herpes simplex encephalitis
Introduction
Introduction to herpes simplex encephalitis Herpes simplex encephalitis, also known as herpes viral encephalitis, can be found in both primary herpes simplex virus infections and in recurrent patients. The disease is sporadic, and it is the most common type among non-epidemic viral encephalitis. According to statistics, it accounts for 10% to 20% of viral encephalitis, and the condition is serious and the prognosis is poor. The pathogenesis of herpes virus encephalitis is complicated. In recent years, studies have shown that part of the mechanism of brain tissue damage caused by viral infection is the result of damage of immunopathological response. basic knowledge The proportion of illness: 0.001% Susceptible people: no specific people Mode of infection: non-infectious Complications: coma
Cause
Causes of herpes simplex encephalitis
Virus infection (45%):
The pathogen of herpes simplex is human herpes simplex virus. It is classified into the human herpesvirus family A subfamily, herpes simplex virus genus, and is divided into two subtypes: HSV-1 and HSV-2. The HSV-1 subtype mainly invades the waist. The above parts, especially the face, brain tissue, etc.; and HSV-2 mainly invade the lower part of the waist, especially the genitals, so it is called genital herpes; but this distinction is not strict.
Secondary infection (25%):
One of the complications caused by the failure of the patient to be cured in time after infection with herpes simplex virus. The pathogenesis of herpes virus encephalitis is complicated. In recent years, studies have shown that part of the mechanism of brain tissue damage caused by viral infection is the result of damage of immunopathological response.
Maternal and child infections (30%):
The mother is infected with the herpes simplex virus and transmitted to the fetus through the placenta or the birth canal. This causes the fetus to carry herpes simplex virus after birth.
Pathogenesis
In children and young people, primary HSV infection can cause encephalitis, which can be a consequence of viremia, but it may also be caused by herpesviruses directly invading the brain along the nascent pharynx. Animal studies have shown that HSV- 2 is more toxic to the nervous system than HSV-1. Since HSV-1 is mainly associated with lip infection, and HSV-2 is mainly caused by genital infection, it is clear that HSV-1 is more accessible and invades the brain, so herpes virus brain More than 95% of inflammation is caused by HSV-1 infection; in neonates, HSV-2 is common.
The encephalitis caused by adult herpes simplex virus is characterized by the most serious damage to the temporal lobe. Most patients have a history of herpes simplex, or serum HSV-1 antibody positive. The occurrence of encephalitis mainly comes from HSV-1 latent infection in vivo. Reactivation, when the body's immune function is low, HSV lurking in the trigeminal ganglion (half-month) or spinal ganglia invades the central nervous system along the axons, causing damage to the brain tissue; or the virus is latent in the central nervous system, in a certain Encephalitis occurs when activated under these conditions, and such patients may have no viremia process.
The pathogenesis of herpes virus encephalitis is complicated. In recent years, studies have shown that part of the mechanism of brain tissue damage caused by viral infection is the result of damage of immunopathological response.
The encephalitis caused by herpes simplex virus is acute necrotic encephalitis, which shows asymmetric diffuse whole brain damage, forming hemorrhagic necrotic foci of different sizes. The damage is caused by the temporal lobe, the frontal lobe and the marginal lobe are the heaviest, and also affect Meninges, lesions can be damaged first and one side of the cerebral hemisphere, and then extended to the contralateral side, half of the case necrosis is limited to one side, about 1/3 of the cases are limited to the temporal lobe; even if the patient's bilateral cerebral hemisphere is damaged, often one Side is heavy, diffuse swelling around the hemorrhagic necrosis, softening, degeneration of nerve cells in the center of the lesion, necrosis, loss, type A eosinophilic inclusions in the nucleus of peripheral neurons and glial cells, with lymphocytes, plasma cell infiltration Under electron microscope, it is observed that there are virus particles in the nucleus of nerve cells in brain tissue specimens.
Prevention
Herpes simplex encephalitis prevention
prevention:
1. Avoid kissing with patients and sharing toiletries;
2, should wash your hands after touching, can not blink your eyes;
3. Avoid eating arginine-containing foods;
4. Eat food rich in lysine or directly supplement lysine;
5, eat more alkaline foods, eat less acidic foods.
Complication
Herpes simplex encephalitis complications Complications coma
Complications are often coma, and cerebral palsy can occur in severe cases.
Symptom
Herpes simplex encephalitis symptoms common symptoms spotted hemorrhoids convulsions fainting hallucinations central fever coma convulsions dynamism
The disease can occur at any age, often acute onset, but also subacute, chronic and recurrent cases.
1. Prodromal period: manifested as dizziness, headache, systemic pain, etc., followed by upper respiratory tract infection symptoms, fever can reach 38 ~ 40 ° C, only some cases of skin herpes, this period generally does not exceed 2 weeks.
2. Neuropsychiatric symptoms: It has a variety of manifestations. Early manifestations of mental symptoms are prominent, including personality changes, behavioral abnormalities, unanswered questions, disorientation, hallucinations, delusions, amnesia, aphasia, etc., may be the virus through the trigeminal nerve And the early olfactory bulb invasion of the temporal lobe, frontal lobe, and marginal system.
As the disease progresses, the brain tissue necrosis appears, and the patient shows disturbance of consciousness, such as drowsiness, lethargy, paralysis, coma, etc.; causes convulsions, convulsions, hemiplegia and cranial nerve dysfunction, such as eyeball deviation, pupillary unequal, hemianopia, etc. With intracranial hypertension, the patient's neck is stiff, the muscle tension is increased, and there is pathological reflex. In some cases, the brain is in a state of tonicity in the early stage. In severe cases, cerebral palsy may occur.
Examine
Herpes simplex encephalitis
EEG examination
Diffuse high-wavelength slow waves often occur, with abnormalities in the unilateral or bilateral sacral area, and even spikes and spikes in the temporal region.
2. Imaging changes
CT scans can be normal, and local low-density areas can also be seen; MRI can help to detect lesions with long T1 and long T2 signals in the brain parenchyma.
3. Cerebrospinal fluid examination
The pressure is normal or slightly increased, the number of cells is increased, the protein is moderately increased, and the sugar and chloride are normal.
4. Detection of herpes simplex virus antigen
Detection of herpes simplex virus-DNA.
5. Display under light microscope
The important feature of brain histopathology is hemorrhagic necrosis. Under electron microscope, it is the core type of CowdryA inclusion body. It can be seen in the oligodendrocytes and nerve nuclei in the necrotic area or nearby, and there may be Doge inclusions in one nucleus. The pathogen examination is that intracellular virus particles can be found under electron microscope; brain tissue specimens can also be used for PCR, in situ hybridization, etc. to detect viral nucleic acids, or to isolate and culture viruses.
Diagnosis
Diagnosis and diagnosis of herpes simplex encephalitis
Herpes zoster viral encephalitis
The disease is rare, mainly invading and lurking in the nerve cells of the posterior root ganglia of the spinal nerve or the sensory ganglion of the brain cells, rarely invading the central nervous system. The clinical manifestations are confusion and ataxia, and the symptoms and signs of focal brain damage. The degree of the lesion is light and the prognosis is good. The patient has a history of herpes zoster in the chest and waist, CT has no hemorrhagic necrosis, and the serum and cerebrospinal fluid are positive for the virus antigen, antibody and viral nucleic acid, which can be identified.
2. Enteroviral encephalitis
More common in summer and autumn, it can be popular or sporadic. Clinical manifestations of fever, disturbance of consciousness, balance disorders, repeated seizures, and paralysis of the limbs. Gastrointestinal symptoms at the beginning of the disease, virus isolation in the cerebrospinal fluid or positive PCR test can help diagnose.
3. Cytomegalovirus encephalitis
It is rare in clinical practice and is common in patients with immunodeficiency or long-term use of immunogenic ampoule.
4. Acute disseminated encephalomyelitis
More acute after infection or vaccination, manifested as symptoms and signs of brain parenchyma, meninges, brainstem, cerebellum and spinal cord. Symptoms and signs are diverse, and critically ill patients may have conscious and psychiatric symptoms.
