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Joseph Junewick, MD FACR
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Herpes Simplex Viral Encephalitis

Case Detail

Anatomy: Brain-Spine
Joseph Junewick, MD FACR
Diagnostic Category: Infectious-Inflammatory
Created: over 11 years ago
Updated: over 9 years ago
Tags: PEDS
Modality/Study Types: MR
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Teenager with headache, fever and progressive confusion.

Case Images


Herpes Simplex Viral Encephalitis

Clinical Notes

CSF evaluation with 55 white blood cells (all monocytes), 51 red blood cells and elevated protein on the 4th vial.


MRI – Thickened left temporal cortical gray matter, hypointense on T1 and hyperintense on T2 and T2 FLAIR sequences.


Herpes simplex accounts for 10-20% of viral encephalitis but is still relatively rare, accounting for approximately 3 new cases per 100,000 people per year. In neonates, herpes simplex encephalitis is usually acquired through the birth canal whereas non-neonatal infection is usually the result of reactivation of latent virus in the trigeminal ganglion.

Headache and fever are the most common presenting features. Intellectual impairment, aphasia, meningeal signs, seizures and parasthesias may occur later and may be rapidly progressive. CSF analysis shows pleocytotic leukocytosis, erythrocytosis and elevated protein. Virus is usually not cultured and HSV antibodies are not usually found for upto 1 – 3 weeks. The polymerase chain reaction is a sensitive and specific test.

Neonatal disease is spread hematogenously and penetrates the blood-brain barrier or directly infects endothelial cells. Neonatal infections are typically secondary to the HSV-1 virus and involve the periventricular white matter and meninges. Non-neonatal disease is usually secondary to the HSV-2 virus and progresses in a retrograde fashion along the orbitofrontal and temporal meningeal branches of the trigeminal ganglion during latent reactivation. Non-neonatal encephalitis predilects limbic disease; typically temporal lobe, hippocampus, parahippocampus and amygdala involvement is seen.

CT is not usually positive for 3 to 5 days after the onset of symptoms. MR is the preferred modality. Early there is T2 hyperintensity in the infrafrontal and insular regions with sparing of the basal ganglia. T1 cortical hyperintensity occurs later and is related to petechial hemorrhage. Parenchymal and leptomeningeal enhancement may be seen. Often there is restricted diffusion. MR spectroscopy will show decreased NAA, increased choline and occasionally elevated lactate peaks.


Barkovich AJ. Pediatric Neuroimaging, 4th Ed. Lippincott, Williams and Wilkins (2005).

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