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Editorial
. 2016 Jun 1;73(6):632-5.
doi: 10.1001/jamaneurol.2016.0576.

Cerebral Microbleeds and Thrombolysis: Clinical Consequences and Mechanistic Implications

Mark Fisher  1
Affiliations
Editorial

Cerebral Microbleeds and Thrombolysis: Clinical Consequences and Mechanistic Implications

Mark Fisher. JAMA Neurol. .
No abstract available

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Conflict of interest statement

Conflict of Interest Disclosures: Dr Fisher receives research grant support from Otsuka Pharmaceutical Company and Boehringer-Ingelheim and is a member of clinical events committees of Covidien.

Figures

Figure
Figure. A Vascular Neurobiology Model of Cerebral Microbleeds
In this model of cerebral microbleeds, the 4 principal vascular comorbidities (hypertension, cerebral amyloid angiopathy, chronic kidney disease, and cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy [CADASIL]) all affect brain arterioles. The consequences are impaired autoregulation (dysfunctional regulation of cerebral blood flow) producing incapacity to accommodate alterations in systemic blood pressure. Further arteriolar injury, ie, necrosis occurring spontaneously or induced by ischemia, results in intracerebral hemorrhage. Concurrently, blood-brain barrier alterations owing to aging, hypertension, cerebral amyloid angiopathy, CADASIL, and possibly chronic kidney disease, create the impaired capillary bed needed for red blood cell extravasation and development of microhemorrhage, the pathologic substrate of microbleeds.
See this image and copyright information in PMC

Comment on

References

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