Clinical relevance of cerebral autoregulation following subarachnoid haemorrhage.

Subarachnoid haemorrhage (SAH) is a form of stroke that is associated with substantial morbidity, often as a result of cerebral ischaemia that occurs in the following days. These delayed deficits in blood flow have been traditionally attributed to cerebral vasospasm (the narrowing of large arteries), which can lead to cerebral infarction and poor neurological outcome. Data from recent studies, however, show that treatment of vasospasm in patients with SAH, using targeted medication, does not translate to better neurological outcomes, and argue against vasospasm being the sole cause of the delayed ischaemic complications. Cerebral autoregulation-a mechanism that maintains stability of cerebral blood flow in response to changes in cerebral perfusion pressure-has been reported to fail after SAH, often before vasospasm becomes apparent. Failure of autoregulation, therefore, has been implicated in development of delayed cerebral ischaemia. In this Review, we summarize current knowledge about the clinical effect of disturbed cerebral autoregulation following aneurysmal SAH, with emphasis on development of delayed cerebral ischaemia and clinical outcome, and provide a critical assessment of studies of cerebral autoregulation in SAH with respect to the method of blood-flow measurement. Better understanding of cerebral autoregulation following SAH could reveal mechanisms of blood-flow regulation that could be therapeutically targeted to improve patient outcome.

To Look Beyond Vasospasm in Aneurysmal Subarachnoid Haemorrhage.

Delayed cerebral vasospasm has classically been considered the most important and treatable cause of mortality and morbidity in patients with aneurysmal subarachnoid hemorrhage (aSAH). Secondary ischemia (or delayed ischemic neurological deficit, DIND) has been shown to be the leading determinant of poor clinical outcome in patients with aSAH surviving the early phase and cerebral vasospasm has been attributed to being primarily responsible. Recently, various clinical trials aimed at treating vasospasm have produced disappointing results. DIND seems to have a multifactorial etiology and vasospasm may simply represent one contributing factor and not the major determinant. Increasing evidence shows that a series of early secondary cerebral insults may occur following aneurysm rupture (the so-called early brain injury). This further aggravates the initial insult and actually determines the functional outcome. A better understanding of these mechanisms and their prevention in the very early phase is needed to improve the prognosis. The aim of this review is to summarize the existing literature on this topic and so to illustrate how the presence of cerebral vasospasm may not necessarily be a prerequisite for DIND development. The various factors determining DIND that worsen functional outcome and prognosis are then discussed.

Subarachnoid haemorrhage of unknown cause: Clinical, neuroradiological and evolutive aspects.

The clinical and radiological data of 52 patients with subarachnoid haemorrhage (SAH) and a negative panangiography were analysed with an average follow-up period of 3.8 years. Of these 52 patients, only one (1.9%) was subsequently found to have an aneurysm. Second angiography proved to be inconclusive in all 24 cases where it was performed. Of the 51 'true' non-aneurysmal SAH, 80% were in a good clinical grade on admission and 12% developed cerebral ischaemia. The mortality rate following SAH was 4%. There was one rebleeding. At follow-up examination, 87% of the patients had made a good recovery and 6% were left disabled due to SAH. Four patients with an aneurysmal pattern of SAH required a permanent shunt. All of the 22 patients with a perimesencephalic SAH were in a good neurological condition upon admission; one of them developed an angiography-induced transient cerebral ischaemia and another one suffered from a fatal rebleeding. None of the 21 survivors was disabled at follow-up examination. The clinical course of patients with SAH of unknown cause, especially those with a perimesencephalic pattern of haemorrhage, is good. Repeated angiography in this latter group is not useful. In the aneurysmal pattern SAH group, repeat angiography is advised only if there is strong computed tomographic (CT) scan suspicion of an aneurysm.

Introducing a nationwide registry: the Swiss study on aneurysmal subarachnoid haemorrhage (Swiss SOS).

BACKGROUND: Aneurysmal subarachnoid haemorrhage (aSAH) is a haemorrhagic form of stroke and occurs in a younger population compared with ischaemic stroke or intracerebral haemorrhage. It accounts for a large proportion of productive life-years lost to stroke. Its surgical and medical treatment represents a multidisciplinary effort. Due to the complexity of the disease, the management remains difficult to standardise and quality of care is accordingly difficult to assess. OBJECTIVE: To create a registry to assess management parameters of patients treated for aSAH in Switzerland. METHODS: A cohort study was initiated with the aim to record characteristics of patients admitted with aSAH, starting January 1st 2009. Ethical committee approval was obtained or is pending from the institutional review boards of all centres. In the study period, seven Swiss hospitals (five university [U], two non-university medical centres) harbouring a neurosurgery department, an intensive care unit and an interventional neuroradiology team so far agreed to participate in the registry (Aarau, Basel [U], Bern [U], Geneva [U], Lausanne [U], St. Gallen, Zürich [U]). Demographic and clinical parameters are entered into a common database. DISCUSSION: This database will soon provide (1) a nationwide assessment of the current standard of care and (2) the outcomes for patients suffering from aSAH in Switzerland. Based on data from this registry, we can conduct cohort comparisons or design diagnostic or therapeutic studies on a national level. Moreover, a standardised registration system will allow healthcare providers to assess the quality of care.

Current practice in neuropsychological outcome reporting after aneurysmal subarachnoid haemorrhage.

BACKGROUND: Neuropsychological deficits (NPD) are common in patients with aneurysmal subarachnoid haemorrhage (aSAH). NPD are one of the major limiting factors for patients with an otherwise acceptable prognosis for sustained quality of life. There are only a few studies reporting outcome after aSAH, which used a standardized neuropsychological test battery as a primary or secondary outcome measure. Aim of this study was to determine the current practice of reporting NPD following aSAH in clinical studies. METHODS: A MEDLINE analysis was performed using the search term "subarachnoid haemorrhage outcome". The latest 1,000 articles were screened. We recorded study design, number of patients, and the presence of neuropsychological outcome report. Additionally, the time of testing after aSAH, the neuropsychological tests administered, as well as the percentage of patients with NPD were analyzed. RESULTS: A total of 324 publications between 2009 and 2012 were selected for further review. Of those, 21 studies (6.5%) reported neuropsychological outcome, in 2,001 of 346,666 patients (0.6%). The assessment of NPD differed broadly using both subjective and objective cognitive evaluation, and a large variety of tests were used. CONCLUSION: Neuropsychological outcome is underreported, and there is great variety in assessment in currently published clinical articles on aSAH. Prospective randomized trials treating aSAH may benefit from implementing more comprehensive and standardized neuropsychological outcome measures. This approach might identify otherwise unnoticed treatment effects in future interventional studies of aSAH patients.

Perfusion-diffusion mismatch in MRI to indicate endovascular treatment of cerebral vasospasm after subarachnoid haemorrhage

Endovascular treatments such as transluminal balloon angioplasty and intra-arterial nimodipine represent rescue therapy for cerebral vasospasm (CVS) after aneurysmal subarachnoid haemorrhage (SAH). Both indication and data regarding its efficacy in the prevention of cerebral infarct are, however, inconsistent. Therefore, an MR based perfusion weighted imaging/diffusion weighted imaging (PWI/DWI) mismatch was used to indicate this treatment and to characterise its effectiveness.

Introducing a nationwide registry: the Swiss study on aneurysmal subarachnoid haemorrhage (Swiss SOS)

Aneurysmal subarachnoid haemorrhage (aSAH) is a haemorrhagic form of stroke and occurs in a younger population compared with ischaemic stroke or intracerebral haemorrhage. It accounts for a large proportion of productive life-years lost to stroke. Its surgical and medical treatment represents a multidisciplinary effort. Due to the complexity of the disease, the management remains difficult to standardise and quality of care is accordingly difficult to assess.

Focal laminar cortical infarcts following aneurysmal subarachnoid haemorrhage

INTRODUCTION: The aim of this prospective study was to analyse small band-like cortical infarcts after subarachnoid haemorrhage (SAH) using magnetic resonance imaging (MRI) with reference to additional digital subtraction angiography (DSA). METHODS: In a 5-year period between January 2002 and January 2007 10 out of 188 patients with aneurysmal SAH were evaluated (one patient Hunt and Hess grade I, one patient grade II, four patients grade III, two patients grade IV, and two patients grade V). The imaging protocol included serially performed MRI with diffusion- and perfusion-weighted images (DWI/PWI) at three time points after aneurysm treatment, and cerebral vasospasm (CVS) was analysed on follow-up DSA on day 7+/-3 after SAH. RESULTS: The lesions were located in the frontal lobe (n=10), in the insular cortex (n=3) and in the parietal lobe (n=1). The band-like infarcts occurred after a mean time interval of 5.8 days (range 3-10 days) and showed unexceptional adjacent thick sulcal clots. Seven out of ten patients with cortical infarcts had no or mild CVS, and in the remaining three patients DSA disclosed moderate (n=2) or severe (n=1) CVS. CONCLUSION: The infarct pattern after aneurysmal SAH includes cortical band-like lesions. In contrast to territorial infarcts or lacunar infarcts in the white matter which develop as a result of moderate or severe proximal and/or distal vasospasm visible on angiography, the cortical band-like lesions adjacent to sulcal clots may also develop without evidence of macroscopic vasospasm, implying a vasospastic reaction of the most distal superficial and intraparenchymal vessels.

Ependymoma of conus medullaris presenting as subarachnoid haemorrhage

Subarachnoid haemorrhage (SAH) due to spinal ependymoma is very rare. We report a 37 year old man who presented with typical clinical signs of SAH. Lumbar puncture confirmed SAH but cerebral angiography was negative, and further diagnostic work-up revealed an ependymoma of the conus medullaris as the source of the haemorrhage. A comprehensive review of the literature was conducted. Only 17 patients with spontaneous SAH due to a spinal ependymoma have been reported since 1958. However, in cases of SAH and negative diagnostic findings for cerebral aneurysms or malformations, this aetiology should be considered and work-up of the spinal axis completed.

Norepinephrine-induced hypertension dilates vasospastic basilar artery after subarachnoid haemorrhage in rabbits

BACKGROUND: Vasopressor-induced hypertension is routinely indicated for prevention and treatment of cerebral vasospasm (CVS) after subarachnoid haemorrhage (SAH). Mechanisms underlying patients' clinical improvement during vasopressor-induced hypertension remain incompletely understood. The aim of this study was to evaluate angiographic effects of normovolaemic Norepinephrine (NE)-induced hypertension therapy on the rabbit basilar artery (BA) after SAH. METHODS: Cerebral vasospasm was induced using the one-haemorrhage rabbit model; sham-operated animals served as controls. Five days later the animals underwent follow-up angiography prior to and during NE-induced hypertension. Changes in diameter of the BA were digitally calculated in mean microm +/- SEM (standard error of mean). FINDINGS: Significant CVS of 14.2% was documented in the BA of the SAH animals on day 5 compared to the baseline angiogram on day 0 (n = 12, p < 0.01), whereas the BA of the control animals remained statistically unchanged (n = 12, p > 0.05). During systemic administration of NE, mean arterial pressure increased from 70.0 +/- 1.9 mmHg to 136.0 +/- 2.1 mmHg in the SAH group (n = 12, p < 0.001) and from 72.0 +/- 3.1 to 137.8 +/- 1.3 in the control group (n = 12, p < 0.001). On day 5 after SAH, a significant dilatation of the BA in response to norepinephrine could be demonstrated in both groups. The diameter of the BA in the SAH group increased from 640.5 +/- 17.5 microm to 722.5 +/- 23.7 microm (n = 12, p < 0.05; ). In the control group the diameter increased from 716.8 +/- 15.5 microm to 779.9 +/- 24.1 microm (n = 12, p < 0.05). CONCLUSION: This study demonstrated that NE-induced hypertension causes angiographic dilatation of the BA in the SAH rabbit model. Based on these observations, it can be hypothesised that clinical improvement during vasopressor-induced hypertension therapy after SAH might be explained with cerebral vasodilatation mechanisms that lead to improvement of cerebral blood flow.

Decompressive hemicraniectomy in subarachnoid haemorrhage: the influence of infarction, haemorrhage and brain swelling

OBJECTIVE: To analyse decompressive hemicraniectomy (DHC) in patients with aneurysmal subarachnoid haemorrhage (SAH) with regard to infarction, haemorrhage or brain swelling. METHODS: DHC was performed in 43 of 787 patients with SAH. Patients were stratified according to (1) primary brain swelling without and (2) with additional intracerebral haematoma, (3) secondary brain swelling without rebleeding or infarcts and (4) with infarcts or (5) with rebleeding. Outcome was assessed according to the modified Rankin scale at 6 months RESULTS: Overall, 36 of 43 patients (83.7%) with DHC and 241 of 744 patients (32.4%) without DHC have been of a poor grade on admission (World Federation of Neurological Societies grading 4-5; p<0.0001). Favourable outcome was achieved in 11 of 43 (25.6%) patients with DHC. There was no difference in favourable outcome after primary (25%) versus secondary (26.1%) DHC (p = 1.0). Subgroup analysis (brain swelling vs bleeding vs infarcts) revealed no difference in the rate of favourable outcome. In a multivariate analysis, acute hydrocephalus (p = 0.02) and clinical herniation (p = 0.03) were significantly associated with unfavourable outcome. CONCLUSIONS: We conclude that primary and secondary hemicraniectomy may be warranted, irrespective of the underlying aetiology-infarction, haemorrhage or brain swelling. The time from onset of intractable ICP to DHC seems to be crucial, rather than the time from SAH to DHC.