NEUROLOGY AND NEUROSURGERY - YU. V. ALEKSEEENKO - 2014

INFECTIOUS DISEASES OF THE NERVOUS SYSTEM

Infectious and Inflammatory Diseases of the Central Nervous system typically present with a general infectious symptom complex, The Development of diffuse cerebral and focal neurological disorders, and CEREBROSPINAL FLUID abnormalities. Symptoms of a general infectious nature include fever, characteristic Blood inflammatory changes (leukocytosis, elevated ESR, etc.), Muscle and joint pain, a sensation of heat and chills, Skin rashes, and others.

Among diffuse cerebral disorders, meningeal syndrome (irritation of the Meninges) is the most critical. It is characterized by widespread, often rapidly escalating and severe headaches. Pain may radiate along the spine down to the lower back and lower extremities. Pain upon movement of the eyeballs occurs, accompanied by nausea, vomiting, and generalized hyperesthesia. Bright light, odors, noise, and tactile stimuli during examination intensify the pain and become intolerable. Meningeal irritation leads to characteristic signs. The most frequent is nuchal rigidity, detected during passive flexion of the neck and inclination of the HEAD toward the Sternum. Kernig's and Brudzinski's signs, along with a few others, are somewhat less common. In certain cases, a characteristic meningeal posture develops, where the patient's head is hyperextended, the abdomen is retracted, and the legs are drawn up toward the abdomen. Depression of consciousness ranging from stupor to coma may occur. Psychomotor agitation, delirium, and hallucinations are less common. Seizure disorders can occasionally develop, predominantly in children.

Focal neurological deficits are diverse and depend on the localization and Nature of the inflammatory process. Most frequently, infectious and inflammatory CNS diseases present with anisoreflexia or hemiparesis, Facial Nerve Asymmetry, gaze disorders, speech impairments, and less commonly, extrapyramidal disorders or sensory disturbances.

Infectious and inflammatory CNS disorders are accompanied by characteristic Changes in the cerebrospinal fluid (CSF), where an increased Cell count—predominantly neutrophils or lymphocytes—comes to the forefront. In some cases, the causative agent may be detected in the CSF. Additionally, elevated CSF pressure, alterations in its color and transparency, and a moderate increase in protein levels are typically observed. The identification of many infectious central nervous system pathologies can be facilitated by bacteriological and serological tests, or virological studies of the CSF and blood.

Meningitis

Meningitis is an infectious and inflammatory disease primarily affecting the membranes of the Brain AND SPINAL cord. The causative agents may include Bacteria, Viruses, Fungi, Protozoa, and others. The disease can be primary, developing without a preceding generalized infection, or secondary, meaning it arises as a complication of a localized or systemic infection. Depending on The Nature of the inflammatory process in the meninges and CSF alterations, meningitis is classified into purulent (typically bacterial) and serous (typically viral) forms. The penetration of infection into the cranial cavity can occur via hematogenous routes (in bacteremia), perineural or lymphatic pathways (in infections of the Paranasal Sinuses, Middle ear, or Orbit), as well as by direct contact (in traumatic brain injury and cerebrospinal fluid leakage).

Morphological changes in meningitis (inflammatory infiltration) predominantly develop in the pia mater, ependyma, adjacent layers of brain tissue, and the choroid plexuses of the cerebral ventricles. The subarachnoid space becomes filled with purulent or relatively clear CSF. Cerebral edema and predominantly internal Hydrocephalus are observed. The thickening of the inflammatory exudate can create an obstruction to CSF Circulation. Among the primary mechanisms of brain damage in meningitis are intoxication, disruption of the blood-brain barrier, cerebral edema and elevated intracranial pressure, impaired CSF circulation with obstructive disorders, and the development of secondary ischemic brain lesions. Direct causes of patient mortality in meningitis can include pronounced intracranial Hypertension and tentorial herniation, as well as infectious-toxic Shock.

The Clinical presentation of meningitis, regardless of Etiology, is quite characteristic. It invariably consists of 1) a general infectious and 2) a meningeal symptom complex, along with 3) inflammatory CSF changes. In meningitis, signs of meningeal irritation and other diffuse cerebral disorders dominate. Potential symptoms of focal brain damage typically recede into the Background against this backdrop. It should be emphasized that the ultimate and decisive criterion for diagnosing meningitis remains inflammatory changes in the CSF. The presence of meningeal irritation signs in the neurological status without inflammatory CSF alterations is referred to as meningism. The presence of meningeal syndrome and signs of an infectious process should be considered the primary indication for CSF analysis. In Purulent meningitis, the CSF predominantly reveals neutrophils, typically numbering in the thousands per 1 µL, which determines the altered color and transparency of the fluid. However, the nature of pleocytosis depends on the stage of the disease. In the earliest stages of meningeal inflammation, lymphocytes may predominate. During convalescence, alongside a decrease in cell count, lymphocytes are once again predominantly found. In serous meningitis, lymphocytic pleocytosis is observed (ranging from several dozen to hundreds of Cells per 1 µL), while the color and transparency of the CSF remain largely unchanged.

Meningococcal meningitis

Meningococcal infection is transmitted via airborne droplets. It is important to bear in mind that meningococcal (purulent) meningoencephalitis is merely one clinical variant of meningococcal disease. The condition affects individuals of all age groups, though most commonly children and young adults. Meningococcal meningitis is characterized by an acute and fulminant onset with high fever and pronounced meningeal syndrome. Patients experience severe headache, nausea, and vomiting, and may present with back or lower back pain. Confusion gradually develops, and delirium sometimes occurs. Some patients experience epileptic seizures. A characteristic feature of the disease is a hemorrhagic rash distributed across the abdomen, buttocks, thighs, and shins. From the first day of illness, the CSF is typically turbid, containing hundreds or thousands of cells—predominantly neutrophils per 1 µL. Meningococci may be identified within these cells. Furthermore, the protein content in the CSF is elevated, and its pressure is increased. Meningococcal meningitis follows a severe clinical course, yet with adequate Treatment, recovery occurs in the vast majority of cases. Dangerous complications of the disease include bacterial (endotoxic) shock and Waterhouse-Friderichsen syndrome (acute adrenal insufficiency caused by destruction of the adrenal cortex).

Meningitis caused by Coxsackie and ECHO Viruses

This is a serous meningitis that predominantly affects children under the age of 15. The transmission mechanism is fecal-oral. The disease has an acute onset and presents with all characteristic features: fever, severe headache, nausea and vomiting, and pronounced meningeal signs. Patients' faces are typically flushed, accompanied by scleral injection, Conjunctivitis, and herpetic labial eruptions. CSF pressure is elevated, revealing lymphocytic pleocytosis and a moderate increase in protein levels. The Diagnosis is confirmed by rising titers of antiviral Antibodies in the blood serum and CSF. The clinical course of this condition is favorable, yet relapses occur in 10–40% of cases.

Meningitis Caused by Mumps Virus

This is an acute serous meningitis that most commonly develops concurrently with or following parotitis. The disease primarily affects preschool and school-aged children. Mumps Meningitis develops acutely and is accompanied by a significant fever, severe headache, and repeated vomiting. Moderate meningeal signs are detectable. In certain cases, depression of consciousness occurs, accompanied by hallucinations. Seizure episodes occasionally develop. Focal neurological signs are rare. A substantial increase in CSF pressure is observed. The cerebrospinal fluid predominantly reveals lymphocytes—numbering in the hundreds or thousands per 1 µL. Serological tests are of great importance in establishing the exact etiology of the meningitis. Patients' well-being generally improves significantly within one to two weeks. Complications of mumps infection include pancreatitis and orchitis.

Tuberculous meningitis

The source of tuberculous infection is usually localized in the Lungs or bronchial Lymph Nodes. Involvement of the meninges occurs via hematogenous spread. Tuberculous meningitis is characterized by The formation of numerous miliary tubercles on the pia mater and a serofibrinoid exudate within the subarachnoid space. Inflammatory changes are most pronounced at the Base of the brain, which dictates certain specific Clinical Features of the disease. Tuberculous inflammation of the meninges involving the choroid plexuses and ventricular ependyma, along with the formation of adhesions and sclerotic changes, contributes to profound disturbances in CSF circulation and hydrocephalus. Tuberculous meningitis is characterized by a slow onset of symptoms. The prodromal period features general malaise, increased fatigue, loss of appetite, mood changes, daytime somnolence, low-grade fever, and headaches. The development of meningeal symptoms may be preceded by cognitive and behavioral impairments. The duration of this period can span several weeks. Subsequently, the patient's condition deteriorates sharply, revealing signs of meningeal irritation and a significant fever. At this stage, cranial nerve involvement (abducens, oculomotor, facial, vestibulocochlear) typically emerges. Other syndromes of focal brain damage and seizure episodes may also appear. In the absence of adequate treatment, patients' conditions progressively worsen, and profound disturbances of consciousness develop. Under such circumstances, a fatal outcome may occur within 4 to 8 weeks.

CSF analysis reveals moderate pleocytosis (initially predominantly neutrophilic, later shifting to lymphocytic)—600–800 cells per 1 µL. Additionally, elevated CSF pressure and protein content are detected, alongside a decreased glucose concentration. Upon standing in a test tube for 12–24 hours, a delicate, web-like fibrin network frequently precipitates, resembling an inverted fir tree in shape. The diagnosis is confirmed by identifying Mycobacterium tuberculosis in the CSF in approximately two-thirds of cases. When tuberculous meningitis is suspected, additional evaluation of the patient is necessary to locate the primary source of infection. A history of prior tuberculosis is documented infrequently—only in 10–50% of cases. CT and MRI scans frequently reveal thickening of the meninges around the base of the brain, hydrocephalus, areas of secondary ischemic brain injury, tuberculomas, or tuberculous abscesses. The mortality rate among patients with tuberculous meningitis remains relatively high, at approximately 10%. However, early recognition of the meningeal etiology and the prompt initiation of targeted therapy significantly improve the chances of recovery.

Encephalitis

Encephalitis is characterized by the predominance of brain parenchymal involvement; nevertheless, it almost invariably proceeds with inflammatory changes in the Spinal Cord, meninges, and CSF, which in many cases allows these conditions to be terminologically defined as meningoencephalitis or encephalomyelitis. Encephalitis is conventionally subdivided into Primary and secondary forms. Primary encephalitis arises as an independent and direct infectious-inflammatory Pathology of the central nervous system resulting from the pathogen breaching the blood-brain barrier. Secondary encephalitis (post- or parainfectious) is predominantly characterized by indirect CNS involvement mediated by autoimmune, toxic-metabolic, and frequently nonspecific mechanisms.

Primary acute encephalitis is caused by viruses in the vast majority of cases, though it may also have other etiologies. Based on the anatomical distribution of the pathological process, encephalitis is subdivided into leukoencephalitis (with predominant involvement of the White matter—subacute progressive encephalitis) and polioencephalitis (with predominant involvement of the Gray matter—poliomyelitis, von Economo encephalitis).

Classification of Encephalitis

   I. Primary Encephalitis

1. Viral

Arboviral, seasonal

   ■ Tick-borne spring-summer

   ■ Mosquito-borne Japanese

   ■ Australian Murray Valley

   ■ American St. Louis

Viral, polyseasonal

   ■ Enteroviral Coxsackie and ECHO

   ■ Herpetic

   ■ Rabies-associated

   ■ Retroviral (associated with neuro-AIDS, etc.)

Caused by an unknown virus

   ■ Economo encephalitis

2. Microbial and rickettsial

   ■ Neurosyphilitic

   ■ Epidemic typhus-associated

   ■ Neuroborreliosis (Lyme disease)

II. Secondary encephalitides

1. Viral

   ■ Measles-associated

   ■ Varicella-zoster (chickenpox)-associated

   ■ Rubella-associated

   ■ Papovavirus (progressive multifocal leukoencephalopathy), cytomegalovirus, and others

2. Post-vaccination

3. Microbial and rickettsial

   ■ Staphylococcal

   ■ Streptococcal

   ■ Malarial

   ■ Toxoplasmic

   III. Encephalitis Caused by Slow Infections

   ■ Subacute Sclerosing Panencephalitis

   ■ Prion Diseases (Creutzfeldt-Jakob Disease, etc.).

The clinical presentation of such conditions comprises well-known symptom complexes: general infectious signs, general cerebral symptoms (including meningeal syndrome), central nervous system focal lesion syndrome, and cerebrospinal fluid (CSF) alterations. However, local brain injury signs occupy a significant (sometimes dominant) place among the clinical manifestations of encephalitis: limb paresis and sensory disturbances, speech disorders and cranial nerve dysfunctions, ataxia, mental function impairments, etc.

CSF analysis in encephalitis may reveal lymphocytic pleocytosis (several hundred cells per 1 µL), a moderate protein elevation, and increased CSF pressure. In hemorrhagic leukoencephalitis, erythrocytes may be present in the CSF. CT and MRI scans typically reveal inflammatory brain lesions with signs of cerebral edema and distortion of CSF-containing spaces. Serological tests using CSF and blood serum help establish a definitive diagnosis, although they frequently confirm it only retrospectively. In approximately 50% of cases, the specific etiology of acute viral encephalitis remains unknown.

Herpes Simplex Encephalitis

Herpes simplex encephalitis is caused by the Herpes simplex virus and is one of the most dangerous forms of herpetic infection. The disease occurs worldwide and can affect individuals of any age. In about one-third of cases (primarily in young adults), herpes encephalitis results from a primary infection, while in the remaining two-thirds, it develops due to the reactivation of a latent infection. Patients with herpes encephalitis do not pose an infection hazard to others and do not require isolation.

Herpes encephalitis is an asymmetric, necrotizing, hemorrhagic inflammatory process accompanied by lymphocytic and plasmacytic infiltration. It predominantly affects the medial temporal lobes and the basal frontal lobes, involving primarily the gray matter and, to a lesser extent, the WHITE MATTER OF the brain.

The disease begins with hyperthermia, headache, nausea, and vomiting. Most patients exhibit distinct meningeal signs. They may rapidly experience a depressed level of consciousness, progressing to stupor or coma. Epileptic seizures or even status epilepticus may develop. The predominant involvement of the temporal and frontal lobes determines the characteristic focal symptomatology of herpes encephalitis. Patients experience impairments in mental Functions and behavior (speech and memory disorders, etc.), olfactory and taste disturbances, autonomic dysfunctions, and complex partial seizures of temporal origin. Hemiparesis, visual field defects, and cranial nerve dysfunctions may also be observed. It should be noted that herpetic eruptions around the Lips are not proof of a herpetic etiology of encephalitis and can occur in various colds and inflammatory diseases. Herpes encephalitis runs a severe course; even with etiotropic therapy, patients' conditions may show no improvement for several days or weeks.

The CSF shows lymphocytic or mixed lymphocytic-neutrophilic pleocytosis and a moderate increase in protein. Some patients present with erythrocytes and xanthochromia in the CSF. In certain cases (5-10% of observations), no significant abnormalities can be detected, especially at the onset of the disease. A CT or MRI scan performed a few days after the initial signs of encephalitis allows the visualization of hypodense areas in the temporal and frontal Regions of the brain with hyperdense components, which may indicate necrotic and hemorrhagic changes in the brain Tissues.

It must be emphasized that clinical symptoms and instrumental research data do not reliably differentiate the etiology of encephalitis, nor can they immediately distinguish this condition from other acute vascular or toxic-metabolic CNS disorders. The results of certain blood and CSF serological tests, aside from the Polymerase Chain Reaction, become available too late to serve as a basis for initiating specific therapy. Therefore, antiviral treatment (acyclovir) must be initiated as early as possible at the slightest suspicion of herpes encephalitis—that is, practically in every case of severe encephalitis of unclear etiology. The mortality rate in herpes encephalitis has recently decreased to 28% with The Use of antiviral drugs. However, approximately half of the patients with a favorable outcome exhibit residual neurological disorders, such as memory and speech deficits, psychiatric disorders, epileptic syndrome, and motor impairments.

Tick-Borne Spring-Summer Encephalitis

The disease is prevalent in the Far East, Siberia, the Urals, as well as parts of Europe. Tick-borne encephalitis is caused by a virus that enters the patient's bloodstream through a tick bite. Another route of transmission is alimentary, associated with the consumption of raw goat milk. At the same time, patients with tick-borne encephalitis themselves pose no danger to others. In endemic foci, only 0.5–5% of ticks carry the virus. The disease induces a lifelong, persistent Immunity.

Following a tick bite, the virus enters the skin and subcutaneous tissue, where it multiplies and subsequently invades the bloodstream. The incubation period lasts 8–20 days. Inflammatory and degenerative changes in tick-borne encephalitis are found in the anterior horns of the cervical thickening of the spinal cord, the motor nuclei of the Brainstem, the Cerebral Cortex, subcortical structures, and the Cerebellum.

The disease typically begins acutely with a fever, chills, myalgia, headache, nausea, and vomiting. In some cases, stupor and delirium may develop. Meningeal signs appear, followed by flaccid paralysis of the shoulder girdle Muscles. Due to neck muscle weakness, the patient's head drops, and bulbar syndrome with dysarthria, dysphagia, and dysphonia may also emerge. Blood tests reveal leukocytosis and an elevated ESR. CSF analysis shows moderate lymphocytic pleocytosis and increased protein levels.

The patient's condition improves by the end of the second week. Subsequently, a gradual recovery of motor functions takes place, which may be incomplete in some cases. This clinical course of tick-borne encephalitis resembles poliomyelitis. The disease can also manifest as meningitis or meningoencephalitis with a predominance of general cerebral symptoms. Later on, Kozhevnikov's Epilepsy may develop, characterized by continuous myoclonic twitching in isolated muscle groups against a background of periodic generalized convulsive seizures. A biphasic clinical variant of tick-borne encephalitis also exists.

A medical history noting a stay in an epidemically unsafe area and a tick bite is of paramount importance in diagnosing tick-borne encephalitis. Characteristic clinical features, such as flaccid paralysis of the Neck Muscles, shoulder girdle, and bulbar musculature, help suspect tick-borne encephalitis. Serological tests confirm the diagnosis. In such circumstances, a Differential diagnosis must be made with neuroborreliosis, which can also occur following a tick bite and sometimes presents with similar clinical symptoms. The Far Eastern variant of tick-borne encephalitis is severe, with a mortality rate reaching 30%. European forms of the disease carry a more favorable prognosis. No adequate etiotropic treatment exists for this condition; therefore, timely vaccination is of immense importance for individuals at high risk of infection. Following a tick bite, tick-borne gamma globulin is administered intramuscularly (3 mL for adults and 2 mL for children aged 10–15 years), and the dose may be repeated after a week.

Epidemic Encephalitis (von Economo Encephalitis)

This disease is currently not diagnosed; however, at the end of World War I, it assumed an epidemic character. The CAUSATIVE AGENT OF von Economo encephalitis has not been identified, although there are grounds to assume its viral nature. Characteristic manifestations of the illness include hypersomnia and oculomotor disorders (diplopia, less commonly supranuclear ophthalmoplegia), indicating primary involvement of the Midbrain. For this reason, von Economo encephalitis is also referred to as lethargic encephalitis. The acute stage typically ended in recovery, but this was followed by the gradual development of a parkinsonian symptom complex.

Principles of Complex Therapy for Meningitis and Encephalitis

The foundation of comprehensive treatment for infectious and inflammatory disorders of The Nervous System is specific etiotropic therapy, which naturally must be prescribed as early as possible. In the absence of data regarding the specific pathogen and its sensitivity to Antibiotics or antivirals, treatment begins empirically. Subsequent adjustments to prescriptions can be made based on the susceptibility of the isolated strain and the clinical response achieved.

In the treatment of purulent meningitis, the correct choice of antibiotics capable of crossing the blood-brain barrier in sufficient quantities is of great significance. In adults, the drugs of choice for empirical therapy and after pathogen identification include ampicillin, third- and fourth-generation Cephalosporins (ceftazidime, cefotaxime, ceftriaxone, cefepime), kanamycin, rifampicin, gentamicin, vancomycin, meropenem, etc. Given the high efficacy of modern antibiotics, the intraluminal administration of antibiotics is generally unnecessary. Intravenous administration is typically recommended, while intramuscular use of antibiotics is acceptable in mild cases. Antibacterial therapy is usually continued for 7–10 days after normalization of body Temperature. Prior to discontinuing antibiotics, a follow-up CSF examination is generally performed. The presence of fewer than 100 cells in the CSF (with at least 75% being lymphocytes) serves as a criterion for stopping antibiotics.

To treat tuberculous meningitis, several drugs are prescribed simultaneously: isoniazid, rifampicin, and pyrazinamide. Treatment is long-term, lasting several months. Vitamin B₆ is additionally administered to prevent isoniazid-induced polyneuropathy.

The treatment of most serous meningitides is symptomatic and pathogenetic. In herpetic meningoencephalitis, acyclovir (Virolex, Zovirax) is the drug of choice. It has a relatively narrow spectrum of activity, exerting effects on herpes simplex viruses and other herpes-group viruses. The duration of treatment should be at least 10–14 days.

To manage cerebral edema and elevated intracranial pressure, repeated administration of mannitol, Lasix, and dexamethasone is used. Careful monitoring of Water, electrolyte, and acid-base balance is essential. In the acute phase of the disease, detoxification therapy is typically performed using Hemodez and other well-known agents. Analgesics from various groups are prescribed to virtually all patients, taking into account The Nature and severity of the cephalic syndrome.

Great importance is attached to the timely recognition and appropriate therapy of systemic complications, such as shock, DIC syndrome, myocardial infarction, Cardiac Arrhythmias, Pneumonia, and thromboembolic events.

For convulsive syndrome, diazepam is administered intravenously, after which carbamazepine may be used to prevent the recurrence of seizures during the acute phase of the disease. At the same time, prescribing antiepileptic drugs to all patients for the purpose of preventing the long-term development of epileptic syndrome is impractical.

In the acute and recovery periods of infectious and inflammatory CNS disorders, metabolic and vasoactive agents, as well as Vitamins, are used. Comprehensive patient rehabilitation involving specialists from related medical fields is of great importance.

Brain Abscesses

A brain abscess is a localized collection of pus within the brain parenchyma. As a rule, it is the outcome of focal meningoencephalitis with liquefaction of brain tissue. The cause of a brain abscess is the spread of infection, which can reach the cranial cavity via contact (e.g., in inflammatory Diseases of the middle ear), hematogenously (metastatic abscesses), or through a pathological communication between the cranial cavity and the external environment (e.g., in open and penetrating TRAUMATIC BRAIN INJURIES).

The formation of a brain abscess goes through several stages. The First stage is the development of focal encephalitis. This is followed by the liquefaction of brain tissue and the formation of a purulent cavity. Subsequently, the gradual formation of a Connective Tissue capsule around the abscess is observed. As the abscess develops, There is a risk of its contents rupturing into the cerebral ventricles, leading to ventriculitis, increasing cerebral edema and intracranial pressure, and causing herniation complications, which ultimately lead to the patient's death.

The clinical picture of an abscess comprises general infectious symptoms, signs of progressive intracranial hypertension, and various focal neurological disorders that correspond to the localization of the abscess. These symptoms usually develop gradually. In typical cases, the signs of the infectious process gradually subside, against which background signs of intracranial hypertension increase and focal neurological deficits appear, resembling the picture of a brain tumor. Epileptic seizures may occur (in 30% of patients). Most patients complain of headaches, sometimes accompanied by nausea and vomiting. Many develop depressed levels of consciousness. Signs of meningeal irritation are occasionally detected. Cerebrospinal fluid (CSF) changes are usually nonspecific and most often boil down to an elevation in protein and a slight increase in cell count.

Suspicion of a brain abscess should arise in the presence of a chronic infection focus, progressive general cerebral disorders, and the onset of focal brain damage signs (including irritation phenomena such as epileptic seizures). CSF examination is not recommended when a brain abscess is suspected, as this Procedure increases the risk of herniation complications. Indirect signs of elevated intracranial pressure are quite frequently detected on fundus examination. Echoencephaloscopy may reveal a midline shift, confirming the presence of a space-occupying process in one of the cerebral hemispheres. However, the definitive solution for diagnosing brain abscesses is the timely performance of CT or MRI scans. These neuroimaging Methods allow for the precise Determination of the abscess Location and size, the presence of a capsule, the tracking of its developmental stages, the detection of signs of herniation complications, and other features of brain damage. Contrast-enhanced CT can be performed to obtain clearer images. In approximately 15% of cases, such examinations reveal multiple brain abscesses. Cerebral angiography also quite frequently detects a space-occupying brain lesion with a shift of CEREBRAL Arteries AND an avascular zone in the brain. Leukocytosis and an elevated ERYTHROCYTE SEDIMENTATION RATE (ESR) may be found in the peripheral blood, but these data are not specific for the diagnosis of brain abscesses. A targeted search for suspected sources of infection is of great importance: pneumonia, inflammatory diseases of the middle ear, frontal sinusitis, maxillary sinusitis, Oral Cavity diseases, inflammatory lesions of the scalp and soft Tissues of the face and neck, and open and penetrating traumatic brain injuries with cerebrospinal fluid leakage, etc. Brain abscesses must be differentiated primarily from neoplastic and parasitic lesions.

When a brain abscess is suspected, antibacterial therapy is initiated immediately. In doing so, the activity spectrum of the drugs and their ability to cross the blood-brain barrier and the abscess capsule must be taken into account. Currently, high doses of third-generation cephalosporins and metronidazole are increasingly used for these purposes. However, Surgical methods remain the primary treatment for brain abscesses. Total excision of the abscess along with its capsule is possible, as well as puncture Treatment of the abscess with aspiration of contents and cavity drainage. It is essential to ensure the identification of the causative agent. The choice of surgical approach depends on the patient's condition and the LOCATION OF THE abscess. In some cases, conservative management of brain abscesses may be performed. This is justified when a brain abscess is detected at the encephalitis stage; when it is small in size (up to 2 cm in diameter) with no signs of elevated intracranial pressure or herniation disorders; when abscesses are located deeply or are multiple, making surgical access technically difficult and fraught with an unacceptable risk of damaging vital CNS structures; or when there are contraindications to surgery.

Conservative therapy must be conducted under CT monitoring for at least 4 weeks. However, once the abscess capsule has formed, such therapy may not be sufficiently effective. Mortality rates for brain abscesses reach 15–25%. In the residual period, even with a favorable outcome, focal neurological deficits often persist, and the probability of developing epileptic syndrome is high.

Complications and Sequelae of Meningitis and Encephalitis

Among the early neurological complications of infectious and inflammatory CNS diseases, the most dangerous are a significant increase in intracranial pressure, hydrocephalus with obstructive disorders, epileptic syndrome and occasionally status epilepticus, secondary cerebrovascular disorders, and the development of subdural effusion. Systemic or somatic complications primarily include septic shock, pneumonia, DIC syndrome, myocardial infarction and cardiac arrhythmias, thromboembolism, pressure ulcers, etc.

The sequelae of infectious CNS lesions in the recovery and long-term periods are no less diverse. These may include residual focal neurological syndromes—limb paresis, cranial nerve dysfunctions (e.g., oculomotor disorders, Hearing impairment, etc.), psychiatric disorders, epileptic syndrome, and vegetative dysfunction syndrome. Most often, these neurological disorders tend to gradually recover with appropriate treatment and rehabilitation measures, but situations do arise where they cause permanent disability in patients.

Neurological Manifestations of HIV Infection

Pathomorphological signs of nervous system involvement are detected in 90% of HIV-infected patients. At the same time, neurological disorders with clearly defined clinical manifestations occur in approximately 50–70% of affected individuals. Moreover, in 10% of cases, neurological disorders are the very first manifestations of HIV infection. THE SPECTRUM OF neurological disorders in HIV infection is exceptionally broad, reflecting both the potential for virtually all PARTS OF THE nervous system to be drawn into the pathological process and the likelihood of all known forms of its damage developing.

Primary and secondary variants of nervous system involvement are possible in HIV infection. The first group is the result of direct, immediate involvement of the central and peripheral nervous systems by the retrovirus. The second group represents various pathological conditions that are consequences of immunodeficiency. These include opportunistic infections affecting the nervous system, central nervous system neoplasms, etc.

In the first weeks after infection with this disease, serous meningitis (or meningoencephalitis) may develop, presenting with meningeal syndrome, sometimes accompanied by cranial nerve involvement and moderate lymphocytic pleocytosis. In some cases, epileptic syndrome develops, and profound alterations of consciousness are possible, though most often such forms of the disease are reversible. Simultaneously, lymphadenopathy, Splenomegaly, and rashes may be detected, but serological tests at this stage frequently yield negative results.

The most frequent variant of CNS involvement is HIV encephalopathy. This condition typically occurs at various intervals following infection, usually against the background of pronounced immunosuppression. It develops gradually, initially manifesting as cognitive disorders. Its signs are diverse: headaches, fatigue, mood changes, memory impairment, difficulty concentrating, reduced work capacity, and Sleep disturbances. A subcortical-frontal type dementia symptom complex gradually forms. Motor disorders arise: ataxia, akinetic-rigid syndrome, oculomotor disorders, gait disturbances, and symptoms of oral automatism appear. As the disease progresses, confusion deepens, and epileptic seizures may occur. Death ensues several months after the onset of dementia. Pleocytosis and a mild increase in protein levels are found in the CSF of some patients. CT or MRI scans reveal cerebral atrophy and ventricular system enlargement, as well as symmetrical diffuse or multi-focal density changes in the white matter within the periventricular region and Basal Ganglia.

Vacuolar myelopathy (HIV myelopathy) is detected in 10–25% of patients. Pathomorphologically, it is characterized by demyelination

and spongy degeneration in the spinal cord. The lateral and posterior columns of the spinal cord are predominantly affected. The clinical manifestations of this nosological form consist of signs of progressive lower spastic paraparesis and proprioceptive sensory impairments in the legs, phenomena of sensory ataxia, paresthesias, and pelvic organ dysfunctions. The absence of pain is characteristic.

In addition, Peripheral Nervous System disorders can develop in HIV infection. One such form of pathology is acute inflammatory demyelinating polyneuropathy (Guillain-Barré syndrome). A feature of this disease is the appearance of mild pleocytosis in the CSF. The most frequent variant of peripheral nervous system involvement in HIV infection is distal symmetric sensorimotor polyneuropathy. It occurs in one-third of all patients and is an axonal neuropathy. Patients are typically troubled by burning and pain in the feet, which intensify with the slightest Touch to the skin of the legs and impair walking. Examination reveals hyperesthesia in the distal parts of the arms and legs, depressed Reflexes, weakness and Atrophy of the small Muscles of the feet, and vegetative-trophic disorders. Some patients develop signs of peripheral autonomic failure with visceral dysfunction—orthostatic hypotension, cardiac arrhythmias, Urinary Incontinence or retention, constipation, impotence, etc. Multiple mononeuropathies involving Cranial and Spinal Nerves are less common. Myopathy may arise at various Stages of the development of HIV infection. Clinically, it resembles polymyositis and is characterized by myalgias, subacutely developing weakness in the proximal limb muscles sometimes accompanied by atrophy, as well as elevated creatine phosphokinase activity.

Aside from neurological complications caused by the direct action of HIV infection, there is a whole range of pathological conditions that result from immunodeficiency. These include toxoplasmic encephalitis (developing in 20–30% of AIDS patients), Cryptococcal meningitis, cytomegalovirus infection with nervous system involvement (meningoencephalitis, polyradiculomyelitis), Various Forms of herpetic infection (encephalitis, radiculoganglionitis, myelitis, neuropathies of Cranial Nerves II and VII), Listeriosis infection leading to meningitis or brain abscess, tuberculosis, and neurosyphilis. Approximately 5% of patients develop progressive multifocal leukoencephalopathy, which is based on a multi-focal demyelinating lesion predominantly of the cerebral white matter of viral origin against the background of immunodeficiency. Neoplastic lesions of the CNS—primary lymphomas—can also occur in immunosuppressed states. They manifest as progressive symptoms of focal brain damage, intracranial hypertension syndrome, and epileptic seizures. Acute ischemic and hemorrhagic cerebrovascular accidents occupy a definite place among the neurological complications of HIV infection.

In diagnosing various neurological complications of HIV infection, a thorough medical history, serological tests, assessment of neuropsychological status, and modern instrumental neurological diagnostic methods, alongside a comprehensive somatic examination, are of paramount importance. Specific treatment includes antiviral agents (such as azidothymidine) and immunotherapy. Corticosteroids, cytostatics, and plasmapheresis are also employed. Management of many neurological disorders can prove effective and, in some cases, helps achieve the regression of symptoms and significantly prolongs patients' lives.

Clinical Cases

Case 1

A 19-year-old male awoke in the morning with a severe diffuse headache, nausea, repeated vomiting, and chills. He reports pain upon moving his eyes, as well as pain in the muscles of the neck, trunk, lower back, and extremities. Body temperature rose to 39°C. Upon examination, the patient appears drowsy and lethargic, is partially disoriented in time and space, and Answers questions with difficulty. He resists examination. There is marked nuchal rigidity and bilateral Kernig's signs. Movements in the arms and legs are unimpaired. Tendon and periosteal reflexes are symmetrical, with inconstant pathological plantar reflexes. Generalized hyperesthesia. Blood pressure is 140/85 mm Hg, pulse is regular at 110 bpm. Blood work: leukocytes 16.0 x 10⁹/L, ESR 28 mm/h. Cerebrospinal fluid is cloudy with a milky-gray color, opening pressure 390 mm H₂O, protein 2.6 g/L, cell count 8000 x 10⁶/L (predominantly neutrophils), meningococci present.

   • List the main neurological and somatic disorders.

   • State the indications for cerebrospinal fluid examination in this patient.

   • Evaluate the cerebrospinal fluid findings.

   • Formulate the topical diagnosis.

   • Formulate and justify the clinical diagnosis.

   • Outline the main directions for differential diagnosis.

   • Outline the instrumental and Laboratory examination plan.

   • List other possible symptoms of the disease.

   • Indicate the Key Components of the therapeutic regimen.

   • Select the optimal initial etiotropic therapy regimen.

   • How to determine the required duration of antibiotic therapy?

   • Determine the prognosis for this condition.

   • Name potential complications and long-term sequelae of the disease.

Case 2

A 12-year-old child developed Swelling in the Cytology/practical/97.html">Parotid salivary gland area a week ago, accompanied by pain upon swallowing and generalized weakness. Body temperature was 37.5–38°C. Mumps (epidemic parotitis) was diagnosed. With treatment, the general condition improved. On the 7th day from the onset of the illness, the child awoke in the morning with a severe headache, nausea, and frequent vomiting. Upon examination, the child is restless and complains of headaches. Nuchal rigidity and moderate bilateral Kernig's signs are elicited. The child cannot tolerate bright light. Noise and loud conversations exacerbate the headache. Resists examination. No distinct focal neurological deficits are identified. Blood tests reveal leukocytosis of 12.0 x 10⁹/L, ESR 23 mm/h. Cerebrospinal fluid is clear, opening pressure 280 mm H₂O, protein 0.66 g/L, lymphocytes 130 x 10⁶/L.

   • List the main neurological and somatic disorders.

   • State the indications for cerebrospinal fluid examination in this patient.

   • Evaluate the cerebrospinal fluid findings.

   • Formulate the topical diagnosis.

   • Formulate and justify the clinical diagnosis.

   • Outline the main directions for differential diagnosis.

  • Outline the plan for instrumental and laboratory investigations.

  • Specify the Main Components of the therapeutic program.

  • Determine the prognosis for this condition.

  • Name the potential complications and long-term consequences of the disease.

Option 3

A 48-year-old man presents with severe generalized headaches, nausea, vomiting, tinnitus, and hearing loss. Upon examination, he is lethargic, responds sluggishly to verbal stimuli, does not recognize relatives, and is disoriented in place and time. His speech is quiet and slurred. Examination reveals moderately pronounced Kernig's signs, nuchal rigidity, and gross facial asymmetry (the palpebral fissure is wider on the left, and the Mouth is deviated to the right). Body temperature is 38.5°C. According to his relatives, he had been complaining of malaise, headaches, somnolence, and low-grade fever for three weeks. He did not seek medical attention. About a year ago, he underwent fluorography regarding some focal pulmonary lesions. Blood tests: ESR 16 mm/h, leukocytes 12.0 x 10⁹/L. Cerebrospinal fluid is clear, opening pressure 340 mm H₂O, protein 2.0 g/L, pleocytosis 160 x 10⁶/L (80% lymphocytes), glucose 1.2 mmol/L. After a few hours, a delicate web-like pellicle forms in the CSF tube.

  • List the neurological and somatic disorders.

  • Outline the indications for cerebrospinal fluid analysis in this patient.

  • Evaluate the changes in the cerebrospinal fluid.

  • Formulate the topographic diagnosis.

  • Formulate and substantiate the clinical diagnosis.

  • Determine the main directions for the differential diagnosis.

  • Outline the plan for instrumental and laboratory investigations.

  • List the characteristic cerebrospinal fluid changes that confirm the etiology of this disease.

  • What additional anamnestic details need to be specifically clarified?

  • Specify the main Components of the therapeutic program.

  • Determine the prognosis for this condition.

  • Name the potential complications and long-term consequences of the disease.

Option 4

A 37-year-old female patient felt moderate headaches and nausea in the morning, with her body temperature rising up to 38°C. By evening, the headaches worsened; she became lethargic and obtunded, complaining of weakness in her arms and legs. The next day, family members noticed oddities in her behavior. Around the same time, she experienced a seizure accompanied by loss of consciousness, generalized convulsions, and foaming at the mouth. Clinical examination revealed somnolence and disorientation to her surroundings. Findings included severe memory impairment and indistinct speech, horizontal nystagmus, nuchal rigidity, positive Kernig's signs, generalized hyperesthesia, heightened and asymmetrical (D>S) deep tendon reflexes, release signs (oral automatism reflexes), as well as pathological hand and FOOT signs. Blood tests: leukocytes 9.0 x 10⁹/L, ESR 15 mm/h. Cerebrospinal fluid: pressure approximately 250 mm H₂O, 15 x 10⁶/L lymphocytes, protein 0.99 g/L. On the third day, her condition worsened. Consciousness is depressed, she does not open her eyes, verbal contact is impossible, and she does not respond to examination. In response to painful stimuli, limb flexion is observed, accompanied by periodic tonic tension of the muscles in the arms and legs. Urinary incontinence is present. A CT scan revealed areas of heterogeneous hypodensity in the brain parenchyma within the basal regions of the left frontal lobe and both temporal lobes.

  • List the main neurological disorders.

  • State the indications for cerebrospinal fluid examination in this patient.

  • Evaluate the cerebrospinal fluid changes.

  • How can the neurological disorders on the third day of the disease be characterized?

  • Explain the CT scan findings.

   • Establish the topical diagnosis.

   • Formulate and justify the provisional clinical diagnosis.

   • Outline the main directions for differential diagnosis.

   • Outline the plan for instrumental and laboratory investigations.

   • What methods can be used to confirm the suspected etiology of the disease?

   • What additional anamnestic details should be specifically clarified?

   • Specify the core components of the therapeutic regimen.

   • Determine the prognosis of the disease.

   • State the potential complications and long-term consequences.

Case 5

   A 52-year-old man fell ill about five years ago, when shooting pains in his legs appeared for no apparent reason. Shortly after, he began to experience tingling and a "crawling sensation" (paresthesia) in his feet. He developed unsteadiness and gait ataxia, which worsened in the dark, along with a sensation of losing support beneath his soles. About a year ago, his Vision deteriorated abruptly. Recently, he has noticed difficulty with urination. Examination revealed anisocoria S>D. Pupillary light reflex is sluggish, whereas convergence and accommodation reactions are normal. Muscle strength in the upper and lower extremities is good. Muscle tone in the legs is somewhat decreased. Tendon and periosteal reflexes from the upper limbs are brisk and symmetrical. Knee and Achilles reflexes are absent. There are no pathological plantar reflexes. He walks unsteadily, with a broad-based gait, lifting his feet high and striking them down on the floor with excessive force. Romberg's test shows that he maintains balance only with his eyes open. Heel-to-knee testing is severely impaired bilaterally. Tactile sensitivity is impaired in the feet. He cannot distinguish the direction of passive movements of his toes. Cerebrospinal fluid analysis reveals a protein level of 0.66 g/L, 30 x 10⁶/L lymphocytes, and a positive Wassermann reaction.

   • List the main neurological disorders.

   • Determine the nature of the sensory disturbances.

   • Determine the nature of the motor disturbances.

   • Explain the nature of the altered pupillary reactions.

   • Evaluate the cerebrospinal fluid findings.

   • Establish the topical diagnosis.

   • Formulate and justify the clinical diagnosis.

   • Outline the main directions for differential diagnosis.

   • Outline the plan for instrumental and laboratory investigations.

   • What additional anamnestic details should be specifically clarified?

   • Specify the core components of the therapeutic regimen.

   • Determine the prognosis for this disease.