Crossed cerebellar diaschisis in patients with acute middle cerebral artery infarction: Occurrence and perfusion characteristics

Abstract

We aimed to investigate the overall prevalence and possible factors influencing the occurrence of crossed cerebellar diaschisis after acute middle cerebral artery infarction using whole-brain CT perfusion. A total of 156 patients with unilateral hypoperfusion of the middle cerebral artery territory formed the study cohort; 352 patients without hypoperfusion served as controls. We performed blinded reading of different perfusion maps for the presence of crossed cerebellar diaschisis and determined the relative supratentorial and cerebellar perfusion reduction. Moreover, imaging patterns (location and volume of hypoperfusion) and clinical factors (age, sex, time from symptom onset) resulting in crossed cerebellar diaschisis were analysed. Crossed cerebellar diaschisis was detected in 35.3% of the patients with middle cerebral artery infarction. Crossed cerebellar diaschisis was significantly associated with hypoperfusion involving the left hemisphere, the frontal lobe and the thalamus. The degree of the relative supratentorial perfusion reduction was significantly more pronounced in crossed cerebellar diaschisis-positive patients but did not correlate with the relative cerebellar perfusion reduction. Our data suggest that (i) crossed cerebellar diaschisis is a common feature after middle cerebral artery infarction which can robustly be detected using whole-brain CT perfusion, (ii) its occurrence is influenced by location and degree of the supratentorial perfusion reduction rather than infarct volume (iii) other clinical factors (age, sex and time from symptom onset) did not affect the occurrence of crossed cerebellar diaschisis.

Crossed cerebellar diaschisis in acute ischemic stroke: Impact on morphologic and functional outcome

“…Recent studies on CCD occurrence and perfusion characteristics suggest that CT perfusion is an appropriate technique to study the phenomenon of CCD. 14,15 Building on this, we could show that the mere presence of CCD in the acute phase has no impact on functional outcome in ischemic stroke patients. The original notion of diaschisis being a reversible condition, either in the form of CCD or transhemispheric diaschisis, 43 is not contradicted by our observations as significant clinical improvement was observed in patients with acute CCD.…”

“…30 Advances in imaging technology meanwhile allow to cover the entire brain tissue at a reasonable radiation dose (whole-brain CT perfusion, WB-CTP). 31 While recent WB-CTP studies on stroke patients have shown the occurrence of CCD in the acute phase to be dependent on the location of the supratentorial perfusion deficit and the severity of supratentorial hypoperfusion, 14 the key question of the clinical impact of CCD in acute ischemic stroke remains unanswered.…”

Changes in structure and perfusion of grey matter tissues during recovery from Ischaemic subcortical stroke: a longitudinal MRI study

“…However, the mechanism for GM atrophy in ipsilesional cerebellar cortex cannot be explained by axonal degeneration through crossed fibres as all lesions located at the same side as cerebellum. We speculated that depression of metabolism at the non‐ischaemic side of hemisphere may result in GM atrophy in the ischaemic side of cerebellum, which was similar to the phenomenon of crossed cerebellar diaschisis (Mah et al ., ; Sommer et al ., ). Further investigation is still required to verify this speculation.…”

Crossed Cerebellar Diaschisis

“…CCD mostly accompanies middle cerebral artery infarctions. Sommer et al (4) found CCD in 35.3% of patients with middle cerebral artery infarction. In particular, it was found to be associated with hypoperfusion involving the left hemisphere, frontal lobe, and thalamus.…”

“…Damage of corticopontocerebellar fibers is usually secondary to cerebral hypoperfusion, but it can also be related with supratentorial hyperperfusion following revascularization (3). Scientific data show that disruption in corticopontocerebellar fibers causes functional deactivation by leading decrease in excitatory input and a decrease in cerebellar blood flow (4).…”