Polyneuritis

Introduction Polyneuritis is also known as multiple peripheral neuritis, which belongs to the category of TCM syndromes and syndromes. It can be caused by various causes such as poisoning, nutritional and metabolic disorders, infection, allergies, allergies, etc., which damage most peripheral nerve endings, causing symmetry or asymmetrical movement of the limbs, and diseases of autonomic dysfunction .

Cause

The pathological changes of the disease are mainly segmental demyelination or axonal degeneration of the peripheral nerve, or both. There are many reasons for this, which are described as follows:

(1) Acute inflammatory demyelinating polyneuritis: a group of autoimmune diseases that may be induced by infection or sera injection or vaccination.

(2) Metabolic and endocrine disorders: diabetes, uremia, hematoporphyria, amyloidosis, gout, hypogonadism, acromegaly, xanthomatosis, hemophilia, cachexia caused by various causes, Burns, etc.

(3) Nutritional disorders: beriberi, pellagra, vitamin B12 deficiency, chronic alcoholism, pregnancy, chronic diseases of the gastrointestinal tract and post-operative.

(4) Chemical factors:

1. Drugs: furan drugs, isoniazid, phenytoin, sulfonamides, vincristine, chloroquine, ethambutol, cytarabine, etc.

2. Chemicals: carbon monoxide, carbon disulfide, carbon tetrachloride, benzene and its derivatives (aniline, dinitrobenzene, etc.), methanol, methyl bromide, n-hexane, acetone, chloroform, chloropropene, chlorobutanol, trichloro Ethylene, organochlorine pesticides, organophosphorus pesticides (trichlorfon, dichlorvos, 1605, 1059).

3. Heavy metals: arsenic, lead, mercury, antimony, antimony, etc.

(5) Infectious diseases:

1. Direct infection of peripheral nerves such as leprosy and herpes zoster.

2. Accompanying or secondary to various acute and chronic infections, such as influenza, measles, chickenpox, mumps, scarlet fever, infectious mononucleosis, leptospirosis, etc.

3. Toxins secreted by bacteria have special affinity for peripheral nerves, such as diphtheria, tetanus, and dysentery.

(6) Connective tissue diseases: such as lupus erythematosus, nodular polyarteritis, scleroderma, rheumatoid arthritis, etc.

(7) Inheritance: such as hereditary ataxia-induced peripheral neuritis (Refsum disease), progressive hypertrophic polyneuritis.

(8) Other causes: such as multiple myeloma, lymphoma, polycythemia vera, cancer, abnormal globulinemia.

(9) The cause is unknown: chronic progressive or recurrent polyneuritis.

an examination

1. Cerebrospinal fluid examination: normal or slightly increased protein content.

2. Electromyography and nerve conduction velocity: If there is only a slight axis mutation, the conduction velocity is still normal. When there is severe axonal degeneration and secondary myelin loss, the conduction velocity is slowed down. The electromyogram has neurological abnormal changes. In the case of segmental myelin loss and axonal degeneration is not significant, the conduction velocity is invaded, but the EMG can be normal; determining the EMG and nerve conduction velocity contributes to the neurogenic damage and myogenicity of the disease. The identification of lesions is also conducive to the differentiation of axonal lesions and segmental demyelination lesions. The axonal lesions show a decrease in amplitude, while the demyelinated lesions show a slower nerve conduction velocity.

3. Immunological examination: For those suspected of having immune diseases, it can be used for detection of immunoglobulin, rheumatoid factor, anti-nuclear antibody, anti-phospholipid antibody, lymphocyte transformation test and flower rectangular test.

4. Neurobiopsy: Neuronal biopsy provides more accurate evidence for determining the nature and extent of neuropathy.

Differential diagnosis

Clinically, it should be identified with the following diseases:

1. Periodic paralysis: no clear gloves, socks-like sensory disturbances, and a short course of disease, rapid recovery.

2. Poliomyelitis (polio sequelae): Most of the muscle spasm is asymmetrical, and there is no sensory defect in the skin.

3. Subacute combined degeneration of the spinal cord: It may have symptoms of multiple neuropathy such as numbness and weak muscles, but it may be identified by increased muscle tone, hyperreflexia and positive pyramidal tract.

diagnosis:

(1) Lower extremity motor neurons in the distal extremity: Severe cases with muscular atrophy and fasciculation, quadriplegia reflexes disappeared or disappeared, tendon reflexes were obvious, and fine tasks could not be performed. The distal end is heavier than the proximal end, the lower extremity tibialis anterior muscle, the tibialis anterior muscle, the upper limb interosseous muscle, the sacral muscle and the intermuscular muscle atrophy, the hand, the foot sag and the cross-threshold gait, and the late muscle contracture is deformed.

(2) Various sensory sensations are distributed in the shape of gloves and socks, which may be accompanied by irritation, abnormal feelings and pain. Pain is a small fiber-damaged neuropathy (such as diabetes alcoholism, porphyria, etc.), as well as AIDS, hereditary sensory neuropathy, paraneoplastic sensory neuropathy, invasive neuropathy, and idiopathic brachial plexus. Hereditary sensory neuropathy, amyloid neuropathy can be seen as a discrete sensory loss.

(3) Autonomic neurological disorders: orthostatic hypotension, cold limbs, excessive sweating or no sweat, fingernails, crisp skin, dry or desquamation, vertical hair disorder, afferent neuropathy leading to tension-free bladder , impotence and diarrhea.

The material in this site is intended to be of general informational use and is not intended to constitute medical advice, probable diagnosis, or recommended treatments.