Clinical Neuroscience

[Neurological aspects of some sleep disorders]

SZŰCS Anna

MARCH 15, 2004

Clinical Neuroscience - 2004;57(03-04)

[My aim is to examine the relation between some sleep disorders and neurological diseases; to analyse their mutual interactions in order to achieve new practical data for clinical use. In the theoretical part I summarise some main points of sleep physiology concentrating on the associations of sleep regulation and neurological diseases. In my examinations, besides clinical methods, the most important tools used are sleep analyses performed by polysomnography and MESAM IV as well as brain imaging methods. To assess clinical state of my stroke patients I utilised NIH Stroke Scale. I found pathological sleep apnoea frequency in more than half of the patients in any type (bleeding/infarction) of acute stroke. In a prospective study, sleep apnoea parameters remain permanent during 3 months in the ischaemic group; on the other hand, sleep apnoea improves during follow up after brain haemorrhages. I showed pathological sleep apnoea frequency in myasthenia gravis among male patients without daytime respiration complaint. I looked for the link between the mechanism of the sleep disorder and the underlying organic lesion in two cases. In this analyses I took into account the function of the affected structure in sleep regulation. I found a basal forebrain tumour, affecting sleep regulating centres underlying severe insomnia and I suggest a neurovascular compression of the lateral preoptic area of the hypothalamus being the reason of sleep related painful erection, a parasomnia of unknown origin.]

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Clinical Neuroscience

[Effect lesions of extrahypothalamic brain structures on testicular functions in rats with special emphasis on asymmetry]

BANCZEROWSKI Péter, GERENDAI Ida

[Introduction - The aim of our studies was to investigate the involvement of extrahypothalamic brain structures in the control of testicular functions with special emphasis on the effect of right- and left-sided structures. Material and method - We performed lesion of the insular cortex, the amygdala, interrupted part of nerve fibers to and from the insular cortex, and cut the major commissural pathway of the brain the corpus callosum in adult male rats and studied the effect of the interventions on testicular steroidogenesis, serum testosterone and gonadotrop hormone concentrations. Results - Following lesion of the insular cortex on the right side serum testosterone level and steroidogenesis of the testes decreased (in the case of the left testis the difference was significant). Similar lesion on the left side did not change the parameters studied. Both right- and left-sided lesion induced a significant increase in serum LH concentration. The effect was more pronounced after right-sided lesion. Interruption of nerve fibers above the amygdala by a paramedian sagittal knife cut on the right or on the left side resulted in opposite effect on testicular steroidogenesis: right-sided intervention increased while left-sided one reduced testosterone secretion. Only left-sided cut influenced (decreased) serum testosterone level. There was no changes in LH concentration. Both right- and left-sided lesion of the amygdala induced a significant decrease in basal testosterone secretion in vitro of both testes and in serum testosterone level. However, serum LH concentration decreased only after left-sided surgery. Interruption of the corpus callosum in animals with leftsided orchidectomy induced a significant rise in steroidogenesis of the remaining (right) testis. Both sham surgery and callosotomy combined with left orchidectomy resulted in a significant increase in serum FSH level. Conclusion - Results of our studies suggest that extrahypothalamic brain structures and interventions influence endocrine functions of the testis through the hypothalamohypophyseal- testicular axis and by a direct neural route.]

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[In ischaemic stroke the two major potential therapeutic strategies are aimed at either improving cerebral blood flow or directly interacting with the cytotoxic cascade - a large body of evidence gained from animal studies is in support of them. In clinical trials direct neuroprotection by blocking the neurotoxic cascade remained ineffective, although there are several clinical trials still in progress. We summarize the experimental data and present the results of clinical trials and also discuss why so many drugs, which were effective in animal studies, failed in human trials. It is emphasized, that 1. in most animal studies the reduction of infarct size, i.e. the amount of saved penumbral tissue, was the outcome measure, whereas neurological function remained unassessed; 2. the recovery of intellectual performance and higher cortical functions are of major importance in the future quality of life in stroke victims; however, it is impossible to examine these parameters appropriately in animal studies; 3. in many clinical trials the patient population was rather heterogenous and low in number, the study protocol was not optimal and the critical analysis of the subacute and chronic phase was lacking or insufficient. We present the major experimental stroke models, discuss their similarities, differencies and limitations as compared to the human pathophysiological processes. The pitfalls of extrapolating data from animal studies to clinical practice are also summarized. The complex network of functional and morphological intercellular connections, the long timescale of neurotoxic and reparative events and the lessons learned from clinical trials suggest, that the use of drug combinations (therapeutic cocktails) targeting multiple steps of the neurotoxic cascade would hopefully result in more effective treatment of ischaemic stroke. Strategies to facilitate brain plasticity and regeneration is an additional promising tool to enhance recovery in brain ischaemia.]

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