Search PubMed⌕ Search

Biomedical subjects

W M Carroll

Publications and source records attributed to W M Carroll.

At least 55 records · Page 3Linked to original sources
PubMed1984

F-response studies: computer analysis and recovery cycle.

A computerized technique has been used for the analysis of F responses in normal subjects. Differences between the dominant and non-dominant upper limb have been found in some subjects and potentiation of the F response by the Jendrassik manoeuvre has been demonstrated. The recovery cycle of the F response has been studied in human subjects and in the rat and has been found to be similar to that of the H reflex. Such studies may be useful for studying alpha motor neurone excitability.

Adult↗
PubMed1983

Visual evoked potential abnormalities in Charcot-Marie-Tooth disease and comparison with Friedreich's ataxia.

Pattern-reversal visual evoked potentials (VEPs), recorded in 15 visually asymptomatic patients fulfilling the clinical and electrophysiological criteria of Charcot-Marie-Tooth disease (CMTD), were abnormal in 5 and possibly abnormal in another 3. Five patients showed a prolongation of P100 latency, one a reduction of amplitude and one a possibly abnormal "scotomatous" waveform. In 9 cases abnormalities were detected on neuro-ophthalmological examination. These were poorly correlated with VEP abnormalities, except for patients with 2 or more clinical eye signs. Relative central scotomata were found in the patient with an abnormal waveform. VEP abnormalities, where present, were usually fairly comparable in the 2 eyes. In comparison with a group of Friedrich's ataxia cases there was a lower overall incidence of VEP abnormalities in CMTD, but little to suggest a qualitative difference in the nature of the visual pathway pathology. All 4 patients with unequivocally abnormal VEPs had experienced atypical symptoms suggestive of CNS involvement. In none of these was it possible to sustain an alternative diagnosis. It is concluded that a minor degree of visual pathway involvement may be present in many CMTD cases, in spite of the fact that optic atrophy is only rarely reported, and that the VEP latency may reflect the degree to which other parts of the CNS are involved.

Adolescent↗
PubMed1983

Peripheral and central sensory nerve conduction in Charcot-Marie-Tooth disease and comparison with Friedreich's ataxia.

Somatosensory evoked potentials were recorded in response to stimulation of the median nerve at the wrist and the elbow in 14 cases of Charcot-Marie-Tooth disease (CMTD). Cervical and cortical latencies were used to derive conduction times and velocities over peripheral and central segments of the pathway. Sensory conduction velocities between the wrist and the elbow were distributed bimodally (12-27 m/s and 36-70 m/s), but did not correspond with the bimodality of motor conduction velocity values in 4 cases. Three patients had severely slowed sensory conduction in one arm but only moderate slowing in the other. In the majority of cases sensory conduction was considerably faster from the elbow to the spinal cord than from the wrist to the elbow. This was most apparent in 2 young patients, suggesting that demyelination secondary to axonal degeneration may gradually progress from distal to proximal segments. Compared with a group of Friedreich's ataxia (FA) patients, almost all CMTD cases could be distinguished by a greater degree of peripheral conduction slowing (not significant in FA). In FA there was a much higher incidence of impaired conduction over central segments of the somatosensory pathway, although evidence of this was also seen in 5 CMTD cases. Three of the latter had presented with atypical symptoms suggestive of CNS involvement, and also had delayed visual evoked potentials.

Adolescent↗
PubMed1983

Relapse of herpes simplex encephalitis after acyclovir therapy.

Acyclovir is a new and well tolerated anti-viral agent whose role in the treatment of herpes simplex encephalitis (HSE) is still being evaluated. Although relapse of adenosine arabinoside treated HSE has been documented, this paper describes the recurrence of encephalitis after treatment with the recommended course of Acyclovir. A more extended course of Acyclovir produced a rapid and sustained improvement with minimal residual neurological deficit. We emphasise the need for more prolonged treatment and an awareness of the possibility of relapse when using Acyclovir for HSE.

Acyclovir↗
PubMed1983

Hemimasticatory spasm--a peripheral paroxysmal cranial neuropathy?

The clinical and electrophysiological features of a case of hemimasticatory spasm are presented. The findings are in many respects similar to those described in hemifacial spasm. A peripheral cranial neuropathy as proposed in hemifacial spasm also may be responsible for hemimasticatory spasm.

Blinking↗
PubMed1983

Hemimasticatory and hemifacial spasm: a common pathophysiology?

The case is described of a 60-year-old woman with a 4-year history of left hemimasticatory spasm. Detailed electrophysiological studies are compared with those from 6 patients with typical idiopathic hemifacial spasm. On the basis of comparable patterns of EMG activity in the 2 conditions, it is concluded that they may have both a common pathophysiology and a peripheral site of involvement.

Aged↗
PubMed1983

Experimental demyelinating optic neuropathy: a model for combined morphological and electrophysiological studies.

A model is described for the morphological and electrophysiological study of demyelinative optic neuropathy in the rat. Cortical visual evoked potentials (VEPs) to flash stimuli were recorded before and after the intraneural microinjection of lysophosphatidyl choline (LPC) and galacto-cerebroside (Gal-C) antiserum. Progress was monitored by calculating the interocular latency differences (ILD) for the N40 and P60 components of the rat VEP, thus allowing a longitudinal evaluation of optic nerve function. Histological examination of the visual pathway using light and electron microscopy was performed at intervals through the course of the study. LPC produced a less selective lesion than did Gal-C antiserum. In lesions induced by the latter there was relatively little accompanying anoxal degeneration and subsequent remyelination was prominent. Control serum did not result in demyelination. This model should permit accurate electrophysiological and morphological correlations to be made during the developing and the reparative phases of demyelinative optic neuropathy and the assessment of potential therapeutic manoeuvres.

Animals↗
PubMed1980

Two distinct patterns of visual evoked response asymmetry in human albinism.

Results are presented which confirm that in human albinos each cerebral hemisphere receives a predominantly monocular input from the contralateral eye, giving rise to an asymmetry of the visual evoked potential (VEP) to whole-field stimulation which is similar to that for stimulation of the temporal half-field in the same individual. The further finding of two distinct, and in some respects opposite, types of topographical asymmetry raises the possibility that there are two anatomically distinct variants in the retinocortical projection in human albinism, as there are in the Siamese cat.

Albinism↗
PubMed1980

Pattern evoked potentials in human albinism. Evidence of two different topographical asymmetries reflecting abnormal retino-cortical projections.

In fifteen subjects with oculo-cutaneous or ocular albinism pattern-reversal visual evoked potentials (VEP) were recorded to monocular whole-field (16 degrees radius) and right and left vertical half-field (16 degrees radius) stimulation from an array of occipital electrodes. In all 15 subjects the VEP was of low amplitude and the monocular response to whole-field stimulation showed abnormal asymmetry in scalp topography. This asymmetry was similar to that produced by stimulation of the temporal half-field in the same eye. Two distinct types of VEP asymmetry were readily identified in different subjects. In 5 the major positivity of the response (P100) was distributed in the channels ipsilateral to the stimulated eye or temporal half-field, being similar in distribution to the P100 from the temporal hemifield or normal individuals. In 9 other subjects the converse occurred; the P100 was distributed contralaterally. The remaining subject was unique in that the responses from each eye had a distribution that resembled one of the two main groups. The nasal half-field responses also differentiated the two groups. On stimulation of the nasal field in the first group the P100 was usually absent or attenuated and when present it had the same topography as the temporal half-field P100. In contrast the nasal half-field P100 from the second group was always present and, although almost invariably smaller than the temporal half-field P100, it had an identical distribution. There was no correlation between these two patterns of VEP asymmetry and clinical or known genetic features. The findings confirm that in human albinos each hemisphere receives a predominantly monocular input from the contralateral eye; i.e. in addition to the temporal, half-field, approximately 20 degrees of the nasal half-field is projected to the hemisphere contralateral to each eye and not, as in normal subjects, to the ipsilateral hemisphere. Furthermore, the findings of two distinct and in some respects opposite types of VEP topographical asymmetry raises the possibility of two variants of the geniculo-cortical projection patterns existing in human albinos similar to those described in the Siamese cat.

Adolescent↗
PubMed1980

The incidence and nature of visual pathway involvement in Friedreich's ataxia. A clinical and visual evoked potential study of 22 patients.

Pattern-reversal visual evoked potentials (VEP) were recorded from 22 patients (mean age 33.7 years) with Friedreich's ataxia, 15 of whom also had a detailed neuro-ophthalmological assessment prior to the VEP examination. None had noted symptomatic visual impairment. Eleven of the 15 (73 per cent) examined clinically had one or more neuro-ophthalmic abnormality and 14/22 (64 per cent) had an abnormal VEP study which was always binocular and comprised absent responses, or most commonly, increased P100 component latencies. The maximum P100 latency was 143 ms and the group mean was 118 ms. The P100 amplitude was also generally reduced particularly in those patients with latencies less than 115 ms (upper limit of normal), while in those with latencies above the normal range there was a significant inverse correlation between the P100 amplitude and latency. The waveform, temporal dispersion and interocular differences were normal in almost all patients with identifiable responses, including those with prolonged VEP latencies. Electroretinograms recorded from three selected patients were either normal or minimally abnormal and suggested secondary rather than primary retinal involvement. The only VEP parameter to correlate with either the duration of the generalized disease or the visual acuity was the P100 amplitude. A good correlation was found between the VEP and the clinical neuro-ophthalmic findings. Temporal pallor of the optic disc was most often associated with an abnormal VEP result and impaired visual acuity or colour vision were uncommon in the absence of VEP abnormalities. The VEP changes and those obtained from 24 age- and acuity-matched cases of demyelinating optic neuritis are contrasted and the probable pathophysiology is discussed. Two main conclusions emerge from this study. First, there is a high incidence of asymptomatic visual pathway involvement in Friedreich's ataxia which can be demonstrated by both clinical and VEP examination. Secondly, the VEP changes in Friedreich's ataxia differ from those found in typical demyelinating optic neuropathy and are consistent with progressive nerve fibre loss and associated slowing of conduction, indicating that the visual pathway is affected by the same widespread process of axonal degeneration found throughout the nervous system.

Adult↗
PubMed1979

'Locked-in coma' in postinfective polyneuropathy.

A patient with postinfective cranial and peripheral polyneuropathy exhibited the electroencephalographic and behavioral features of "alpha coma". The relation of this form of extensive peripheral disconnection to those cases with central disconnection due to pontomesencephalic lesions is discussed. We conclude that in both situations further evaluation of brain stem and cortical function is necessary to determine whether or not consciousness is preserved, rather than relying solely on the presence of ocular movements and reactivity of the electroencephalogram.

Coma↗
PubMed1979

Alpha and beta coma in drug intoxication uncomplicated by cerebral hypoxia.

Four patients who were rendered comatose or stuporous by drug intoxication, but who were not hypoxic, are described. Three patients received high doses of chlormethiazole for alcohol withdrawal symptoms, and one took a suicidal overdose of nitrazepam. The patient with nitrazepam overdose and two of those with chlormethiazole intoxication conformed to the criteria of 'alpha coma', showing non-reactive generalized or frontally predominant alpha activity in the EEG. The fourth patient who was unconscious after chlormethiazole administration exhibite generalized non-reactive activity in the slow beta range. All four recovered completely without neurological sequelae following the withdrawal of the offending agents. The similarities between the effects of structural lesions and pharmacological depression of the brain stem reticular formation are discussed. It is suggested that in both situations disturbed reticulo-thalamic interactions are important in the pathogenesis of alpha coma. It is concluded that when this electroencephalographic and behavioural picture is seen in drug intoxication, in the absence of significant hypoxaemia, a favourable outcome may be anticipated.

Adult↗
PubMed1979

Leber's optic neuropathy: a clinical and visual evoked potential study of affected and asymptomatic members of a six generation family.

Fourteen clinically affected and 40 asymptomatic members of a six generation family with Leber's optic neuropathy have been studied clinically and by recording pattern-reversal visual evoked potentials. While 12 of the affected members had suffered the typical sequential bilateral failure of vision, in 2 the condition was still monocular after periods of 12 and 14 years. Reduced vascularity of the optic nerve head was found in 11 of these cases, all of whom had some degree of optic atrophy, and showed a significant correlation with the visual acuity. Excessive tortuosity of peripheral retinal vessels was noted in 6 cases and was a prominent feature in the unaffected eye of one of the subjects with monocular visual impairment. In cases with advanced visual impairment the VEP was absent bilaterally, while in those with less severe involvement responses which were delayed, desynchronized and much small than normal could still be recorded. Two subjects with early bilateral clinical involvement had normal or minimally abnormal responses. Repeat studies in 6 subjects after intervals of up to fifteen months showed no change in 4 and a deterioration in 2. It is concluded that the VEP findings in clinically affected subjects are in keeping with a severe demyelinating lesion of the optic nerve with associated nerve fibre loss. Mild impairment of colour vision, pallor or reduced vascularity of the optic nerve head, excessive tortuosity of retinal vessels, a small central scotoma, and/or mild abnormalities or atypical features of the VEP were found in 16 of the 40 asymptomatic family members studied. Such abnormalities were present in 50 per cent of descendants from the female lineage who were at risk of developing the disease, and also in 30 per cent of descendants from male lineages who were not at risk. These findings suggest that there is a stage prior to the onset of visual impairment during which subtle abnormalities may be detected in individuals at risk of developing or transmitting the disease. The finding of asymptomatic abnormalities in descendants from male lineages could be accounted for by transmission of a partial form of the disease by affected or unaffected males, which would be in accord with a cytoplasmic mechanism of transmission for the disease.

Adolescent↗