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1225 Hiccups in pure lateral medullary infarction
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Poster Abstracts
Thursday, November 10, 2005
Symptoms subsided. Two weeks later she was readmitted with a worsening of the headache. Cerebral venography was attempted through a femoral access but only the left IJV could be entered Milch showed multiple collaterals drainilig into it with non visualizatioli of the sigmoid silius. She also developed Deep vein thrombosis of the right leg and Pulliloliary embolism during the course of stay. We will be discussing the management of the complications and successful management of raised ICP with regression of papilledema. 1222 Neuroproteetive etti~ct of Hyperbaric Oxygenation abet Embolie Stroke in rats Kueppers-Tiedt, L ~, Henninger, N 2'3, Guenther, A a, Sicard, K M 4, Kollmar, R a, Schwab, S a, Wagner, A 1, Schneider, D :. 1Department of
Neurology, University of Leipzig, Leipzig, Germany; 2Department of Neurology and E,~perimental Neurology, University of Heidelberg, Heidelberg, Germany; 3Department of Neurology, University of iVlassaehusetts Medical School, Worcester, MA, USA; 4Centerfor Comparative Neurolmaging, Department of Psychiatry, University of iVlassaehusetts Medical School Worcester, MA, USA Backgrouml: Hyperbaric oxygeli treatment (HBO) in acute stroke remains controversial. This study investigated potential IIeuroprotectire properties of HBO in a model of embolic middle cerebral artery occlusion (MCAO) in rats that simulates human stroke with its different degrees of inadvertent reperfusion. Methods: 3 h after MCAO, 30 male Wistar rats were randomly exposed to either 1 h of 100% oxygen at 2.5 atmospheres pressure (HBO group; II -- 15) or normobaric room air (colitrol group; n - 15). Cerebral blood flow (CBF), apparent diffusion coefficient (ADC) and T2-weighted images were acquired at 30 min, 5 h, 24 h (1"2 only), and 7 d (T2 only) post-MCAO. Lesion volumes were calculated by using viability thresholds or by visual inspection. After the last scan, animals were sacrificed and brains stained with hematoxylili & eosili (H&E) for infarct measurement. Results: In both groups, CBF withili the infarct core was reduced 95°,5 relative to the corresponding contralateral region immediately after MCAO and remained 55?,'; subnormal at 5 h. Within HBO group, the ADC-derived lesion volume was 73.4?,'; at 5 h, T2-derived lesion volumes were 82.2"/0 and 76.7°,5 at 1 d and 7 d respectively, and histologically-derived lesion volume was 62.4"/0 at 7 d (all values are with respect to control). Lastly, mortality tended to be lower in the HBO group (data not shown). Conclusion: HBO treatment is neuroprotective for up to 7 d after embolic MCAO when initiated within 3 h after ischemia.
1223 Cerebral hnbolism as a cause of Lacunar Stroke Kuznetsov, A l, Vinogradov, 01, Kucherenko, S2, Odinak, M ~.
1National Pirogov Centre of Therapy and Surgery, ivIoseow, Russia; 2Military Medical Academy, Saint-Petersburg, Russia Lacunar stroke is one of subtypes of ischemic stroke. The main cause of lacunar ilifarctioli is cerebral microaligiopathy due to arterial hypertension or diabetes mellitus. The purpose of this study was the estimation o f cerebral embolism as a possible cause of lacunar infarction. Material anti Methods: We studied 4g uliselected patients with various subtypes of acute ischemJc stroke, 26 patients with atrial fibrillation and ischemJc stroke, and 6 patients with infective elidocarditis and ischernic stroke. We used MRI ("Magnetom Impact", Germany) or CT ("Somatom+4"', Germany) of the brain, transthoracJc echocardiography, duplex sonography ("Acuson 128XP", USA) and M R A ("Magnetom Impact", Germany) for estimation of cerebral arteries, and microemboli detection ("Soliomed-300", Russia). Results: Pattern of lacunar infarction on MRI or CT was detected in 13 patients (127,1'%). Four of 13 patients had potential cardiac and
arterial sources o f cerebral embolism, and they had not other causes of stroke. In these patients lacunar infarction were larger, and it had more lateral localization, near froli1 ilisula. In the patients with atrial fibrillation lacunar infarction was very rare (7,7°,5). Most of the patients with infective elidocarditis had IImltiple small infarction with cortical and subcortical localization (83,3%). Microembolic signals were detected in all o f these patients. Conclusions: Cerebral embolism can cause lacunar infarction if the size of embolic material is small (about 200 mcTn). Possible sources are heart valve disease and unstable atherosclerotic plaques. In these patients the alitiplatelet agents should be used. Carotid elidarterectomy should be indicated if there is unstable carotid atherosclerotic plaque. 1224 A ease of infarction restricted to unilateral hypothalamus with symptoms of hyperphagia and hypersomnolence Kwon, YS ~, Seo, M JÀ, Yu, HJ ~, Roh, SY a. 1PundangJaesaeng General
Hospital, Korea Background: It is well known that brain infarction restricted to unilateral hypothalamus is very rare because of abundant blood supply from circle of Willis. Results: We report a case of right hypothalamic infarction. A 63-yearold woman developed hyperphagia, hypersomnolence and hemihypertfidrosis limited to the left face. Conclusion: Brain M R imaging revealed the high signal intensities in right aliteromedial hypothalamus. 1225 Hiccups in Pure Lateral Medullary Infarction
Kwon, SB a, Hwang, SH ~, Yun, SH ~, Jung, S a, Lee, BC a. 1Department
of Neurology, Hallym University College of Medicine, SeouL Korea Background: Hiccups are not a frequent but disabling condition of lateral medullary infarction (LMI). Unlike other sSaliptoms and signs of LMI, the attatomJcal lesions of hiccups are not well known. Although there were studies about clinical-radiological correlation studies using MRI, few studies have evaluated the relation between the lesional location of LMI and hiccups. Therefore, we performed this study to clarify the lesiolial correlation with hiccups in LML Method: Between 1997 and 2004, we identified 12 patients with pure LMI (LMI without concomitant politilie or cerebellar infarction) who presented with hiccups in addition to typical lateral medullary syndrome. Eighteen patients without hiccups were included as a control. Clinical and radiologic findings were compared between two groups. Results: The patients with hiccups significalitly IIlore ofteli had dorsolateral rather than ventral lesions at horizontal levels (P < 0.05, likelihood ratio test for trend). But, there were no rosto-caudal differences at vertical levels. Conclusion: We suggest that LMI associated with hiccups often locates in the dorsolateral medulla at horizontal correlation. This comparative study using MRI helps us to expand the uliderstalidilig of the neural substrate for hiccups in LMI. 1226 Isolated CerebeUar Infarction in tile territory of tile medial branch of the Superior Cerebellar Artery Hyung Lee ~, Hyon-Ah Kim 1, Sung-II Sohn ~, Robert W Baloh 2.
1Defiartment of Neurology, Keimyung University School of Medicine, Daegu, South Korea; 2Department of Neurology UCLA School of Medicine, Los Angeles, CA, USA Background: The clinical syndrolire associated with dorsomedial infarction of the rostral cerebellulir in the territory of the medial
Poster Abstracts
Thursday, November 10, 2005
Symptoms subsided. Two weeks later she was readmitted with a worsening of the headache. Cerebral venography was attempted through a femoral access but only the left IJV could be entered Milch showed multiple collaterals drainilig into it with non visualizatioli of the sigmoid silius. She also developed Deep vein thrombosis of the right leg and Pulliloliary embolism during the course of stay. We will be discussing the management of the complications and successful management of raised ICP with regression of papilledema. 1222 Neuroproteetive etti~ct of Hyperbaric Oxygenation abet Embolie Stroke in rats Kueppers-Tiedt, L ~, Henninger, N 2'3, Guenther, A a, Sicard, K M 4, Kollmar, R a, Schwab, S a, Wagner, A 1, Schneider, D :. 1Department of
Neurology, University of Leipzig, Leipzig, Germany; 2Department of Neurology and E,~perimental Neurology, University of Heidelberg, Heidelberg, Germany; 3Department of Neurology, University of iVlassaehusetts Medical School, Worcester, MA, USA; 4Centerfor Comparative Neurolmaging, Department of Psychiatry, University of iVlassaehusetts Medical School Worcester, MA, USA Backgrouml: Hyperbaric oxygeli treatment (HBO) in acute stroke remains controversial. This study investigated potential IIeuroprotectire properties of HBO in a model of embolic middle cerebral artery occlusion (MCAO) in rats that simulates human stroke with its different degrees of inadvertent reperfusion. Methods: 3 h after MCAO, 30 male Wistar rats were randomly exposed to either 1 h of 100% oxygen at 2.5 atmospheres pressure (HBO group; II -- 15) or normobaric room air (colitrol group; n - 15). Cerebral blood flow (CBF), apparent diffusion coefficient (ADC) and T2-weighted images were acquired at 30 min, 5 h, 24 h (1"2 only), and 7 d (T2 only) post-MCAO. Lesion volumes were calculated by using viability thresholds or by visual inspection. After the last scan, animals were sacrificed and brains stained with hematoxylili & eosili (H&E) for infarct measurement. Results: In both groups, CBF withili the infarct core was reduced 95°,5 relative to the corresponding contralateral region immediately after MCAO and remained 55?,'; subnormal at 5 h. Within HBO group, the ADC-derived lesion volume was 73.4?,'; at 5 h, T2-derived lesion volumes were 82.2"/0 and 76.7°,5 at 1 d and 7 d respectively, and histologically-derived lesion volume was 62.4"/0 at 7 d (all values are with respect to control). Lastly, mortality tended to be lower in the HBO group (data not shown). Conclusion: HBO treatment is neuroprotective for up to 7 d after embolic MCAO when initiated within 3 h after ischemia.
1223 Cerebral hnbolism as a cause of Lacunar Stroke Kuznetsov, A l, Vinogradov, 01, Kucherenko, S2, Odinak, M ~.
1National Pirogov Centre of Therapy and Surgery, ivIoseow, Russia; 2Military Medical Academy, Saint-Petersburg, Russia Lacunar stroke is one of subtypes of ischemic stroke. The main cause of lacunar ilifarctioli is cerebral microaligiopathy due to arterial hypertension or diabetes mellitus. The purpose of this study was the estimation o f cerebral embolism as a possible cause of lacunar infarction. Material anti Methods: We studied 4g uliselected patients with various subtypes of acute ischemJc stroke, 26 patients with atrial fibrillation and ischemJc stroke, and 6 patients with infective elidocarditis and ischernic stroke. We used MRI ("Magnetom Impact", Germany) or CT ("Somatom+4"', Germany) of the brain, transthoracJc echocardiography, duplex sonography ("Acuson 128XP", USA) and M R A ("Magnetom Impact", Germany) for estimation of cerebral arteries, and microemboli detection ("Soliomed-300", Russia). Results: Pattern of lacunar infarction on MRI or CT was detected in 13 patients (127,1'%). Four of 13 patients had potential cardiac and
arterial sources o f cerebral embolism, and they had not other causes of stroke. In these patients lacunar infarction were larger, and it had more lateral localization, near froli1 ilisula. In the patients with atrial fibrillation lacunar infarction was very rare (7,7°,5). Most of the patients with infective elidocarditis had IImltiple small infarction with cortical and subcortical localization (83,3%). Microembolic signals were detected in all o f these patients. Conclusions: Cerebral embolism can cause lacunar infarction if the size of embolic material is small (about 200 mcTn). Possible sources are heart valve disease and unstable atherosclerotic plaques. In these patients the alitiplatelet agents should be used. Carotid elidarterectomy should be indicated if there is unstable carotid atherosclerotic plaque. 1224 A ease of infarction restricted to unilateral hypothalamus with symptoms of hyperphagia and hypersomnolence Kwon, YS ~, Seo, M JÀ, Yu, HJ ~, Roh, SY a. 1PundangJaesaeng General
Hospital, Korea Background: It is well known that brain infarction restricted to unilateral hypothalamus is very rare because of abundant blood supply from circle of Willis. Results: We report a case of right hypothalamic infarction. A 63-yearold woman developed hyperphagia, hypersomnolence and hemihypertfidrosis limited to the left face. Conclusion: Brain M R imaging revealed the high signal intensities in right aliteromedial hypothalamus. 1225 Hiccups in Pure Lateral Medullary Infarction
Kwon, SB a, Hwang, SH ~, Yun, SH ~, Jung, S a, Lee, BC a. 1Department
of Neurology, Hallym University College of Medicine, SeouL Korea Background: Hiccups are not a frequent but disabling condition of lateral medullary infarction (LMI). Unlike other sSaliptoms and signs of LMI, the attatomJcal lesions of hiccups are not well known. Although there were studies about clinical-radiological correlation studies using MRI, few studies have evaluated the relation between the lesional location of LMI and hiccups. Therefore, we performed this study to clarify the lesiolial correlation with hiccups in LML Method: Between 1997 and 2004, we identified 12 patients with pure LMI (LMI without concomitant politilie or cerebellar infarction) who presented with hiccups in addition to typical lateral medullary syndrome. Eighteen patients without hiccups were included as a control. Clinical and radiologic findings were compared between two groups. Results: The patients with hiccups significalitly IIlore ofteli had dorsolateral rather than ventral lesions at horizontal levels (P < 0.05, likelihood ratio test for trend). But, there were no rosto-caudal differences at vertical levels. Conclusion: We suggest that LMI associated with hiccups often locates in the dorsolateral medulla at horizontal correlation. This comparative study using MRI helps us to expand the uliderstalidilig of the neural substrate for hiccups in LMI. 1226 Isolated CerebeUar Infarction in tile territory of tile medial branch of the Superior Cerebellar Artery Hyung Lee ~, Hyon-Ah Kim 1, Sung-II Sohn ~, Robert W Baloh 2.
1Defiartment of Neurology, Keimyung University School of Medicine, Daegu, South Korea; 2Department of Neurology UCLA School of Medicine, Los Angeles, CA, USA Background: The clinical syndrolire associated with dorsomedial infarction of the rostral cerebellulir in the territory of the medial