Crossed cerebellar diaschisis due to intracranial hematoma in basal ganglia or thalamus

Citation
Js. Lim et al., Crossed cerebellar diaschisis due to intracranial hematoma in basal ganglia or thalamus, J NUCL MED, 39(12), 1998, pp. 2044-2047
Citations number
20
Categorie Soggetti
Radiology ,Nuclear Medicine & Imaging","Medical Research Diagnosis & Treatment
Journal title
JOURNAL OF NUCLEAR MEDICINE
ISSN journal
01615505 → ACNP
Volume
39
Issue
12
Year of publication
1998
Pages
2044 - 2047
Database
ISI
SICI code
0161-5505(199812)39:12<2044:CCDDTI>2.0.ZU;2-O
Abstract
The purpose of our study was to evaluate the remote effects on the cerebell um and cerebral cortex from subcortical hematoma without cortical structura l abnormality. Methods: Our study included 23 patients with hematoma, stric tly confined either to the basal ganglia (n = 12) or thalamus (n = II) with out cortical abnormality on CT or MRI. Twenty psychiatric patients without structural abnormality on MRI were selected as control subjects. Technetium -ethyl cysteinate dimer brain SPECT was performed in patients and control s ubjects. Regional cerebral blood flow (rCBF) was visually and semiquantitat ively assessed. Asymmetry index (AI) was determined using data from regions of interest at the basal ganglia, thalamus, cerebellum, frontal, parietal and temporal cortex to support the semiquantitative analysis. The criteria for defining hypoperfusion that reflected diaschisis was based on an Al > t he mean + 2 s.d. of Al in control subjects. Results: In the basal ganglia h ematoma, rCBF was reduced significantly in the contralateral cerebellum (10 /12), ipsilateral thalamus (12/12), ipsilateral frontal (6/12), parietal (1 2/12) and temporal cortex (10/12). As for thalamic hematoma, significantly reduced perfusion was seen in the contralateral cerebellum (10/11), ipsilat eral basal ganglia (7/11), ipsilateral frontal (5/11), parietal (11/11) and temporal cortex (3/11). Conclusion: Crossed cerebellar diaschisis (CCD) an d cortical diaschisis frequently were observed in patients with subcortical hematoma without cortical structural abnormality. This suggested that CCD can develop regardless of interruption of the corticopontocerebellar tract, which is the principal pathway of CCD.