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Pathology- Cerebral Infections
I. Encephalitis
A. Definition: Infection of the brain parenchyma (functional tissue of the brain).
B. Etiology: Primarily viral, most commonly Herpes Simplex Virus (HSV).
C. Pathogenesis: HSV encephalitis typically results from reactivation of latent HSV in the trigeminal ganglion, leading to infection of the temporal lobe.
D. Presentation: * Confusion * Behavioral changes * Altered consciousness * Seizures (severe cases) * Key diagnostic clue: Simultaneous perioral (around the mouth) involvement.
E. Diagnosis: * Imaging: Brain imaging (e.g., MRI) may show temporal lobe abnormalities. * Laboratory: Polymerase chain reaction (PCR) on cerebrospinal fluid (CSF) to identify HSV DNA. * Histology: Necrotizing inflammation with characteristic herpetic intranuclear inclusions in neurons and glial cells (post-mortem).
F. Treatment: Urgent antiviral treatment is essential.
II. Cerebral Abscess
A. Definition: Localized brain infection with tissue destruction.
B. Etiology: Primarily bacterial, often mixed infections.
C. Pathogenesis: * Direct spread: From paranasal sinuses, middle ear, or teeth. * Hematogenous spread: From septic emboli (e.g., infective endocarditis).
D. Presentation: Symptoms of an infected intracranial mass: * Headache * Nausea * Vomiting * Fever * Seizures * Focal neurological signs (depending on abscess location).
E. Diagnosis: Primarily through CT scan.
F. Treatment: Surgical drainage and prolonged antibiotic therapy.
G. Prognosis: High mortality (20%) and significant morbidity (50% of survivors have persistent neurological deficits or epilepsy).
III. Progressive Multifocal Leukoencephalopathy (PML)
A. Definition: Demyelinating disease of the central nervous system white matter.
B. Etiology: JC virus (polyomavirus).
C. Risk Factors: Virtually exclusive to immunocompromised individuals (e.g., HIV/AIDS, transplant recipients).
D. Pathogenesis: JC virus infection leads to multiple foci of demyelination in the white matter, which can coalesce.
E. Histology: Viral inclusions in the nuclei of astrocytes, macrophages, and oligodendrocytes within demyelinated areas.
F. Diagnosis: * Clinical presentation: Neurological symptoms. * Imaging: Characteristic MRI findings. * Laboratory: Detection of JC virus DNA in CSF.
G. Prognosis: High mortality (up to 50% within 3 months).
I. Encephalitis
A. Definition: Infection of the brain parenchyma (functional tissue of the brain).
B. Etiology: Primarily viral, most commonly Herpes Simplex Virus (HSV).
C. Pathogenesis: HSV encephalitis typically results from reactivation of latent HSV in the trigeminal ganglion, leading to infection of the temporal lobe.
D. Presentation: * Confusion * Behavioral changes * Altered consciousness * Seizures (severe cases) * Key diagnostic clue: Simultaneous perioral (around the mouth) involvement.
E. Diagnosis: * Imaging: Brain imaging (e.g., MRI) may show temporal lobe abnormalities. * Laboratory: Polymerase chain reaction (PCR) on cerebrospinal fluid (CSF) to identify HSV DNA. * Histology: Necrotizing inflammation with characteristic herpetic intranuclear inclusions in neurons and glial cells (post-mortem).
F. Treatment: Urgent antiviral treatment is essential.
II. Cerebral Abscess
A. Definition: Localized brain infection with tissue destruction.
B. Etiology: Primarily bacterial, often mixed infections.
C. Pathogenesis: * Direct spread: From paranasal sinuses, middle ear, or teeth. * Hematogenous spread: From septic emboli (e.g., infective endocarditis).
D. Presentation: Symptoms of an infected intracranial mass: * Headache * Nausea * Vomiting * Fever * Seizures * Focal neurological signs (depending on abscess location).
E. Diagnosis: Primarily through CT scan.
F. Treatment: Surgical drainage and prolonged antibiotic therapy.
G. Prognosis: High mortality (20%) and significant morbidity (50% of survivors have persistent neurological deficits or epilepsy).
III. Progressive Multifocal Leukoencephalopathy (PML)
A. Definition: Demyelinating disease of the central nervous system white matter.
B. Etiology: JC virus (polyomavirus).
C. Risk Factors: Virtually exclusive to immunocompromised individuals (e.g., HIV/AIDS, transplant recipients).
D. Pathogenesis: JC virus infection leads to multiple foci of demyelination in the white matter, which can coalesce.
E. Histology: Viral inclusions in the nuclei of astrocytes, macrophages, and oligodendrocytes within demyelinated areas.
F. Diagnosis: * Clinical presentation: Neurological symptoms. * Imaging: Characteristic MRI findings. * Laboratory: Detection of JC virus DNA in CSF.
G. Prognosis: High mortality (up to 50% within 3 months).
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