Cerebral venous malformation complicated by spontaneous thrombosis

A case of spontaneous thrombosis and infarction leading to death as complications of a cerebral venous malformation in a 13-yearold boy is reported. This is the first published report of this type of complication occurring in a case of venous angioma. While the biologic behavior of cerebral venous malformations has suggested that they are benign in nature, and the results of surgical management have encouraged a conservative approach, the present case illustrates a potential complication and argues against the assumption that these malformations are completely benign in nature.     

等密度硬膜下血肿的CT诊断(附47例分析)

本文分析了47例等密度硬膜下血肿的CT表现,观测的各种CT征象,发现(1)bolus增强扫描显示的血肿、血肿膜及表面移位血管;(2)中线结构的特征性偏移;(3)表面脑回聚拢内移;(4)脑灰白质界面内移;(5)侧脑室变形和脑—脑室指数变小,对等密度硬膜下血肿的诊断和鉴别诊断有重要意义。     

Acute cerebral infarction: pathophysiology and modern treatment concepts

Summary This review focuses on the pathophysiological changes in acute cerebral ischemia, with special emphasis on disturbances of the cerebral blood flow (CBF) and the associated penumbra concept. Alternatively, the model of peri-infarct depolarization is demonstrated. Metabolic and molecular changes caused by cerebral ischemia and reperfusion are discussed, namely energy failure, release of glutamate with an excitatoric burst, calcium influx in neurons, generation of free radicals, activation of different proteases, disturbances of protein synthesis, induction of gene expression and apoptosis, loss of membrane integrity, edema formation and microvascular disturbances. In summary, the pathophysiological changes after focal cerebral ischemia and reperfusion are most adequately described by a network of interacting different mechanisms of tissue alterations. The simple concept of a cascade of ischemic effects which would be easy to block seems to be less applicable. A time window of approximately 6 h for the acute stroke therapy is postulated on the base of the above mentioned pathophysiological changes. The recently introduced treatment regimen with optimized basic treatment, recanalization using thrombolysis and neuroprotection by different agents is presented. Different modes of a possible intervention are discussed. Modern concepts of stroke therapy including stroke-unit care and thrombolysis with add-on neuroprotection seem to have potential for improving the outcome of acute stroke patients.      

Ruptured aneurysm with intracerebral hemorrhage in an 8 year old boy

Report on a case of aneurysm in a child and its treatment with discussion of its rarity and origin.     

不同脑缺血和再灌流过程中大鼠脑组织NO含量的动态变化

采用线栓法制成大鼠大脑中动脉梗塞 ( MCAO)模型 ,依 Hb O2 - NO法测定持续性脑缺血和缺血 /再灌流脑组织内 NO含量的变化 ,以探讨不同脑缺血和再灌流过程中 NO的变化规律及其意义。结果 :缺血 3小时受损脑组织 NO水平即增高 ,再灌流后 NO逐步升高 ,而持续性缺血状态下 NO则表现降低后再升高的变化。虽然两组 NO在 7天时均有明显降低 ,但仍高于缺血前水平。认为持续性脑缺血和缺血 /再灌流情况下 NO的变化规律有所不同 ,与缺血脑组织的缺氧及产生 NO所需底物供应缺乏有关 ,且可能与脑组织的损害密切相关     

Channges in regional cerebral blood flow after hyperventilation in the pig with an induced focal cerebral contusion

Summary Changes in regional cerebral blood flow in anaesthetized pigs with an induced focal cerebral contusion were studied before and after two grades of hyperventilation. A reduction in arterial tension of CO₂ with 0.70mmHg and a further reduction of 0.55mmHg did not change the CO₂ reactivity. Reactivity in both injured and macroscopically normal regions was the same, revealing an average of 39.3% flow change per kPa change in CO₂ tension. Regions with low flow after the contusion had an equally big reduction apparently leading to hypoxia because global metabolic rate was unchanged.     

Hyperaemia prior to acute cerebral swelling in severe head injuries: The role of transcranial doppler monitoring

Summary Acute cerebrovascular congestion after a closed head injury is significantly related to intracranial hypertension. As an indirect method of cerebral blood flow measurement, transcranial doppler sonography (TCD) provides a rapid and noninvasive assessment of cerebral haemodynamics, including hyperaemic conditions.TCD examinations was serially performed in 35 patients with severe head injury with intact cerebral circulation; i.e. the mean flow velocity (MFV) patterns of the middle cerebral artery (MCA) did not show signs of cerebral circulatory arrest such as systolic spike, to and fro, or no flow. The results showed that the MFV of the MCAs and ipsilateral extracranial internal carotid arteries (ICAs) in 9 of these patients increased sharply and pulsatility index (PI) decreased during 48–96 hours after the injury. This was soon followed by patterns of high intracranial resistance, consistent with elevated intracranial pressure (ICP) in monitored patients and acute brain swelling on repeated computed tomographic (CT) scans. The correlation between increased MFVs, decreased PIs, and cerebral haemodynamic changes leading to acute brain swelling is discussed.The number of patients who ended with severe disability, vegetative state, or death was 66% in this group of 9 patients, compared to only 34% for the 35 patients overall with severe head injury. Though the morbidity and mortality rates largely depend on the primary injury, the presence of acute cerebral swelling aggravate the grave course in these patients. And the ability of TCD to monitor the hyperaemic state prior to oedema should lead us to adjust the therapy in order to minimize the secondary insult related to intracranial hypertension.     

Injection of botulinum A toxin into the gastrocnemius muscle of patients with cerebral palsy: a 3-dimensional motion analysis study

Botulinum A toxin (BOTOX^®) was injected into the gastrocnemius muscle of 26 cerebral palsy subjects with equinus gait. All subjects were equinus walkers without fixed contracture of the triceps-surae muscle. Injections were performed at 3 month intervals, if needed, as determined by the treating clinician. There were 14 subjects with spastic hemiplegia, 11 subjects with spastic diplegia and 1 subject with spastic quadriplegia. In the case of those subjects with bilateral equinus gait the dose was divided and given into both the right and left gastrocnemius muscle. Gait analysis data was collected prior to the first injection and subsequently at 3 month intervals for 1 year. Kinematic and electromyographic data was obtained. This data was analyzed to provide objective information about the outcome of treatment. Four subjects moved away and were lost to follow-up. Seven subjects left the study to have surgery. The data collected revealed statistically significant improvements in dynamic ankle dorsiflexion in both stance and swing phases, stride length, and electromyography of the tibialis anterior. There were no complications. While the results of this study are promising, additional prospective studies are needed to determine the feasibility of preventing muscle contractures over a longer time period. Furthermore, there is a need for inclusion of other muscles in future research. Future research should also compare BOTOX^® treatment with alternative methods of dealing with muscle spasticity such as: casting, orthotic devices, physical therapy, selective dorsal rhizotomy, and surgical lengthening.     

严重鼻衄行颌内动脉栓塞术并发脑梗塞死亡

报道１例严重鼻衄伴高血压、动脉硬化患者，经常规方法止血无效，行患侧颌内动脉超选择性栓塞术。术后鼻出血停止，但出现脑梗塞、昏迷，经抢救无效，于术后第９天死亡。认为对有动脉硬化的患者，应不用或慎用超选择性动脉栓塞术。     

Vasodilator effects of C-type natriuretic peptide on cerebral arterioles in rats

The vasodilator effects of C-type natriuretic peptide (CNP) were investigated in isolated rat cerebral arterioles. CNP caused dose-dependent vasodilation, maximally by 10.0±2.2% at 10⁻⁶ M. The median effective concentration (EC₅₀) was 5.2×10⁻¹⁰ M. In contrast, atrial natriuretic peptide and B-type natriuretic peptide, other members of the natriuretic peptide family, produced little or no vasodilation. Pretreatment with methylene blue (10⁻⁴ M) abolished CNP-induced vasodilation, whereas pretreatment with N^G-monomethyl-

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-arginine or indomethacin did not inhibit vasodilation. Thus, CNP is suggested to cause significant vasodilation in cerebral arterioles via a cyclic guanosine monophosphate-dependent mechanism. © 1997 Elsevier Science B.V. All rights reserved.