OVERVIEW
Herpes simplex encephalitis is the most common viral infectious disease of the central nervous system caused by herpes simplex virus. It often involves the temporal and frontal lobes of the brain and the limbic system, causing hemorrhagic necrosis of brain tissue and metaplastic brain damage.
Causes
Herpes simplex virus is a neurophilic DNA virus, which is divided into type I and type II. Nearly 90% of herpes simplex virus is caused by type I virus, and the rest is caused by type II. The virus first causes primary infection in the oral cavity and the respiratory tract for 2-3 weeks, and then retrogrades along the branches of the trigeminal nerve through the axon to the trigeminal ganglion, where it lurks. When the body’s immunity decreases, virus activation is induced, and the virus directly invades the lobes of the brain from the olfactory bulb and olfactory tract, or the virus enters the brain via the trigeminal nerve after oral infection and causes encephalitis.
Symptoms
1. The disease can develop at any age, more than 50% in adults over 20 years old, with onset in all seasons. There are symptoms such as fever, headache, myalgia, drowsiness, abdominal pain and diarrhea in the early stage.
2. Most acute onset of disease, may have a history of herpes on the lips and mouth, body temperature up to 38.4 ℃ ~ 40.0 ℃, and headache mild consciousness and personality changes, sometimes with generalized or partial motor seizures as the first symptom. Subsequently, the disease slowly progresses, mental symptoms are prominent, such as inattention, slow reaction, speech reduction, emotional indifference and dull expression, the patient sits, action lazy, even can not take care of their own life, or performance of wooden stiffness, reticence, or increased movement, behavior peculiar and impulsive behavior, intellectual disability is also more obvious.
3. Neurological symptoms can be manifested as hemianopsia, hemiparesis, aphasia, oculomotor paralysis, ataxia, hyperactivity, meningeal irritation and other diffuse and focal brain damage. Most of the patients have consciousness disorders, about 1/3 of the patients may have generalized or partial epileptic seizures, and severe cases may die due to increased intracranial pressure caused by extensive cerebral parenchymal necrosis and cerebral edema, and formation of brain hernia. The course of the disease ranges from a few days to 1 to 2 months.
Examination
1. Electroencephalography
Diffuse high amplitude slow waves are often seen, which are obvious in unilateral or bilateral temporofrontal region, and even spike waves and spikes in temporal region can be seen.
2. Imaging changes
CT scan: it can be normal, or localized low-density areas can be seen; MRI can help to find foci with long T1 and long T2 signals in the brain parenchyma.
3. Cerebrospinal fluid examination
Normal or mildly increased pressure, increased cell count, moderately increased protein, normal sugar and chloride.
4. Detection of herpes simplex virus antigen
Detection of herpes simplex virus-DNA.
5. Light microscopic display
Important features of brain histopathology are hemorrhagic necrosis, and electron microscopy of intranuclear CowdryA-type inclusion bodies, which can be seen in the nuclei of oligodendrocytes and neuronal cells in the necrotic area or its vicinity, and there can be multigoligomer inclusion bodies in the nucleus of one cell. Pathogenetic examination is, electron microscopy can be found in intracellular viral particles; can also have brain tissue specimens for PCR, in situ hybridization and other checks of viral nucleic acid, or virus isolation and culture.
Diagnosis
History of herpes of the lips and mouth or genital tract, or herpes of the skin and mucous membranes in the current episode; fever, obvious mental abnormality, impaired consciousness, and signs of focal neurological damage in the early stage; diffuse cerebral abnormalities of the electroencephalogram with predominantly temporal and frontal damage; focal hemorrhagic cerebral softening foci in the temporal lobe detected by CT or MRI of the head; and the effectiveness of specific antiviral medication can indirectly support the diagnosis.
Differential diagnosis
1. Herpes zoster virus encephalitis
This disease is rare, mainly invading and latent in the nerve cells of the posterior root ganglion of the spinal nerve or the nerve cells of the sensory ganglion of the brain cells, rarely invading the central nervous system. Clinical manifestations are blurred consciousness, ataxia, and signs and symptoms of focal brain damage. The extent of the lesion is mild and the prognosis is good. Most patients have a history of herpes zoster in the chest and waist, no hemorrhagic necrosis on CT, and serum and cerebrospinal fluid are positive for antigen, antibody and nucleic acid of the virus, which can be identified.
2. Enteroviral encephalitis
Mostly seen in summer and fall, can be epidemic or sporadic. Clinical manifestations include fever, impaired consciousness, imbalance, recurrent seizures and limb paralysis. Gastrointestinal symptoms early in the course of the disease and positive virus isolation in cerebrospinal fluid (CSF) or PCR can help make the diagnosis.
3. Cytomegalovirus encephalitis
It is rare in clinical practice and is common in patients with immunodeficiency or long-term use of immunosuppressive drugs.
4. Acute disseminated encephalomyelitis
Acute disseminated encephalomyelitis usually develops acutely after infection or vaccination, and is characterized by symptoms and signs in the brain parenchyma, meninges, brainstem, cerebellum and spinal cord. Symptoms and signs are varied, and patients with severe disease may have consciousness disorder and mental symptoms.
Treatment
The main treatment includes etiologic treatment, supplemented by immunotherapy and symptomatic supportive treatment.
1. Antiviral chemotherapy
(1) Cyclic guanosine should be used for 14-21 days. Side effects include delirium, tremor, skin rash, hematuria, and temporary elevation of serum aminotransferases.
(2) Ganciclovir Intravenous drip for 10 to 14 days. The efficacy of anti-HSV is 25 to 100 times that of acyclovir.
2. Immunotherapy
(1) Interferon and its inducers α-interferon therapy, intramuscular injection.
(2) Transfer factor Subcutaneous injection.
(3) adrenocorticotropic hormone For critical condition, CT shows hemorrhagic necrotic foci, as well as cerebrospinal fluid leukocytes and erythrocytes increased significantly can be used as appropriate, with dexamethasone plus sugar saline intravenous drip; on the clinical condition of less serious, MRI shows that there is scattered distribution of punctate demyelination foci of the white matter around the ventricles of the brain, suggesting that there is virus-induced metamorphic damage, advocating high-dose hormone shock treatment, often obtaining satisfactory results. In order to achieve satisfactory therapeutic effect, methylprednisolone should be added into sugar saline for intravenous drip, and then changed to prednisone for oral administration.
3.Systemic supportive therapy
It is crucial for critically ill and comatose patients to maintain nutritional and water-electrolyte balance, and keep the airway unobstructed. If necessary, small amount of blood transfusion, or give intravenous high nutrition or compound amino acid, or large dose of immunoglobulin intravenous drip, to prevent pressure sores and respiratory tract infection and other complications.
4.Symptomatic treatment
Physical hypothermia, anticonvulsant sedation, dehydration and lowering of cranial pressure should be carried out for patients with high fever, and adrenocorticotropic hormone should be given to patients with severe cerebral edema at an early stage in large quantities and for a short period of time. Rehabilitation can be carried out during the recovery period.
Questions you may be concerned about
What should be done about herpes simplex encephalitis in children?
Herpes simplex encephalitis in children should be diagnosed and treated promptly.
Herpes simplex encephalitis in children is caused by the herpes simplex virus and manifests as fever, dizziness, convulsions and seizures, accompanied by personality changes and behavioral abnormalities. Examination of viral DNA or RNA from cerebrospinal fluid and serologic detection of antibodies are important methods of diagnosing herpes simplex encephalitis in children.
Herpes simplex encephalitis in children who have been diagnosed or are highly suspected should be treated promptly. General treatment includes cooling, anticonvulsant, and reducing edema. Etiologic treatment includes the application of antiviral drugs, such as ganciclovir, acyclic guanosine, and interferon, to control further disease progression.
Specific treatment should follow medical advice. The disease should be detected, diagnosed and treated early to avoid neurological sequelae.