Neurological Lyme disease

Introduction to neurological Lyme disease Lyme's disease (LD) is a kind of vector-borne disease that has been recognized in recent years as a natural epidemic of humans and animals and involving multiple organs of the human body. About 15% and 8% of patients showed significant signs of neurological symptoms and heart involvement, respectively. The nervous system can be manifested as meningitis, encephalitis, chorea, cerebellar ataxia, encephalitis, motor and sensory radiculitis, and myelitis, but with meningitis, encephalitis and radiculitis More common. The lesion can be recurrent, and occasionally. basic knowledge The proportion of illness: 0.002% Susceptible people: no special people Mode of infection: non-infectious Complications: joint pain

Cause of neurological Lyme disease

(1) Causes of the disease

The pathogen of Lyme disease is BB, which is 10 to 39 m in length and 0.2 to 0.25 m in width. Gram staining is negative, and Giemsa staining is purple-red. It grows well in BSK medium at 30-37 °C. A hard bite carrying BB causes infection and causes clinical symptoms.

(two) pathogenesis

1. Pathogenesis BB enters the human body and spreads to the whole body with blood flow, and can exist in the body for a long time, thus inducing complex inflammatory reactions. The histological damage of Lyme disease mainly manifests as inflammatory exudation. The exudate mainly contains lymphocytes, tissue cells and plasma cells. BB can be isolated from a variety of specimens of patients with Lyme disease such as blood, skin, central nervous system, ocular, synovial fluid, and myocardium. BB is mainly a pathogen of extracellular parasitism. But there is growing evidence that BB can adhere to and invade human cells such as fibroblasts and endothelial cells. Experimental studies have shown that BB can enter the CNS through the blood-cerebrospinal fluid barrier in the early stage of Lyme disease. BB entering the cell can escape the effects of host immune response and antibiotics, proliferate and cause clinical symptoms.

In addition, BB antigenic variation or OspA/OspC changes may be the mechanism by which extracellular BB evades host immune responses, causing relapsed Lyme disease. BB can stimulate the production of a variety of inflammatory cytokines such as IL-1, TNF-, cytokines may play a role in the pathogenesis of Lyme arthritis. BB-induced cytokines, especially IL-6 and autoimmune mechanisms are involved in the development of Lyme neuropathy. Therefore, it is currently believed that the pathogenesis of this disease is related to the direct effects of BB and the abnormal immune response.

2. The pathologically damaged skin is characterized by eosinophil infiltration, occasionally vasculitis or vascular changes; the surrounding skin is mainly around the perivascular and interstitial lining of lymphocytes with a small number of eosinophils and Plasma cell infiltration. In the synovial fluid of patients with arthritis, lymphocytes and plasma cells are contained. A small number of patients may develop chronic lesions similar to rheumatoid arthritis, such as synovial membrane, vascular proliferation, and erosion of bone and cartilage. Endocardial biopsy revealed extensive lymphocytic infiltration around the myocardial blood vessels.

Neurological Lyme disease prevention

1. Strengthen personal protection and eliminate cockroaches and rodents.

2. Strengthen the education of this disease, travel in the wild, especially in the forest areas and mountainous areas, should pay attention to self-protection, wear long-sleeved clothes and trousers, use insect repellent on clothing to prevent cockroaches, most Good not to sleep.

3. If you find a bite, or if your skin has erythema, you should go to the hospital for examination. Don't be numb. Early diagnosis and treatment are the key to curing Lyme disease. Since the disease was officially named in 1984, many patients and even medical workers in China are still unfamiliar, and they should be vigilant to avoid misdiagnosis and missed diagnosis.

Neurological Lyme disease complications Complications joint pain

The disease invades multiple organs and systems of the human body. It is both a complex clinical manifestation and can be considered as a variety of complications. Early signs of chronic migratory erythema, accompanied by fever, sweating, fatigue, weakness, headache, neck stiffness and muscle, bone and joint pain and other symptoms; later, joint, heart and nervous system damage. If left untreated after illness, it can cause permanent disability.

Symptoms of neurological Lyme disease Common symptoms Local erythema erythema, lymphadenopathy, nausea, chills, fever

Lyme disease has the same clinical features as other spirochetes, usually with staged seizures, alternating with remission and seizures. The incubation period is 3 to 32 days, with an average of 7 days. Clinical manifestations are diverse and can be divided into three phases. Early clinical manifestations include stage I and stage II. Stage I is mainly characterized by systemic infections (fever, headache, nausea, vomiting, and local lymphadenopathy) and characteristic skin lesions (chronic migratory erythema). Chronic migratory erythema of the skin, found in most cases. At the beginning, it is common to have erythema or papules in the bite area, gradually expanding, forming a ring shape, with an average diameter of 15 cm, the center is slightly hardened, and the outer red boundary is unclear. The lesions are in one or more locations. More common in the thigh, groin and armpits. Partially hot and itchy. At the beginning of the disease, there are often symptoms such as fatigue, chills and fever, headache, nausea, vomiting, joint and muscle pain, and meningeal irritation. Local and systemic lymph nodes can be swollen. Occasionally splenomegaly, hepatitis, pharyngitis, conjunctivitis, iritis or testicular swelling. Skin lesions generally last 3 to 8 weeks. Stage II is a few weeks or months after onset, and approximately 15% and 8% of patients have significant signs of neurological symptoms and heart involvement, respectively. The nervous system can be manifested as meningitis, encephalitis, chorea, cerebellar ataxia, encephalitis, motor and sensory radiculitis, and myelitis, but with meningitis, encephalitis, and radiculitis More common. The lesion can be recurrent, and occasionally it can develop into dementia and personality disorder.

In a few cases, 3 to 10 weeks after the onset of skin lesions, different degrees of atrioventricular block, myocarditis, pericarditis and left ventricular dysfunction were involved. Heart damage usually lasts only a few weeks, but can recur. A few weeks after the stage III infection, about 80% of patients have varying degrees of joint symptoms, such as joint pain, arthritis or chronic aggressive synovitis. Large joints such as knees, elbows, and hips are often present, and tissues around the facet joints can also be affected. The main symptoms are joint pain and swelling, and the knee joint can have a small amount of fluid. Frequent recurrent attacks, a small number of patients with large joint lesions can become chronic, accompanied by destruction of cartilage and bone tissue. A small number of patients in this period may have chronic neurological damage and chronic atrophic dermatitis. Some patients may also have mental abnormalities. Cases with impaired eyes, early manifestations of conjunctivitis, late manifestations of uveitis, optic neuritis, iridocyclitis, keratitis. This period generally begins 2 months or more after the illness and lasts for several months to several years.

Examination of neurological Lyme disease

1. Blood routine examination of white blood cells is mostly normal, individual can be moderately increased, 60% of patients with increased lymphocyte percentage.

2. About half of the patients had a mild, moderate increase in erythrocyte sedimentation rate.

3. CSF pressure increases, white blood cells count to hundreds, of which lymphocytes are dominant, accounting for 70% to 100%, protein content is slightly elevated, sugar and chloride are normal or slightly lower.

4. Specific IgM and IgG antibodies in blood and CSF generally reach a peak 4 to 6 weeks after onset, and decrease with the antibiotic treatment titer in about 10 weeks, but need to be alert to false positive and false negative reactions. ELISA indirect immunofluorescence (IFA), immunoblotting (WB) and other methods are generally used to detect specific antibodies in blood.

5. Pathogen detection There are PCR and isolation of pathogens from blood, CSF, and skin samples using BSKII medium. X-ray of the skull base, chest X-ray, electrocardiogram, brain CT, MRI examination, etc., have important clinical significance for differential diagnosis.

Diagnosis and diagnosis of neurological Lyme disease

The early symptoms of this disease are not typical, the incidence of insidious attacks, the incubation period can be as long as several months to one year, the course of recurrence and remission, sometimes misdiagnosed as tuberculosis, viral meningitis, Bell palsy, multiple sclerosis. It is also necessary to distinguish skin, heart, joint and nervous system diseases caused by various other causes, such as rheumatic fever, erythema multiforme, rheumatoid arthritis and the like.

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