Multiple sclerosis

Multiple sclerosis is characterized by the appearance in the brain and spinal cord of disseminated foci of demyelination.

Among the characteristic symptoms, visual and oculomotor disorders, paresthesia, weakness, impaired pelvic organs and cognitive impairment.

Typically, the neurological deficit is multiple, with remissions and exacerbations, gradually leading to disability. The diagnosis of multiple sclerosis is posed in the presence of remissions and exacerbations, at least 2 topically selected neurological disorders, clinically or instrumentally identified, changes in MRI or other criteria (depending on the complaints). Treatment of multiple sclerosis: glucocorticoids with exacerbations, immunomodulators for the prevention of exacerbations and symptomatic therapy.

Read also: Multiple sclerosis: face to face

Multiple sclerosis is the most common cause of the acquired demyelination of the central nervous system, which, in fact, is an inflammatory process directed against the myelin of the brain and spinal cord. As a fairly common disease in the Western Hemisphere and Europe, multiple sclerosis is one of the main causes of disability in the streets of middle and young age. For the majority, if not for all patients, multiple sclerosis is a source of significant physical and emotional suffering, and to society, it causes significant economic and social damage. In the US, multiple sclerosis affects 300-400 thousand people. Although the exact cause of multiple sclerosis remains unknown and the disease can not be completely cured, in recent years there have been funds that affect the course of the disease, affecting the pathogenetic processes underlying it, and are capable of improving the quality of life and health.

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Epidemiology of multiple sclerosis

Probably with multiple sclerosis (PC) an immunological mechanism is involved, it is possible that there is an infection (an unidentified latent virus) triggering a secondary immune response. The increased prevalence in some families and certain allotypes of the main histocompatibility complex (HLA-DR2) testifies to the genetic predisposition. Multiple sclerosis is more common in people who have spent the first 15 years of life in a temperate climate (1/2000) than in the tropics (1/10 000). Increases risk and smoking. The debut of the disease at the age of 15-60 years, typically 20-40 years. Women are sick more often.

Multiple Sclerosis - Epidemiology

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Causes of Multiple Sclerosis

Demyelination sites are identified (they are called plaques), inside and around which is degradation of oligodendroglia, perivascular inflammation, chemical changes in lipid and protein components of myelin. Perhaps axonal lesion, but the cell bodies and axons are sufficiently preserved. In the plaques scattered over the central nervous system, fibrinous gliosis develops, first in white matter, in particular in the lateral and posterior columns (especially in the cervical region), optic nerves and periventricular zones. Affect the pathways of the midbrain, bridge and cerebellum. The gray matter of the brain and spinal cord suffers less.

Multiple sclerosis - Causes and pathogenesis

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Symptoms of Multiple Sclerosis

For multiple sclerosis, remissions and exacerbations of neurological deficits are characteristic. The frequency of exacerbations varies, on average, about 3 times a year. The most common initial symptoms are paresthesia in one or more extremities, the trunk or one side of the face; weakness or awkwardness in the arm or leg and visual impairment (eg, partial loss of vision and pain in one eye due to retrobubear neuritis, diplopia due to paralysis of the oculomotor nerves, scotoma). Other frequent early symptoms of multiple sclerosis include numbness or fatigue of the limb, abnormalities in gait and pelvic organs, dizziness. These signs, indicating the mosaic involvement of the central nervous system, may be barely noticeable. When the temperature rises (heat, hot bath, fever), the symptoms can be aggravated.

Usually a slight cognitive decline, apathy, a decrease in criticism and attention, as well as affective disorders, including emotional lability, euphoria or, more often, depression. Depression can be reactive or develop due to brain damage. Epileptic seizures are possible.

Cranial nerves

Typical unilateral (asymmetric) optic neuritis and bilateral interocular ophthalmoplegia. Neuritis of the optic nerve leads to poor eyesight (from livestock to blindness), pain in the eye, sometimes narrowing of the visual fields, edema of the optic disc, partial or complete afferent pupillary defect. Internuclear ophthalmoplegia is the result of a lesion of the medial longitudinal fascicle that unites the nuclei of III, VI pairs of cranial nerves. At a glance in a horizontal plane adduction of one eye decreases and nystagmus of another appears; Convergence is not violated. Fast, low-amplitude oscillations of the eye with a direct look (peduncular nystagmus) are characteristic of multiple sclerosis, but are infrequent. Dizziness is common. Intermittent unilateral facial numbness, pain (similar to the trigeminal neuralgia), paralysis or spasm are possible. Mild dysarthria may occur due to bulbar disorders, cerebellar lesions, or cortical control disorders. The defeat of other cranial nerves is uncharacteristic, but may complicate brain stem lesions.

[15], [16], [17], [18]

Motor sphere

The bilateral spastic paresis of the predominantly lower extremities usually develops as a result of the defeat of the corticospinal pathways at the level of the spinal cord. The tendon reflexes (knee and Achilles) are increased, extensor plantar reflexes (Babinsky reflex) and clonus of feet and kneecaps are often revealed. Gait disturbances over time can pin the patient to a wheelchair. In later stages, in response to sensory stimuli (for example, the touch of bed linen), painful spasm of the flexor arises. Brain lesions can lead to hemiplegia.

Intensive tremor - limb oscillates during movement - can simulate cerebellar dysmetry (ataxic limb movements). There is also a tremor of rest, especially noticeable, when the head loses additional support.

Cerebellum

In far-reaching stages of multiple sclerosis, cerebellar ataxia and spasticity lead to persistent disability. Among other manifestations of cerebellar involvement, dysarthria, chanted speech (slow pronunciation with stumbles at the beginning of a word or syllable), intentional tremor and nystagmus are possible.

[19], [20], [21], [22], [23]

Sensitivity

Characteristic of paresthesia and partial loss of sensitivity of any type (for example, on the hands or feet). Various sensory disturbances (for example, burning sensation or pain, as with an electric shock) can occur spontaneously or in response to a touch, especially when the spinal cord is affected. An example is the symptom of Lermitt, when, with the head tilted forward, the pain by the type of electric shock irradiates from the top down along the spine and into the legs. Objective signs of sensory disturbances are transient.

Spinal cord.

Involving the spinal cord leads to disruption of the pelvic organs (for example, imperative urges, delay or incontinence). Constipation, erectile dysfunction in men and anesthesia of the genitals in women are possible.

Optiocoelitis (Devik's disease ) - a variant of multiple sclerosis - acute, sometimes bilateral neuritis of the optic nerve in combination with demyelination in the cervical or thoracic spinal cord; leads to loss of vision and paraparesis. Another option is isolated motor weakness due to spinal cord injury without other neurological deficits (progressive myelopathy).

Multiple Sclerosis - Symptoms

Diagnosis of multiple sclerosis

Multiple sclerosis should be suspected in optic neuritis, internuclear ophthalmoplegia and other symptoms compatible with multiple sclerosis, especially if the deficit is multifocal or intermittent. Most diagnostic criteria for multiple sclerosis require anamnestic exacerbations and remissions, as well as objective data indicating the presence of two or more focal lesions of the central nervous system. Conduct an MRI of the head and sometimes the spinal cord. If the MRI data and the clinical picture are not convincing, an additional examination may be required to provide an objective demonstration of the foci of the foci. It is usually started with CSF analysis and, if necessary, evoked potentials.

MRI is the most sensitive method of non-visualization. It allows the elimination of multiple-sclerosis-imitating potentially reversible diseases. Among them, non-myelinizing lesions in the area of the transition of the spinal cord to the oblong (eg, subarachnoid cysts and tumors in the region of the large occipital orifice). Contrast enhancement with gadolinium helps to distinguish active inflammation from old plaques. Alternatively, CT with contrast is possible. The sensitivity of MRI and CT can be increased by reintroducing contrast and delayed scanning.

Usually, the content of IgG in relation to protein (norm <11%), albumin (norm <27%) and other parameters is increased in CSF. The level of IgG correlates with the severity of the disease. CSF electrophoresis in agarose usually reveals a zone of oligoclonal clusters. In the phase of active demyelination, the main protein of myelin can increase. The content of lymphocytes and protein in the CSF can be increased.

The method of evoked potentials (latent periods of responses to sensory stimulation) for the diagnosis of multiple sclerosis is often more sensitive than complaints. Spotted evoked potentials reveal latent brain lesions (eg, in confirmed foci only in the spinal cord). Somatosensory evoked potentials are sometimes evaluated, including at the level of the brainstem. Routine blood tests sometimes exclude, for example, systemic lupus erythematosus, Lyme disease, etc.

Multiple Sclerosis - Diagnosis

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Treatment of multiple sclerosis

The goal of the treatment is to reduce the duration of exacerbations, reduce their frequency and severity of complaints; especially the ability to walk. In cases of exacerbations leading to an objective deficiency (eg, loss of vision, strength or coordination), short courses of glucocorticoids are prescribed (prednisolone 60-100 mg orally once a day with a decrease in dose 2-3 weeks, methyl prednisolone 500-1000 mg intravenously 1 time / day for 3-5 days). Cotricosteroids can shorten the duration of acute attack, but do not give a lasting effect. However, methylprednisolone can delay the progression of acute neuritis of the optic nerves.

Immunomodulatory therapy reduces the frequency of exacerbations and can delay the threat of disability. Among the immunomodulating drugs interferon beta 1b 8 million ME subcutaneously every other day, interferon-beta 1a 6 million ME intramuscularly weekly. Side effects: flu-like symptoms, depression (eventually decreases), the appearance of neutralizing antibodies after months of treatment and cytopenia. You can use glatiramer acetate 20 mg subcutaneously 1 time / day. Interferon-beta and glatiramer acetate are not immunosuppressants, and with progressively progressive PC, an immunosuppressant mitoxantrone, 12 mg / m ^{2, can be} administered intravenously every 3 months throughout the year. Natalizumab - antibodies to alpha ₄ -integrin - inhibits the passage of leukocytes across the blood-brain barrier; with monthly infusions, it helps to reduce the frequency of exacerbations and the appearance of new foci, but its admission to the market is suspended until the completion of a study of its association with progressive multifocal leukoencephalopathy. If immunomodulatory therapy is ineffective, monthly intravenous immunoglobulin administration can help. With expressed, progressive multiple sclerosis, immunosuppressants (methotrexate, azathioprine, mycophenolate, cyclophosphamide, cladribine) are used, but the justification for their use remains a matter of debate.

When spasticity is prescribed baclofen, gradually increasing the dose from 10 to 20 mg orally 3-4 times / day or tizanidine 4-8 mg orally 3 times / day. Gait training and physical exercises are effective. With neuropathic pain, gabapentin is prescribed 100-600 mg orally 3 times a day, alternatively tricyclic antidepressants (for example, amitriptyline 25-75 mg orally at bedtime, if amitriptyline causes anticholinergic side effects, then desipramine 25-100 mg orally at bedtime), carbamazepine 200 mg orally 3 times / day and opioids. For violations of the functions of the pelvic organs, treatment depends on their specific mechanism.

Help is encouraged and supported. Even at far advanced stages the training muscles and heart are shown regular physical exercises (exercise bike, running track, swimming). They reduce spasticity, help prevent the development of contractures and are useful psychologically. Patients should, if possible, maintain an active lifestyle, but avoid overwork and overheating. Vaccinations do not increase the risk of exacerbation. Weakened patients need to prevent bedsores and urinary tract infections; sometimes an intermittent self-catabolization of the bladder is needed.

• Treatment of exacerbations of multiple sclerosis
• Interferons and Multiple Sclerosis
• Symptomatic treatment of multiple sclerosis

Forecast for multiple sclerosis

The course of the disease is unpredictable and changeable. More often, usually when the disease makes its debut with optic neuritis, remission can last more than 10 years. In other cases, especially in men who have fallen ill in middle age, there are frequent exacerbations, which leads to disability. The course of the disease can speed up smoking. Life expectancy is reduced only in the most severe cases.

[29], [30]