Bailliere's clinical neurology最新文献

{"title":"The cause and management of bladder, sexual and bowel symptoms in multiple sclerosis.","authors":"C J Fowler","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Neurological control of bladder, bowel and sexual function depends on intact innervation between cerebral controlling centres and the conus of the cord. It is probably the spinal cord disease in multiple sclerosis (MS) which is the main cause of the pelvic organ dysfunctions that occur. Essential to bladder management is understanding to what extent the patient has incomplete emptying while complaining predominantly of symptoms of bladder overactivity. Anticholinergic medication can be highly effective for treatment of detrusor hyperreflexia but if incomplete emptying is also part of the problem intermittent catheterization or some other means of improving emptying will be necessary. Although there is an increasing range of treatments available for erectile failure there is still little that can be done to help women with sexual dysfunction. However, patients of both sexes are likely to welcome the opportunity to discuss their problem. The prevalence of bowel dysfunction is higher in patients with MS than in the general population and there are a number of possible pathophysiological mechanisms for both the constipation and the faecal incontinence that occur. However, there are as yet few specific effective treatments.</p>","PeriodicalId":77030,"journal":{"name":"Bailliere's clinical neurology","volume":"6 3","pages":"447-66"},"PeriodicalIF":0.0,"publicationDate":"1997-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20973440","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interferon beta 1a.","authors":"C Pozzilli,&nbsp;T Koudriavtseva","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>An improved understanding of the immunopathogenesis of multiple sclerosis (MS) has led to therapeutic attempts using immunoregulatory agents in patients with MS, including interferon beta. IFN-beta 1a has been tested in relapsing-remitting MS and its effectiveness in reducing exacerbation rate and in slowing sustained worsening of disability after 2 years has been shown. Magnetic resonance imaging results supported the clinical findings, showing a significant reduction in Gd-enhancing lesion frequency and new lesion formation on T2-weighted images. This type of interferon is well tolerated and most adverse events are mild and transient. Further trials are in progress to amplify and clarify the observed benefits of IFN-beta 1a.</p>","PeriodicalId":77030,"journal":{"name":"Bailliere's clinical neurology","volume":"6 3","pages":"481-93"},"PeriodicalIF":0.0,"publicationDate":"1997-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20973442","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neurocardiology. Stress and atherosclerosis.","authors":"J D Spence","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Until recently, there has been little evidence substantiating the belief that mental stress provokes myocardial infarction and stroke, and aggravates atherosclerosis. However, recent advances in methodology for demonstrating effects of stress are now beginning to build a foundation of evidence that supports those beliefs. In monkeys, social stress doubles coronary atherosclerosis, and increases coronary spasm, and treatment with oestrogen, which improves endothelial function, reduces coronary spasm in relation to stress. In human beings, mental stress provokes myocardial ischaemia, and haemodynamic responses to mental stress predict progression of left ventricular enlargement, and progression of carotid atherosclerosis. These findings suggest that it may not be safe to withhold treatment of high office pressures in patients with white coat hypertension. There is now some evidence that stress management in the form of individualized cognitive behavioural interventions reduces blood pressure. Further work is needed to determine whether it is safe to withhold treatment in white-coat syndrome, and whether stress management can reduce atherosclerosis and ischaemic events.</p>","PeriodicalId":77030,"journal":{"name":"Bailliere's clinical neurology","volume":"6 2","pages":"275-82"},"PeriodicalIF":0.0,"publicationDate":"1997-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20408049","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of acute emotional stress on the brain and autonomic variables.","authors":"K V Sudakov","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Under emotional stress (ES) the brain limbic-reticular structures are shown to change first. The integrative interaction of brain structures determines the secondary changes of cardiovascular functions. The effects of ES on autonomic functions are mediated primarily by chemical changes of brain limbic-reticular neurons to neurotransmitters and oligopeptides. Genetic and individual cardiovascular disorders under ES have been demonstrated. Mechanisms of sustained arterial blood hypertension under experimental ES are considered. It has been established that the resistance to ES is strongly dependent on the basic levels of oligopeptides and norepinephrine in the hypothalamus. Additional injections of oligopeptides enhance the resistance to ES.</p>","PeriodicalId":77030,"journal":{"name":"Bailliere's clinical neurology","volume":"6 2","pages":"261-74"},"PeriodicalIF":0.0,"publicationDate":"1997-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20408048","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neural regulation in experimental heart failure.","authors":"K P Patel","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The hallmarks of the chronic heart failure state are alterations in autonomic reflexes, neurohumoral drive and fluid balance. The available evidence suggests that several factors contribute to these alterations. These may include peripheral as well as central nervous system abnormalities. However, recent evidence from animals with experimental heart failure suggests that alterations in central neural sites involved in regulating sympathetic outflow may be important in the alterations in autonomic reflexes, neurohumoral drive and fluid balance commonly observed in heart failure. Many of these central mechanisms have not been extensively studied; a comprehensive understanding of these mechanisms will enhance our ability to treat the heart failure condition and its cardiovascular complications.</p>","PeriodicalId":77030,"journal":{"name":"Bailliere's clinical neurology","volume":"6 2","pages":"283-96"},"PeriodicalIF":0.0,"publicationDate":"1997-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20408050","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardiovascular consequences of clinical stroke.","authors":"J Klingelhöfer,&nbsp;D Sander","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>In clinical stroke cardiovascular abnormalities are frequently neglected although they occur more often than it is generally assumed. However, cardiac arrhythmias, pathological ECG findings, and changes of circadian blood pressure patterns are significantly increased in patients with acute cerebrovascular lesions and are associated with an increased mortality. Several clinical studies have shown that cerebral infarctions may cause different cardiovascular abnormalities depending on the location and the size of the stroke. Hereby, the prolongation of the QT interval and the expansion of the QRS-complex as the most frequent ECG abnormalities are regarded as indicators of the electrical instability of the ventricular myocardium. Furthermore, cardiac enzyme increases are interpreted as an indicator of myocardial damage during the acute phase after cerebral ischaemia. Since the autonomic nervous system plays a major role in the regulation of blood pressure, alterations of sympatho-adrenergic activity can also affect the diurnal blood pressure profile. Some studies report frequent changes of the circadian blood pressure patterns with a decreased night-time blood pressure decline or a pathological night-time blood pressure elevation. Several studies proved the importance of infarct location. The insular cortex in particular has an important role in the genesis of the pathological activation of the sympathetic nervous system. Hence, a highly significant relationship between the extent of circadian blood pressure variation and percentage insular infarction could be found. Some findings implied that the mechanism of cardiovascular instability following stroke relates to the disinhibition of the insular cortex and a reacting augmentation of the sympathetic tone. A further important aspect is given by the strong evidence that sympathetic activation ] is lateralized following hemispheric brain infarction. Accordingly, patients with a right-sided hemispheric infarction showed a significantly diminished circadian blood pressure variation as compared with patients with left-sided hemispheric infarction. The results in patients with brain stem infarction were heterogeneous. On the one hand, patients with brain stem infarction had substantially higher mean plasma norepinephrine levels than did patients with hemispheric infarction; on the other hand, hemispheric lesions were associated with a significantly higher incidence of cardiac arrhythmias when compared to patients with brain stem infarction.</p>","PeriodicalId":77030,"journal":{"name":"Bailliere's clinical neurology","volume":"6 2","pages":"309-35"},"PeriodicalIF":0.0,"publicationDate":"1997-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20408052","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neurological complications of heart disease.","authors":"R T Cheung","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Focal deficits, seizures and epilepsy, altered consciousness, and disturbed behaviours can complicate heart diseases and their medical treatment as well as cardiological procedures and cardiac surgery. Neurological complications of common cardiac conditions are discussed. These cardiac conditions are acute myocardial infarction and ischaemic heart disease, atrial fibrillation and cardiac arrhythmias, congestive heart failure, valvular heart diseases, infective endocarditis, congenital heart disease, invasive cardiological procedures and cardiac surgery. As transient ischaemic attack, stroke, seizures and epilepsy are the most common neurological complications, their management is also reviewed. Precautions should be taken to prevent neurological complications of heart disease. Regular surveillance for these complications would allow early diagnosis and initiation of appropriate management.</p>","PeriodicalId":77030,"journal":{"name":"Bailliere's clinical neurology","volume":"6 2","pages":"337-55"},"PeriodicalIF":0.0,"publicationDate":"1997-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20408053","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neural control of cardiac function.","authors":"M N Levy","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The principal functions of the heart are regulated by the sympathetic and parasympathetic divisions of the autonomic nervous system. In general, the sympathetic nerves to the heart are facilitatory, whereas the parasympathetic (vagus) nerves are inhibitory. The kinetics of the two autonomic divisions differ substantially. The vagal effects develop very rapidly, often within one heartbeat, and they decay quickly as well. Hence, the vagus nerves can exert beat-by-beat control of cardiac function. Conversely, the onset and decay of the sympathetic effects are much more gradual; only small changes are effected within the time of one cardiac cycle. When both autonomic systems act concomitantly, the effects are not additive algebraically, but complex interactions prevail. Such interactions may be mediated either pre-junctionally or post-junctionally with respect to the neuro-effector junction.</p>","PeriodicalId":77030,"journal":{"name":"Bailliere's clinical neurology","volume":"6 2","pages":"227-44"},"PeriodicalIF":0.0,"publicationDate":"1997-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20408847","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardiovascular consequences of anger and other stress states.","authors":"R L Verrier,&nbsp;M A Mittelman","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Anger is the affective state most commonly associated with myocardial ischaemia and infarction and life-threatening arrhythmias, with at least 36,000 (2.4% of 1.5 million) heart attacks precipitated annually by anger in the United States. Fear, anxiety and bereavement are also implicated in increased vulnerability to cardiac events. The lethal cardiovascular consequences of these behavioural stress states in patients with ischaemic heart disease are attributable to activation of high-gain central neurocircuitry and the sympathetic nervous system, provoking acute sinus tachycardia, hypertension, impaired myocardial perfusion and cardiac electrical instability. The fields of epidemiology, behavioural medicine and cardiovascular physiology have generated new methodologies for studying the pathophysiology of anger and other behavioural stress states with the goal of developing means to sever the link between the anger and its life-threatening consequences.</p>","PeriodicalId":77030,"journal":{"name":"Bailliere's clinical neurology","volume":"6 2","pages":"245-59"},"PeriodicalIF":0.0,"publicationDate":"1997-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20408047","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardiovascular consequence of experimental stroke.","authors":"D F Cechetto,&nbsp;V Hachinski","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Clinically, it has been observed that stroke causes a number of cardiovascular disturbances that are detrimental to prognosis and may cause death. We have developed an experimental model of stroke, a middle cerebral artery occlusion in the rat, that can mimic the acute cardiovascular responses observed clinically. This model has clearly demonstrated that the insular cortex is necessary to produced the autonomic changes and that these changes are exacerbated by right-sided infarcts and increasing age. In addition, we have demonstrated that there are neurochemical changes associated with our stroke model that may mediate the cardiovascular complications. In particular, an increase in dynorphin in the central nucleus of the amygdala occurs with a peak at 3 to 5 days after the stroke and is directly due to damage in the insular cortex. Finally, we have shown that there is a similar time course in the exaggerated cardiovascular responses to stress following middle cerebral artery occlusion. Direct injection of dynorphin into the central nucleus of the amygdala can enhance the cardiovascular response obtained by stimulation of the acoustic stress pathway. These observations have direct relevance to clinical stroke.</p>","PeriodicalId":77030,"journal":{"name":"Bailliere's clinical neurology","volume":"6 2","pages":"297-308"},"PeriodicalIF":0.0,"publicationDate":"1997-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20408051","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}