Carla S. Jung

European Stroke Organization Guidelines for the Management of Intracranial Aneurysms and Subarachnoid Haemorrhage

Background: Intracranial aneurysm with and without subarachnoid haemorrhage (SAH) is a relevant health problem: The overall incidence is about 9 per 100,000 with a wide range, in some countries up to 20 per 100,000. Mortality rate with conservative treatment within the first months is 50–60%. About one third of patients left with an untreated aneurysm will die from recurrent bleeding within 6 months after recovering from the first bleeding. The prognosis is further influenced by vasospasm, hydrocephalus, delayed ischaemic deficit and other complications. The aim of these guidelines is to provide comprehensive recommendations on the management of SAH with and without aneurysm as well as on unruptured intracranial aneurysm. Methods: We performed an extensive literature search from 1960 to 2011 using Medline and Embase. Members of the writing group met in person and by teleconferences to discuss recommendations. Search results were graded according to the criteria of the European Federation of Neurological Societies. Members of the Guidelines Committee of the European Stroke Organization reviewed the guidelines. Results: These guidelines provide evidence-based information on epidemiology, risk factors and prognosis of SAH and recommendations on diagnostic and therapeutic methods of both ruptured and unruptured intracranial aneurysms. Several risk factors of aneurysm growth and rupture have been identified. We provide recommendations on diagnostic work up, monitoring and general management (blood pressure, blood glucose, temperature, thromboprophylaxis, antiepileptic treatment, use of steroids). Specific therapeutic interventions consider timing of procedures, clipping and coiling. Complications such as hydrocephalus, vasospasm and delayed ischaemic deficit were covered. We also thought to add recommendations on SAH without aneurysm and on unruptured aneurysms. Conclusion: Ruptured intracranial aneurysm with a high rate of subsequent complications is a serious disease needing prompt treatment in centres having high quality of experience of treatment for these patients. These guidelines provide practical, evidence-based advice for the management of patients with intracranial aneurysm with or without rupture. Applying these measures can improve the prognosis of SAH.

CSF and Serum Biomarkers Focusing on Cerebral Vasospasm and Ischemia after Subarachnoid Hemorrhage

Delayed cerebral vasospasm (CVS) and delayed cerebral ischemia (DCI) remain severe complications after subarachnoid hemorrhage (SAH). Although focal changes in cerebral metabolism indicating ischemia are detectable by microdialysis, routinely used biomarkers are missing. We therefore sought to evaluate a panel of possible global markers in serum and cerebrospinal fluid (CSF) of patients after SAH. CSF and serum of SAH patients were analyzed retrospectively. In CSF, levels of inhibitory, excitatory, and structural amino acids were detected by high-performance liquid chromatography (HPLC). In serum, neuron-specific enolase (NSE) and S100B level were measured and examined in conjunction with CVS and DCI. CVS was detected by arteriography, and ischemic lesions were assessed by computed tomography (CT) scans. All CSF amino acids were altered after SAH. CSF glutamate, glutamine, glycine, and histidine were significantly correlated with arteriographic CVS. CSF glutamate and serum S100B were significantly correlated with ischemic events after SAH; however, NSE did not correlate neither with ischemia nor with vasospasm. Glutamate, glutamine, glycine, and histidine might be used in CSF as markers for CVS. Glutamate also indicates ischemia. Serum S100B, but not NSE, is a suitable marker for ischemia. These results need to be validated in larger prospective cohorts.

Helmet use in winter sport activities-attitude and opinion of neurosurgeons and non-traumatic-brain-injury-educated persons

PurposeDuring the last winter season, some fatal sport injuries with severe traumatic brain injury (TBI) prompted major discussions about protective helmet use. Although ski helmets reportedly lead to a 60% decrease of risk to incur TBI, little is known about the distribution of helmet users and which factors are crucial for the decision to wear a helmet. Especially, it is unknown whether knowledge or experience concerning TBI in winter sports influences the use of helmets, as well as the attitude and opinion of people.MethodsSince treatment of TBI is a major field in neurosurgery, 55 neurosurgical departments (NS) in Germany, Switzerland and Austria were addressed and asked to answer anonymous questionnaires. A “non-trauma-educated” control cohort (NTP) was interviewed in ski resorts in Austria as well as sports equipment stores in Germany.ResultsQuestionnaires were returned by 465 NS and 546 NTP. Half of NS and NTP wore helmets in winter sports. Although some interviewees showed cognitive dissonant behaviour, experience in TBI after ski or snowboard accidents significantly affected the decision to wear helmets. After the fatal ski accidents, and increased media coverage 15.4% NS and 13.2% NTP bought their helmet. Furthermore, incidence of helmet use in children was correlated with the actual use and disposition of their parents to make the use of helmet compulsory.ConclusionsThis study indicates that brain-trauma education affects ones attitude and opinion concerning protective helmet use in winter sports. However, without neglecting educational measures, emotional arguments should be added in the promotion of helmets to make them a popular integral part of winter sport outfits.

The CSF concentration of ADMA, but not of ET-1, is correlated with the occurrence and severity of cerebral vasospasm after subarachnoid hemorrhage

Under physiological conditions, vasoconstrictors and vasodilators are counterbalanced. After aneurysmal subarachnoid hemorrhage (SAH) disturbance of this equilibrium may evoke delayed cerebral vasospasm (CVS) leading to delayed cerebral ischemia (DCI). Most studies examined either the vasoconstrictor endothelin-1 (ET-1) or the vasodilative pathway of nitric oxide (NO) and did not include investigations regarding the relationship between vasospasm and ischemia. Asymmetric dimethyl-L-arginine (ADMA), an endogenous inhibitor of nitric oxide synthase (NOS), decreases the concentration of NO. Studies have correlated increasing concentrations of ADMA with the course and degree of CVS after SAH. We sought to determine, if ADMA and endothelin-1 (ET-1) are associated with CVS and/or DCI after SAH. CSF concentrations of ADMA and ET-1 were retrospectively determined in 30 patients after SAH and in controls. CVS was detected clinically and by arteriogaphy. DCI was monitored by follow-up CT scans. 17 patients developed arteriographic CVS and 4 patients developed DCI. ADMA but not ET-1 concentrations were correlated with occurrence and degree of CVS. However, ET-1 concentrations were correlated with WFNS grade on admission. Neither ADMA nor ET-1 correlated with DCI in this cohort. ET-1 concentrations seem to be associated with the impact of the SAH bleed. ADMA may be directly involved in the development and resolution of CVS after SAH via inhibition of NOS disturbing the balance of vasodilative and -constrictive components.

Does suboccipital decompression and evacuation of intraparenchymal hematoma improve neurological outcome in patients with spontaneous cerebellar hemorrhage

OBJECTIVE Spontaneous cerebellar hemorrhages (SCH) can lead to life-threatening complications with high mortality rates of 20-50%. Although complications of SCH can be prevented by surgical therapy, there is a lack of consensus concerning the optimal surgical technique for evacuating SCH. METHODS In this retrospective study 85 patients with SCH were divided into four treatment groups: (1) Decompression and Hematoma Evacuation via suboccipital craniectomy and removal of the posterior arch of C1 (DHE). (2) Hematoma Evacuation Only via craniotomy (HEO). (3) External Ventricular Drainage (EVD). (4) Conservative treatment (C). To ascertain the level of consciousness, Glasgow Coma Scale (GCS) was calculated. To evaluate the clinical and neurological outcome, modified Rankin Score, Glasgow Outcome Scale and mortality rate were recorded after 6months. RESULTS The mean volume of hematoma was significant larger in the DHE- and HEO-group compared to the EVD- and C-group before treatment. DHE and HEO could significantly reduce the volume comparing pre- and postoperative measurements. Larger preoperative volume was a strong predictor of worse neurological outcome and high mortality. Overall mortality was 25.9%. After subdivision into the treatment groups, a comparison of the DHE- and HEO-groups showed a trend towards lower mortality and better neurological outcome in the DHE-group. Patients with the worst preoperative GCS scores profited significantly from DHE with respect to regaining consciousness. CONCLUSIONS Patients with SCH should receive surgical therapy when hemorrhages are space-occupying and when the patients neurological condition deteriorates. With regards to surgical technique, and limited by the retrospective design of the study, our results indicate that patients might benefit most from DHE.

Role of endogenous monomethylated L-arginine (L-NMMA) after subarachnoid hemorrhage.

Abstract Objectives: Monomethylated L-arginine (L-NMMA) has been proven to be a strong inhibitor of nitric oxide synthase (NOS) and has been used as an exogenous tool in experimental evaluation of cerebrovascular reactivity leading to vasoconstriction. However, L-NMMA is also produced endogenously and belongs, as does asymmetric dimethylated L-arginine (ADMA), to a family of endogenous NOS inhibitors. While ADMA has been associated with cerebral vasospasm (CVS) but not with delayed cerebral ischemia (DCI) after subarachnoid hemorrhage (SAH), no results are available concerning endogenous L-NMMA and SAH. We therefore decided to investigate the role of endogenous L-NMMA with regard to CVS and DCI after SAH. Methods: Retrospective analysis of cerebro-spinal fluid (CSF) and serum of SAH patients and controls was performed by high performance liquid chromatography (HPLC) and chemiluminescence. Delayed CVS was detected by arteriography and cerebral ischemic events by follow-up computed tomography (CT) scans. Results: Cerebro-spinal fluid and serum L-NMMA concentrations neither correlated with CVS nor with NO2− levels (P > 0·05, in both cases). However, endogenous L-NMMA concentrations correlated with cerebral ischemic events and with the size of infarction (cc  =  0·459, P  =  0·032, 95% CI: 0·046–0·738). Conclusions: This study shows that endogenous L-NMMA is associated with the occurrence of cerebral ischemic events, but seems not to be involved in CVS after SAH. Therefore, endogenous L-NMMA after SAH features intriguing differences compared with previous reports on exogenous L-NMMA and ADMA after SAH.