A 75 year old man presented with fever and altered sensorium for one week. The patient had no history of tuberculosis, diabetes or hypertension. Laboratory tests including CSF analysis were normal. His HIV status was negative. At the time of initial presentation ,a plain & contrast CT scan of the brain was performed.

Fig 1

The patient did not respond to conservative management and an MRI of the brain was performed 10 days later.

Fig 2

The patient was followed up with a CT scan of the brain two weeks later.

Fig 3

Radiological Findings :

The initial CT scan films are unremarkable.

The MR examination done 10 days after the admission shows high signal intensity in both temporal lobes extending into insular cortices on T2 weighted images. Hyperintense signals are also seen in inferior frontal lobes bilaterally. The involvement is asymmetrical with right side more severely involved. There is no hydrocephalus, mass effect or midline shift.

The second CT examination of the brain shows nonenhancing, hypodense areas bilaterally in the temporal, frontal & occipital lobes suggestive of encephalomalacic changes. There is no ventricular dilation or mass effect.

Diagnosis :

On the basis of clinical presentation, course of the patient in the hospital and typical radiological findings in serial imaging studies, a diagnosis of herpes simplex encephalitis was made.

 

Differential Diagnosis :

The differential diagnosis of the above condition may include other inflammatory brain parenchymal diseases causing demyelination particularly HIV encephalopathy and CMV encephalitis.

HIV ENCEPHALOPATHY:

This condition develops in around 60% of seropositive patients. The imaging signs of HIV encehalopathy most frequently are cerebral atrophy as manifested by ventricular enlargement & sulcal widening and/or cerebellar atrophy in a relatively young individual; diffuse hyperintensity in the periventricular white matter and centrum semiovale on T2 weighted images and sometimes patchy focal areas of hyperintensity on T2 weight images on MRI. CT will demonstrate these areas as being of diminished attenuation. The frontal lobes are more frequently involved than the temporal lobes.

CMV ENCEPHALITIS:

CMV encephalitis sometimes occurs in immunocompromised adult hosts and may represent reactivation of previously silent infection. CT & MRI findings are of thick, somewhat nodular, confluent periventricular rims. Subependymal enhancement is sometimes seen following contrast administration.

Discussion :

Herpes encephalitis is the most common cause of sporadic viral encephalitis in immunocompetent individuals. It is common in both in the pediatric age group as well as in adults. Neonatal herpes simplex encephalitis is usually caused by HSV 2(genital herpesvirus) whereas in older patients is caused by HSV 2(oral herpes virus).The mechanism by which the virus reaches the brain is controversial. The herpes virus appears to live in the trigeminal ganglion in a latent state, having reached the ganglion by an initial infection in the face.Under certain conditions, which sometimes may be related to immunocompetence, the virus may reach the inferior frontal and temporal areas of brain.

HSV 1 has a predilection for the limbic system. Infection is therefore localized to the temporal lobes, insular cortex, subfrontal areas and cingulate gyri. Involvement may initially appear to be unilateral but is typically followed by less severe contralateral disease. This 'sequential bilaterality' is highly suggestive of herpes simplex Encephalitis. Infrequently, cranial nerve inflammation occurs - involvement of trigeminal the nerve being the most common.

Patients typically present with altered mental status. Seizures, fever and headaches are also common. The mortality rate with HSE is between 50% to 60% with significant long term morbidity. A rise in antibody titre is diagnostic, but may take as long as 10 to 20 days to develop. Though, done rarely, identification of viral antigen on brain biopsy is definitive.

The primary role of cross sectional imaging in the evaluation of HSE is to confirm the clinical diagnosis, indicate best site for biopsy if imaging findings are inconclusive and to exclude tumour or abscess. The findings on CT or MRI may be present within 2 or 3 days after the initiation of symptoms. The diagnosis of HSE is not proven by CT or MRI but involvement of unilateral or bilateral temporal lobe and/or frontal lobe is sufficiently typical of HSE, that an active treatment with antiviral agent is recommended.

Imaging findings on CT scan early in the course of the disease may be normal or subtly abnormal. Low density lesions in temporal lobes with mild mass effect are common initial abnormalities. There may be ill defined patchy or gyriform enhancement. MRI is more sensitive than CT in detecting early changes of HSE 1.Typical early findings include high signal intensity in the temporal lobe or cingulate gyrus on T2 weighted scans. The signal abnormalities often extend into the insular cortex and spare the putamen. Enhancement following contrast administration is unusual. Follow up scans obtained 1 to 2 weeks after the onset of the disease demonstrate progressively more widespread abnormalities with involvement of the contralateral temporal lobe, insula and cingulate gyrus. Encephalomalacia,atrophy and dystrophic calcifications are common late sequele..