimulus) were reinforced and releases to a second frequency (negative stimulus) were extinguished. Median latencies to the negative stimulus slowly increased as did the variability of the latency distribution for the negative stimulus. There was no evidence of a concurrent decrease in latencies to the positive stimulus indicative of behavioral contrast. The third part of the experiment consisted of determining maintained generalization gradients by increasing the number of nonreinforcement stimuli. The gradients that eventually resulted showed approximately equal latencies to all frequencies of the negative stimulus and shorter latencies to the positive stimulus frequency.

Animals↗

Global increase in response latencies by early middle age: complexity effects in individual performances.

Ten young women (age 20 to 22 years) and 10 middle-aged women (age 36 to 44 years) served as subjects in choice reaction time, letter classification, and abstract matching-to-sample tasks. In each of seven conditions, the older group responded more slowly than the younger group. Age differences showed a complexity effect. That is, differences between the latencies of young and old subjects increased as the latency of the young subjects increased. Both linear and power functions accurately described the relation between the latencies of the middle-aged and young adult groups. This was true not only for the relation between average latencies but also for the relation between corresponding quartiles of latency distributions. Similar results were observed at the individual level: All middle-aged subjects showed complexity effects, and, for each middle-aged subject, the relation between her latencies and those of the average young adult was well described by linear and power functions. These findings indicate that age-related slowing is apparent by age 40, and that complexity effects are observable in individual performances. This slowing is global and not specific to particular tasks, as indicated by the fact that the latencies of older adults can be predicted directly from those of younger adults without regard to the nature of the task.

Adult↗

Latency of saccadic eye movement during contraction of bilateral and unilateral shoulder girdle elevators.

We compared the timed latencies of saccadic eye movement during isometric contraction of the bilateral and unilateral shoulder girdle elevators in a sitting posture. Muscle contraction force was increased in 10% increments from 0% to 60% of the maximal voluntary contraction (MVC) of each side. Saccadic latency was measured as the latency to the beginning of eye movement toward the lateral target that was moved at random intervals in 20 degree amplitude jumps. Eye movement was measured using the electro-oculogram technique. During bilateral contraction, saccadic latency decreased until 30% MVC and then began to increase at 40% MVC. During unilateral contraction, saccadic latency decreased until 30% MVC in a similar pattern as in bilateral condition, was constant from 30% MVC to 50% MVC, followed by a slight increase at 60% MVC. The saccadic latencies at 10% and 40-60% MVC were significantly shorter during unilateral contraction than bilateral contraction. Thus, the relative force for producing a marked shortening of saccadic latency is observed within a wider range during unilateral contraction than bilateral contraction.

Adolescent↗

ABR latency in infants: properties and applications of various measures.

ABR latency ratios have been proposed as useful clinical tools in the assessment of infants at risk for auditory or neurologic deficits. These parameters, together with classical absolute and interwave latency measures, were examined in 131 infants with normal ABR thresholds at 48-64 weeks post-conceptional age, and with no conventional risk factor for hearing impairment or neurological abnormality. Latency of wave I is unaffected by age or gender, but that of waves III and V decreases linearly with age and is smaller in females. These effects must be accounted for in clinical evaluation. However, latency ratios V/I, V/III and III/I show no significant age or gender effects. Wave I latency and the V/I latency ratio both permitted very good discrimination between normal infants and those with presumed conductive hearing losses, but the effects of sensorineural impairment have yet to be determined. On a priori grounds it seems improbable that latency ratios will outperform classical ABR parameters, at least for the goals and age range considered in this study.

Acoustic Stimulation↗

2f1-f2 distortion product otoacoustic emission latency: changes with frequency and level of primaries.

Distortion product otoacoustic emissions (DPOAEs) provide a non-invasive and relatively direct method for evaluating cochlear travel time in humans. In the present study, the 2f1-f2 DPOAE latency was deduced from DPOAE phase shift according to f2 frequency shift, with f1 being fixed, using the ILO92 system. Latencies of 2f1-f2 DPOAEs were recorded at various primary frequencies and levels. Results were not wholly consistent with previous latency estimates. This study showed that the functions describing both 2f1-f2 DPOAE latency decrease with primary frequency increase, at several primary-tone levels, and 2f1-f2 DPOAE latency decrease with primary-level increase, at various frequencies, are best fit by exponential equations. The results of the evaluation of the latency-frequency-level relationship indicated the possibility of linking these three variables by the following expression: Latency = 68.30 exp (-0.027I -0.000434 f)+1.13.

Acoustic Stimulation↗

Association of serum testosterone levels with latencies of somatosensory evoked potentials from right and left posterior tibial nerves in right-handed young male and female subjects.

The relationships between serum testosterone levels and somatosensory evoked potential (SEPs) latencies from the right and left posterior tibial nerves (PTNs) were studied in right-handed young men and women. The corrected P1 (P39) and N1 (N49) latencies from the right PTN (left hemisphere) were found to be significantly longer in females than males. The corrected P2 and N2 latencies from both PTNs were longer in females than males. Testosterone was not associated with N1 latencies. In females, there was a negative linear correlation between testosterone and latencies from the right and left PTNs. These relationships were complex in males depending upon foot and eye preferences. The following results were obtained from males: no correlation with P1, N1, and P2, but a direct relation with P2 from left PTN in total sample; in males with right eye and right foot preference, a direct correlation only with P1 from right and left PTNs; in mixed- and left-eyed males, inverse correlations with P1, N1, and P2 latencies especially from right PTN; in right-eyed males, direct correlation with P1, inverse correlation with P2 from left PTN; in right-footed males, direct correlation with P1 and N2 waves from right and left PTNs. The interpeak latencies also showed sex-related differences. The overall results suggested that the left brain would be the main target for testosterone effects in both sexes, which may be beneficial for females but mainly disadvantageous for males.

Adolescent↗

Relation of nonverbal intelligence assessed by Cattell's Culture Fair Intelligence Test to latencies of the somatosensory evoked potentials elicited by stimulation of the posterior tibial nerves in right-handed male and female subjects.

The association of nonverbal intelligence (NVI) with latencies of the somatosensory evoked potentials from the right and left posterior tibial nerves (PTNs) was studied in right-handed male and female subjects without familial sinistrality (FS-). There was a significant negative linear correlation between N49-P39 interpeak latencies from the right and left PTNs in females and a significant positive linear correlation between these parameters in males. There was no significant correlation between P58-N49 interpeak latencies and NVI in females, but a significant negative linear correlation in males. The N76-P58 interpeak latencies were found to be positively linearly related to NVI only in females; there was no correlation between these parameters in males. There was no significant correlation between IQ and side differences in SEP latencies in females. The right minus left P39 latencies from the right and left PTN were found to be negatively linearly related to IQ in males. In females with nearly equal heights, latencies of N49 waves were found to be negatively linearly related to IQ. In males with nearly equal heights, only P39 and P58 waves from the right PTN were found to be negatively linearly related to IQ. These results did not support the hypothesis of speed of information processing by the brain in behavioral intelligence. An asymmetrical organization of the male brain seems to be disadvantageous for nonverbal intelligence; the female brain appeared to be independent of the degree of asymmetrical organization of the brain in this respect.

Adult↗

Middle latency auditory evoked potentials in intensive care patients and normal controls.

Evoked potentials have been introduced into intensive care unit to objectively measure parameters of coma. In particular, auditory brainstem evoked potentials have been useful for localizing brainstem dysfunction in comatose patients. The middle latency auditory evoked potentials (MLAEPs) believed to be a response of subcortical auditory radiations and the primary auditory cortex. MLAEPs were measured in 40 adults (mean age 24.9 +/- 2.9 years; range: 19-34 years) with normal hearing and in 102 intensive care patients (mean age: 48.4 +/- 18.9 years; range: 14-86 years) under the influence of biological variables. Latencies (control group, mean +/- SD: V = 5.74 +/- .29 ms, N0 = 9.11 +/- 1.74 ms, P0 = 12.94 +/- 1.87 ms, Na = 17.23 +/- 1.77 ms, and Pa = 29.22 +/- 3.43 ms), amplitudes (control group, mean +/- SE: N0-P0 = 2.00 +/- .34 microV, P0-Na = 3.88 +/- .67 microV, Na-Pa = 2.83 +/- .29 microV) and the amplitude ratio (control group, mean +/- SE: P0-Na/Na-Pa = 1.53 +/- .39) were calculated. In the control group in both females and males, right-sided stimulation produced shorter average MLAEP latencies and higher amplitudes than left-sided stimulation (Pa-right 28.26 +/- 3.53 ms; Pa-left 30.17 +/- 3.33 ms). MLAEPs showed significant differences according to sex but did not depend significantly on age. A temperature dependence was found for the latency of wave V (short latency AEP), which was prolonged at lower temperatures and for the amplitude Na-Pa, which was increased at decreased temperatures between 38.9 and 35.4 degrees C. There was a significant association between the amplitude Na-Pa and PO2 (P = .017). Alterations of PCO2 in the range of 26 to 54 mmHg did not influence the MLAEPs. Also, renal dysfunction or hepatic dysfunction and alterations of mean arterial pressure (range: 50-102 mmHg) did not affect MLAEP latencies and amplitudes significantly. Increases in latencies and decreases in amplitude were seen in sedated patients. These results in intensive care patients suggest that the combination of early AEP (acute phase) and MLAEP (post acute phase) may be useful to monitor comatose patients.

Adolescent↗

Treatment with AC pulsed electromagnetic fields normalizes the latency of the visual evoked response in a multiple sclerosis patient with optic atrophy.

Visual evoked response (VER) studies have been utilized as supportive information for the diagnosis of multiple sclerosis (MS) and may be useful in objectively monitoring the effects of various therapeutic modalities. Delayed latency of the VER, which reflects slowed impulse transmission in the optic pathways, is the most characteristic abnormality associated with the disease. Brief transcranial applications of AC pulsed electromagnetic fields (EMFs) in the picotesla flux density are efficacious in the symptomatic treatment of MS and may also reestablish impulse transmission in the optic pathways. A 36 year old man developed an attack of right sided optic neuritis at the age of 30. On presentation he had blurring of vision with reduced acuity on the right and fundoscopic examination revealed pallor of the optic disc. A checkerboard pattern reversal VER showed a delayed latency to right eye stimulation (P100 = 132 ms; normal range: 95-115 ms). After he received two successive applications of AC pulsed EMFs of 7.5 picotesla flux density each of 20 minutes duration administered transcranially, there was a dramatic improvement in vision and the VER latency reverted to normal (P100= 107 ms). The rapid improvement in vision coupled with the normalization of the VER latency despite the presence of optic atrophy, which reflects chronic demyelination of the optic nerve, cannot be explained on the basis of partial or full reformation of myelin. It is proposed that in MS synaptic neurotransmitter deficiency is associated with the visual impairment and delayed VER latency following optic neuritis and that the recovery of the VER latency by treatment with pulsed EMFs is related to enhancement of synaptic neurotransmitter functions in the retina and central optic pathways. Recovery of the VER latency in MS patients may have important implications with respect to the treatment of visual impairment and prevention of visual loss. Specifically, repeated pulsed applications of EMFs may maintain impulse transmission in the optic nerve and thus potentially sustain its viability.

Adult↗

Changes in the auditory middle latency responses during all-night sleep recording.

The middle latency response (MLR) using wide band-pass filters shows marked changes in amplitude, latency and configuration in sleep. The components with latencies greater than 20 ms show the greatest variability. There is a significant increase in Pa latency in stages 2 and stages 3/4, and in some cases a disappearance of the Nb component with the development of a broad positivity of latency intermediate to Pa and Pb which dominates the response. The responses in REM are of similar latency and configuration as in wakefulness but of reduced amplitude. The 40 Hz response is markedly reduced in amplitude in all sleep stages reflecting a decrease in the contribution of the middle latency components to this composite response. This appears to arise through a loss of 40 Hz periodicity in slow wave sleep and an increase in the slow 10 Hz component. In REM sleep, there is an overall reduction in amplitude. Much of the reported variability of the MLR in the literature arises from the widely differing band-pass filters used and the inadequate control for level of arousal. Both these factors have been shown to produce significant changes in the response.

Adult↗