The American Academy of Neurology (AAN) Annual Meeting was held in Toronto, Canada from 10 to 17 April, 2010. As usual, multiple sclerosis (MS) featured prominently with about 450 poster and platform presentations on various aspects. Highlights were presentations on the controversial theory of venous obstruction as a cause of MS and updates on promising oral treatments, particularly fingolimod, cladribine and teriflumomide.

Lenercept, a tumour necrosis factor (TNF) capture molecule, was tested in a double- blind, placebocontrolled Phase II trial in multiple sclerosis (MS). Most patients had relapsing-remitting disease. The code was broken once all patients had been treated for at least 24 weeks. Patients on the drug experienced one and a half times as many MS attacks as those on placebo. MS attacks lasted one and a half times as long in those on the drug as those on placebo. Additionally, MS-related complaints voiced by patients on drug were much increased. Prior studies of TNF capture molecules in animals with experimental autoimmune encephalomyelitis turned out to have been counter-predictive. Surprisingly, magnetic resonance imaging scans performed every 4 weeks over the course of the trial, immediately prior to intravenous dosing, were uninformative. The lenercept trial findings raise concerns about other agents that lower TNF levels and that are sometimes given to MS patients. As an example, the possibility is discussed that cyclo propyl-substituted fluoroquinolone antibiotics, of which ciprofloxacin is the most studied, may provoke worsening of MS because of their TNF-inhibiting properties.

Although the diagnostic value of magnetic resonance imaging (MRI) in multiple sclerosis (MS) is widely accepted, the clinical usefulness of routine MRI for monitoring the evolution of patients with MS is less widely accepted. It is not uncommon for clinicians to say that they treat the patient, not the MRI. In this review, we highlight some of the evidence that routine MRI surveillance of patients with MS provides important information about disease activity that is not evident clinically, and that this information can help with prognosis and management decisions. Specific recommendations for MRI surveillance of MS patients are provided.

Psychiatric disorders have been commonly recognized to be associated with multiple sclerosis (MS) during the course of the illness or as a result of the side effects of the drugs used for its management. There have been reports of MS patirents, presenting initially with pure psychiatric symptoms. Amongst these, atypical psychosis has been infrequently reported to be a feature of MS; presentation with typical features of acute psychosis associated with stress appears to be very rare. Hence, this should always prompt for consideration of other diagnoses, including functional psychosis. Nonetheless, as illustrated by the following case report, acute onset of demyelinating diseases with the clinical phenotype of acute psychosis associated with stress may.

In 1930 there were many conflicting views on the cause, incidence, precipitating factors, inheritance and treatment of multiple sclerosis (MS). A young, London neurologist summarized the state of understanding of the disease with his personal view of many of the uncertain areas, and clarified the thinking for the neurological community at that time. Although his later career was influential in many fields of medicine, and his personal influence was extraordinary in many areas as an author, educator, administrator, opinion leader and historian, his review was an important milestone in the history of MS.

The search for the aetiology of multiple sclerosis (MS) has led to many theories over the years. It has become clear, however, that MS is complex and multifactorial, involving many interlacing mechanisms, many of which appear to be playing a role in the causation and evolution of the disease. In the large part for epidemiological reasons, an infectious aetiology has always been a prime suspect in this search. Although many agents have been examined over the years, the Epstein-Barr virus (EBV) has re-emerged as a candidate pathogen, based to a large degree on sero-epidemiological evidence, and on the knowledge of the effects this virus is capable of producing in other situations.

Epstein-Barr virus (EBV) infection, particularly symptomatic infection, is closely associated with multiple sclerosis (MS). The strength of this association, the interaction of EBV infection with genetic risk factors and emerging immunological data have resulted in some investigators arguing that this association may be causative. Causation, however, is a complex science and more extensive and definitive data is required to convince the wider community that EBV is the pivotal factor in the complex causal pathway that ultimately leads to the development of MS.

The American Academy of Neurology (AAN) Annual Meeting was held in Toronto, Canada from 10-17 April, 2010. As usual, multiple sclerosis (MS) featured prominently with about 450 poster and platform presentations on various aspects. Highlights were presentations on the controversial theory of venous obstruction as a cause of MS and updates on promising oral treatments, particularly fingolimod, cladribine and teriflumomide.

The ability to cope emotionally and experience quality of life (QoL) do not appear to be correlated with severity of disease or disability amongst people with multiple sclerosis (MS). An exploration of the health-related literature (trauma, chronic illness, disability, loss) from a resiliency perspective identifies a constellation of variables: personality and environmental characteristics, resiliency processes and drives for growth and healing which can guide the health-care practitioner wishing to enable QoL despite MS.

Local skin reactions to subcutaneous injections of interferon beta (IFNB) or glatiramer acetate (GA) in multiple sclerosis (MS) are frequent, while severe cutaneous toxicity is rare. Both IFNB and GA are immunomodulatory drugs that have excellent safety profiles and are currently used for treatment of MS. They are administered by SC injection every other day for IFNB-1b, three times a week for IFNB-1a or daily for 20 mg for GA. The most common adverse effects, which occur in approximately 20-60% of patients, include pain, inflammation and induration at the injection sites. Another adverse effect is frank panniculitis followed by localized lipoatrophy at the injection sites, which has been described in half of the patients receiving GA injections but is also described with Subcutaneous IFNB-1b. No guidelines have yet been established for the treatment of skin reactions, which is a frequent point for discussion between neurologists and dermatologists. In addition, no treatment has been found for established lipoatrophy. The prevention and management of cutaneous side-effects include patient education, regular examination and manual palpation of all injection sites. Non-steroid antiinflammatory gels, local corticosteroids or endermology can help patients to resolve side-effects and to continue immunomodulatory treatment.

Since multiple sclerosis (MS) has its onset at a young age, it is valuable to know how it affects life plans and future perspectives of patients. Through two narratives, this aspect is discussed in this article. The first is the autobiographical journal: The Journal of a Disappointed Man by WNP Barbellion, published in 1920, and the other one is from a contemporary patient. Despite the fact that both narratives are derived from different centuries, clear similarities have been perceived in the patients life plans and future perspectives. The narratives show that the life plans of both patients were adjusted due to physical limitations. Additionally, both patients experienced sorrows for losing the ability to perform passionate hobbies during their life. Moreover, a strong sense of uncertainty was expressed in both narratives concerning their future.

More than 3000 neurologists attended the 20th Meeting of the European Neurological Society (ENS) and participated in the exciting and highly scientific programme. Eighty per cent of the submitted abstracts, which covered all aspects of neurology, were accepted. One major symposium, 16 oral presentations and 112 posters on multiple sclerosis (MS) were included in the programme. Additionally, there were three teaching courses and one interactive case presentation on MS.

At its final meeting, the MS Forum Executive Committee reviewed highlights of where things stood prior to the immunomodulatory era, and how things have evolved subsequently. What the future might hold was discussed in a second session. Prior to 1990: Genetic predisposition to multiple sclerosis (MS), as determined by human leukocyte antigen expression, was established and an environmental trigger (Epstein-Barr virus?) was suspected, as was lack of sunshine. Substantial evidence for activated T-cells as relapse initiators had accumulated. Defective regulatory cell function that correlated with disease activity was shown. Adrenocorticotropic hormone lessened relapse severity as did its steroid replacement. A trial of cyclosporine, a T-cell inhibitor, in progressive MS failed. The drug, not the patients chosen, was blamed. 1990-2010: Approval of interferon-beta (IFNB)-1b was followed promptly by IFNB-1a, glatiramer acetate, mitoxantrone and then by natalizumab and fingolimod. All reduce MS attack frequency and new lesion accumulation. None have reduced disability progression in progressive MS. Brain atrophy, cognitive loss and axonal interruption in progressive MS depend on innate immune system activation rather than on T-cells. New strategies are needed.

When The International MS Journal (IMSJ) first appeared in 1994 multiple sclerosis (MS) was an under-recognized disease of little interest therapeutically. Its frequency was not great enough to interest the major pharmaceutical companies, its cause was unknown and evidence of any major therapeutic effect was lacking.

The majority of patients with Multiple Sclerosis (MS) experience fatigue and for many susabjects concerned it is the most disabling symptom. Fatigue is most prominent in the afternoon and may be aggravated by heat. It has a tremendous negative impact on quality of life and is often one of the major reasons for early retirement and unemployment. Against further assumptions, fatigue can occur at all stages and is often present at the onset of the disease. Reliable assessment however, is difficult as it is a subjectively perceived lack of physical and/or mental energy interfering with intended activities and has to be differentiated from depression, consequences of sleep disorders, cognitive decline, and side-effects of medication. Moreover, fatigue is not directly related to overall disease evolution, to disability levels or localized lesions, although an association with dysfunction of fronto-thalamo-basal-ganglia circuits seems likely. Several therapeutic approaches including pharmacological as well as non-pharmacological strategies are available but an evidence-based specific gold-standard for the treatment of fatigue is still missing.