.png){kind=icon}
Return
Multiple sclerosis
.png){kind=icon}
PRE
AI
DOI：10.1016/S0140-6736(08)61620-7.png)
.png){kind=icon}
Original request for help.png){kind=icon}
Share.png){kind=icon}
Save
Abstract
En 中文
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 pathological changes 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 (evoked electrophysiological 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 accumulation of 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.
Keywords:
EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS
STEM-CELL TRANSPLANTATION
DOUBLE-BLIND
INTERFERON BETA-1B
GLATIRAMER ACETATE
NEUROMYELITIS-OPTICA
IN-VITRO
DIAGNOSTIC-CRITERIA
RECURRENCE RISKS
AXONAL DAMAGE
AI Summary
Key information extracted from the uploaded paper, including a brief overview, abstract, background, key highlights, visual analysis, and future outlook.
Journal
IF:
88.5
Papers:
5.4W
Citations:
34.8W
Organization
Cited Papers
ShareSaveDivergent Modulation of Nociception by Glutamatergic and GABAergic Neuronal Subpopulations in the Periaqueductal Gray.png)
eneuro
OAAI
eneuroIF0
OAAIShareSaveShareSaveShareSaveLoss of aquaporin 4 in lesions of neuromyelitis optica: distinction from multiple sclerosisBRAINOAAI
BRAINIF11.7
OAAIShareSaveNormal-appearing white matter in multiple sclerosis is in a subtle balance between inflammation and neuroprotectionBRAIN
OAAI
BRAINIF11.7
OAAIShareSave
View more