A positive polymerase chain reaction for herpes in the cerebrospinal fluid usually establishes the diagnosis of herpetic meningitis. A negative polymerase chain reaction makes the diagnosis of herpetic meningitis very unlikely. Viral cultures from the affected brain tissue remain the most reliable diagnostic method but they are seldom done because of the inherent risk of brain biopsy. Magnetic resonance imaging of the brain may reveal typical changes depending on the time of diagnosis (Figure 69.1).

A	B	C

Figure 69.1.— Evolution of MRI changes in a patient with herpetic meningitis. [A] First MR, T1 axial image shows temporal pole asymmetry; [B] MRI contrast T1 axial, seven days later shows white matter and vascular interhemisphere asymmetry; and [C] MRI T1 axial image one month after the first MRI shows hypointensity in the right temporal pole.

Atypical changes such as diffuse edema or posterior fossa abnormalities (Figure 69.2) may prevail early in the course of herpetic meningitis.

A	B	C

Figure 69.2.— Patient with herpetic meningitis. [A] Contrast CT demonstrating a non enhancing low density area in the left cerebellar dentate nucleus and abnormal increased enhancement of the cerebellar folia extending into the parenchyma; [B] Coronal T2 weighted image at the level of the cerebellum. Note bilateral high signal abnormality of the cerebellar hemispheres and left cerebellar peduncle; [C] Coronal T1 weighted image at the level of the cerebellum. Note gyriform enhancement of the cerebellar hemisphere bilaterally and signal abnormality compromising the folia and the underlying white matter of the cerebellum.

Acyclovir 20 mg/kg every 8 hours for 21 days is the treatment of choice in term neonates with normal renal function.

Sepsis may cause coma in neonates even without evidence of meningitis. The exact mechanism for encephalopathy is not clear. Fever, metabolic alterations, and hypotension are contributing factors. Sepsis is diagnosed on clinical grounds and confirmed by blood culture.

Intraparenchymal, subdural, and epidural hematomas may produce coma in neonates. The mechanisms of coma are transtentorial and subfalcial herniations with supratentorial hematomas and direct brainstem compression with infratentorial hematomas. Infratentorial (Figure 69.2) and supratentorial hematomas are diagnosed by CT scan of the brain. Intraparenchymal bleeding most often occurs in the cerebral hemispheres. Coagulation disorders are the most frequent cause of intraparenchymal bleeding. Correction of the bleeding diathesis is imperative. Evacuation of the intraparenchymal hematoma is seldom possible or needed. Subdural and epidural hemorrhages are due to trauma or coagulation disorders. Subdural and epidural supratentorial hematomas are due to a tear in a meningeal artery or cerebral bridging vein. Eye deviation responsive to caloric testing and focal seizures may be present. Supratentorial subdural and epidural hematomas are treated by evacuation if they are considered clinically significant. Infratentorial subdural hematomas are usually due to tentorial lacerations or occipital osteodiastasis due to difficult deliveries.

Figure 69.2.— T1 axial MRI of the brain demonstrates an infratentorial subdural hematoma.