Bailliere's clinical neurology最新文献

{"title":"Tropical neuropathies.","authors":"G C Román","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Peripheral neuropathies constitute an important cause of neurological disability in the tropics. The clinical manifestations of tropical peripheral neuropathies are identical to those observed by neurologists elsewhere and their aetiologies are also similar. However, the frequency of occurrence, or prevalence, of the different types of neuropathy is clearly different from that observed in developed nations, ranging from epidemic outbreaks of optic and peripheral sensory neuropathy caused by malnutrition--such as in the outbreak recently observed in Cuba--to the endemic problems of leprosy and HTLV-1 infection. A large variety of plant and animal poisons and industrial neurotoxins frequently affect the peripheral nervous system in warm climates. In addition to their public health importance, tropical neuropathies constitute unexplored natural models of disease worthy of clinical and laboratory studies.</p>","PeriodicalId":77030,"journal":{"name":"Bailliere's clinical neurology","volume":"4 3","pages":"469-87"},"PeriodicalIF":0.0,"publicationDate":"1995-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19579079","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":"Toxic neuropathies and their treatment.","authors":"A C Ludolph,&nbsp;P S Spencer","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Peripheral neuropathy triggered by therapeutic drugs, workplace chemicals and environmental pollutants continues to be one of the most common pathological responses of the human nervous system to chemical attack. While some agents seem to damage the nerve cell directly, and a few induce primary demyelination, the large majority produces distal axonal degeneration simultaneously in long peripheral nerves and spinal tracts. Glove-and-stocking sensory loss typically precedes the development of a similar distribution of motor weakness. Clinical signs usually appear weeks after exposure has commenced; the condition continues to evolve after chemical exposure has ceased, and recovery spans a period of months or years. Careful clinical and laboratory assessment is needed to identify environmental agents responsible for human neuropathy, and reports of cases that claim a chemical causation require verification from experimental animal studies of suspect agents. Treatment of peripheral neuropathy continues to be limited, although a new therapeutic approach to patients with neuropathy-producing heavy metal intoxication is promising. Novel methods to limit nerve degeneration and promote regeneration are under study, but none has produced a convincing therapeutic effect. These are urgently needed to prevent and control the neuropathies that limit the therapeutic usefulness of drugs used in cancer chemotherapy and AIDS treatment.</p>","PeriodicalId":77030,"journal":{"name":"Bailliere's clinical neurology","volume":"4 3","pages":"505-27"},"PeriodicalIF":0.0,"publicationDate":"1995-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19579081","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":"Vascular cognitive impairment: a new approach to vascular dementia.","authors":"J V Bowler,&nbsp;V Hachinski","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Vascular dementia has remained a confused concept since its origin over a century ago. Recently developed criteria, which have not met with universal acceptance, erroneously base their description of vascular dementia on Alzheimer's disease, an error that is founded in the historical confusion of the two conditions. These errors include requirements for prominent memory loss and the occurrence of a substantial degree of cognitive impairment before dementia can be diagnosed. They also treat vascular dementia as a single condition and fail to address the question of aetiology. Furthermore, these criteria largely ignore such data as is already available regarding vascular dementia. Vascular dementia is preventable. Thus cases need to be detected as soon as possible to avoid unnecessary deterioration. To correct these errors a new concept, that of vascular cognitive impairment, is proposed. This concept seeks to identify cognitive impairment due to cerebrovascular disease at the very earliest stage and, by identifying the aetiology, enable the institution of appropriate preventive therapy.</p>","PeriodicalId":77030,"journal":{"name":"Bailliere's clinical neurology","volume":"4 2","pages":"357-76"},"PeriodicalIF":0.0,"publicationDate":"1995-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18503964","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":"Carotid endarterectomy: emerging indications.","authors":"H E Meldrum,&nbsp;H J Barnett,&nbsp;M Eliasziw","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Several randomized trials have recently reported on the benefit of carotid endarterectomy for symptomatic or asymptomatic patients. A positive benefit has been found for symptomatic patients with > or = 70% stenosis measured by angiogram with a particular formula and performed with high surgical skill. Symptomatic patients with < 70% stenosis continue to be randomized and followed. The answer for this group is expected in the next two years. The randomized trials of asymptomatic patients have not established the benefit for carotid endarterectomy clearly. The most recent trial shows the absolute risk reduction at 5 years is only 5.9% or less than 1.5% risk reduction per year. A fifth trial continues in Europe.</p>","PeriodicalId":77030,"journal":{"name":"Bailliere's clinical neurology","volume":"4 2","pages":"339-55"},"PeriodicalIF":0.0,"publicationDate":"1995-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18503963","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":"Recovery from stroke: rehabilitation.","authors":"D P Speach,&nbsp;M L Dombovy","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Most of the neurological and functional recovery following stroke occurs during the first 3-6 months, although some patients show prolonged and unexpected levels of recovery. Research shows that the determination of outcome is multifactorial and includes demographics and psychosocial as well as medical factors. New information on how the brain recovers from injury has given us insights into which therapy approaches theoretically might be beneficial. In some cases recovery may be facilitated by the interaction of appropriate therapies and pharmacological interventions. Comprehensive rehabilitation programmes and integrated acute care rehabilitation stroke units appear to produce improved functional recovery over the standard of care. The reasons are unclear, but may include coordination and standardization of care as well as the early start of rehabilitation. Future research should continue to enhance the mechanisms of recovery from stroke and the approaches to facilitating the recovery process.</p>","PeriodicalId":77030,"journal":{"name":"Bailliere's clinical neurology","volume":"4 2","pages":"317-38"},"PeriodicalIF":0.0,"publicationDate":"1995-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18503962","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":"Advances in atherosclerosis.","authors":"J D Spence","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>In the past few years major advances have changed the way we think about atherosclerosis. Treatments for hyperlipidaemia not only regress angiographic stenosis and reduce coronary mortality; in meta-analysis, and in large trials of secondary prevention, they appear to reduce overall mortality. Reduction in events precedes regression of stenosis, partly through stabilization of plaque, and partly by reversal of the endothelial dysfunction caused by oxidized LDL. The study of lipid disorders has been advanced by new understanding of the role of apolipoproteins and lipoprotein (a). Significant advances have also been made in the understanding of effects of angiotensin, fibrinogen, homocysteinaemia, platelets, genetics of atherosclerosis, autoimmunity, flow disturbances and wall stress. Most importantly, because of a revolution in our understanding of the endothelium, we can now begin to make sense of some of the effects of risk factors such as lipids, menopause, flow disturbances, and pressure, to begin to understand atherosclerosis, arterial remodelling and the protective effect of oestrogen in a new light. These changes will profoundly affect the way we practise vascular medicine and neurology, and will give us powerful new ways to help our patients.</p>","PeriodicalId":77030,"journal":{"name":"Bailliere's clinical neurology","volume":"4 2","pages":"191-205"},"PeriodicalIF":0.0,"publicationDate":"1995-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18504654","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":"The proximal aorta: a source of stroke.","authors":"E F Jones,&nbsp;G A Donnan","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The availability of the sophisticated imaging techniques of transoesophageal echocardiography and epiaortic ultrasound scanning have drawn attention to the ascending aorta and aortic arch as a potential source of embolic stroke. Several studies have shown an association between atheroma in this region and cerebral ischaemic events. Although aortic atheroma is associated with vascular disease in other arterial territories, two large controlled studies have shown it to be a risk factor for stroke, independently of other major risk factors such as carotid vascular disease, cardiac disease and hypertension. In observational and case-control studies, the risk of stroke is higher in the presence of certain echocardiographic appearances of atheromatous plaque--these include plaque thickness of > 4-5 mm, surface irregularity suggesting plaque ulceration and mobile elements suggesting superimposed thrombus. However, longitudinal studies are required to evaluate the prognostic significance of such findings. Several therapeutic options have been described or suggested in patients with and without stroke in whom aortic atheroma is demonstrated, but the optimal management of such patients is yet to be determined in prospective controlled trials.</p>","PeriodicalId":77030,"journal":{"name":"Bailliere's clinical neurology","volume":"4 2","pages":"207-20"},"PeriodicalIF":0.0,"publicationDate":"1995-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18504655","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":"The genetics of cerebrovascular disease.","authors":"L M Brass,&nbsp;M J Alberts","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Genetics contribute to all aspects of cerebrovascular disease from the underlying pathology, through acute neuronal injury, to recovery and long-term prognosis. By understanding better the genetic contribution to the risk for cerebrovascular disease we can work toward the day when simple genetic tests can be used to assess an individual's risk for stroke (and cardiovascular disease) in the same way that we now use routine screening of blood pressure or cholesterol (Harrap, 1994b). Finally, it is worth noting that genetic effects do not work 'in vacuo'. They are subject to environmental influences which impact on the individual's phenotypic characteristics. Modification of these environmental factors may have a significant effect on the action of certain expressed genes and their putative mutations.</p>","PeriodicalId":77030,"journal":{"name":"Bailliere's clinical neurology","volume":"4 2","pages":"221-45"},"PeriodicalIF":0.0,"publicationDate":"1995-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18504656","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":"The penumbra, therapeutic time window and acute ischaemic stroke.","authors":"M Fisher,&nbsp;K Takano","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>There is a great deal of evidence that an ischaemic penumbra exists in animals and humans after the occurrence of focal brain ischaemia (Hossmann, 1994). The concept of the penumbra leads to the idea of a therapeutic time window. Because, if the region of irreversible injury (infarction) after focal ischaemia evolves in time and space, then the possibility of therapy to interfere becomes a tenable hypothesis. All of the acute stroke therapies given after onset have their basis from this hypothesis of a therapeutic time window (Fisher, 1995). As previously alluded to, a more apt term might be a window-shade, because this metaphor suggests a more dynamic event. The time and location of potentially salvageable ischaemic brain tissue after ischaemic stroke is a moving target and many unanswered questions remain. The data from animal stroke models support 2-3 hours as the time when intervention is likely to be beneficial in rats. Non-human primate data are scarce, but the few studies available do imply that at 3-4 hours after stroke onset some ischaemic tissue remains potentially salvageable. In humans, we really do not know what the time window is and we must remember that it is likely to be highly variable among individuals. This variability relates to many factors including the status of collateral flow, patient age, coexistent metabolic abnormalities (i.e. hyperglycaemia), premorbid medications and many other confounding variables. All acute stroke intervention trials are trying to initiate therapy within 6-8 hours after onset and the earlier, presumably the better. However, this approach is based upon population averaging, since we have had no convenient and reliable mechanism to determine, if an individual patient has viable tissue when therapy can be started. The availability of an imaging modality that could distinguish the presence and extent of salvageable ischaemic tissue would greatly facilitate stroke therapy trials and ultimately the selection of patients when proven therapies are available. The new MRI techniques might afford this possibility. As we enter the exciting era of effective therapy for acute ischaemic stroke, the issues surrounding the therapeutic time window(shade) will become more critical, because it is this critical time that will define the success or failure of our interventions. Therefore it is incumbent upon basic stroke researchers and clinicians to continue to define the ischaemic penumbra and to develop readily applicable mechanisms to identify and treat this moving target.</p>","PeriodicalId":77030,"journal":{"name":"Bailliere's clinical neurology","volume":"4 2","pages":"279-95"},"PeriodicalIF":0.0,"publicationDate":"1995-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18504658","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":"Intracerebral haemorrhage.","authors":"C S Kase","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Intracerebral haemorrhage accounts for 15% of strokes. Its mechanisms include hypertension, cerebral amyloid angiopathy, rupture of vascular malformations, bleeding into primary or metastatic brain tumours, coagulopathies (due to the use of anticoagulants and thrombolytic agents), sympathomimetic drug effect (amphetamines, phenylpropanolamine, and cocaine), and vasculitis. The clinical presentation reflects both the general effects of increased intracranial pressure, and the neurological deficits that result from the specific location of the haemorrhage. Its diagnosis is based on computerized tomography, which identifies haemorrhage as a high-attenuation mass within the brain substance, and magnetic resonance imaging, which in addition estimates the age of the haemorrhage by identifying sequential patterns of transformation of the haemoglobin molecule within the haematoma. The mortality in intracerebral haemorrhage is dependent on the size and location of the haematoma. A reliable clinical parameter for the prediction of outcome is the Glasgow Coma Scale score at presentation. The management of intracerebral haemorrhage involves: (a) the prevention and treatment of increased intracranial pressure; and (b) the choice between surgical and nonsurgical treatment, a clinical decision that is still controversial as a result of the paucity of controlled clinical data comparing both treatment modalities.</p>","PeriodicalId":77030,"journal":{"name":"Bailliere's clinical neurology","volume":"4 2","pages":"247-78"},"PeriodicalIF":0.0,"publicationDate":"1995-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18504657","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}