Multiple sclerosis
Multiple sclerosis [41, 69, 86, 187, 212] (MS) is a chronic autoimmune inflammatory neurological disease. It is a multifactorial pathology whose clinical manifestations are linked to the demyelination [213] of nerve fibers in the white matter of the central nervous system (comprising the brain, spinal cord, and optic nerve, the latter being part of the CNS [41]). The definition of MS is primarily anatomical; the description of the lesions is what gave the disease its name [74].
Pathophysiology :
It is a demyelinating pathology; its symptoms are linked to the destruction of myelin [107, 185] while sparing the axons (myelin-axonal dissociation [31, 36, 107, 179]). Early lesions confirm its inflammatory nature [182], showing edema and inflammatory infiltrates alongside active myelin disintegration [31]. In older lesions, inflammation is found at the periphery - in the zones of progression - consisting of T lymphocytes (CD4), followed by macrophages and B lymphocytes that secrete immunoglobulins (IgM and then IgG) [74].
Older lesions are the site of astrocytic proliferation, which characterizes the sclerosis of nerve tissue (plaques). What Charcot described in 1868 [214] is only the scarring phase of the lesions. These multiple plaques are disseminated throughout the central nervous system. They can affect any part of the white matter, but they have sites of predilection: the brainstem and periventricular zones [36].
The unique feature of this disease is its progression, marked by phases of relapses [178] (during the formation of a new zone of demyelination) and remission (when the plaque heals), with partial remyelination [107] and sometimes dramatic improvement in symptoms. During a relapse, the myelin sheath is destroyed. This demyelination leads to an alteration in electrical conduction within the axon, resulting in various clinical signs that appear over a few days.
Unfortunately, over time, new relapses heal less effectively, and neurological alterations eventually stop regressing, forming permanent lesions. The rhythm of the relapsing-remitting phases varies significantly from one individual to another; for some, the disease remains without major impact outside of relapses for a long time, while for others, a rapid deterioration in quality of life occurs due to frequent relapses with poor recovery.
There is also a progressive form that consists of a permanent worsening. In patients suffering from MS, heat impairs nerve conduction and thus worsens symptoms during relapses (Uhthoff's phenomenon) [215].
Causes :
There is likely no single cause of MS; rather, it is recognized as a multifactorial disease for which several factors are being identified: autoimmunity, genetic factors, and environmental factors [213] ...
It is an autoimmune disease linked to the abnormal activity of certain antibodies directed against the myelin sheath of nerve fibers, triggered by a likely viral event [75] in an individual genetically predisposed to the disease [216]. MS has an increased incidence among women and young adults.
Diagnosis :
Often, the first signs of the disease include a temporary decrease in visual acuity and paresthesia (tingling or "pins and needles") in the arms. After a few days, these symptoms disappear, only for diplopia and balance disorders to set in later.
Patients with MS may present with motor disorders (muscle weakness, muscle contractions and spasms, paralysis of one or more limbs, ataxia, and speech or writing disorders) sometimes associated with sensory disturbances (tingling, abnormal sensations in a part of the body, extremities, hands, feet, or face, pain, diffuse headaches, dizziness and imbalance).
There is no specific test for multiple sclerosis [212]. Modern examinations allow for early diagnosis, but clinical data are often sufficient: a progression through successive relapses is highly suggestive of the diagnosis. A duration of 24 hours is necessary to qualify an event as a relapse.
Dissemination in space is the second criterion [212]; this involves demonstrating that the patient has at least two lesions in the central nervous system. The ideal clinical situation for diagnosis is the concomitant involvement of the neuraxis and the optic nerve. In other cases, recourse to complementary examinations is necessary to demonstrate this multifocality. It should be noted that the identified lesions are often more disseminated than clinical symptoms suggest.
Analysis of the cerebrospinal fluid (CSF) [91, 215] provides valuable diagnostic evidence when it highlights inflammation.
Evoked potentials (EP) [31, 216] - visual, auditory, sensory, and more recently motor EPs - allow for the detection of subclinical distress in the corresponding axonal pathways. The goal is to demonstrate the multifocality of the lesions; if clinical data alone achieve this, these tests are unnecessary.
Magnetic Resonance Imaging (MRI) [183] is the second examination of choice; it allows for the early detection of lesion multifocality, even before the onset of symptoms [215].
Treatment :
The treatment of multiple sclerosis aims for two objectives: to slow the progression of the disease and to relieve the patient. However, it is still impossible to cure MS [217]. Treatment is therefore symptomatic [216], although it can influence the course of the disease: corticosteroids, immunosuppressants, antispasmodics, muscle relaxants, antidepressants, and interferon-beta…
Medical treatment is accompanied by rest, physiotherapy sessions, therapeutic massage, and rehabilitation (occupational therapy and physiotherapy). However, one must remain critical regarding the efficacy of treatments, especially at the beginning of the disease, while taking into account the naturally regressive nature of relapses. For individuals with the disease, it is possible to slow the onset of symptoms by getting enough rest [212], avoiding stress, heat and sunlight, exercising regularly, and maintaining a healthy, balanced diet.