5 Within the posterior fossa, cerebral edema can rapidly obstruct the fourth ventricle, causing hydrocephalus. The cerebellum and brain stem are tightly constrained by the tentorium cerebelli superiorly, and the occipital bone and foramen magnum posteriorly. The superior cerebellar artery supplies most of the cerebellar cortex, the cerebellar nuclei, and the superior cerebellar peduncles.Ĭerebellar infarcts require special attention because of the danger of cerebral edema within the posterior fossa. AICA supplies the anterior portion of the inferior cerebellum, the middle cerebellar peduncle, and the facial and vestibulocochlear nerves. PICA supplies the lateral medulla, the inferior cerebellum, and the inferior cerebellar peduncle. The blood supply of the cerebellum consists of the posterior inferior cerebellar arteries (PICAs), branches of the vertebral artery, and the anterior inferior cerebellar arteries (AICAs) and the superior cerebellar arteries (SCAs), which arise from the basilar artery. 3 The reasons for disproportionate embolization to the posterior circulation are unclear, but may, in part, be because of manipulation of the catheter within the subclavian arteries near the vertebral origins while catheterizing the internal mammary arteries. 1 – 4Īlthough 80% to 90% of ischemic infarctions occur in the anterior circulation, >50% of infarcts after cardiac catheterization affect the posterior circulation. 1, 2 Potential pathogeneses include cardiac emboli, large-vessel atherosclerosis, vertebral artery dissection, local arterial disease, and less commonly hypercoagulable conditions, vasculitis, venous sinus thrombosis, and drug use. This case demonstrates several important points about cerebellar infarcts including the disproportionate number of posterior circulation strokes after cardiac catheterization, the difficulty recognizing cerebellar infarctions and, most importantly, the potential for rapid deterioration requiring urgent neurosurgical intervention.Ĭerebellar infarcts are relatively uncommon and represent ≈2% of all ischemic strokes. C, Within 48 hours, cerebral edema effaced the fourth ventricle, enlarged the temporal horns of the lateral ventricles, and compressed the brain stem. B, Infarcts were clearly evident on MRI at 6 hours. A, Initial computed tomography head showed questionable cerebellar infarcts at 5 hours of symptoms. At the time of discharge, she had severe bilateral upper extremity dysmetria and was nonambulatory.įigure. After surgery, her mental status improved. Forty-eight hours after the catheterization, she became obtunded, and CT of the head showed worsening posterior fossa edema and obstructive hydrocephalous ( Figure), requiring placement of an external ventricular drain (EVD) followed by urgent suboccipital decompressive. The next morning aspirin and clopidogrel were held in favor of heparin, in case she required neurosurgical intervention. She was started on low-dose aspirin and clopidogrel and transferred to the Neurological Intensive Care Unit for monitoring. Emergent noncontrasted computed tomography (CT) of the head showed questionable bilateral cerebellar infarcts that MRI confirmed ( Figure). Her examination was significant for lethargy, dysarthria, bilateral upper extremity ataxia, and bilateral inferomedial gaze deviation. She was nauseated with continued vomiting. Initially, the patient’s systolic blood pressure was >180 mm Hg. Initially, her symptoms were attributed to sedation however, after failing to improve four hours later despite treatment with opioid antagonists, urgent neurological consultation was obtained. Customer Service and Ordering InformationĪn 80-year-old woman was admitted for lethargy and vomiting after diagnostic cardiac catheterization.Stroke: Vascular and Interventional Neurology.Journal of the American Heart Association (JAHA).Circ: Cardiovascular Quality & Outcomes.Arteriosclerosis, Thrombosis, and Vascular Biology (ATVB).
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