Superior MRI outcomes with alemtuzumab compared with subcutaneous interferon β-1a in MS.

Objective: To describe detailed MRI results from 2 head-to-head phase III trials, Comparison of Alemtuzumab and Rebif Efficacy in Multiple Sclerosis Study I (CARE-MS I; NCT00530348) and Study II (CARE-MS II; NCT00548405), of alemtuzumab vs subcutaneous interferon β-1a (SC IFN-β-1a) in patients with active relapsing-remitting multiple sclerosis (RRMS).

Methods: The impact of alemtuzumab 12 mg vs SC IFN-β-1a 44 μg on MRI measures was evaluated in patients with RRMS who were treatment-naive (CARE-MS I) or who had an inadequate response, defined as at least one relapse, to prior therapy (CARE-MS II).

Results: Both treatments prevented T2-hyperintense lesion volume increases from baseline.

Should MS be treated by escalation or induction therapy?

MS is a chronic, increasingly disabling disease whose long-term outcomes determine the key social, medical and economic impact of this disease. Disease-modifying therapies (DMTs) for multiple sclerosis (MS) are prescribed to delay disease progression and to protect a patient's functional capability. The concepts of escalation and induction immunotherapy in MS represent different therapeutic strategies for the treatment of MS.

Alemtuzumab versus interferon beta 1a as first-line treatment for patients with relapsing-remitting multiple sclerosis: a randomised controlled phase 3 trial.

Background: The anti-CD52 monoclonal antibody alemtuzumab reduced disease activity in a phase 2 trial of previously untreated patients with relapsing-remitting multiple sclerosis. We aimed to assess efficacy and safety of first-line alemtuzumab compared with interferon beta 1a in a phase 3 trial.

Methods: In our 2 year, rater-masked, randomised controlled phase 3 trial, we enrolled adults aged 18-50 years with previously untreated relapsing-remitting multiple sclerosis.

Early-onset ataxia with progressive external ophthalmoplegia associated with POLG mutation: autosomal recessive mitochondrial ataxic syndrome or SANDO?

Autosomal recessive ataxias caused by mutations of the polymerase γ (POLG) gene make an important group of progressive ataxias accompanied by a diverse spectrum of neurological disorders. Because the clinical picture can be quite miscellaneous, it is challenging to assort patients to any of the currently described syndromes; therefore, to provide such a patient with a conclusive diagnosis can be challenging for the neurologist. A typical magnetic resonance imaging finding is probably the most useful landmark in the diagnostic process, which will steer the clinician toward POLG gene testing.

Diagnostic approach of patients with longitudinally extensive transverse myelitis.

The aim of this study is to present a diagnostic and therapeutic approach in patients with LETM. In a period between June 2008 and June 2010, all patients who fulfilled criteria for LETM were included in the study. All patients underwent a standardized protocol of investigations presented in this paper.

Sporadic CJD in a patient with relaplsing-remitting multiple sclerosis on an immunomodulatory treatment.

Creutzfeld-Jacob disease (CJD) is a degenerative, invariably fatal brain disorder. Multiple sclerosis (MS) is a chronic, potentially disabling, immune-mediated inflammatory demyelinating disease of the central nervous system. Here, we report a 50-year-old woman who, two years after the diagnosis of relapsing remitting MS, developed altered consciousness, dystonic posture of the left hand and myoclonic jerks.

Spinal cord tumor versus transverse myelitis.

Background Context: Longitudinally extensive transverse myelitis (LETM) is one of the defining features of neuromyelitis optica (NMO). Despite the well-established criteria, clinical and paraclinical features, the disease is often misdiagnosed and erroneously treated.

Purpose: We report on a case of LETM in a patient with spatially limited NMO spectrum disorder that was misdiagnosed as spinal cord tumor and underwent spinal cord biopsy.

Central positioning upbeat nystagmus and vertigo due to pontine stroke.

We present a female patient with central positioning nystagmus and vertigo (c-PPV) due to a pontine stroke. To our knowledge this is the first report of central upbeat positioning nystagmus caused by pontine lacunar stroke. This report, together with those published previously, supports the existence of a crossing ventral tegmental tract in humans.

Downbeat nystagmus, ataxia and spastic tetraparesis due to coeliac disease.

A 25-year-old female presented to a university neurology clinic with a 1-month history of progressive ataxia, downbeat nystagmus and spastic tetraparesis. Personal history revealed polyarthralgias and weight loss. Family history was negative.

Genes associated with multiple sclerosis: 15 and counting.

Evaluation of: The International Multiple Sclerosis Genetics Consortium (IMSGC). IL12A, MPHOSPH9/CDK2AP1 and RGS1 are novel multiple sclerosis susceptibility loci. Genes Immun.

Treatment of steroid unresponsive relapse with plasma exchange in aggressive multiple sclerosis.

The options for treating steroid unresponsive relapses in relapsing remitting multiple sclerosis (RRMS) are modest. We present a small series of patients with an aggressive course of RRMS whose steroid unresponsive relapses were treated with plasma exchange. In the period from January 2007 until February 2009 we identified four patients with steroid unresponsive relapses.

Genomics in multiple sclerosis.

Multiple sclerosis (MS) is chronic, inflammatory disease of the central nervous system that mainly affects young adults and is characterized with dissemination of demyelinating lesions in time and space. It is well known that MS is very heterogeneous disease, so biomarkers that would reliably determine disease course, outcome or treatment response in early stages of the disease (preferentially clinically isolated syndrome) are desperately needed. Genome-wide expression analysis represents the profile of all genes in a certain tissue or cell population in a certain time point.

Nutrition in multiple sclerosis.

Multiple sclerosis (MS) is a chronic idiopathic inflammatory demyelinating disease that causes neurological disability in young adults. Etiology of the disease is still unknown, but it has an immune-mediated basis and occurs in genetically susceptible individuals. Nutritional status and dietary habits in MS patients have not been extensively studied or reported, however individual findings suggest that many patients suffer from various forms of malnutrition.

Rare infections mimicking MS.

The diagnosis of multiple sclerosis (MS), despite well defined clinical criteria is not always simple. On many occasions it is difficult to differentiate MS from various non-MS idiopathic demyelinating disorders, specific and infectious inflammatory diseases or non-inflammatory demyelinating diseases. Clinicians should be aware of various clinical and MRI "red flags" that may point to the other diagnosis and demand further diagnostic evaluation.

Primary diffuse meningeal melanomatosis.

Primary diffuse meningeal melanomatosis can clinically mimic a wide variety of other conditions, including lymphoma, leukemia, neurosarcoidosis, metastatic carcinoma, acute disseminated encephalomyelitis, subacute meningitis, viral encephalitis, and idiopathic hypertrophic cranial pachymeningitis. We report on a young patient with primary diffuse meningeal melanomatosis who presented with papilledema, flaccid paraparesis, and cognitive impairment. The importance of imaging of the whole central nervous system, cerebrospinal fluid analysis, and pathohistological examination is emphasized in making the appropriate diagnosis.

Diagnostic imaging in acute disseminated encephalomyelitis.

Acute disseminated encephalomyelitis is an idiopathic inflammatory demyelinating disease of the CNS that is particularly difficult to differentiate from the first episode of multiple sclerosis, so called clinically isolated syndrome. Currently, no diagnostic criteria exist that could reliably differentiate these two diseases. More importantly no single clinical, neuroimaging or cerebrospinal fluid feature defines a disorder with absolute certainty.

Subacute brainstem angioencephalopathy: favorable outcome with anticoagulation therapy.

We present a patient who developed progressive neurological disease caused by lesions histologically compatible with those observed in subacute brainstem angioencephalopathy. The patient was treated with low-molecular weight heparin, and treatment response was monitored clinically and with MRI. Anticoagulation therapy stopped progression of the neurological deficit and led to improvement of MRI findings.