Diagnosis and treatment of neurosyphilis
Nervous system involvement by *Treponema pallidum* requires a comprehensive diagnostic approach. The physician relies on the patient's history, specific neurological and psychiatric abnormalities, as well as mandatory cerebrospinal fluid (CSF) analysis and serological tests.
Key specific reactions:
- Wassermann reaction (WR) is a classical detection method.
- In doubtful and diagnostically challenging cases, highly sensitive methods are used: the fluorescent treponemal antibody absorption (FTA-ABS) test and the *Treponema pallidum* immobilization (TPI) test.
During neuroimaging (brain CT or MRI), specialists often detect ventricular enlargement (hydrocephalus), signs of cortical atrophy, and, in the meningovascular form, characteristic focal brain lesions.
The drug of choice for treatment is benzylpenicillin (intravenously 12–24 million IU daily for 14 days). Alternatively, the cephalosporin ceftriaxone can be used (1 g 4 times a day, also for 14 days). In asymptomatic cases or syphilitic meningitis, the patient's prognosis remains favorable.
Nervous system involvement in HIV infection
Neurological complications occur in more than half of patients with the human immunodeficiency virus. In one out of ten patients, nervous system disorders are the very first symptoms of AIDS, and sometimes remain the only manifestations of the disease until death. At autopsy, CNS structural damage is detected in nearly 100% of cases.
Dynamics of complication development:
- Early phase (2–4 weeks after infection). Resulting meningitis, myelopathy, or encephalitis may be transient and completely resolve within days or weeks.
- Advanced AIDS stage. Disorders become persistent, steadily progressive, and lead to the patient's death.
Spectrum of neurological pathologies in HIV:
- Encephalopathies and myelopathies (often manifesting as central lower paraparesis and loss of deep sensation).
- Opportunistic infections (cytomegalovirus, herpes, cryptococcosis, and especially toxoplasmosis).
- Peripheral nervous system disorders (sensory polyneuropathy with distal pain, as well as Herpes zoster affecting the spinal ganglia).
- Tumor processes (primary CNS lymphoma).
AIDS dementia and opportunistic infections
Progressive multifocal leukoencephalopathy and AIDS dementia complex develop in half of patients at late stages. They are characterized by a steady decline in memory and attention, apathy, lethargy, and behavioral shifts up to psychosis and seizures. MRI reveals diffuse white matter changes and atrophy. After the development of severe dementia, life expectancy usually does not exceed six months.
A special place is occupied by toxoplasmic encephalitis. Its early diagnosis via blood serum and CSF is critical, as it is one of the few potentially treatable neurological complications.
It is important to note that standard antiretroviral therapy (a combination of transcriptase blockers, such as zidovudine, and protease inhibitors) reduces viral load and prolongs life, but has no effect on already established neurological disorders (with the exception of progressive multifocal leukoencephalopathy, which is amenable to correction).
Creutzfeldt-Jakob disease
This fatal disease belongs to the group of spongiform encephalopathies. The causative agent is a pathologically altered prion protein. Unlike classical viruses, the prion contains no nucleic acids, is not recognized by the immune system, and does not trigger a typical inflammatory response.
Forms of the disease:
- Sporadic (about 90% of cases). The normal prion protein spontaneously converts into the pathological one. Its accumulation leads to neuronal death, gliosis, and vacuolization of brain tissue (sponge-like structure). The latent period can last for decades.
- Hereditary (about 10% of cases).
- Iatrogenic. More than 200 cases of transmission through medical procedures have been documented: corneal transplants from infected donors or the use of inadequately sterilized brain electrodes.
Despite its rarity (1 case per million people), in recent years there has been an upward trend in incidence, partly due to the emergence of "new" forms of the disease.
Briefly: answers to topical questions
What family and genus does the poliomyelitis virus belong to?
The poliomyelitis causative agent belongs to the family Picornaviridae and the genus Enterovirus. The virus is a typical representative of this genus and is classified as the species Enterovirus C. Structurally, it is an RNA-containing virus with three known serotypes (1, 2, and 3). There is no cross-immunity between these serotypes, so immunity to one type does not protect against infection by the others. All serotypes are pathogenic to monkeys and cause a similar clinical picture in them.
What transmission routes are typical for the poliomyelitis virus?
The poliomyelitis virus is characterized by fecal-oral (alimentary) and airborne transmission routes.
- Fecal-oral route is the main mechanism of infection, in which the virus is excreted in feces for a prolonged period (an average of about 30 days).
- Airborne route acts as an additional route and occurs only in the first days of the disease, when the virus is excreted from the mucous membranes of the nasopharynx.
Which structures of the central nervous system does the poliomyelitis virus selectively affect?
The poliomyelitis virus selectively affects motor neurons (motoneurons) located in the anterior horns of the spinal cord, as well as motor nuclei of the brainstem. As a result of the rapid and irreversible death of these cells, motor functions are lost. Neurons in the cervical and lumbar enlargements of the spinal cord are most frequently affected. The damage is mosaic in nature, as the anterior horn cells are grouped in long vertical columns, meaning not all muscles are involved in the pathological process.
What periods are distinguished in the clinical course of the paralytic form of poliomyelitis?
Four consecutive periods are strictly distinguished in the clinical course of the paralytic form of poliomyelitis.
- Preparalytic period — lasts from 3 to 6 days, manifests with fever, and is accompanied by catarrhal, dyspeptic, and pronounced pain syndromes.
- Paralytic period — lasts from a few days to 2 weeks, characterized by the development of flaccid paresis and paralysis with complete preservation of sensation.
- Recovery period — lasts up to 1 year.
- Residual period — the stage of persistent residual effects, including muscle atrophy and contracture formation.
What are the characteristics of motor disorders in the spinal form of poliomyelitis?
Motor disorders in the spinal form of poliomyelitis are characterized by the development of acute asymmetrical flaccid paresis and paralysis with complete preservation of sensation.
- Localization — predominantly one or both lower extremities are affected, less commonly the upper extremities, trunk, and neck muscles are involved.
- Topography — proximal limb segments are affected more severely than distal ones.
- Specificity — a peculiar "mosaicism" of damage is observed, meaning not all limb muscles are involved in the pathological process.
- Trophic changes — accompanied by pronounced muscle atrophy and concomitant pain syndrome.
Which cranial nerves are most commonly affected in the bulbar form of poliomyelitis?
In the bulbar form of poliomyelitis, sources indicate involvement of the facial nerve and the development of bulbar syndrome. It manifests as dysarthria, dysphagia, choking, nasal voice, palatal paresis, hypersalivation, and respiratory disorders. The specific list of the most commonly affected cranial nerves is not specified in the cited sources.
What types of vaccines are used for the specific prevention of poliomyelitis?
Two types of vaccines are used for the specific prevention of poliomyelitis: the live oral poliovirus vaccine (OPV) and the inactivated poliovirus vaccine (IPV). Mass vaccination has established high herd immunity and led to the near-total disappearance of poliomyelitis cases in developed countries. Booster doses are administered at 1 and 4 years of age following the primary vaccination series completed at 8 weeks.
To memorize the causative agents of opportunistic infections in HIV (T-G-C-C): Toxoplasma, Herpes, Cytomegalovirus, Cryptococcus.
Class and exam questions
Does antiretroviral therapy affect neurological complications in AIDS?
In most cases, therapy does not affect already developed neurological disorders. The only exception is progressive multifocal leukoencephalopathy, in which cART has a positive effect.
How does a prion differ from a virus?
A prion is an exclusively infectious protein that lacks nucleic acids in its structure. Furthermore, it does not induce an immune response or signs of inflammation in the body.
Which neurological complication in HIV is considered potentially reversible?
Toxoplasma encephalitis (cerebral toxoplasmosis). Early diagnosis via examination of cerebrospinal fluid and blood serum is extremely critical.
What changes are visible on MRI in neurosyphilis?
Characterized by hydrocephalus (enlargement of the ventricular system), signs of cortical atrophy, and focal brain lesions, particularly in the meningovascular form.
What else to study on this topic
- Pathogenesis of spongiform encephalopathy and mechanisms of prion accumulation
- Differential diagnosis of sensory polyneuropathy in HIV
- Antiretroviral therapy regimens and blood-brain barrier penetration of drugs
- Characteristics of CSF examination in opportunistic infections
- Clinical manifestations of meningovascular neurosyphilis
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Other topics in "Chapter 23. Infectious Diseases of the Nervous System"
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