Esclerosis muy bueno

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Seminar

Multiple sclerosis
Alastair Compston, Alasdair Coles
Lancet 2008; 372: 1502–17 Department of Clinical Neurosciences, University of Cambridge Clinical School, Addenbrooke’s Hospital, Cambridge, UK (A Compston FRCP, A Coles FRCP) Correspondence to: Dr Alasdair Coles, University of Cambridge Clinical School, Addenbrooke’s Hospital, Hills Road, Cambridge CB2 2QQ, UKajc1020@medschl.cam.ac.uk

Multiple sclerosis is primarily an inflammatory disorder of the brain and spinal cord in which focal lymphocytic infiltration leads to damage of myelin and axons. Initially, inflammation is transient and remyelination occurs but is not durable. Hence, the early course of disease is characterised by episodes of neurological dysfunction that usually recover. However, over time the pathologicalchanges become dominated by widespread microglial activation associated with extensive and chronic neurodegeneration, the clinical correlate of which is progressive accumulation of disability. Paraclinical investigations show abnormalities that indicate the distribution of inflammatory lesions and axonal loss (MRI); interference of conduction in previously myelinated pathways (evokedelectrophysiological potentials); and intrathecal synthesis of oligoclonal antibody (examination by lumbar puncture of the cerebrospinal fluid). Multiple sclerosis is triggered by environmental factors in individuals with complex genetic-risk profiles. Licensed disease modifying agents reduce the frequency of new episodes but do not reverse fixed deficits and have questionable effects on the long-term accumulationof disability and disease progression. We anticipate that future studies in multiple sclerosis will provide a new taxonomy on the basis of mechanisms rather than clinical empiricism, and so inform strategies for improved treatment at all stages of the disease.

Introduction
“…the chief curse of the illness...I must ask constant services of people I love most closely...it is an illnessaccompanied by frustration...it is an illness that inflicts awareness of loss...sporadically it is, in its manifestations, a disgusting disease” Brigid Brophy, 1929–952

The principle of diagnosis is to establish from clinical evidence, supplemented by laboratory investigations, that disease activity which is consistent with focal demyelination has affected more than one part of the CNS and on more than oneoccasion.

Diagnosis
In most patients, clinical manifestations indicate the involvement of motor, sensory, visual, and autonomic systems but many other symptoms and signs can occur (table). Few of the clinical features are disease-specific, but particularly characteristic are Lhermitte’s symptom (an electrical sensation running down the spine or limbs on neck flexion) and the Uhthoff phenomenon(transient worsening of symptoms and signs when core body temperature increases, such as after exercise or a hot bath). New criteria allow for safe and early diagnosis, which avoids incorrect attribution of symptoms and signs in young adults to multiple sclerosis, and allows timely discussion about management before tissue injury has compromised the ability to undertake activities of daily living(figure 1).5,6 In many situations, clinical evidence is sufficient for establishment of the diagnosis and laboratory studies are superfluous; but, when the diagnosis is ambiguous, paraclinical features can decide the matter. MRI shows focal or confluent abnormalities in white matter in more than 95% of patients. Their presence alone, however, does not make the diagnosis of multiple sclerosis;characteristic radiological lesions can appear in people without clinical signs of disease and

The depiction of “a remarkable lesion of the spinal cord accompanied with atrophy” by Robert Carswell in 18383 anticipated a more or less complete description of the pathological anatomy and clinical features of multiple sclerosis (named thus in 1955) by the last decades of the 19th century. Over the next 100...
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