Crossed cerebellar hyperperfusion without restricted diffusion in status epilepticus

Abstract

Crossed cerebellar diaschisis (CCD) has originally been reported as metabolic depression on positron emission tomography in the cerebellar hemisphere contralateral to supratentorial infarction [1]. CCD has currently been documented in status epilepticus using magnetic resonance imaging (MRI) and single-photon emission computed tomography (SPECT) [2]. However, combined diffusion and perfusion profiles have remained controversial in CCD with status epilepticus. A 46-year-old woman was admitted to our hospital for the treatment of status epilepticus. Nine days before admission, she had presented with convulsion in the left limbs and been admitted to another hospital. Her convulsion was initially controlled with intravenous diazepam, but subsequent treatment with several anti-epileptic drugs was unsuccessful and she was diagnosed with drug-induced rash. Upon admission to our hospital, a brain MRI revealed a small cyst in the right mesial temporal lobe, which was speculated as the seizure focus. T2-weighted MRI (T2WI) showed mild hyperintensity and edematous changes in the right frontal, posterior temporal, parietal, and occipital cortices, and the left cerebellar hemisphere (Fig. 1a). Diffusion-weighted MRI (DWI) revealed mild hyperintensity and apparent diffusion coefficient (ADC) showed a slight increase in the T2WI hyperintensity regions of the right cerebral cortex; ADC values were mildly higher in the right temporal cortex (8.37 9 10 ± 7.04 9 10 mm/s) than in the contralateral area (7.90 9 10 ± 1.77 9 10 mm/s). On the other hand, ADC values were similar in the bilateral cerebellar hemispheres (right, 6.07 9 10 ± 4.06 9 10 mm/s; left, 6.08 9 10 ± 5.43 9 10 mm/s; Fig. 1b). I-Iodoamphetamine (IMP) SPECT, which reflects brain perfusion, revealed hyperperfusion in these regions (Fig. 1c). Carbamazepine, which had been spared because of the druginduced skin lesions, was prescribed in combination with steroids, and her seizures were finally controlled. T2WI intensity was normal 2 weeks after admission (Fig. 1d). I-IMP SPECT performed on the same day showed mild hyperperfusion in the right cerebral cortex and symmetric perfusion in the cerebellar hemispheres (Fig. 1e). MRI studies were performed on a 3-T instrument (Signa EXCITE HD 3.0T, GE Medical Systems, Milwaukee, WI, USA) with a standard quadrature head coil. The parameters of DWI were as follows: time of repetition = 10,000 ms, time of echo = 86.6 ms, field of view = 24 cm, matrix size = 128 9 128 with echo planar sequence, b value = 1,500 s/mm, and slice thickness/gap = 5/1 mm. This study has been performed in accordance with the ethical standards laid down in the 1964 Declaration of Helsinki. Neuroimaging studies of the present case demonstrated crossed hyperintensity on T2WI concurrent with hyperperfusion on SPECT. Of note, ADC was mildly increased, not decreased, in the present case. Previous reports of CCD in status epilepticus have documented DWI hyperintensity of the ipsilateral cortical ribbon and the contralateral cerebellar hemisphere [2, 3]. Restricted diffusion (reduced ADC) has been speculated, without clear evidence, in the DWI hyperintensity lesions of CCD in status epilepticus [2, 3], which contradicts our observations. K. Fujita (&) Y. Izumi R. Kaji Department of Clinical Neuroscience, Institute of Health Biosciences, The University of Tokushima Graduate School, 3-18-15 Kuramoto-cho, Tokushima 770-8503, Japan e-mail: kof@clin.med.tokushima-u.ac.jp