Model of cerebral palsy in the perinatal rabbit

Perinatal brain injury results in one of the highest burdens of disease in view of the lifelong consequences and is of enormous cost to society. This makes it imperative to develop better animal models that mimic the human condition. Many neurodevelopmental deficits, such as cerebral palsy, are believed to be a result of prenatal hypoxia-ischemia in humans. Fetal global hypoxia-ischemia is most commonly a consequence of acute placental insufficiency. Our laboratory has modeled in utero sustained and repetitive hypoxia-ischemia in the pregnant rabbit to mimic the insults of abruptio placenta and labor, respectively. Sustained hypoxia-ischemia at 70% (22 days' gestation) and 79% (25 days' gestation) and repetitive hypoxia-ischemia at 90% gestation (28 days' gestation) caused stillbirths and multiple deficits in the postnatal survivors. The deficits included impairment in multiple tests of spontaneous locomotion, reflex motor activity, motor responses to olfactory stimuli, and the coordination of suck and swallow. Hypertonia was observed in the 22 and 25 days' gestation survivors but not in the 28 days' gestation group. Hypertonic survivors were artificially fed and found to have the motor deficits persist for at least 11 postnatal days. A spectrum of brain abnormalities is found on magnetic resonance imaging. This is the first animal model to mimic cerebral palsy. The findings also suggest a window of vulnerability during brain development when the injury results in hypertonia in newborn pups.     

Magnetic resonance imaging in diplegic form of cerebral palsy

Eighteen children with diplegic form of cerebral palsy (CP) underwent magnetic resonance imaging (MRI) because of the enlarged occipital horns of both lateral ventricles found on previous computerized tomography (CT). In 16 of them squint was present. MRI in flow attenuated inversion recovery (FLAIR) and turbo spin echo (TSE) modes (T2 weighted images) best showed white matter lesions in occipital areas in all patients with squint, while no white matter changes could be detected in CT (in retrospect), thus proving the superiority of MRI in examining CP children. The authors postulate that the hemispheric occipital lesion causing impairment of visual co-ordination may result in squint.     

Ante- and perinatal factors for cerebral palsy: case-control study in Estonia

Establishing consistency between cerebral palsy registries in reporting of new cases enables more effective collaboration in terms of researching predisposing factors. To identify antenatal and intrapartum risk factors for cerebral palsy in the Estonian population, we undertook a matched case-control study of 153 children with cerebral palsy, ascertained from a population-based survey. One hundred two maternal, antenatal, and intrapartum variables were initially retrieved from medical records. Main outcome measures were the odds ratio estimates of relative risk of cerebral palsy. As a result of the study, and considering the whole spectrum of severity, the relevant risk factors during pregnancy were bleeding after 20 weeks, anemia in the second half of pregnancy, pregnancy-induced hypertension in the second half of pregnancy, and preeclampsia. The most important intrapartum factors were premature birth, placental abruption, an acute hypoxic event during delivery, and any fetal presentation other than vertex. Predisposing factors related to neonatal condition were an Apgar score < or = 7 at the first and fifth minutes of life, hypoxic-ischemic encephalopathy, and assisted ventilation. Our findings suggest that intrapartum factors, including those hypothetically realized through hypoxic-ischemic pathways, are not of low importance in the etiology of cerebral palsy.     

A case of cardiac arrest encephalopathy in athetotic cerebral palsy]

A 25-year-old woman with cerebral palsy of spastic quadriplegia and athetosis showed typical cardiac arrest encephalopathy on neuropathology. The etiology of cerebral palsy was perinatal origin including prematurity, asphyxia and hyperbilirubinemia. Ventricular premature beats had developed since about 20 years of age. Muscle tone also increased with aging and symptoms of vago-vagal reflex were occasionally observed after eating. At 25 years, cardiac arrest occurred and cardiopulmonary resucitation was done immediately. She remained unconscious with absent corneal reflex and irregular respiration. EEG or auditory brain stem response showed flat activity. She died of respiratory failure 53 days after the episode of cardiac arrest. Neuropathology showed bilaterally symmetrical necrosis in the superior colliculi, gracilis nuclei, cuneate nuclei and spinotrigeminal nuclei accompanied with severe necrosis in the cerebrum and cerebellum. These findings in this adult case of total asphyxia were compatible with those observed in total plus partial asphyxia in the neonates. This discrepancy may be due to difference in cerebral maturity. Children or young adults with athetotic type cerebral palsy have a high risk of sudden death. Sudden cardiac arrest seems to play an important role in sudden death of these patients.     

Homozygous factor-V mutation as a genetic cause of perinatal thrombosis and cerebral palsy

A 5-year old girl with cerebral palsy (CP), preterm birth, postnatal aortic thrombus, and cerebellar venous infarction who is homozygous for the thrombophilic factor-V Leiden (fVL) mutation is reported. The role of hereditary thrombophilic disorders in the development of perinatal vascular lesions such as aortic thrombi, renal-vein thrombosis, venous-sinus thrombosis, and cerebral infarction is unknown. This case report brings into question a potential association between fVL, perinatal vascular lesions, perinatal stroke, and CP.     

韦尼克脑病16例临床分析

目的探讨韦尼克脑病(Wernicke’s encephalopathy,WE)的病因、发病机制、临床表现及治疗。方法回顾性分析我院2002~2009年16例WE患者的临床资料。结果 WE病因复杂,饮酒为其最常见的病因。主要临床表现包括行走不稳、眼征、精神神志障碍三联征,但典型的WE三联征很少同时出现,往往以其中一种或两种表现为主。头部MRI大多为腔隙性脑梗死、脑萎缩等非特异性表现,丘脑、下丘脑、乳头体及脑室周围等部位对称性长T1、长T2信号的特征性表现并不多见。绝大多数患者经大剂量补充Vit-B1后疗效显著。结论 WE病因及临床表现复杂多样,早期诊断困难,头部MRI可作为WE重要的辅助检查。及时补充大剂量Vit-B1预后良好。     

表现为脑梗死的41例神经梅毒的临床表现和治疗分析

目的 观察表现为腩梗死的神经梅毒临床特点,探讨其治疗及预后. 方法 分析41例此类患者的临床表现、心理量表评分、实验室检查和影像学等资料. 结果 41例中有智能下降23例;表现肢体瘫痪30例,肢体麻痹8例,眩晕2例,癫痫样发作1例;头颅MRI显示脑萎缩及多发梗死灶,脑水肿占位表现不显著;血液及脑脊液梅毒螺旋体血凝试验(TPHA)阳性;用大剂量青霉素治疗后,95.1%临床症状得到改善. 结论 神经梅毒临床表现多样,易误诊;MR显示多发脑梗死、脑萎缩、占位效应不明显;青霉素治疗有效,且疗效较好,但合并大面积脑梗死预后较差.     

表现为脑梗死的41例神经梅毒的临床表现和治疗分析

目的 观察表现为腩梗死的神经梅毒临床特点,探讨其治疗及预后. 方法 分析41例此类患者的临床表现、心理量表评分、实验室检查和影像学等资料. 结果 41例中有智能下降23例;表现肢体瘫痪30例,肢体麻痹8例,眩晕2例,癫痫样发作1例;头颅MRI显示脑萎缩及多发梗死灶,脑水肿占位表现不显著;血液及脑脊液梅毒螺旋体血凝试验(TPHA)阳性;用大剂量青霉素治疗后,95.1%临床症状得到改善. 结论 神经梅毒临床表现多样,易误诊;MR显示多发脑梗死、脑萎缩、占位效应不明显;青霉素治疗有效,且疗效较好,但合并大面积脑梗死预后较差.     

表现为脑梗死的41例神经梅毒的临床表现和治疗分析

目的 观察表现为腩梗死的神经梅毒临床特点,探讨其治疗及预后. 方法 分析41例此类患者的临床表现、心理量表评分、实验室检查和影像学等资料. 结果 41例中有智能下降23例;表现肢体瘫痪30例,肢体麻痹8例,眩晕2例,癫痫样发作1例;头颅MRI显示脑萎缩及多发梗死灶,脑水肿占位表现不显著;血液及脑脊液梅毒螺旋体血凝试验(TPHA)阳性;用大剂量青霉素治疗后,95.1%临床症状得到改善. 结论 神经梅毒临床表现多样,易误诊;MR显示多发脑梗死、脑萎缩、占位效应不明显;青霉素治疗有效,且疗效较好,但合并大面积脑梗死预后较差.     

表现为脑梗死的41例神经梅毒的临床表现和治疗分析

目的 观察表现为腩梗死的神经梅毒临床特点,探讨其治疗及预后. 方法 分析41例此类患者的临床表现、心理量表评分、实验室检查和影像学等资料. 结果 41例中有智能下降23例;表现肢体瘫痪30例,肢体麻痹8例,眩晕2例,癫痫样发作1例;头颅MRI显示脑萎缩及多发梗死灶,脑水肿占位表现不显著;血液及脑脊液梅毒螺旋体血凝试验(TPHA)阳性;用大剂量青霉素治疗后,95.1%临床症状得到改善. 结论 神经梅毒临床表现多样,易误诊;MR显示多发脑梗死、脑萎缩、占位效应不明显;青霉素治疗有效,且疗效较好,但合并大面积脑梗死预后较差.     

表现为脑梗死的41例神经梅毒的临床表现和治疗分析

目的 观察表现为腩梗死的神经梅毒临床特点,探讨其治疗及预后. 方法 分析41例此类患者的临床表现、心理量表评分、实验室检查和影像学等资料. 结果 41例中有智能下降23例;表现肢体瘫痪30例,肢体麻痹8例,眩晕2例,癫痫样发作1例;头颅MRI显示脑萎缩及多发梗死灶,脑水肿占位表现不显著;血液及脑脊液梅毒螺旋体血凝试验(TPHA)阳性;用大剂量青霉素治疗后,95.1%临床症状得到改善. 结论 神经梅毒临床表现多样,易误诊;MR显示多发脑梗死、脑萎缩、占位效应不明显;青霉素治疗有效,且疗效较好,但合并大面积脑梗死预后较差.     

表现为脑梗死的41例神经梅毒的临床表现和治疗分析

目的 观察表现为腩梗死的神经梅毒临床特点,探讨其治疗及预后. 方法 分析41例此类患者的临床表现、心理量表评分、实验室检查和影像学等资料. 结果 41例中有智能下降23例;表现肢体瘫痪30例,肢体麻痹8例,眩晕2例,癫痫样发作1例;头颅MRI显示脑萎缩及多发梗死灶,脑水肿占位表现不显著;血液及脑脊液梅毒螺旋体血凝试验(TPHA)阳性;用大剂量青霉素治疗后,95.1%临床症状得到改善. 结论 神经梅毒临床表现多样,易误诊;MR显示多发脑梗死、脑萎缩、占位效应不明显;青霉素治疗有效,且疗效较好,但合并大面积脑梗死预后较差.     

表现为脑梗死的41例神经梅毒的临床表现和治疗分析

目的 观察表现为腩梗死的神经梅毒临床特点,探讨其治疗及预后. 方法 分析41例此类患者的临床表现、心理量表评分、实验室检查和影像学等资料. 结果 41例中有智能下降23例;表现肢体瘫痪30例,肢体麻痹8例,眩晕2例,癫痫样发作1例;头颅MRI显示脑萎缩及多发梗死灶,脑水肿占位表现不显著;血液及脑脊液梅毒螺旋体血凝试验(TPHA)阳性;用大剂量青霉素治疗后,95.1%临床症状得到改善. 结论 神经梅毒临床表现多样,易误诊;MR显示多发脑梗死、脑萎缩、占位效应不明显;青霉素治疗有效,且疗效较好,但合并大面积脑梗死预后较差.