The role of the substantia nigra on amygdaloid kindling

The role of the substantia nigra on amygdaloid kindling

5100 ent levels. Five patients had lesions caused by spinal cord injury, 2 had ischaemic and 1 an inflammatory lesion. All patients had a neurogenic b...

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5100 ent levels. Five patients had lesions caused by spinal cord injury, 2 had ischaemic and 1 an inflammatory lesion. All patients had a neurogenic bladder as demonstrated by urodynamic evaluation. The results showed a precise correlation (according to the level of the lesion) between the neurophysiological and the urodynamic data. This demonstrates that sacral evoked potentials and pudendal-cortical somatosensory evoked potentials are diagnostic methods which, with other clinical data, contribute to a more precise definition of the entity and level of spinal cord lesions. These methods also provide a better understanding of vesico-sphincter problems demonstrated by urodynamic investigation.

during the intermediate and late stages of drug administration Total sleep time increase was comprised of larger amounts 01 stage 2 NREM sleep and REM sleep. Withdrawal of moclobemide was followed by a further increase of REM sleep although values did not surpass those observed in adults with normal sleep. Clinical efficacy of moclobemide was confirmed by the results from the Hamilton depression rating scale, Beck scale and self-evaluation rating scale all of which showed significant improvements in symptoms of depression. There were no stgnificant changes in vital signs including blood pressure and heart rate.

SLEEP LABORATORY STUDY OF THE ZOLPIDEM IN INSOMNIAC PATIENTS.

THE ROLE OF THE SUBSTANTIA DALOID KINDLING.

EFFECTS

OF

J. M. Monti (Hospital

de Clinicas,

M. Murasaki, A. Takahashi, Montevideo,

Uruguay)

We determined the effects of zolpidem on the sleep cycle of insomniac patients by means of polysomnographic recordings following short- and intermediate-term administration. The study involved patients with moderate sleep disturbances. The period of observation involved 21 nights, 14 of which were spent in the sleep laboratory. Zolpidem 10 mg was given just before turning off the lights. An improvement in sleep with no rebound insomnia was observed during the 2-week period of drug administration. Zolpidem markedly increased the duration of stage 2 sleep without affecting either slow wave sleep or REM sleep. Subjective evaluations of sleep improvement correlated well with sleep laboratory findings. In addition, the compound did not impair patients’ memory or psychomotor performance the morning after its administration. In conclusion, zolpidem shares some of the properties of the short- to intermediate-term BZD hypnotics. Accordingly, it quickly induced sleep, reduced time spent awake and improved the subjective quality of sleep. In addition, sleep architecture was preserved.

THE RELATIONSHIP BETWEEN EEG SLEEP AND CLINICAL IMPROVEMENT IN DEPRESSED PATIENTS TREATED WITH MOCLOBEMIDE. J.M. Monti. P. Altetwain (Hospital

de Clinicas,

(Kitasato

Medical

School,

NIGRA ON AMVG-

M. Suzuki and S. Watanabe Kanagawa,

Japan)

The present study was designed to examine the role of the substantia nigra (SN) on amygdaloid kindling. Two experiments were performed as follows: Experiment 1: Influence of bilateral SN destruction upon developed amygdaloid kindling. Eight male Wistar rats with fully developed amygdaloid kindling, received bilateral SN destruction by thermocoagulation. Twenty-four hours after treatment, electrical brain stimulation was delivered at the grand mal threshold once a day for over 4 days. Nigral destruction retarded the onset of generalized motor convulsions, while it did not affect other kindling parameters including seizure stage, latency of generalized convulsion and postictal phenomena. These findings appear to suggest that the SN may be involved in triggering of motor convulsions and their modulation. Experiment 2: Influence of bilateral SN destruction upon the development of amygdaloid kindling. Seven male Wistar rats received bilateral SN destruction by thermocoagulation before they were submitted to the amygdaloid kindling paradigm. Bilateral SN destruction failed to affect the development of amygdaloid kindling and other kindling parameters. The results might imply the complexity of the mediation of the seizure activity in the SN rather than disagree with the involvement of the SN in epileptic seizures.

and D. Monti

Montevideo,

Uruguay)

The effect of moclobemide, a short-acting, reversible, preferential type-A MAO inhibitor (300 mg daily in 3 divided doses) in a 4 week therapeutic trial on the sleep of 10 depressed patients was assessed by polysomnographic recordings. Compared to placebo, patients receiving moclobemide showed improved sleep continuity as judged by the decrease of wake time after sleep onset and total wake time, particularly

MAGNETIC STIMULATION IN VASCULAR MVELINATING DISORDERS.

AND

DE-

N. M. F. Murray (The National

Hospital,

London,

UK)

A single stimulus to the motor cortex through a magnetic coil excites transversely oriented afferents onto the corticomotoneuron to produce a series of descending volleys (I-waves) in

SlOl corticospinal is necessary

tract fibres. Spatiotemporal summation of I-waves for depolarisation of the alpha motoneuron. Thus,

in addition to processes such as demyelination which cause actual slowing of conduction in large myelinated corticospinal axons, any disorder which reduces the size or increases dispersion of the I-wave volley can cause delay in or failure of anterior horn cell discharge. Abnormalities of central motor conduction (CMC) are therefore not specific to any pathophysiological process, though marked prolongation of CMC time is suspicious of demyelination whereas loss of corticomotoneurons or their axons tends to cause low amplitude responses with less delay. CMC studies are abnormal in over 70% of patients with multiple sclerosis and may be helpful for quantification and follow-up purposes, as well as for confirmation of mild motor signs. CMC is less effective than SEPs for demonstrating subclinical lesions of their respective pathways, perhaps reflecting the greater sensitivity of clinical motor testing. CMC studies performed within a few days of acute stroke are of prognostic value, very small responses predicting poor outcome, but are of less value for localisation of the site of the lesion.

ELECTROPHYSIOLOGICAL MYOTONIC DYSTROPHY.

L. Murri, R. Massetani,

(University

ABNORMALITIES

IN

B. Rossi and F. Sartucci

of Pisa, Pisa, Italy)

The involvement of the nervous system in myotonic dystrophy (MD) is supported by numerous data, both clinical and laboratory. We report findings of a multimodal electrophysiological evaluation of the peripheral as well as central nervous system in patients with MD. Brain-stem auditory evoked potentials (BAEPs) were performed in 18 patients, somatosensory evoked potentials (SEPs) in 16 patients and visual evoked potentials (VEPs) in 6 (without retinopathies or cataract). Evoked potentials were found abnormal in 53%, 62.5% and 71.4% of these cases. In 9 the maximal and minimal motor nerve conduction and the percentage of fibres with intermediate velocity using Hopfs technique in the posterior tibial nerve were evaluated. A reduction of maxima1 and minimal conduction velocities was found; the distribution of fibres with intermediate velocity was nearly identical to that of the control group and the dispersion values were normal. Moreover, topographic EEG analysis and brain mapping during wakefulness showed a significant increase of theta band over the entire scalp in 12 patients. The EEG polygraphic recording during sleep showed an apnoea syndrome in 1 case. The various abnormalities observed using different electrophysiological approaches reveal a diffuse involvement of the nervous system in patients with MD.

EEG MAPPING STROKE.

IN

VASCULAR

DISORDERS

AND

K. Nagata (Brain Research

Institute,

Akita,

Japan)

Previous studies in stroke patients suggested a close relationship between reduction of cerebral blood flow (CBF) and slowing of the background EEG as evaluated by visual inspection. Correlation studies have been performed utilizing both topographic quantitative EEG mapping and positron emission tomography (PET) providing quantitative three-dimensional images of CBF and metabolism. The topographic focus of slow-wave activity and the depression of background EEG activity correlated well with the localization of ischemic lesions as shown on CT as well as on PET images in patients with neurological disorders. In the present report, topographic EEG data was compared statistically with cortical CBF and oxygen metabolism (CMRO,) as measured by PET. Confirming the previous knowledge, delta and theta activities increased as CBF and CMRO,, whereas alpha and beta activities decreased. In the acute stage, EEG slowing may reflect reduced CBF more closely than reduced CMRO,. In contrast, in the subacute stage, EEG slowing tends to correlate more closely with CMRO, than with CBF. In the chronic stage, highly significant correlations are seen with both CBF and CMRO,. When the pathophysiological characteristics and stage of discrete cerebra1 infarction are taken into consideration, quantitative EEG mapping provides useful information reflecting the depressed cortical blood flow and/or metabolism of ischemic brain tissue.

SIMULATION OF EARLY CORTICAL SEPs WITH GAUSSIAN DISTRIBUTIONS. R. Nakanishi, M. Harada, Yonemitsu and T. Ideta

H. Yamanaga,

(Kumamoto

Kumamoto,

Kino Hospital,

N. Murayama,

H.

Japan)

In five normal subjects, 16-channel recordings of cortical SEPs evoked by median nerve stimulation were simulated with some Gaussian distribution curves. We kept the peak latency and width of each curve fixed for each individual, changing only the amplitude. Simulations were done by using a computer to the extent of 40 msec in SEPs. Four negative and four positive elements were needed for each simulation. In all five subjects the peak latencies, widths and topographical distributions of each element were similar. Therefore, we named each Gaussian distribution for three factors: electric polarity (N or P), mean peak latency (msec) and mean half width (msec). P14-4, N17-3 and P19-2 were distributed widely on the scalp with low amplitudes. N20-4 and N32-9 were localized in the parietal area contralateral to the stimulation. P22-4 was located in the frontal area and P24-7 was localized in the central area. N24-8