Dystrophic polyneuropathy

Introduction to dystrophic polyneuropathy Dystrophic polyneuropathy (symstrophic polyneuropathy) is a common type of polyneuropathy, caused by nutritional deficiencies or metabolic disorders, characterized by distal sympathetic sensory disturbances of the extremities, lower motor neuron spasm and/or autonomic dysfunction. . Lack of nutrients caused by various reasons, especially the lack of specific nutrients (such as vitamins), can affect certain functions of the central nervous system and/or peripheral nerves or cause pathological damage, produce some neuropsychiatric symptoms, and the lack of nutrients usually Something is mainly related to the lack of several substances. The causes of nutrient deficiencies are inadequate intake, excessive consumption, and increased physiological needs. Internal organs such as liver, pancreas and other diseases can cause abnormal metabolism of certain substances in the body. basic knowledge The proportion of illness: the incidence rate is about 0.007%-0.008% Susceptible people: no special people Mode of infection: non-infectious Complications: dysphagia, edema, hypotension

The cause of dystrophic polyneuropathy

Lack of nutrition (30%):

The disease is due to lack of nutrition, such as chronic alcoholism, pregnancy, chronic gastrointestinal diseases and post-operative B vitamin deficiency, the typical disease is vitamin B1 deficiency caused by vitamin B1 deficiency (beetle), some people think that vitamin B6 and Pantothenic acid deficiency can also cause peripheral nerve degeneration.

Metabolic disorders (20%):

Metabolic disorders such as diabetes, uremia, hematoporphyria, mucinous edema, acromegaly, amyloidosis and cachexia can also cause dystrophies and cause polyneuropathy. Thus, metabolic diseases have a great impact on the disease.

Pathological changes (20%):

The basic lesion is peripheral axonal degeneration with segmental demyelination, usually the longest myelinated nerve fiber lesions in the foot, followed by the myelinated fibers of the arm, and the late demyelinating lesions can extend to the nerve roots. It may also involve the vagus nerve, the phrenic nerve and the paraspinal sympathetic trunk. The anterior horn cells and dorsal root ganglion cells may have Nisslolyticism, suggesting that the axonal damage may occur. In some cases, the posterior column degeneration may occur, which may be secondary to the posterior root of the spinal cord. Lesion.

Nutritional disorder polyneuropathy prevention

Early treatment of primary diseases, reasonable diet, and alcohol withdrawal.

Nutritional polyneuropathy Complications, difficulty swallowing, edema, hypotension

There are no special records, depending on the degree of nutritional disorders, the severity of the disease is also different, so the symptoms and signs are diverse and the performance is different.

Symptoms of dystrophic polyneuropathy Common symptoms Nutritional disorders Sensory disturbances Powerless dysphagia Hypotension Edema Muscle tenderness Dull pain cachexia

1. Most patients have obvious symptoms, complaining of weakness, paresthesia and pain, usually insidious onset, slow progress, and even worse in a few days, the symptoms often start at the distal end of the limb, and can slowly involve the proximal end without symptoms. It usually appears earlier and heavier than the upper limbs.

The most common complaint is dyskinesia, and 1/4 of those with paresthesia and pain are characterized by persistent dull pain in the foot or lower extremity, transient tearing or stinging similar to spinal cord spasm, or pressure or tightness of the foot or gastrocnemius. The feeling of the lower limbs, etc., the patient feels cold feet or soles, the burning sensation of the foot, the degree of sensation abnormality is fluctuating, and some patients can not walk because they can not bear the friction of the clothes, and the touch can be aggravated is a characteristic performance. The type of sensation is not fixed, and the boundary between the affected part and the normal part is unclear.

2. Physical examination showed visible movement, sensory and reflex abnormalities, and the signs were mostly symmetrical. The distal end was more severe than the proximal end, the lower limbs were heavier, the foot was drooping or the wrist was drooping, sometimes the proximal muscles were weak, the squat standing difficulties, and the complete lower extremity paralysis Rare, more common knees, contractures can not cause exercise.

Gastrocnemius and deep tenderness of the foot are specific signs. The lower extremity tendon reflexes disappear early, and mild muscle weakness can occur. A few patients have symptoms of paresthesia and pain, knee reflexes and tendon reflexes can be preserved, and peripheral sympathetic nerves are involved. Signs include the soles of the feet, excessive secretion of sweat from the back of the feet and palms (a common manifestation of alcoholic dystrophic neuropathy) and orthostatic hypotension. Most patients have only limb involvement, normal chest, abdomen and ball muscles, and vagus nerve involvement in the late course of the disease. There are hoarseness and dysphagia.

3. Severe patients with stagnant edema in the lower extremities, pigmentation and thinning of the skin; and plantar penetrating ulcers and painless destruction of the foot and joints, namely ulcer-osteolytic neuropathy or Charcot forefoot (Charcot's forefeet) is rare, and it is a major cause of neuropathic arthropathy that recurrent trauma and co-infection in a dull area.

Some asymptomatic patients need physical examination or electromyography to find evidence of peripheral neuropathy, which is characterized by lower extremity muscle tenderness, decreased muscle volume, weakened or disappeared tendon reflexes.

4. There is no abnormality in cerebrospinal fluid. The CSF protein is slightly increased in a few patients. The EMG is mild to moderately moving. The sensory conduction velocity is slowed down, the amplitude of the sensory action potential is significantly reduced, the conduction velocity of the proximal nerve is normal, and the distal end is slowed down. Denervation muscles may have fibrillation potential and the like.

Examination of dystrophic polyneuropathy

1. There was no abnormality in cerebrospinal fluid examination, and a small number of patients had a slight increase in CSF protein.

2. Hematuria routine, blood sugar, electrolytes, blood vitamin B level and suspected poison detection, have differential diagnosis significance.

3. The electromyogram showed mild to moderate movement, the sensory conduction velocity slowed down, the sensory action potential amplitude decreased significantly, the proximal nerve motor conduction velocity was normal, the distal end slowed down, and the denervated muscles had fibrillation potential.

Diagnosis and differentiation of dystrophic polyneuropathy

1. Mainly based on medical history, such as chronic alcoholism, pregnancy, chronic gastrointestinal diseases and post-operative, there are various causes of nutrient deficiency, or metabolic disorders such as diabetes, uremia, cachexia and other secondary nutritional disorders .

2. Clinical features such as distal sympathetic sensory disturbances, lower motor neuron sputum and/or autonomic dysfunction.

Attention should be paid to the identification of multiple neuropathy caused by infection, immune diseases and certain metal poisoning.

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