Leprosy peripheral neuropathy

Introduction to leprosy peripheral neuropathy Leprosy peripheral neuropathy primarily affects the posterior root ganglia or sensory fibers, producing sensory symptoms. Leprosy is a chronic infectious disease caused by M. leprae, and the skin and peripheral nerves are the main target tissues of M. leprae. The clinical manifestations are numb skin lesions, large nerves, severe cases and even limb disability. Peripheral neuropathy has a loss of sensation, muscle weakness and atrophy, a decrease in tendon reflexes, and vasomotor symptoms, either alone or in any combination. basic knowledge The proportion of the disease: the incidence is rare, the incidence rate is about 0.001% Susceptible people: no special people Infection: Through nasal and oral secretions, sweat, tears, milk, semen and vaginal secretions Complications: erythema, iridocyclitis, neuritis

Causes of leprosy peripheral neuropathy

(1) Causes of the disease

Leprosy is mainly transmitted through nasal and oral secretions, sweat, tears, milk, semen and vaginal secretions and other minor fluid damages. After the leprosy invades the human body, it first lurks in the macrophages and peripheral nerves. In the cell, whether the pathogenesis after the infection or the evolution process after the disease depends on the immune state of the body. The human body's response to M. leprae is mainly cellular immunity, although it can also produce specific antibodies, but inhibit and kill. M. leprae does not work.

(two) pathogenesis

In the state of strong cellular immunity, M. leprae is eliminated by macrophages without disease. In the case of abnormal cellular immune function, depending on the tissue response to M. leprae, it can be evolved into three different pathological types, namely tuberculosis. Type (tuberculous leprosy), lepromatous leprosy and borderline leprosy.

Patients with tuberculosis-type leprosy have strong cellular immunity and can control the lesions in a limited lesion, mainly involving the peripheral nerves and skin. The internal organs are rarely affected. Because the lesions contain very few bacteria, the disease progresses slowly and the infection progresses. Low in nature, the body of patients with lepromatous leprosy is deficient in the cellular immunity of M. leprae. A large number of M. leprae in the lesions breed, which is highly contagious. It not only affects the skin and peripheral nerves, but also invades the nasal mucosa, liver and spleen. Lymph nodes and testes, the cell immune status of patients with borderline leprosy is between the tumor type and the tuberculosis type. It can have both types of pathological changes, or it can be more biased to a certain type, called metamorphosis or partial tuberculosis. type.

The mechanism of peripheral nerve damage in leprosy is related to peripheral nerves such as caseous necrosis, fibrosis, proliferative inflammation, and ischemic damage caused by vasculitis. Vasculitis mainly involves small blood vessels of the epicardium, which can be expressed as Neoplastic vasculitis of granulomatous vasculitis or immune complex type, immunohistochemical staining revealed mycobacterial antibody deposition on peripheral nerves and blood vessel walls, and Chimelli et al also found that the adventitial blood vessels were occluded by inflammatory tissue, resulting in occlusion The nerve tissue is a focal ischemic infarction.

Tuberculosis type leprosy often invades the auricular nerve, ulnar nerve and phrenic nerve, causing nerve enlargement. Tuberculosis-like necrosis can be seen in nerve biopsy. There are granuloma formed by lymphocytes and epithelioid cells. Necrosis can liquefy to form so-called nerve abscess. Both the inner and outer membranes showed a large number of lymphocytic infiltration, small blood vessel hyperplasia, endothelial cell swelling, luminal stenosis, granulomatous vasculitis in the epicardium, fibrosis in the recovery period, nerve enlargement, texture hardening, acid-fast staining It is generally difficult to find acid-fast bacilli, both myelinated and unmyelinated fibers are severely damaged, and the number is significantly reduced. The remaining nerve fibers are characterized by axonal degeneration and segmental demyelination.

The affected nerves of lepromatous leprosy also became thicker, diffuse lymphocytic infiltration was observed in the neuroendocardium, and the type of epicardial vasculitis was different from that of tuberculosis. Most of them were immune complex type necrotizing vasculitis, and the number of nerve fibers was significantly reduced. Myelin and axonal coexistence coexist, acid-fast staining can be found in Schwann (Snow) cells and macrophages, and macrophages phagocytose a large number of M. leprae to form a so-called "leprobe", leprosy Lipids accumulate in macrophages to form so-called foam cells.

Chimelli (1997) analyzed 53 cases of gastrocnemius neuropathy, the dorsal branch of the ulnar nerve, and the biopsy pathology of the superficial branch of the radial nerve. The results showed that 40 cases (75%) of inflammatory lesions and 7 cases of granulomatous reaction (1.3%) There were 35 cases (66%) with different degrees of fibrosis and 7 cases (1.3%) with intimal vascular hyperplasia. Most of them had different degrees of axonal degeneration and nerve fiber loss, and some were completely lost, 9 cases (1.7 cases) %) visible myelin degeneration and regenerative response, 15 cases (28%) were found in vascular endothelial cells, Schwann cells and macrophages.

Leprosy peripheral neuropathy prevention

To control and eliminate leprosy, we must adhere to the principle of prevention first, implement the principle of active prevention and control, control infection, and implement the practice of investigating, segregating, and treating, discovering and controlling infectious diseases, and cutting off infection. Ways, giving regular medications, while improving the immunity of the surrounding natural population, can effectively control infection and eliminate leprosy.

In view of the current prevention of leprosy, the lack of effective preventive vaccines and ideal preventive drugs, it is necessary to apply various methods to early detection of patients in prevention and treatment methods, and to promptly give regular joint chemical treatment to patients found, Children in endemic areas, family members of patients, and close contacts with both lepronin and tuberculin reactions can be given BCG vaccination or given effective chemotherapy for prophylactic treatment.

Leprosy peripheral neuropathy complications Complications, erythema, iridocyclitis, neuritis

Skin lesions can be one or more, usually in a lighter color than the surrounding normal skin. Sometimes the damage can be red or copper, with macules, papules, plaques, diffuse infiltration, nodules, Ulcers are common, most skin lesions are numb and sweat-free, but a few have itching or itching.

The immunoreactive damage induced by leprosy antigen refers to the release of antigen after death of leprosy in the body, which induces immune response and tissue damage, such as leprosy nodular erythema, iridocyclitis and neuritis. Appears before skin and peripheral nerve damage, but sometimes it can occur earlier, becoming a first-time and prominent performance, often causing misdiagnosis.

Symptoms of leprosy peripheral neuropathy Common symptoms Inability to dystrophic sensation Separation of sensory impairments Perforation of toes and short bones to dissolve peripheral nerve damage

1. Characteristics of peripheral nerve damage

The peripheral nerve damage of leprosy is most prominent in tuberculosis type, the tumor type is lighter, and the boundary type is between the first two types. The most commonly involved nerves are the auricular nerve, ulnar nerve, phrenic nerve, phrenic nerve and sural nerve. The cranial nerves can also be affected, with the facial nerve and the trigeminal nerve being common.

2. Sensory damage manifestations of leprosy peripheral neuropathy

Most of them suffer from loss of feeling and cause attention due to painless limb damage. The degree of sensory involvement is temperature, pain and touch. Deep feeling is rarely affected. Clinically, there are sometimes deep sensory separation and painful touch separation. The syringomyelia is confused. The distribution of sensory disturbances is mostly flaky. Because the autonomic nerve endings are also destroyed, it is accompanied by local sweating. This is a feature of intradermal nerve involvement. The nerve trunk and nerve roots are rare. Type leprosy can have a glove-like sensory disturbance, accompanied by a noticeable coldness at the distal end of the limb, which is different from the sensory disturbance of gloves and socks caused by other peripheral neuropathy.

3. Exercise involvement of leprosy peripheral neuropathy

When the sensory disturbance develops to a certain extent, exercise can be involved. When the ulnar nerve is violated, the interosseous muscle atrophy can occur, which is a claw-like hand. When the common peroneal nerve is paralyzed, there is a foot drop, and the muscle weakness rarely exceeds the elbow and knee joint. .

4. Peripheral autonomic involvement

It can cause skin dystrophy at the end of the limb, which is characterized by short finger toe, shedding, osteolysis, foot perforation and Charcot joint, leprotic peripheral neuropathy is chronic proliferative inflammation, subcutaneous sensory nerve can reach hypertrophy, and common to the auricular nerve and ulnar nerve .

5. Neuromuscular electrophysiological examination

Neurogenic damage, motor and sensory conduction velocity are slowed down. According to Becx-Bleumink's experience, 65% of leprosy patients with neurological damage have no symptoms, so electrophysiological examination is very important for the detection of preclinical peripheral nerve damage.

Examination of leprosy peripheral neuropathy

1. Leprosy smear examination

It mainly scrapes the tissue fluid from the skin and mucous membranes, and can be used for lymph node puncture if necessary.

2. Blood test

Including blood sugar, liver function, kidney function, erythrocyte sedimentation routine examination; rheumatism series, immunoglobulin electrophoresis and other serological tests related to autoimmunity; serum heavy metal (lead, mercury, arsenic, antimony, etc.) concentration detection, important for differential diagnosis significance.

3. Skin lesions can not be diagnosed, pathological biopsy of skin lesions should be done. Histopathological examination has important significance for the diagnosis, classification and efficacy evaluation of leprosy. The active lesions should be selected, and the fat layer should be deep, such as damage. Differently, it is necessary to cut two inspections at the same time, which is valuable for the diagnosis of boundary leprosy.

4. Neuromuscular electrophysiological examination is very important for the detection of preclinical peripheral nerve damage.

Diagnosis and diagnosis of leprosy peripheral neuropathy

diagnosis

Diagnostic criteria for leprosy:

1 skin lesions with or no numbness.

2 surrounding or cutaneous nerves are thick.

3 skin lesions were positive.

4 lesion biopsy has leprosy-specific changes.

Among these 4 criteria, it is necessary to meet more than 2 criteria to diagnose leprosy; on the basis of skin damage, according to the clinical characteristics of nerve damage around leprosy, leprosy may be considered, and the diagnosis may be based on skin biopsy or scraping to find leprosy. Neurobiopsy is also of great value in understanding peripheral nerve damage and the diagnosis of leprosy. The leprosy test can help with diagnosis.

Differential diagnosis

The differential diagnosis of this disease includes ischemic peripheral neuropathy, toxic peripheral neuropathy, spinal muscular atrophy and dystrophic peripheral neuropathy.

Nerve coarsening needs to be differentiated from amyloid peripheral neuropathy and hereditary peripheral neuropathy, and sensory separation. Hand and foot ulcers should be distinguished from syringomyelia and hereditary sensory neuropathy.

The diagnosis of biopsy disease should be distinguished from vascular inflammatory peripheral neuropathy and sarcoidosis with peripheral neuropathy.

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