INTRODUCTION: Intracranial hypertension (ICHT) is the most frequent presenting syndrome of dural vein sinus thrombosis (CVT). A transient ischemic attack as an acute mode of onset is exceptional. CASE REPORT: A right handed, forty years old man with a medical history of recurrent headaches, microcephalia and calcifications in his brain, presenting to the emergency department with left paresis that lasted a few minutes and with a complete recovery. The cerebral and neck magnetic resonance (MR) including MR angiography showed superior sagittal sinus, both transverse sinuses and right sigmoid sinus thrombosis with an increase in size of superficial cerebral venous that drained to the left sigmoid sinus. There was no evidence of intracranial dural malformations. The cerebral MR did not show any abnormal parenchymal enhancement (edema, arterial or venous infarctions, hemorrhage) including diffusion-weighted IMR. The digital subtraction angiography (ADC) confirmed the same findings as the MR angiography. The diagnosis was a chronic CVT. We studied stroke in a young adult and we did not find other irregularities. The neurological examination was normal when the patient left the hospital with an antiplatelet drug. CONCLUSIONS: Focal neurological deficit is an exceptional event of a chronic vein sinus thrombosis during follow-up. Isolated cases regarding an acute time course have been described. The interest of this case lies in the fact that venous sinus thrombosis rarely has transitory focal deficit in its course and we found no such description as onset symptoms.
INTRODUCTION: Intracranial hypertension (ICHT) is the most frequent presenting syndrome of dural vein sinus thrombosis (CVT). A transient ischemic attack as an acute mode of onset is exceptional. CASE REPORT: A right handed, forty years old man with a medical history of recurrent headaches, microcephalia and calcifications in his brain, presenting to the emergency department with left paresis that lasted a few minutes and with a complete recovery. The cerebral and neck magnetic resonance (MR) including MR angiography showed superior sagittal sinus, both transverse sinuses and right sigmoid sinus thrombosis with an increase in size of superficial cerebral venous that drained to the left sigmoid sinus. There was no evidence of intracranial dural malformations. The cerebral MR did not show any abnormal parenchymal enhancement (edema, arterial or venous infarctions, hemorrhage) including diffusion-weighted IMR. The digital subtraction angiography (ADC) confirmed the same findings as the MR angiography. The diagnosis was a chronic CVT. We studied stroke in a young adult and we did not find other irregularities. The neurological examination was normal when the patient left the hospital with an antiplatelet drug. CONCLUSIONS: Focal neurological deficit is an exceptional event of a chronic vein sinus thrombosis during follow-up. Isolated cases regarding an acute time course have been described. The interest of this case lies in the fact that venous sinus thrombosis rarely has transitory focal deficit in its course and we found no such description as onset symptoms.