Add to favorites

How to get tested for multiple sclerosis. Multiple sclerosis

Multiple sclerosis is represented by the following methods:

blood analysis– collection of venous blood for testing according to various parameters;
MRI– magnetic resonance imaging, allows you to identify foci of inflammation and damage to brain tissue and blood vessels using magnetic waves and fields;
superposition electromagnetic scanner– intended for early detection of MS based on the activity of nervous tissue;
potential measurement(neurological method) – testing sensory conditions, sensitivity and brain activity;
spinal puncture (lumbar)– analysis of the spinal cord substance;
proton magnetic resonance spectroscopy– study of the chemical composition of nervous tissue.

It's sad that this disease spares neither young people nor children.

Types of studies of biological fluids

When taking tests, it is important to follow all prescribed measures regarding:

physical activity;
smoking;
psycho-emotional state.

Let's look at what types of tests are taken and what their results show.

Cerebrospinal fluid examination

Examination of the cerebrospinal fluid (CSF) to determine the extent of damage to this part. A puncture is made with a needle at the lumbar level, the analysis is carried out immediately (no later than half an hour) in four stages:

biochemical research– study of the qualitative and quantitative composition of cerebrospinal fluid for the diagnosis of tumors;
microscopic– counting elements at the cellular level;
macroscopic– by color (normally transparent), red indicates the presence of red blood cells (inflammation), green or yellow indicates the presence of meningitis, subarachnoid hemorrhage, fibrinous film (normally absent);
bacterioscopic and bacteriological– allows you to determine the presence of bacteria (tuberculosis bacilli, meningococci, streptococci and staphylococci), determine immune reactions (Kahn, Wasserman, RIBT, Wright, etc.).

Oligoclonal IgG relationships

In multiple sclerosis, oligoclonal immunoglobulin G is detected in the cerebrospinal fluid, which indicates the influence of the immune system on the brain (infection). Cerebrospinal fluid and venous blood (serum and cerebrospinal fluid) are taken for analysis.

IMPORTANT! The results are obtained within half an hour after collection and the answer is positive in the presence of IgG.

Quantitative IgG

It is done when collecting venous blood to check for the presence of infections, rubella or its history in the past, to count the number of antibodies (oligoclonal immunoglobulin G indicates the presence of MS at any of its stages), the execution period is about ten days.

IgG value:

Reference values- This is a polyclonal type of IgG synthesis.
Positive result– MS, pathologies and damage to the nervous system, vascular inflammation.
Negative result- the norm.

Myelin basic protein

The analysis takes serum from venous blood (peripheral vein) or cerebrospinal fluid, and the analysis takes nine days.

Its increased concentration indicates the presence of destruction and inflammation. Used to predict and monitor the development of MS.

Study results – negative (normal), positive (RS)

Albumin index

Sampling of venous blood and CSF to assess nutritional status and protein-synthetic liver function. It is done immediately after sampling using the calculation of the index - the amount of albumin in the blood plasma is divided by the amount of albumin in the esophageal fluid. Its low rate indicates the presence of pathologies and diseases.

Total protein in cerebrospinal fluid

REFERENCE! CSF is used immediately after collection for the assessment and diagnosis of infectious and inflammatory diseases, oncological changes, and diseases of the central nervous system.

If the analysis results increase, they indicate a disease:

bacterial (0.4-4.4 g/l);
cryptococcal (0.3-3.1 g/l);
tuberculous (0.2-1.5 g/l) meningitis and neuroborreliosis.

Gamma globulin

A venous blood test is performed to assess the amount of immunoglobin antibodies or immune gamma globulins. A certain amount indicates the presence of various infections and inflammations.

The norm is IgA (0.4–2.5 g/l), IgG (7–16 g/l).
IgM in women over 10 years of age (0.7–2.8 g/l).
In men over 10 years of age (0.6–2.5 g/l), IgD (0.008 g/l or lower), IgE (20–100 kU/l).

IgG concentration in cerebrospinal fluid

Comparing the concentration of gamma globulin in the blood and CSF helps to assess the stage of development of MS, as well as the nature of its manifestation, the execution period is 11 working days.

The norm for a healthy person is from 7 to 16 g/l. An increase in the norm indicates the presence of diseases (MS, infections).

IgG ratio

Normally, IgG in blood serum is 70-80/about all immunoglobulins. The content of the main part of the antibodies indicates resistance to a number of viruses and bacteria. Oligoclonal accumulations in the cerebrospinal fluid are found in 98% of MS patients. The ratio is CD4+/CD8+ 2:1.

IgG rate in CSF

The analysis is taken using a puncture in the lower back and is done within half an hour; the spinal cord cerebrospinal fluid is analyzed. The rate of IgG synthesis in MS is increased; it is > 3.3 mg/day.

PCR

Polymerase chain reaction based on venous blood or CSF, which is treated with special enzymes, results are obtained within 24 hours.

ATTENTION! After the introduction of the enzyme, the RNA and DNA of the pathogenic cells are divided. Their calculation gives results about the presence of various diseases.

Peripheral blood

Venous blood from the peripheral zone is taken for analysis. When determining multiple sclerosis, lymphocytes are counted (more than 62%).

Prices

Analysis	Moscow	Saint Petersburg	Novosibirsk	Rostov-on-Don
Oligoclonal IgG relationships	3500	5240	3350	3595
Quantitative IgG analysis	440	505	360	370
IgG value	545	500	450	440
Myelin basic protein	560	550	360	370
Albumin index	300	300	180	185
Total protein in cerebrospinal fluid	290	240	220	160
Gamma globulin	360	355	160	230
IgG concentration in cerebrospinal fluid	3500	5240	3350	3595
IgG ratio	1150	1000	1100	950
Rate of IgG synthesis in cerebrospinal fluid	895	775	430	545
PCR	500	500	470	490
Peripheral blood tests	160-3500	150-5240	150-3350	140-3595

Clinical, laboratory and instrumental research methods in the diagnosis of multiple sclerosis. MRI in the diagnosis of multiple sclerosis. Diagnostic criteria for multiple sclerosis

Diagnosis of multiple sclerosis

Multiple sclerosis It is quite easily diagnosed in young patients with recurrent focal symptoms of white matter lesions in various regions of the central nervous system.

It is much more difficult to diagnose multiple sclerosis during the first attack of the disease and during the primary progressive course of multiple sclerosis (sometimes in such cases, careful questioning can reveal signs of a previous exacerbation of multiple sclerosis), as well as in mild disorders (for example, sensitivity disorders) in the absence of objective signs of damage CNS.

The first signs of multiple sclerosis can appear several years before the patient first consulted a doctor. In this case, a patient with suspected multiple sclerosis may:

or forget about these first manifestations of multiple sclerosis (if the symptoms did not cause significant inconvenience - for example, transient paresthesia)
or not link past symptoms of multiple sclerosis to the current condition (eg, a patient's past history of urinary frequency or urgency has been associated with a suspected urinary tract infection)

Therefore, when collecting anamnesis from a patient with suspected multiple sclerosis, it is necessary to purposefully ask the patient additional questions and talk with his relatives and close people who can provide additional data.

Accurate The diagnosis of multiple sclerosis is made on average 2–3 years after the appearance of the first symptoms of multiple sclerosis, and almost 50% of patients at the time of diagnosis of multiple sclerosis, as it turns out in a retrospective analysis, have been sick with multiple sclerosis for at least 5 years.

Diagnosis of multiple sclerosis traditionally based on clinical manifestations characteristic of multiple sclerosis and anamnesis data indicating previously existing focal symptoms of damage to the white matter of the central nervous system, “separated in time and different (migrating) in localization.”

As with other diseases, the first step to a correct diagnosis of multiple sclerosis is a thorough history. It is very important to find out the time of the first attack of multiple sclerosis and the manifestations of this attack, which in the case of multiple sclerosis is not always easy.

When clinically examining a patient with suspected multiple sclerosis, it is necessary to conduct a thorough full neurological examination in order not to miss such subtle signs of the disease as a slight decrease in vibration sensitivity, a slight disturbance in color perception, mild nystagmus, loss of superficial abdominal reflexes, etc.

Laboratory and instrumental studies in the diagnosis of multiple sclerosis

Among the instrumental methods for diagnosing multiple sclerosis, the following are currently widely used: the study of evoked potentials and magnetic resonance imaging (MRI).

Study of evoked potentials in the diagnosis of multiple sclerosis

Evoked potential (EP) testing in multiple sclerosis can detect slowing or disruption of conduction in the visual, auditory, somatosensory and motor pathways.

In this study, repeated stimuli of the same type are applied and the electrical signals arising in response to these stimuli in different parts of the nervous system are recorded using computer averaging.

A change in one or more types of evoked potentials is observed in 80–90% of patients with multiple sclerosis.

The study of evoked potentials sometimes makes it possible to determine the localization and extent of the pathological process in multiple sclerosis, even if there are no obvious clinical manifestations of multiple sclerosis.

In multiple sclerosis, auditory EPs, somatosensory EPs, and visual EPs are usually examined for checkerboard pattern reversal.

The results of this method are especially valuable when, for example, in a patient with multiple sclerosis with signs of damage to some structures of the central nervous system, asymptomatic damage to other structures is detected, or the presence of neurological disorders is confirmed in a patient with complaints, but without objective symptoms during a neurological examination.

The lengthening of the latent periods of evoked potentials is due to a violation of the spasmodic propagation of excitation along unmyelinated fibers.

Extension of the latent periods of evoked responses is the earliest sign of pathology in multiple sclerosis, and in advanced stages of multiple sclerosis, responses can disappear completely.

The study of visual EPs for reversal of a chess pattern has very high sensitivity. In retrobulbar neuritis, MPT detects damage to the optic nerve in approximately 80% of cases, while optic EPs detect damage in 100%. In general, visual EPs are changed in 75-97% of cases of significant multiple sclerosis, somatosensory EPs - in 96%, and auditory EPs of the brain stem - in 30-67%.

Neuroimaging methods of examination in the diagnosis of multiple sclerosis

The introduction of neuroimaging research methods - magnetic resonance imaging (MRI) and computed tomography (CT) - into clinical practice is the greatest achievement in the diagnosis of multiple sclerosis in recent years.

Magnetic resonance imaging in the diagnosis of multiple sclerosis

The most sensitive method is MRI, which is 10 times more effective than CT for detecting lesions of multiple sclerosis. The sensitivity of MPT for multiple sclerosis is estimated at 95-99% and thus, the absence of changes in MPT of the brain and spinal cord excludes the diagnosis of multiple sclerosis with a high degree of certainty.

The widespread use of MPT has revolutionized the diagnosis of multiple sclerosis.

Pathological changes according to MRI are observed in more than 95% of patients who meet the diagnostic criteria for multiple sclerosis.

When using the inversion-recovery sequence or on T1-weighted images, there may be no changes, or dark (low intensity) punctate lesions in the white matter are detected. Changes characteristic of multiple sclerosis are better seen on T2-weighted images with a spin-echo sequence on average-weighted images. In this case, foci of increased intensity are clearly visible against the background of surrounding brain tissue. Some of them appear to extend from the ventricular wall and correspond to periventricular demyelination lesions characteristic of multiple sclerosis. Lesions are often found in the brainstem, cerebellum, and spinal cord. Unlike most cerebrovascular diseases, in multiple sclerosis, pathological changes are often detected in the corpus callosum.

Foci of demyelination, defined as hyperintense on T2, are found in 95% of cases of definite multiple sclerosis. If MPT reveals the presence of lesions in patients with “probable multiple sclerosis” (in the case of a clinically isolated syndrome), then in 65% of cases they are predictors of the development of definite multiple sclerosis over the next 5 years.

The size of lesions typical for multiple sclerosis is usually 3 mm or more. These lesions can be found periventricularly, in the corpus callosum (with a characteristic spread of lesions from it into the white matter - “Dawson's fingers”), in the brain stem, cerebellum, spinal cord and in the optic nerves.

The detection of hyperintense foci in several areas of the central nervous system in T2 mode reflects the multifocal nature of neurological damage in multiple sclerosis. The most typical distribution of multiple sclerosis lesions in the brain with definite multiple sclerosis (according to MPT data) is presented in Table 1.

Table 1. Localization of multiple sclerosis lesions in the brain.

Gadolinium-enhanced MPT may show areas of increased intensity in the white matter as a result of the contrast agent passing through the disrupted blood-brain barrier. A transient increase in intensity on T1-weighted gadolinium images usually accompanies or precedes the appearance of new lesions on T2-weighted images. Autopsy data indicate that areas of gadolinium leakage correspond to perivenular foci of inflammation. Lesions that appear on T2-weighted and average-weighted images after gadolinium administration are not specific for any type of morphological abnormality– they may reflect swelling, inflammation, demyelination, gliosis or axonal death.

With repeated MPT, it is clear that new lesions arise much more often than would be expected based on the clinical picture. This suggests that asymptomatic exacerbations are common in multiple sclerosis. The volume of the lesion on T2-weighted images weakly correlates with the patient's condition.

In relapsing-remitting multiple sclerosis and secondary progressive multiple sclerosis, the disease activity determined by MRI data is approximately 10 times higher than the activity of the process according to clinical signs, i.e. only 1 in 10 lesions detected by MRI manifest clinically. This is probably due to the fact that not all lesions are located in clinically manifested areas of brain damage

A more accurate correspondence between the results of neuroimaging research methods and the real clinical picture can be achieved using modern research methods that make it possible to distinguish between edema, demyelination and axonal death - for example, the magnetization transfer contrast method and proton magnetic resonance spectroscopy - PMRS or +N MRS. PMRS is a modern method for visualizing biochemical processes occurring in the brain.

Proton magnetic resonance spectroscopy in the diagnosis of multiple sclerosis

PMRS method uses the effect of a “chemical shift” of the resonant frequencies of hydrogen nuclei (protons) in various chemical compounds relative to the resonant frequency of a proton in a water molecule. It allows in vivo determination of the content of various metabolites in brain tissue.

The use of high-field PMRS (1.5 - 2.0 T) makes it possible to clearly visualize eight peaks of metabolites in healthy people: myoinositol/inositol (Ins), choline, creatine (Cr)/phosphocreatine, N-acetylaspartate (NAA), glutamine, glutamate, gamma-aminobutyl, and in a certain research mode - acetate. The concentration of these metabolites in brain tissue is indicated in conventional units for subsequent mathematical processing of the data obtained.

Thus, in multiple sclerosis, PMP spectroscopy makes it possible to identify the degree and extent of axonal damage using the determination of a decrease in the concentration of N-acetylaspartate, a specific axonal and neuronal marker. A decrease in the NAA/Cr index indicates secondary damage to axons and the transition from the phase of reversible inflammation and demyelination to the phase of progressive degeneration. A decrease in the concentration of N-acetylaspartate in brain tissue in multiple sclerosis reflects a decrease in the number of axons and metabolic disorders in them. In multiple sclerosis, the content of N-acetylaspartate (NAA) decreases not only in the lesions (by 80%), but also in the “unchanged white matter” (by 50%), i.e. Axonal loss in multiple sclerosis is diffuse and begins before the plaque formation process. This supports the notion that axonal damage is not only a consequence of gross demyelination, but can occur early in the disease, even before myelin damage.

In “chronic foci” in patients with benign multiple sclerosis, the concentration of N-acetylaspartate is significantly higher than in “chronic foci” in patients with secondary progressive multiple sclerosis, which indicates a greater possibility of restoration of damaged axons in patients of the first group. It has been shown that in secondary progressive multiple sclerosis, a decrease in the level of N-acetylaspartate is present not only in the “normal-looking white” matter, but also in the “normal-looking gray” matter - the cerebral cortex, thalamus opticum and even in the gray matter of the spinal cord. This indicates a significant prevalence of not only axonal, but also neuronal damage during chronicity of the pathological process.

The introduction of the PMRS method into practice has made it possible to predict the stage of multiple sclerosis. And the joint use and parallel analysis of the results obtained from PMRS and MRI allows us to characterize the functional and morphological status of multiple sclerosis - Table 2.

Table 2. Functional and morphological diagnosis of stages of multiple sclerosis

* inositol is a structural component of myelin, released during its breakdown

** choline is a structural component of myelin, released during its breakdown

*** creatine is a marker of energy metabolism and is used to assess basal metabolic activity

Superposition electromagnetic scanner (SPEMS) in the diagnosis of multiple sclerosis

Recently, a new domestic method of studying the brain has been introduced into research practice using superposition electromagnetic scanner(SPEMS), developed by academician. N.P. Metkin (patent for invention 2290869). The components of the scanner are a personal computer, digital recording and calibration units, a 120-channel sensor that allows you to simultaneously apply frequency, time and amplitude calibration signals and indicators of electrodynamic activity to the surface of the head and record them in a wide range, and an output device. By determining the functional activity of brain tissue the method is comparable to positron emission tomography(PET) and allows you to obtain data on the spectrum of activity of enzymes, neurotransmitters, the density of ion channels, and in multiple sclerosis, the level and nature of the process of total and focal demyelination.

As a result of an examination using SPMS of 60 patients with secondary progressive multiple sclerosis in the phase of unstable remission with EDSS from 2.0 to 5.5 points, data were obtained indicating profound metabolic changes, consisting of lactic acidosis, tissue hypoxia, due to dysfunction of the respiratory cascade enzymes ubiquinone and cytochrome, increased peroxidation with the appearance of hydroperoxides, and a decrease in the functional activity of neurotransmitters.

Because the lesions of small vessels of the white matter of the brain in T2 mode look the same as lesions of multiple sclerosis, and is much more common, a diagnosis of multiple sclerosis cannot be made based solely on the presence of lesions on T2 MPT.

Diagnostic criteria are used to confirm the diagnosis of multiple sclerosis using MPT.

Diagnostic criteria for multiple sclerosis according to MRI studies

Various diagnostic criteria for multiple sclerosis based on MPT data have been proposed.

For patients under 50 years of age:

The diagnosis of multiple sclerosis is considered highly probable when a patient has four or more lesions or three lesions, at least one of which is located periventricularly (the diameter of the lesions is at least 3 mm), on average-weighted or T2-weighted images.

For patients over 50 years of age:

Two of the following additional criteria are also required:

the diameter of the lesions is at least 3 mm;
one or more lesions in the posterior cranial fossa.

Diagnostic MPT criteria for multiple sclerosis according to F.H. Fazekas

To confirm the diagnosis of multiple sclerosis using MPT, the diagnostic criteria of MPT F.H. are used. Fazekas:

the presence of at least 3 lesions, 2 of which must be located periventricularly and their size must be more than 6 mm, or 1 lesion can be localized subtentorially.

Diagnostic MPT criteria for multiple sclerosis according to Barkhof

For the purpose of even more accurate neuroimaging diagnosis of multiple sclerosis, F. Barkhof et al. proposed criteria according to which lesions must meet 3 of 4 conditions:

one lesion accumulating contrast or 9 hyperintense lesions in T2 mode
there must be at least 1 subtentorial lesion
at least 1 lesion must be located near the cerebral cortex
there must be at least 3 periventricular lesions

In this case, 1 spinal lesion can replace 1 cerebral one. The lesions must be more than 3 mm in diameter. Spinal lesions should not cause thickening of the spinal cord, spread over more than 3 segments and occupy the entire diameter of the spinal cord.

MPT of the spinal cord is recommended for all patients with multiple sclerosis. In it, unlike the brain, in the absence of clinical signs of circulatory disorders, nonspecific vascular foci are not detected, which makes it possible to clarify the diagnosis in elderly patients.

The effectiveness of treatment for multiple sclerosis is usually assessed by reducing the frequency of exacerbations and slowing the increase in disability. But exacerbations in multiple sclerosis in many cases are not very frequent (therefore long-term observation is necessary), and in primary progressive multiple sclerosis they are not at all. In addition, both in determining exacerbations of multiple sclerosis and in assessing the degree of disability of the patient, there is a lot of subjectivity. That's why It is very important to conduct repeated MPT studies over time, which make it possible to objectify the results of treatment. To do this, it is sufficient to estimate only two parameters:

the number of new lesions accumulating contrast in the Tl-mode, and
total area of lesions in T2 mode

Cerebrospinal fluid examination in multiple sclerosis

The CSF reveals:

lymphocytosis
oligoclonal antibodies
increased concentration of immunoglobulins

Typically, the number of cells in the CSF does not exceed 20 μl -1, but at the beginning of multiple sclerosis it can reach 50 μl -1 and higher. Lymphocytosis above 75 μl -1 or the appearance of neutrophils in the CSF are not characteristic of multiple sclerosis.

Cytosis is more common in young patients with a remitting course than in older patients with a progressive course.

The protein concentration is usually normal, and only sometimes slightly increased.

The most definitive confirmation of the presence of multiple sclerosis is the determination of oligoclonal antibodies (OAT) to myelin proteins and an increase in the concentration of immunoglobulin G in the cerebrospinal fluid (CSF) compared to its content in the blood serum.

In 80% of cases, there is an increased concentration of IgG against the background of normal protein concentration as a result of the selective synthesis of IgG in the central nervous system. An increase in the concentration of IgG in the central nervous system in multiple sclerosis reflects the process of increasing titer of specific autoimmune IgG autoantibodies.

A number of indicators have been proposed to distinguish such formation of IgG in the central nervous system from their passive penetration through the damaged blood-brain barrier. One of them is the liquor IgG index (the ratio of the concentrations of IgG and albumin in the CSF, divided by the ratio of the same concentrations in the serum).

OAT is detected in patients in 90 - 95% of cases. They may not be present at the onset of the disease, but once they appear, OATs always remain, although they do not correlate with disease activity. In order to exclude other causes of the appearance of oligoclonal antibodies, it is necessary to examine paired sera.

The use of corticosteroids leads to a decrease in the concentration of immunoglobulin G, but does not affect the content of OAT.

However, changes in the composition of CSF are not specific to multiple sclerosis.

OAT is also determined in other inflammatory and immunological diseases, many of which must be differentiated from multiple sclerosis (Table 2).

Table 3. Diseases in which oligoclonal antibodies to CNS myelin proteins are detected in the CSF

Autoimmune diseases:

multiple sclerosis;
systemic lupus erythematosus;
Sjögren's syndrome;
Behçet's disease;
periarteritis nodosa;
acute disseminated encephalomyelitis;
Guillain-Barré syndrome

Infectious diseases:

viral encephalitis;
neuroborreliosis;
chronic fungal meningitis;
neurosyphilis;
subacute sclerosing panencephalitis

Sarcoidosis

Cerebrovascular diseases

Markers of inflammatory activity in progressive multiple sclerosis, circulating adhesion molecules (sE-selectin, sICAM-1 and sVCAM), as well as soluble receptors (sTNF-R), serve in the peripheral blood and cerebrospinal fluid. There is a correlation between titers of circulating markers of inflammatory activity and the degree of activity of multiple sclerosis, the degree of disability and visible foci of CNS lesions determined using magnetic resonance imaging. This is equally true for both primary progressive and secondary progressive types of multiple sclerosis.

Differential diagnosis of multiple sclerosis

Due to the variety of manifestations, multiple sclerosis must be differentiated from many other diseases.

For multiple sclerosis, there are no pathognomonic symptoms, laboratory or instrumental data that clearly indicate a diagnosis of multiple sclerosis. However, there are manifestations that are not typical for multiple sclerosis that cast doubt on the diagnosis, for example, aphasia, parkinsonism, chorea, isolated dementia, amyotrophy with fasciculations, neuropathy, epileptic seizures and coma. In doubtful cases, it is better not to rush into a diagnosis of multiple sclerosis, but to first rule out other diseases.

The diagnosis of multiple sclerosis should be questioned and a careful differential diagnosis should be carried out if:

with complaints of increased fatigue and muscle weakness, no objective neurological symptoms are detected
one lesion is determined (especially when it is localized in the posterior cranial fossa: tumors and vascular malformations of this localization are the most common cause of erroneous diagnosis of multiple sclerosis)
spinal symptoms progress from the very onset of the disease in a patient under 35 years of age without dysfunction of the pelvic organs
there is a normal composition of the CSF or, on the contrary, a very significant increase in the number of cells
the leading symptom is pain (although various pain syndromes are not uncommon in multiple sclerosis, they are not the main symptom of the disease)
there is a decrease or loss of tendon reflexes (reflexes disappear only in the later stages of multiple sclerosis due to a sharp increase in muscle tone)

The diagnosis of multiple sclerosis remains doubtful, if 5 years after the onset of symptoms suggestive of multiple sclerosis:

no oculomotor disorders;
no sensory or pelvic disorders;
no remissions in patients under 40 years of age;
there is no “multifocality” of symptoms

In the vast majority of patients with multiple sclerosis, neurological examination reveals objective symptoms. Often there are many more of them than one would expect based on the complaints - for example, a patient complaining of dysfunction in one leg has neurological disorders in both. This allows us to exclude diseases caused by a single lesion in the central nervous system. Sometimes, on the contrary, objective symptoms are not identified, and complaints are mistakenly regarded as a manifestation of conversion disorder - forgetting that compelling reasons are needed to make this diagnosis.

Sometimes systemic lupus erythematosus (SLE) is accompanied by recurrent or progressive central nervous system lesions, similar to multiple sclerosis. However, other signs of SLE are also observed: symptoms of a systemic disease, increased ESR, the presence of autoantibodies, etc.

Behçet's disease may be accompanied by optic neuritis and myelitis or, more often, acute or subacute multifocal damage to the central nervous system. The distinctive signs of this disease are iridocyclitis, aphthous stomatitis, genital ulcers, and increased ESR.

Neurological disorders that occur with exacerbations and remissions occur in Sjögren's syndrome.

With sarcoidosis, damage to the cranial nerves (especially the facial nerve), progressive atrophy of the optic nerve, and myelitis are possible. Sarcoidosis can be distinguished by enlarged lymph nodes, damage to the lungs and liver, increased ACE levels and hypercalcemia.

Lyme disease may involve damage to the optic nerve, brain stem, or spinal cord in the absence of the characteristic rash, fever, and meningoradiculopathy.

Differential diagnosis is also carried out with other chronic infectious diseases, in particular with meningovascular syphilis, HIV infection, etc.

Tropical spastic paraparesis is characterized by back pain, progressive spasticity (mainly in the legs) and impaired bladder function. Diagnosis is based on detection of antibodies to human T-lymphotropic virus type 1 in serum and CSF and isolation of the virus itself.

Human T-lymphotropic virus type 2 can cause a similar progressive myelopathy.

With the sudden development of focal symptoms, multiple sclerosis sometimes has to be differentiated from stroke and migraine.

Progressive focal neurological symptoms are characteristic of a space-occupying lesion. Thus, in primary CNS lymphoma, single or multiple lesions appear that accumulate contrast on MPT and look like fresh plaques of multiple sclerosis. However, in rare cases of multiple sclerosis, inflammation and swelling lead to the appearance of a large lesion resembling a tumor.

Arteriovenous malformations in the posterior fossa can cause progressive or recurrent brainstem disorders.

Unlike multiple sclerosis, pontine glioma develops progressive symptoms, indicating damage to neighboring parts of the central nervous system.

Osteochondrosis of the cervical spine, tumors and arteriovenous malformations of the spinal cord can lead to progressive myelopathy.

With funicular myelosis and related hereditary diseases - homocystinuria type cbl G and deficiency of plasma R-proteins - the same neurological disorders as with multiple sclerosis can occur. In this case, megaloblastic anemia may be absent, and the serum concentration of vitamin B12 cannot always be used to judge clinically significant vitamin B12 deficiency. In such cases, serum concentrations of methylmalonic acid and total homocysteine are determined.

In order to exclude mitochondrial diseases (Leigh disease, MELAS syndrome, Leber syndrome), the lactate content in the blood and CSF is determined, a muscle biopsy or gene diagnosis is performed.

Multiple sclerosis must be differentiated from hereditary ataxias, which are accompanied by progressive symmetrical damage to the dorsal funiculi, corticospinal and spinocerebellar tracts and, sometimes, damage to the peripheral nervous system.

Differential diagnosis of multiple sclerosis is also carried out with other monogenic diseases: metachromatic leukodystrophy, Krabbe disease, Fabry disease and adrenoleukodystrophy. The latter is accompanied by pronounced inflammatory changes in the CSF.

With neuromyelitis optica (Devic's disease), transverse myelitis develops several days or weeks after acute bilateral optic neuritis. Sometimes neuritis is unilateral or occurs after the first attack of myelitis. The severe form may be accompanied by necrosis. Asians are most often affected, whites rarely. The CSF reveals cytosis with a predominance of neutrophils and an increase in protein concentration. Neuromyelitis optica often goes away on its own. However, it may be the first attack of multiple sclerosis, as well as a manifestation of SLE or Behçet's disease.

In each case of suspicion of multiple sclerosis, a thorough differential diagnosis is necessary to exclude any other, often curable, disease. This is especially important at the beginning of the disease, since there are no formalized diagnostic criteria that allow us to make a diagnosis of multiple sclerosis with 100% certainty during the first attack of the disease.

Thus, the diagnosis of multiple sclerosis should be based on a comprehensive analysis of the clinical picture, MRI data, EP, reflecting the nature and “dispersal of the process in time and space,” and, if necessary, a study of the CSF.

Currently, many useful clinical and laboratory diagnostic criteria for multiple sclerosis have been proposed that allow verification of the diagnosis of multiple sclerosis - tables 3 and 4.

Table 4. Clinical and laboratory diagnostic criteria for multiple sclerosis

Objective symptoms during neurological examination
Damage to pathways, especially:
1. corticospinal;
2. spinocerebellar;
3. medial longitudinal fasciculus;
4. optic nerve;
5. posterior cords
Damage to two or more parts of the central nervous system according to anamnesis or examination
1. presence of a second lesion can be confirmed using MPT . About multifocal lesions based on MPT alone can be judged if:
  - 4 lesions in white matter
  - or 3 lesions, one of which is located periventricularly (focus diameter ≥ 3 mm).
  - For patients over 50 years of age, two of the following are also required. additional criteria:
    - lesion diameter ≥ 3 mm.
    - one or more lesions adjacent to the wall of the lateral ventricle;
    - one or more lesions in the posterior fossa
2. If a neurological examination reveals only one lesion, then the presence of the second can be confirmed by studying evoked potentials
Course of multiple sclerosis:
1. two or more separate exacerbations of neurological disorders, reflecting damage to different parts of the central nervous system, lasting ≥24 hours each, with an interval between them ≥1 month, or
2. gradual or stepwise increase in neurological symptoms over ≥6 months, accompanied by signs of increased IgG synthesis in the central nervous system or the appearance of ≥2 oligoclonal antibodies
Onset between 15 and 60 years of age
Neurological disorders cannot be caused by another disease. To exclude such diseases, it is recommended to use the following studies and indicators (depending on the situation):
1. CSF examination;
2. MPT of the head and spine;
3. serum concentration of vitamin B 12;
4. antibody titer to human T-lymphotropic virus type 1;
5. rheumatoid factor, antinuclear antibodies, anti-DNA antibodies (SLE)
6. precipitation reaction of inactivated serum with cardiolipin antigen;
7. ACE (sarcoidosis);
8. serological tests for Borrelia burgdorferi (Lyme disease);
9. very long chain fatty acids (adrenoleukodystrophy);
10. Serum and CSF lactate, muscle biopsy, mitochondrial DNA analysis (mntochondria diseases)

Diagnostic groups of multiple sclerosis, verified according to the criteria given in Table 3:

The diagnosis of multiple sclerosis is reliable: meeting all 6 criteria
The diagnosis of multiple sclerosis is likely: meets all 6 criteria, but:
1. a neurological examination revealed only one lesion, although 2 exacerbations were observed, or
2. only one exacerbation was observed, although ≥ 2 lesions were identified
The diagnosis of multiple sclerosis is possible: full compliance with all 6 criteria, but only one exacerbation was observed and only one lesion was identified

Table 5. Criteria for diagnosing multiple sclerosis (W.I McDonald, 2005)

Clinical manifestations	Additional data required for verification of multiple sclerosis
1 or more attacks with clinical signs of 2 or more lesions	Not required 1
2 attacks or more with clinical signs of 1 lesion	– Dissemination in space: MPT 2 – 2 or more lesions consistent with multiple sclerosis, plus detection of OAT in the CSF; – or wait for another attack with different clinical manifestations
1 attack with clinical signs of 2 or more lesions	– Dissemination over time
1 attack and 1 outbreak (monosymptomatic onset, CIS)	– Dissemination in space: – MPT or 2 or more lesions plus CSF and dissemination over time; – MPT or 2nd clinical attack
Progressive symptoms similar to PC	Year of progression and 2 of the following three features: – positive MPT data of the head (9 lesions in T2 mode or at least 4 in combination with altered visual EP); – 2 lesions in T2 mode in the spinal cord; – changes in the CSF

1 However, if additional examinations (MRI, CSF) are done and changes characteristic of MS are not detected, other possible diagnoses should be considered.

Literature

Bisaga G.N., Pozdnyakov A.V. Magnetic resonance spectroscopy // Multiple sclerosis / ed. I.A. Zavalishin, V.I. Golovkin. M., 2000. pp. 244-249.
Internal medicine according to Tinsley R. Harrison. Ed. E. Fauci, Y. Braunwald, K. Isselbacher, J. Wilson, J. Martin, D. Kasper, S. Hauser and D. Longo. In two volumes. Per. from English – M., Practice – McGraw – Hill (joint publication), 2002.
New technologies for prediction of therapy for multiple sclerosis / Golovkin V.I., Pozdnyakov A.V., Kamynin Yu.F., Martens // Bulletin of Siberian Medicine. – 2010, No. 4. – S. – 138 – 144.
Pozdnyakov A.V. Proton magnetic resonance spectroscopy of the brain in the diagnosis of remission and exacerbation of the disease // Immune-mediated relapsing-remitting multiple sclerosis / ed. IN AND. Golovkin, N.M. Kalinina. St. Petersburg: “Rose of the World”, 2003. pp. 35-50.
Pozdnyakov A.V. The role of proton magnetic resonance spectroscopy in the diagnosis of brain diseases: abstract. dis. ...Dr. med. Sci. St. Petersburg, 2001. 32 p.
Multiple sclerosis: a guide for doctors / T.E. Schmidt, N.N. Yakhno. -2nd ed. - M.: MEDpress-inform, 2010. - 272 p.
Adhesion molecules in multiple sclerosis / Elovaara I., Ukkonen M., Leppakynnas M. et al. Arch. Neurol. – 2000. – v.57. – P.546-551
Assessment of MRI criteria for a diagnosis of MS./ Offenbacher H, Fazekas F, Schmidt R, et al. // Neurology. – 1993 May;43(5):905-9.
Belair M, Girard M. Diagnostic criteria in clinical evaluation of multiple sclerosis: role of magnetic resonance imaging. //Can. Assoc. Radiol. J. – 2004. – v.55, No. 1. – P.29-33.
Comparison of MRI criteria at first presentation to predict conversion to clinically definite multiple sclerosis. / Barkhof F., Filippi M., Miller D.H., et al. //Brain. – 1997 – v.120. – P. 2059 – 2069.
Criteria for an increased specificity of MRI interpretation in elderly subjects with suspected multiple sclerosis. / Fazekas F, Offenbacher H, Fuchs S, et al. // Neurology. – 1988 Dec;38(12):1822-5.
Droogan, A. G., McMillain, S. A., Dougkas, J. R., Hawkins, S. A.: Serum and cerebrospinal fluid levels of soluble adhesion molecules in multiple sclerosis: predominant intrathecal release of vascular cell adhesion molecule-1 J. Neuroimmunol. – 1996, 64: 185-191
Fatigue, depression and progression in multiple sclerosis / Koch M., Uyttenboogaart M. et al. //Mult. Scler. – 2008. – v.14, No. 6. – P. 815 – 822
Magnetic resonance imaging in multiple sclerosis. / Haller S, Pereira VM, Lalive PH, et al. // Top. Magn. Reason. Imaging. – 2009. – v.20, No. 6. – P. 313-323.
Magnetic resonance spectroscopy of multiple sclerosis: in vivo detection of myelin breakdown products / Koopmans R.A., Li D., Zhu GT. et al. // Lancet. 1993. V. 341. P. 631-632.
Recommended diagnostic criteria for multiple sclerosis: guidelines from the International Panel on the diagnosis of multiple sclerosis. / McDonald W.I., Compston A., Edan G., et al. //Ann. Neurol. – 2001. – v.50. – P. 121 – 127.
Recommended standard of cerebrospinal fluid analysis in the diagnosis of multiple sclerosis: a consensus statement. / Freedman M.S., Thompson E.J., Deisenhammer F., et al. //Arch. Neurol. – 2005. – v.62, No. 6. – P.865-870.

25.10.2016

Multiple sclerosis develops as a result of damage to the myelin tissue that protects the spinal cord and brain from external influences, like duct tape around wires.

This type of disease should not be confused with senile sclerosis. The word “scattered” means multiple lesions, as if scattered over the entire surface. Multiple sclerosis also occurs at a young age - from 15 to 40 years. Of course, there are cases of the disease occurring at 50 years of age, but this is an exception.

According to statistics, the disease occurs twice as often in women as in men.

Causes

Additional reasons may be:

Increased intoxication of the body;
Radiation exposure;
Abuse of ultraviolet radiation (sunbathers);
Unsuitable climatic conditions (cold);
Mental stress;
Allergies;
Genetic factor;
Measles virus (the condition of patients improves after a dose of interferons).

Some researchers suggest that multiple sclerosis can be triggered by the hepatitis B vaccine. But this theory has not been confirmed.

Symptoms

The signals given by the body about the onset of multiple sclerosis are different. The process depends on the form and phase of the disease. The first symptoms can occur in different ways - either moderately and unclearly, or progress rapidly.

The following symptoms are reasons to consult a doctor:

weakness in all limbs (or in just one);
gradual decrease in vision or sudden loss (in one or both eyes);
constant feeling of fatigue;
dizziness that occurs for no apparent reason;
uncontrolled urination;
pain in the spine when tilting the head;
nervous tics (eye twitching, eyebrow twitching);
epilepsy attacks.

Symptoms of multiple sclerosis can appear alternately or as a group (several). Those at risk should immediately consult a specialist, even if the symptoms are mild. Multiple sclerosis progresses gradually.

Who to contact

At the first signs of the disease, you must visit a neurologist or neurologist at the clinic.

At the first appointment, the doctor diagnoses:

evaluates the functional functioning of cranial nerve endings;
determines muscle tone affecting the motor system;
assesses sensitivity and reflexivity.

After the initial examination, the specialist will prescribe a number of mandatory tests. For the final diagnosis of multiple sclerosis, patients are usually sent to a hospital, where additional diagnostics and immediate treatment are carried out.

Types of diagnostics

It includes:

Hardware examination (MRI, tomography).

This study helps to assess the beginning changes in the spinal cord and brain. Before the procedure begins, the patient is injected with a contrast liquid (gadolinium), which makes it possible to increase the clarity of the image of the affected tissue.

Gadolinium accumulating in lesions indicates the progression of multiple sclerosis.

Lumbar puncture.

CSF collection(cerebrospinal fluid) from the lumbar region is necessary for laboratory analysis, during which an unacceptable increase in the antibody index is detected. Contrary to various rumors, this procedure is not dangerous for the patient. A needle placed inside the vertebrae does not touch the spinal cord.

Measuring the potential activity of brain cells.

This type of diagnosis analyzes three important potentials: hearing, vision and sensory functions.

During the procedure, electrodes attached to the patient's head record the brain's response to certain stimuli. The doctor's job is to assess the speed with which the brain responds to the signals given. A slow reaction indicates a “problem” in the functioning of the brain.

SPEMS.

Diagnosing a disease using a medical scanner is the youngest and most modern diagnostic method. Its advantage lies in identifying the disease in the early stages, when external manifestations are almost invisible. Using a brain scan, the functioning of all metabolic processes in brain tissue is revealed. Based on the indicators, the nature of the predisposition to multiple sclerosis is determined.

Blood tests.

It is impossible to diagnose multiple sclerosis using a blood test. But this analysis helps to identify diseases in the patient whose symptoms are similar to the disease being detected.

These diseases include: lupus erythematosus, ostiomyelitis, Lyme disease, sarcoma.

The blood test is carried out in combination with the above methods.

Differential diagnosis.

There are many diseases similar to multiple sclerosis. After completing the examination and studying the patient’s tests, the specialist needs to make an appropriate diagnosis. The method of differential diagnosis consists in the fact that the doctor, having compared all the facts with each other, identifies the main ones and establishes a single conclusion. Currently, there are computer programs that allow accurate differential diagnosis.

Treatment

Treatment options for multiple sclerosis depend on its stage. However, in medicine there are general principles prescribed by a specialist:

The most effective and latest technology has been and remains the transplantation of stem cells, which, when entering the patient’s blood, actively restore the myelin sheath to its normal state. But unfortunately this method is not available to everyone.

How long do you live with the disease?

Unfortunately, multiple sclerosis cannot be cured. The life expectancy of such patients does not have an exact figure. It all depends on the factors influencing the progression of the disease:

timeliness of the diagnosis;
age at which the disease begins;
effectiveness of treatment measures;
complications;
accompanying pathologies.

Life expectancy with multiple sclerosis often does not exceed 30 years. With serious complications and rapid progression, a person may not live even 5 years. But most often this figure is 12-16 years.

Sometimes, to determine the correct diagnosis at an early stage, the doctor needs time to monitor the course of the disease. But this does not negatively affect the patient’s condition.

Methods for diagnosing multiple sclerosis at an early stage updated: October 27, 2016 by: vitenega

Stroke Probability Calculator

Is there a risk of stroke?

Prevention

Age

1. Increased (over 140) blood pressure:

3. Smoking and alcohol:

4. Heart disease:

5. Undergoing medical examination and MRI diagnostics:

Total: 0%

Stroke is a rather dangerous disease that affects people not only of old age, but also of middle age and even very young people.

A stroke is a dangerous emergency that requires immediate help. It often ends in disability, in many cases even death. In addition to blockage of a blood vessel in the ischemic type, the cause of an attack can also be a hemorrhage in the brain against the background of high blood pressure, in other words, a hemorrhagic stroke.

Risk factors

A number of factors increase the likelihood of having a stroke. For example, genes or age are not always to blame, although after 60 years the threat increases significantly. However, everyone can do something to prevent it.

1. Avoid hypertension

High blood pressure is a major risk factor for stroke. Insidious hypertension does not show symptoms at the initial stage. Therefore, patients notice it late. It is important to measure your blood pressure regularly and take medications if levels are elevated.

2. Quit smoking

Nicotine constricts blood vessels and increases blood pressure. The risk of stroke for a smoker is twice as high as for a non-smoker. However, there is good news: those who quit smoking noticeably reduce this danger.

3. If you are overweight: lose weight

Obesity is an important factor in the development of cerebral infarction. Obese people should think about a weight loss program: eat less and better, add physical activity. Older adults should discuss with their doctor how much weight loss they would benefit from.

4. Keep your cholesterol levels normal

Elevated levels of “bad” LDL cholesterol lead to deposits of plaques and emboli in blood vessels. What should the values be? Everyone should find out individually with their doctor. Since the limits depend, for example, on the presence of concomitant diseases. Additionally, high values of “good” HDL cholesterol are considered positive. A healthy lifestyle, especially a balanced diet and plenty of exercise, can have a positive effect on your cholesterol levels.

5. Eat healthy food

A diet that is generally known as “Mediterranean” is beneficial for blood vessels. That is: lots of fruits and vegetables, nuts, olive oil instead of frying oil, less sausage and meat and lots of fish. Good news for gourmets: you can afford to deviate from the rules for one day. It is important to eat healthily in general.

6. Moderate alcohol consumption

Excessive alcohol consumption increases the death of stroke-affected brain cells, which is not acceptable. It is not necessary to abstain completely. A glass of red wine a day is even beneficial.

7. Move actively

Movement is sometimes the best thing you can do for your health to lose weight, normalize blood pressure and maintain the elasticity of blood vessels. Endurance exercises such as swimming or brisk walking are ideal for this. Duration and intensity depend on personal fitness. Important note: Untrained individuals over 35 years of age should be initially examined by a physician before starting to exercise.

8. Listen to the rhythm of your heart

A number of heart diseases contribute to the likelihood of a stroke. These include atrial fibrillation, birth defects, and other rhythm disorders. Possible early signs of heart problems should not be ignored under any circumstances.

9. Control your blood sugar

People with diabetes are twice as likely to suffer a cerebral infarction than the rest of the population. The reason is that elevated glucose levels can damage blood vessels and promote plaque deposits. In addition, people with diabetes often have other risk factors for stroke, such as hypertension or too high blood lipids. Therefore, diabetic patients should take care to regulate their sugar levels.

10. Avoid stress

Sometimes stress has nothing wrong with it and can even motivate you. However, prolonged stress can increase blood pressure and susceptibility to disease. It can indirectly cause the development of a stroke. There is no panacea for chronic stress. Think about what is best for your psyche: sports, an interesting hobby, or perhaps relaxation exercises.

Multiple sclerosis is a chronic autoimmune disease that manifests itself through damage to the myelin sheath of the nerve endings of the patient’s spinal cord and brain. In medical practice, there are currently no cases of complete recovery of patients suffering from this disease, but there are ways to achieve a sufficiently long remission. Damaged tissues are difficult to restore. This explains the need to diagnose multiple sclerosis during the early stages of the disease. In order to suspect the disease and contact a neurologist, you need to know the main signs of multiple sclerosis.

As a rule, the age of onset of the first symptoms of multiple sclerosis is 16-20 years. It is during the initial stage of development of the disease that treatment will have the most beneficial effect, however, most patients see a doctor too late.

The main problem with early diagnosis is that patients notice changes in the behavior of their own body late. The early symptoms of multiple sclerosis are quite vague, so the individual is able to attribute them to a banal lack of sleep or fatigue.

The first signs of the development of the disease

In order to be able to diagnose MS on time, it is necessary to know the first signs of multiple sclerosis. It is worth noting that MS manifests itself in women and men equally, although women are statistically affected more often.

Symptoms of multiple sclerosis at the initial stage include the following:

Chronic fatigue is the most common sign of how multiple sclerosis manifests itself in patients in the early stages. Fatigue becomes more noticeable in the afternoon. The patient often feels mental fatigue, weakness throughout the body, a desire to sleep, and general lethargy;
Muscle weakness - the patient finds it more difficult to perform usual physical activities, it is more difficult for him to perform everyday tasks associated with muscle loads;
Dizziness is one of the most common symptoms of multiple sclerosis.
Muscle spasms - usually noticeable in the muscles of the arms and legs. this symptom is leading in the development of disability in patients during the progression of the disease.

The primary symptoms of multiple sclerosis occur as a result of demyelination, a process of damage to the myelin sheath of nerve fibers in the brain and spinal cord. The destructive process leads to a deterioration in the transmission of brain signals to the muscles, as well as the internal organs of the patient.

Also, the first symptoms of multiple sclerosis include tremors, slight tingling in the muscles of the arms and legs, partial loss of vision, impaired bowel and bladder function, and loss of coordination. Such early symptoms of progressive multiple sclerosis are corrected with medication.

Problems in diagnosing MS in the early stages

How to recognize multiple sclerosis and seek help? As can be seen from the above signs of the development of the disease, the symptoms are quite vague. It is almost impossible to determine an accurate diagnosis on your own; moreover, there are various diseases similar to multiple sclerosis. They begin in exactly the same way as MS begins; to exclude them, the neurologist prescribes special tests (biopsy, blood test, MRI). Only a qualified specialist can determine whether a person has multiple sclerosis or not.

The list of diseases similar to multiple sclerosis is huge. Diseases similar to multiple sclerosis:
Infections affecting the central nervous system. These include:

Lyme disease.
AIDS virus.
Syphilis.
Leukoencephalopathy

Inflammatory processes affecting the central nervous system:

Sjögren's syndrome.
Vasculitis.
Lupus.
Behçet's disease.
Sarcoidosis.

Genetic disorders:

Myelopathy.
Cerebral arteriopathy is autosomal dominant.
Leukodystrophy.
Mitochondrial disease.

Brain tumors:

Metastases.
Lymphoma.

Deficiency of vital microelements:

Copper deficiency.
Vitamin B12 deficiency.

Lesions to tissue structure:

Cervical spondylosis.
Disc herniation.

Demyelinating disorders:

Devic's disease.
Disseminated encephalomyelitis.

In addition to these diseases, the first manifestations of the disease may be similar to the symptoms of vegetative-vascular dystonia, and it, unlike MS, is completely harmless to the human body. VSD is not fatal. It, like multiple sclerosis, is also characterized by dizziness, loss of coordination, spasms, and weakness. What problem attacked the patient - VSD or multiple sclerosis - will be determined by a qualified neurologist. The main thing is not to delay visiting the clinic.

Reasons to see a doctor as soon as possible

The signs of MS vary from person to person. If you notice increasing fatigue that appears in the afternoon, an overly sensitive reaction to heat (for example, headaches may appear after taking a hot shower), dizziness, numbness in the limbs, deterioration in visual acuity, immediately go to the doctor.

Remember that it is important to start the treatment process before MS attacks begin. Even if MS is diagnosed, your doctor will help determine the true causes of your symptoms and prescribe the right treatment that can save your life.

How does the disease manifest and progress?

Manifestations of multiple sclerosis depend on the form and course of the disease. The course of the disease is:

remitting;
progressive-remitting course;
primary progressive;
secondary progressive course.

In the case of a primary progressive course, the manifestations of multiple sclerosis are gradual. They increase with moderate frequency. Thus, dizziness in multiple sclerosis is complemented by poor coordination, then disabling spasms. There are both periods of stabilization of the body (remission) and periods of exacerbations.
A gradual increase in symptoms is also characteristic of the secondary progressive course of the disease. Attacks of multiple sclerosis usually appear after acute stress or infectious diseases.

Onset of the disease

As a rule, the debut of the disease is the first clinical manifestation of the disease. By that time, the attacks of multiple sclerosis themselves may have been present for several years. Almost the debut of multiple sclerosis is noted within the first 5 years of the autoimmune process. This period is quite late, it reduces the chances of improving the patient’s condition, but this does not mean that achieving long-term remission becomes impossible.

One of the most typical debuts of MS is considered to be complete or partial damage to the optic nerve. Manifestations of such a debut are:

sudden deterioration of vision;
sudden onset of color blindness;
cloudiness or blurred vision;
a black dot flashing in front of the eye;
constant feeling of the presence of a foreign body;
pain in the eyeball, increasing when the pupil moves;
impaired reaction to light (increased photosensitivity);
flashing objects before the eyes;
blurred contours of visible objects.

As a rule, visual impairment occurs very suddenly. In this case, symptoms may appear for about a week, then pass. Complete restoration of vision occurs in 70% of cases.

How is multiple sclerosis diagnosed?

So, the main question: how to identify multiple sclerosis? After all manifestations have been analyzed and similar diseases have been eliminated, the doctor must move on to a more accurate analysis, which with almost 100% probability confirms or refutes the diagnosis of MS.

The first step is a neurological examination. Thanks to the examination, the doctor has the opportunity to determine the level of sensitivity impairment and determine whether the patient is disabled.

After a neurological examination, the patient is prescribed an MRI. This study is considered the most effective method of diagnosis. Thanks to the results of an MRI, medical personnel are able to determine the presence of focal inflammation in the brain, characteristic of this disease, causing disturbances in the transmission of nerve impulses. The MRI method of operation is based on a magnetic field that causes resonance in the tissues being examined, allowing one to obtain an accurate, high-quality image of all structures of the organs being examined.

At the onset of MS, magnetic resonance imaging is performed exclusively with the use of a contrast agent. The injected contrast accumulates in areas of inflammation, or areas of demyelination. Thus, the doctor is able to establish an accurate diagnosis and record the current level of damage to the fibers of the nerve endings. These data are subsequently used to study the dynamics of the disease.

Immunological testing is also used as one of the methods for determining the disease.

Remember that this disease is a very serious autoimmune disease that has an extremely high rate of progression without appropriate treatment. If you experience even minor symptoms, consult your doctor.

Be healthy, spend enough time on your body and don’t ignore the symptoms that bother you.

Most often, the lesion is localized at the level of the white matter of the cerebral hemispheres, but can also be observed in the cerebellum, brain stem, and spinal cord. The lesions have a denser consistency, they are called multiple sclerosis plaques. On CT scans they appear as lighter lesions in the substance of the brain or spinal cord. The symptoms of the lesion largely depend on the area affected by autoimmune inflammation.

Symptoms and signs of multiple sclerosis

Chronic fatigue. May manifest as constant drowsiness and decreased performance. Symptoms of fatigue most often appear in the afternoon. In this case, the patient feels signs of asthenia - a decrease in the strength of muscle contraction, rapid fatigue during physical activity. Mental stress is also difficult for such patients; mental acuity, attentiveness, and the ability to assimilate new information are lost.
Increased sensitivity to increased body temperature - taking a hot bath or shower, being in a bathhouse or in a heated room can provoke an exacerbation of symptoms of the disease, a sharp deterioration in overall health.
Muscle spasms can occur as complications of the inflammatory process of the central nervous system pathways. In this case, a tendency to spasm of certain muscle groups develops.
Dizziness occurs against the background of normal blood supply to the brain and normal blood glucose levels. Typically, patients complain that it is difficult for them to maintain balance due to the fact that the environment is in motion.
Impaired intelligence and cognitive ability. Increased fatigue leads to the fact that it becomes difficult for the patient to perceive new information, but at the same time, even once perceived information can be lost by the patient after a short period of time. This manifestation of multiple sclerosis, along with movement disorders, is the main reason for the patient’s loss of ability to work.
Visual impairment is usually felt acutely by the patient. Most often, only one eye is affected. First of all, the patient loses the color of the image and says that the surrounding objects have faded. He also complains that the vision in the affected eye is blurry and lacks clarity. As a rule, after a course of treatment, visual acuity is restored, but color impairment may remain at the same level.
Tremors in the limbs - involuntary hand tremors. It is, of course, not as pronounced as in Parkinson's disease and differs from it in that it has a small amplitude. It is difficult for the patient to do delicate work - thread a needle into the eye, draw, change handwriting, draw, etc.
Gait disturbance – from the outside, such patients walk as if they are very tired. This is associated with a pronounced feeling of fatigue, although the patient did not have any physical activity during the day.

Diagnosis of multiple sclerosis, MRI diagnostics, spinal puncture, cerebrospinal fluid analysis, evoked potentials

Nuclear magnetic resonance in the diagnosis of multiple sclerosis

This research method allows you to obtain layer-by-layer images of sections of certain parts of the body. To diagnose the topography of lesions in multiple sclerosis, MNRs are performed in the head region or certain areas of the spinal column.

The tomogram reveals foci of increased density with clearly defined edges of a rounded shape, about 5 mm in size. , no more than 25 mm. The lesions are usually located near the ventricles of the brain in the area where the white medulla is located.

Currently, when performing MRI, preference is given to a technique in which preliminary contrasting of lesions is performed by introducing a special contrast agent (gadolinium), which reveals lesions that have arisen as a result of the blood-brain barrier being broken. When the blood-brain barrier is disrupted, blood plasma, which normally should not penetrate the brain tissue, leaves the vascular bed and penetrates the brain tissue. Violation of this barrier is the main sign of the inflammatory process in brain tissue. Therefore, it is possible to detect the activity of the inflammatory process.

Cerebrospinal fluid examination

To confirm the diagnosis of multiple sclerosis, in some cases, against the background of an exacerbation of the disease, a spinal puncture, sampling of cerebrospinal fluid and its biochemical and microscopic examination are required.

What is a spinal tap?

A spinal puncture is a manipulation performed by a neurologist. During a spinal puncture, a puncture is made with a long special needle in the lumbar region of the spine between the vertebrae. When a needle enters the spinal canal, cerebral fluid flows out of the canal, which washes the spinal cord and brain.

What is revealed by microscopy of cerebrospinal fluid?

After the spinal fluid is collected, it is sent to the laboratory for special analysis.

Microscopic examination of the spinal fluid determines the color and cellular composition of the fluid.

In multiple sclerosis, as a rule, the number of red blood cells in the fluid is normal, but a moderate increase in the level of lymphocytes is observed.

What does a biochemical analysis of cerebrospinal fluid reveal?

The protein content in multiple sclerosis in the acute phase may be slightly increased. However, the increase in protein levels rarely exceeds 1.0 grams/liter

Determination of myelin basic protein is a key indicator in diagnosing multiple sclerosis and assessing its activity at the time of examination. The fact is that with multiple sclerosis, the myelin sheath is damaged by the immune system. Accordingly, during an active process, the first thing that occurs is the breakdown of myelin tissue with the release of free myelin protein into the cerebrospinal fluid. Therefore, during the first two weeks from the moment of exacerbation of the autoimmune process in multiple sclerosis, myelin basic protein is found in large quantities in the spinal fluid. This indicator is the most reliable criterion in the diagnosis of multiple sclerosis.

Study of bioelectrical activity of the brain (evoked potentials)

When examining visual, somatosensory or auditory evoked potentials, signs may be observed that indicate this. That there is a violation in the conduction of tactile, auditory or visual information along the pathways.

Treatment of multiple sclerosis, drugs used in treatment

Unfortunately, curing multiple sclerosis is currently an impossible task. The thing is that damage to the nervous tissue that led to the destruction of certain areas takes a long time to recover, and in some cases cannot be restored at all. Therefore, the consequences of multiple sclerosis can lead to irreversible consequences. All that a neurologist can do for this disease is to reduce the likelihood of re-exacerbation of multiple sclerosis, minimize the consequences of damage to the brain pathways, and stimulate the regenerative properties of nervous tissue.

Treatment tactics for different forms and stages of the disease are different and are determined individually by the attending neurologist, depending on the dynamics of the process and the general condition of the patient.

Prevention of exacerbations of multiple sclerosis

It is produced using drugs that suppress the activity of the immune system.

The drugs in this group are varied: steroid hormones, drugs that slow down cell division processes (cytostatics), certain types of interferons.

Steroid drugs(prednisolone, Kenalog, dexamethasone) have an immunosuppressive effect. These drugs reduce the activity of the entire immune system, suppress the processes of immune cell division, the activity of antibody synthesis, and reduce the permeability of the vascular wall. But along with all the positive properties, steroid drugs have a number of side effects that do not allow the use of this group of drugs for long-term treatment. Side effects of steroid drugs: gastritis, increased intraocular and blood pressure, increased body weight, psychosis, etc.

Drugs from the group of cytostatics(azathioprine, cyclophosphamide and cyclosporine, methotrexate and cladribine). I have an immunosuppressive effect, but the high level of side effects similar to those when using steroid drugs makes this class of medications unsuitable for long-term use.

Interferon-r(IFN-p) This drug has an immunomodulatory effect, influencing the activity of the immune system. The list of side effects is acceptable in order to recommend this drug as a preventive treatment for multiple sclerosis.