CASE REPORT 
Annals of Nuclear Medicine Vol. 15, No.4, 369-372, 2001 
Interictal crossed cerebellar hyperperfusion on Tc-99m ECD SPECT 
Takao SAGIUCHI,* Katsumi ISHII,* Yuuji ASANO,* Yuki AOKI,* Kei KIKUCHI,** Kouji JlNGUUJI,** Hisashi YANAIHARA,* Reiko WOODHAMS* and Kazushige HAYAKAWA* 
*Department of Radiology, Kitasato University School of Medicine * *Division of Nuclear Medicine, Kitasato University Hospital
Crossed cerebellar hyperperfusion (CCH) in epilepsy is a rare condition that is observed on ictal cerebral perfusion SPECT. The mechanism of CCH assumes that hyperperfusion in the epileptic foci of the unilateral supratentorium causes hyperperfusion secondary to the corticopontocerebellar pathway (CPCP)-mediated remote effect in the contralateral cerebellar hemisphere. This phenomenon is similar to that of crossed cerebellar diaschisis (CCD). In this report we demonstrated interictal CCH in a patient with epilepsy in technetium-99m-ethyl cysteinate dimer (Tc-99m ECD) SPECT of the brain. To the best of our knowledge, interictal CCH has not been reported in the literature. This is the first report to describe the phenomenon with interictal Tc-99m ECD SPECT. 
Key words: crossed cerebellar hyperperfusion, crossed cerebellar diaschisis, epilepsy, single photon emission computed tomography, technetium-99m-ethyl cysteinate dimer 
INTRODUCTION 
A UNILATERAL CEREBRAL HEMISPHERIC LESION such as cerebral infarction sometimes causes a reduction in cerebral circulation and metabolism secondary to the corticopontocerebellar pathway (CPCP)-mediated remote effect in the contralateral cerebellar hemisphere. This phenomenon is known as crossed cerebellar diaschisis (CCD)1 on single photon emission computed tomography (SPECT) or positron emission tomography (PET) studies of the brain. In recent years a reversed phenomenon of CCD has been reported in the literature.2-6 These reversible phenomena of CCD have been called "reversible CCD2", "reverse CCD3" and "crossed cerebellar hyperperfusion (CCH)4,5", by investigators. These phenomena are rare conditions. In this report, we describe a case of "crossed cerebellar hyperperfusion," in a patient with epileptic seizure visualized with interictal technetium-99m ethyl cysteinate dimer (Tc-99m ECD) SPECT of the brain. 
Received February 15, 2001 , revision accepted April 16, 2001 . For reprint contact: Takao Sagiuchi. M.D., Department of Radiology, Kitasato University School of Medicine, 1-15-1 , Kitasato, Sagamihara, Kanagawa 228-8555, JAPAN. 
CASE REPORT 
This patient was a 79-year-old man with hypertension. In the night of November 7, 2000, he was alert and well oriented, but he noticed transient repeated aphasic episodes intermittently. Because this condition continued for 1 day, he was brought to a local physician at 18 : 30 on November 8, 2000. During emergency computerized tomography (CT) of the brain, he suddenly had a tonic convulsion with conjugate eye divisions to the right side at 19 : 45. Diazepam was administered intravenously to control his seizure. To clarify the cause of the seizure, he was immediately transported to our hospital at 21 : 30. Neurological examinations on admission revealed mild disorientation and conjugate eye divisions to the left side. His verbal response was normal. His cranial nerves, motor and sensory showed no abnormalities. Emergency CT of the brain was obtained immediately after admission. CT showed multiple low density lesions related to old multiple cerebral infarctions. After admission, he had an anticonvulsant therapy. His consciousness became clear by the morning of November 9, 2000. Magnetic resonance (MR) imaging of the brain was obtained 14 hours after the seizure. Diffusion-weighted MR images (b-value = 1000) showed no signal abnormalities (Fig. 1a). Fluid-attenuated inversion recovery (FLAIR) images showed brain atrophy and old multiple cerebral infarctions in the white matter around the bilateral ventricles and in the centrum semiovales (Fig. 1b). MR imagings showed no evidence of acute cerebral infarction. Immediately after MR imagings, interictal cerebral perfusion SPECT with Tc-99m ECD (740 MBq) was obtained 15 hours after the seizure. Interictal Tc-99m ECD SPECT showed significant diffuse hyperperfusion in the left frontal cortex, the left basal ganglia and the right cerebellar hemisphere, indicating the existence of CCH (Fig. 2). Electroencephalography 17 hours after the seizure showed no seizure discharges or waves. Thereafter, he had no epileptic episode. MR imaging on the second study obtained again 6 days after the seizure. Diffusion-weighted MR, T2-weighted MR (Fig. 3) and FLAIR images showed no new intracranial lesion such as acute cerebral infarction. In the second SPECT study, cerebral perfusion SPECT with I-123-N-isopropyl-p-iodoamphetamine (I-123 IMP) of 167 MBq was obtained 22 days after the seizure. Interictal 1-123 IMP SPECT showed normal cerebral perfusion in most of the left frontal cortex and left basal ganglia, but showed slightly hyperperfusion still persisting in a part of left frontal cortex and hypoperfusion in the right cerebellar hemisphere (Fig. 4). On the basis of these repeated SPECT and MR findings and his clinical course, it was suggested that his episode was epileptic seizure, and interictal hyperperfusion in the left frontal lobe on Tc-99m ECD SPECT were the epileptic foci.
DISCUSSION 
Excitatory afferent impulses from the unilateral cerebral cortex via the CPCP pass through the internal capsule to reach the pontine nuclei. From the pontine nuclei, the pathway runs through the middle cerebellar peduncle and then terminates in the contralateral cerebellar cortex. CCD may be caused by functional disconnection between the unilateral cerebral hemisphere and the contralateral cerebellar hemisphere via the CPCP. It is assumed that CCH is also correlated with CPCP. A reversed phenom-enon of CCD called CCH is a rare condition. Since the first described by Duncan et al.2 in 1987, CCH has been re-ported in 14 patients with the seizure in the ictal state 2~ Won et al.,4 however, reported that CCH was observed in 75% (8 of the 12 patients) on the ictal SPECT and was a frequent phenomenon in the ictal state. These ictal SPECT findings in the literature showed hyperperfusion in the unilateral cerebral hemisphere identifying on the epilep-tic foci and the contralateral cerebellar hemisphere. The epileptic focus in CCH involves the frontal lobe 2,4~5 the temporal lobe3'4 and the occipital lobe.4 Ictal hyperperfu-sion of the unilateral cerebral hemisphere and contralat-eral cerebellar hemisphere have returned to the baseline4 or hypoperfusion4~6 in the postictal or interictal state. Concerning the mechanism of CCH, it is suggested that in the ictal state the neuronal overaction of the epileptic foci in the unilateral cerebral hemisphere spreads through the CPCP to the contralateral cerebellar hemisphere, and this neuronal overaction may lead to ictal hyperperfusion in both areas. In the present case, 15 hours after the seizure, interictal Tc-99m ECD SPECT showed CCH in the left frontal cortex, Ieft basal ganglia and the right cerebellar hemisphere. Twenty-two days after the seizure, interictal I-123 IMP SPECT showed hypoperfusion due to the excitotoxic neuronal damage caused by seizure activity7 in the right cerebellar hemisphere, and moreover, slightly interictal hyperperfusion in the frontal cortex was ob-served. In a similar case, Lang et al.6 reported that interictal hyperperfusion had been prolonged for 14 days after the seizure. In general, ictal SPECT shows hyperperfusion caused by seizure activity, and interictal SPECT shows the baseline or hypoperfusion in the epileptic focus 8,9 Cerebral perfusion SPECT, therefore, has been used to confirm the localization of epileptic focus and the evaluation of seizure activity.8,9 Newton et al.10 reported that the postictal blood flow changes gradually returned to normal within 10-30 minutes. As far as we know, interictal CCH has not been reported in the literature. This is the first report to describe this phenomenon with interictal cerebral perfusion SPECT. Interictal hyperperfusion on SPECT6,11 or PET,12 and postictal and interictal hypermetabolism on PET13 in the epileptic focus have been observed by investigators. Although these significant mechanisms are not clear, it is suggested that postictal and interictal hyperperfusion may be related to seizure activity prolonged by additional factors, such as glucose metabolisum14 or increased lactate12 produced by anaerobic metabolism13 in the epileptic focus during the ictal state. We suggested that interictal CCH was caused by seizure activity prolonged from the ictal state to the interictal state. The interictal hyperperfusion in the right cerebellar hemisphere had become hypoperfusion 22 days later, but the patients had no neurological symptoms involving the right cerebellum and no morphologic changes in the right cerebellar hemisphere. In epilepsy, it is known that patients with long-standing intractable or chronic epilepsy have cerebellar atrophy.7,15 The cerebellar atrophy may be consequent on chronic and the repeated excitotoxic neuronal damage mediated through the CPCP caused by seizure activity in the unilateral cerebral cortex.5 The existence of CCH may predict cerebellar atrophy. In epilepsy, the seizure activity in the epileptic focus spreads to the remote area associated with the epileptic focus via the neural tract. The secondary to the neural tract-mediated remote effects such as CCH and CCD, may therefore be important phenomena in predicting the hypofunction of cerebral perfusion and metabolism in the remote area. To clarify the remote effect and remote area caused by seizure activity, it is necessary to evaluate the CCH with the quantitative flow-mapping and the statistical images such as statistical parametric mapping (SPM) and three-dimensional stereotactic surface projections (3D-SSP). 
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