Pearls & Oy-sters: INO Plus From Downward Herniation-A Cautionary Tale Regarding Neuro-Ophthalmologic Signatures of Brainstem Compression.

Pupillary assessment is a quintessential part of the clinical examination in neuro-intensive care patients because it provides insight into the integrity of midbrain reflex arcs. Abnormal pupils, particularly anisocoria and later bilateral fixed mydriasis, are classically used to assess expansive intracranial processes because they are frequently considered early indicators of transtentorial midbrain compression due to elevated intracranial pressure. Complex ocular motor deficits mapping to the midbrain are rarely described in the setting of high transtentorial pressure. This is likely because ocular motor deficits typically occur in conjunction with decreased consciousness and corticospinal tract dysfunction reflecting advanced midbrain compromise. We present a case of left midbrain compression due to downward herniation in a patient with acute-on-chronic bilateral subdural hematoma. Ocular motor assessment demonstrated left internuclear ophthalmoplegia (INO) and an ocular tilt reaction, termed INO plus. However, pupillary, mental status, and sensorimotor examinations were unremarkable. Head magnetic resonance imaging revealed acute perforator ischemia in the left pontomesencephalic tegmentum, localizing to the ipsilateral medial longitudinal fasciculus and graviceptive oculocephalic circuits. Microvascular compromise secondary to mechanical pressure is discussed as a causative mechanism. We caution against overreliance on "telltale pupils" in suspected brainstem compression and recommend checking for other oculomotor signs.

Investigating the relationship between high-dose norepinephrine administration and the incidence of delayed cerebral infarction in patients with aneurysmal subarachnoid hemorrhage: A single-center retrospective evaluation.

BACKGROUND: One of the longest-standing treatments to prevent delayed cerebral infarction (DCI) in patients with aneurysmal subarachnoid hemorrhage (aSAH) remains raising the blood pressure to a certain level of mean arterial pressure. This may require high doses of norepinephrine, which has been associated with severe end organ damage. With this study, we aimed to investigate the effects of norepinephrine on the incidence of DCI in a clinical setting. METHODS: We conducted a retrospective evaluation of patients with aSAH admitted to our institution between November 2018 and March 2021. Potential risk factors for DCI were analyzed and significant predictors were assessed by means of a logistic regression analysis to account for potential confounders. RESULTS: In this study, 104 patients were included. Hereof, 39 (38%) showed radiologic signs of DCI between day three and 14 post-intervention. These patients had more frequent vasospasms (n = 37 vs. 30, p = 0.022), a higher Hunt & Hess score (3 ± 2 vs. 2 ± 1, p = 0.004), a lower initial Glasgow Coma Scale score (9 ± 5 vs. 12 ± 4, p = 0.003) and received a higher median norepinephrine dose (20,356µg vs. 6,508µg, p < 0.001). A logistic regression analysis revealed that only high-dose norepinephrine administration (OR 2.84, CI 1.56-7.8) and vasospasm (OR 3.07, CI 1.2-7.84) appeared to be significant independent risk factors for DCI. CONCLUSION: Our results indicate a significant association between higher dose norepinephrine administration and the occurrence of DCI. Future research including greater sample sizes and a prospective setting will be necessary to further investigate the relationship.

[Pregnancy and Irreversible Loss of Brain Functions - Case Report]. / Intensivtherapie bei Schwangerer mit irreversiblem Hirnfunktionsausfall.

A 29-year-old woman suffered major traumatic brain injury caused by a car accident. As diagnostic measures had revealed an early pregnancy (9th week), treatment on the intensive care unit was continued for 5 months, after unfavourable cerebral prognosis was followed by an irreversible loss of brain function in the 10th week of pregnancy. After assisted vaginal delivery of a healthy child in the 31th week of pregnancy on the critical care unit, organ procurement took place according to the presumed will of the patient. The article presents the details of the critical care therapy and discusses the supportive medical measures. Those measures served primarily to uphold the pregnancy und support the healthy development and delivery of the fetus and only in second instance the organ preservation aiming on organ donation. Necessary measures included maintenance of vital functions, hemostasis of electrolytes, nutrition, treatment of infection, prevention of adverse effects on the fetus, substitution of hormones and vitamins as well as the preparation of a planned or an unplanned delivery.

Therapeutic hypercapnia for prevention of secondary ischemia after severe subarachnoid hemorrhage: physiological responses to continuous hypercapnia.

Temporary hypercapnia has been shown to increase cerebral blood flow (CBF) and might be used as a therapeutical tool in patients with severe subarachnoid hemorrhage (SAH). It was the aim of this study was to investigate the optimum duration of hypercapnia. This point is assumed to be the time at which buffer systems become active, cause an adaptation to changes of the arterial partial pressure of carbon dioxide (PaCO2) and annihilate a possible therapeutic effect. In this prospective interventional study in a neurosurgical ICU the arterial partial pressure of carbon dioxide (PaCO2) was increased to a target range of 55 mmHg for 120 min by modification of the respiratory minute volume (RMV) one time a day between day 4 and 14 in 12 mechanically ventilated poor-grade SAH-patients. Arterial blood gases were measured every 15 min. CBF and brain tissue oxygen saturation (StiO2) were the primary and secondary end points. Intracranial pressure (ICP) was controlled by an external ventricular drainage. Under continuous hypercapnia (PaCO2 of 53.17 ± 5.07), CBF was significantly elevated between 15 and 120 min after the start of hypercapnia. During the course of the trial intervention, cardiac output also increased significantly. To assess the direct effect of hypercapnia on brain perfusion, the increase of CBF was corrected by the parallel increase of cardiac output. The maximum direct CBF enhancing effect of hypercapnia of 32% was noted at 45 min after the start of hypercapnia. Thereafter, the CBF enhancing slowly declined. No relevant adverse effects were observed. CBF and StiO2 reproducibly increased by controlled hypercapnia in all patients. After 45 min, the curve of CBF enhancement showed an inflection point when corrected by cardiac output. It is concluded that 45 min might be the optimum duration for a therapeutic use and may provide an optimal balance between the benefits of hypercapnia and risks of a negative rebound effect after return to normal ventilation parameters.Trial registration: The study was approved by the institutional ethics committee (AZ 230/14) and registered at ClinicalTrials.gov (Trial-ID: NCT01799525). Registered 01/01/2015.

Neuroprotective Strategies in Aneurysmal Subarachnoid Hemorrhage (aSAH).

Aneurysmal subarachnoid hemorrhage (aSAH) remains a disease with high mortality and morbidity. Since treating vasospasm has not inevitably led to an improvement in outcome, the actual emphasis is on finding neuroprotective therapies in the early phase following aSAH to prevent secondary brain injury in the later phase of disease. Within the early phase, neuroinflammation, thromboinflammation, disturbances in brain metabolism and early neuroprotective therapies directed against delayed cerebral ischemia (DCI) came into focus. Herein, the role of neuroinflammation, thromboinflammation and metabolism in aSAH is depicted. Potential neuroprotective strategies regarding neuroinflammation target microglia activation, metalloproteases, autophagy and the pathway via Toll-like receptor 4 (TLR4), high mobility group box 1 (HMGB1), NF-κB and finally the release of cytokines like TNFα or IL-1. Following the link to thromboinflammation, potential neuroprotective therapies try to target microthrombus formation, platelets and platelet receptors as well as clot clearance and immune cell infiltration. Potential neuroprotective strategies regarding metabolism try to re-balance the mismatch of energy need and supply following aSAH, for example, in restoring fuel to the TCA cycle or bypassing distinct energy pathways. Overall, this review addresses current neuroprotective strategies in aSAH, hopefully leading to future translational therapy options to prevent secondary brain injury.

Magnesium Protects in Episodes of Critical Perfusion after Aneurysmal SAH.

BACKGROUND: To analyze whether magnesium has a neuroprotective effect during episodes that indicate a critical brain perfusion after aneurysmal subarachnoid hemorrhage (SAH). METHODS: 107 patients with aSAH were randomized to continuously receive intravenous magnesium sulfate with target serum levels of 2.0 - 2.5 mmol/l (n = 54) or isotonic saline (n = 53). Neurological examination and transcranial Doppler sonography (TCD) were performed daily, Perfusion-CT (PCT) was acquired in 3-day intervals, angiography in case of suspected vasospasm. The primary endpoint was the development of secondary infarction following episodes of delayed ischemic neurological deficit (DIND), elevated mean flow velocity (MFV) in TCD or pathological findings in PCT. RESULTS: In the magnesium group, 9 episodes of DIND were registered, none was followed by secondary infarction. In the control group, 23 episodes of DIND were registered, 9 were followed by secondary infarction (p < 0.05). In the magnesium group, 114 TCD-measurements showed an elevated MFV(> 140 cm/s). 7 were followed by new infarction. In control patients, 135 measurements showed elevated MFV, 32 were followed by new infarction (p < 0.05). 10 of 117 abnormal PCT-findings were followed by new infarction, compared to 30 of 122 in the control-group (p < 0.05). CONCLUSION: DIND, elevated MFV in TCD and abnormal PCT are findings which are associated with an increased risk to develop delayed secondary infarction. The results of this analysis suggest that magnesium-treatment may reduce the risk to develop infarction in a state of critical brain perfusion.

Cellular infiltrates in skin and sural nerve of patients with polyneuropathies.

INTRODUCTION: The aim of this study was to determine the diagnostic usefulness of skin punch biopsies with emphasis on visualization and quantification of T-cells and macrophages in patients with polyneuropathies. METHODS: We quantified inflammatory cells in skin samples (lower leg, upper thigh) in 187 patients and compared data with counts in their sural nerve biopsies and with skin biopsies from 32 healthy volunteers. RESULTS: Vessel-bound T-cells and macrophages were increased in proximal and distal skin samples of neuropathy patients compared with controls (P < 0.001 in both). Patients with vasculitic neuropathy had increased T-cell and macrophage counts in distal skin compared with controls (P < 0.01; for scattered macrophages/mm2 diagnostic sensitivity 71% and specificity 79%). In patients with vasculitic neuropathy, distal skin perivascular inflammatory cell counts also correlated with those in sural nerve biopsies (P < 0.001). CONCLUSION: Neuropathy per se may lead to skin inflammation. In cases of possible vasculitic neuropathy, skin biopsy may be an additional tool to support the diagnosis. Muscle Nerve 55: 884-893, 2017.

Controlled Hypercapnia Enhances Cerebral Blood Flow and Brain Tissue Oxygenation After Aneurysmal Subarachnoid Hemorrhage: Results of a Phase 1 Study.

BACKGROUND: This study investigated if cerebral blood flow (CBF) regulation by changes of the arterial partial pressure of carbon dioxide (PaCO2) can be used therapeutically to increase CBF and improve neurological outcome after subarachnoid hemorrhage (SAH). METHODS: In 12 mechanically ventilated poor-grade SAH-patients, a daily trial intervention was performed between day 4 and 14. During this intervention, PaCO2 was decreased to 30 mmHg and then gradually increased to 40, 50, and 60 mmHg in 15-min intervals by modifications of the respiratory minute volume. CBF and brain tissue oxygen saturation (StiO2) were the primary and secondary endpoints. Intracranial pressure was controlled by an external ventricular drainage. RESULTS: CBF reproducibly decreased during hyperventilation and increased to a maximum of 141 ± 53 % of baseline during hypercapnia (PaCO2 60 mmHg) on all days between day 4 and 14 after SAH. Similarly, StiO2 increased during hypercapnia. CBF remained elevated within the first hour after resetting ventilation to baseline parameters and no rebound effect was observed within this time-span. PaCO2-reactivities of CBF and StiO2 were highest between 30 and 50 mmHg and slightly decreased at higher levels. CONCLUSION: CBF and StiO2 reproducibly increased by controlled hypercapnia of up to 60 mmHg even during the period of the maximum expected vasospasm. The absence of a rebound effect within the first hour after hypercapnia indicates that an improvement of the protocol is possible. The intervention may yield a therapeutic potential to prevent ischemic deficits after aneurysmal SAH.

Effects of Fluid Treatment With Hydroxyethyl Starch on Renal Function in Patients With Aneurysmal Subarachnoid Hemorrhage.

BACKGROUND: Recent reports have doubted the efficacy and safety of hydroxyethyl starch (HES) for volume resuscitation. HES has been reported to promote renal insufficiency particularly in sepsis and trauma patients. This analysis investigated the effects of HES 6% 130/0.4 for fluid therapy in patients with intact renal function who suffered aneurysmal subarachnoid hemorrhage (SAH). METHODS: This retrospective analysis included 107 patients and was conducted in the framework of a clinical trial assessing the efficacy of magnesium sulfate in SAH. Because magnesium is renally eliminated, patients with renal insufficiency had been excluded. Standard therapy after aneurysm occlusion included the daily administration of HES 6% 130/0.4. Serum and urine creatinine and fluid balance were measured daily. RESULTS: Patients received a daily mean of 1101±524 mL HES and 3353±1396 mL Ringer's solution. The highest creatinine values were recorded on day 3 after admission (0.88±0.25 mg/100 mL) and continuously decreased thereafter. In 6 patients, creatinine values temporarily increased by >0.3 mg/100 mL but recovered to admission values at the end of the observation period. CONCLUSIONS: Concerning renal function, the first days after SAH seem to be a vulnerable phase in which a variety of interventions are performed, including contrast-enhanced neuroradiologic procedures. In this period, HES 6% 130/0.4 should be administered with caution. However, no patient suffered from renal failure and required temporary or permanent renal replacement therapy. These results suggest that the administration of HES 6% 130/0.4 is safe in SAH patients without preexisting renal insufficiency.

Trauma- and distress-associated mental illness symptoms in close relatives of patients with severe traumatic brain injury and high-grade subarachnoid hemorrhage.

BACKGROUND: Close relatives (CR) of patients with severe traumatic brain injury (TBI) and high-grade subarachnoid hemorrhage (SAH) suffer extraordinary distress during the treatment: Distress may lead to persisting mental illness symptoms within the spectrum of post-traumatic stress disorder (PTSD), anxiety disorders, and depression. The primary goal of this study was to determine the prevalence and severity of these symptoms in CR. The secondary goal was identification of associated factors. METHOD: Standardized interviews were conducted with 53 CR (mean age of 57.7 ± 11.4 years) of patients with TBI °III (n = 27) and high-grade SAH H&H °III-V (n = 26) between 5 and 15 months after the event. The interviews contained a battery of surveys to quantify symptoms of PTSD, anxiety disorders, and depression, i.e., Impact of Event Scale (IES-R), 36-item Short-Form General Health Survey (SF-36), and Hospital Anxiety and Depression Scale (HADS). Fixed and modifiable possibly influencing factors were correlated. RESULTS: Twenty-eight CR (53 %) showed IES-R scores indicating a probable diagnosis of PTSD. Twenty-five CR (47 %) showed an increased anxiety score and 18 (34 %) an increased depression score using HADS. Mean physical component summary of SF-36 was not abnormal (49.1 ± 9.1), whereas mean mental component summary was under average (41.0 ± 13.2), indicating a decreased quality of life caused by mental effects. Perception of the interaction quality with the medical staff and involvement into medical decisions correlated negatively with severity of mental illness symptoms. Evasive coping strategies were highly significantly associated with symptoms. CONCLUSIONS: This study quantifies an extraordinarily high prevalence of mental illness symptoms in CR of patients with critical acquired brain injury due to SAH and TBI. Modifiable factors were associated with severity of mental illness symptoms. Prospective studies testing efficiency of early psychotherapeutic interventions are needed.

Controlled transient hypercapnia: a novel approach for the treatment of delayed cerebral ischemia after subarachnoid hemorrhage?

OBJECT: The authors undertook this study to investigate whether the physiological mechanism of cerebral blood flow (CBF) regulation by alteration of the arterial partial pressure of carbon dioxide (PaCO2) can be used to increase CBF after aneurysmal subarachnoid hemorrhage (aSAH). METHODS: In 6 mechanically ventilated patients with poor-grade aSAH, the PaCO2 was first decreased to 30 mm Hg by modification of the respiratory rate, then gradually increased to 40, 50 and 60 mm Hg for 15 minutes each setting. Thereafter, the respirator settings were returned to baseline parameters. Intracerebral CBF measurement and brain tissue oxygen saturation (StiO2), measured by near-infrared spectroscopy (NIRS), were the primary and secondary end points. Intracranial pressure (ICP) was controlled by external ventricular drainage. RESULTS: A total of 60 interventions were performed in 6 patients. CBF decreased to 77% of baseline at a PaCO2 of 30 mm Hg and increased to 98%, 124%, and 143% at PaCO2 values of 40, 50, and 60 mm Hg, respectively. Simultaneously, StiO2 decreased to 94%, then increased to 99%, 105%, and 111% of baseline. A slightly elevated delivery rate of cerebrospinal fluid was noticed under continuous drainage. ICP remained constant. After returning to baseline respirator settings, both CBF and StiO2 remained elevated and only gradually returned to pre-hypercapnia values without a rebound effect. None of the patients developed secondary cerebral infarction. CONCLUSIONS: Gradual hypercapnia was well tolerated by poor-grade SAH patients. Both CBF and StiO2 reacted with a sustained elevation upon hypercapnia; this elevation outlasted the period of hypercapnia and only slowly returned to normal without a rebound effect. Elevations of ICP were well compensated by continuous CSF drainage. Hypercapnia may yield a therapeutic potential in this state of critical brain perfusion. Clinical trial registration no.: NCT01799525 ( ClinicalTrials.gov ).

Routine follow-up cranial computed tomography for deeply sedated, intubated, and ventilated multiple trauma patients with suspected severe head injury.

BACKGROUND: Missed or delayed detection of progressive neuronal damage after traumatic brain injury (TBI) may have negative impact on the outcome. We investigated whether routine follow-up CT is beneficial in sedated and mechanically ventilated trauma patients. METHODS: The study design is a retrospective chart review. A routine follow-up cCT was performed 6 hours after the admission scan. We defined 2 groups of patients, group I: patients with equal or recurrent pathologies and group II: patients with new findings or progression of known pathologies. RESULTS: A progression of intracranial injury was found in 63 patients (42%) and 18 patients (12%) had new findings in cCT 2 (group II). In group II a change in therapy was found in 44 out of 81 patients (54%). 55 patients with progression or new findings on the second cCT had no clinical signs of neurological deterioration. Of those 24 patients (44%) had therapeutic consequences due to the results of the follow-up cCT. CONCLUSION: We found new diagnosis or progression of intracranial pathology in 54% of the patients. In 54% of patients with new findings and progression of pathology, therapy was changed due to the results of follow-up cCT. In trauma patients who are sedated and ventilated for different reasons a routine follow-up CT is beneficial.

Value of transcranial Doppler, perfusion-CT and neurological evaluation to forecast secondary ischemia after aneurysmal SAH.

INTRODUCTION: This study was conducted to prospectively evaluate the diagnostic value of detailed neurological evaluation, transcranial Doppler sonography (TCD) and Perfusion-CT (PCT) to predict delayed vasospasm (DV) and delayed cerebral infarction (DCI) within the following 3 days in patients with aneurysmal subarachnoid hemorrhage (SAH). METHODS: A total of 61 patients with aneurysmal SAH were included in the study. All patients were amenable for neurological evaluation throughout the critical phase to develop secondary ischemia after SAH. The neurological status was assessed three times a day according to a detailed examination protocol. Mean flow velocities (MFV) in intracranial vessel trunks were measured daily by TCD. Native CT and PCT were routinely acquired at 3-day intervals and, in addition, whenever it was thought to be of diagnostic relevance. The predictive values of abnormal PCT and accelerations in TCD (MFV > 140 cm/s) to detect angiographic DV and DCI within the following 2 days were calculated and compared to the predictive value of delayed ischemic neurological deficits (DIND). RESULTS: The accuracy of TCD and PCT to predict DV or DCI was 0.65 and 0.63, respectively. In comparison, DIND predicted DV or DCI with an accuracy of 0.96. Pathological PCT findings had a higher sensitivity (0.93) and negative predictive value (0.98) than TCD (0.81 and 0.96). CONCLUSION: Neurological assessment at close intervals is the most accurate parameter to detect DV and DCI in the following 3 days. However, DIND may not be reversible. The routine acquisition of PCT in addition to daily TCD examinations seems reasonable, particularly in patients who are not amenable to a detailed neurological examination since it has a higher sensitivity and negative predictive value than TCD and leaves a lower number of undetected cases of vasospasm and infarction.

Magnesium treatment for neuroprotection in ischemic diseases of the brain.

This article reviews experimental and clinical data on the use of magnesium as a neuroprotective agent in various conditions of cerebral ischemia. Whereas magnesium has shown neuroprotective properties in animal models of global and focal cerebral ischemia, this effect could not be reproduced in a large human stroke trial. These conflicting results may be explained by the timing of treatment. While treatment can be started before or early after ischemia in experimental studies, there is an inevitable delay of treatment in human stroke. Magnesium administration to women at risk for preterm birth has been investigated in several randomized controlled trials and was found to reduce the risk of neurological deficits for the premature infant. Postnatal administration of magnesium to babies after perinatal asphyxia has been studied in a number of controlled clinical trials. The results are promising but the trials have, so far, been underpowered. In aneurysmal subarachnoid hemorrhage (SAH), cerebral ischemia arises with the onset of delayed cerebral vasospasm several days after aneurysm rupture. Similar to perinatal asphyxia in impending preterm delivery, treatment can be started prior to ischemia. The results of clinical trials are conflicting. Several clinical trials did not show an additive effect of magnesium with nimodipine, another calcium antagonist which is routinely administered to SAH patients in many centers. Other trials found a protective effect after magnesium therapy. Thus, it may still be a promising substance in the treatment of secondary cerebral ischemia after aneurysmal SAH. Future prospects of magnesium therapy are discussed.

Value of Perfusion CT, Transcranial Doppler Sonography, and Neurological Examination to Detect Delayed Vasospasm after Aneurysmal Subarachnoid Hemorrhage.

Background. If detected in time, delayed cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH) may be treated by balloon angioplasty or chemical vasospasmolysis in order to enhance cerebral blood flow (CBF) and protect the brain from ischemic damage. This study was conceived to compare the diagnostic accuracy of detailed neurological examination, Transcranial Doppler Sonography (TCD), and Perfusion-CT (PCT) to detect angiographic vasospasm. Methods. The sensitivity, specificity, positive and negative predictive values of delayed ischemic neurological deterioration (DIND), pathological findings on PCT-maps, and accelerations of the mean flow velocity (MVF) were calculated. Results. The accuracy of DIND to predict angiographic vasospasm was 0.88. An acceleration of MFV in TCD (>140 cm/s) had an accuracy of 0.64, positive PCT-findings of 0.69 with a higher sensitivity, and negative predictive value than TCD. Interpretation. Neurological assessment at close intervals is the most sensitive and specific parameter for cerebral vasospasm. PCT has a higher accuracy, sensitivity and negative predictive value than TCD. If detailed neurological evaluation is possible, it should be the leading parameter in the management and treatment decisions. If patients are not amenable to detailed neurological examination, PCT at regular intervals is a helpful tool to diagnose secondary vasospasm after aneurysmal SAH.

Prolonged heparin-free extracorporeal membrane oxygenation in multiple injured acute respiratory distress syndrome patients with traumatic brain injury.

BACKGROUND: Extracorporeal membrane oxygenation (ECMO) can be used as an "ultima ratio" strategy in multiple injured patients with severe thoracic trauma. However, systemic anticoagulation during ECMO is recommended and thus traumatic brain injury (TBI) and intracranial bleeding are well-accepted contraindications for ECMO therapy. METHODS: This report describes three cases of prolonged heparin-free venovenous ECMO in multiple injured acute respiratory distress syndrome patients with severe TBI failing conventional mechanical ventilation. RESULTS: : Using this strategy, neither ECMO-associated bleeding nor clotting of the extracorporeal circuit occurred. All patients survived. CONCLUSIONS: Based on our experience, we recommend the use of heparin-free ECMO in multiple injured patients with pulmonary failure that is not successfully controlled by lung-protective ventilation even if severe TBI is present. LEVEL OF EVIDENCE: IV, therapeutic study.

The temporal profile of cerebral blood flow and tissue metabolites indicates sustained metabolic depression after experimental subarachnoid hemorrhage in rats.

BACKGROUND: Derangement of cerebral metabolism occurs after various insults such as ischemia, traumatic brain injury, and subarachnoid hemorrhage (SAH). OBJECTIVE: To investigate the course of cerebral blood flow and metabolic parameters in the first hours after experimental SAH. METHODS: Sixteen Sprague-Dawley rats were subjected to SAH using the endovascular filament model or served as controls (8 rats in each group). Local cerebral blood flow and intracranial pressure were measured continuously. Microdialysis samples were acquired in 30-minute intervals for 6 hours after SAH. Concentrations of glucose, lactate, pyruvate, and glutamate were determined. RESULTS: After induction of SAH, cerebral perfusion pressure and local cerebral blood flow sharply decreased. The decrease in local cerebral blood flow exceeded the decrease in cerebral perfusion pressure throughout the observation period. Glutamate concentrations in microdialysis samples increased sixfold and recovered to baseline levels. Lactate concentrations immediately increased after SAH, recovered incompletely, and remained above the levels of control animals until the end of the sampling period. Pyruvate concentrations showed a delayed increase starting 2 hours after SAH. CONCLUSION: The course of cerebral blood flow after SAH resembles global ischemia followed by a continuous low-flow state caused by a sudden decrease in cerebral perfusion pressure and acute vasoconstriction. The courses of lactate and pyruvate concentrations indicate a persistently deranged aerobic metabolism.

Spectral iEEG markers precede SSEP events during surgery for subarachnoid hemorrhage.

OBJECTIVE: During neurosurgical intracranial vascular manipulations, surgeons need early feed-back on the effects of temporary vascular occlusion. In surgical practice, commonly the amplitude of somatosensory evoked potentials (SSEP) is monitored. However, the latency between an ischemic event and the drop of SSEP amplitude may amount to several minutes. Therefore intracranial electroencephalogram (iEEG) is tested for its predictive value. METHODS: During surgery in 13 patients, SSEP was recorded simultaneously with iEEG. iEEG was analyzed real-time in the frequency domain. Spectral observables of the iEEG were validated on the basis of SSEP by computing the statistical correlation first for the whole data set, then for salient events occurring in the SSEP in the group of patients, and finally for salient events occurring in single patients. RESULTS: Placement of subdural strip electrodes was compatible with standard surgical routine. Maximal correlation between time series of iEEG and SSEP was found for relative alpha power, which preceded the drop of SSEP by 7min. CONCLUSIONS: iEEG is feasible during neurosurgical intracranial vascular manipulations. Monitoring relative alpha power detects salient events earlier than SSEP. SIGNIFICANCE: Early detection of salient events facilitates early reaction of the surgeon and may thereby aid to further reduce intraoperative morbidity.

Prophylactic intravenous magnesium sulfate for treatment of aneurysmal subarachnoid hemorrhage: a randomized, placebo-controlled, clinical study.

OBJECTIVE: To examine whether the maintenance of elevated magnesium serum concentrations by intravenous administration of magnesium sulfate can reduce the occurrence of cerebral ischemic events after aneurysmal subarachnoid hemorrhage. DESIGN: Prospective, randomized, placebo-controlled study. SETTING: Neurosurgical intensive care unit of a University hospital. INTERVENTIONS: One hundred ten patients were randomized to receive intravenous magnesium sulfate or to serve as controls. Magnesium treatment was started with a bolus of 16 mmol, followed by continuous infusion of 8 mmol/hr. Serum concentrations were measured every 8 hrs, and infusion rates were adjusted to maintain target levels of 2.0-2.5 mmol/L. Intravenous administration was continued for 10 days or until signs of vasospasm had resolved. Thereafter, magnesium was administered orally and tapered over 12 days. MEASUREMENTS AND MAIN RESULTS: Delayed ischemic infarction (primary end point) was assessed by analyzing serial computed tomography scans. Transcranial Doppler sonography and digital subtraction angiography were used to detect vasospasm. Delayed ischemic neurologic deficit was determined by continuous detailed neurologic examinations; clinical outcome after 6 months was assessed using the Glasgow outcome scale. Good outcome was defined as Glasgow outcome scale score 4 and 5.The incidence of delayed ischemic infarction was significantly lower in magnesium-treated patients (22% vs. 51%; p = .002); 34 of 54 magnesium patients and 27 of 53 control patients reached good outcome (p = .209). Delayed ischemic neurologic deficit was nonsignificantly reduced (9 of 54 vs. 15 of 53 patients; p = .149) and transcranial Doppler-detected/angiographic vasospasm was significantly reduced in the magnesium group (36 of 54 vs. 45 of 53 patients; p = .028). Fewer patients with signs of vasospasm had delayed cerebral infarction. CONCLUSION: These data indicate that high-dose intravenous magnesium can reduce cerebral ischemic events after aneurysmal subarachnoid hemorrhage by attenuating vasospasm and increasing the ischemic tolerance during critical hypoperfusion.

An anatomical assessment of the supracerebellar midline and paramedian approaches to the inferior colliculus for auditory midbrain implants using a neuronavigation model on cadaveric specimens.

The inferior colliculus (IC) is an alternative site for electrode placement in neural deafness due to its surgical accessibility and its well-known tonotopic stratification. In patients where tumor surgery has already occurred and the cerebellopontine angle contains scar tissue or tumor-remnants, midline and paramedian supracerebellar approaches are alternative routes. They are often avoided due to concerns regarding the venous drainage of the cerebellum, the electrode trajectory and the course of the electrode cable. We studied these surgical routes in five neuronavigated fixed cadaveric specimens. For paramedian and midline approaches, the transverse sinus was exposed 5.8mm on average. A mean of 1.6 cerebellar veins, with an average diameter of 2.0mm, draining to the tentorium were transected to reach the tentorial notch. Only 0.4 arterial branches were met. We conclude that the supracerebellar midline and paramedian approaches provide a good exposure of the IC and offer safe and viable alternative routes to the IC. Additionally, they provide a wider angle of action for optimal electrode placement.