My name is Daniela
The missing impulse
Multiple sclerosis
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MULTIPLE SCLEROSIS .

<back> In older individuals the spastic paraparesis increases with time up to the impossibility of independent locomotion. Bladder impairment is common as well as cognitive impairment. At least 70% of patients should to improve in the days to months following their initial bout, with the degree of improvement ranging from slight to virtual disappearance of the neurologic dysfunction. Unfortunately as time goes by, recovery from individual bouts decreases, fixed impairment and disability remain and the course became chronically progressive. The average interval time from clinical onset is 35-45 years.





- Etiopathogenesis.

The initiating cause or causes of MS are unknown, but it is now widely believed that pathogenesis involves immune-mediated inflammatory demyelination and axonal injury ( the immune system of the patients mounts, wrongly, an inflammatory-immune response against own myelin components recognized as non-self). The immune system (9) components involved in this anomalous inflammatory response consist of blood cells :T linfocytes and monocytes ( white blood cells or leucocytes, produced by the bone marrow (10), responsible of fighting the non-self ). Such cells infiltrate the perivascular spaces of CNS by extravasating and secrete certain substances that destroy broad areas of CNS myelin. Such regions represent multiple patches of myelin degeneration, from which the name of MS. The patches of myelin degeneration can develop in any myelinated area of the CNS but most frequently in the optic nerves, periventricular white matter (11) ( the periventricular region is located around the cerebral ventricles containing the liquor), and spinal white substance. The ematoancephalic barrier (the barrier of the cells of the cerebral vessels) prevents the extravasation of the T lynfocytes and monocytes into spaces of white substance. Due to unknown causes, the ematoencephalic barrier is compromised in MS patients.

 

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