What Is Polyneuritis?

[Cause and Pathology]

Acute polyneuritis

Acute polyneuritis is also called acute polyradiculoneuritis or Guillain-Barre syndrome. It mainly damages most of the spinal nerve root and peripheral nerves, and often involves the cranial nerve. It is a special type of polyneuritis.

[Cause and Pathology]

The etiology of acute polyneuritis is unknown. Most patients have symptoms of upper respiratory intestinal infection a few days to several weeks before the onset, or secondary to certain viral diseases such as influenza. Therefore, the disease is suspected to be related to viral infection Relevant, but no virus has been isolated so far. In addition, this disease is considered to be an autoimmune disease, which may be caused by immune disorders after infection. Symptoms have also been reported after vaccination. It is also believed that the disease is not caused by a single cause, but by multiple causes, including even a syndrome caused by poisoning.

The main pathological changes of acute polyneuritis are in the spinal nerve root (previously the root is more common and obvious), ganglia and peripheral nerves, and occasionally the spinal cord is involved. The pathological changes were edema, congestion, infiltration of lymphocytes around the blood vessels, segmental demyelination and axonal degeneration of nerve fibers.

[Clinical manifestations]

Can be seen at any age, but more common in young and middle-aged men. Onset occurs in all four seasons, and it is more common in summer and autumn. The onset is acute or subacute, and a few have a slow onset. The main performance is as follows:

1. Dyskinesia

(1) Limb paralysis: Motor limbs are paralyzed under the symmetry of the extremities, and often start from the lower limbs, gradually spread to both upper limbs, and can also go from one side to the other. The disease usually reaches its peak within 1 to 2 weeks, and then stabilizes. The weakness of the limbs often develops from the distal end to the proximal end, or from the proximal end to the distal end. Extremity muscle tension is low, tendon reflexes weaken or disappear, abdominal wall, cremaster test reflexes are more normal. A few may have pathological reflex signs due to the involvement of the pyramidal tract. Muscle atrophy gradually develops 2-3 weeks after onset.

(2) Paralysis of the trunk muscles: The cervical muscles, trunk muscles, intercostal muscles, and diaphragm muscles may also be paralyzed. When the respiratory muscles are paralyzed, chest tightness, shortness of breath, low speech, cough weakness, reduced chest or abdominal breathing movement, and reduced breathing sounds can cause coma and death due to hypoxia, respiratory failure, or respiratory complications. .

(C) cranial nerve palsy: about half of the patients may have cranial nerve damage, the most common are parapharyngeal, vagus and peripheral paralysis of one or both sides of the nerve, followed by eye movement, car crash, abductor nerve. Occasionally, optic nerve papillary edema may be caused by inflammation of the optic nerve itself or cerebral edema, or it may be associated with a significant increase in cerebrospinal fluid protein, blocking the arachnoid villi, and affecting the absorption of cerebrospinal fluid. With the exception of the trigeminal sensory branch, other sensory nerves are rarely affected.

Sensory disorders

May be the first symptom, mainly subjective sensory disturbance, mostly starting from the numbness and acupuncture at the extremities. Pulling the nerve root during examination can often aggravate the pain (such as Kernig's sign is positive), the muscles can have obvious tenderness, especially bilateral gastrocnemius muscles. Objective examination is more normal, and only some patients may have gloves and sock-type sensory disturbances. Occasionally, segmental or conduction beam sensory disorders. Sensory disorders are much lighter than motor disorders and are one of the characteristics of this disease.

Third, autonomic dysfunction

In the initial or recovery period, there is often sweating and a strong sweat odor, which may be the result of 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 the spinal nerve that governs the external sphincter. Stool is often secretive. Some patients may experience cardiovascular dysfunction such as blood pressure instability, tachycardia, and abnormal electrocardiogram. ^[1]