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Medicolegal and ethical issues in neurology
In this issue of Neurologic Clinics, guest editors Drs. Joseph S. Kass and Michael A. Rubin bring their considerable expertise to the topic of medicolegal issues in neurology. Top experts in the field provide up-to-date, focused guidance on how to identify and approach the major medicolegal and ethical issues that neurologists confront in today's clinical practice.
Book
Antibodies to the GABAB receptor in limbic encephalitis with seizures: case series and characterisation of the antigen
Summary Background Some encephalitides or seizure disorders once thought idiopathic now seem to be immune mediated. We aimed to describe the clinical features of one such disorder and to identify the autoantigen involved. Methods 15 patients who were suspected to have paraneoplastic or immune-mediated limbic encephalitis were clinically assessed. Confocal microscopy, immunoprecipitation, and mass spectrometry were used to characterise the autoantigen. An assay of HEK293 cells transfected with rodent GABAB1 or GABAB2 receptor subunits was used as a serological test. 91 patients with encephalitis suspected to be paraneoplastic or immune mediated and 13 individuals with syndromes associated with antibodies to glutamic acid decarboxylase 65 were used as controls. Findings All patients presented with early or prominent seizures; other symptoms, MRI, and electroencephalography findings were consistent with predominant limbic dysfunction. All patients had antibodies (mainly IgG1) against a neuronal cell-surface antigen; in three patients antibodies were detected only in CSF. Immunoprecipitation and mass spectrometry showed that the antibodies recognise the B1 subunit of the GABAB receptor, an inhibitory receptor that has been associated with seizures and memory dysfunction when disrupted. Confocal microscopy showed colocalisation of the antibody with GABAB receptors. Seven of 15 patients had tumours, five of which were small-cell lung cancer, and seven patients had non-neuronal autoantibodies. Although nine of ten patients who received immunotherapy and cancer treatment (when a tumour was found) showed neurological improvement, none of the four patients who were not similarly treated improved (p=0·005). Low levels of GABAB1 receptor antibodies were identified in two of 104 controls (p<0·0001). Interpretation GABAB receptor autoimmune encephalitis is a potentially treatable disorder characterised by seizures and, in some patients, associated with small-cell lung cancer and with other autoantibodies. Funding National Institutes of Health.
Journal Article
The biology of multiple sclerosis
\"Multiple sclerosis is the most common debilitating neurological disease in people under the age of forty in the developed world. Many publications cover medical and clinical approaches to the disease; however, The Biology of Multiple Sclerosis provides a clear and concise up-to-date overview of the scientific literature on the various theories of MS pathogenesis. Covering the main elements of scientific research into multiple sclerosis, the book contains chapters on the neuropathology of the disease as well as an account of the most extensively used animal model experimental autoimmune encephalomyelitis. The book contains chapters regarding the role of viruses in the development of multiple sclerosis. Viruses have long been implicated and chapters on animal models based on virus infection, as well as their possible role in the etiology of MS, are included. Of interest to MS researchers, the book is written to also be of value to postgraduate and medical students\"-- Provided by publisher.
Book
Stroke treatment with alteplase given 3·0–4·5 h after onset of acute ischaemic stroke (ECASS III): additional outcomes and subgroup analysis of a randomised controlled trial
In the European Cooperative Acute Stroke Study III (ECASS III), alteplase administered 3·0–4·5 h after the onset of stroke symptoms resulted in a significant benefit in the primary endpoint (modified Rankin scale [mRS] score 0–1) versus placebo, with no difference in mortality between the treatment groups. Compared with the 0–3 h window, there was no excess risk of symptomatic intracranial haemorrhage. We assessed the usefulness of additional endpoints and did subgroup and sensitivity analyses to further investigate the benefit of alteplase.
In a double-blind, multicentre study in Europe, patients with acute ischaemic stroke were randomly assigned to intravenous alteplase (0·9 mg/kg bodyweight) or placebo. Additional outcome analyses included functional endpoints at day 90 or day 30 (mRS 0–1 [day 30], mRS 0–2, Barthel index ≥85, and global outcome statistic [day 30]) and treatment response (8-point improvement from baseline or 0–1 score on the National Institutes of Health stroke scale [NIHSS], and a stratified responder analysis by baseline NIHSS score). The subgroup analyses were based on the mRS 0–1 at day 90, symptomatic intracranial haemorrhage, and death. Analyses were by intention to treat and per protocol. This study is registered with ClinicalTrials.gov, number NCT00153036.
418 patients were assigned to alteplase and 403 to placebo. Although not significant in every case, all additional endpoints showed at least a clear trend in favour of alteplase. Alteplase was effective in various subgroups, including older patients (<65 years: odds ratio 1·61, 95% CI 1·05–2·48; ≥65 years: 1·15, 0·80–1·64; p=0·230), and the effectiveness was independent of the severity of stroke at baseline (NIHSS 0–9: 1·28, 0·84–1·96; NIHSS 10–19: 1·16, 0·73–1·84; NIHSS ≥20: 2·32, 0·61–8·90; p=0·631). The incidence of symptomatic intracranial haemorrhage seemed to be independent of previous antiplatelet drug use (no: 2·41, 1·09–5·33; yes: 2·33, 0·79–6·90; p=0·962) and time from onset of symptoms to treatment (181–210 min: 1·62, 0·26–10·25; 211–240 min: 1·97, 0·82–4·76; 241–270 min: 3·15, 1·01–9·79; p=0·761), but not of age dichotomised at 65 years (<65 years: 0·74, 0·28–1·96; ≥65 years: 5·79, 2·18–15·39; p=0·004).
Our results support the use of alteplase up to 4·5 h after the onset of stroke symptoms across a broad range of subgroups of patients who meet the requirements of the European product label but miss the approved treatment window of 0–3 h.
Boehringer Ingelheim.
Journal Article