MR imaging of human herpesvirus-6 encephalopathy after hematopoietic stem cell transplantation in adults

Abstract

Background and purpose: Human herpesvirus-6 (HHV-6)-associated encephalopathy tends to develop in immunocompromised patients. Neurologic symptoms, such as disorientation, short-term memory loss, convulsion, coma, and hypopnea could occur, but they may be nonspecific. We retrospectively reviewed MR images of 6 adults with HHV-6-associated encephalopathy to study characteristic imaging findings that could be useful in making the diagnosis.

Materials and methods: Between 2003 and 2005, we encountered 6 cases of HHV-6-associated encephalopathy (3 men and 3 women; age range, 36-55 years) in 3 hospitals. The diagnosis was made clinically according to the neurologic symptoms accompanied by high-level copies of HHV-6 DNA in CSF or peripheral blood by quantitative polymerase chain reaction without the detection of any other infectious pathogen.

Results: All 6 patients had abnormal hippocampus/amygdala findings on presentation, and no other regions were involved. In the early period (0-2 days from onset), abnormal high signal intensity on fluid-attenuated inversion recovery (FLAIR) imaging (2 of 3, 67%) and on diffusion-weighted images accompanied by apparent diffusion coefficient (ADC) reduction (2 of 2, 100%) were observed. In the middle period (3-30 days), abnormal low signal intensity on T1-weighted images (5 of 6, 83%) and abnormal high signal intensity on T2-weighted images (4 of 6, 67%) and FLAIR (5 of 6, 83%) were confirmed. In the late period (> 30 days), we saw the resolution of signal intensity abnormalities and the appearance of atrophic change (4 of 4, 100%) of the affected regions.

Conclusion: HHV-6-associated encephalopathy in adults tends to affect the mesial temporal lobe. MR imaging is useful for detecting HHV-6 encephalopathy and distinguishing it from the other diseases of the central nervous system in immunocompromised patients.

Fig 1.

Axial MR images of an HHV-6 encephalopathy patient (patient 2) obtained on the second day after the onset of neurologic symptoms. A, T1WI (TR/TE = 466/11 ms). B, T2WI (2650/93 ms). C, FLAIR (TR/TE/TI = 9000/97/2300 ms). D, DWI (TR/TE = 3100/119 ms, b = 1000). E, ADC map. F, postcontrast T1WI (TR/TE = 558/17 ms). An abnormal low signal intensity on T1WI (A) and high signal intensity on T2WI (B) and FLAIR (C) are shown in the bilateral amygdalae and hippocampi. High signal intensity on DWI (D) with ADC reduction (E) is also shown. However, no abnormal enhancement is seen on postcontrast T1WI (F).

Fig 2.

Serial axial MR images of a 49-year-old woman (patient 1) including FLAIR (TR/TE/TI = 9000/110/2200 ms [A, B, D] or 9000/97/2300 ms [C]), DWI (TR/TE = 4000/137 ms [E, F, H] or 3100/119 ms [G]), and ADC maps on days 1, 13, 26, and 98 after the onset of neurologic symptoms (I-L). On FLAIR, high signal intensity in the bilateral amygdalae and hippocampi appears on day 1, peaks on day 13, and becomes less pronounced on day 26, disappearing on day 98 but leaving marked atrophy. High signal intensity on DWI is observed until day 26, whereas ADC value reduction is seen only on days 1 and 13.