22. European Stroke Conference 162 Interesting and challenging cases Cisplatin-related Cerebral Infarction in Testicular Germ Cell Cancer: 2 Case Reports J. Lange1, M. Endres2, H. J. Audebert3, A. Rocco4 Department of Neurology, Charité – Universitätsmedizin Berlin, Campus Benjamin Franklin, Berlin, GERMANY1, Department of Neurology, Charité – Universitätsmedizin Berlin, Campus Charité Mitte, Berlin, GERMANY2, Department of Neurology, Charité – Universitätsmedizin Ber-lin, Campus Benjamin Franklin, Berlin, GERMANY3, Department of Neurology, Charité – Univer-sitätsmedizin Berlin, Campus Benjamin Franklin, Berlin, GERMANY4 Background: Ischemic stroke following cisplatin-based chemotherapy in testicular germ cell cancer (GCC) patients have been reported only in very rare case reports. We describe 2 cases of cerebrovas-cular occlusive disease (COD) associated with cisplatin-combined treatment (cisplatin, bleomycin, etoposid; PEB) and provide an overview of recent literature and possible pathophysiology. Results: Case 1: A 44 year old man with metastasized seminoma was admitted to our hospital. During the 1st chemotherapy cycle he suffered multiple infarctions in the middle cerebral artery (MCA) territory of both hemispheres. No vascular risk factors were known. Case 2: A 56 year old men presented with metastasized seminoma. After the 1st PEB-cycle he suf-fered from multiple infarctions in both MCA-territories. Vascular risk factors consisted of hyper-tension, hyperlipidemia and smoking. Angiography revealed multiple intracranial stenoses. Despite dual antiplatelet therapy and management of risk factors he experienced re-infarction after a second dose of cisplatin. The patient died after suffering from a subdural hematoma and occlusion of the right M1-stenosis. Various causes of COD after cisplatin therapy have been suggested. Most frequently, occlusions of cerebral arteries are explained with procoagulatory effects and increasing aggregation due to cell damage and endothelial activation. In our cases, multiple infarctions in different vascular territories argue for thromboembolic mechanisms. However, local thrombosis and vasospasm suspected in course of observing rapidly progressive arterial stenosis may also be involved. Conclusion: COD can be a severe complication of cisplatin treatment in GCC patients although prognosis might be good concerning tumor remission. Early detection and close interdisciplinary cooperation especially at initiation of chemotherapy may help in reducing mortality and long-term morbidity. 368 © 2013 S. Karger AG, Basel Scientific Programme 163 Interesting and challenging cases ATYPICAL PRESENTATION OF MOYA MOYA DISEASE A. Cerino1, D. Mittino2, L. Coppo3, G. Strigaro4, R. Cantello5 Department of Neurology, University of Piedmont East A. Avogadro, Novara, ITALY1, De-partment of Neurology, University of Piedmont East A. Avogadro, Novara, ITALY2, Department of Neurology, University of Piedmont East A. Avogadro, Novara, ITALY3, Department of Neurology, University of Piedmont East A. Avogadro, Novara, ITALY4, Department of Neurology, University of Piedmont East A. Avogadro, Novara, ITALY5 Background Moya Moya disease (MMD) was first described in 1957 as “hypoplasia of the bilateral internal ca-rotid arteries”. It’s a rare cerebrovascular condition with progressive stenosis of bilateral distal inter-nal carotid artery (ICA) and development of compensatory collateral small vessels, which appear as smoky-puffs (moya moya in Japanese) at the cerebral angiography. Methods We report the case of a 48-year-old caucasic woman with acute onset of language disturbances. The day after she was admitted to the Emergency Department of our Hospital. At the neurologic examination she was apathetic with no spontaneous speech production (only few correct words in response to questions), no other neurological alterations. She didn’t have fever, blood tests were unremarkable, blood pressure was normal. In the previous two years, she had two similar episodes lasted about 24 hours, never investigated. A brain CT demonstrated bilateral frontal lobe ipodensi-ty and a subsequent MRI scan confirmed the acute ischemic nature of the lesions. We performed a brain angiography that showed intracranial occlusion of the right ICA and severe stenosis of the left ICA, with a “smoky-puff” collateral network. We performed echocardiogram, abdominal echogra-phy, hematic and CSF examination to exclude associated conditions like vasculitis, congenital cardi-ac anomaly, renal-artery stenosis, hyperthyroidism. We diagnosed MMD. The patient was started on acetylsalicylic acid 100 mg and sertraline 50 mg daily. Few weeks later the symptoms improved: she was more cooperative, she could walk alone and answer with short sentences. Conclusion MMD in adults usually presents with haemorrhagic stroke due to the rupture of the collateral ves-sels; frontal signs are long-term manifestation of the disease. This is an atypical case with bilateral frontal ischemic stroke and acute onset of frontal lobe syn-drome.
Karger_ESC London_2013
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