Neurological Research A Journal of Progress in Neurosurgery, Neurology and Neurosciences

ISSN: 0161-6412 (Print) 1743-1328 (Online) Journal homepage: https://www.tandfonline.com/loi/yner20

Cerebellar blood flow involvement in temporal post-ictal epilepsy: a TC-Hm PA0 Spect study L. Septien, R. DiDi-roy, J.L. Pelletier & M. Giroud To cite this article: L. Septien, R. DiDi-roy, J.L. Pelletier & M. Giroud (1992) Cerebellar blood flow involvement in temporal post-ictal epilepsy: a TC-Hm PA0 Spect study, Neurological Research, 14:2, 127-127, DOI: 10.1080/01616412.1992.11740030 To link to this article: https://doi.org/10.1080/01616412.1992.11740030

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Cerebellar blood flow involvement in temporal post-ictal epilepsy: a TC-Hm PAO Spect study L. Septien*1 , R. DiDi-roy1 , J.L. Pelletier2 and M. Giroud 3 1 Centre

Hospitalier Specialise de Ia Chartreuse, 2 Centre de Medecine Nuc/eaire du Pare and 3Service de Neurologie, Hopital General, Dijon, (ranee

A decrease in cerebellar blood flow, during a marked decrease in interictal uptake of _ the contralateral temporal lobe-as shown by TC-Hm PAO Spect imaging-in epilepsy, has been reported in the past1 . In this paper the authors describe a case of increased post-ictal uptake in a right temporal epileptic focus and the two cerebellar lobes.

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CASE REPORT G . . . Suzanne, female, was born in December 1939. Since the age of 5 years, she presented partial complex seizures with loss of consciousness, hypersialorrhea, lip twitching and automatic swallowing. EEG showed spikes in right temporal lobe. The CT-scan was normal. Under phenobarbital and then carbamazepine alone, the patient experienced one epileptic crisis per month, without generalized seizures. No aetiology was determined. Neurological examinations remained normal. In July 1991, a TC-Hm PAO Spect imaging was performed 8 hours after a complex seizure confirmed by a right temporal discharge in the EEG recording. The Spect localized a hyperperfusion focus in the right temporal lobe and in the 2 cerebellar lobes (Figure 1 ).

COMMENTS We_have never observed such a finding in our personal series of 52 epileptic patients. Forty-one were studied by Spect in inter-ictal period with either no abnormalities (25 cases), a zone of hypoperfusion (14 cases) or a zone of hyperperfusion (2 cases). Eleven patients were studied by Spect in post-ictal period with a zone of hyperperfusion in 6 cases, and a zone of hypoperfusion in 5. The rate of abnormalities observed in our series are quite similar to those reported by Duncan et a/. 3 . In the cases where a zone of hyperperfusion was observed, we didn't find a zone of hyperperfusion in the cerebellar lobes. In this case, the zone of hyperperfusion in the right temporal lobe corresponds to the epileptic focus localized by several inter-ictal and ictal EEG. The explanation for the cerebellar hyperperfusion with no clinical traduction, rem ains obscure. The hyperperfusion observed in the 2 cerebellar lobes was as intense as in the right temporal lobe. There was no tumour, nor

Hyperperfusion focus in t he right t emporal lobe and in the 2 cerebellar lobes

Figure 1:

vascular malformation in the cerebellum, there was no status epilepticus, no anoxia and the patient never took a phenytoin treatment. This image is quite different from the more usual unilateral crossed cerebellar diaschisis4 reported in 2 epileptic patients by Ryding et a/.5 and Duncan et a/. 2 , where a zone of hypoperfusion in one temporal lobe was associated with the same abnormality in the contralateral cereb ellar lobe. We only found one previous case report of association of similar abnormalities in one temporal lobe and the 2 cerebellar lobes, but it was not a Spect study, but a positron emission tomographic scan, and the result was a decrease of the metabolism of these areas 1 . The question this observation raises is about the origin of the neurophysiological pathways that explain the increase of cerebellar perfusion during an increase in the temporal one, both induced by one epileptic discharge. In the meantime, we would like to point out the possibility of finding a marked cerebellar hyperperfusion in such patients.

REFERENCES 2

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4 • Present address: Department of Psychiatry, UNAM Mexico-City, Mexico. Address correspondence to : Dr M. Giraud, Service de Neurologie, Hopital General, 3 rue du Faubourg Raines, 21000 Dijon, France. Accepted for publication November 1991.

© 1992 Forefront Publishing Group 0161-6412 /92/020127- 01

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Bairamian D, di Chiro G, Theodore WH. Epilepsy and cerebel lar hypometabolism. Ann Neurol1986; 5: 649 Duncan R, Patterson ), Hadley OM, MacPherson P, Brodie M), Bone I, MacGeorge AP, Wyper D). CT, MR and Spect imaging in temporal lobe epilepsy. I Neural Neurosurg Psychiat 1990; 53: 11 - 15 Duncan R, Patterson J, Hadley OM, MacPherson P, Bone I, Wyper OJ. Tc 99 m Hm- PAO single photon emission computed tomography in temporal lobe epilepsy. Acta Neural Scand 1990; 81 : 287-293 Patronas N), di Chiro G, Smith BH. Depressed cerebellar glucose metabolism in supratentorial tumors. Brain Res 1984; 291: 93- 101 Ryding E, Rosen I, Elmgnist D, lnguard H. SPECT measurements with 99 m TC- Hm PAO in focal epilepsy. I Cereb Blood Flow M etab 1988; 8: S95- S100

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Cerebellar blood flow involvement in temporal post-ictal epilepsy: a TC-Hm PAO Spect study.

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