What Is Inflammatory Neuropathy?

Polyneuropathy refers to a clinical syndrome mainly manifested as symmetrical peripheral sensory disturbances of the extremities, paralysis of lower motor neurons, and / or autonomic nerve disorders.

Polyneuropathy refers to a clinical syndrome mainly manifested as symmetrical peripheral sensory disturbances of the extremities, paralysis of lower motor neurons, and / or autonomic nerve disorders.

Chinese name

Polyneuropathy

Foreign name

polyneuropathy

Polyneuropathy I. Causes and common diseases:

There are many causes of peripheral neuropathy, including poisoning, nutritional deficiencies or metabolic disorders, inflammatory or vasculitis, heredity, infection, and distant tumor effects.

Polyneuropathy 2. Differential diagnosis:

1. Periodic paralysis: more recurrent attacks, no sensory disturbances; serum potassium below 3.5 mmol / L during the onset, and low potassium manifestations on the electrocardiogram; the potassium supplementation soon improved.

2. Subacute joint degeneration: numbness and weakness in the distal extremities, but mainly deep sensory disturbances; cone bundle sign and tendon reflex enhancement.

3. Acute poliomyelitis: limb paralysis is distributed in spinal cord segments and is more asymmetric; there is no sensory disturbance; cerebrospinal fluid protein and cells are increased; electromyography has denervation.

Polyneuropathy 3. Inspection:

(1) Physical examination:

1. Distal symmetry of the distal limb is lacking in various senses, and it is distributed like gloves and socks.

2. May have paramotor neuron paralysis, showing muscle weakness, muscle atrophy and muscle bundle tremor, etc., the distal end is heavier than the proximal end; lower limb muscle atrophy, hand and foot sagging and walking gait when walking.

3. The tendon reflexes of the extremities weakened and disappeared.

4. The skin on the distal extremities is cold, sweaty or non-sweat, the nails of the fingers (toes) are crisp, the skin is thin, dry or desquamated, and the vertical hair is disturbed.

(2) Laboratory inspection:

1. Cerebrospinal fluid examination: Generally normal, if it is a demyelinating lesion, protein-cell separation can occur.

2. Blood tests: such as blood routine, blood biochemical and immunological tests, etc., help to determine the cause.

(3) Special inspections:

1. Electrophysiological examination: EMG showed denervation, sensory conduction velocity (SCV), and motor conduction velocity (MCV) slowed down.

2. Peripheral nerve biopsy: Degeneration of various myelin sheaths or axons can be seen.

Polyneuropathy 4. Principles of treatment:

(1) General treatment:

Severe cases in the acute phase, especially those with myocardial involvement, must stay in bed. People with quadriplegics should turn over regularly, passively exercise and massage, and put their limbs in a functional position. Splints or braces should be used on sagging hands and feet to prevent joint contracture and deformity.

(2) Drug treatment:

1. Neurotrophic drug treatment: Vitamin drugs such as vitamin B ₁ 100mg, once / day, intramuscular injection; vitamin B ₁₂ 250 500g, once / day, intramuscular injection. And treated with coenzyme A, adenosine triphosphate and so on.

2. Glucocorticoids: suitable for patients in the acute phase. Available dexamethasone, 10-15mg, once / day, intravenous infusion, for 7-10 days in a row; or prednisone 30mg / day, oral administration in the morning or in divided doses. Symptoms are gradually reduced after control.

3. Pain treatment: carbamazepine 0.1g, 3 times a day, orally; or oxcarbazepine or gabapentin or pregabalin, start with a small amount, increase the dose, orally.

4. More specific treatments: Nerve growth factor, good for nerve axonal damage (significant muscle weakness and muscle atrophy, low amplitude of NCV examination) and n-hexane poisoning peripheral neuropathy; Micopro or other vitamin B ₁₂ preparation Damage mainly caused by demyelination (numbness and other paresthesia are obvious, muscle atrophy is not obvious, and NCV examination slows down the conduction rate) and B vitamin deficient neuropathy are effective; thiozincate is effective for diabetic neuropathy (numbness and other paresthesia) (Obviously) works well.

(3) Other treatments:

1. Etiology treatment: Different treatments can be selected for different causes, such as anti-infection, promotion of toxin excretion, lowering blood sugar, application of glucocorticoids, etc.

2. Physiotherapy: Infrared, ultra-short wave is applied in the acute phase, and calcium ion and procaine ion are infiltrated after stabilization. Pulsed current and electrical stimulation therapy can be used during recovery and chronic periods.