ABSTRACT
A 75-year-old woman with a dural arteriovenous fistula (DAVF) presented with progressive cognitive impairment including amnesia and alexia. Neuroradiological studies showed a relatively confined DAVF lesion in the left temporal lobe. The patient did not have a history of trauma and did not complain of headache or tinnitus. Amnesia and alexia dramatically improved upon treatment of the DAVF, and this was associated with attenuation of an abnormal MRI signal in the left temporal lobe. The results suggest that gradually impaired cerebral circulation due to focal venous hypertensive encephalopathy localized to the left temporal lobe and resulting from a DAVF could be involved in slowly progressive amnesia and alexia. The case also shows that an intracranial DAVF may present as a variety of neurological symptoms, depending on its localization, size and clinical stage.
Subject(s)
Central Nervous System Vascular Malformations/diagnosis , Cognition Disorders/etiology , Aged , Amnesia/etiology , Central Nervous System Vascular Malformations/complications , Central Nervous System Vascular Malformations/diagnostic imaging , Central Nervous System Vascular Malformations/physiopathology , Cerebral Angiography , Disease Progression , Dyslexia, Acquired/etiology , Female , Humans , Magnetic Resonance Imaging , Tomography, Emission-Computed, Single-PhotonABSTRACT
The patient was 47 years old on his first visit in 1969 and has been treated at our outpatient clinic until now, at the age of 79. The initial blood pressure was 164/98 mmHg without abnormalities on electrocardiogram or urinalysis. He was followed-up for 8 years with non-pharmacologic treatment, which was eventually changed to antihypertensive drug treatment. At the age of 71 he was admitted because blood pressure increased to 210/110 mmHg, with marked fluctuation. At admission bilateral ocular (right < left) and carotid bruits (right < left) were detected. At the age of 75 he had cerebellar infarction with reversible neuro-logic deficits. At the age of 76 he was again addmitted because the labile hypertension was difficult to control. Cerebral angiography which was performed to clarify the relationship between labile hypertension and cerebral ischemia revealed significant bilateral stenosis at the portion of the cavernous sinus in the internal carotid arteries. The stenosis was more remarkable on the left side than the right side. Based on the angiographic findings we considered the ocular bruits to be not a murmur of augmentation flow but a stenotic murmur.
