London, United Kingdom 2013 Poster Session Red Cerebrovasc Dis 2013; 35 (suppl 3)1-854 381 185 Interesting and challenging cases Spontaneous and complete thrombosis of a giant unruptured PICA aneurysm: an unusual cause of cerebellar stroke R. Hourez1, K. Papadopoulos2, G. Bruninx3 CHU Charleroi, Charleroi, BELGIUM1, CHU Charleroi, Charleroi, BELGIUM2, CHU Charleroi, Charleroi, BELGIUM3 Background: The mechanisms of most PICA occlusion are equally divided into cardioembolic and atherosclerotic causes; other reported causes are vertebral artery dissection, ulcerated plaques on the aortic arch and occlusion of the PICA by tonsilar herniation due to raised posterior fossa pressure. Methods: We present a 57-year-old female who woke up with left occipital headache and gait un-steadiness, followed by one episode of vomiting. The examination showed very slight left upper limb dysmetria, ataxic gait, the tandem walk test was impossible to perform and the Romberg’s test demonstrated falls to the left side with eyes open. Results: CT showed a hyperdense lesion surrounded by hypodense tissue in the left cerebellar hemi-sphere (11x22x19mm) with a mass effect on the medulla. MRI revealed a left cerebellar extra-axial nodular T2 and Flair hypointense lesion (20x24mm) with peripheral annular gadolinium enhance-ment, surrounding edema and acute ischemic lesions in the PICA territory. MRA showed normal posterior circulation except that the left PICA could not be seen. Cerebral arteriography demonstrat-ed a left PICA thrombosis. The patient fully recovered and was treated conservatively. One-year after the event, the patient did not experience further symptom and arteriography did not show reca-nalization of the completely thrombosed giant PICA aneurysm. Conclusion: We describe a case of PICA stroke caused by a spontaneous and complete thrombosis of a giant PICA aneurysm. Conservative treatment and imaging follow-up is an option as recanaliza-tion appears to be rare. 186 Interesting and challenging cases Excessive Upper Body Sweating after Bilateral Anterior Cerebral Artery Infarct – A Case Re-port K. Khadjooi1, G.M. Smith2, K. Boyle3, E. Warburton4, E. O’Brien5 Cambridge University Hospitals, Addenbrooke’s Hospital, Cambridge, UNITED KINGDOM1, Cambridge University Hospitals, Addenbrooke’s Hospital, Cambridge, UNITED KINGDOM2, Cambridge University Hospitals, Addenbrooke’s Hospital, Cambridge, UNITED KINGDOM3, Cambridge University Hospitals, Addenbrooke’s Hospital, Cambridge, UNITED KINGDOM4, Cambridge University Hospitals, Addenbrooke’s Hospital, Cambridge, UNITED KINGDOM5 Introduction Excessive sweating as a result of stroke has been reported rarely and its mechanisms and clinical significance are not fully understood. We describe a case of severe hyperhydrosis after bilateral ACA infarct. Case report A 78-year old fit and well man was admitted following sudden loss of consciousness. He was on no medications. His GCS was 9/15 (E3V1M5) with aphasia and quadriparesis. All bloods were normal and ECG showed atrial flutter. Imaging (Fig. 1) confirmed bilateral large acute ischaemic frontal infarct (cardioembolic), with both left and right ACA arising from the left ICA. He spent around 7 weeks in Stroke Unit and remained in the state of akinetic mutism with flaccid quadriparesis. On day of admission he was sweaty but apyrexial. Sweating was confined to face, trunk and upper limbs and over the following days it became more pronounced to the extent that bed sheets were drenched and he became clinically and biochemically dehydrated (Urea started to rise from day 3, to maximum 21 on day 11). He needed extra fluids, initially 2 litres of intravenous fluids to keep elec-trolytes stable. Thyroid function was normal, and apart from an episode of pneumonia, sepsis was not a contributory factor. From week 5, sweating became less pronounced and at the time of dis-charge to an overseas rehabilitation unit (day 62), he needed around 1 litre positive balance through NG tube. Conclusion Post-stroke hyperhydrosis in the affected limbs is rare, reported in only 3 of 633 cases by Labar et al. Disruption of a neural pathway of cortical origin, inhibitory to sweating, is a proposed mecha-nism. In our case, confinement of hyperhydrosis to upper body, bilateral sweating and severity of fluid loss that led to dehydration were unique features. We decided to treat him conservatively, and as far as we know there is no evidence-based treatment for controlling post-stroke hyperhydrosis. This emphasises the need for increasing awareness and further research into this condition.
Karger_ESC London_2013
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