Abstract

An 80-year-old woman was admitted for lethargy and vomiting after diagnostic cardiac catheterization. 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. Initially, the patient’s systolic blood pressure was >180 mm Hg. She was nauseated with continued vomiting. Her examination was significant for lethargy, dysarthria, bilateral upper extremity ataxia, and bilateral inferomedial gaze deviation. Emergent noncontrasted computed tomography (CT) of the head showed questionable bilateral cerebellar infarcts that MRI confirmed (Figure). She was started on low-dose aspirin and clopidogrel and transferred to the Neurological Intensive Care Unit for monitoring. The next morning aspirin and clopidogrel were held in favor of heparin, in case she required neurosurgical intervention. 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. After surgery, her mental status improved. At the time of discharge, she had severe bilateral upper extremity dysmetria and was nonambulatory. Figure. A , Initial computed tomography head showed questionable cerebellar infarcts at 5 hours of symptoms. B , Infarcts were clearly evident on MRI at 6 hours. C , Within 48 hours, cerebral edema effaced the fourth ventricle, enlarged the temporal horns of the lateral ventricles, and compressed the brain stem. 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. Cerebellar infarcts are relatively uncommon and represent ≈2% of all ischemic strokes.1,2 Potential pathogeneses include cardiac …

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