Abstract

Introduction To describe a unique case of pial arteriovenous fistula presenting as left hemispheric cerebral edema with hemianopsia, sensory change and ataxia. Methods Case report Results Our patient is a 38 year old male with a history of diabetes, hyperlipidemia and congenital deafness with a left cochlear implant who presented to an outside hospital for visual complaints. Non‐contrast CT of the head was negative at that time; he could not obtain an MRI due to his cochlear implant. He developed worsening right hemianopia and aphasia, prompting his transfer to our facility. Upon arrival, repeat imaging was done, including a CTA of the head and neck. This revealed a large region of hypodensity involving the left PCA and distal MCA territories. An MRI was attempted but artifact from his implant obscured visualization of the left hemisphere. Post‐contrast CT was negative for evidence of tumor. CT venogram was negative for veno‐occlusive disease. He complained of worsening headache and demonstrated worsening word‐finding ability. He received100g total of mannitol divided across 3 boluses which improved his symptoms mildly. Over the following days he began to become ataxic and clumsy in the right upper extremity and his headache worsened further and he began to develop focal seizures electrographically localized to the left parietal lobe. Repeat CTA demonstrated expanding hypodensity with marked vascular engorgement in the left hemisphere. He underwent 6‐vessel digital subtraction angiography (DSA) of the head which revealed gross left hemispheric venous congestion with early filling of the left hemispheric venous system by a parasagittal pial ateriovenous fistula believed to be responsible for his hemispheric edema. He was discharged on acetazolamide and acetaminophen for headache management and plans for outpatient follow‐up and potential intervention. Follow‐up DSA revealed improvement in his venous congestion and reduction in the degree of his early venous filling with some symptomatic improvement by medical management. Conclusions Pial arteriovenous fistulae (pAVF) are a rare entity and can present in a variety of ways, with symptomatic intracranial hemorrhage and ischemia being two of the most common. This case illustrates an unusual instance of hemispheric edema initially mistaken for venous infarct caused by a pAVF, and prompts the physician to consider angiography and further exploration when initial workup for cerebral edema and/or venous infarct is initially unrevealing.

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