Answer for BIR CoW 25 Feb 2024
HHV encephalitis
Findings
FLAIR hyperintensity noted in the dorsomedial nucleus of bilateral thalamus and in bilateral medial temporal cortex showing diffusion restriction with low ADC values. On contrast administration, there is no abnormal enhancement. After 3 weeks of intensive care admission and intravenous antivirals – Complete resolution of the FLAIR hyperintensities noted with no abnormal diffusion restriction.
Discussion
Hb – 13.2 gm/dl TC – 14,350 cells/mm3 Platelets – 3,02,040 platelets/microlitre Lumbar puncture and CSF analysis – Appearance – clear Proteins – low Glucose – normal CBNAAT - negative Viral panel workup – HSV = negative Enterovirus = negative Adenovirus = negative The CSF analysis confirmed viral aetiology and the viral panel workup was negative for most of the common causes of viral encephalitis.
Etiology - More than 90% of the general population is seropositive for HHV-6 by 2 years of age. Most primary infections are asymptomatic, after which the virus remains latent. Clinical Issues - HHV-6 can become pathogenic in immunocompromised patients, especially those with hematopoietic stem cell or solid organ transplantation. The median interval between transplantation and onset of neurologic symptoms is 3 weeks. Patients typically present with altered mental status, short term memory loss, and seizures Imaging - NECT scans are typically normal. MR shows predominant or exclusive involvement of one or both medial temporal lobes (hippocampus and amygdala) (12-54). Extrahippocampal disease is less common than with HSE. Transient hyperintensity of the mesial temporal lobes on T2WI and FLAIR with restriction on DWI is typical. T2* (GRE, SWI) scans show no evidence of hemorrhage. HHV-6 encephalitis usually involves just the medial temporal lobes, but, if extrahippocampal lesions are present, it may be difficult to distinguish from HSE solely on the basis of imaging findings.
Differential Diagnosis
1) The major differential diagnosis is HSE. The disease course of HSE is more fulminant. Extratemporal involvement and hemorrhagic necrosis are common in HSE but rare in HHV-6 encephalopathy. In contrast to HSE, in HHV-6, MR abnormalities tend to resolve with time.
2) Postictal hippocampal hyperemia is transient, and extrahippocampal involvement is absent. References - Osborn's brain - 2nd edition
Findings
FLAIR hyperintensity noted in the dorsomedial nucleus of bilateral thalamus and in bilateral medial temporal cortex showing diffusion restriction with low ADC values. On contrast administration, there is no abnormal enhancement. After 3 weeks of intensive care admission and intravenous antivirals – Complete resolution of the FLAIR hyperintensities noted with no abnormal diffusion restriction.
Discussion
Hb – 13.2 gm/dl TC – 14,350 cells/mm3 Platelets – 3,02,040 platelets/microlitre Lumbar puncture and CSF analysis – Appearance – clear Proteins – low Glucose – normal CBNAAT - negative Viral panel workup – HSV = negative Enterovirus = negative Adenovirus = negative The CSF analysis confirmed viral aetiology and the viral panel workup was negative for most of the common causes of viral encephalitis.
Etiology - More than 90% of the general population is seropositive for HHV-6 by 2 years of age. Most primary infections are asymptomatic, after which the virus remains latent. Clinical Issues - HHV-6 can become pathogenic in immunocompromised patients, especially those with hematopoietic stem cell or solid organ transplantation. The median interval between transplantation and onset of neurologic symptoms is 3 weeks. Patients typically present with altered mental status, short term memory loss, and seizures Imaging - NECT scans are typically normal. MR shows predominant or exclusive involvement of one or both medial temporal lobes (hippocampus and amygdala) (12-54). Extrahippocampal disease is less common than with HSE. Transient hyperintensity of the mesial temporal lobes on T2WI and FLAIR with restriction on DWI is typical. T2* (GRE, SWI) scans show no evidence of hemorrhage. HHV-6 encephalitis usually involves just the medial temporal lobes, but, if extrahippocampal lesions are present, it may be difficult to distinguish from HSE solely on the basis of imaging findings.
Differential Diagnosis
1) The major differential diagnosis is HSE. The disease course of HSE is more fulminant. Extratemporal involvement and hemorrhagic necrosis are common in HSE but rare in HHV-6 encephalopathy. In contrast to HSE, in HHV-6, MR abnormalities tend to resolve with time.
2) Postictal hippocampal hyperemia is transient, and extrahippocampal involvement is absent. References - Osborn's brain - 2nd edition
Note:
We do not discourage differential diagnosis. But all the differentials must satisfy the findings noted in the case.
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Did you Know?
The order in which the names appear in this winner's list is based on the time of submission. The first person to send the correct answer gets his/her name on top of the list!
We do not discourage differential diagnosis. But all the differentials must satisfy the findings noted in the case.
If you feel you have answered rightly but cannot find your name in the above list, please call 09551942599.
Did you Know?
The order in which the names appear in this winner's list is based on the time of submission. The first person to send the correct answer gets his/her name on top of the list!