Classification and mechanisms of development
Depending on their origin, encephalitides are divided into two main groups:
- Primary encephalitis. The infectious agent (usually a neurotropic virus) crosses the blood-brain barrier and directly affects the brain parenchyma, as well as the pia and arachnoid mater. Such a process is called meningoencephalitis. Causative agents are frequently herpes simplex virus, cytomegalovirus, Epstein-Barr virus, arboviruses (tick-borne and mosquito-borne encephalitis viruses), enteroviruses, and rabies virus.
- Secondary (parainfectious) encephalitis. Develops against the background of a general systemic infection (measles, rubella, chickenpox, mumps, influenza) or as a post-vaccination reaction (usually on days 7–14). The pathogenesis is based on microvascular disorders and autoimmune reactions, which lead to focal or diffuse demyelination of nerve fibers.
Symptoms and clinical course
The disease debuts with fever and headache. Within a few hours or days, moderate meningeal signs join.
A severe course is characterized by profound impairment of consciousness — from obtundation to coma. Depending on which areas of the brain are affected, focal neurological and psychiatric disorders occur:
- Speech disorders (aphasia).
- Central paresis (weakness) of the limbs.
- Coordination disorders (ataxia).
- Behavioral disorders and psychomotor agitation.
- Epileptic seizures.
Some surviving patients retain persistent neurological deficits, and a severe course can be fatal.
Herpetic and tick-borne encephalitis
These are two specific and frequently encountered types of the disease with their own features.
Herpes simplex encephalitis Caused by herpes simplex virus type I or II. Inflammation predominantly affects the inferior and medial parts of the temporal lobes. Patients complain of headache, experience epileptic seizures, behavioral disorders, memory impairment, aphasia, as well as gustatory and olfactory hallucinations. The disease can rapidly lead to stupor and coma. Without treatment, mortality reaches 50–70%, with treatment it drops to 20%, but the risk of persistent disorders and the development of symptomatic epilepsy is high.
Tick-borne spring-summer encephalitis Characteristic of Siberia and the Russian Far East, less common in the European part of the Russian Federation. Infection can occur via a tick bite (incubation period 8–20 days) or by consuming raw contaminated milk (7 days). The onset is always acute: chills, temperature spike to 39–40 °C, severe headache, vomiting, and myalgia. A distinctive feature is peripheral paresis of the neck, shoulder girdle, and arm muscles due to damage to the anterior horns of the spinal cord.
Diagnostics and treatment
The diagnosis is established based on clinical presentation, anamnesis, and additional studies. The decisive role is played by:
- Lumbar puncture: cerebrospinal fluid reveals elevated pressure, increased protein levels, and lymphocytic pleocytosis (10–100 cells per mm³).
- CSF PCR: allows rapid identification of the pathogen in the first days.
- CT and MRI: visualize inflammatory lesions and help rule out other pathologies (stroke, abscess).
Treatment depends on the etiology. In herpes simplex encephalitis, intravenous acyclovir is prescribed immediately for 10–14 days. For tick-borne encephalitis, homologous gamma globulin or serum immunoglobulin is used.
Briefly: answers to topical questions
What clinical forms is tick-borne encephalitis classified into?
Tick-borne encephalitis is classified into two broad groups: non-focal and focal forms.
- Non-focal forms — include febrile (about 20% of cases) and meningeal (30–50%) forms.
- Focal forms — include meningoencephalitis (involvement of brain structures), polioencephalitis (involvement of brain neurons), myelitis (involvement of the spinal cord), and poliomyeloencephalitis.
Sources also mention polyradiculoneuritic and progressive forms of the disease.
What specific changes are visualized on brain MRI in herpes encephalitis?
In herpes encephalitis, brain MRI visualizes bilateral edema, hyperintense signal, and hemorrhage foci.
- T2-weighted images — demonstrate a hyperintense signal from the medial sections of both temporal lobes.
- Edema — bilateral edema is detected in the hippocampal region, temporal lobes, and cingulate gyri.
- Hemorrhages — dynamic imaging visualizes the formation of hemorrhage foci within the edema zones.
The pathological process may also involve the left thalamus and the lateral part of the temporal lobe.
What are the absolute contraindications to performing a lumbar puncture in suspected encephalitis?
Contraindications to performing a lumbar puncture in suspected encephalitis are:
- infectious process at the puncture site;
- brain space-occupying lesion;
- increased intracranial pressure, since CSF extraction is associated with a high risk of brain herniation.
Class and exam questions
What is the difference between primary and secondary encephalitis?
Primary encephalitis is caused by a virus that directly invades the brain (e.g., herpes, tick-borne encephalitis virus). Secondary develops as an autoimmune or vascular complication following other infections (measles, influenza) or after vaccination.
Which brain region is most frequently affected in herpes encephalitis?
The inferior, medial, and orbital parts of the temporal lobes are predominantly affected.
Which specific symptom indicates tick-borne encephalitis?
It is characterized by peripheral paresis of the neck and shoulder girdle muscles due to damage to the anterior horns of the cervical spinal cord segments.
What will CSF analysis show in viral encephalitis?
There will be elevated pressure, increased protein count, and lymphocytic pleocytosis (usually 10 to 100 cells per cubic millimeter).
What else to study on this topic
- Mechanism of viral penetration across the blood-brain barrier
- Pathogenesis of autoimmune demyelination in parainfectious encephalitides
- Features of differential diagnosis between encephalitis and meningitis using MRI and CT
- Specific neurological syndromes in tick-borne encephalitis (involvement of accessory nerve nuclei)
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Other topics in "Chapter 23. Infectious Diseases of the Nervous System"
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