Guillain-Barre syndrome is an acute demyelinating disease that causes the rapid development of weakness in the extremities. A condition defined as demyelinating implies that it destroys the myelin plates (a protein that surrounds the nerve endings and allows the transmission of nerve stimulation). The dysfunction or destruction of myelin prevents the correct transmission of sensory and motor information from the nerves to the brain and vice versa.
Guillain-Barre syndrome is a pathology in which patients develop a motor paralysis of an ascending type since it begins in the lower limbs and progresses in hours or days to the muscles of the trunk, upper limbs, neck, and hips. Cranial innervation and often facial, respiratory, and swallowing muscles.
This entity was diagnosed and discovered in 1859 by Landry and in 1916 by Guillain, Barre , and Strohl and has classically included multiple subtypes within its definition. Currently, the spectrum of clinical variants of the syndrome is extensive, supported by advances in molecular biology and immunology that have made it possible to characterize these forms of GBS better.
In about two-thirds of patients, Guillain-Barre syndrome begins five days to three weeks after a trivial infectious disorder, surgery, or vaccination. Infection is the trigger in more than 50% of patients; The most common pathogens are:
Campylobacter jejuni, enteric viruses Herpesviruses (including cytomegalovirus and Epstein-Barr virus) Mycoplasma spp…
It usually affects people of any age and sex. Two peaks of presentation are recorded: one in the young adult stage (15 to 34 years) and another in the elderly (60-74 years), rare in children under one year of age.
Clinical forms according to symptoms and signs.
Guillain-Barre Syndrome (GBS) is configured by the progressive appearance of neurological and autonomic symptoms such as:
A predominant flaccid weakness in most patients with Guillain-Barre syndrome is usually more evident in the upper portion. Relatively symmetric weakness with paresthesias usually begins in the legs and progresses to the arms but occasionally begins in the arms or head. In 90% of patients, weakness is maximal, usually at 3 to 4 weeks. Deep tendon reflexes are lost. The sphincters are generally spared. The liability remains the same for a variable period, usually a few weeks, and then resolves. The facial or oropharyngeal muscles are weak in more than 50% of patients with severe disease. Dehydration and malnutrition may appear. On numerous occasions, respiratory paralysis is severe enough to require endotracheal intubation, and mechanical ventilation is performed in 5% to 10% of patients. Some patients have significant, potentially fatal autonomic dysfunction resulting in blood pressure fluctuations, cardiac arrhythmias, gastrointestinal stasis with nausea and vomiting, urinary retention, and pupillary changes.
Taking into account the significant variability in the appearance of symptoms and signs and the diverse location of the condition, we can currently divide each of the subgroups into four predominant clinical forms:
Fisher syndrome is characterized by areflexia, ataxia (lack of coordination), and ophthalmoparesis (weakness (-paresis) or paralysis (-plegia) of one or more extraocular muscles). Pure motor Guillain-Barre syndrome, with exclusive pathological involvement of the anterior roots. Pure sensory Guillain-Barre syndrome, with locations of inflammatory lesions and demyelination in the posterior roots of the central nervous system and sensory nerves. Cranial Guillain-Barre syndrome, usually with eye palsy and facial palsy.
Guillain-Barré Syndrome: Doctor explaining its health effects Guillain-Barre Syndrome
The primary diagnosis of Guillain-Barre syndrome is clinical and through speed tests of the peripheral nervous system (assessment of nerve demyelination) and study of cerebrospinal fluid (CSF). To this end, many tests or tables with diagnostic criteria have been created. The most relevant in the health world are usually the Asbury criteria, divided into three large groups: characteristics necessary for the diagnosis, standards that support the diagnosis, and aspects that cast doubt on or rule out the diagnosis.
Support measures in the acute phase of the disease such as:
Prevention and treatment of complications (respiratory failure, infections, autonomic dysfunction, and pulmonary thromboembolism). Assess and support and vital depending on the clinical status, in case mechanical ventilation is required. Arterial blood gases before and after connection to a ventilator. Evaluate possible intubation time and possible tracheostomy. Define enteral feeding route. Specific treatment directed in large directions: Specific immunoglobulin at a dose of (2 g/kg/total amount) divided into two doses (1 g/kg/day. Plasmapheresis: its use is based on the reduction of antibodies and the elimination of other immunoregulatory elements such as lymphokines, complement components, immune complexes, and other reactants of the acute phase.
What prognosis do you have?
Recovery from Guillain-Barre syndrome symptoms can take weeks, months, or years. Most people recover completely, with a minor and mild motor weakness remaining in a relatively small percentage of those affected. The prognosis is generally good when the symptoms disappear immediately after onset and is slightly worse the longer the motor symptoms persist and are more severe.