Lancet neurology
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Multiple sclerosis (MS) is probably aetiologically heterogeneous. Systematic genetic epidemiological and molecular genetic studies have provided important insights. Both genetic and non-genetic (environment, stochastic) factors may be involved in susceptibility as well as outcome, but we have yet to understand their relative roles. ⋯ There are, however, many genes that seem to be associated with MS. These include, but are in no way limited to, HLA classes I and II, T-cell receptor beta, CTLA4, ICAM1, and SH2D2A. The future of MS genetics, as for most common complex disorders, will be dependent on the resources available, ranging from biological samples and comprehensive databases of clinical and epidemiological information to the development of new technologies and statistical methods.
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15 years ago, the treatment of incidentally discovered intracranial aneurysms was straightforward with a good evidence base behind it. When intracranial aneurysms were identified, people were referred to neurosurgeons who would offer surgical repair if the patient was in reasonable health and had a good life expectancy. Since that time, several studies have given contradictory evidence for what should be done with these lesions, and a new technique for the repair of aneurysms, endovascular coil embolisation, has been developed. ⋯ Second, people with remaining life expectancy of less than 20 years or so (ie, those over age 60 years) should be informed that from a statistical point of view the benefits of treatment do not outweigh the risks. Third, in all other cases treatment with surgical clipping or coil embolisation should be advised. And finally, if surgical treatment is not feasible then medical hypotensive treatment may be a viable alternative.
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Multiple system atrophy (MSA) is a sporadic neurodegenerative disorder characterised clinically by any combination of parkinsonian, autonomic, cerebellar, or pyramidal signs and pathologically by cell loss, gliosis, and glial cytoplasmic inclusions in several CNS structures. Owing to the recent advances in its molecular pathogenesis, MSA has been firmly established as an alpha-synucleinopathy along with other neurodegenerative diseases. ⋯ Although the diagnosis of this disorder is largely based on clinical expertise, several investigations have been proposed in the past decade to assist in early differential diagnosis. Symptomatic therapeutic strategies are still limited; however, several candidate neuroprotective agents have entered phase II and phase III clinical trials.