Purulent CNS Infections: Meningitis and Abscess
Inflammation of the meninges is classified into leptomeningitis (inflammation of the pia and arachnoid maters, most common) and pachymeningitis (inflammation of the dura mater).
Acute purulent meningitis is the most frequent manifestation of pyogenic CNS infection. Causative agents vary by age: group B streptococci and Escherichia coli predominate in the perinatal period, whereas Neisseria meningitidis, Streptococcus pneumoniae, and Haemophilus influenzae are more common in adults. In meningococcal infection, the pathogen enters hematogenously, and severe septicemia can complicate into disseminated intravascular coagulation (DIC) with acute adrenal insufficiency (Waterhouse-Friderichsen syndrome).
Pathogenesis of Purulent Meningitis:
- Impaired intracranial hemodynamics and increased blood-brain barrier permeability.
- Increased cerebrospinal fluid (CSF) production and development of brain edema.
- Direct toxic effects on neural tissue.
Macroscopically, the brain in purulent meningitis is edematous with flattened gyri. The exudate is localized in the subarachnoid space. In pneumococcal and meningococcal infections, it covers the basal and convex surfaces (frontal and parietal lobes) in the shape of a 'cap' or 'hood'. Over time, the exudate thickens and contains fibrin. Inadequate early treatment leads to edema, brain herniation, and death due to tonsillar herniation (coning). A late complication is the obliteration of CSF outflow pathways, leading to hydrocephalus.
Brain abscess is a localized purulent infection of the brain parenchyma. Macroscopically, it appears as a pus-filled cavity, most frequently located in the frontal lobes, parietal lobes, or cerebellum. Within a few weeks, a dense fibrous-glial capsule forms around the lesion.
Specific Infections: Tuberculosis and Neurosyphilis
Non-purulent infections are characterized by specific granulomatous or atrophic changes that can lead to the destruction of myelin sheaths and neuronal cell death.
Tuberculous meningitis and CNS tuberculosis have a subacute course and present in two primary forms:
- Tuberculous meningitis: Hematogenous dissemination from the lungs. A gelatinous, caseous exudate accumulates at the base of the brain. Microscopic examination reveals a fibrinous-caseous exudate with Langhans giant cells and thrombo-necrotic vasculitis. Mortality reaches 50%, and hydrocephalus is a frequent outcome.
- Tuberculoma: An encapsulated focus of caseous necrosis (more common in the cerebral hemispheres in adults, and in the cerebellum in children).
Neurosyphilis (Treponema pallidum infection) often presents atypically today. Two late forms are distinguished:
- Tertiary syphilis: Meningovascular form characterized by the formation of miliary gummas (foci of necrosis surrounded by a lymphoplasmacytic infiltrate and Langhans giant cells).
- Parenchymatous (quaternary) syphilis:
- General paresis (general paralysis of the insane): Develops 10–15 years after infection. Characterized by subacute encephalitis, syphilitic capillaritis, ischemia, and progressive cortical atrophy (especially of the frontal lobes).
- Tabes dorsalis: Occurs after 8–12 years. Morphologically manifested by demyelination and shrinkage of the posterior (dorsal) columns of the spinal cord due to Wallerian degeneration. Clinically, this causes loss of proprioception, lancinating pains, and absent deep tendon reflexes.
Viral CNS Infections
Viral infections typically manifest as serous meningitis or encephalitis.
Viral meningitis is mainly caused by enteroviruses. Macroscopically, meningeal edema is observed, while microscopic examination reveals lymphocytic infiltration. The disease follows a benign course, with recovery in 2–3 weeks.
Acute viral encephalitis (herpes simplex, arboviruses, rhabdoviruses) has distinct pathohistological features:
- Perivascular infiltrates (lymphocytes, monocytes).
- Microglial hyperplasia forming glial nodules.
- Neuronophagia (phagocytosis of necrotic neurons by macrophages).
Definitive diagnosis of viral encephalitis requires the identification of specific intracellular inclusion bodies within the neural tissue, whereas recovering the virus itself from the CSF is extremely rare.