Contralateral cerebellar diaschisis 7 hours after MCA-occlusion in primates

1995 ◽  
Vol 17 (2) ◽  
pp. 109-112 ◽  
Author(s):  
Christian Dettmers ◽  
Alexander Hartmann ◽  
Thomas Rommel ◽  
Sandra Hartmann ◽  
Sabina Pappata ◽  
...  
Keyword(s):  
Mca Occlusion ◽  
Cerebellar Diaschisis

Crossed Cerebellar Diaschisis in Alzheimer’s Disease

2018 ◽  
Vol 15 (13) ◽  
pp. 1267-1275 ◽  
Author(s):  
F.E. Reesink ◽  
D. Vállez García ◽  
C.A. Sánchez-Catasús ◽  
D.E. Peretti ◽  
A.T. Willemsen ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Left Hemisphere ◽  
Pet Imaging ◽  
Fdg Pet ◽  
Pathophysiological Mechanism ◽  
Crossed Cerebellar Diaschisis ◽  
Amyloid Accumulation ◽  
Cerebellar Diaschisis ◽  
18F Fdg

Background: We describe the phenomenon of crossed cerebellar diaschisis (CCD) in four subjects diagnosed with Alzheimer’s disease (AD) according to the National Institute on Aging - Alzheimer Association (NIA-AA) criteria, in combination with 18F-FDG PET and 11C-PiB PET imaging. Methods: 18F-FDG PET showed a pattern of cerebral metabolism with relative decrease most prominent in the frontal-parietal cortex of the left hemisphere and crossed hypometabolism of the right cerebellum. 11C-PiB PET showed symmetrical amyloid accumulation, but a lower relative tracer delivery (a surrogate of relative cerebral blood flow) in the left hemisphere. CCD is the phenomenon of unilateral cerebellar hypometabolism as a remote effect of supratentorial dysfunction of the brain in the contralateral hemisphere. The mechanism implies the involvement of the cortico-ponto-cerebellar fibers. The pathophysiology is thought to have a functional or reversible basis but can also reflect in secondary morphologic change. CCD is a well-recognized phenomenon, since the development of new imaging techniques, although scarcely described in neurodegenerative dementias. Results: To our knowledge this is the first report describing CCD in AD subjects with documentation of both 18F-FDG PET and 11C-PiB PET imaging. CCD in our subjects was explained on a functional basis due to neurodegenerative pathology in the left hemisphere. There was no structural lesion and the symmetric amyloid accumulation did not correspond with the unilateral metabolic impairment. Conclusion: This suggests that CCD might be caused by non-amyloid neurodegeneration. The pathophysiological mechanism, clinical relevance and therapeutic implications of CCD and the role of the cerebellum in AD need further investigation.

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

2015 ◽  
Vol 36 (4) ◽  
pp. 743-754 ◽  
Author(s):  
Wieland H Sommer ◽  
Christine Bollwein ◽  
Kolja M Thierfelder ◽  
Alena Baumann ◽  
Hendrik Janssen ◽  
...  
Keyword(s):  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Symptom Onset ◽  
Ct Perfusion ◽  
Clinical Factors ◽  
Middle Cerebral Artery Infarction ◽  
Whole Brain ◽  
Crossed Cerebellar Diaschisis ◽  
Brain Ct ◽  
Cerebellar Diaschisis

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.

Selective MCA occlusion: A precise embolic stroke model

2006 ◽  
Vol 154 (1-2) ◽  
pp. 233-238 ◽  
Author(s):  
Vincent A. DiNapoli ◽  
Charles L. Rosen ◽  
Tomoaki Nagamine ◽  
Todd Crocco
Keyword(s):  
Embolic Stroke ◽  
Stroke Model ◽  
Mca Occlusion

scholarly journals Crossed Cerebellar Diaschisis: Insights into Oxygen Challenge MRI

2012 ◽  
Vol 32 (12) ◽  
pp. 2114-2117 ◽  
Author(s):  
Krishna A Dani ◽  
Celestine Santosh ◽  
David Brennan ◽  
Donald M Hadley ◽  
Keith W Muir
Keyword(s):  
Magnetic Resonance Imaging ◽  
Cerebral Blood Volume ◽  
Oxygen Extraction Fraction ◽  
Resonance Imaging ◽  
Crossed Cerebellar Diaschisis ◽  
Relative Contribution ◽  
Extraction Fraction ◽  
Signal Change ◽  
Cerebellar Diaschisis ◽  
Weighted Magnetic Resonance Imaging

Hyperoxia during T2∗-weighted magnetic resonance imaging (oxygen challenge imaging (OCI)) causes T2∗-weighted signal change that is dependent on cerebral blood volume (CBV) and oxygen extraction fraction (OEF). Crossed cerebellar diaschisis (CCD), where CBV is reduced but OEF is maintained, may be used to understand the relative contributions of OEF and CBV to OCI results. In subjects with large hemispheric strokes, OCI showed reduced signal change in the contralesional cerebellum ( P = 0.027, n = 12). This was associated with reduced CBV in contralesional cerebellum ( P = 0.039, n = 9). CCD may be a useful model to determine the relative contribution of CBV to signal change measured by OCI.

Abstract P730: MCA Stroke Chronically Disrupts Hippocampal Activity and Cortico-Hippocampal Communication

Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Zachary Ip ◽  
Gratianne Rabiller ◽  
Jiwei He ◽  
Shivalika Chavan ◽  
Yasuo Nishijima ◽  
...  
Keyword(s):  
Structural Integrity ◽  
Memory Function ◽  
Brain Regions ◽  
Male Rats ◽  
Brain State ◽  
Signal Power ◽  
Hippocampal Function ◽  
Electrode Arrays ◽  
Mca Occlusion ◽  
Hippocampal Activity

Introduction: Cognition and memory deficits are common sequelae following middle cerebral artery (MCA) stroke, one of the most common strokes in humans. However MCA stroke does not compromise the structural integrity of the hippocampus, which is highly involved in memory function, because the MCA does not supply blood flow to the hippocampus. We previously reported on the acute effect of MCA stroke, where we observed increased hippocampal activity and cortico-hippocampal communication. Here we investigate chronic changes to local oscillations and cortico-hippocampal communication following MCA occlusion in rats two weeks and one month following stroke. Hypothesis: Cortical stroke affects remote brain regions, disrupting hippocampal function and cortico-hippocampal communication. Methods: We subjected male rats (n=28) to distal MCA occlusion compared to controls (n=19). We recorded local field potentials simultaneously from cortex and hippocampus two weeks and one month following stroke using 16-site linear electrode arrays under urethane anesthesia. We analyzed signal power, brain state, CFC, and sharp wave SPW-Rs to assess hippocampal function and cortico-hippocampal communication. Results: Our results show disruptions to local oscillations; lowered delta (1-3 Hz) signal power in the cortex and hippocampus, increased signal power in gamma (30-60 Hz) and high gamma (60-200 Hz) in cortex and hippocampus. Theta/delta brain state is disrupted, and SPW-Rs increase in power at two weeks, before returning to baseline levels at one month. Communication is also disrupted; Theta-gamma coupling, a measure of information being communicated between regions, breaks down after stroke. Conclusions: These results suggest that chronic stroke causes significant changes to hippocampal function, which can be characterized by these electrophysiological biomarkers, establishing putative targets for targeted stimulation therapies.

Abstract 3438: Intracranial Arterial Occlusion and Extent of Hypoattenuation on CT Angiography Source Images may Modify the Benefit of Thrombolysis

Stroke ◽  
2012 ◽  
Vol 43 (suppl_1) ◽  
Author(s):  
Imanuel Dzialowski ◽  
Volker Puetz ◽  
Jasmin Renger ◽  
Andrei Khomenko ◽  
Ulf Bodechtel ◽  
...  
Keyword(s):  
Functional Outcome ◽  
Ct Angiography ◽  
Time Window ◽  
Brain Infarction ◽  
Randomized Study ◽  
Arterial Occlusion ◽  
Extended Time ◽  
Anterior Circulation ◽  
Nihss Score ◽  
Mca Occlusion

Background: CT angiography source images (CTASI) improve diagnostic accuracy for ischemic brain infarction compared to non-contrast CT (NCCT). We studied whether CTASI alone or combined with the CTA occlusion status may improve patient selection for thrombolysis in an extended time window. Methods: We prospectively observed patients presenting with anterior circulation ischemic stroke within 12 hours from symptom onset and an NIHSS score ≥ 3. All patients underwent cranial NCCT and CTA. Patients were treated with intravenous and/or intra-arterial thrombolysis at the discretion of the treating stroke neurologist and neuroloradiologist. We determined intracranial occlusion status and applied the Alberta Stroke Program Early CT Score (ASPECTS) to CTASI. Primary clinical outcome measure was independent outcome at 3 months, defined as mRS scores 0-2. We calculated unadjusted risk ratios to assess the effect of thrombolysis on functional outcome in patients with: 1) minor ischemic changes on CTASI (CTASI-ASPECTS >5) and 2) patients with minor ischemic changes on CTASI and middle cerebral artery (MCA) occlusion. Results: We enrolled 102 patients with a mean age of 71 +/- 12 years, median onset-to-CTA time of 112,5 (range 37-898) min, a median NIHSS score of 9.5 (3-39), and a median CTASI-ASPECTS of 8. Sixty-two patients (61%) received any thrombolysis (56 IV, 5 IV/IA, 1 IA). MCA occlusion was present in 57 patients (56%), 80/101 (80%) assessable patients had a CTASI-ASPECTS >5 and 37/101 (37%) patients had a CTASI-ASPECTS >5 in the presence of a MCA occlusion. At 3 months, 52 (51%) patients had an independent functional outcome. When patients with CTA-SI ASPECTS > 5 received thrombolysis, 30/46 (65%) achieved an independent functional outcome, whereas 20/35 (57%) without thrombolysis were functionally independent (RR 1.1, CI 95 0.8-1.6). In patients with CTASI-ASPECTS > 5 and additional MCA-occlusion, 13/24 (54%) with thrombolysis and 3/13 (23%) without thrombolysis achieved an independent functional outcome (RR 2.3, CI 95 0.8-6.8). Conclusion: In our non-randomized study, the extent of CTASI hypoattenuation alone did not identify patients benefiting from thrombolysis. In the presence of an MCA-occlusion, however, CTASI might identify patients with benefit from thrombolysis in an extended time window.

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