What Is the Connection Between Guillain-Barre Syndrome and Vaccination?

Guillian-Barre syndrome is a common demyelinating disease of the spinal and peripheral nerves. Also known as acute idiopathic polyneuritis or symmetric polyradiculitis. Clinical manifestations are progressive asymmetry paralysis, limb paralysis, and sensory impairment of varying degrees. Patients have acute or subacute clinical course, and most of them can completely recover. A few severe cases can cause fatal respiratory palsy and bilateral paralysis. Cerebrospinal fluid examination, a typical increase in protein and normal cell count, also known as protein cell separation phenomenon.

Basic Information

nickname: Acute idiopathic polyneuritis, symmetric polyradiculitis
English name: Guillain-Barre syndrome
English alias: acute infectious polyneuritis

Visiting department: Neurology
Common causes: CMV, Epstein-Barr virus, or Mycoplasma infections
Common symptoms: Sudden onset of severe nerve root pain, delayed paralysis of limbs, and abnormalities in limbs, such as numbness, tingling, burning, etc.

Causes of Guillain-Barre Syndrome

Most patients have infections such as cytomegalovirus, Epstein-Barr virus, or mycoplasma before the onset of the disease, but the cause is unknown in a few cases. The nature of the disease is unclear and may be related to immune damage. Injection of animal serum into animal nerves can produce perivenous demyelinating lesions. In addition, C3b and immunoglobulin C are mainly present in the patient's nervous tissue (IgG or IgM). The above facts suggest that this disease may be related to humoral immunity. However, antibodies to myelin have not yet been proposed from patients' blood. One of the side effects of the vaccine is the possibility of Guillain-Barre syndrome.

Guillain-Barre Syndrome

1 to 4 weeks ago with symptoms of gastrointestinal or respiratory infections and a history of vaccination, sudden severe nerve root pain, mainly neck, shoulder, waist and lower limbs, others with acute progressive symmetrical limb paralysis, subjective sensory disorders, tendons Reflex diminishes or disappears.

Dyskinesia

Limb palsy of the extremities is the main symptom of this disease. Generally, the trunk, upper limbs and cranial nerves are gradually spread from the lower limbs, the muscle tension is low, and the proximal end is often heavier than the distal end. Usually within a few days to 2 weeks, the condition develops to a peak, and the critically ill patients quickly aggravate within 1 to 2 days, complete limb paralysis, paralysis of the respiratory muscles and swallowing muscles, dyspnea, and swallowing disorders are life threatening.

Sensory disturbance

It is generally lighter than movement disorders, but common physical dysfunctions, such as numbness and burning sensation, can precede paralysis or appear at the same time. About 30% of patients have muscle pain and feel abnormal. And joint movement is usually saved.

3. Reflex disorder

The tendon reflexes of the extremities are mostly symmetrically weakened or disappeared, and the abdominal wall cremaster testis more normal. A few patients may have pathological reflex signs due to the involvement of the pyramidal tract.

4. Autonomic dysfunction

In the initial or recovery period, there is often sweating, and the sweat smell is strong, which may be the result of the sympathetic nerve stimulation. A small number of patients may have short-term urinary retention at the beginning, which may be caused by a temporary imbalance of the autonomic nerve function that governs the bladder or damage to the spinal nerve that governs the external sphincter; the stool is often constipated; and some patients may have unstable blood pressure and tachycardia.

5. Cranial nerve symptoms

Half of the patients had cranial nerve damage, and peripheral paralysis of the vagus-pharyngeal vagus nerve and one or both sides of the nerve was more common, followed by eye movement, pulley, abductor nerve, and occasional optic nerve papillary edema, which may be caused by changes in optic nerve inflammation or cerebral edema. It may also be related to the significant increase in cerebrospinal fluid protein blocking the arachnoid villi and affecting cerebrospinal fluid absorption.

Guillain-Barre Syndrome

Cerebrospinal fluid examination

The protein is elevated, and the number of cells is not high or slightly elevated, showing a "protein-cell separation".

2. Blood white blood cell count and classification may increase during co-infection.

3. Severe cases

Electrocardiogram is abnormal, sinus tachycardia and T wave changes are common, and QRS wave voltage is increased.

4. Electrophysiological examination

Evidence of slowed motor and sensory nerve conduction velocity (NCV), denervation, or axonal degeneration. Early F-waves or H-reflexes may only be seen delayed or disappeared (F-wave abnormalities represent proximal nerve or nerve root damage, which is helpful in the diagnosis of segmental lesions, and multiple nerves should be examined). Demyelinating lesions showed slow NCV, prolonged distal latency, normal or mild abnormal amplitude, and axonal injury showed decreased distal amplitude.

5. Sural nerve biopsy

Demyelination and inflammatory cell infiltration can be seen. This result is for diagnostic reference only.

Guillain-Barre Syndrome

Diagnosis can be confirmed based on clinical manifestations and examinations.

Guillain-Barre Syndrome Differential Diagnosis

The disease needs to be distinguished from the following diseases: polio; acute myelitis; hypokalemia paralysis; peripheral neuritis (peripheral neuritis); polymyositis; porphyria with peripheral neuropathy.

Guillain-Barre syndrome complications

Because patients with this disease often stay in bed for a long time, they are prone to complications such as septal pneumonia sepsis, deep vein thrombosis of bedsores, pulmonary embolism, urinary retention, anxiety, depression, etc., and if the disease involves respiratory muscles, it can be fatal.

Guillain-Barre Syndrome Treatment

1. Comprehensive treatment and nursing

Keeping the airway open and preventing secondary infections is the key to treatment. Swallowing muscles and respiratory muscles are coughing weakly, phlegm is not good, if necessary, tracheostomy, ventilator assisted breathing; strengthen care, turn over more to prevent pressure ulcers; facial paralysis need to protect the cornea to prevent ulcers. Myocarditis may be associated with this disease, and the condition of the heart should be closely observed. The amount of fluid replacement is not easy to be too large.

Hormone

The application is controversial. It can be applied for short time in the early stage, and the treatment course should not be too long. Generally, it is about 1 month. Short-term impact treatment with hydrocortisone and dexamethasone can be used for acute severe cases.

3. Intravenous application of high-dose gamma globulin. Should be used as soon as possible.

4. Plasma exchange therapy

It is a new treatment launched in recent years. It is initially considered effective and expensive.

5. Appropriate application of neurotrophic drugs

Metabolic drugs such as coenzyme A, ATP, and cytochrome C can also be used with vitamin B ₁₂ at the same time. Micobo and others.