The need to curb the rising costs of health care has led policy-makers in many countries to consider widespread generic substitution of brand-name drugs as an effective means to cut costs. For example, on January 5, 2010, the NHS in England began a 3-month consultation to seek views on plans to automatically substitute branded drugs with generic versions in primary care. However, doctors, patients, and advocacy groups—in England and elsewhere—are concerned that generic antiepileptic drugs (AEDs) might not be therapeutically equivalent to branded drugs, which could put patients at risk of breakthrough seizures or other adverse events.

Although a rare neuropathy, chronic inflammatory demyelinating polyneuropathy (CIDP) causes substantial disability in untreated patients. There is compelling data from randomised controlled trials that intravenous immunoglobulin, plasma exchange, and corticosteroids cause meaningful clinical improvement in most patients.1 About one-third of cases are refractory to these conventional therapies, and there therefore remains a need for more effective treatments. In addition, current treatments can be time consuming, inconvenient, and costly.

Bacterial meningitis causes 170 000 deaths worldwide per year and, in low-income and middle-income countries, is ranked fourth as a cause of disability,1 emphasising the need for clear evidence-based recommendations to guide acute management. Despite more than 20 clinical trials of adjunctive corticosteroid therapy in bacterial meningitis over the past 50 years,2 absence of significant benefit in most individual studies, diverse steroid and antibiotic regimens, and concerns about generalisability to all causative organisms have fuelled continued debate.

The availability of natalizumab for the treatment of multiple sclerosis has revolutionised the practice of neurology in at least one salient way: we now spend much more time thinking about progressive multifocal leukoencephalopathy (PML). The reasons for this increased attention are not difficult to identify. Many patients with multiple sclerosis have ongoing disease activity while receiving the first-line drugs interferon beta and glatiramer acetate, and natalizumab offers a second-stage medication for these patients.

Coeliac disease is regarded as an autoimmune small bowel disorder that is triggered by the ingestion of wheat gliadins and other cereal prolamins in genetically susceptible individuals.1 Although the small bowel is one of the main targets of the disease, increasing evidence indicates that coeliac disease can affect other organs, including the nervous system, thus changing the clinical scenario from what was once thought of as an intestinal disorder to a broader systemic disease. In this context, the term gluten sensitivity was coined to take into account the various extraintestinal gluten-dependent manifestations, even in patients with an apparently normal intestinal mucosa.

Currently available treatments for Alzheimer's disease (acetylcholinesterase inhibitors and memantine) improve cognitive function, but do not slow the long-term progression of this disorder. Despite several attempts with therapies aimed at reducing the brain amyloid load, or that target other pathological mechanisms, no treatment has been shown to slow the progression of Alzheimer's disease in a phase 3 trial. Results from a phase 2 study of tarenflurbil, a compound that inhibits γ-secretase and has positive effects on cognition in animals, seemed promising in slowing decline in Alzheimer's disease assessment scale-cognitive (ADAS-cog) scores in patients with mild Alzheimer's disease.

Stroke accounts for about 10% of deaths worldwide each year. Although the incidence of stroke in high-income countries has fallen by about 40% over the past four decades, the incidence in low-income and middle-income countries has more than doubled during this timeframe, and 85% of all strokes now occur in developing countries.1,2 Advances in the management of stroke during the past decade have improved outcomes for patients who have had a stroke.3 However, stroke continues to present many challenges, not least of which is the gross underfunding of stroke research compared with coronary heart disease and cancer.

Bushby K, Finkel R, Birnkrant DJ, et al. Diagnosis and management of Duchenne muscular dystrophy, part 2: implementation of multidisciplinary care. Lancet Neurol 2010; 9: 177–89. On page 185 of this Review (published Online First on Nov 30, 2009), in the paragraph entitled ‘Emergency-care considerations’ the sentence on the use of opiates should have read “Care in the use of opiates and other sedating medication is essential, as is care in the use of oxygen without ventilation owing to the risk of hypercapnia.

After the Human Genome Project there came proteomes, transcriptomes, and epigenomes. There was even a Human Microbiome Project launched last year by the US National Institutes of Health. Are neuroscientists just jumping on the 'ome bandwagon, or is there truly a benefit to deciphering and detailing the human connectome? Ruth Williams reports.

It would surely be impossible for someone who works at a place called Rainbow Babies and Children's Hospital to be anything but joyful and benevolent. Max Wiznitzer, director of the Rainbow Autism Center at the hospital in Cleveland (OH, USA), certainly lives up to that expectation. Wiznitzer is also an associate professor of paediatrics and neurology at Case Western Reserve University in Cleveland.

Epigenetic mechanisms (Review, November)Urdinguio RG, Sanchez-Mut JV, Esteller M. Epigenetic mechanisms in neurological diseases: genes, syndromes, and therapies. Lancet Neurol 2009; 8: 1056–72.Duchenne muscular dystrophy (Review, January)Bushby K, Finkel R, Birnkrant DJ, et al. Diagnosis and management of Duchenne muscular dystrophy, part 1: diagnosis, and pharmacological and psychosocial management. Lancet Neurol 2010; 9: 77–93.Initial features of PD (Review, December)Rodriguez-Oroz MC, Jahanshahi M, Krack P, et al.

Renaud Du Pasquier obtained his MD from the University of Geneva, Switzerland. After a Swiss Board certification in neurology and internal medicine, he did a research fellowship in neurovirology and neuroimmunology at the Beth Israel Deaconess Medical Center, Boston, MA, USA. Back in Switzerland, he established his laboratory at the Centre Hospitalo-Universitaire Vaudois, Lausanne. His group studies the physiopathogenesis of multiple sclerosis and the link between viruses and demyelination.

The fundamental rules of medicine—take a thorough history and, if unsure, always phone a friend—are well illustrated in this collection of unusual medical cases. The Deadly Dinner Party presents cases that all required a certain level of detective work and lateral thinking to reach the eventual diagnosis. Each scenario is unravelled in an almost forensic fashion to finally untangle why the patient became infected or afflicted with a particular illness in the first place.

International Neurology: A Clinical Approach offers a wide ranging and exhaustive view of neurological pathology around the world. This book deals with the diversity that now characterises the approaches to and management of neurological disorders in terms of geography, racial and ethnic groups, economic aspects, environmental matters, and pathological features. Wherever they practise, neurologists face the usual diseases found in their region, but they are also facing more and more aetiological patterns imported from abroad.

Neuro-ophthalmology—a subspecialty at the intersection of ophthalmology, neurology, neurosurgery, and general medicine—deals with ocular diseases as well as myriad neurological and systemic conditions with ophthalmic manifestations. More than ever before, successful practice of neuro-ophthalmology requires both careful clinical observation (aided by familiar tools such as slit-lamp microscopes and stereoscopic ophthalmoscopes) and use of increasingly sophisticated technologies, such as neuroradiological imaging and optical coherence tomography.

Short-course cladribine is effective for providing rapid and sustained treatment benefits for patients with relapsing-remitting multiple sclerosis. In the phase 3, double-blind CLARITY (Cladribine Tablets Treating Multiple Sclerosis Orally) study, 1326 patients received short courses of placebo or 3·5 mg/kg or 5·25 mg/kg cladribine in two 48-week periods ( N Engl J Med 2010; published online Jan 20. DOI:10.1056/NEJMoa0902533). Compared with placebo, both doses of the immunomodulator reduced yearly relapse rates (0·14 and 0·15 vs 0·33; p<0·001), increased relapse-free rates (79·7% and 78·9% vs 60·9%; p<0·001), reduced risk of 3-month disability progression (3·5 mg: 33%, p=0·02; 5·25 mg: 31%, p=0·03), and reduced lesion disease activity (p<0·001).

Pulsed high-dose dexamethasone treatment did not induce remission more often than prednisolone treatment. A substantial proportion of patients were in remission at 12 months in both treatment groups. High-dose dexamethasone could be considered as induction therapy in CIDP, but comparison with intravenous immunoglobulin treatment is needed.

Adjunctive dexamethasone in the treatment of acute bacterial meningitis does not seem to significantly reduce death or neurological disability. There were no significant treatment effects in any of the prespecified subgroups. The benefit of adjunctive dexamethasone for all or any subgroup of patients with bacterial meningitis thus remains unproven.

Natalizumab increases cellular immune responses specific to viruses and myelin proteins in the peripheral blood after 1 year, without evidence of viral reactivation.

Aspirin is widely used for the prevention of recurrent stroke in patients with transient ischaemic attack (TIA) and ischaemic stroke of arterial origin, because it is effective and inexpensive. Clopidogrel and the combination of aspirin and extended-release dipyridamole are more effective than aspirin, but are also much more expensive. No other antithrombotic regimens provide significant advantages over aspirin, although cilostazol and the novel platelet protease activated receptor-1 antagonist, SCH 530348, are currently being evaluated.

Migraine is a common and disabling brain disorder with a strong inherited component. Because patients with migraine have severe and disabling attacks usually of headache with other symptoms of sensory disturbance (eg, light and sound sensitivity), medical treatment is often required. Patients can be managed by use of acute attack therapies (eg, simple analgesics or non-steroidal anti-inflammatory drugs) or specific agents with vasoconstrictor properties (ie, triptans or ergot derivatives). Future non-vasoconstrictor approaches include calcitonin gene-related peptide receptor antagonists.

Multiple sclerosis (MS) is an autoimmune disease of the CNS. It is the most common non-traumatic cause of neurological disability among young adults in western Europe and North America. Existing MS therapies are partly effective in halting ongoing inflammatory tissue damage and clinical progression. MS pathogenesis is complex and probably heterogeneous among patients, suggesting that combination therapy strategies that target a range of disease mechanisms might be more effective than medications used as monotherapy.

Migraine attacks with auras are sometimes associated with underlying hereditary or acquired cerebrovascular disorders. A unifying pathophysiological explanation linking migraine to these conditions has been difficult to identify. On the basis of genetic and epidemiological evidence, we suggest that changes in blood vessels, hypoperfusion disorders, and microembolisation can cause neurovascular dysfunction and evoke cortical spreading depression, an event that is widely thought to underlie aura symptoms.

Gluten sensitivity is a systemic autoimmune disease with diverse manifestations. This disorder is characterised by abnormal immunological responsiveness to ingested gluten in genetically susceptible individuals. Coeliac disease, or gluten-sensitive enteropathy, is only one aspect of a range of possible manifestations of gluten sensitivity. Although neurological manifestations in patients with established coeliac disease have been reported since 1966, it was not until 30 years later that, in some individuals, gluten sensitivity was shown to manifest solely with neurological dysfunction.