Cerebral Vasospasm: Mechanisms, Pathomorphology, Diagnostics, Treatment

Cerebral vessels constriction is one of the leading causes of mortality and disability in patients with acute cerebral circulatory disorders. The most dangerous type of acute cerebrovascular disease accompanied by high mortality is ruptured cerebral aneurysms with subarachnoidal hemorrhage (SAH). Following a constriction of the cerebral vessels on the background of SAH is the reason for brain ischemia. This chapter will focus on the mechanisms of formation of cerebral vascular spasm, pathomorphological aspects of the cerebral vessels constriction, and the stages of vascular spasm—the development of constrictive-stenotic arteriopathy, contractural degeneration of smooth muscle cells, and endothelial damage. We will cover classifications of cerebral vessels constriction by prevalence and severity, modern methods of clinical and instrumental diagnostics and treatment including paroxysmal sympathetic hyperactivity syndrome associated with the development of secondary complications, a longer stay of the patients in the ICU, higher disability and mortality.

Elevation Mechanisms and Diagnostic Consideration of Cardiac Troponins under Conditions Not Associated with Myocardial Infarction. Part 2

This article proceeds with a discussion of the causes and mechanisms of an elevation in cardiac troponins in pathological conditions not associated with acute myocardial infarction. The second part of the article discusses the causes and mechanisms of cardiac troponins elevation in diabetes mellitus, arterial hypertension, hereditary cardiomyopathies, cardiac arrhythmias (atrial fibrillation, supraventricular tachycardia), acute aortic dissection, and diseases of the central nervous system (strokes, subarachnoidal hemorrhage). The final chapter of this article discusses in detail the false-positive causes and mechanisms of elevated cardiac troponins.

Sequence Variation in the DDAH1 Gene Predisposes for Delayed Cerebral Ischemia in Subarachnoidal Hemorrhage

Delayed cerebral ischemia (DCI) often causes poor long-term neurological outcome after subarachnoidal hemorrhage (SAH). Asymmetric dimethylarginine (ADMA) inhibits nitric oxide synthase (NOS) and is associated with DCI after SAH. We studied single nucleotide polymorphisms (SNPs) in the NOS3, DDAH1, DDAH2, PRMT1, and AGXT2 genes that are part of the L-arginine–ADMA–NO pathway, and their association with DCI. We measured L-arginine, ADMA and symmetric dimethylarginine (SDMA) in plasma and cerebrospinal fluid (CSF) of 51 SAH patients at admission; follow-up was until 30 days post-discharge. The primary outcome was the incidence of DCI, defined as new infarctions on cranial computed tomography, which occurred in 18 of 51 patients. Clinical scores did not significantly differ in patients with or without DCI. However, DCI patients had higher plasma ADMA and SDMA levels and higher CSF SDMA levels at admission. DDAH1 SNPs were associated with plasma ADMA, whilst AGXT2 SNPs were associated with plasma SDMA. Carriers of the minor allele of DDAH1 rs233112 had a significantly increased relative risk of DCI (Relative Risk = 2.61 (1.25–5.43), p = 0.002). We conclude that the DDAH1 gene is associated with ADMA concentration and the incidence of DCI in SAH patients, suggesting a pathophysiological link between gene, biomarker, and clinical outcome in patients with SAH.

Therapy results of pericallosal aneurysms: A retrospective unicenter study

This retrospective study aims to compare treatment results of ruptured and unruptured pericallosal artery aneurysms (PAAs) regarding patient outcome and aneurysm recurrence after endovascular treatment (EVT) and neurosurgical treatment (NT). A total of 67 patients with PAA were admitted to our hospital, 44 patients with subarachnoidal hemorrhage (SAH) due to a ruptured PAA and 23 patients with unruptured PAA. The radiographic features of PAA were collected from pre-treatment digital subtraction angiography. In addition, demographic, clinical and radiographic parameters of all patients were recorded. Outcome was measured based on the modified Rankin scale (mRS) at 6 months after admission (favorable mRS score, 0-2 vs unfavorable mRS score, 3-6). Overall 46 patients underwent EVT and 21 patients NT. Six months after discharge 24 patients with SAH had a favorable outcome (mRS 0-2) and 16 patients an unfavorable outcome (mRS 3-6). Mortality rate of patients with SAH was 9.1% (4/44). Overall aneurysm recurrence was treated in 13 % of patients in the EVT cohort (6/46), whereas patients treated with NT had no recurrence. All patients with unruptured PAA had a favorable outcome. EVT and NT of PAA show comparable good results, although aneurysm recurrence occurs more often after EVT.

Liquorpunktion – Schritt für Schritt

Performing a diagnostic lumbar puncture is an essential clinical skill for the clinician. The procedure is of high importance for both, the emergency care for patients with suspected infection of the cerebral nervous system or subarachnoidal hemorrhage, as well as the elective diagnostic work up of chronic disease including multiple sclerosis and dementia. Furthermore the technique’s principles are applied for spinal anesthesia or the intrathecal administration of drugs. This article describes a Standard Operating Procedure for the lumbar puncture step by step. Based on the latest evidence, it particularly focusses on clinically relevant questions and practical aspects.