Biomedical subjects
Publications and source records attributed to N A Shaw.
The present investigation shows how, in certain circumstances, electroencephalography is capable of detecting the presence of cerebral dysfunction when CT head scanning fails to reveal that any abnormality is present.
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The effect of electroconvulsive shock on the cervical somatosensory evoked potential was studied in 20 male rats. Shock (80 mA for 600 ms) had no detectable effect on either the latency or amplitude of the cervical potential. This contrasts with the total loss of the cortical somatosensory evoked potential following electroconvulsive shock.
Experimental acceleration concussion was induced in 30 male rats who were immobilized with curare, artificially ventilated but not anaesthetised. Serial recordings of cortical somatosensory evoked potentials (SEPs) were made from the onset of concussion and for the following 30 min. Immediately after the head blow the initial three components of the SEP (P1, N1 and P2) were all either absent or markedly increased in latency. The late negative component (N2) was always abolished. All components reappeared and returned to approximately pre-concussion latencies within 5-6 min. The most persisting abnormality was in N2 whose post-concussion amplitude stabilized and remained depressed at only 50% of baseline value. The results suggest that experimental head injury produces a significant abnormality in every component of the evoked potential. The findings are therefore inconsistent with the theory that concussion differentially affects the diffuse nonspecific pathways whose activity is mediated by the reticular formation while leaving the lemniscal system comparatively intact. It is also shown that the morphology of the post-concussion SEP waveform can be quite accurately simulated by recording SEPs from normal animals at high rates of stimulation (50/s). This implies that the pathophysiology of concussion involves a temporary dysfunction in synaptic transmission although the level at which this is occurring has yet to be determined.
The calculation of central somatosensory conduction time by subtracting the peak latency of the cervical potential from that of the initial cortical response in patients in posttraumatic coma provides both a reliable indication of outcome plus an assessment of brain damage. The interpretation of such recordings is confounded in a minority of patients by the presence in the cortical SEP of a biphasic cortical negativity, giving the impression that the initial cortical response (N20) has bifurcated into two subcomponents. Depending upon which subcomponent is assumed to be N20, an individual recording may ambiguously appear to have a central conduction time either within normal limits or very abnormally prolonged. The aetiology and significance of this double peak phenomenon was studied in 30 patients with severe head trauma. It is concluded that the first of the subcomponents invariably represents the genuine N20 potential irrespective of its relative amplitude. The second subcomponent is assumed to be N25, a minor cortical potential which can be recorded in only a limited number of normal subjects. The double peak effect appears to be created by a distortion in the early cortical waveform probably due to the characteristic reduction in its amplitude following head injury.
The effect of pentobarbital on the auditory evoked response in the brainstem was studied in 20 male rats. Auditory evoked responses were recorded at regular intervals from the onset of a surgical level of anaesthesia until the return of spontaneous movement. There were small (less than 0.1 msec) but significant increases in the mean latency of each of the four major waves of the auditory evoked response under barbiturate anaesthesia. This is consistent with the effect of pentobarbital on far-field potentials generated from subthalamic locations in the somatosensory system. The mean transmission time in the brainstem, measured as the wave I-IV interpeak latency, increased significantly from 2.11 msec when the animals were awake to 2.15 msec when they were anaesthetized. The effect of pentobarbital on the amplitudes of the four waves was more complex than that on the latencies. Overall, there was an increase in the amplitude of wave I under barbiturate anaesthesia while wave II remained constant and wave III decreased. Wave IV was the component most affected by pentobarbital. In most animals there was either a marked reduction in amplitude or a complete abolition of this wave for one or more intervals during the period of anaesthesia.
The relative prognostic value of short-latency somatosensory evoked potentials (SEPs) and brain-stem auditory evoked potentials (BAEPs) was assessed in 35 patients with post-traumatic coma. Analysis of the evoked potentials was restricted to those recorded within the first 4 days following head injury. Abnormal SEPs were defined as an increase in central somatosensory conduction time or an absence of the initial cortical potential following stimulation of either median nerve. Abnormal BAEPs were classified as an increase in the wave I-V interval or the loss of any or all of its 3 most stable components (waves I, III and V) following stimulation of either ear. SEPs reliably predicted both good and bad outcomes. All 17 patients in whom SEPs were graded as normal had a favourable outcome and 15 of 18 patients in whom SEPs were abnormal had an unfavourable outcome. Although abnormal BAEPs were associated with an unfavourable outcome in almost all patients (6 of 7), only 19 of 28 patients with normal BAEPs had a favourable outcome. The finding of normal BAEPs was therefore of little prognostic significance. These results confirm the superiority and greater sensitivity of the SEP in detecting abnormalities of brain function shortly after severe head trauma.
Somatosensory evoked potentials (SEPs) were recorded from a 63 year old male who had sustained severe right sided cortical damage including infarction of the primary sensory hand area. When SEPs were recorded following right median nerve stimulation, both cervical and cortical waveforms were of normal configuration. When SEPs were recorded following left median nerve stimulation, the cervical potential was intact but the cortical waveform was absent and replaced with a positive-negative complex which was probably a far field reflection of thalamic activity. These findings suggest that the first negative component of the cortical SEP (N20) is not generated in the diencephalon but represents the initial response of the somatosensory cortex.
The effect of the regular administration of ibuprofen on pain following abdominal surgery was investigated in a double-blind placebo-controlled study. The analgesic action of ibuprofen was measured by a reduction in the amount of morphine self-administered from an On-Demand Analgesic Computer. Pain scores, nausea scores and blood loss were similar in both groups, but patients receiving ibuprofen demanded significantly less morphine in the 24 h after surgery.
Somatosensory evoked potentials (SEPs) were recorded simultaneously from scalp and neck locations following median nerve stimulation. By subtracting the latency of the major negative peak of the cervical SEP (N13) from that of the primary cortical response (N20), the central somatosensory conduction time was calculated (5.9 ms). On the descending slope of the cervical SEP was superimposed a positive potential of probable thalamic origin (P17). By subtracting the latency of N13 from that of P17 and P17 from that of N20 respectively, the transit time for the afferent volley both within the brainstem (3.9 ms) and the thalamo-cortical radiation (2.0 ms) was obtained.
The effect of electroconvulsive shock (ECS) on the cortical somatosensory evoked potential (SEP) was studied in 25 male rats. SEPs were recorded after stimulation of the contralateral forepaw. Animals were curarized and artificially ventilated but not anesthetized. The magnitude of the ECS was 80 mA for 600 ms which produced tonic-clonic convulsions lasting an average 54 s in noncurarized control animals. SEPs were recorded during the ictal period and then at intervals for 20 min. ECS initially caused the total abolition of all components of the SEP implying a significant but transient effect on activity propagated in specific and also possibly diffuse somatosensory pathways. The reappearance of the SEP coincided with the cessation of convulsive movements and the return of the corneal reflex. The return of the waveform to near baseline condition corresponded to the regaining of the righting reflex at approximately 3 min in the control animals. The most persisting change in the SEP waveform was in the shape of the late high-amplitude component (N2) which may reflect activity in the reticular formation. Following ECS, N2 reappeared with a peak latency notably decreased (approximately 1 ms) in comparison with the mean baseline recording. There was also an attenuation in the amplitude of N2 which remained significantly depressed (at less than 50% of mean baseline amplitude) throughout the post-ECS recording period. The results are compared with the relatively few studies of the acute effects of ECS on evoked potentials in psychiatric patients and also with a neuroendocrine theory which argues that the principal site and mode of action of ECS lies in the diencephalon.
A device is described for eliciting acceleration concussion in the awake rat. Animals, which were manually restrained, were struck on the occipital crest by a rubber knob attached to the striker wire of a spring-loaded rat trap. This method produced concussion with survival in over 50% of animals tested. The remainder were either simply stunned or else died shortly after the blow to the head. The device is compared with a number of alternate techniques designed to concuss the rat.
Cortical and lumbar somatosensory evoked potentials (SEPs) were recorded following unilateral stimulation of the tibial, peroneal and sural nerves in 20 normal adults. The active cortical electrode (Cz) was referred to either a cephalic (mid-forehead, contralateral central scalp, linked ears) or a non-cephalic (contralateral shoulder) site. The configuration of the short-latency cortical SEP waveforms was nearly identical irrespective of the nerve stimulated or the location of the reference. Central conduction times (CCTs) were also calculated by subtracting the peak latency of the lumbar SEP from that of the primary cortical response following stimulation of the tibial and peroneal nerves. A stronger relationship was consistently observed between the absolute cortical latency and height than between CCT and height. The potential clinical applications of the results are discussed.
Cortical somatosensory evoked potentials (SEPs) were recorded following experimental acceleration concussion in the rat. Immediately after head injury there was a general reduction in the amplitude of the SEP, and all its components were either temporarily abolished or increased in latency. The early components of the SEP recovered much more rapidly than did the amplitude and latencies of the later potentials. The purpose of the study was to investigate the relative effects of concussion on the lemniscal system (whose activity is reflected by the discrete early components of the SEP) and the reticular activating system (whose activity is reflected by the diffuse high amplitude late component of the SEP). Contrary to a widely accepted theory, there was a delay in transmission of somatosensory information through the lemniscal pathways as well as through the reticular system following head injury. Such an observation is consistent with recent studies of SEPs recorded from humans comatose after head trauma. As the changes in the morphology of the waveform of the SEP following concussion can be simulated by simply recording evoked potentials at high rates of stimulation, this suggests that the delays are caused by a failure or malfunction of synaptic transmission, but the level at which this is occurring remains to be determined.
Pattern visual evoked potentials (PVEPs) were recorded from 177 normal subjects aged 11-87 years. The purpose was to determine age-dependent changes in the latency of the individual components of the waveform. The initial components of the PVEP, which are thought to reflect activity in the primary visual (striate) cortex, showed no change in latency from 11-50 years followed by an abrupt increase occurring during the sixth decade. It is probable that this delay in the PVEP is mediated largely by pathophysiological changes occurring either in the eye or visual pathways, or both. The secondary components of the PVEP, which are presumed to be generated in the visual association areas of the extrastriate cortex, showed a progressive although initially very limited increase in latency starting after adolescence. It is suggested that those delays occurring between 21 and 50 years in the secondary components are mediated largely by intracortical factors. The more pronounced delays occurring for the older age groups (over 50 years) appear to be caused by a combination of cortical, subcortical and ocular changes in visual function. The prolongation of the later components in the age group 11-20 years seems to reflect maturational changes almost entirely confined to intracortical processes. The results are discussed in terms of the many conflicting reports of the effects of age on the PVEP.
Compressed spectral array (CSA) transforms the electroencephalogram into a succinct graphic display of changes in frequency and amplitude. We used CSA to monitor 51 comatose patients for at least 15 hours daily for up to 49 days. The crucial CSA feature was the presence or absence of a peak of activity within the theta or alpha frequency range (4.0 to 13 Hz). Persistence or return of this peak in the first 10 days of coma was seen in all patients who made a good recovery; continued absence of the peak for 10 days, or its return and loss, was associated with death or a residual disability.
Somatosensory evoked potentials were recorded simultaneously from the neck and scalp following stimulation of the median nerve at the wrist in 83 normal subjects aged 10-79 years. The central somatosensory conduction time was measured by subtracting the peak latency of the major response from the upper cervical area (N14) from that of the primary cortical response (N20). The central conduction time remained constant between 10 and 49 years but increased abruptly by approximately 0.3 msec between the fifth and sixth decades. Following this increase there was no further change in the central conduction time. Changes with age in the amplitude of N14 and N20 differed both from the changes in latency and from each other. The amplitude of N14 was stable between 10 and 39 years but then declined progressively. The amplitude of N20 deceased between 10 and 39 years and then increased until the end of the seventh decade.