Carotid endarterectomy is the gold standard surgical intervention for stroke prevention in patients with symptomatic internal carotid stenosis. Early intervention is crucial for a good outcome. However, according to a recent UK audit from the Vascular Society and the Royal College of Physicians, two-thirds of patients face an unacceptable delay. Although there are examples of timely service provision from centres of excellence in the UK and elsewhere, it is thought that many countries are struggling to reduce the time to carotid surgery.

Every year, about 15 million people worldwide have an acute stroke. If widespread treatment with a simple, inexpensive vitamin pill for a few years among stroke survivors had even a small effect on the risk of subsequent vascular events, the effect on the global burden of vascular disease could be very large. From the perspective of efforts to tackle the ever increasing global burden of non-communicable diseases, the results of the VITAmins TO Prevent Stroke (VITATOPS) trial, published in this issue of The Lancet Neurology,1 are of great interest.

Seven randomised, placebo-controlled trials combined in a recent pooled analysis1 reported that thrombolysis with intravenous alteplase (recombinant tissue plasminogen activator; rt-PA) is efficacious in the treatment of acute ischaemic stroke. The window of opportunity is up to 4·5 h after onset, although much earlier is much better.2 There has been some concern as to whether the results of trials could be replicated in broad-based clinical practice, and support for such generalisability has come from a number of registries, the largest of which is the Safe Implementation of Treatment in Stroke-International Stroke Thrombolysis Registry (SITS-ISTR).

Spinal and bulbar muscular atrophy (SBMA), also known as Kennedy's disease,1–3 is a slowly progressive, X-linked motor neuron disease caused by a triplet repeat expansion in the androgen receptor gene. SBMA can easily be confused with amyotrophic lateral sclerosis (ALS) in its early stages because of bulbar signs, muscle wasting, and fasciculations. Although the prognosis of SBMA is more favourable than that of ALS, the life expectancy of patients with SMBA can be shortened by aspiration pneumonia in later stages4 and the disorder can interfere with patients' independence.

Medical dictionaries commonly define an epidemic either as a condition that affects or tends to affect an atypically large number of individuals within a population, community, or region at the same time, or as the occurrence of more cases of a disease than would be expected in a community or region during a specific time period. If these definitions for an epidemic are applied to global stroke—for which 85% of stroke burden is in low-income and middle-income countries,1 with an incidence that has increased by more than 100% over the past four decades to exceed stroke incidence rates in high-income countries2—it should be agreed that we are experiencing a global stroke epidemic.

The editorial team publicly acknowledges its gratitude once a year to peer reviewers who have appraised manuscripts for the journal. Yet we owe our advisers a debt of gratitude that keeps growing at the pace of the journal's success. According to the 2009 Journal Citation Report, for the sixth successive year The Lancet Neurology held the number 1 position in the clinical neurology category, and the journal's impact factor reached 18·126.

Populations are ageing, and the burden of neurodegenerative disease is increasing. By 2030, the global burden of Parkinson's disease is expected to have increased by 25% from 2005 levels,1 and by 2040 the number of people with dementia worldwide is expected to reach 81·1 million.2 Yet effective disease-modifying treatments remain elusive, not only for Alzheimer's and Parkinson's diseases but also for the many other neurodegenerative disorders that, although less common, can be just as devastating for the people affected.

With an epidemic of Alzheimer's disease lying in wait, some researchers are calling for a new era of prevention research—research in which people with a particular genetic fate would be vital participants. Adrian Burton reports.

Francisco Cardoso, professor of internal medicine at the Universidade Federal de Minas Gerais (UFMG) in Belo Horizonte, Brazil, insists he should not be acclaimed as the pioneer of movement disorder research in his country. However, via his extensive promotion and dissemination of modern methodologies and developments in this field, he could justly claim to be responsible for its great growth in Brazil since the mid-1990s.

Vitamin D and MS (Review, June)Ascherio A, Munger KL, Simon KC. Vitamin D and multiple sclerosis. Lancet Neurol 2010; 9: 599–612.Drugs for Alzheimer's disease (Review, July)Mangialasche F, Solomon A, Winblad B, et al. Alzheimer's disease: clinical trials and drug development. Lancet Neurol 2010; 9: 702–16.Cerebral small vessel disease (Review, July)Pantoni L. Cerebral small vessel disease: from pathogenesis and clinical characteristics to therapeutic challenges. Lancet Neurol 2010; 9: 689–701.

Gen Sobue graduated in medicine and trained as a neurologist at Nagoya University, Japan. He then completed a PhD in neurology at Nagoya University Graduate School of Medicine, after which he became an assistant professor at the University of Pennsylvania, USA, and then a lecturer and associate professor at Aichi Medical University, Japan. He is now dean and professor of neurology at the Nagoya University Graduate School of Medicine. He is interested in neurodegenerative diseases, particularly motor neuron diseases and peripheral neuropathies.

Delirium is common among elderly patients, and new data link this syndrome to poor long-term outcome. A review and meta-analysis of published studies revealed an association between delirium and risk of death over an average follow-up time of about 2 years (hazard ratio 1·95, 95% CI 1·51–2·52). The risk of institutionalisation over a follow-up of about 15 months (odds ratio [OR] 2·41, 1·77–3·29) and developing dementia over about 4 years (OR 12·52, 1·86–84·21) were also increased ( JAMA 2010; 304: 443–51).

Daily administration of folic acid, vitamin B6, and vitamin B12 to patients with recent stroke or transient ischaemic attack was safe but did not seem to be more effective than placebo in reducing the incidence of major vascular events. These results do not support the use of B vitamins to prevent recurrent stroke. The results of ongoing trials and an individual patient data meta-analysis will add statistical power and precision to present estimates of the effect of B vitamins.

Since October, 2008, thrombolysis within 3–4·5 h after stroke has been implemented rapidly, with a simultaneous increase in the number of patients treated within 3 h; admission-to-treatment time has not increased. Safety and functional outcomes are less favourable after 3 h, but the wider time window now offers an opportunity for treatment of those patients who cannot be treated earlier. Thrombolysis should be initiated within 4·5 h after onset of ischaemic stroke, although every effort should be made to treat patients as early as possible after symptom onset.

48 weeks of treatment with leuprorelin did not show significant effects on swallowing function in patients with spinal and bulbar muscular atrophy, although it was well tolerated. Disease duration might influence the efficacy of leuprorelin and thus further clinical trials with sensitive outcome measures should be done in subpopulations of patients.

Cerebellar ataxias with autosomal dominant transmission are rare, but identification of the associated genes has provided insight into the mechanisms that could underlie other forms of genetic or non-genetic ataxias. In many instances, the phenotype is not restricted to cerebellar dysfunction but includes complex multisystemic neurological deficits. The designation of the loci, SCA for spinocerebellar ataxia, indicates the involvement of at least two systems: the spinal cord and the cerebellum. 11 of 18 known genes are caused by repeat expansions in the corresponding proteins, sharing the same mutational mechanism.

Stroke remains a primary cause of morbidity throughout the world mainly because of its effect on cognition. Individuals can recover from physical disability resulting from stroke, but might be unable to return to their previous occupations or independent life because of cognitive impairments. Cognitive dysfunction ranges from focal deficits, resulting directly from an area of infarction or from hypoperfusion in adjacent tissue, to more global cognitive dysfunction. Global dysfunction is likely to be related to other underlying subclinical cerebrovascular disease, such as white-matter disease or subclinical infarcts.

Imaging techniques are important for accurate diagnosis and follow-up of patients with gliomas. T1-weighted MRI, with or without gadolinium, is the gold standard method. However, this technique only reflects biological activity of the tumour indirectly by detecting the breakdown of the blood–brain barrier. Therefore, especially for low-grade glioma or after treatment, T1-weighted MRI enhanced with gadolinium has substantial limitations. Development of more advanced imaging methods to improve outcomes for individual patients is needed.

Optical coherence tomography (OCT) is a new method that could aid analysis of neurodegeneration in multiple sclerosis (MS) by capturing thinning of the retinal nerve fibre layer (RNFL). Meta-analyses of data for time domain OCT show RNFL thinning of 20·38 μm (95% CI 17·91–22·86, n=2063, p<0·0001) after optic neuritis in MS, and of 7·08 μm (5·52–8·65, n=3154, p<0·0001) in MS without optic neuritis. The estimated RNFL thinning in patients with MS is greater than the extent expected in normal ageing, probably because of retrograde trans-synaptic degeneration and progressive loss of retinal ganglion cells, in addition to the more pronounced thinning caused by optic neuritis if present.

The prevalence of hypertension in children is increasing but its neurological effects are under-recognised. Here, we describe acute and chronic effects of childhood hypertension on the nervous system. Acute neurological involvement ranges from posterior reversible encephalopathy syndrome to, possibly, infarction and haemorrhage. Children with chronic hypertension are likely to have learning disabilities and deficiencies in executive function, which are potentially reversible with antihypertensive treatment.