Chapters 7 - Neurological Disorders 08. Multiple sclerosis

08. Multiple sclerosis

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Multiple sclerosis [ 41 , 69 , 86 , 187 , 212 ] (MS) is a neurological chronic inflammatory autoimmune disease.

It is a multifactorial disease whose clinical manifestations are related to demyelination [ 213 ] nerve fibers of the white matter of the central nervous system (brain, spinal cord and optic nerve, the latter part of the CNS [ 41 ]).

The definition of MS is primarily anatomical, this is the description of the injuries that led to his name [ 74 ].

1. Pathophysiology:

This is a demyelinating disease, the symptoms are related to the destruction of myelin [ 107 , 185 ] while maintaining the axons (axonal dissociation myélino-[ 31 , 36 , 107 , 179 ]).

It is an inflammatory disease [ 182 ] as evidenced by the early lesions where edema and inflammatory infiltrate accompanying the active disintegration of myelin sheaths [ 31 ].

In less early lesions is at the periphery of the lesions, in their areas of progress, found inflammation: T lymphocytes (CD4) and macrophages and B lymphocytes that secrete immunoglobulins (IgM and IgG) [ 74 ].

Old lesions are the seat of astrocytic proliferation characteristic sclerosis of nervous tissue (sclerosis). That Charcot described in 1868 [ 214 ], only the scar phase lesions.

The plates are numerous and scattered over the central nervous system. They can affect any area of the white matter, but with predilection sites: brainstem and periventricular areas [ 36 ].

The characteristic of this disease is its evolution, marked by phases of relapses [ 178 ] (when the formation of a new area of demyelination) and remission (when the plate heals) with partial remyelination [ 107 ] and sometimes dramatic improvement symptoms.

During an outbreak of the disease, the myelin sheath is destroyed. This alteration results in demyelination of axons in the electrical conduction, which results in a variety of clinical signs which appear in a few days. Unfortunately, over time, new outbreaks heal less, and neurological alterations end up not regress, forming permanent damage.

The pace of the relapsing-remitting phase is highly variable from one individual to another, so that for some the disease is very long without major impact outside attacks, while for others a rapid deterioration in the quality occurs in life compared with frequent relapses and little limiting. There is also a trend shape which consists of a permanent thrust.

Patients that suffer from MS, Heat alters nerve conduction and thus aggravates the symptoms during flares (Uhthoff phenomenon) [ 215 ].

2. Causes:

There is probably no single cause of MS, rather we must admit that this is a multifactorial disease in which certain factors are beginning to be demonstrated: autoimmunity, genetic factors, environmental factors [ 213 ] ...

It is an autoimmune disease associated with abnormal activity of some directed against the myelin sheath of nerve fibers, probably triggered after a viral event [antibody 75 ], in a genetically predisposed to the disease [ 216 ]. MS has a greater impact on women and young adults.

3. Diagnosis:

Often the first signs of the disease include a temporary reduction in visual acuity and paresthesia (tingling or pins and needles) in the arms. After a few days, these symptoms disappear, then diplopia and balance disorders settle.

Patients with MS may have motor problems (muscle weakness, twitching and muscle spasms, paralysis of one or more limbs, ataxia, slurred speech or writing) sometimes associated with sensory symptoms (tingling, abnormal sensations in one part of the body, the ends in the hands, feet and face, pain, headache diffuse, dizziness, imbalance).

There is no specific test for multiple sclerosis [ 212 ]. Modern tests allow early but often clinical data are generally adequate diagnosis: a change in crops is highly suggestive of the diagnosis. A period of 24 hours is necessary to speak of a push.

Dissemination in space is the second criterion [ 212 ], then it is to demonstrate that the patient has at least two lesions of the central nervous system. The ideal clinical setting for the diagnosis is concurrent involvement of the central nervous system and optic nerve. In other cases, the use of additional tests necessary to demonstrate that multifocality. Note that the lesions seen are often more scattered than is suggested by the clinic.

Analysis of the cerebrospinal fluid (CSF) [ 91 , 215 ] is an input value when diagnostic highlights inflammation.

Evoked potentials (EP) [ 31 , 216 ] visual, auditory, sensory, and more recently PE allow engines to detect subclinical suffering corresponding axonal pathways. It is therefore to identify the multifocal lesions. If the clinic only achieves that goal, their practice is useless.

The magnetic resonance imaging (MRI) [ 183 ] is the second test of choice, it can highlight the multifocal lesions at an early stage before the onset of symptoms [ 215 ].

4. Treatment:

The treatment of multiple sclerosis has two objectives: Slow the progression of the disease and relieve the patient. However, it is still impossible to cure MS [ 217 ].

Treatment is symptomatic [ 216 ] though can influence the evolution of the disease, corticosteroids, immunosuppressants, antispasmodics, muscle relaxants, antidepressants, beta-interferon ...

The medication comes with rest, physiotherapy, massage therapy and rehabilitation (occupational therapy, physiotherapy).

It should however remain critical of the effectiveness of treatment, particularly at the beginning of the disease, taking into account the spontaneously regressive outbreaks.

For people with the disease, it is possible to slow the onset of symptoms by resting enough [ 212 ], avoiding sources of stress and exposure to heat and sun, doing regular exercises and maintaining a healthy and balanced diet.