Lancet neurology
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Arteriovenous malformations of the brain (AMB) can cause stroke when they rupture. Epidemiological and imaging research has found that about 50% of patients with AMB present with haemorrhage, and the other 50% either present with non-focal symptoms, such as headache, seizure, or focal neurological deficit, or have no symptoms and the lesion is found during unrelated investigations. Treatment for arteriovenous malformations aims to prevent and resolve haemorrhage and is a growing interdisciplinary challenge. Although treatment uses enormous resources, there have been few studies on the risk-benefit ratios for treatment of unruptured AMB and the best approaches.
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Thrombolysis for stroke is still not widely used as current recommendations restrict treatment to selected patients. In general, these are patients who can be assessed quickly by specialised stroke teams, have intracranial haemorrhage excluded by appropriate brain imaging, and are treated with alteplase (recombinant tissue plasminogen activator; rt-PA) within 3 h of symptom onset. There is, however, still much debate regarding the scope of treatment and the reorganisation of services required to support an effective service. ⋯ Two recent publications have helped clarify some issues. The first was an individual-patient data meta-analysis of the alteplase trials. These analyses suggest treatment effects beyond the usual 3 h time window, but other than time to treatment no other factors influenced the effects of treatment. The second publication was a reanalysis of the original National Institute of Neurological Disorders and Stroke (NINDS) alteplase trial, done after criticism of the original study. The reanalysis confirmed that there was significant baseline imbalance of stroke severity between treatment and control groups in the NINDS trial, but established that this did not materially affect the positive results of the trial. However, the recording of blood pressure in the study was found to be inconsistent and therefore unsuitable for reanalysis. The previously published data on recommendations for blood-pressure control, arising from the NINDS trial, needs to be reconsidered in this light. Both studies included too few patients to provide reliable data on which clinical and radiological features influence the response to alteplase. WHERE NEXT?: The individual-patient data meta-analysis and reanalysis of the NINDS trial have probably exhausted the potential of previous trials to answer questions on the effects of thrombolysis. Further randomised trials comparing thrombolysis with control will be required to determine whether elderly people benefit from treatment or whether there are worthwhile benefits from alteplase beyond 3 h (and in such patients, whether advanced magnetic resonance imaging is an effective way to select those most likely to benefit). Various new approaches to reperfusion also require assessment in large-scale trials: new thrombolytic drugs, the combination of intravenous and intra-arterial thrombolytic drugs, combinations of thrombolytics with new antiplatelet agents, and augmentation of thrombolysis either with mechanical devices or with transcranial ultrasound.
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Multiple sclerosis (MS) is a serious chronic neurological disorder in which demyelination and inflammation occur in the white matter of the CNS. The findings of many epidemiological studies and a discordance of MS in monozygotic twins suggest that the disorder is acquired. The most likely cause is a virus because more than 90% of patients with MS have high concentrations of IgG, manifest as oligoclonal bands, in the brain and CSF. ⋯ Nevertheless, no virus has been isolated from the brains of patients who had MS. Molecular analysis of IgG gene specificity in the brain and CSF of those with MS has shown features of an antigen-driven response: clonal amplification and extensive somatic mutations. A viral antigen against which the IgG in MS brain and CSF is directed might be identified.
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Tuberculous meningitis (TM) is difficult to diagnose and treat; clinical features are non-specific, conventional bacteriology is widely regarded as insensitive, and assessment of newer diagnostic methods is not complete. Treatment includes four drugs, which were developed more than 30 years ago, and prevents death or disability in less than half of patients. ⋯ There are many important unanswered questions about the pathophysiology, diagnosis, and treatment of TM. Here we review the available evidence to answer some of these questions, particularly those on the diagnosis and treatment of TM.
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Tourette's syndrome (TS) is a chronic neuropsychiatric disorder characterised by motor and vocal tics. Diagnosis is based solely on clinical criteria. The prevalence of this syndrome is estimated to be between one and ten per 1000 children and adolescents and the outcome is generally favourable; most patients improve by their late teens or early adulthood. ⋯ Brain imaging, neurophysiological, and post-mortem studies support involvement of cortical-striatal-thalamocortical pathways, but the definitive pathophysiological mechanism or neurotransmitter abnormality is unknown. Recent evidence, however, suggests a prefrontal dopaminergic abnormality. Traditional neuroleptics are the standard treatment for TS, but there is increasing interest in non-neuroleptic drugs, behavioural therapies, and surgical approaches.