The neurologic complications of HSV-2 infection are reviewed by researchers at University of Kentucky College of Medicine, Lexington. HSV-2-associated neurologic disease results from primary infection or reactivation of latent HSV-2. Primary infection occurs in neonates but is usually delayed until adolescence and adulthood, following sexual activity. HSV-2 latency and reactivation is centered in sacral ganglia, but may also be widespread in the CNS. Approximately 90% of infections are unrecognized. Neurological complications of HSV-2 infection involve any part of the neuraxis. Encephalitis (HSE) is the most frequent manifestation of HSV-2 in neonates, and onset is heralded by focal or generalized seizures. CSF shows a lymphocytic pleocytosis, increased protein, and PCR positive for HSV-2. Compared to HSV-1 infection, HSV-2 encephalitis has a higher frequency of seizures, greater pleocytosis and protein level in CSF, and more severe structural brain damage on imaging. Other neurological complications of HSV-2 infection occur mainly in adults and include acute aseptic meningitis, recurrent aseptic meningitis (sometimes called Mollaret meningitis), ascending myelitis, lumbosacral radiculopathy, cranial neuropathy (Bell palsy), and acute retinal necrosis. HSV-2 CNS complications appear early in the course of HIV/AIDS. Diagnosis of HSV infection of the nervous system is made by PCR assays of CSF. Viral culture and serological assays for HSV antibodies may also be useful. Acyclovir is standard therapy. [1]

COMMENT. American Academy of Pediatrics Red Book (27th ed, 2006) finds that one third of cases of HSV infection in the neonate involve the CNS. CNS disease usually manifests between the second and third weeks of life. HSV-2 is the most common cause of disease in neonates, and accounts for 75% of cases.