Peripheral neuropathy

2021-02-05 12:00 AM

Polyneuritis due to lack of vitamin B1 is axonal damage, common in heavy workers with overly milled rice, pregnant women or postpartum diets.


Nerve roots are classified into the following 3 main groups:


Inflammation of multiple nerve roots.

Inflammation of one or more non-systemic nerves.

Types of polyneuritis

Polyneuritis due to lack of nutrition

Polyneuritis due to lack of vitamin B1

Polyneuritis due to lack of vitamin B1 is axonal damage, common in heavy workers with overage milled rice diet, pregnant women or postpartum dieting ... Start often from with a feeling of numbness in the lower extremities is mainly, sometimes there is cramping or pain in the calf at night with soft white oedema in the legs, especially in the legs and feet, maybe transient at first. Then the patient moves weakly. Sometimes it is difficult to breathe due to heart failure. On examination, the decrease or loss of sensation may be shallow and deep in the legs, opposite sides of the side. Muscle power is reduced or completely lost. The tendon reflex is reduced or evenly lost legs. Vitamin B1 treatment high dose of 100-400 mg/day intramuscularly.

Polyneuritis due to lack of vitamin PP

Often accompanied by vitamin B deficiency, sensory dominant disorders, mental disorders such as confusion, dementia with signs of skin symptoms such as erythema, platelets. There may be diarrhoea. Vitamin group B treatment with 2 capsules daily.

Polyneuritis caused by alcohol

Common in long time alcoholics (10 years or more) due to axon damage often in the lower extremities. It starts with a sensation of mainly the legs with a tingling or aching sensation and then difficulty walking. On examination, the decrease in sense of shallow feeling is mainly accompanied by decreased muscle tone in the legs. The tendon reflex is reduced or lost in the lower extremities. Often accompanied by Korsakoff syndrome include tremor, near memory loss and making up stories. Sometimes there is a paralysis of the cranial nerves. Treatment is by quitting alcohol and giving a high dose of vitamin B1.

Polyneuritis caused by intoxication

Lead poisoning

Common in glass coaters, plumber, battery factory ... Causing movement disturbances are mainly the upper limb stretching muscles, more rarely the paralysis of the anterior and outer paralysis of the lower leg. feet in combination with abdominal cramps, gums with grey rims, alkaline granulocyte anaemia, sometimes increased blood pressure. Treatment with BAL (dimercaprol) 200 mg syringe dose of 3 mg/kg intramuscularly for the first two days every 4 hours, on the third day every 6 hours and for ten days, twice-daily injection.

Arsenic poisoning

Symptoms are similar to alcohol poisoning, but the pain is often acute poisoning, often accompanied by digestive symptoms such as nausea, vomiting. The back of the hands and feet are thickened and horny, and the nails are thick and jellyfish. Determined by quantitative arsenic in urine, in hair and nails. Treatment with BAL

Other drugs

INH, Almitrine, metronidazole, vincristine, nitrofurantoin, cisplatin, disulfiram, amiodarone, dapsone, platinum, chloramphenicol, Taxol, Taxotere, ethambutol, hydralazine, imipramine, chloroquine, gold salt, indomethacin, phenytoin, thalidomide...

Polyneuritis caused by infection


Now rare thanks to extensive vaccination. Occurs only in malignant diphtheria forms due to diphtheria toxin. The first is paralysis of the pharyngeal muscle, then the eye muscle paralysis, then the limbs are paralyzed by the third or fifth week, dominant in the lower extremities. The disease is gradual and there is no specific treatment.

HIV infection

The lesions are mainly axonal, disorders mainly on the extremities and often associated with cytomegalovirus. There may be an antiviral response to HIV.

Metabolic polyneuritis


Complicated polyneuritis of diabetes is common. The early clinical manifestation is a feeling disorder in the legs and is symmetrical. No movement disorders occurred after a very long time. The examination has decreased or lost tendon reflexes, mainly in the lower extremities. Treatment is mainly blood sugar balance. Analgesic can use one of the following nonsteroidal anti-inflammatory drugs, tricyclic depression, carbamazepine, phenytoin, tramadol, lidocaine intravenous, alpha-lipoic acid.

Acute porphyria

Usually occurs after using barbituric with manifestations mainly weak movements of the limbs accompanied by paraesthesia, but examination found no objective sensory disturbances. The urine is red and then turns black in a moment. There is no specific treatment.

High blood urea, hypothyroidism, blood globulin disorder, degenerative starch disease, cancer

These are rare diseases.

Due to hereditary degenerative disease

Diseases Charcot- Marie- Tooth

Muscle atrophy and deformity of the foot with disturbances of feeling and lower limb movement.

Déjerine- Sotas disease

Thickening of peripheral nerves causes pain and also disturbs other sensations, sometimes accompanied by wobbly.

Inflammation of multiple nerve roots

There are no definitive data on the prevalence so far. This pathology is divided into two main groups: acute polyneuropathy (Guillain - Barré Syndrome) and chronic.

Guillain - Barré syndrome

The anatomical causes and characteristics of the disease

The Guillain-Barré syndrome is an acute inflammatory myelin multi-rooted neuropathy that causes major motor disorders, most of which are benign. This pathology has been described by Guillain since 1916. There is no difference between the sexes, appearing at any age but rarely before 5 years old. The incidence rate is 0.6 - 1.9 / 100,000 people. Diseases are sporadic, rarely into an epidemic. An outbreak has also been seen in Colombia following the rabies strain, in Jordanian following E. coli infection. Guillain-Barré syndrome usually occurs after an infection of the upper respiratory tract, ear, nose and throat rather than gastrointestinal infection. About 70% of cases appear after 1-3 weeks of infection. The identified agents were Campylobacter jejuni (32%), cytomegalovirus (13%), Epstein-Bar virus (10%) and Mycoplasma pneumonia (5%). Also seen 1-3 weeks after infection due to herpes virus, measles, erythema,

This syndrome is the immune response to a pre-existing infection because antibodies against gangliosides have been found. The molecular pathogenesis mechanism shows that there is a molecular similarity between the myelin epitope and the glycolipids of campylobacter, mycoplasma and other infectious agents, which is the starting point of the immune response. Antibodies against infectious agents cross-react with specific antigens of Schwann cells or axolemma (axolemma). The antibody binding to the target peripheral nerve induces inhibition of neurotransmission. Partial or full-length myelin destruction of the nerve axon, most pervasive and symmetrical, is associated with nonspecific inflammatory processes, there is oedema of small lymphocyte infiltration and subsequently activated lymphocytes and macrophages in the interstitial and periostitis regions in the nerve bundle. Lesions that normally destroy myelin start at the Ranvier node and then progress toward the cytoplasm of Schwann cells. Damage to myelin anterior and more than axon, that is why the majority of cases can be completely recovered. Only a few severe cases can damage the axon bed and of course it is difficult or impossible to recover.

Classification of Guillain - Barré syndrome

Acute inflammatory demyelinating polyneuropathy (AIDP) mainly degenerates myelin.

Acute motor axonal neuropathy (AMAN) mainly damages axons.

Acute motor-sensory axonal neuropathy (AMSAN) causes damage to the axon.

Miller-Fisher syndrome


Guillain - Barré syndrome has a shaping disease of a sensory and motor neuron syndrome, usually diffuse, mainly associated with decreased or lost tendon reflexes with the following stages:

Stage of symptom-setting: Onset is usually quiet but sudden with paraesthesia of the extremities, pain in the limbs or back pain and gradually the most difficult movement is the lower extremities. But sometimes there is only one weakness or asymmetric symptoms. The initial disorders then gradually spread from the top of the limb to the base of the limb or from the bottom of the foot to the top. There are also cases of limb initiation. Sometimes at first just nerve paralysis on the sides. This setting time depends on each case, usually in 6-10 days, sometimes only 24-48 hours. According to Castaigne et al. 1966 of 258 cases, 72% from 3-20 days, 8.1% over 20 days, 4.7% over 40 days and 14.3% less than 3 days. This period on average lasts 12 days. During this period there is no muscle atrophy, but attention may be present with respiratory failure.

Full-release phase: Usually after a week to 12 days, it will progress to full release. If typical, there is paralysis and systemic sensory disturbances, bilateral symmetry, possibly with damage to the cranial nerves. Sensory disturbances that spread to the base of the limbs or spread to the body. If the sensation spreads to the chest area, be alert for signs of respiratory distress. Examination shows that pain when squeezing into muscles is the pain of the nerve and also when tensioning it is pain caused by nerve roots. It is the root pain symptom that is not present in polyneuritis that helps us distinguish from Guillain - Barré syndrome. Severe cases can be disturbed to deep feeling with signs of decrease/loss of vibration, recognition of objects, position. Regarding movement, limb weakness or only localized in two lower limbs with different degrees from mild paralysis to complete paralysis. There is no muscle atrophy and jerking muscles. Sometimes cases of respiratory muscle paralysis causing acute respiratory failure need immediate emergency. Paralysis and swallowing account for about 30%, from mild to severe, with signs of choking, difficulty swallowing or complete failure to swallow. Before patients suffering from either of these disorders must be kept close to the emergency room. Other rarer cranial nerves are II, III, V (10-15%), XII (1.5-7%). The levels of sensory and motor disturbances are often inconsistent, unbalanced and disproportionate. The tendon reflex is reduced or lost in the extremities or just the legs. Rarely has a circular muscle disorder, if any, it is very discreet that is temporary difficulty urinating due to muscle weakness in the abdominal wall. Nervous plant disorders are often manifested by increased sweating, increased secretion of bronchial fluid and saliva, oedema of the extremities, heat disturbances in the apical extremities; even severe cardiac arrest or milder tachycardia, low blood pressure. May see dysregulation of blood sugar or hyponatremia due to increased secretion of ADH. This phase lasts about 1-3 weeks.

Recovery phase: Symptom recovery is the opposite of symptom-setting meaning which symptoms appear first after recovery, before recovery, and recovery is usually slow and slow. long weeks to months. Completely recoverable. If after 18 months the recovery becomes more difficult and less likely.


Cerebrospinal fluid: in the first week of the disease, cerebrospinal fluid can be normal, but from the second week on, there is a phenomenon of protein-cell dissociation and lasts for 4-6 weeks, then gradually decreases. Cells are typically less than 12 cells / mm3, protein (50 mg%. There is no association between increased protein and clinical severity, but when the protein increases for more than 6 weeks, the clinical progression is unfavourable. Gamma globulin level measurement shows that 88% of cases increase and it increases from week 1 If the cells in the CSF are more than 10 lymphocytes / mm3, especially more than 50 cells / mm3, peripheral neuropathy must be considered. Guillain - Barré syndrome itself caused by Lyme disease, recent HIV infection, or sarcoidosis.

Liver function tests: Increased liver enzymes should think of hepatitis A, B, C, Epstein - Barr virus infection or cytomegalovirus.

Anti-ganglioside antibodies especially anti-GM1 antibodies.

Electromyography: Typically, the sign of reduced apical motor conduction. The F-wave potential time is long and has a small motor action potential amplitude.


Table: Diagnostic standards.

Criteria needed

Support standards

- Weakness/paralysis diffuse and symmetrical

- Decreased/lost tendon reflexes in the lower extremities or both extremities

- Progression less than 4 weeks

- Eliminate porphyria, diphtheria, polio, myelitis, myasthenia gravis.

- Mild sensory disturbances

- Bilateral peripheral VII paralysis (50%)

- Nervous plant disorders: tachycardia

- Protein increases in cerebrospinal fluid from the second week, cells under 12 children.

- Electrical diagnosis: myelin damage


As usual, after 2 months, full recovery accounts for 57.3%, some are faster but also about 1 month (11.4%). About 80% recover completely. The frequency of recovery in 2 weeks is 50%, 3 weeks is 80% and 4 weeks is 90%. However, there are also 20% of cases that last longer, with incomplete recovery, leaving behind paraesthesia, or dyskinesia, of which 5% leave severe sequelae. If symptoms and signs progress for more than 8 weeks, the Guillain-Barré syndrome is virtually ruled out. After 18 months, there is no possibility of recovery. There are cases of movement disorders, feeling from the legs spread to the abdomen and to the chest ... called the Landry body. The first recovery is sensation followed by movement and finally the tendon reflex. Very rarely recurrence. The scary complications are respiratory paralysis (about 16-22% sometimes up to 30%) and pulmonary artery obstruction.


Usually, the prognosis of this pathology is good, benign, but there are also severe prognostic factors such as complete quadriplegia, duration of full development lasting more than 2 weeks, axon damage recorded by electricity. musculoskeletal, age over 50, must be ventilated or arrhythmia especially bradycardia and swallowing disturbances.


There is no specific treatment. If the respiratory muscles are paralyzed, then ventilate if the vital capacity decreases by about 30%. Should monitor vital capacity every 4 hours, if <1 litter (reduced below 12-15 ml/kg), respiration, positive pressure ventilation. As for swallowing disorder, then put in the stomach. Monitoring heart rate by monitoring if less than 60 times min, then atropine, if <50 times min, should be set to a pacemaker. Attention emergency cardiac arrest. In case of complete paralysis, it must be preoccupied every 1-2 hours to avoid the list of entries. Prophylaxis of embolism and limb deformity with heparin 5,000 units subcutaneously every 12 hours and elevation of the leg position about 100. Prednisolone 0.5 mg/kg daily for 5 to 10 days but results are unclear. Vitamin group B high dose combined with folic acid 5-10 mg/day. Now active treatment by plasma filtration with 250ml / kg 5 times every 7-10 days is also effective. If ineffective, add human immunoglobin 0.4g / kg daily for 5 days. Should incorporate physical therapy early.

Chronic multi-root neuropathy


The pathogenesis and clinical practice are similar to Guillain-Barré syndrome, but rarely, males more than females, typically appear between the ages of 40-60 and are associated with HLA DR3. Often weak limbs, intercostal muscles and cranial nerves VII, IX, X, XI and XII accompanied by numbness, stinging, and crawling, burning burn in the extremities. Bone tendon reflexes are reduced or lost. There may be popular oedema. Progressive periods lasting more than 2 months can be intermittent especially during pregnancy or advancement.


 Increased blood gamma globulin IgA, IgG or IgM. There is also the phenomenon of protein-cell dissociation 80-95%. The diagnostic electrolyte has a decreased transmission rate. Nerve biopsy showed degeneration of myelin and a decrease in the number of axons. Especially, magnetic resonance imaging with gadolinium can show root and peripheral nerve enlargement.


Prednisolone 1-1.5 mg/kg for 2 to 4 weeks alone or in combination with plasma filtration. Immunoglobulin intravenous injection showed quite good results. In case of non-response to corticosteroids, azathioprine should be given 2-3 mg/kg daily. Mycophenolate mofetil can be used as a starting dose of 1g twice daily, which can be increased to 500mg per month up to 1.5g twice daily. It is also possible to use cyclophosphamide 50-150mg daily and monthly intravenously for an additional 1g / m2. Or use cyclosporine 4-6 mg/kg daily. About 80% of patients responded well to the above treatments.

Inflammation of one or more nerves


Common damage to the cylindrical nerve, external sternum sciatic nerve, branch V1. Nerve thickening and irregularity. May see muscle atrophy of the affected area with a decrease or loss of pain sensation in the macules. There may be a tingling sensation. Biopsy of the skin of the affected area is recommended to confirm the diagnosis.

Colloid disease

Inflammation of the node around the arteries. Scattered nerve damage. Diagnosed by detecting antinuclear antibodies. Treatment with steroid or cyclophosphamide.

Pathology of near cancer

Nerve compression caused by metastasis causes pain along the damaged nerve.

Peripheral neuropathy caused by cup pressure

Causes of trauma, bursitis, arthritis ... Most commonly carpal tunnel syndrome (carpal tunnel syndrome). Treatment with topical corticosteroids or pressure surgery.