Acute anterior poliomyelitis (Heine-Medin disease)
The disease is caused by an RNA virus from the enterovirus group. Infection most commonly occurs via the alimentary route, after which the pathogen multiplies in lymphoid tissue. In only 1% of cases does the virus penetrate the central nervous system, where it binds to motor neuron receptors in the anterior horns of the spinal cord. Viral RNA blocks normal protein synthesis within the cell, leading to neuronal death.
Macroscopically, the meninges are hyperemic, the spinal cord tissue swells, and the normal "butterfly" pattern of the gray matter becomes blurred. At the microscopic level, neuronophagocytic nodules (clusters of polymorphonuclear leukocytes and microglia) form around the destroyed cells, which are subsequently replaced by glial scars.
In the residual stage of the disease, small cysts appear at the site of the destroyed areas. Due to the irreversible death of motor cells, atrophy of the nerve roots and secondary neurogenic atrophy of the skeletal muscles develop, leading to severe disability.
Neuroinfections: herpes and rabies
Herpes simplex virus type 1 (Herpes simplex virus type 1) enters the nervous system via retrograde axonal transport. It causes acute necrotizing encephalitis, predominantly affecting the temporal lobes and orbitofrontal gyri. Specific intranuclear Cowdry type A viral inclusions form within neurons. The outcome of such encephalitis is fatal in 80% of cases.
The causative agent of chickenpox and shingles (Varicella-zoster virus) can remain in a latent phase in sensory spinal ganglia for a prolonged period. Upon reactivation, it causes neuronal necrosis in the ganglion and spreads along nerve fibers, provoking intraneural neuritis with the formation of vesicular (papulovesicular rash) lesions.
Rabies is an anthropozoonosis transmitted through the bite of an infected animal. The rhabdovirus spreads along perineural spaces. Edema and the clinical picture of severe encephalitis develop in the brain. A pathognomonic sign of rabies is Babes-Negri bodies—eosinophilic cytoplasmic inclusions most commonly localized in the neurons of the hippocampus.
Tick-borne encephalitis
An acute natural-focal disease caused by an RNA-containing flavivirus. The primary reservoir and vector are ixodid ticks (Ixodes persulcatus, Ixodes ricinus).
Routes of transmission:
- Transmissible — via tick bite (incubation period 7–14 days, depending on the duration of attachment).
- Alimentary — through raw milk from infected goats or cows (often causes biphasic meningoencephalitis).
Clinically, the disease begins with sudden chills, fever, facial and ocular hyperemia. In the severe poliomyelitic form, flaccid paralysis of the neck and upper extremity muscles develops (characteristic "hanging head" sign). Morphologically, hemorrhages, edema, and neuronophagia are detected in the acute stage, while demyelination and fibrillary gliosis are found in the chronic course (characteristic of the Siberian subtype of the virus).
Slow infections, prion diseases, and HIV
In addition to acute infections, there are processes with a prolonged latent period:
- Persistent viral infections. These include subacute sclerosing panencephalitis (caused by the measles virus, accompanied by white matter condensation of the brain) and progressive multifocal leukoencephalopathy (caused by a polyomavirus against the background of severe immunodeficiency, leading to multiple demyelination).
- Prion diseases. Neurodegenerative pathologies with inevitable fatal outcomes (e.g., Creutzfeldt-Jakob disease). They are characterized by spongiform degeneration of tissue, neuronal loss, amyloid plaques, and a complete absence of inflammation.
- HIV infection. The human immunodeficiency virus directly causes aseptic meningitis or vacuolar myelopathy, and also paves the way for opportunistic central nervous system infections (toxoplasmosis, cytomegalovirus, cryptococcosis).
Demyelinating diseases
A distinct group of nervous system pathologies. They share a specific pathogenesis: selective destruction of the myelin (Schwann) sheath of nerve fibers in the central nervous system occurs, while the axon (axis cylinder) itself remains relatively undamaged.
Briefly: answers to topical questions
Which nosological forms belong to the group of central nervous system demyelinating diseases?
The group of central nervous system demyelinating diseases (myelinopathies) includes the following nosological forms:
- Multiple sclerosis — the primary demyelinating disease with a chronic, slowly progressive course.
- Acute disseminated encephalomyelitis — a monophasic, self-limiting disease developing as a complication of viral infections or vaccinations.
- Acute hemorrhagic leukoencephalitis — a rare form of demyelinating disease.
- Central pontine myelinolysis — a rare form of pathology.
- Toxic demyelination — a rare form of myelin damage.
What stages are distinguished in the morphogenesis of acute anterior poliomyelitis?
Four successive stages are distinguished in the clinical course and morphogenesis of acute anterior poliomyelitis.
- Preparalytic stage — characterized by the disappearance of tigroid substance in motor neurons, nuclear pyknosis, vascular congestion, diapedesis of erythrocytes, and brain tissue edema.
- Paralytic stage — necrosis of motor neurons, softening of the brain gray matter, and formation of neuronophagocytic and glial nodules occur.
- Recovery stage — a period of reparative processes.
- Residual stage (stage of residual changes) — small cysts and gliosis form at the sites of softening, accompanied by neurogenic atrophy of skeletal muscles.
What types of human prion diseases exist besides Creutzfeldt-Jakob disease?
In addition to Creutzfeldt-Jakob disease, human prion diseases include:
- Kuru disease.
- Gerstmann-Sträussler-Scheinker syndrome — a hereditary familial disease.
- Fatal familial insomnia — a genetically determined prion disease.
Class and exam questions
What is the main morphological difference between prion diseases and viral encephalitis?
In viral encephalitis, an inflammatory response is always present (lymphoid infiltration, microglial nodules). Prion diseases present exclusively with a pattern of degeneration (spongiform change, gliosis) without signs of inflammation.
How do pathological intracellular inclusions differ between rabies and herpes simplex?
In herpes simplex and CMV infection, intranuclear Cowdry type A inclusion bodies form within neurons and glial cells. In rabies, viral inclusions (Babes-Negri bodies) form in the cytoplasm of hippocampal cells.
Why does muscle atrophy occur in poliomyelitis?
The virus destroys motor neurons in the anterior horns of the spinal cord. This leads to Wallerian degeneration of the corresponding nerve roots, cessation of muscle innervation, and, consequently, secondary neurogenic atrophy.
What changes in the central nervous system are caused by cytomegalovirus?
In intrauterine infection, CMV causes periventricular necrosis, calcification, and microcephaly. In adults against the background of AIDS, subacute encephalitis with microglial nodules develops.
What else to study on this topic
- Classification and clinical stages of acute poliomyelitis
- Mechanism of Varicella-zoster virus reactivation and the development of intraneural neuritis
- Comparative characteristics of tick-borne encephalitis forms
- Opportunistic neuroinfections in terminal stages of HIV
- Pathogenesis of progressive multifocal leukoencephalopathy
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