The Effect of Packed Red Blood Cell Transfusion on Cerebral Oxygenation and Metabolism After Subarachnoid Hemorrhage.

BACKGROUND: Anemia adversely affects cerebral oxygenation and metabolism after subarachnoid hemorrhage (SAH) and is also associated with poor outcome. There is limited evidence to support the use of packed red blood cell (PRBC) transfusion to optimize brain homeostasis after SAH. The aim of this study was to investigate the effect of transfusion on cerebral oxygenation and metabolism in patients with SAH. METHODS: This was a prospective observational study in a neurological intensive care unit of a university hospital. Nineteen transfusions were studied in 15 consecutive patients with SAH that underwent multimodality monitoring (intracranial pressure, brain tissue oxygen, and cerebral microdialysis). Data were collected at baseline and for 12 h after transfusion. The relationship between hemoglobin (Hb) change and lactate/pyruvate ratio (LPR) orbrain tissue oxygen (PbtO2) was tested using univariate and multivariable analyses. RESULTS: PRBC transfusion was administered on the median post-bleed day 8. The average Hb concentration at baseline was 8.1 g/dL and increased by 2.2 g/dL after transfusion. PbtO2 increased between hours 2 and 4 post-transfusion and this increase was maintained until hour 10. LPR did not change significantly during the 12-h monitoring period. After adjusting for SpO2, cerebral perfusion pressure, and LPR, the change in Hb concentration was independently and positively associated with a change in PbtO2 (adjusted b estimate = 1.39 [95% confidence interval 0.09-2.69]; P = 0.04). No relationship between the change in Hb concentration and LPR was found. CONCLUSIONS: PRBC transfusion resulted in PbtO2 improvement without a clear effect on cerebral metabolism prior to SAH.

Systemic glucose variability predicts cerebral metabolic distress and mortality after subarachnoid hemorrhage: a retrospective observational study.

INTRODUCTION: Cerebral glucose metabolism and energy production are affected by serum glucose levels. Systemic glucose variability has been shown to be associated with poor outcome in critically ill patients. The objective of this study was to assess whether glucose variability is associated with cerebral metabolic distress and outcome after subarachnoid hemorrhage. METHODS: A total of 28 consecutive comatose patients with subarachnoid hemorrhage, who underwent cerebral microdialysis and intracranial pressure monitoring, were studied. Metabolic distress was defined as lactate/pyruvate ratio (LPR) >40. The relationship between daily glucose variability, the development of cerebral metabolic distress and hospital outcome was analyzed using a multivariable general linear model with a logistic link function for dichotomized outcomes. RESULTS: Daily serum glucose variability was expressed as the standard deviation (SD) of all serum glucose measurements. General linear models were used to relate this predictor variable to cerebral metabolic distress and mortality at hospital discharge. A total of 3,139 neuromonitoring hours and 181 days were analyzed. After adjustment for Glasgow Coma Scale (GCS) scores and brain glucose, SD was independently associated with higher risk of cerebral metabolic distress (adjusted odds ratio = 1.5 (1.1 to 2.1), P = 0.02). Increased variability was also independently associated with in hospital mortality after adjusting for age, Hunt Hess, daily GCS and symptomatic vasospasm (P = 0.03). CONCLUSIONS: Increased systemic glucose variability is associated with cerebral metabolic distress and increased hospital mortality. Therapeutic approaches that reduce glucose variability may impact on brain metabolism and outcome after subarachnoid hemorrhage.

Fluid responsiveness and brain tissue oxygen augmentation after subarachnoid hemorrhage.

BACKGROUND: The objective of this study was to investigate the relationship between cardiac index (CI) response to a fluid challenge and changes in brain tissue oxygen pressure (PbtO(2)) in patients with subarachnoid hemorrhage (SAH). METHODS: Prospective observational study was conducted in a neurological intensive care unit of a university hospital. Fifty-seven fluid challenges were administered to ten consecutive comatose SAH patients that underwent multimodality monitoring of CI, intracranial pressure (ICP), and PbtO(2), according to a standardized fluid management protocol. RESULTS: The relationship between CI and PbtO(2) was analyzed with logistic regression utilizing generalized estimating equations. Of the 57 fluid boluses analyzed, 27 (47 %) resulted in a ≥ 10 % increase in CI. Median absolute (+5.8 vs. +1.3 mmHg) and percent (20.7 vs. 3.5 %) changes in PbtO(2) were greater in CI responders than in non-responders within 30 min after the end of the fluid bolus infusion. In a multivariable model, a CI response was independently associated with PbtO(2) response (adjusted odds ratio 21.5, 95 % CI 1.4-324, P = 0.03) after adjusting for mean arterial pressure change and end-tidal CO(2). Stroke volume variation showed a good ability to predict CI and PbtO(2) response with areas under the ROC curve of 0.86 and 0.81 with the best cut-off values of 9 % for both responses. CONCLUSION: Bolus fluid resuscitation resulting in augmentation of CI can improve cerebral oxygenation after SAH.

Dysmorphic features, cognitive disability, chronic inflammation, and predisposition to vascular disease in two sisters: a new autosomal recessive disorder?

A 20-year-old woman presented with mental retardation and a history of stroke related to moyamoya disease at the age of 8 years. She had cognitive impairment which became more pronounced after the stroke. This patient's parents were first cousins and six close family relatives had strokes in their 60s or 70s. The patient's 16-year-old sister had learning disability, chronic muscle pain, and an ECG suggestive of previous hypoxemic heart injury. The two sisters had similar dysmorphic facial appearance including a prominent philtrum, bulbous nose, and severe acne. They both had increased subcutaneous tissue in their faces, whereas their bodies were slim. Both sisters were found to have elevated levels of rheumatoid factor, C-reactive protein, and erythrocyte sedimentation rate on repeat measurements. Partial autoimmunity screening in one of the patients was negative. Chromosome analysis and array comparative genomic hybridization analyses were also normal. Nerve conduction findings in the younger sister were consistent with distal, predominantly motor, demyelinating neuropathy localized to the lower extremities. We propose that these two sisters suffer from a new autosomal recessive syndrome. Carrier status for this condition may predispose to later onset stroke.

Prolonged intracerebral convection-enhanced delivery of topotecan with a subcutaneously implantable infusion pump.

Intracerebral convection-enhanced delivery (CED) of chemotherapeutic agents currently requires an externalized catheter and infusion system, which limits its duration because of the need for hospitalization and the risk of infection. To evaluate the feasibility of prolonged topotecan administration by CED in a large animal brain with the use of a subcutaneous implantable pump. Medtronic Synchromed-II pumps were implanted subcutaneously for intracerebral CED in pigs. Gadodiamide (28.7 mg/mL), with or without topotecan (136 µM), was infused at 0.7 mL/24 h for 3 or 10 days. Pigs underwent magnetic resonance imaging before and at 6 times points after surgery. Enhancement and FLAIR+ volumes were calculated in a semi-automated fashion. Magnetic resonance spectroscopy-based topotecan signature was also investigated. Brain histology was analyzed by hematoxylin and eosin staining and with immunoperoxidase for a microglial antigen. CED of topotecan/gadolinium was well tolerated in all cases (n = 6). Maximum enhancement volume was reached at day 3 and remained stable if CED was continued for 10 days, but it decreased if CED was stopped at day 3. Magnetic resonance spectroscopy revealed a decrease in parenchymal metabolites in the presence of topotecan. Similarly, the combination of topotecan and gadolinium infusion led to a FLAIR+ volume that tended to be larger than that seen after the infusion of gadolinium alone. Histological analysis of the brains showed an area of macrophage infiltrate in the ipsilateral white matter upon infusion with topotecan/gadolinium. Intracerebral topotecan CED is well tolerated in a large animal brain for up to 10 days. Intracerebral long-term CED can be achieved with a subcutaneously implanted pump and provides a stable volume of distribution. This work constitutes a proof of principle for the safety and feasibility for prolonged CED, providing a means of continuous local drug delivery that is accessible to the practicing neuro-oncologist.

Cerebral perfusion pressure thresholds for brain tissue hypoxia and metabolic crisis after poor-grade subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: To identify a minimally acceptable cerebral perfusion pressure threshold above which the risks of brain tissue hypoxia (BTH) and oxidative metabolic crisis are reduced for patients with subarachnoid hemorrhage (SAH). METHODS: We studied 30 poor-grade SAH patients who underwent brain multimodality monitoring (3042 hours). Physiological measures were averaged over 60 minutes for each collected microdialysis sample. Metabolic crisis was defined as a lactate/pyruvate ratio>40 with a brain glucose concentration≤0.7 mmol/L. BTH was defined as PbtO2<20 mm Hg. Outcome was assessed at 3 months with the Modified Rankin Scale. RESULTS: Multivariable analyses adjusting for admission Hunt-Hess grade, intraventricular hemorrhage, systemic glucose, and end-tidal CO2 revealed that cerebral perfusion pressure≤70 mm Hg was significantly associated with an increased risk of BTH (OR, 2.0; 95% CI, 1.2-3.3; P=0.007) and metabolic crisis (OR, 2.1; 95% CI, 1.2-3.7; P=0.007). Death or severe disability at 3 months was significantly associated with metabolic crisis (OR, 5.4; 95% CI, 1.8-16; P=0.002) and BTH (OR, 5.1; 95% CI, 1.2-23; P=0.03) after adjusting for admission Hunt-Hess grade. CONCLUSIONS: Metabolic crisis and BTH are associated with mortality and poor functional recovery after SAH. Cerebral perfusion pressure levels<70 mm Hg was associated with metabolic crisis and BTH, and may increase the risk of secondary brain injury in poor-grade SAH patients.

Effect of mannitol on brain metabolism and tissue oxygenation in severe haemorrhagic stroke.

BACKGROUND: The impact of osmotic therapies on brain metabolism has not been extensively studied in humans. The authors examined if mannitol treatment of raised intracranial pressure will result in an improvement in brain metabolism together with the expected drop in intracranial pressure (ICP). METHODS: This is a retrospective review of prospectively collected data. Twenty episodes of raised ICP (>20 mm Hg) resistant to standard therapy that required infusions of mannitol were studied in 12 comatose patients with multimodality monitoring including ICP, PbtO(2) and microdialysis. The authors compared mean arterial blood pressure, ICP, cerebral perfusion pressure, PbtO(2), brain lactate, pyruvate and glucose using cerebral microdialysis, for 3 h preceding and 4 h after hyperosmolar therapy. Time-series data were analysed using a multivariable general linear model utilising generalised estimating equations for model estimation to account for within-subjects and between-subjects variations over time. RESULTS: 20% mannitol solution (1 g/kg) was administered at the discretion of the attending neurointensivist. ICP decreased 30 min (from 27 ± 13 to 19 ± 16 mm Hg, p<0.001) and cerebral perfusion pressure increased 45 min (from 73 ± 18 to 85 ± 22 mm Hg, p=0.002) after the start of mannitol infusions, whereas mean arterial blood pressure and PbtO(2) did not change significantly. The peak lactate-pyruvate ratio was recorded at the time of initiating osmotherapy (44 ± 20) with an 18% decrease over 2 h following mannitol therapy (35 ± 16; p=0.002). Brain glucose remained unaffected. CONCLUSIONS: Mannitol effectively reduces ICP and appeared to benefit brain metabolism as measured by the lactate-pyruvate ratio.

High-dose intra-arterial verapamil for the treatment of cerebral vasospasm after subarachnoid hemorrhage: prolonged effects on hemodynamic parameters and brain metabolism.

BACKGROUND: Studies attempting to establish the safety and efficacy of standard and high-dose intra-arterial infusions of calcium channel blockers for treatment of cerebral vasospasm have focused on hemodynamic changes during the angiographic procedure. OBJECTIVE: To evaluate longer-term drug effects over the hours following infusion and the effects on brain tissue oxygen tension or cerebral metabolism. METHODS: We studied 11 patients with poor-grade aneurysmal subarachnoid hemorrhages who underwent multimodality brain monitoring and angiography with infusion of high-dose intra-arterial verapamil (≥15 mg total dose). Hourly intracerebral microdialysis measurements and continuously recorded mean arterial pressure (MAP), intracranial pressure (ICP), cerebral perfusion pressure (CPP), and Pbto2 were analyzed for 6 hours before and 12 hours following treatment. RESULTS: A median dose of 23 mg (range, 15-55 mg) of intra-arterial verapamil was given. Compared with baseline values, reductions in CPP and MAP were maximal at 3 hours postangiography (from 105 ± 13 mm Hg to 95 ± 15 mm Hg and from 116 ± 12 mm Hg to 106 ± 16 mm Hg, P < .01) and persisted for up to 6 hours (P < .04); increases in vasopressor therapy were required in 8 procedures (53%). ICP significantly increased during the first 3 hours post angiography (P < .03). Brain glucose increased by 33% by hour 9 (P < .001). There were no significant changes in Pbto2 or the lactate/pyruvate ratio. CONCLUSION: High-dose intra-arterial verapamil causes increases in ICP and reductions in CPP, followed by an increase in brain glucose levels, without altering brain oxygen tension or oxidative metabolism. Patients undergoing high-dose intra-arterial verapamil therapy warrant close hemodynamic and ICP monitoring for at least 12 hours following treatment.

Intracortical EEG for the detection of vasospasm in patients with poor-grade subarachnoid hemorrhage.

BACKGROUND: To study the feasibility of utilizing intracortical electroencephalography (ICE) including quantitative EEG (qEEG) analysis for the detection of vasospasm in five consecutive poor-grade SAH patients. METHODS: Intracortical electroencephalography (ICE) was obtained via a single miniature parenchymal 8-contact depth electrode placed at the bedside. Quantitative EEG parameters, calculated on surface EEG and ICE, included alpha/delta ratio (ADR), mean amplitude, suppression percent, and total power. Percent changes between averaged values over 4-6 h of baseline EEG and EEG prior to angiography were calculated. The entire continuous qEEG recording for each patient was then reviewed to determine optimal automated alarm criteria. RESULTS: ICE ADR was the most accurate for predicting angiographic vasospasm (5/5). ICE ADR decreased between baseline and follow-up by 42% (from 0.56 ± 0.07 to 0.32 ± 0.03) for those with vasospasm (N = 3) compared to 17% (0.62 ± 0.06 to 0.51 ± 0.03) for those without (N = 2). A sustained decrease in the ICE ADR from baseline (>25% for ≥ 4 h) occurred in all three patients with angiographically confirmed vasospasm and not in the two without; this decline occurred 1-3 days prior to angiographic confirmation. CONCLUSIONS: Intracortical EEG is promising for detecting ischemia from vasospasm in poor-grade SAH patients, may be superior to scalp EEG, and allow automated detection, particularly using the ADR. Larger studies are needed to better define the effectiveness of this approach.

Relationship between brain interstitial fluid tumor necrosis factor-α and cerebral vasospasm after aneurysmal subarachnoid hemorrhage.

Tumor necrosis factor-alpha (TNF-alpha) has a crucial role in the onset of hemolysis-induced vascular injury and cerebral vasoconstriction. We hypothesized that TNF-alpha measured from brain interstitial fluid would correlate with the severity of vasospasm following aneurysmal subarachnoid hemorrhage (aSAH). From a consecutive series of 10 aSAH patients who underwent cerebral microdialysis (MD) and evaluation of vasospasm by CT angiogram (CTA) or digital subtraction angiography (DSA), TNF-alpha levels from MD were measured at 8-hour intervals from aSAH days 4-6 using enzyme-linked immunosorbent assay. An attending neuroradiologist blinded to the study independently evaluated each CTA and DSA and assigned a vasospasm index (VI). Five patients had a VI<2 and 5 patients had a VI>2, where the median VI was 2 (range 0-13). The median log TNF-alpha area under the curve (AUC) was 1.64pg/mL *day (interquartile range 1.48-1.71) for the VI<2 group, and 2.11pg/mL *day (interquartile range 1.95-2.47) for the VI>2 group (p<0.01). Thus, in this small series of poor-grade aSAH patients, the AUC of TNF-alpha levels from aSAH days 4-6 correlates with the severity of radiographic vasospasm. Further analysis in a larger population is warranted based on our preliminary findings.

Anemia is associated with metabolic distress and brain tissue hypoxia after subarachnoid hemorrhage.

BACKGROUND: Anemia is frequently encountered in critically ill patients and adversely affects cerebral oxygen delivery and brain tissue oxygen (PbtO2). The objective of this study is to assess whether there is an association between anemia and metabolic distress or brain tissue hypoxia in patients with subarachnoid hemorrhage. METHODS: Retrospective study was conducted in a neurological intensive care unit in a university hospital. Patients with subarachnoid hemorrhage that underwent multimodality monitoring with intracranial pressure, PbtO2 and microdialysis were analyzed. The relationships between hemoglobin (Hb) concentrations and brain tissue hypoxia (PbtO2 < or = 15 mmHg) and metabolic distress (lactate/pyruvate ratio > or =40) were analyzed with general linear models of logistic function for dichotomized outcomes utilizing generalized estimating equations. RESULTS: A total of 359 matched neuromonitoring hours and Hb measurements were analyzed from 34 consecutive patients. The median hemoglobin was 9.7 g/dl (interquartile range 8.8-10.5). After adjusting for significant covariates, reduced hemoglobin concentration was associated with a progressively increased risk of brain tissue hypoxia (adjusted OR 1.7 [1.1-2.4]; P = 0.01 for every unit decrease). Also after adjusting for significant covariates, hemoglobin concentrations below 9 g/dl and between 9.1 and 10 g/dl were associated with an increased risk of metabolic distress as compared to concentrations between 10.1 and 11 g/dl (adjusted OR 3.7 [1.5-9.4]; P = 0.004 for Hb < or = 9 g/dl and adjusted OR 1.9 [1.1-3.3]; P = 0.03 for Hb 9.1-10 g/dl). CONCLUSIONS: Anemia is associated with a progressively increased risk of cerebral metabolic distress and brain tissue hypoxia after subarachnoid hemorrhage.

Systemic glucose and brain energy metabolism after subarachnoid hemorrhage.

BACKGROUND: Brain energy metabolic crisis (MC) and lactate-pyruvate ratio (LPR) elevations have been linked to poor outcome in comatose patients. We sought to determine if MC and LPR elevations after subarachnoid hemorrhage (SAH) are associated with acute reductions in serum glucose. METHODS: Twenty-eight consecutive comatose SAH patients that underwent multimodality monitoring with intracranial pressure and microdialysis were studied. MC was defined as lactate/pyruvate ratio (LPR) > or = 40 and brain glucose < 0.7 mmol/l. Time-series data were analyzed using a multivariable general linear model with a logistic link function for dichotomized outcomes. RESULTS: Multimodality monitoring included 3,178 h of observation (mean 114 +/- 65 h per patient). In exploratory analysis, serum glucose significantly decreased from 8.2 +/- 1.8 mmol/l (148 mg/dl) 2 h before to 6.9 +/- 1.9 mmol/l (124 mg/dl) at the onset of MC (P < 0.001). Reductions in serum glucose of 25% or more were significantly associated with new onset MC (adjusted odds ratio [OR] 3.6, 95% confidence interval [CI] 2.2-6.0). Acute reductions in serum glucose of 25% or more were also significantly associated with an LPR rise of 25% or more (adjusted OR 1.6, 95% CI 1.1-2.4). All analyses were adjusted for significant covariates including Glasgow Coma Scale and cerebral perfusion pressure. CONCLUSIONS: Acute reductions in serum glucose, even to levels within the normal range, may be associated with brain energy metabolic crisis and LPR elevation in poor-grade SAH patients.

Intracranial multimodal monitoring for acute brain injury: a single institution review of current practices.

BACKGROUND: Critical care management of patients with severe acute brain injury has undergone tremendous advances. Neurosurgeons and neurointensivists have a large armamentarium of invasive monitoring devices available to help detect secondary brain injury and guide therapy. No consensus exists regarding patient specific selection of monitoring devices, the placement of devices in relation to injured brain tissue, or the preferred insertion technique. Here we review our experience in a consecutive series of acutely brain injured patients who underwent multimodality monitoring. METHODS: Sixty-one patients admitted to the Neurological Intensive Care Unit underwent multimodality intracranial monitoring between January 2005 and October 2008. Patient demographics, hospital length of stay, types of monitoring devices and modalities monitored, insertion techniques, device placement location relative to injury, and complications are reported. RESULTS: Monitored modalities included brain tissue oxygen (PbtO(2)) in 97% (N = 59), microdialysis (MD) in 79% (N = 48), intracranial electroencephalography in 31% (N = 19), brain temperature in 18% (N = 11), and cerebral blood flow in 11% (N = 7). On average, monitoring started within 2 days (0-8) of admission and was continued for 7 days (1-17). The majority of probes (56%; N = 35) were placed into patients with focal brain injuries, while in 43% N = 26 the injury was diffuse. Among those with focal injury, probe placement was categorized as peri-lesional in 46% (N = 16), and within a clot or infarct in 17% (N = 6). The most frequent complication of multimodality brain monitoring was device malfunction or dislodgement (43%; N = 26). Rates of hematoma and infection were 3 and 5%, respectively. Average NICU length of stay was 17 days (3-48) and 26% (N = 16) of patients were dead at discharge. CONCLUSIONS: Collaboration among institutions is necessary to establish practice guidelines for the choice and placement of multimodal monitors. Further advancement in device technology is needed to improve insertion techniques, inter-device compatibility, and device durability. Multimodality data needs to be analyzed to determine the preferable device location.

Intracortical electroencephalography in acute brain injury.

OBJECTIVE: Continuous electroencephalography (EEG) is used in patients with neurological injury to detect electrographic seizures and clinically important changes in brain function. Scalp EEG has poor spatial resolution, is often contaminated by artifact, and frequently demonstrates activity that is suspicious for but not diagnostic of ictal activity. We hypothesized that bedside placement of an intracortical multicontact electrode would allow for improved monitoring of cortical potentials in critically ill neurological patients. METHODS: Sixteen individuals with brain injury, requiring invasive neuromonitoring, underwent implantation of an eight-contact minidepth electrode. RESULTS: Intracortical EEG (ICE) was successfully performed and compared with scalp EEG in 14 of these 16 individuals. ICE provided considerable improvement in signal-to-noise ratio compared with surface EEG, demonstrating clinically important findings in 12 of 14 patients (86%) including electrographic seizures (n = 10) and acute changes related to secondary neurological injury (n = 2, 1 ischemia, 1 hemorrhage). In patients with electrographic seizures detected by ICE, scalp EEG demonstrated no concurrent ictal activity in six, nonictal-appearing rhythmic delta in two, and intermittently correlated ictal activity in two. In two patients with secondary neurological complications, ICE demonstrated prominent attenuation 2 to 6 hours before changes in other neuromonitoring modalities and more than 8 hours before the onset of clinical deterioration. INTERPRETATION: ICE can provide high-fidelity intracranial EEG in an intensive care unit setting, can detect ictal discharges not readily apparent on scalp EEG, and can identify early changes in brain activity caused by secondary neurological complications. We predict that ICE will facilitate the development of EEG-based alarm systems and lead to prevention of secondary neuronal injury.

Neurostimulation techniques for painful peripheral nerve disorders.

Disorders of the peripheral nervous system often present a unique challenge to the clinician or surgeon, because the neuropathic pain associated with them can be extremely resistant to typical pain treatments. Painful peripheral nerve disorders often have pain in a particular peripheral nerve distribution, and thus an optimal treatment modality is one that delivers targeted relief to the precise distribution of the pain. To that end, peripheral nerve stimulation (PNS) has undergone several refinements in recent years. New types of stimulation, such as techniques for cranial nerve stimulation and spinal nerve root stimulation (SNRS), have enabled the treatment of painful peripheral nerve problems that until fairly recently were either untreatable or poorly treated with traditional spinal cord stimulation (SCS) techniques. In this article, PNS techniques are described in detail for the stimulation of the occipital and trigeminal nerves for intractable craniofacial pain, as well as emerging techniques for the selective stimulation of spinal nerve roots and subcutaneous peripheral nerve stimulation. The increasing spectrum of disorders and pain syndromes amenable to PNS also is discussed.

Novel use of a custom stereotactic frame for placement of depth electrodes for epilepsy monitoring.

The authors describe the first reported application of a miniature, customized, one-time use, skull-mounted stereotactic frame for the implantation of depth electrodes for epilepsy monitoring. Using a platform template, 4 skull fiducial markers were placed 1 week prior to surgery. A brain MR image and a CT scan were subsequently obtained. All planning (longitudinal trajectories into the hippocampi) was done preoperatively using personal computers in the office. No further workstation planning was necessary on the day of the operation. The StarFix microTargeting Platform system was secured to the previously implanted skull fiducial screws. Pin fixation was not required. The platform was used to identify the area of entry for the depth electrodes on the right and left sides. On each side, a 12-contact depth electrode was advanced to the depth of the targets without difficulty. A temporal craniotomy was then performed to place subdural electrodes. The desired location of the electrodes was confirmed on postoperative imaging studies. There were no complications associated with the electrode implantation. The depth electrodes demonstrated symmetrical, robust coverage of each hippocampus, with epileptiform discharges observed bilaterally. This first application of the StarFix platform for placing depth electrodes for epilepsy monitoring was both safe and feasible. With this technique, the patient does not need to be pinned or placed in a head holder, no imaging or computer planning is required on the day of implantation (which means there is no time pressure when the meticulous target/trajectory planning is done), and with bilateral posterior implants both bur holes can be made simultaneously. For these reasons this system may be preferable to existing methods of depth electrode implantation.

Effect of antibiotic-impregnated shunt catheters in decreasing the incidence of shunt infection in the treatment of hydrocephalus.

OBJECT: The majority of shunt infections occur within 6 months of shunt placement and chiefly result from perioperative colonization of shunt components by skin flora. Antibiotic-impregnated shunt (AIS) systems have been designed to prevent such colonization. In this study, the authors evaluate the incidence of shunt infection after introduction of an AIS system in a population of children with hydrocephalus. METHODS: The authors retrospectively reviewed all pediatric patients who had undergone cerebrospinal fluid (CSF) shunt insertion at their institution over a 3-year period between April 2001 and March 2004. During the 18 months prior to October 2002, all CSF shunts included standard, nonimpregnated catheters. During the 18 months after October 2002, all CSF shunts included antibiotic-impregnated catheters. All patients were followed up for 6 months after shunt surgery, and all shunt-related complications, including shunt infection, were evaluated. The independent association of AIS catheter use with subsequent shunt infection was assessed via multivariate proportional hazards regression analysis. A total of 211 pediatric patients underwent 353 shunt placement procedures. In the 18 months prior to October 2002, 208 (59%) shunts were placed with nonimpregnated catheters; 145 (41%) shunts were placed with AIS catheters in the 18 months after October 2002. Of patients with nonimpregnated catheters, 25 (12%) experienced shunt infection, whereas only two patients (1.4%) with antibiotic-impregnated catheters experienced shunt infection within the 6-month follow-up period (p < 0.01). Adjusting for intercohort differences via multivariate analysis, AIS catheters were independently associated with a 2.4-fold decreased likelihood of shunt infection. CONCLUSIONS: The AIS catheter significantly reduced incidence of CSF shunt infection in children with hydrocephalus during the early postoperative period (< 6 months). The AIS system used is an effective instrument to prevent perioperative colonization of CSF shunt components.

An electrophysiologic model for functional assessment of effects of neurotrophic factors on facial nerve reinnervation.

OBJECTIVES: To establish a sound objective model for assessing the effects of neurotrophic factors on facial nerve function after injury and to compare the effects of brain-derived neurotrophic factor (BDNF) with its neutralizing antibody on facial nerve function after injury. DESIGN: Prospective electrophysiologic analysis of recovery of function 4 weeks after axotomy involving facial nerve transection and primary end-to-end reanastomosis in adult rats and blind comparison with randomized intramuscular injection of either BDNF, monoclonal antibody to BDNF in neutralizing concentration, or control solution. RESULTS: There were no statistically significant differences between groups in latencies, duration, amplitude, area, or conduction velocity before axotomy, and recorded conduction velocities were consistent with previously reported values, which suggests that the recordings were reliable and reproducible. After transection, there was a mean increase in latency 1 and decreases in latency 2, integrated average area, muscle action potential duration, amplitude, and conduction velocity for all 3 groups. When the groups were compared after transection, the anti-BDNF group showed a significant decrease in conduction velocity and muscle action potential duration (Kruskal-Wallis P = .01 and P = .008, respectively) compared with the other groups. There were no statistically significant differences in latencies, amplitude, or area among the groups. CONCLUSIONS: We have established an electrophysiologic model for objective assessment of facial nerve function in the rat. Future studies should combine functional electrophysiologic assessment and histologic examination to provide a more robust model for studying the effects of neurotrophic factors on facial nerve reinnervation and synkinesis.