Viral Infections
After viral multiplication in extraneural tissues, dissemination to CNS occurs by hematogenous route or spread along nerve fibers.
General Comments
CNS Viral Syndromes
Meningitis: headache, photophobia, stiff neck; no brain symptoms; usually self-limited.
Encephalitis: brain parenchyma involved with seizures, impaired consciousness, focal signs.
Myelitis: spinal cord inflammation.
CSF findings similar in all 3 syndromes: increased pressure, lymphocytic pleocytosis, moderate increase in protein content, normal glucose content.
Biologic properties differ: myxoviruses attack ependymal cells; herpes simplex produces latent infection, preference for frontal and temporal lobes; enteroviruses, togaviruses epidemic.
Diagnostic clues: epidemics, seasonal occurrence.
Diagnosis: virus isolation, antibody tests, polymerase chain reaction for viral nucleic acids. Some viruses (e.g., mumps) can be isolated from CSF; others (e.g., poliovirus, herpes simplex virus [HSV] type 1) rarely recovered.
Serology: antibodies rise 4-fold from first few days to convalescent phase (3–5 weeks).
If brain biopsy done: immunostaining, electron microscopy, injection of tissue into susceptible animals or cultured cell lines.
Treatment
Specific antiviral agents: acyclovir for HSV; acyclovir, famciclovir, foscarnet for varicella-zoster virus (VZV); ganciclovir,
foscarnet for cytomegalovirus (CMV); reverse transcriptase, protease inhibitors for human immunodeficiency virus (HIV).
foscarnet for cytomegalovirus (CMV); reverse transcriptase, protease inhibitors for human immunodeficiency virus (HIV).
Immunization available for rabies, poliomyelitis, hepatitis A and B, mumps, influenza, rubella, measles, chickenpox (varicella), smallpox.
Vector control, mass immunization: most practical means of control.
Acute Viral Infections
Herpesvirus Infections
HSV type 1, HSV type 2, VZV, Epstein-Barr virus, CMV, human herpes virus (HHV)-6, HHV-7, HHV-8 (also known as Kaposi sarcoma herpes virus). All cause neurologic disease. Occur sporadically or as opportunistic infection in immunocompromised people.
Herpes Simplex Encephalitis
Epidemiology: most common cause of fatal sporadic encephalitis in United States. Early diagnosis crucial because antiviral treatment is available and usually effective. Mostly caused by HSV-1.
Clinical findings: fever, headache, altered consciousness and personality, usually abrupt onset; sometimes seizures, meningism. Behavioral changes vary from withdrawal to agitation with hallucinations. Course progressive for hours to days, with increasing obtundation, focal signs. Herpetic labial lesions in few cases.
CSF: increased pressure, lymphocytic pleocytosis, red blood cells (typical of herpes but not diagnostic), usually normal glucose. First CSF sample normal in 5% to 10%. Detection of viral DNA by PCR is diagnostic.
EEG abnormal in 80%: diffuse slowing or focal changes over temporal areas; periodic complexes against slow-wave background.
Imaging. CT, low-density abnormality (temporal lobe), mass effect, or linear contrast enhancement in 90%. Often normal in first week of disease. MRI: focal abnormalities often present in first week.
Treatment: if clinical picture suggests HSV encephalitis, start intravenous acyclovir immediately after CSF sent for HSV PCR. Continue for 14 days unless initial PCR negative. Treat brain edema with corticosteroids.
Prognosis: mortality 70–80% without treatment; 28% with treatment. Outcome depends on patient’s age, level of consciousness, prompt treatment.
Herpes Zoster (Shingles)
Inflammatory lesions in dorsal root ganglia due to VZV. Often seen with systemic illness or immunosuppression.
Neuralgic pain or dysesthesia in distribution of affected root. Followed in 3–4 days by characteristic vesicular rash in same distribution. Resolves in 10–14 days. Simultaneous painless adenopathy. Spinal ganglia most often affected; cranial ganglia in 20%. Almost always unilateral.
Ophthalmic zoster: ophthalmic division of trigeminal ganglion. Complications: permanent eye changes after panophthalmitis or corneal scarring; temporary or permanent paresis of ocular muscles.
Geniculate herpes: otic zoster with involvement of geniculate ganglion (Ramsay Hunt syndrome); facial paralysis, loss of taste over anterior two thirds of tongue. Rash confined to tympanic membrane and external auditory canal.
Treatment: systemic acyclovir (oral or intravenous) or newer formulations (famciclovir, valacyclovir), depending on severity; analgesics, nonspecific topical medications for rash. Postherpetic neuralgia difficult to treat: amitriptyline, anticonvulsants (carbamazepine, phenytoin, gabapentin). Refractory to usual analgesics.
Cytomegalovirus Infection
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