Guillain-Barré Syndrome
At the beginning of the twentieth century, researchers Barre, Guillain and Strohl described an unknown disease in soldiers of the French army. The fighters were paralyzed, they did not have tendon reflexes, and there was a loss of sensitivity. Scientists examined the cerebrospinal fluid of patients and determined that it contained an increased protein content, while the number of other cells was absolutely normal. On the basis of the protein-cell association, as evidenced by the result of the analysis of cerebrospinal fluid, Guillain-Barré syndrome was diagnosed, which differs from other demyelinating diseases of the nervous system by a rapid course and a favorable prognosis. The studied soldiers recovered earlier than 2 months later.
Subsequently, it turned out that Guillain-Barré syndrome is not as harmless as the discoverers described it. For 20 years before the appearance of the description of the disease, the neuropathologist Landry observed patients with similar diseases. They also had flaccid paralysis, rapidly developing along the ascending nerve tracts. The rapid development of the disease was fatal. The damage to the nervous system was called Landry's palsy. Subsequently, it turned out that Guillain-Barré syndrome can also be fatal due to the shutdown of muscle transmission in the diaphragm. But even in such patients, a laboratory pattern of protein-cell association in the cerebrospinal fluid was observed.
Then they decided to combine both diseases and assign the pathology one name Landry-Guillain-Barre syndrome, and to this day neuropathologists use the proposed terminology. However, the international classification of diseases has registered only one name: Guillain-Barré syndrome or acute post-infectious polyneuropathy.
Guillain-Barré syndrome, causes
Since the disease develops after infection, there is an assumption that it is she who causes the process of demylination of nerve fibers. However, no direct infectious agent has yet been found. The antigen-antibody complexes are deposited on the myelin fibers of the nervous tissue, which cause the destruction of myelin.
The myelin sheaths are located along the nerve trunk at regular intervals. They play the role of capacitors, so nerve impulses are transmitted several tens of times faster and reach the "addressee" unchanged. When Guillain-Barré syndrome develops, its causes lie in a decrease in the capacity of the "capacitors". As a result, the nerve transmission is delayed and becomes ineffective. The person intends to clench his fingers, but can only move them.
This is the essence of all demilienizing diseases of the nervous system. When a person develops Guillain-Barré syndrome, impulse transmission to major vital organs suffers, such as:
- Cardiac muscle;
- Diaphragm;
- Swallowing muscles.
With the paralysis of these organs, the vital activity of the organism stops.
Guillain-Barré syndrome, symptoms
The paradox of the disease lies in the fact that in acute development, a successful outcome falls on two-thirds of patients, and in the chronic course, the prognosis is poor.
Guillain-Barré syndrome begins after acute viral infections, most often respiratory. In the form of complications after the flu, a person develops general weakness, which is transmitted to the arms and legs. Subsequently, the subjective feeling of weakness progresses to flaccid paralysis. In an acute course, the following symptoms develop:
- The disappearance of the swallowing reflex;
- Paradoxical type of breathing - during inhalation, the abdominal wall does not expand, but, on the contrary, falls;
- Violation of the sensitivity of the distal extremities of the type of "gloves" and "stockings".
In severe cases, breathing is shut off due to paralysis of the diaphragm.
When primary chronic Guillain-Barré syndrome develops, symptoms build up slowly over several months, but at their peak they are difficult to treat. As a result, the effects of paralysis remain for the rest of your life.
The clinical course of Guillain-Barré syndrome
During the course of the disease, 3 stages are determined:
- Prodromal;
- Razgara;
- Exodus.
The prodromal period is characterized by general malaise, muscle pain in the arms and legs, and a slight increase in temperature.
During the peak period, all the symptoms characteristic of Guillain-Barré syndrome appear, which reach their peak by the end of the phase.
The outcome stage is characterized by a complete absence of signs of any infection, but manifests itself only with neurological symptoms. The disease ends with either complete restoration of all functions, or disability.
Guillain-Barré syndrome, treatment
With an acute onset, especially when Guillain-Barré syndrome develops in children, first of all, resuscitation measures are found. Timely connection of the artificial respiration apparatus saves the patient's life.
A long stay in the intensive care ward requires additional treatment, bedsores are prevented and the fight against infections, including hospital ones.
The uniqueness of Guillain-Barré disease lies in the fact that with adequate artificial ventilation of the lungs, the regeneration of the myelin sheaths occurs without any medication.
Modern methods of treatment of Guillain-Barré syndrome, in children in particular, involve plasmapheresis. Cleansing blood plasma from autoimmune complexes prevents the progression of demyelination of nerve fibers and significantly shortens the period of artificial ventilation.
Currently, Guillain-Barré syndrome is treatable with immunoglobulin infusions. The method is expensive but effective. In the recovery period, methods of physiotherapy, physiotherapy exercises and massage are used.
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The information is generalized and provided for informational purposes only. At the first sign of illness, see your doctor. Self-medication is hazardous to health!