- Email: [email protected]
Intraoperative monitoring: The brainstem
s4
Plenary
general issues are raised. Does “normal” mean representative of a particular age or absence of specific sleep disorders? Are sleep related respiratory disturbances and periodic limb movement disorder, which increase markedly with elderly, part of normal aging? To what extent do reduced activity levels, ambient, light decreases, ease of taking naps, masked depression and other frequent accompaniments of aging deteriorate sleep, independent of structural brain changes? Where does the interface lie between normal aging and dementia in relation to sleep? Some of the well documented features of sleep in the elderly are: Sleep Architecture: Decrease (minor) in time asleep, longer sleep latency increased wakefulness after sleep onset, decreased slow wave sleep (SWS). Decreased SWS consists of lowered amplitude rather than number of slow waves. It begins in early adulthood, is greater in males and has been reported in lower mammals. Sleep Homeostasis: Sleep deprivation followed by recuperation shows a more rapid (then in younger Ss) return to habitual sleep length, SWS, daytime sleepiness on MSLT. and performance. Circadian Rhythms: There is general realignment of circadian rhythms in the elderly. Sleep is often phase advanced relative to clock time and sometimes combined with daytime napping. The circadian temperature rhythm is phase advanced relative to sleep and lower in amplitude. Neuropathological studies and animal experiments point to reduced efficiency of the pacemaker in the suprachiasmatic nuclei plus possible impaired entrainment. Sleep Disorders: There is a very high incidence (45%) of periodic limb movement disorder, with or without restless legs. Either may cause insomnia or simply be a co-morbid condition. As well, snoring and sleep apnoea become very common, especially in elderly males. Obesity, hypertension and death in sleep remain obscure.
Corticomotoneuronal
Connections:
D. Burke. Institute of NeurologicalSciences, Street, Sydney, NSW.2031, Australia
Physiological
Studies
Prince of Wales Hospital, High
While magnetic stimulation has largely superseded electrical as the preferred method for transcranial activation of corticospinal pathways in diagnostic studies, electrical stimulation remains superior for monitoring purposes in anaesthetized patients, and both are useful in studies of physiological mechanisms. 1. The compound muscle action potential evoked by motor cortex stimulation is due to the fast conducting component of the corticospinal system with conduction velocity of 60-80 m/s in the spinal cord. 2. Single magnetic and electrical stimuli produce complex descending volleys which contain both D waves and I waves. With both magnetic and electrical stimuli (but particularly with magnetic), some l-wave activity may occur in corticospinal axons that have not responded in the D wave. 3. The D and I waves lead to temporal summation of monosynaptic EPSPs (and disynaptic IPSR) in the spinal motoneuronal pool, such that the latency and intensity of the motoneurone discharge reflect (i) the background excitability of the motoneurone pool, (ii) the amplitudes of individual components of the cotticospinal volley, and (iii) the complexity of the volley. 4. Electrical stimulation can evoke a much more intense corticospinal volley than magnetic. As confirmed by direct recording from the pyramids and by stimulation applied between the mastoids, electrical stimulation on the scalp over the motor cortex can access the corticospinal system at the pyramidal decussation. 5. Anaesthetics can profoundly depress corticospinal activation of the motoneurone pool, such that epidural recordings of the descending spinal volley provide more reproducible recordings for spinal cord monitoring than the compound muscle action potential.
Epileptic Transformation
of Neuronal Activity
G. Buzsaki. A. Bragin. institution Rutgers, The State University ofN.J., CML3N Aidekman Research Ctc, 197 UniversityAvenue, Newark, NJ 07102, USA lnterictal spikes (IIS) are believed to emerge as a result of synchronous discharge of large neuronal populations. However, the identity of neuronal populations in the various types of IIS, and the mechanism of the fast neuronal recruitment is unknown. Based on various epilepsy models we suggest that (a) two basic forms of IIS emerge in the hippocampus (Type 1 and 2). (b) they reflect excessively fast recruitment of different classes of
Abstracts
cells and (c) the physiological basis for both types of interictal spikes are present in the intact hippocampus (sharp waves, SPW, and dentate spikes, DS, respectively). SPW and DS occur simultaneously in both hemispheres, SPW reflect summated EPSPs of the apical dendrites of CA1 pyramidal neurons as a result of cooperative synchrony in the CA3 recurrent network. SPW-associated network bursts spread to the subiculum and the entorhinal cortex. The spatial distribution and cellular generation of SPW and Type 1 IIS are identical. DS emerge as a result of synchronous discharge of hilar interneurons and consequent synchronous inhibition of granule cells. We hypothesize that Type 2 IIS reflect excessive synchronization of the interneurons that underlie the generation of DS.
Intraoperative
Monitoring: The Brainstem
G.-E. Chatrian. University of Washington, Seattle, WA 98195, USA
NN282A, Medical
Center RC-97,
Removal of cerebella-pontine angle (CPA) tumors, especially suboccipital removal of acoustic neuromas. and other posterior fossa surgeries variously threaten the integrity of the cochlea, the auditory nerve, and the brainstem. We simultaneously monitor intraoperatively click-evoked potentials from: (1) the cochlea (cochlear microphonics [CM] and summating potentials [SP]), (2) the auditory nerve (Nl component of the auditory nerve compound action potential [API), and (3) the brainstem (BAEPs). Cochlear and auditory nerve responses are detected by a pretragal transtympanic promontory needle electrode (Prass et al., 1987) and BAEPs are recorded by surface leads. We alternate blocks of responses to excitation of the ear ipsilateral to surgery with BAEPs to stimulation of the contralateral ear. When hearing and BAEPs are inadequately preserved preoperatively on the side of surgery, we monitor BAEPs to stimulation of the contralateral ear, short-latency median nerve-evoked potentials, or both. EVPs and video images of the surgical field are viewed and assessed remotely in the EEG laboratory. Monitoring of responses from multiple levels of the auditory pathways is crucial in determining whether BAEP alterations indicate brainstem to cochlear or auditory nerve dysfunction (Levine dysfunction or are secondary et al. 1984). Certain changes may be reversed by prompt remedial action. Extreme, lasting alterations of latencies. interpeak intervals and amplitudes are often associated with postoperative deficits. However, because complex factors influence outcome, formulation of simple interpretative criteria is an elusive goal. Irreversible electrophysiologic alterations associated with postoperative deficits have increased awareness of potentially harmful effects of certain operative manipulations and prompted beneficial modifications of surgical technique.
Electrophysiology
of Tropical Neuropathies
J.S. Chopra, S.K. Bansal, V. Lal. S. Prabhakar. Postgraduate institute of Medical Education EtResearch, Chandigarh, Dept. of Neurology Pgimer Chandigarh, tndia Peripheral neurophaties (PN) constitute a neglected aspect of epidemiological and clinical research in tropical countries of Asia, Africa and South America. Community surveys are limited and hospital based studies do not provide a true picture of the pattern of peripheral nerve disorders. Diabetes, Leprosy and Guillian Barre Syndrome (GBS) are among the commonest causes of PN. Other distinctive causes of tropical PNs include infectious disorders - paralytic rabies, tetanus, Chagas disease and other parasitosis; nutritional disorders - protein energy malnutrition, tropical sprue. pellagra and Beri-Beri: toxins - lead, arsenic, organ0 phosphates, drugs, plant and animal toxins. Geographical predilections observed in the case of certain disorders are Chagas disease, plant and animal toxin induced paralysis in Central America, Arsenic neuropathy in North India and Tropical ataxic neuropathy in East Africa. Two hundred and sixty five patients of peripheral neuropathies due to various causes were studied electrophysiologically at Postgraduate Institute of Medical Education Et Research, Chandigarh, India in 7 years (1985-1991) which excluded 70 patients of diabetic neuropathy. Diabetic neuropathy is not being discussed since its patterns are similar to the developed Western world. Thirty six of total 48 leprosy patients had mononeuritis multiplex while 12 had mononeuropathy. Electromyographic (EMG) and nerve conduction (NC) studies of median, ulnar 8 common peroneal revealed a diffuse lesion affecting motor nerves equally common as compared to sensory, Clinical silent lesion were also demonstrated. In Leprosy EMG 8 NC studies suggested mixed demyelinating and axonal insult. However in 125 patients of GBS. demyelination of the peroneal nerves was
Plenary
general issues are raised. Does “normal” mean representative of a particular age or absence of specific sleep disorders? Are sleep related respiratory disturbances and periodic limb movement disorder, which increase markedly with elderly, part of normal aging? To what extent do reduced activity levels, ambient, light decreases, ease of taking naps, masked depression and other frequent accompaniments of aging deteriorate sleep, independent of structural brain changes? Where does the interface lie between normal aging and dementia in relation to sleep? Some of the well documented features of sleep in the elderly are: Sleep Architecture: Decrease (minor) in time asleep, longer sleep latency increased wakefulness after sleep onset, decreased slow wave sleep (SWS). Decreased SWS consists of lowered amplitude rather than number of slow waves. It begins in early adulthood, is greater in males and has been reported in lower mammals. Sleep Homeostasis: Sleep deprivation followed by recuperation shows a more rapid (then in younger Ss) return to habitual sleep length, SWS, daytime sleepiness on MSLT. and performance. Circadian Rhythms: There is general realignment of circadian rhythms in the elderly. Sleep is often phase advanced relative to clock time and sometimes combined with daytime napping. The circadian temperature rhythm is phase advanced relative to sleep and lower in amplitude. Neuropathological studies and animal experiments point to reduced efficiency of the pacemaker in the suprachiasmatic nuclei plus possible impaired entrainment. Sleep Disorders: There is a very high incidence (45%) of periodic limb movement disorder, with or without restless legs. Either may cause insomnia or simply be a co-morbid condition. As well, snoring and sleep apnoea become very common, especially in elderly males. Obesity, hypertension and death in sleep remain obscure.
Corticomotoneuronal
Connections:
D. Burke. Institute of NeurologicalSciences, Street, Sydney, NSW.2031, Australia
Physiological
Studies
Prince of Wales Hospital, High
While magnetic stimulation has largely superseded electrical as the preferred method for transcranial activation of corticospinal pathways in diagnostic studies, electrical stimulation remains superior for monitoring purposes in anaesthetized patients, and both are useful in studies of physiological mechanisms. 1. The compound muscle action potential evoked by motor cortex stimulation is due to the fast conducting component of the corticospinal system with conduction velocity of 60-80 m/s in the spinal cord. 2. Single magnetic and electrical stimuli produce complex descending volleys which contain both D waves and I waves. With both magnetic and electrical stimuli (but particularly with magnetic), some l-wave activity may occur in corticospinal axons that have not responded in the D wave. 3. The D and I waves lead to temporal summation of monosynaptic EPSPs (and disynaptic IPSR) in the spinal motoneuronal pool, such that the latency and intensity of the motoneurone discharge reflect (i) the background excitability of the motoneurone pool, (ii) the amplitudes of individual components of the cotticospinal volley, and (iii) the complexity of the volley. 4. Electrical stimulation can evoke a much more intense corticospinal volley than magnetic. As confirmed by direct recording from the pyramids and by stimulation applied between the mastoids, electrical stimulation on the scalp over the motor cortex can access the corticospinal system at the pyramidal decussation. 5. Anaesthetics can profoundly depress corticospinal activation of the motoneurone pool, such that epidural recordings of the descending spinal volley provide more reproducible recordings for spinal cord monitoring than the compound muscle action potential.
Epileptic Transformation
of Neuronal Activity
G. Buzsaki. A. Bragin. institution Rutgers, The State University ofN.J., CML3N Aidekman Research Ctc, 197 UniversityAvenue, Newark, NJ 07102, USA lnterictal spikes (IIS) are believed to emerge as a result of synchronous discharge of large neuronal populations. However, the identity of neuronal populations in the various types of IIS, and the mechanism of the fast neuronal recruitment is unknown. Based on various epilepsy models we suggest that (a) two basic forms of IIS emerge in the hippocampus (Type 1 and 2). (b) they reflect excessively fast recruitment of different classes of
Abstracts
cells and (c) the physiological basis for both types of interictal spikes are present in the intact hippocampus (sharp waves, SPW, and dentate spikes, DS, respectively). SPW and DS occur simultaneously in both hemispheres, SPW reflect summated EPSPs of the apical dendrites of CA1 pyramidal neurons as a result of cooperative synchrony in the CA3 recurrent network. SPW-associated network bursts spread to the subiculum and the entorhinal cortex. The spatial distribution and cellular generation of SPW and Type 1 IIS are identical. DS emerge as a result of synchronous discharge of hilar interneurons and consequent synchronous inhibition of granule cells. We hypothesize that Type 2 IIS reflect excessive synchronization of the interneurons that underlie the generation of DS.
Intraoperative
Monitoring: The Brainstem
G.-E. Chatrian. University of Washington, Seattle, WA 98195, USA
NN282A, Medical
Center RC-97,
Removal of cerebella-pontine angle (CPA) tumors, especially suboccipital removal of acoustic neuromas. and other posterior fossa surgeries variously threaten the integrity of the cochlea, the auditory nerve, and the brainstem. We simultaneously monitor intraoperatively click-evoked potentials from: (1) the cochlea (cochlear microphonics [CM] and summating potentials [SP]), (2) the auditory nerve (Nl component of the auditory nerve compound action potential [API), and (3) the brainstem (BAEPs). Cochlear and auditory nerve responses are detected by a pretragal transtympanic promontory needle electrode (Prass et al., 1987) and BAEPs are recorded by surface leads. We alternate blocks of responses to excitation of the ear ipsilateral to surgery with BAEPs to stimulation of the contralateral ear. When hearing and BAEPs are inadequately preserved preoperatively on the side of surgery, we monitor BAEPs to stimulation of the contralateral ear, short-latency median nerve-evoked potentials, or both. EVPs and video images of the surgical field are viewed and assessed remotely in the EEG laboratory. Monitoring of responses from multiple levels of the auditory pathways is crucial in determining whether BAEP alterations indicate brainstem to cochlear or auditory nerve dysfunction (Levine dysfunction or are secondary et al. 1984). Certain changes may be reversed by prompt remedial action. Extreme, lasting alterations of latencies. interpeak intervals and amplitudes are often associated with postoperative deficits. However, because complex factors influence outcome, formulation of simple interpretative criteria is an elusive goal. Irreversible electrophysiologic alterations associated with postoperative deficits have increased awareness of potentially harmful effects of certain operative manipulations and prompted beneficial modifications of surgical technique.
Electrophysiology
of Tropical Neuropathies
J.S. Chopra, S.K. Bansal, V. Lal. S. Prabhakar. Postgraduate institute of Medical Education EtResearch, Chandigarh, Dept. of Neurology Pgimer Chandigarh, tndia Peripheral neurophaties (PN) constitute a neglected aspect of epidemiological and clinical research in tropical countries of Asia, Africa and South America. Community surveys are limited and hospital based studies do not provide a true picture of the pattern of peripheral nerve disorders. Diabetes, Leprosy and Guillian Barre Syndrome (GBS) are among the commonest causes of PN. Other distinctive causes of tropical PNs include infectious disorders - paralytic rabies, tetanus, Chagas disease and other parasitosis; nutritional disorders - protein energy malnutrition, tropical sprue. pellagra and Beri-Beri: toxins - lead, arsenic, organ0 phosphates, drugs, plant and animal toxins. Geographical predilections observed in the case of certain disorders are Chagas disease, plant and animal toxin induced paralysis in Central America, Arsenic neuropathy in North India and Tropical ataxic neuropathy in East Africa. Two hundred and sixty five patients of peripheral neuropathies due to various causes were studied electrophysiologically at Postgraduate Institute of Medical Education Et Research, Chandigarh, India in 7 years (1985-1991) which excluded 70 patients of diabetic neuropathy. Diabetic neuropathy is not being discussed since its patterns are similar to the developed Western world. Thirty six of total 48 leprosy patients had mononeuritis multiplex while 12 had mononeuropathy. Electromyographic (EMG) and nerve conduction (NC) studies of median, ulnar 8 common peroneal revealed a diffuse lesion affecting motor nerves equally common as compared to sensory, Clinical silent lesion were also demonstrated. In Leprosy EMG 8 NC studies suggested mixed demyelinating and axonal insult. However in 125 patients of GBS. demyelination of the peroneal nerves was