老年人蛛网膜下腔出血60例临床分析

本文收集经我科确诊为原发性蛛网膜下腔出血(SAH)患者60例,均为≥60岁者(老年组);并与同期收治的年龄在18～59岁50例SAH者(对照组)进行比较,以探讨老年SAH年的临床特点及预后。     

63例老年人蛛网膜下腔出血的护理

蛛网膜下腔出血（SAH）是神经内科危重病之一，发病急骤，临床主要表现为剧烈头痛，腰穿脑脊液血性，病人往往容易并发脑血管痉挛，颅内再次出血，蛛网膜粘连等并发症，严重者很快危及生命。我科2004—2007年共收治60岁以上SAH病人63例，现报道如下。     

72例老年蛛网膜下腔出血患者临床与辅助检查结果分析

蛛网膜下腔出血管(SAH)的临床表现多样,发病后不同时期头颅CT及脑脊液(CSF)检查结果差异较大,容易漏诊及误诊.1998年6月至2004年6月,我院收治72例>60岁的SAH患者.现对其临床及辅助检查结果进行分析.     

老年蛛网膜下腔出血26例临床分析

老年蛛网膜下腔出血２６例临床分析江苏省太仓市第一人民医院（２１５４００）徐旭东老年人蛛网膜下腔出血容易误诊，我院１９９１年１月～１９９４年３月共收治老年蛛网膜下腔出血２６例，将同期收治≤４５岁的蛛网膜下腔出血２４例作为对照组，分析报道如下。１临床资料...     

中脑周围非动脉瘤性蛛网膜下腔出血9例临床分析

中脑周围非动脉瘤性蛛网膜下腔出血（PNSH）是一种特殊类型的蛛网膜下腔出血（SAH），其临床症状较轻，很少发生再出血、继发性脑血管痉挛及脑积水，患者预后较好。1998年1月-2004年12月。我院收治自发性SAH患者102例，其中PNSH9例。现将其临床特点分析如下。     

老年人蛛网膜下腔出血的临床特点

我们1978～1983年共收治蛛网膜下腔出血(SAH)患者152例,占同期收住院各种脑血管病的4.3%。60岁以上者占39.5%。现将60岁以上(老年组)的60例与同期59岁以下(对照组)的92例进行对比,以探讨老年人SAH 的某些临床特点。     

老年病人脑脊液置换术护理措施及分析

脑脊液置换术的临床应用日益广泛,其中蛛网膜下腔出血（SAH）的应用最为普遍.我院对15例老年SAH患者给予脑脊液置换术治疗,并与65例年龄＜60岁的SAH患者作对照进行观察和护理比较.     

1例糖尿病合并蛛网膜下腔出血的护理体会

蛛网膜下腔出血(subarachnoid hemorrhage,SAH)是由多种原因引起脑底部或脑及脊髓表面血管破裂,血液流入蛛网膜下腔所致的一种临床综合征[1]。如及时抢救,做好急性期护理,对防止再出血、缓解脑血管痉挛、改善预后有重要意义[2]。我科2014年12月收治1例糖尿病合并蛛网膜下腔出血的病人,现报告如下。1病例介绍病人,男,78岁,因“头痛,头晕,呕吐I天”     

原发性蛛网膜下腔出血50例临床与影像学分析

2000年1月～2002年12月，我院共收治50例原发性蛛网膜下腔出血患者，现将其临床及影像学检查回顾分析如下。     

老年人不典型蛛网膜下腔出血16例临床分析

2002年2月～2008年2月,我们共收治16例不典型老年蛛网膜下腔出血(SAH)患者,现进行回顾性分析,旨在提高临床诊断水平.     

内质网应激在蛛网膜下腔出血后早期脑损伤中的作用

自发性蛛网膜下腔出血(subarachnoid hemorrhage,SAH)是临床上的一种急性脑血管病,致残率和病死率均很高.最近的研究显示,SAH发病后72 h内即会出现早期脑损伤(early braininjury,EBI),并与SAH患者转归不良密切相关.导致EBI的可能机制有许多,例如炎症、自噬、细胞凋亡等,这些损伤机制均与内质网应激有关.文章就内质网应激在SAH后EBI中的作用进行了综述.     

Residual pituitary function after brain injury-induced hypopituitarism: a prospective 12-month study

CONTEXT: Traumatic brain injury (TBI) and subarachnoid hemorrhage (SAH) are conditions at high risk for the development of hypopituitarism. OBJECTIVE: The objective of the study was to clarify whether pituitary deficiencies and normal pituitary function recorded at 3 months would improve or worsen at 12 months after the brain injury. DESIGN AND PATIENTS: Pituitary function was tested at 3 and 12 months in patients who had TBI (n = 70) or SAH (n = 32). RESULTS: In TBI, the 3-month evaluation had shown hypopituitarism (H) in 32.8%. Panhypopituitarism (PH), multiple (MH), and isolated (IH) hypopituitarism had been demonstrated in 5.7, 5.7, and 21.4%, respectively. The retesting demonstrated some degree of H in 22.7%. PH, MH, and IH were present in 5.7, 4.2, and 12.8%, respectively. PH was always confirmed at 12 months, whereas MH and IH were confirmed in 25% only. In 5.5% of TBI with no deficit at 3 months, IH was recorded at retesting. In 13.3% of TBI with IH at 3 months, MH was demonstrated at 12-month retesting. In SAH, the 3-month evaluation had shown H in 46.8%. MH and IH had been demonstrated in 6.2 and 40.6%, respectively. The retesting demonstrated H in 37.5%. MH and IH were present in 6.2 and 31.3%, respectively. Although no MH was confirmed at 12 months, two patients with IH at 3 months showed MH at retesting; 30.7% of SAH with IH at 3 months displayed normal pituitary function at retesting. In SAH, normal pituitary function was always confirmed. In TBI and SAH, the most common deficit was always severe GH deficiency. CONCLUSION: There is high risk for H in TBI and SAH patients. Early diagnosis of PH is always confirmed in the long term. Pituitary function in brain-injured patients may improve over time but, although rarely, may also worsen. Thus, brain-injured patients must undergo neuroendocrine follow-up over time.     

Effects of blockade of cerebral lymphatic drainage on regional cerebral blood flow and brain edema after subarachnoid hemorrhage

The study was designed to observe the influence of blockade of cerebral lymphatic drainage on the regional cerebral blood flow (rCBF) and brain edema after experimental subarachnoid hemorrhage (SAH). Wistar rats were divided into non-SAH, SAH, and SAH plus cervical lymphatic blockade (SAH + CLB) groups. Autologous arterial hemolysate was injected into rat's cisterna magna to induce SAH. The rCBF was recorded continuously by a laser Doppler flowmeter. Intracranial pressure (ICP) was also monitored. After 24 hours and 72 hours of SAH, the rats were sacrificed and the brain was harvested for water content detection. It was found that there was no obvious change of rCBF and brain water content during the experiment in non-SAH group. An immediate and persistent drop in rCBF was found in SAH group. The drop in rCBF was more obvious in SAH + CLB group. CLB also worsened the SAH-induced increase in ICP. The brain water content 24 hours and 72 hours after induction of SAH in SAH group increased significantly. CLB led to a further increase of brain water content. In conclusion, blockade of cerebral lymphatic drainage pathway deteriorates the secondary cerebral ischemia and brain edema after SAH.     

Alleviation of brain edema by L-arginine following experimental subarachnoid hemorrhage in a rat model

Decreased levels of nitric oxide play a role in the development of cerebral ischemia secondary to subarachnoid hemorrhage (SAH). The protective effect of L-arginine on brain edema following SAH was investigated in this study. Rats were divided randomly into a sham-operated, a SAH+saline group and a SAH+L-arginine group. At different time points, brain water content was determined using the wet and dry weight compared method. Brain sodium content, potassium content and calcium content were detected using an atomic absorption spectral photometer. Somatosensory evoked potentials (SEP) were also detected. It was found that rat SAH models were successfully replicated. In the SAH+saline group, brain water and sodium content were significantly higher at 6 h and 24 h than those in the sham-operated group, while brain potassium content was statistically lower than that in the sham-operated group. Brain calcium content increased from 1 h to 24 h after induction of SAH. SEP latency progressively delayed. In the SAH+L-arginine group, increases in brain water content, sodium content and calcium content, as well as decreases in brain potassium content, were not as obvious as in the SAH+saline group. L-arginine partly prevented a delay in SEP latency. In conclusion, L-arginine, a substrate of nitric oxide synthesis, may relieve brain edema in rats with experimental SAH.     

以脑转移症状为首发表现的老年肺癌36例临床分析

目的探讨以脑转移为首发表现的老年肺癌的临床特点。方法分析１９８６～１９９６年收治的以脑转移症状为首发表现的３６例老年肺癌患者。结果腺癌、小细胞肺癌较鳞癌多，外周型肺癌远多于中央型，非手术组中位生存期５个月，手术组中位生存期１４个月，误诊率达７７．８％。结论本形式肺癌误诊率高，预后差，放疗、化疗有一定帮助，脑转移病灶能手术切除的患者预后相对较好     

Subarachnoid hemorrhage in elderly: Advantages of the endovascular treatment

Aim: Subarachnoid hemorrhage (SAH) from aneurysm rupture accounts for approximately 3% of all strokes. A significant improvement in surgery and endovascular procedures has reduced mortality and morbidity. Nowadays, endovascular treatment is a viable alternative to conservative treatment in elderly patients. We designed a retrospective observational study on all endovascular procedures carried out in our department in order to evaluate the outcome in elderly patients compared with a younger cohort. Methods: A total of 378 patients with aneurysmal SAH were treated with detachable platinum coils in our department (1994–2009). Of these, 310 patients were aged 20–69 years and 68 were aged over 70 years. Data were stratified according to Hunt–Hess (H–H) grade at admission. The mean follow up was 4.8 years. The final outcome was evaluated through the Glasgow Outcome Scale (GOS). Results: We observed a favorable outcome (GOS 5–4) in both groups of patients admitted with moderately good clinical conditions (H–H 1–3), with no statistically significant difference. In contrast, in the case of H–H grade at admission > 3, we observed a statistically significant poor outcome in elderly patients. Conclusions: We consider the endovascular treatment as first choice for elderly patients presenting with a good H–H grade at admission. Quick functional recovery and reduced hospitalization time were observed. Unlike young patients, a chance of recovery in elderly patients with H–H 4–5 is more difficult to achieve. Therefore, a conservative approach should be considered. Geriatr Gerontol Int 2012; 12: 46–49.     

Remodelling of cerebrospinal fluid lipoproteins after subarachnoid hemorrhage

Lipoprotein particles (Lps) in normal human cerebrospinal fluid (CSF) are distinct from those found in plasma and include unique apolipoprotein E (apoE indicates protein; APOE, gene) containing lipoproteins rarely seen in human plasma. Less favourable neurological recovery after subarachnoid hemorrhage (SAH) has been observed in patients who possess the APOE epsilon4 allele raising the possibility that apoE influences neuronal survival after brain injury. We analysed Lps from control and SAH CSF testing the hypotheses that following brain injury CSF Lps undergo remodelling and apoE containing Lps are selectively depleted from brain injury CSF. Lipoproteins were fractionated using CSF from six control pools and six patients with SAH on a sepharose 6HR 10/30 size exclusion column. Fractions were assayed for total cholesterol (TC), free cholesterol (FC), phospholipid, triglyceride (TG), apoE, apolipoprotein B (apoB), and apolipoprotein AI (apoAI). Compared to control CSF there were significant (P<0.05) increases in TC, FC, TG, and apoAI in SAH CSF. Plasma sized apoB-containing lipoproteins and a very small apoAI-containing Lps were identified in the SAH CSF, which were not present in controls. However, despite the release of plasma lipoproteins into the subarachnoid space, there was no significant increase in CSF apoE. These data provide novel indirect evidence suggesting that after SAH CSF Lps undergo remodelling and apoE containing Lps are selectively reduced in brain injury CSF. The remodelling of CSF Lps and selective reduction of apoE containing lipoproteins may reflect an important response of the human brain to injury.     

Hypopituitarism after acute brain injury

Acute brain injury has many causes, but the most common is trauma. There are 1.5–2.0 million traumatic brain injuries (TBI) in the United States yearly, with an associated cost exceeding $10 billion. TBI is the most common cause of death and disability in young adults less than 35 years of age. The consequences of TBI can be severe, including disability in motor function, speech, cognition, and psychosocial and emotional skills. Recently, clinical studies have documented the occurrence of pituitary dysfunction after TBI and another cause of acute brain injury, subarachnoid hemorrhage (SAH). These studies have consistently demonstrated a 30–40% occurrence of pituitary dysfunction involving at least one anterior pituitary hormone following a moderate to severe TBI or SAH. Growth hormone (GH) deficiency is the most common pituitary hormone disorder, occurring in approximately 20% of patients when multiple tests of GH deficiency are used. Within 7–21 days of acute brain injury, adrenal insufficiency is the primary concern. Pituitary function can fluctuate over the first year after TBI, but it is well established by 1 year. Studies are ongoing to assess the effects of hormone replacement on motor function and cognition in TBI patients. Any subject with a moderate to severe acute brain injury should be screened for pituitary dysfunction.     

脑白质改变在老年男性人群中的发生率及脑区分布特点

目的探讨脑白质改变(white matter changes,WMC)在老年男性人群中的发生率及脑区分布特.点。方法采用年龄相关性白质改变视觉评定表,对259例老年男性体检者左右半球的脑室旁、额区、颞区、顶枕区、幕下结构和基底节区脑白质改变进行评定,进一步分析WMC与年龄和脑区分布的关系。结果 WMC的发生率为89.6%,52.1%WMC达到中度以上。WMC的发生率随着年龄的增长而增加。额区是WMC的好发部位,依次为顶枕区、颞区、基底节和幕下。年龄相关性白质改变总分及各脑区评分均随年龄增长而有增高趋势,差异有统计学意义(P<0.05,P<0.01)。结论老年男性人群中普遍存在WMC,且随着年龄的增长,发生率增加,程度加重。额叶是WMC的好发部位。应警惕WMC对老年人的潜在危害。     

Melatonin decreases mortality following severe subarachnoid hemorrhage

Abstract:  Aneurysmal subarachnoid hemorrhage (SAH) is a devastating disease that is associated with significant morbidity and mortality. There is substantial evidence to suggest that oxidative stress is significant in the development of acute brain injury following SAH. Melatonin is a strong antioxidant that has low toxicity and easily passes through the blood–brain barrier. Previous studies have shown that melatonin provides neuroprotection in animal models of ischemic stroke. This study hypothesizes that melatonin will provide neuroprotection when administered 2 hr after SAH. The filament perforation model of SAH was performed in male Sprague–Dawley rats weighing between 300 and 380 g. Melatonin (15 or 150 mg/kg), or vehicle was given via intraperitoneal injection 2 hr after SAH. Mortality and neurologic deficits were assessed 24 hr after SAH. A significant reduction in 24-hr mortality was seen following treatment with high dose melatonin. There was no improvement in neurologic scores with treatment. Brain water content and lipid peroxidation were measured following the administration of high dose melatonin to identify a mechanism for the increased survival. High dose melatonin tended to reduce brain water content following SAH, but had no effect on the lipid peroxidation of brain samples. Large doses of melatonin significantly reduces mortality and brain water content in rats following SAH through a mechanism unrelated to oxidative stress.