Bilateral crossed cerebello-cerebral diaschisis and mutism after surgery for cerebellar medulloblastoma

Citation
T. Sagiuchi et al., Bilateral crossed cerebello-cerebral diaschisis and mutism after surgery for cerebellar medulloblastoma, ANN NUCL M, 15(2), 2001, pp. 157-160
Citations number
24
Categorie Soggetti
Radiology ,Nuclear Medicine & Imaging
Journal title
ANNALS OF NUCLEAR MEDICINE
ISSN journal
09147187 → ACNP
Volume
15
Issue
2
Year of publication
2001
Pages
157 - 160
Database
ISI
SICI code
0914-7187(200104)15:2<157:BCCDAM>2.0.ZU;2-7
Abstract
A 7-year-old boy developed mutism after surgery for cerebellar medulloblast oma. Postoperative magnetic resonance imaging (MRI) showed atrophy of the c erebellar vermis and both cerebellar hemispheres, predominantly on the righ t side. Single photon emission computed tomography (SPECT) with technetium- 99m-ethyl cysteinate dimer (Tc-99m ECD) revealed decreased cerebral blood f low (CBF) in the bilateral thalami, bilateral medial frontal lobes, and lef t temporal lobe in addition to the cerebellar vermis and both cerebellar he mispheres when mutism was manifest, indicating the existence of bilateral c rossed cerebello-cerebral diaschisis (BCCCD). Circulatory disturbance in bo th cerebellar hemispheres secondary to tumor resection probably caused BCCC D in both cerebral hemispheres, predominantly in the left, via the dentatot halamocortical pathway (DTCP). With recovery of his mutism, CBF increased i n the right thalamus, bilateral medial frontal lobes and left temporal lobe . Thus BCCCD was improved, with only a slight decrease in CBF still persist ing in the left thalamus. The mechanism of mutism may have involved damage to the cerebellar vermis (the site of incision at operation), the left dent ate nucleus (heavily infiltrated by the tumor) and the right dentate nucleu s of the cerebellum (affected by circulatory disturbance secondary to acute postoperative edema). The SPECT findings suggested that mutism was associa ted with BCCCD-induced cerebral circulatory and metabolic hypofunction in t he supplementary motor area mediated via the DTCP.