Viral meningitis is a relatively common form of meningitis. The characteristic of this type of meningitis is that it develops very quickly, causing great pain to patients. If it is not treated well, it may lead to some sequelae and even have a greater impact on the patient's future life. There are many causes of viral encephalitis, the most common of which is enterovirus infection, as well as mumps virus and lymphocytic choriomeningitis virus. What causes viral encephalitis? With the development of virological research, especially tissue cell culture, blood and cerebrospinal fluid infection etiology detection technology, it has been made clear that most of the diseases are enterovirus infections, followed by mumps virus and lymphocytic choriomeningitis virus, and a few are herpes viruses including herpes simplex virus and varicella-zoster virus. In addition, viruses such as infectious mononucleosis virus and cytomegalovirus can occasionally cause this disease. Enterovirus is a smallest non-enveloped RNA virus that can survive in sewage for a long period of time. Humans are the natural host of enterovirus. Once enterovirus enters the human body, it can enter the cell cytoplasm and damage and kill the cell. Enteroviruses are generally divided into three types, namely poliovirus, coxsackievirus and echovirus. In addition, there are enteroviruses that have not yet been classified. Each of these enteroviruses has many subtypes. For example, Coxsackievirus has type A and type B, but both types can cause viral meningitis, and occasionally encephalitis and acute cerebellar ataxia. Echovirus can be isolated from normal feces through cell culture and is generally not pathogenic. There are more than 30 serotypes of echovirus. Pathogenesis of viral meningeal diseases The virus enters the lymphatic system through the intestines (such as enterovirus) or respiratory tract (such as adenovirus and rash disease) to multiply, and then infects certain extracranial organs through the bloodstream (arboviruses enter the bloodstream directly). At this time, the patient may have systemic symptoms such as fever. In the later stage of viremia, it enters the central nervous system and enters the cerebrospinal fluid through the choroid plexus, causing central nervous system symptoms. If the host develops a strong immune response to viral antigens, it will further lead to demyelination and damage to vascular and perivascular brain tissue. The virus can also cause myocarditis, pharyngitis, intercostal muscle pain and skin damage in the human body. Pathological changes are mostly diffusely distributed, but may also be prominent in certain cerebral lobes and tend to be relatively localized. Gross observation of the brain generally shows no special abnormalities, except for engorgement of blood vessels on the surface of the brain and cerebral edema. Extensive congestion and edema of the meninges and/or brain parenchyma, accompanied by infiltration of lymphocytes and plasma cells. The lesions are mainly in the pia mater. Mononuclear cell infiltration can be seen in the arachnoid membrane. In the superficial layer of the brain, there may be vascular cuffs formed by perivascular inflammatory cell infiltration. The nerve cells in the perivascular tissues may degenerate and necrotize, and the myelin sheath may collapse. However, there was no evidence of inflammatory changes or neuronal necrosis in the deep brain and spinal cord tissues. Moreover, in patients with encephalitis, obvious demyelinating pathology is seen, but the related neurons and axons are relatively intact. This pathological feature represents the body's immune response stimulated by viral infection, suggesting the pathological characteristics of "post-infectious" or "allergic" encephalitis. Warm reminder: With the above introduction to the causes of viral meningitis, I believe everyone has a deeper understanding of the disease. The patient's life may be in danger due to brain herniation caused by increased intracranial pressure, so the observation and care of intracranial hypertension is very important. Closely monitor vital signs and pupil changes; observe the location, duration, and severity of headache; pay attention to the frequency and characteristics of vomiting; ensure early detection and treatment of intracranial hypertension. |
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