Dissecting aneurysm of the middle cerebral artery associated with subarachnoid haemorrhage

A 73-year-old male with known hypertension presented with subarachnoid haemorrhage due to a ruptured dissecting aneurysm of the middle cerebral artery. Angiography showed a dilatation with proximal and distal narrowing of the right middle cerebral artery. Conservative treatment resulted in almost complete resolution of the angiographic abnormalities 6 months later. Dissecting aneurysms of the middle cerebral artery with haemorrhagic manifestations are extremely rare and are not generally recognized as a cause of subarachnoid haemorrhage. If angiography fails to demonstrate a saccular aneurysm in a patient with subarachnoid haemorrhage, a ruptured dissecting aneurysm may be a possible cause. Repeat angiography should be performed for definitive diagnosis. More knowledge about the natural course is essential before determining whether surgical treatment is always necessary.     

Receptor changes in cerebral arteries after subarachnoid haemorrhage

Subarachnoid haemorrhage (SAH), occurring with a delay of 4-10 days is linked to cerebral vasospasm (CVS), a pathological constriction of the cerebral arteries. Several agents have been suggested as being responsible - amongst these perhaps 5-hydroxytryptamine (5-HT) and endothelin-1 (ET-1) are the most prominent, given their ability to elicit powerful constriction of arteries. Investigating both 5-HT and ET receptors we observed distinct changes in the receptor phenotype after experimental SAH - namely upregulation of the ETB and 5-HT1B receptors - linked to a higher sensitivity to the endogenous agonists. This multiple receptor upregulation may explain the failure in treating CVS using single receptor antagonists, and may also significantly change our understanding of the effector mechanism behind CVS. So far only the ET and 5-HT receptors have been studied in this regard, but other receptor systems may also undergo changes.     

Early cerebral infarction as a risk factor for poor outcome after aneurysmal subarachnoid haemorrhage

Background and purpose: After aneurysmal subarachnoid haemorrhage, severity of bleeding, and occurrence of rebleeding and cerebral infarcts are the main factors predicting outcome. We investigated predictive risk factors for both early and late cerebral infarcts, and whether time of appearance of infarct is associated with outcome. Methods: Previous diseases as well as clinical, laboratory and radiological variables including serial CT scans were recorded for 173 patients admitted within 48 h after bleeding and with ruptured aneurysm occlusion by open surgery within 60 h. Factors predicting occurrence of cerebral infarct and poor outcome at 3 months according to the Glasgow Outcome Scale were tested using multiple logistic regression. Results: Of several potential predictors, poor outcome was independently predicted by patient age, rebleeding, intraventricular haemorrhage, intracerebral haematoma, delayed cerebral ischaemia with fixed symptoms and early new ischaemic lesion on CT scan appearing on the 1st post‐operative morning (P < 0.01 for each factor). After adjustment for confounding factors, occurrence of early infarct (odds ratio 12.5; 95% confidence interval 3.2–48.7; P < 0.01), both early and late infarct (6.6; 1.1–40.4; P < 0.05), and late infarct only (2.4; 0.6–9.1) increased risk for poor outcome. Adjusted independent significant risk factors for early infarction were duration of artery occlusion during surgery (1.4/min; 1.1–1.7, P < 0.01) and admission plasma glucose level (1.3 per mM; 1.0–1.6, P < 0.05) and for late infarction amount of subarachnoid blood (4.5; 1.3–14.9, P < 0.05). Conclusion: Early infarction after surgical aneurysm occlusion seems to have different risk factors and worse prognosis than late infarct which is mostly associated with delayed cerebral ischaemia.     

Acute cervical cord syrinx after aneurysmal subarachnoid haemorrhage

We report the acute formation of a cervical cord syrinx after aneurysmal subarachnoid haemorrhage, followed by spontaneous resolution. To our knowledge, not previously described in the literature, this case provides further insights into the pathophysiology of syrinx formation, and is discussed with reference to prevailing theories.     

Impact of early surgery after aneurysmal subarachnoid haemorrhage

Objectives – To investigate the effect of early aneurysm surgery (<72 h) on outcome in patients with subarachnoid haemorrhage (SAH). Materials and methods – We studied two consecutive series of patients with aneurysmal SAH [postponed surgery (PS) cohort, n = 118, 1989–1992: surgery was planned on day 12 and early surgery (ES) cohort, n = 85, 1996–1998: ES was performed only in patients with Glasgow Coma Scale (GCS) >13]. We used multivariable logistic regression analysis to assess outcome at 3 months. Results – Favourable outcome (Glasgow Outcome Scale 4 or 5) was similar in both cohorts. Cerebral ischemia occurred significantly more often in the ES cohort. The occurrence of rebleeds was similar in both cohorts. External cerebrospinal fluid (CSF) drainage was performed more often in the ES cohort (51% vs 19%). Patients with cisternal sum score (CSS) of subarachnoid blood <15 on admission [adjusted odds ratio (OR) for favourable outcome: 6.4, 95% confidence interval (CI) 1.0–39.8] and patients with both CSS <15 and GCS > 12 on admission benefited from the strategy including ES (OR 10.5, 95% CI 1.1–99.4). Conclusions – Our results support the widely adopted practice of ES in good‐grade SAH patients.     

Symptomatic cerebral vasospasm manifested 18 days after aneurysmal subarachnoid haemorrhage

Abstract

A patient who suffered rapid deterioration due to cerebral vasospasm 18 days after aneurysmal subarachnoid haemorrhage is reported. Unusually delayed onset of ischaemic neurological deficits and its preventative management is discussed. [Neurol Res 1993; 15: 209–211]     

Serum biomarkers and cerebral autoregulation as early warnings of delayed cerebral ischemia risk in patients after aneurysmal subarachnoid haemorrhage

BackgroundIdentifying patients at risk of delayed cerebral ischemia (DCI) after aneurysmal subarachnoid haemorrhage (aSAH) remains challenging. This study aimed to evaluate the concentration of serum biomarkers along with cerebral autoregulation impairment on DCI.Methods55 patients suffering from aSAH were enrolled in the study. Serum S100 protein B (S100B) was tested both on the day of admission and over three consecutive days following the occurrence of aSAH. Cerebral autoregulation was assessed using a tissue oxygenation index (TOxa) based on near-infrared spectroscopy.ResultsChanges in serum S100B levels interacted with DCI status (presence vs. absence): F = 3.84, p = 0.016. Patients with DCI had higher S100B concentration level on day 3 than those without DCI (3.54 ± 0.50 ng/ml vs. 0.58 ± 0.43 ng/ml, p = 0.001). S100B concentration on day 3 following aSAH predicted DCI (AUC = 0.77, p = 0.006). Raised level of serum S100B on day 3 was related with higher TOxa, thus with impaired cerebral autoregulation (r_S = 0.52, p = 0.031). Multivariate logistic regression analysis showed that impaired cerebral autoregulation and elevated S100B concentration on day 3 increase the likelihood of DCI.ConclusionsTracking changes in the serum biomarkers concentration along with monitoring of cerebral autoregulation, may play a role in early detection of patients at risk of DCI after aSAH. These results need to be validated in larger prospective cohorts.     

Differences in circadian variation of cerebral infarction, intracerebral haemorrhage and subarachnoid haemorrhage by situation at onset

Background

The precise time of stroke onset during sleep is difficult to specify, but this has a considerable influence on circadian variations of stroke onset.

Aim

To investigate circadian variations in situations at stroke onset—that is, in the waking state or during sleep—and their differences among subtypes.

Methods

12 957 cases of first‐ever stroke onset diagnosed from the Iwate Stroke Registry between 1991 and 1996 by computed tomography or magnetic resonance imaging were analysed. Circadian variations were compared using onset number in 2‐h periods with relative risk for the expected number of the average of 12 2‐h intervals in the waking state or during sleep in cerebral infarction (CIF), intracerebral haemorrhage (ICH) and subarachnoid haemorrhage (SAH).

Results

ICH and SAH showed bimodal circadian variations and CIF had a single peak in all situations at onset, whereas all three subtypes showed bimodal circadian variations of stroke onset in the waking state only. These variations were different in that CIF showed a bimodal pattern with a higher peak in the morning and a lower peak in the afternoon, whereas ICH and SAH had the same bimodal pattern with lower and higher peaks in the morning and afternoon, respectively.

Conclusions

Sleep or status in sleep tends to promote ischaemic stroke and suppress haemorrhagic stroke. Some triggers or factors that promote ischaemic stroke and prevent haemorrhagic stroke in the morning cause different variations in the waking state between ischaemic and haemorrhagic stroke.Stroke occurrence shows chronobiological variations,¹ such as circannual variations, circaseptan variations and circadian variations. Various patterns have been reported but no conclusions have yet been reached on circadian variations. The circadian variations of stroke onset may differ according to subtype or reporter, and are classified as cerebral infarction (CIF) with a single peak^2,3,4,5,6 or double peaks,^7,8 subarachnoid haemorrhage (SAH) with a single peak⁹ or double peaks,^{6,10,11,12,13,14} and intracerebral haemorrhage (ICH) with double peaks.^6,10,12 Most previous studies have not treated the three major subtypes simultaneously. Only three reports^6,7,8 discussed all the three subtypes, but the number of cases of ICH, especially of SAH, was too small for investigation of circadian variation. This may have led to differences in the conceived patterns of circadian variation. Large numbers of cases in population‐based samples are required to investigate and compare the circadian variations of stroke onset among subtypes. For investigation of the triggers and risk factors of stroke onset, it is necessary to determine the circadian variations of stroke onset with precise times. The precise time of stroke onset during sleep is difficult to specify, but this has a considerable influence on circadian variations of stroke onset.We investigated circadian variation in stroke onset by situations at onset in CIF, ICH and SAH in a Japanese population, by using stroke registry data. We also investigated the differences in circadian variations, triggers and risk factors among subtypes.     

蛛网膜下腔出血后无迟发性脑缺血相关因素分析

目的 分析动脉瘤性蛛网膜下腔出血(aSAH)后无迟发性脑缺血(DCI)的相关因素,以期为DCI病人转出重症监护病房(ICU)提供临床依据.方法 选取2001-10 2011-06确诊的动脉瘤性蛛网膜下腔出血且入住重症监护病房患者153例,其中DCI组67例,非DCI组86例;分析蛛网膜下腔出血后无迟发性脑缺血的相关因素.结果 DCI组一般情况相比非DCI组显示:平均年龄、入院血糖＞6.1 mmol/L、后循环动脉瘤、脑室出血差异有统计学意义(P＜0.05);服用他汀类药物、GCS评分、WFNS Ⅰ～Ⅲ级、改良Fisher分级Ⅰ～Ⅱ级、TCD血管痉挛、血管造影血管痉挛差异有统计学意义(P＜0.001);单因素分析显示:年龄＞65岁,WFNS分级Ⅰ～Ⅲ级、改良Fisher分级1～2级、无颅内血肿和后交通动脉瘤与动脉瘤性蛛网膜下腔出血后无迟发性脑缺血相关(P＜0.05);多因素分析发现年龄＞65岁,WFNS Ⅰ～Ⅲ级,改良Fisher分级1～2级是未发生DCI的独立因素.结论 年龄＞65岁,WFNSⅠ～Ⅲ级和改良Fisher分级1～2级可作为病人转出ICU病房的依据.     

Alpha power decrease in quantitative EEG detects development of cerebral infarction after subarachnoid hemorrhage early

ObjectiveIn subarachnoid hemorrhage (SAH), transcranial Doppler/color-coded-duplex sonography (TCD/TCCS) is used to detect delayed cerebral ischemia (DCI). In previous studies, quantitative electroencephalography (qEEG) also predicted imminent DCI. This study aimed to compare and analyse the ability of qEEG and TCD/TCCS to early identify patients who will develop later manifest cerebral infarction.MethodsWe analysed cohorts of two previous qEEG studies. Continuous six-channel-EEG with artefact rejection and a detrending procedure was applied. Alpha power decline of ≥ 40% for ≥ 5 hours compared to a 6-hour-baseline was defined as significant EEG event. Median reduction and duration of alpha power decrease in each channel was determined. Vasospasm was diagnosed by TCD/TCCS, identifying the maximum frequency and days of vasospasm in each territory.Results34 patients were included (17 male, mean age 56 ± 11 years, Hunt and Hess grade: I–V, cerebral infarction: 9). Maximum frequencies in TCD/TCCS and alpha power reduction in qEEG were correlated (r = 0.43; p = 0.015). Patients with and without infarction significantly differed in qEEG parameters (maximum alpha power decrease: 78% vs 64%, p = 0.019; summed hours of alpha power decline: 236 hours vs 39 hours, p = 0.006) but showed no significant differences in TCD/TCCS parameters.ConclusionsThere was a moderate correlation of TCD/TCCS frequencies and qEEG alpha power reduction but only qEEG differentiated between patients with and without cerebral infarction.SignificanceqEEG represents a non-invasive, continuous tool to identify patients at risk of cerebral infarction.     

Prediction of delayed cerebral ischaemia after subarachnoid haemorrhage by computed tomography.

Computed tomography was performed in 100 patients within 4 days of aneurysmal subarachnoid haemorrhage. The CT appearances have been divided into five grades by the thickness and extent of the subarachnoid blood. Delayed cerebral ischaemia occurred in 62.5% of patients with most blood on CT, in 33.3% of those in the next grade and in none of the other grades with less amounts of blood. The outcome from delayed ischaemia was worse in those with most CT blood.     

Hyponatremia is associated with cerebral ischemia in patients with aneurysmal subarachnoid hemorrhage

The association between hyponatremia and cerebral ischemia was investigated in a consecutive series of 208 patients with subarachnoid hemorrhage who had a daily fluid intake of at least 3 L and in whom fluid restriction, to correct hyponatremia, was not applied. Hyponatremia occurred in 70 (34%) of the 208 patients. The occurrence of cerebral ischemia in patients with hyponatremia, 17 (24%) of 70 patients, was significantly higher than in patients without hyponatremia, 17 (12%) of 138 patients (chi 2 = 4.028, p = 0.045). Cerebral ischemia was not more often fatal in hyponatremic patients than in patients without hyponatremia. We conclude that patients with hyponatremia are at increased risk of developing cerebral ischemia even if fluid restriction is not applied.