iFlow成像技术对中脑周围非动脉瘤性蛛网膜下腔出血后脑血管痉挛的评估

目的 探讨iFlow成像技术在中脑周围非动脉瘤性蛛网膜下腔出血（PNSAH）后脑血管痉挛评估中的价值。方法 收集经CT及两次血管造影明确诊断为PNSAH 60例为观察组,收集我院同期颅内动脉瘤单纯弹簧圈栓塞治疗后半年以上随访复查造影时未见复发60例为对照组。利用西门子公司iFlow软件测量首次造影和复查造影时双侧颈内动脉分叉部、双侧大脑中动脉分叉部、双侧椎动脉造影基底动脉末端相同部位的造影剂达峰时间（TTP）。结果 与对照组相比,观察组首次造影中双侧椎-基底动脉末端造影剂TTP明显增高（P<0.05）,观察组复查造影中双侧椎-基底动脉末端、右侧颈内分叉部、右侧大脑中分叉部造影剂TTP均明显增高（P<0.05）。与首次造影相比,观察组复查造影双侧椎-基底动脉末端造影剂TTP明显增高（P<0.05）。结论 PNSAH后存在血管痉挛,且以基底动脉最明显,应用iFlow技术评估脑血管痉挛的具有可行性。     

大脑中动脉动脉瘤的血管内治疗

目的探讨血管内治疗大脑中动脉动脉瘤的可行性、安全性和有效性。方法回顾性分析采用血管内治疗的24例大脑中动脉动脉瘤患者的临床资料,包括患者年龄、临床分级、动脉瘤出血量、部位、形态、瘤颈宽度、血管痉挛程度及术中应用技术等。结果100%栓塞17例,95%栓塞4例,90%栓塞3例。1例患者术中血管痉挛加重致不完全失语。随访无动脉瘤再破裂出血病例,1例患者出现迟发性血管痉挛。结论血管内治疗大脑中动脉动脉瘤是一种安全、有效的方法。     

Intra-arterial Dantrolene for Refractory Cerebral Vasospasm After Aneurysmal Subarachnoid Hemorrhage

Background

Intravenous dantrolene has been used to prevent and treat cerebral vasospasm. We report a case of refractory cerebral vasospasm treated with intra-arterial dantrolene after aneurysmal subarachnoid hemorrhage.

Methods

A 56-year-old woman suffered a diffuse subarachnoid hemorrhage from a ruptured anterior communicating artery aneurysm which was successfully treated with coil embolization. She subsequently developed bilateral severe angiographic vasospasm which was treated with intra-arterial vasodilators. However, owing to the recurrence of vasospasm, intra-arterial dantrolene followed by balloon angioplasty was used.

Results

There was moderate improvement of the severe vasospasm in bilateral A1 segments of the anterior cerebral arteries after microcatheter-based intra-arterial infusion of 30?ml (1?mg/ml) dantrolene. Patient??s hemodynamic parameters were monitored during and after the procedure and no significant changes were seen after dantrolene infusion. A follow up cerebral angiogram after 1?day demonstrated the persistence of therapeutic effect.

Conclusion

Intra-arterial dantrolene induced a sustained improvement in cerebral vasospasm secondary to ruptured aneurysm. No significant side effects were observed during or after the infusion of the drug.     

Intracranial Extension of Spinal Subarachnoid Hematoma Causing Severe Cerebral Vasospasm

Spinal subarachnoid hemorrhages (SAH) can extend into the intracranial subarachnoid space, but, severe cerebral vasospasm is rare complication of the extension of intracranial SAH from a spinal subarachnoid hematoma. A 67-year-old woman started anticoagulant therapy for unstable angina. The next day, she developed severe back pain and paraplegia. MRI showed intradural and extramedullar low signal intensity at the T2-3, consistent with intradural hematoma. High signal intensity was also noted in the spinal cord from C5 to T4. We removed subarachnoid hematoma compressing the spinal cord. The following day, the patient complained of severe headache. Brain CT revealed SAH around both parietal lobes. Three days later, her consciousness decreased and left hemiplegia also developed. Brain MRI demonstrated multiple cerebral infarctions, mainly in the right posterior cerebral artery territory, left parietal lobe and right watershed area. Conventional cerebral angiography confirmed diffuse severe vasospasm of the cerebral arteries. After intensive care for a month, the patient was transferred to the rehabilitation department. After 6 months, neurologic deterioration improved partially. We speculate that surgeons should anticipate possible delayed neurological complications due to cerebral vasospasm if intracranial SAH is detected after spinal subarachnoid hematoma.     

Angiographic vasospasm and release of platelet thromboxane after subarachnoid hemorrhage

We studied adenosine diphosphate-induced platelet aggregation and the associated release of thromboxane B2 in 49 patients with subarachnoid hemorrhage in relation to angiographic vasospasm. Postoperative cerebral angiography was performed less than or equal to 3 (median 1) days after surgery for an aneurysm 5-14 days after subarachnoid hemorrhage. Correspondingly, one sample from each patient was taken within 24 hours either before or after angiography. The occurrence of severe as well as diffuse, moderate, or severe angiographic vasospasm was associated with the presence of delayed cerebral ischemia (p less than 0.05). Patients with diffuse angiographic vasospasm had significantly higher (p less than 0.05) values for thromboxane B2 release than the others, even after adjustment by the clinical grades on admission and before surgery, the timing of surgery, the time from subarachnoid hemorrhage to angiography and blood sampling, and nimodipine therapy. Severe and diffuse angiographic vasospasm were also associated with poor outcome at 1 year (p less than 0.05). Our results suggest that augmented release of platelet thromboxane may be involved in the pathogenesis of vasospasm in large cerebral arteries.     

The importance of traumatic subarachnoid haemorrhage

Post-traumatic cerebral vasospasm is being increasingly recognised as a possibly significant complication after head injury. To assess the relationship between post-traumatic subarachnoid haemorrhage (tSAH) and post-traumatic vasospasm, 63 patients with severe head injury (GCS 3-8) were studied. Forty-seven patients had cerebral contusion on the initial CT scan. In 25 of these (Group I) there were only contusions, while 22 (Group II) also had tSAH. All patients had daily measurements of blood flow velocity in the basal cerebral arteries using transcranial Doppler ultrasound (TCD). The incidence of vasospasm detected by TCD was significantly higher in Group II. Furthermore there were significantly fewer good outcomes (GOS 1 and 2) in this group. These results suggest that the presence of subarachnoid blood in patients with severe head injury is associated with a risk of vasospasm, and with poorer outcome.     

Impact of cerebral microcirculatory changes on cerebral blood flow during cerebral vasospasm after aneurysmal subarachnoid hemorrhage

BACKGROUND AND PURPOSE: Cerebral microcirculatory changes during cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH) are still controversial and uncertain. The aim of this study was to investigate the changes of cerebral microcirculation during cerebral vasospasm and to clarify the roles of microcirculatory disturbances in cerebral ischemia by measuring cerebral circulation time (CCT) and regional cerebral blood flow (rCBF). METHODS: In 24 cases with aneurysmal SAH, rCBF studies by single-photon emission CT and digital subtraction angiography (DSA) were performed on the same day between 5 and 7 days after SAH and/or within 4 hours after the onset of delayed ischemic neurological deficits. CCT was obtained by analyzing the time-density curve of the contrast media on DSA images and was divided into proximal CCT, which was the circulation time through the extraparenchymal large arteries, and peripheral CCT, which was the circulation time through the intraparenchymal small vessels. They were analyzed in association with rCBF and angiographic vasospasm. RESULTS: Severe angiographic vasospasm statistically decreased rCBF, and correlation between the degree of angiographic vasospasm and rCBF was seen (r=0.429, P=0.0006). Peripheral CCT showed strong inverse correlation with rCBF (r=-0.767, P<0.0001). Even in none/mild or moderate angiographic vasospasm, prolonged peripheral CCT was clearly associated with decreased rCBF. CONCLUSIONS: In addition to the marked luminal narrowing of large arteries detected as severe angiographic vasospasm, microcirculatory changes detected as prolonged peripheral CCT affected cerebral ischemia during cerebral vasospasm. These results suggested that impaired autoregulatory vasodilation or decreased luminal caliber in intraparenchymal vessels may take part in cerebral ischemia during cerebral vasospasm.     

Transcranial Doppler detection of anterior cerebral artery vasospasm.

The performance of transcranial Doppler in the detection of anterior cerebral artery vasospasm and vasospasm in patients after subarachnoid haemorrhage was analysed. Transcranial Doppler and cerebral angiography were performed within the same 24 hours on each of 41 patients with acute subarachnoid haemorrhage. Sensitivity and specificity of transcranial Doppler to classify middle cerebral arteries, anterior cerebral arteries, and patients with angiographic vasospasm were determined at mean velocities of 120 and 140 cm/s. Accuracy of transcranial Doppler was better at 140 than at 120 cm/s. For the middle cerebral artery, sensitivity was 86%, specificity 98%. For the anterior cerebral artery, sensitivity was 13%, specificity 100%. Among all patients, sensitivity was 45%, specificity 96%. Among patients with anterior communicating artery aneurysms, sensitivity was 14%, specificity 90%. Therefore, transcranial Doppler accurately differentiates between middle cerebral arteries with and without vasospasm on angiography, but has a very low sensitivity for detecting anterior cerebral artery vasospasm and vasospasm in patients with anterior communicating artery aneurysms. Since vasospasm may involve anterior cerebral arteries while sparing middle cerebral arteries, especially after rupture of an anterior communicating artery aneurysm, caution should be exercised in using negative transcranial Doppler results to make treatment decisions based on the assumed absence of vasospasm.     

脑血管痉挛中差异表达蛋白质的实验研究

目的 建立兔脑血管痉挛(CVS)基底动脉和正常兔基底动脉双向凝胶电泳图谱,鉴定差异表达蛋白,从中发现有意义的CVS相关标志物.方法 采用双向凝胶电泳(2-DE)分离痉挛基底动脉和正常基底动脉总蛋白,银染显色,通过imagemaster5.0软件分析,从中选取差异表达蛋白质点,应用基质辅助激光解析飞行时间串联质谱(MALDI-TOF/TOF)鉴定差异表达的蛋白质.结果 获得重复性和分辨率较好的兔基底动脉双向凝胶电泳图谱;发现49个差异表达点,其中35个点得到鉴定,在CVS中高表达的有24个,其余11个在CVS中呈低表达.结论 建立了痉挛基底动脉和正常基底动脉双向凝胶电泳图谱,并应用质谱技术鉴定了35个差异表达点,这些差异表达蛋白质可能与CVS的发生相关.     

Blindness of cerebral origin in acute intermittent porphyria. Report of a case and postmortem examination.

Sudden permanent blindness of cerebral origin, in addition to severe abdominal pain, hypertension, convulsions, and peripheral neuropathy developed in a 21-year-old woman, a victim of acute intermittent porphyria. Findings of the pathological examination of the brain showed extensive infarction in both occipital lobes. The pathological changes were consistent with anoxia. We discuss and review the literature of the possibility of "vasospasm" of both posterior cerebral arteries. Follow-up studies with serial EEG showed either focal epileptogenic activity or diffuse slow waves. The most consistent epileptic discharges were found in the occipital regions. The favorable response to the treatment of seizures with carbamazepine in this patient might encourage further clinical trials.     

Therapeutic potential of peroxisome proliferator-activated receptor γ agonist rosiglitazone in cerebral vasospasm after a rat experimental subarachnoid hemorrhage model

The pathogenesis of cerebral vasospasm is closely associated with inflammation and immune response in arterial walls. Recently, the authors proved the key role of Toll-like receptor (TLR)4 in the development of vasospasm in experimental subarachnoid hemorrhage (SAH) model. Because peroxisome proliferator-activated receptor (PPAR) gamma agonists are identified as effective inhibitors of TLR4 activation, we investigated the anti-inflammation properties of PPAR-gamma agonist rosiglitazone in basilar arteries in a rat experimental SAH model and evaluated the effects of rosiglitazone on vasospasm. Inflammatory responses in basilar arteries were assessed by immunohistochemical staining for intercellular molecule (ICAM)-1 and myeloperoxidase (MPO). Expression of TLR4 was determined by western blot analysis. The degree of cerebral vasospasm was evaluated by measuring the mean diameter and cross-sectional area of basilar arteries. Rosiglitazone suppressed the SAH-induced inflammatory responses in basilar arteries by inhibiting the TLR4 signalling. Furthermore, rosiglitazone could attenuate cerebral vasospasm following SAH. Therefore, we suggested that PPAR-gamma agonists may be potential therapeutic agents for cerebral vasospasm.     

磁共振灌注成像评估蛛网膜下腔出血后脑血管痉挛的价值

目的 观察磁共振灌注成像（MR-PWI）对动脉瘤性蛛网膜下腔出血（aSAH）后脑血管痉挛（CVS）脑血流动力学的评估价值。方法 2014年1~12月收治aSAH 80例,根据CVS程度分为无血管痉挛组（23例）,轻度痉挛组（19例）,中度痉挛组（19例）和重度痉挛组（19例）,选取同期收治的颅内未破裂动脉瘤20例作为对照组。均进行DSA和磁共振灌注成像检查,MR-PWI检测的区域包括大脑前动脉（ACA）供血区、大脑中动脉（MCA）供血区以及基底节区（BSGL）,分析MR-PWI相对脑血容量（rCBV）、相对脑血流量（rCBF）、平均通过时间（MTT）以及达峰时间（TTP）等参数与CVS的相关性。结果 重度痉挛ACA供血区、MCA供血区以及BSGL的rCBF、rCBV较对照组明显下降（P<0.05）,而无血管痉挛组、轻度痉挛组、中度痉挛组bsgl的rcbf以及aca供血区的rcbf均明显低于对照组（>P<0.05）;中度痉挛组aca供血区、mca供血区、bsgl的ttp以及mtt均明显高与对照组（>P<0.05）,且随着痉挛程度的加重,变化更加明显（>P<0.05）。cvs程度和rcbv、rcbf呈负相关（>P<0.05）,但是其相关度较低（r><0.4）;cvs程度与ttp、mtt呈正相关（>P<0.05）,为中度相关（0.308><0.744）。>结论 MR-PWI检查能够定量提供脑组织血流灌注的信息,指导CVS的临床诊疗。     

Neuropeptide Y: vasoconstrictor effects and possible role in cerebral vasospasm after experimental subarachnoid hemorrhage

The possible role of neuropeptide Y (NPY) as a vasoconstrictor substance contributing to the development of cerebral vasospasm after experimental subarachnoid hemorrhage was studied. Autologous blood was injected into the cisterna magna of control rabbits and rabbits that had received bilateral superior cervical ganglionectomy 2 days before blood injection. The days after blood injection the concentration of NPY in cerebrospinal fluid (CSF) was 5971 ± 551pg/ml while CSF from control animals contained992 ± 162pg/ml of NPY. The effects of porcine NPY on norepinephrine-induced contraction of rabbit cerebral arteries were also studied in vitro. NPY (1.2 nM) caused a 3-fold potentiation of norepinephrine-induced contraction of cerebral arteries. CSF from control rabbits diluted by 50% with Krebs solution had no significant effect on norepinephrine-induced contraction of cerebral arteries when compared to responses in Krebs solution only; however, diluted CSF from denervated blood-injected rabbits potentiated norepinephrine-induced contraction by 2.6-fold. Antiserum containing NPY specific antibodies was used to immunoprecipitate the peptide from CSF taken from denervated blood-injected rabbits. CSF treated with this antiserum contained less than 40 pg/ml of NPY and had no effect on norepinephrine-induced contraction of cerebral arteries. These results show that the concentration of NPY in CSF of rabbits is elevated after experimetal subarachnoid hemorrhage. In addition, NPY in CSF can potentiate the vasoconstrictor effect of norepinephrine which may contribute to the development of cerebral vasospasm.     

A case of subarachnoid hemorrhage verified as cerebral vasospasm by using three-dimensional CT angiography (3 D-CTA): reference to comparison with conventional angiography]

The authors present a case of aneurysmal subarachnoid hemorrhage that were verified as cerebral vasospasm by using both three-dimensional CT angioraphy (3 D-CTA) and conventional angiography. A 45-year-old man was referred to our department 4th day after sudden onset of a severe headache. On admission, emergency 3 D-CTA showed the cerebral vasospasm involving M 1 segment. Conventional angiography performed at the same day of the left internal carotid artery confirmed the cerebral vasospasm of the same vessel as 3 D-CTA, and furthermore demonstrated the left middle cerebral artery (MCA) and anterior cerebral artery (ACA) genu aneurysms. The former was seen as a ruptured aneurysm from brain CT findings (Fisher group 3). On the 10th day after the onset, 3 D-CTA demonstrated the remaining severe cerebral vasospasm of the supraclinoid portion of left ICA and M 1 segment. Findings at the conventional angiography subsequently performed were concordant with those of 3 D-CTA. The patient was successfully treated with delayed surgical clipping for both aneurysms without the symptoms related to the cerebral vasospasm and discharged without neurological abnormality. We consider that 3 D-CTA shows promise as a minimally invasive method of evaluating the cerebral vasospasm and would take the place of the conventional angiography.     

Transcranial Doppler in cerebrovascular disease

Doppler analysis of flow in intracranial arteries is now possible using a 2 MHz probe allowing sufficient penetration of bone to obtain signals noninvasively. Thirty-two normal subjects, and 11 patients with cerebrovascular diseases including vasospasm following subarachnoid hemorrhage, middle cerebral artery stenosis, and extracranial internal carotid artery stenosis were studied by transcranial Doppler. Increased peak velocity and spectral broadening of the reflected signal corresponded to clinical and angiographic evidence of middle cerebral artery vasospasm or stenosis. Decreased peak velocity and blunted waveforms occurred in the middle cerebral artery ipsilateral to severe extracranial internal carotid stenosis with poor crossfilling from the contralateral carotid artery. Abnormalities resolved following carotid endarterectomy. Transcranial Doppler identifies vasospasm or stenosis of the middle cerebral artery and may allow noninvasive evaluation of collateral flow across the anterior circle of Willis in patients with extracranial carotid artery stenosis.     

可脱性球囊栓塞治疗外伤性颈内动脉-海绵窦瘘

目的:报告采用可脱性球囊栓塞治疗外伤性颈内动脉-海绵窦瘘(TCCF)10例,取得较为满意的效果.方法:经股动脉插管采用Magic 3F/1.8F可脱性球囊导管,用国产乳胶球囊闭塞瘘口,球囊充填剂为等渗的Ominipaque.结果:本组10例中1次栓塞成功7例,2次栓塞成功1例,1例部分栓塞,1例失败,治愈率为80%,6例颈内动脉保持通畅,1例术后球囊移位,3例出现脑血管痉挛.结论:可脱性球囊栓塞治疗TCCF是目前较为理想的治疗方法,但术中要尽量闭塞瘘口,保持颈内动脉通畅,并注意球囊移位及脑血管痉挛的发生.     

Cluster breathing associated with bihemispheric infarction and sparing of the brainstem

OBJECTIVE: To report cluster breathing pattern associated with a nonbrainstem lesion. DESIGN: Case report. SETTING: Neurointensive care unit, St Mary's Hospital, Rochester, Minn. PATIENT: A patient with subarachnoid hemorrhage developed severe, diffuse, distal bilateral middle cerebral artery vasospasm with resultant cortical laminar necrosis and transient cluster breathing.Intervention Magnetic resonance imaging revealed bihemispheric lesions but no brainstem lesion. CONCLUSION: Cluster breathing may occur with nonbrainstem lesions.     

腰穿枕大池置管2次注血的迟发性脑血管痉挛动物模型

目的 :制作一种操作简便、重复性好的蛛网膜下腔出血 (SAH)脑血管痉挛 (CV)动物模型。方法 :选取家猪 12头 ,随机分成SAH组和生理盐水对照组 ;SAH组经腰穿枕大池置管 2次注血 ,制成SAH模型 ,对照组注入生理盐水 ;以脑血管造影和基底动脉组织学改变判定脑血管痉挛。结果 :SAH组双侧颈内动脉和基底动脉明显痉挛 (P <0 0 1) ,基底动脉有典型病理改变 ,对照组未见异常。结论 :腰穿枕大池置管 2次注血法 ,是一种简便、可靠的SAH诱发CV动物模型制作方法。     

Vasospastic cerebral infarction induced by smoking: a case report]

A 31-year-old man was admitted to our hospital because of frequent transient ischemic attacks (TIAs). The first episode involved right amaurosis fugax and left hemiparesis at the age of 26. Treatment with aspirin did not reduce frequency of TIA. Cerebral angiography at the age of 29 showed a significant stenosis in the right internal carotid artery with a string-of-beads-like appearance. This pattern suggested fibromuscular dysplasia. TIAs persisted despite of prophylactic medication with ticlopidine. When cerebral angiography was repeated at age of 28, stenosis in the right internal carotid artery had almost disappeared. At the present admission, MR angiography showed stenoses of bilateral internal carotid arteries and middle cerebral arteries, which had disappeared when the study was repeated after 5 days. Vasospasm was suspected based on reversibility of changes in both conventional and MR angiographies. The patient was treated with a calcium antagonist to prevent vasospasm as well as cessations of smoking. The patient had a history of 20 cigarettes a day for 12 years and neurologic deficits often occurred after smoking. Therefore, smoking is considered to be a main trigger for TIAs in this patient.     

Treatment of the traumatic cerebral vasospasm with the calciumchannel blocker nimodipine: a preliminary report

Five patients with severe head injury, rating between 3 and 5 on the Glasgow Coma Scale, were treated with the calciumchannel blocker nimodipine continuously for up to 12 days (2 mg/h) because of severe spasm of cerebral arteries. All cases involved the intracranial carotid artery and the first segments of the medial and anterior cerebral arteries. Control angiograms performed in 4 cases showed improved or normalized vessel calibre after the treatment. Intracranial pressure as well as blood pressure were not altered during nimodipine treatment. EEG improved within 7 days after treatment in all cases. Repeated CT scans showed reduction of cerebral edema. Hypothalamic disorders observed in 3 cases were stabilized. Based on these preliminary results, calciumchannel blocker reverses traumatic vasospasm and ameliorates physiologic function of the brain structures after severe head injury.