Acta neurochirurgica. Supplement
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Acta Neurochir. Suppl. · Jan 2015
Multicenter StudyCharacteristics of patients without neuropsychological deficits following aneurysmal subarachnoid haemorrhage.
Previous studies have shown that the incidence of neuropsychological deficits (NPD) after aneurysmal subarachnoid haemorrhage (aSAH) is high despite excellent outcome evaluated by traditional neurological grading scales. The aim of this study was to elucidate the clinical characteristics in patients presenting with aSAH who had a good clinical outcome without NPD. ⋯ Patients without NPD after aSAH are likely to present with mild admission scores, develop neither chronic hydrocephalus nor DCI. In this series the aneurysm occlusion modality did not influence the cognitive outcome.
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Acta Neurochir. Suppl. · Jan 2015
Tenascin-C is a possible mediator between initial brain injury and vasospasm-related and -unrelated delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage.
Tenascin-C (TNC), a matricellular protein, exerts diverse functions, including tissue remodeling and apoptosis, and is induced in cerebrospinal fluid (CSF) after aneurysmal subarachnoid hemorrhage (SAH). The purpose of this study was to examine the relationships among CSF TNC levels, initial brain injury, delayed cerebral ischemia (DCI), and vasospasm after SAH. ⋯ SAH (initial brain injury) that is more severe induces more TNC, which may cause the subsequent development of both vasospasm and vasospasm-unrelated secondary brain injury, leading to DCI.
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Acta Neurochir. Suppl. · Jan 2015
Relationship between angiographic vasospasm, cerebral blood flow, and cerebral infarction after subarachnoid hemorrhage.
Delayed cerebral ischemia (DCI) and cerebral infarction are major contributors to poor functional recovery after subarachnoid hemorrhage (SAH). Cerebral vasospasm, the narrowing of proximal intracranial arteries after SAH, has long been assumed to be the primary cause of DCI, and has therefore been the primary therapeutic target in attempts to diminish disability after SAH. However, emerging evidence has questioned the strength and causality of the relationship between vasospasm and DCI. ⋯ We found that regional hypoperfusion was common in the absence of proximal vasospasm and that some patients without any significant vasospasm still could have hypoperfused brain regions. Similarly, our parallel study demonstrated that both patients and brain territories without vasospasm could develop delayed cerebral infarction, and that such vasospasm-independent infarcts account for more than a quarter of the infarct burden from DCI. These findings suggest that other processes, perhaps at a microvascular level, contribute at least part of the burden of DCI and future interventions should also address these other pathophysiologic processes.
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Acta Neurochir. Suppl. · Jan 2015
Case Reports Clinical TrialEarly identification of brain tissue at risk for delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage.
Delayed cerebral ischemia (DCI) continues to be a major cause of morbidity and mortality in patients with aneurysmal subarachnoid hemorrhage (aSAH) because it can only be diagnosed after the onset of clinical symptoms, contributing to poor clinical outcomes and huge use of clinical resources. We hypothesized that early disturbances in cerebrovascular reactivity, noninvasively measured with functional MRI + CO₂, can be a sensitive marker of brain tissue at risk for DCI. ⋯ In this feasibility study, functional MRI measurements of cerebrovascular reactivity showed a spatial correspondence between impaired cerebrovascular reactivity and the onset of DCI in patients with aSAH.
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Acta Neurochir. Suppl. · Jan 2015
Comparative StudyProximal arterial diameters on CT angiography and digital subtraction angiography correlate both at admission and in the vasospasm period after aneurysmal subarachnoid hemorrhage.
Comparison of artery diameters between CT angiography (CTA) and subtraction arteriography (DSA) has the limitation that measurements on DSA are provided as relative units, making a quantitative comparison difficult. On CTA, artery diameters may depend on windowing settings and may lead to false measurements. This study assesses the correlation between CTA and DSA based on measurements in a basic imaging viewer using normalized DSA values, and assesses whether the validity is time dependent. ⋯ Using basic imaging viewers, mostly accessible for clinicians, CTA is a noninvasive and reliable method to assess proximal arterial diameters of the brain in the management of cerebral vasospasm in the acute phase after aSAH. Significance is reached, independent of whether CTA is obtained in the acute phase or during the period of vasospasm, by normalization of basal cerebral artery diameters to a non-variable anatomic landmark, i.e., the petrous or cavernous internal carotid artery diameter.