Showing papers in "Canadian Journal of Neurological Sciences in 1975"

Motor responses to sudden limb displacements in primates with specific CNS lesions and in human patients with motor system disorders.

Abstract: Central feedback pathways for motor control were studied by recording EMG responses to sudden upper limb displacements in humans and monkeys using a precision torque motor to generate step load changes. Normal human subjects showed three short-latency EMG responses (M1, M2 and M3) which appear to correspond to those recorded from trained monkeys. The M2 and M3 components, thought to represent feedback in supraspinal pathways, were significantly increased when the subjects were instructed to actively compensate for the load changes. Parkinsonian patients with rigidity showed evidence of markedly increased feedback over the interval for the M2 and M3 responses and appeared to have lost the ability to modulate feedback according to the motor task being performed. The results are discussed with reference to recent research on motor control mechanisms in primates and a tentative model for the basis of Parkinsonian rigidity is proposed.

Does the Engram of Kindling Model the Engram of Normal Long Term Memory

Abstract: The kindling effect is a relatively permanent alteration in brain function which results from repeated electrical or chemical stimulation and culminates in the appearance of electrographic and behavioral convulsions whenever the original stimulus is reapplied. The effect results from tetanic activation in the anterior cortex, limbic system or associated areas of the adult mammalian brain, and the lasting alterations are transynaptic and quite widespread. They are based in part on synaptic facilitation, and they are accompanied by specific alterations in normal behavior. In these and other respects, kindling is analogous to normal learning. It is possible that the stored component (engram) of kindling involves the same physiological mechanism as the engram of normal long term memory. Morphological study of identified synapses has not provided conclusive evidence for an anatomical substrate of kindling, but physiological experiments demonstrate a lasting potentiation of the excitatory post-synaptic potential.

Principles underlying new methods for chronic neural recording.

Abstract: Chronic recording is possible from nerve fibers which have grown through holes in an insulating medium (regeneration electrodes) or which are enclosed by an insulating sheath (cuff electrodes). Use of three electrodes in a balanced configuration permits good rejection of electromyographic (EMG) signals and other sources of electrical interference (fluorescent lights, 60 Hz signals from the mains, etc.). Equations are derived and tested for predicting the amplitude and form of the signals expected for a given cuff length and diameter. These equations can be used to design electrode units optimally for a given application. Finally, the use of transformers permits the neural signals to be carefully matched to the recording apparatus and further optimizes the neural signal-to-noise and signal-to-EMG ratios. Use of these methods in several physiological and clinical applications, as well as potential abuses, are discussed.

Kindling, unit discharge patterns and neural plasticity.

Abstract: Two approaches to the study of the kindling phenomenon were discussed: 1) an attempt to identify the pattern of neural activity required to produce the changes underlying kindling and 2) an investigation into the nature of those changes. Three experiments were reported that used the neocortical transcallosal system as a monosynaptic model system in which to study possible synaptic mechanisms of the kindling effect. Experiment I showed an increase in the transcallosal evoked potential following neocortical kindling. Experiment II showed an increase in the strength of the transcallosal evoked cell discharge following neocortical kindling. Experiment III reported the results of an histological examination of neocortical tissue in kindled and non-kindled animals using the Golgi-Cox technique. Spine density, spine dimension and branching were measured for pyramidal cell apical dendrites. No differences were found between primary and secondary (contralateral) foci or between kindled and non-kindled animals.

Generality of the kindling phenomenon: some clinical implications.

Abstract: The purpose of the present investigations was to explore the generality of the kindling phenomenon and its applicability to clinical situations. Whether local brain stimulation, electroconvulsive shock (ECS), or metrazol the consequence of periodic administration of convulsive agents was found to be the same; in each case repeated application of the agent resulted in the gradual development and intensification of convulsive symptoms (kindling). Moreover, in each case the resulting intensification was not specific to the agent being used and seemed to increase the responsiveness to convulsive agents in general. In the present studies this interaction was seen in the form of an intensified alcohol withdrawal syndrome observed 18 days after cessation of a series of metrazol injections, amygdaloid stimulations, of ECS. Thus, it appears that one of the hazards of the convulsive therapies is that they may induce enduring changes in brain function which leave the patient in a state of increased susceptibility to a variety of potentially convulsive agents.

Primary and "transfer" seizure development in the kindled rat.

Abstract: An investigation was made of both primary and "transfer" kindling as they occur in ipsilateral limbic sites. Primary kindling was found to involve progressive growth of afterdischarge (AD), propagation and convulsive behavior. It was noted that AD growth did not take place gradually but occurred in sudden, large increments. "Transfer" (a significant acceleration of secondary kindling) was found at every secondary limbic site. It was associated with the early appearance of full-blown AD's, super-normal propagation, and well-developed seizures. The post-transfer interference of primary site function previously reported by Goddard et al was also found, but it occurred in significant amounts only after transfer kindling of the amygdala. It is believed that the data offer some support for both of the hypothetical mechanisms of transfer which have been proposed.

Kindling: secondary epileptogenesis, sleep and catecholamines.

Abstract: Seizure development and transference phenomenon were investigated in hippocampal and amygdaloid kindled cats. The behavioral and electrographic findings during the kindling procedures showed that motor seizure development in hippocampal seizures occurred with the emergence of independent discharging in the amygdala, globus pallidus and contralateral hippocampus. Furthermore, secondary site convulsions developed upon the first stimulation of these structures in the hippocampal group but only after over a month of hippocampal stimulation in the amygdaloid group. It was, therefore, concluded that role of the amygdala and globus pallidus in hippocampal seizure development was more essential than that of hippocampal stimulation in amygdaloid seiqure development. The common findings between the hippocampal and amygdaloid kindled animals were the systematic progression to seizures, the all-or-nothing nature of the electrical response and the relative permanency of the seizure susceptibility. Seizure susceptibility increased during slow wave sleep and decreased during REM sleep. These latter findings were examined with preliminary data of brain bioassays of catecholamines.

Behavioral and Epileptic Determinants of Predatory Attack Behavior in the Cat

Abstract: This report presents studies which relate limbic epileptic excitability to behavioral measures of defensive suppression of predatory attack in cats. Correlated with heightened defensiveness to environmental stimuli among non-killer cats is a heightened amygdaloid epileptic excitability, as well as a heightened conduction of amygdaloid epileptic activity to thalamic and hypothalamic substrates of predatory response in the amygdala to the complex visual stimuli presented by rat prey. These neurosensory responses correlate well with measures of epileptic excitability. Brain and behavior measures appear related since enhancement of excitability in the amygdala and of projection of epileptic activity by repeated electrical stimulation of predatory attacks. Furthermore, the ventral hippocampus seems capable of antagonizing the behaviorally suppressive effects of heightened amygdaloid excitability perhaps at points of convergence of amygdaloid and hippocampal output.

Split-brain rat: transfer and interference of kindled amygdala convulsions.

Abstract: Rats were subjected to varying degrees of commissurotomy, followed by implantation of a bipolar electrode into each amygdala. After the kindling of six convulsions at one electrode (primary site), the procedure was applied to the contralateral amygdala (secondary site). Convulsions were observed to develop more rapidly, independent of the degree or kind of transection. After 6 secondary site convulsions, the primary site was re-tested and convulsion-triggering was blocked, except in animals with transection of the rostral portion of the corpus callosum (CC). Collectively, the data indicate: (i) amygdala kindling develops a lasting trace which operates through the midbrain or brainstem; (ii) kindling from a second site utilizes this trace; (iii) a series of 6 convulsions produces negative after-effect which manifests itself at the convulsion level via the anterior CC; (iv) the anterior CC is important in determining the laterality of the forelimb clonus; and (v) the inter-amygdala propagation of after-discharge is blocked by the combined sectioning of the anterior CC and the anterior commissure.

Recurrent spontaneous seizure state induced by prefrontal kindling in senegalese baboons, Papio papio.

Abstract: In our earlier study of amygdaloid kindling in Papio papio (Pp), the development of partial complex seizure and of focal motor seizure was correlated with bifrontal theta discharge and increasing Rolandic spike discharge respectively and the final stage was characterized by primary generalized convulsive seizure. Since the latter seizure pattern is known to originate from the frontal focus in man, the frontal cortex became suspect in the development of the final stage seizure pattern. Daily prefrontal stimulation showed that Pp can be kindled from this site, culminating in a recurrent spontaneous seizure state identical to that induced by amygdaloid kindling in this species. However, our observation did not support our original assumption regarding the genesis of primary generalized convulsive seizure. Prefrontal and amygdaloid kindling are significantly different with respect to morphology, distribution and propagation of after discharge and interictal spike discharge, and speed and pattern of clinical seizure development. Most intriguingly, inter-ictal behavioral aberration associated with depth EEG changes was observed only in the prefrontal animals and not in the amygdaloid animals.

Frontal lobe and kindling in the rat.

Abstract: To test the hypothesis that the cortex participates in amygdaloid kindling in rats, bilateral aspiration lesions were made in various cortical areas in rats prior to kindling. Lesions in orbital cortex (on the dorsal lip of the rhinal sulcus) or prefrontal cortex (area 10) significantly retarded the rate of amygdaloid kindling; lesions in motor cortex, anterior cingulate cortex, or visual cortex were without effect. Detailed analysis indicated that the orbital lesioned and frontal-lesioned rats kindled relatively normally up to the second-last stage of amygdaloid kindling, in which stage they perseverated significantly longer than the controls and the other lesioned rats. These results suggest that areas of the frontal lobe participate in the elaboration and generalization of amygdaloid seizures in rats. Although retarded in rate, kindling nonetheless occurred in the lesioned rats, indicating that these cortical areas are not essential for the development of amygdaloid seizures.

The dorsomedial hypothalamic nucleus in autonomic and neuroendocrine homeostasis.

Abstract: Median eminence and ventromedial hypothalamus have in the past been the principal foci of research in neuroendocrine and neurovisceral control mechanisms. The present report provides an overview of work involving the dorsomedial hypothalamic nucleus (DMN). This structure is located dorsal to the ventromedial hypothalamic nucleus (VMN) and extends anteroposteriorly from the plane of the largest cross section of the VMN to the plane of the dorsal premammillary nucleus. Fibers from the DMN pass with the periventricular system and the dorsal longitudinal fasciculus of Schutz and have been traced to the midbrain tegmentum and reticular formation. Intrahypothalamic connections involve intensive networks between DMN, lateral hypothalamic nucleus (LHN) and VMN. Regarding neurotransmitters, recent studies indicate that the DMN receives noradrenergic innervation along two pathways, a dorsal and a ventral one. Monoamine-containing systems approach the DMN from the lateral hypothalamus and the bulk of these fibers are carried in the medium forebrain bundle from their cells of origin in the brain stem. Studies of the vascular supply indicate that both VMN and DMN receive their blood supply from the internal carotid artery. It has been recently demonstrated that the DMN is involved in the control of food intake and possibly water intake as well. Discrete lesions in the DMN have caused hypophagia and hypodipsia, and implantation of epinephrine and norepinephrine in this area has initiated eating. Many years ago, electrical stimulation of this area was reported to cause eating. Although DMN lesions cause hypodipsia, they do not result in the reduced water/food intake ratios that are so characteristic of the VMN syndrome. DMN lesions are also followed by reduced spontaneous activity (running wheel), but this reduced activity is not accompanied by increased weight gain and accretion of adipose tissue, the latter being consistently observed in the VMN rat. Rather, carcass fat remains normal in the DMN rat and carcass protein is either normal or slightly increased. Many of the aforementioned changes in weanling rats with DMN lesions, however, are not matched by similar alterations in the intermediary metabolism of carbohydrate and lipid. Possibly this is due to a “resetting” of a central autonomic control system that makes it possible for the DMN rat to adapt more efficiently to a reduced influx of substrate, i.e. the consistent hypophagia. From a review of the literature it appears that the DMN and their circuitry are involved in only a few neuroendocrine, i.e. hypothalamohypophyseal control mechanisms. Both lesion and cervical stimulation experiments suggest an involvement of the DMN in the control of LTH. Circumstantial evidence points to the DMN as a possible formation and/or storage site of growth hormone inhibiting factor (GIF). Although DMN rats show reduced ponderal and linear growth, they have been found to have normal or elevated plasma growth hormone (GH) levels. Both lesion and stimulation studies have yielded the impression that the DMN is not involved in thyroid, i.e., thyrotropin stimulating hormone releasing factor (TSHRF) control. Electrical stimulation of the DMN has been reported to result in a positive correlation between adrenal blood flow and adrenal corticoid release in hypophysectomized dogs. This has been interpreted as a coordinated response at the level of a “dorsomedial sympathetic vasodilator relay” rather than a “true” neuroendocrine effect via corticotropin releasing factor (CRF). Experiments that failed to demonstrate a relationship between the DMN and the tonic and cyclic control of luteinizing hormone releasing factor (LHRF) are discussed. The data reviewed indicate the existence in the dorsomedial hypothalamus of an area that exerts a profound influence on many aspects of neurovisceral and some neuroendocrine control systems.

Secondary epileptogenesis in frog forebrain: effect of inhibition of protein synthesis.

Abstract: Secondary epileptogenesis was induced in the hippocampal cortex of the paralyzed bullfrog by means of localized, unilateral, intermittent electrical stimulation (kindling). Stimuli were designed to yield a brief but definite after-discharge. In control animals a progressive increase in after-discharge duration occurred at the 1 degree (stimulated) site and then at the 2 degrees site (contralateral hippocampus). Spontaneous epileptiform potentials (SEP's) occurred between stimuli, eventually independently on both sides. Cycloheximide (50 mg/kg) caused 88-99% reduction in protein synthesis, measured by 14C-leucine incorporation into brain protein. Cycloheximide-treated animals revealed no evidence of progressive prolongation of after-discharge duration when subjected to the kindling procedure (p = 0.1205 X 10(-7)). SEP's were reduced in the cycloheximide-treated animals, and confined to 1 degree hemisphere (p = 0.6 X 10(-10)). Since cycloheximide did not disturb normal electrogenesis or disrupt the after-discharges, this experiment distinguishes processes dependent upon electrical events from those requiring macromolecular synthesis. Protein synthesis seems critical to the emergence of spontaneous and autonomous epileptiform behavior of neural aggregates.

A model for the future care of acute spinal cord injuries.

Abstract: This is a review of the total care of those acute spinal cord injury patients in Ontario during the years 1969 and 1970, from extrication and transportation following the accident to death, or the completion of primary definitive rehabilitation. Information was extracted from the available ambulance records, the patients and many of the responsible physicians were interviewed personally. The study was detailed and intensive and included a review of each patient's hospital records in each hospital up to discharge from the rehabilitation programme into the community, or to a chronic care unit. The data was compiled in accordance with a detailed and lengthy questionnaire developed for this study. The incidence of acute cord injuries in Ontario in 1969 and 1970 amounted to 244; in 1969, 15.9 per million population and in 1970, 13.6 per million. As in other studies road accidents took first place, followed by falls from a height; sports injuries ranked third and 65.7% of these were caused by diving into shallow water. Age incidence, and incidence by month, day of week and time of day were identified. Fridays and Saturday afternoons in July and August are particularly hazardous. The study continued to the end of 1974 by which time 34 deaths had been recorded. Peak incidence of death occurred within fourteen days of injury. The most common cause of death was respiratory in origin. Geographical distribution was identified and the type of hospital treating the acutely injured patient. Fourteen percent of persons with spinal column injury suffered progressive or sequential spinal cord damage both prior to and following medical contact. The incidence of pressure sores and genitourinary sepsis and calculosis was high in all types of hospitals. The effect of operative treatment was noted in cases of complete quadriplegia and paraplegia. Of the 133 survivors who undertook a rehabilitation program, 84% returned to their homes and 59% achieved gainful employemnt or ongoing education. The cost was determined of general hospital services and rehabilitation programmes. A new model for the care of the spinal cord injury patients in Ontario was proposed.

Memory and growth in the superior temporal gyri.

Abstract: The superior temporal gyri were measured in 33 infants and in 33 adults. In the adults, most right superior temporal gyri were larger. This asymmetry was not found in infants, a difference which suggests greater growth of the right superior temporal gyri in the population from which our sample was taken. The asymmetry may be related to the functional asymmetry found by Penfield: some of his patients reported re-experiencing of past sensory experiences with electrical stimulation of the temporal lobe. This response was more frequently evoked from the right hemisphere.

Why transcortical reflexes

Abstract: Experiments in humans and in monkeys have indicated that load perturbations, occurring during voluntary movements and postural activity, may be automatically compensated for. Overall muscle stiffness opposing load changes is determined by the visco-elastic properties of the muscle, by segmental reflex actions and finally by long-loop reflexes. Under certain circumstances, for instance when the subject or the experimental monkey is "prepared" to counteract perturbations which are unpredictable in time, the long-loop "reflexes" appear to be responsible for most of the corrective muscle tension. Experiments in anaesthetized monkeys revealed that signals from stretch afferents reach neurons of the motor cortex, possibly via a relay in the cortical area 3a. The latencies of these responses to well controlled muscle stretches were in the same range as motor cortical cell discharges recorded in alert monkeys subjected to load perturbations. Furthermore, these responses of cells in the motor cortex also had the appropriate timing to indicate a causal relationship with the long-latency electromyographic responses to load changes referred to above. These experimental results therefore strongly support the hypothesis, first proposed by Phillips (1969), of a transcortical servo-loop adjusting motor cortical output according to the load conditions in which movements are performed. The major advantage of transcortical regulations as opposed to segmental regulations, seems to be a powerful gain control acting at the cortical level; it was repeatedly shown that the long-loop reflexes are strongly modifiable and under voluntary control. It is suggested that an adaptive gain control at the cortical level is a prerequisite to preserve the complex capabilities of the motor cortex as the chief "executive" for skilled, preprogrammed movements. A loss of this adaptive gain control may be, at least partly, the cause of motor disorders such as rigidity in Parkinsonian patients, as reported by Tatton and Lee (1975). It is suggested that further investigations of the control of transcortical reflexes may aid in the understanding of the pathophysiology of motor disabilities.

The Nature of Primary Vocal Tremor

Abstract: Three elderly women with marked progressive voice tremor, without other neurological symptoms, and negative family histories were investigated. All had a 4-5 Hz respiratory tremor in expiration and, to a lesser degree, in inspiration; and all had vocal tremulousness synchronous with their respiratory irregularity. Articulation of phonemes was normal. In two cases the neurological examination was otherwise normal; in the third case there was a minimal 71/2 Hz tremor in the left thumb and index finger. Simultaneous speech and vocal air pressure recordings, as well as cinematographic studies of the vocal apparatus and diaphragm were carried out. It is suggested that these cases represent primarily an action tremor of respiration, that they belong in the spectrum of essential tremor, and hence may be amenable to treatment with propranolol.

Relative efficacy of alcohol and propranolol in action tremor.

Abstract: Thirty-nine patients with a variety of diseases, including essential tremor, Parkinson's Disease, olivopontocerebellar degeneration, ataxia telangiectasia, and cervical cord injury with action tremor, were evaluated for the effect of one ounce of absolute alcohol ingestion. Tremor significantly subsided in 61.9% of E.T.; 46.6% of P.D.; one patient with A.T.; and one patient with C6 lesion. The tremor became worse in one patient with O.P.C.D. Twenty of these patients were treated with propranolol, an average dose of 92 mgm. per day, and re-evaluated three to six months later. All those who improved on alcohol improved on propranolol and the one whose tremor accentuated with alcohol had a similar response to propranolol. It is concluded that the tremorilytic effect of alcohol is neither specific for, nor limited to, essential tremor and is of no value in differentiating various neurological disorders which manifest as action tremor. It is recommended that one ounce of absolute alcohol by mouth be used as an office procedure to predict the response of patients' tremor to propranolol.

Sleep, subcortical stimulation and kindling in the cat.

Abstract: A longitudinal study of the effects of sleep on amygdaloid kindling showed that kindling disrupted normal sleep patterns by reducing REM sleep and increasing awake time. Few interictal spike discharges were observed during the awake stage, while a marked increase in discharge was observed during the light and deep sleep stages. No discharges were observed during REM sleep. During the immediate post-stimulation period the nonstimulated amygdala showed a much higher rate of spike discharge. On the other hand, there was an increase in spike discharge in the stimulated amygdala during natural sleep without preceding amygdaloid stimulation. Amygdaloid stimulation at the generalized seizure threshold during each sleep stage resulted in a generalized convulsion. The influence of subcortical electrical stimulation on kindled amygdaloid convulsions was investigated in a second experiment. Stimulation of the centre median and the caudate nucleus was without effect on kindled convulsions, while stimulation of the mesencephalic reticular formation at high frequency (300 Hz) reduced the latency of onset of kindled generalized convulsions. Stimulation of the nucleus ventralis lateralis of the thalamus at low frequency (10 Hz) prolonged the convulsion latency, and at high current levels blocked the induced convulsion. Stimulation in the central gray matter at low frequency (10 Hz) also blocked kindled amygdaloid convulsions.

Central mechanisms of tremor in some feline and primate models.

Abstract: For several years our interest has been in a postural Parkinson-like tremor at 4-6/sec. which can be produced in the monkey by lesions of the central nervous system. We have also studied the effects of harmaline, a drug which evokes or intensifies the Parkinson-like tremor in lesioned animals and which also induces a fine, generalized tremor at 7-12/sec. in normal animals. The results obtained so far indicate that these two types of tremor are generated by two independent central mechanisms which do not require the integrity of peripheral feedback loops. The experimental Parkinson-like tremor is generated by a thalamo-cortical mechanism while the olivo-cerebellar system is responsible for the faster "physiological" tremor. Similar tremor mechanisms may be involved in some movement disorders in man.

Technical report: method of fixation of subluxed or dislocated cervical spine below C1-C2.

Abstract: A method of internal fixation of adjacent vertebrae that have been dislocated or subluxed has been presented In the author's hands and in the hands of associates this has proven to be a satisfactory method of fixation in this type of injury It has the advantage over many other posterior techniques that only two verbebrae are fixed together

Cellular hypersensitivity to basic myelin (P2) protein in the Guillain-Barré syndrome.

Abstract: Lymphocytes of 29 subjects were assayed for MIF production in response to P 2 peripheral nerve protein, crude human peripheral nerve and human central nervous system Al basic myelin protein. Seven were performed in normal control subjects, 12 in Guillain-Barre patients (GB), 5 with other polyneuropathies and 5 in patients with multiple sclerosis (MS). Only GB patients with acute illness produced MIF in response to neuritogenic P 2 protein and crude human nerve. Two MS patients in the acute phase of an exacerbation and one GB patient produced MIF in Response to Al protein. The results of this study demonstrate cellular hypersensitivity to a neuritogenic constituent in peripheral nervous tissue and support the concept that this may be important in the pathogenesis of GB.

Relative prognostic significance of vasospasm following subarachnoid hemorrhage.

Abstract: A retrospective analysis of 274 patients with intracranial aneurysms, diagnosed either angiographically or at autopsy between 1968 and 1973 at the University of Alberta, was carried out. One hundred and forty-six patients had intracranial clipping of the aneurysm. Clinical and radiologic data were abstracted from the chart and the angiographic studies. Probability of survival curves were constructed. Associations between various clinical factors and survival at two months were demonstrated. The most important prognostic factors were the clinical grade at angiography or surgery, followed by the presence of preoperative spasm, hematoma or focal edema, elevated blood pressure on admission, time of interval from hemorrhage to surgery and age. The data lends some support to the policy of operating on patients in good neurological condition, even if their pre-operative angiogram shows spasm.

Skin punch biopsies and lymphocytes in the diagnosis of lipidoses.

Abstract: Skin punch biopsies and buffy coats of white blood cells were examined electron microscopically in patients suffering from a variety of storage diseases. No specific abnormalities could be detected in Gaucher's disease and adreno-leucodystrophy. While characteristic deposits were found in cutaneous nerves in globoid and metachromatic leucodystrophy, this method was deemed inferior to sural nerve biopsy. In gangliosidoses, on the other hand, pathognomonic membranous cytoplasmic bodies were common in axons of cutaneous nerves, and in generalized gangliosidoses marked vacuolation of many other cells was prominent. Specific deposits were found in various cells in skin punch biopsies and in lymphocytes of children suffering from ceroid lipofuscinoses, and in lymphocytes of their parents. This constitutes the easiest diagnostic laboratory procedure in such cases.

Meningo-encephalomyelitis due to the saprophagous nematode, Micronema deletrix.

Abstract: A five-year-old boy succumbed 24 days following an unusual farm accident in which considerable manure was deposited in multiple lacerations. Death was due to an extensive meningo-encephalomyelitis caused by a nematode that is ordinarily saprophagous.

Neurophysiological Changes Following Spinal Cord Lesions in Man

Abstract: A study has been made of the neurophysiological changes that follow spinal cord lesions in man. The Achilles tendon reflex (ATR) is used to estimate transmission in the Ia monosynaptic pathway, and the tonic vibration reflex (TVR) to estimate transmission in the Ia polysynaptic pathway to motoneurons. The inhibition of the H reflex by vibration is used as an estimate of presynaptic inhibition of the Ia monosynaptic pathway. Immediately following a complete lesion of the spinal cord presynaptic inhibition of the Ia monosynaptic pathway appears to be greatly increased. This enhanced inihibition may last several months but it eventually declines and in some instances becomes less than normal. Transmission in the Ia polysynaptic pathway is permanently abolished by a complete spinal lesion. A hypothesis is developed from these findings to explain the evolution of some of the clinical features that follow complete spinal lesions in man. Distinct differences are observed when the spinal lesion is incomplete. Transmission in the Ia polysynaptic pathway may be preserved and there may be no increase in presynaptic inhibition. These differences may depend upon the integrity of certain spinal long tracts which cannot be tested clinically.

Laying the ghost of 'muscles versus movements'.

Abstract: It is certainly a mark of great wisdom to the organizer of this meeting to have chosen Charles Phillips as our Guest Lecturer for this meeting.Whilst I am grateful for this opportunity of saying a few words of introduction, I am sure it can be said of Charles Phillips that very little introduction is necessary, since we meet him at the most important meetings in Neurophysiology around the world. Any meeting on the motor system, of course, is not complete without the participation of Dr. Phillips. However, some of the less old-timers than myself, and the students, might be interested in the beginnings of Dr. Phillips’ career in neurophysiology and to know that he was first a clinical neurologist beginning his medical studies in Oxford just before the war, where he came under the influence of Sir Charles Sherrington with Jack Eccles as his tutor.

Roles of cerebellum and basal ganglia in initiation and control of movements

Abstract: Theories of function of the cerebellum and basal ganglia are examined in the light of recent experimental findings obtained with the local cooling method, and both are matched against clinical observations. Evidence is summarized for a programming and initiating role in monkeys' elbow movements of the lateral, and to a lesser degree, intermediate, cerebellum. Cooling either nuclei affected movements, but neither seemed to be important for precentral cortical unit discharge accompanying compensation for suddenly applied load pulses. The globus pallidus seemed to be importantly involved in movement guidance in the absence of vision.

Frontal cortical kindling in cats.

Abstract: Our observaiton of amygdoloid seizure development in cats indicated early afterdischarge propagation into basal cortical areas prior to the development of bifrontal sharp theta discharge. In view of the implied participation of the frontal lobe in amygdaloid kindling, both fractional lesioning and kindling of selective areas were performed. This paper summarizes out stimulation study involving premotor, prefrontal, mesial frontal and orbital cortices. Except for the orbital series which showed a rather strikingly similar pattern of seizure development to that of amygdaloid kindling, all areas showed significantly different features in terms of the speed of seizure development, afterdischarge propagation, fragility of developing seizure, final stage 5 seizure and post-ictal behavior pattern, interictal discharge morphology and propagation, and generalized seizure triggering threshold intensity. All these findings suggest that the frontal lobe participates in, but is not essential for, the amygdaloid seizure development. The results of ongoing fractional lesion series support such a conclusion.

Supersensitivity of central neurons--a brief review of an emerging concept.

Abstract: The concept that "denervation" or "pharmacological disuse" supersensitivity develops in central neuronal systems subsequent to sustained attenuation of normal neurohumoral mechanisms is reviewed. Particular emphasis is placed on biochemical and electrophysiological parameters of supersensitivity in dopaminergic (striatal) neuronal systems. The possible applicability of theories invoking changes in receptor sensitivity to the phenomenon of narcotic tolerance and physical dependence and to psychoactive drug therapy is discussed.