Search

Purpose Recurrent lumbar disk herniation (rLDH) following lumbar microdiscectomy is common. While several risk factors for primary LDH have been described, risk factors for rLDH have only sparsely been investigated. We evaluate the effect of Body mass index (BMI) and smoking on the incidence and timing of rLDH. Methods From a prospective registry, we identified all patients undergoing primary tubular microdiscectomy (tMD), with complete BMI and smoking data, and a minimum 12-month follow-up. We defined rLDH as reherniation at the same level and side requiring surgery. Overweight was defined as BMI > 25, and obesity as BMI > 30. Intergroup comparisons and age- and gender-adjusted multivariable regression were carried out. We conducted a survival analysis to assess the influence of BMI and smoking on time to reoperation. Results Of 3012 patients, 166 (5.5%) underwent re-microdiscectomy for rLDH. Smokers were reoperated more frequently (6.4% vs. 4.0%, p = 0.007). Similarly, rLDH was more frequent in obese (7.5%) and overweight (5.9%) than in normal-weight patients (3.3%, p = 0.017). Overweight smokers had the highest rLDH rate (7.6%). This effect of smoking (Odds ratio: 1.63, 96% CI: 1.12–2.36, p = 0.010) and BMI (Odds ratio: 1.09, 95% CI: 1.02–1.17, p = 0.010) persisted after controlling for age and gender. Survival analysis demonstrated that rLDH did not occur earlier in overweight patients and/or smokers. Conclusions BMI and smoking may directly contribute to a higher risk of rLDH, but do not accelerate rLDH development. Smoking cessation and weight loss in overweight or obese patients ought to be recommended with discectomy to reduce the risk for rLDH.

Recurrent lumbar disk herniation (rLDH) following lumbar microdiscectomy is common. While several risk factors for primary LDH have been described, risk factors for rLDH have only sparsely been investigated. We evaluate the effect of Body mass index (BMI) and smoking on the incidence and timing of rLDH.From a prospective registry, we identified all patients undergoing primary tubular microdiscectomy (tMD), with complete BMI and smoking data, and a minimum 12-month follow-up. We defined rLDH as reherniation at the same level and side requiring surgery. Overweight was defined as BMI 25, and obesity as BMI 30. Intergroup comparisons and age- and gender-adjusted multivariable regression were carried out. We conducted a survival analysis to assess the influence of BMI and smoking on time to reoperation.Of 3012 patients, 166 (5.5%) underwent re-microdiscectomy for rLDH. Smokers were reoperated more frequently (6.4% vs. 4.0%, p = 0.007). Similarly, rLDH was more frequent in obese (7.5%) and overweight (5.9%) than in normal-weight patients (3.3%, p = 0.017). Overweight smokers had the highest rLDH rate (7.6%). This effect of smoking (Odds ratio: 1.63, 96% CI: 1.12-2.36, p = 0.010) and BMI (Odds ratio: 1.09, 95% CI: 1.02-1.17, p = 0.010) persisted after controlling for age and gender. Survival analysis demonstrated that rLDH did not occur earlier in overweight patients and/or smokers.BMI and smoking may directly contribute to a higher risk of rLDH, but do not accelerate rLDH development. Smoking cessation and weight loss in overweight or obese patients ought to be recommended with discectomy to reduce the risk for rLDH.

Object Traumatic brain injury (TBI) is a leading cause of injury, hospitalization, and death among pediatric patients. Admission CT scans play an important role in classifying TBI and directing clinical care, but little is known about the differences in CT findings between pediatric and adult patients. The aim of this study was to determine if radiographic differences exist between adult and pediatric TBI. Methods The authors retrospectively analyzed TBI registry data from 1206 consecutive patients with nonpenetrating TBI treated at a Level 1 adult and pediatric trauma center over a 30-month period. Results The distribution of sex, race, and Glasgow Coma Scale (GCS) score was not significantly different between the adult and pediatric populations; however, the distribution of CT findings was significantly different. Pediatric patients with TBI were more likely to have skull fractures (OR 3.21, p < 0.01) and epidural hematomas (OR 1.96, p < 0.01). Pediatric TBI was less likely to be associated with contusion, subdural hematoma, subarachnoid hemorrhage, or compression of the basal cisterns (p < 0.05). Rotterdam CT scores were significantly lower in the pediatric population (2.3 vs 2.6, p < 0.001). Conclusions There are significant differences in the CT findings in pediatric versus adult TBI, despite statistical similarities with regard to clinical severity of injury as measured by the GCS. These differences may be due to anatomical characteristics, the biomechanics of injury, and/or differences in injury mechanisms between pediatric and adult patients. The unique characteristics of pediatric TBI warrant consideration when formulating a clinical trial design or predicting functional outcome using prognostic models developed from adult TBI data.

Object Decompressive craniectomy plays an important role in the management of patients with traumatic brain injury (TBI) and stroke. Risks of decompressive craniectomy include those associated with cranioplasty, and may be related to adhesions that develop between the brain surface and overlying scalp and temporalis muscle. The authors report their institutional experience using a multilayered technique (collagen and gelatin film barriers) to facilitate safe and rapid cranioplasty following decompressive craniectomy. Methods The authors conducted a retrospective chart review of 62 consecutive adult and pediatric patients who underwent decompressive craniectomy and subsequent cranioplasty between December 2007 and January 2011. Diagnoses included TBI, ischemic stroke, intraparenchymal hemorrhage, or subarachnoid hemorrhage. A detailed review of clinical charts was performed, including anesthesia records and radiographic study results. Results The majority of patients underwent unilateral hemicraniectomy (n = 56), with indications for surgery including midline shift (n = 37) or elevated intracranial pressure (n = 25). Multilayered decompressive craniectomy was safe and easy to perform, and was associated with a low complication rate, minimal operative time, and limited blood loss. Conclusions Decompressive craniectomy repair using an absorbable gelatin film barrier facilitates subsequent cranioplasty by preventing adhesions between intracranial contents and the overlying galea aponeurotica and temporalis muscle fascia. This technique makes cranioplasty dissection faster and potentially safer, which may improve clinical outcomes. The indications for gelatin film should be expanded to include placement in the epidural space after craniectomy.

More than 5,000,000 survivors of traumatic brain injury (TBI) live with persistent cognitive deficits, some of which likely derive from hippocampal dysfunction. Oscillatory activity in the hippocampus is critical for normal learning and memory functions, and can be modulated using deep brain stimulation techniques. In this pre-clinical study, we demonstrate that lateral fluid percussion TBI results in the attenuation of hippocampal theta oscillations in the first 6 days after injury, which correlate with deficits in the Barnes maze spatial working memory task. Theta band stimulation of the medial septal nucleus (MSN) results in a transient increase in hippocampal theta activity, and when delivered 1 min prior to training in the Barnes maze, it significantly improves spatial working memory. These results suggest that MSN theta stimulation may be an effective neuromodulatory technique for treatment of persistent learning and memory deficits after TBI.

Incisional cerebrospinal fluid (CSF) leakage after cranial surgery is a significant cause of morbidity due to poor wound healing and infection, meningitis, and pseudomeningocele formation. Many common dural closure techniques, such as sutures, autologous grafts, gelatin or collagen sponges, and fibrin glues, are used to achieve watertight closure, although none are US Food and Drug Administration approved for this use. DuraSeal Dural Sealant System is a polyethylene glycol (PEG) hydrogel approved by the U.S. Food and Drug Administration for obtaining watertight dural closure when applied after standard dural suturing. This multicenter, prospective randomized study further evaluated the safety of a PEG hydrogel compared with common dural sealing techniques.A total of 237 patients undergoing elective cranial surgery at 17 institutions were randomized to dural closure augmented with the PEG hydrogel or a control "standard of care" dural sealing technique after Valsalva maneuver demonstrated an intraoperative nonwatertight dural closure. Data were collected on complications resulting in unplanned postoperative interventions or reoperations, surgical site infections, CSF leaks, and other neurological complications within 30 days. Surgeons also provided data on the ease of use of the dural sealing techniques, as well as preparation and application times.The incidences of neurosurgical complications, surgical site infections, and CSF leaks were similar between treatment and control groups, with no statistically significant difference between the measures. In the PEG hydrogel group (n = 120), the incidence of neurosurgical complications was 5.8% (n = 7), the incidence of surgical site infections was 1.7% (n = 2), and the incidence of CSF leak was 0.8% (n = 1). In the control group (n = 117), the incidence of neurosurgical complications was 7.7% (n = 9), the incidence of surgical site infection was 2.6% (n = 3), and the incidence of CSF leak was 1.7% (n = 2). Sealant preparation time was less than 5 minutes in 96.6% of the PEG hydrogel group compared with 66.4% of controls (P

Object Posttraumatic vasospasm (PTV) is an underrecognized cause of ischemic damage after severe traumatic brain injury (TBI) that independently predicts poor outcome. There are, however, no guidelines for PTV screening and management, partly due to limited understanding of its pathogenesis and risk factors. Methods A database review of 46 consecutive cases of severe TBI in pediatric and adult patients was conducted to identify risk factors for the development of PTV. Univariate analysis was performed to identify potential risk factors for PTV, which were subsequently analyzed using a multivariate logistic regression model to calculate odds ratios (ORs) and 95% confidence intervals (CIs). Results Fever on admission was an independent risk factor for development of PTV (OR 22.2, 95% CI 1.9–256.8), and patients with hypothermia on admission did not develop clinically significant vasospasm during their hospital stay. The presence of small parenchymal contusions was also an independent risk factor for PTV (OR 7.8, 95% CI 0.9–69.5), whereas the presence of subarachnoid hemorrhage or other patterns of intracranial injury were not. Other variables, such as age, sex, ethnicity, degree of TBI severity, or admission laboratory values, were not independent predictors for the development of clinically significant PTV. Conclusions Independent risk factors for PTV include parenchymal contusions and fever. These results suggest that diffuse mechanical injury and activation of inflammatory pathways may be underlying mechanisms for the development of PTV, and that a subset of patients with these risk factors may be an appropriate population for aggressive screening. Further studies are needed to determine if treatments targeting fever and inflammation may be effective in reducing the incidence of vasospasm following severe TBI.

Anemia is recognized as a possible cause of secondary injury following traumatic brain injury (TBI). Cogent arguments can be made for both liberal and restrictive blood transfusion practices in this setting. In this narrative review, we summarize available knowledge regarding the risks of anemia and transfusion in patients with TBI. Laboratory studies using animal models and healthy human subjects suggest that anemia below a hemoglobin (Hb) concentration of 7 g/dL results in impaired brain function and below 10 g/dL may be detrimental to recovery from TBI. Clinical studies that have evaluated the association of anemia with clinical outcomes have not consistently demonstrated harm, but they generally have important methodological weaknesses. Alternatively, studies that have analyzed transfusion as a predictor of worse outcome have consistently identified such an association, but these studies may involve residual confounding. What little information exists from randomized trials that have included patients with TBI and evaluated liberal versus restrictive transfusion strategies is inconclusive. Since anemia in the setting of TBI is relatively common and there is considerable variation in transfusion preferences, greater study of this topic - preferably with one or more rigorous, adequately powered, non-inferiority randomized trials - is desirable.

Chronic memory deficits are a major cause of morbidity following traumatic brain injury (TBI). In the rat, the hippocampal theta rhythm is a well-studied correlate of memory function. This study sought to investigate disturbances in hippocampal theta rhythm following lateral fluid percussion injury in the rat. A total of 13 control rats and 12 TBI rats were used. Electrodes were implanted in bilateral hippocampi and an electroencephalogram (EEG) was recorded while the rats explored a new environment, and also while navigating a modified version of the Barnes maze. Theta power and peak theta frequency were significantly attenuated in the injured animals. Further, injured rats were less likely to develop a spatial strategy for Barnes maze navigation compared to control rats. In conclusion, rats sustaining lateral fluid percussion injury demonstrated deficits in hippocampal theta activity. These deficits may contribute to the underlying memory problems seen in chronic TBI.

Significant progress has been made in lumbar and cervical disc replacement therapy. Several cervical disc prostheses have recently gained FDA approval. Although arthroplasty has not been previously described in the thoracic spine, selected patients with long-segment fusion to the level of C-7 have altered cervicothoracic and upper thoracic biomechanics and may benefit from motion-preservation therapy for T1–2 disc herniation. Currently, FDA-approved prostheses are indicated only for patients with single-level degenerative disc disease between C-3 and C-7 and no history of cervical arthrodesis. The authors describe a 52-year-old woman who had previously undergone C3–7 fusion and returned 4 years later with symptoms of C-8 myeloradiculopathy and radiological evidence of T1–2 degenerative disc disease. She underwent T1–2 arthroplasty in which a Prestige artificial cervical disc was placed via an anterior cervicothoracic approach. Motion at C7–T1 and T1–2 was preserved, and the patient made an excellent clinical recovery.

Background and Purpose— In clinical trials and observational studies there is considerable inconsistency in the use of definitions to describe delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage. A major cause for this inconsistency is the combining of radiographic evidence of vasospasm with clinical features of cerebral ischemia, although multiple factors may contribute to DCI. The second issue is the variability and overlap of terms used to describe each phenomenon. This makes comparisons among studies difficult. Methods— An international ad hoc panel of experts involved in subarachnoid hemorrhage research developed and proposed a definition of DCI to be used as an outcome measure in clinical trials and observational studies. We used a consensus-building approach. Results— It is proposed that in observational studies and clinical trials aiming to investigate strategies to prevent DCI, the 2 main outcome measures should be: (1) cerebral infarction identified on CT or MRI or proven at autopsy, after exclusion of procedure-related infarctions; and (2) functional outcome. Secondary outcome measure should be clinical deterioration caused by DCI, after exclusion of other potential causes of clinical deterioration. Vasospasm on angiography or transcranial Doppler can also be used as an outcome measure to investigate proof of concept but should be interpreted in conjunction with DCI or functional outcome. Conclusion— The proposed measures reflect the most relevant morphological and clinical features of DCI without regard to pathogenesis to be used as an outcome measure in clinical trials and observational studies.

Acute elevation in intracellular calcium ([Ca(2+)](i)) following traumatic brain injury (TBI) can trigger cellular mechanisms leading to neuronal dysfunction and death. The mechanisms underlying these processes are not completely understood, but calcium influx through N-type voltage-gated calcium channels (VGCCs) appears to play a central role. The present study examined the time course of [Ca(2+)](i) flux, glutamate release, and loss of cell viability following injury using an in vitro neuronal-glial cortical cell-culture model of TBI. The effects of N-channel blockade with SNX-185 (e.g. omega-conotoxin TVIA) before or after injury were also examined. Neuronal injury produced a transient elevation in [Ca(2+)](i), increased glutamate release, and resulted in neuronal and glial death. SNX-185 administered before or immediately after cell injury reduced glutamate release and increased the survival of neurons and astrocytes, whereas delayed treatment did not improve cell survival but significantly facilitated the return of [Ca(2+)](i) to baseline levels. The new findings that N-type VGCCs are critically involved in injury-induced glutamate release and recovery of [Ca(2+)](i) argue for continued investigation of this treatment strategy for the clinical management of TBI. In particular, SNX-185 may represent an effective class of drugs that can significantly protect injured neurons from the secondary insults that commonly occur after TBI.

Posttraumatic vasospasm (PTV) is a relatively common event following traumatic brain injury (TBI) that has been strongly correlated with worse neurological outcome in many studies. However, vasospasm continues to be an under-recognized source of secondary injury following TBI, and currently published guidelines do not address screening or management strategies for PTV. Brain tissue oxygen (P(bt)O(2)) monitoring probes allow for continuous screening for cerebral hypoxia following TBI, but their use as a monitor for PTV has not been previously described.Case report and literature review.We present a case of PTV identified by persistent low P(bt)O(2) despite aggressive medical therapy. Computed tomography and digital subtraction angiography confirmed severe cerebral arterial vasospasm involving both anterior and posterior circulations. The patient was successfully treated with serial intraarterial therapy including balloon angioplasty and verapamil infusion.Posttraumatic vasospasm should be included in the differential diagnosis of cerebral hypoxia (e.g., low P(bt)O(2)) following TBI. Management strategies for PTV may include early, aggressive intraarterial therapies including drug infusion and balloon angioplasty.

Background and Purpose— Cerebral vasospasm continues to be a major cause of poor outcome in patients with ruptured aneurysms. Prophylactic Transluminal Balloon Angioplasty (pTBA) appeared to prevent delayed ischemic neurological deficit in a pilot study. A phase II multicenter randomized clinical trial was subsequently designed. Methods— One hundred and seventy patients with Fisher Grade III subarachnoid hemorrhage were enrolled in the study. Of these, 85 patients were randomized to the treatment group and underwent pTBA within 96 hours after subarachnoid hemorrhage. Main end points of the study included the 3-month dichotomized Glasgow Outcome Score (GOS), development of delayed ischemic neurological deficit (DIND), occurrence of Transcranial Doppler (TCD) vasospasm, and length of stay in the ICU and hospital. Results— The incidence of DIND was lower in the pTBA group ( P =0.30) and fewer patients required therapeutic angioplasty to treat DIND ( P =0.03). Overall pTBA resulted in an absolute risk reduction of 5.9% and a relative risk reduction of 10.4% unfavorable outcome ( P =0.54). Good grade patients had absolute and relative risk reductions of respectively 9.5 and 29.4% ( P =0.73). Length of stay in ICU and hospital was similar in both groups. Four patients had a procedure-related vessel perforation, of which three patients died. Conclusions— While the trial is unsuccessful as defined by the primary end point (GOS), proof of concept is confirmed by these results. Fewer patients tend to develop vasospasm after treatment with pTBA and there is a statistically significantly decreased need for therapeutic angioplasty. pTBA does not improve the poor outcome of patients with Fisher grade III subarachnoid hemorrhage.

OBJECTIVE: To determine whether moderate hypothermia (HYPO) (32-33°C) begun in the early period after severe traumatic brain injury (TBI) and maintained for 48 hours is safe compared with normothermia (NORM) (36.5-37.5°C). METHODS: After severe (Glasgow Coma Scale score ≤8) nonpenetrating TBI, 48 children less than 13 years of age admitted within 6 hours of injury were randomized after stratification by age to moderate HYPO (32-33°C) treatment in conjunction with standardized head injury management versus NORM in a multicenter trial. An additional 27 patients were entered into a parallel single-institution trial of excluded patients because of late transfer or consent (delayed in transfer >6 h but within 24 h of admission), unknown time of injury (e.g., child abuse), and adolescence (e.g., aged 13-18 yr). Assessments of safety included mortality, infection, coagulopathy, arrhythmias, and hemorrhage as well as ability to maintain target temperature, mean intracranial pressure (ICP), and percent time of ICP less than 20 mm Hg during the cooling and subsequent rewarming phases. Additionally, assessments of neurocognitive outcomes were obtained at 3 and 6 months of follow-up. RESULTS: Moderate HYPO after severe TBI in children was found to be safe relative to standard management and NORM in children of all ages and in children with delay of initiation of treatment up to 24 hours. Although there was decreased mortality in HYPO in both studies, there was an increased potential for arrhythmias with HYPO, although they were manageable with fluid administration or rewarming. Additionally, there was a reduction in mean ICP during the first 72 hours after injury in both studies, although rebound ICP elevations in HYPO compared with those in NORM were noted for up to 10 to 12 hours after rewarming. Although functional outcome at 3 or 6 months did not differ between treatment groups, functional outcome tended to improve from the 3- to 6-month cognitive assessment in HYPO compared with NORM, although the sample size was too small for any definitive conclusions. CONCLUSION: HYPO is likely a safe therapeutic intervention for children after severe TBI up to 24 hours after injury. Further studies are necessary and warranted to determine its effect on functional outcome and intracranial hypertension.

The behavioral and histological effects of the lateral fluid percussion (LFP) brain injury model were compared with the weight drop impact-acceleration model with 10 min of secondary hypoxia (WDIA + H). LFP injury resulted in significant motor deficits on the beam walk and inclined plane, and memory deficits on the radial arm maze and Morris water maze. Motor deficits following LFP remained throughout 6 weeks of behavioral testing. WDIA + H injury produced significant motor deficits on the beam walk and inclined plane immediately following injury, but these effects were transient and recovered by 14 days post-injury. In contrast to the LFP injury, the WDIA + H injured animals showed no memory deficits on the radial arm maze and Morris water maze. In order to determine if the differences in behavioral outcome between models were due to differences in injury mechanism or injury severity, 10 LFP-injured animals were matched with 10 WDIA-injured animals based on injury severity (i.e., time to regain righting reflex after brain injury). The LFP-matched injury group showed greater impairment than the WDIA + H matched injury group on the radial arm maze and Morris water maze. Histological examination of LFP-injured brains with Fluoro-Jade staining 24 h, 48 h, and 7 days post-injury revealed degenerating neurons in the cortex, thalamus, hippocampus, caudate-putamen, brainstem, and cerebellum, with degenerating fibers tracts in the corpus callosum and other major tracts throughout the brain. Fluoro-Jade staining following WDIA+H injury revealed damage to fibers in the optic tract, lateral olfactory tract, corpus callosum, anterior commissure, caudate-putamen, brain stem, and cerebellum. While both models produce reliable and characteristic behavioral and neuronal pathologies, their differences are important to consider when choosing a brain injury model.

Neuronal-glial interactions are important for normal brain function and contribute to the maintenance of the brain's extracellular environment. Damage to glial cells following traumatic brain injury (TBI) could therefore be an important contributing factor to brain dysfunction and neuronal injury. We examined the early fate of astrocytes and neurons after TBI in rats. A total of 27 rats were euthanized at 0.5, 1, 2, 4, or 24 h after moderate lateral fluid percussion TBI or after sham TBI. Ipsilateral and contralateral hippocampi were examined in coronal sections from -2.12 to -4.80 mm relative to bregma. Adjacent sections were processed with markers for either astrocytes or degenerating neurons. Astrocytes were visualized using glial fibrillary acidic protein (GFAP) or glutamine synthetase immunohistochemistry. Neuronal degeneration was visualized using Fluoro-Jade (FJ) histofluorescence. At 30 min, there was a significant loss of GFAP immunoreactivity in ipsilateral hippocampal CA3 with some loss of normal astrocyte morphology in the remaining cells. The number of normal staining astrocytes decreased progressively over time with extensive astrocyte loss at 24 h. At 4 h, lightly stained FJ-positive neurons were scattered in the ipsilateral CA3. The intensity and number of FJ-positive neurons progressively increased over time with moderate numbers of degenerating neurons in the ipsilateral hippocampal CA3 evident at 24 h. We conclude that astrocyte loss occurs in the hippocampus early after TBI. The data suggest that loss of supporting glial cell may contribute to subsequent neuronal degeneration.

Traumatic brain injury (TBI) remains a major public health problem globally. In the United States the incidence of closed head injuries admitted to hospitals is conservatively estimated to be 200 per 100,000 population, and the incidence of penetrating head injury is estimated to be 12 per 100,000, the highest of any developed country in the world. This yields an approximate number of 500,000 new cases each year, a sizeable proportion of which demonstrate significant long-term disabilities. Unfortunately, there is a paucity of proven therapies for this disease. For a variety of reasons, clinical trials for this condition have been difficult to design and perform. Despite promising pre-clinical data, most of the trials that have been performed in recent years have failed to demonstrate any significant improvement in outcomes. The reasons for these failures have not always been apparent and any insights gained were not always shared. It was therefore feared that we were running the risk of repeating our mistakes. Recognizing the importance of TBI, the National Institute of Neurological Disorders and Stroke (NINDS) sponsored a workshop that brought together experts from clinical, research, and pharmaceutical backgrounds. This workshop proved to be very informative and yielded many insights into previous and future TBI trials. This paper is an attempt to summarize the key points made at the workshop. It is hoped that these lessons will enhance the planning and design of future efforts in this important field of research.

Data from the "National Acute Brain Injury Study: Hypothermia" were examined to identify the impact of hypothermia on admission. In all patients, temperature was measured at randomization using bladder catheters with thermistors. Patients assigned to hypothermia were cooled using fluid-circulating pads. Outcome was assessed at 6 months using the dichotomized Glasgow Outcome Scale (good outcome = good recovery/moderate disability; poor outcome = severe disability/vegetative/dead). One-hundred and two patients (hypothermia, 62; normothermia, 40) were hypothermic on admission (or =35.0 degrees C). Hypothermia-on-admission patients assigned to normothermia (n = 40) had a 78% poor outcome, and normothermia-on-admission patients assigned to normothermia had a 52% poor outcome (p0.004). Hypothermia-on-admission patients assigned to hypothermia had a lower percentage of poor outcomes than those assigned to normothermia (hypothermia, 61%; normothermia, 78%; p = 0.09). Patients over 45 years of age had an adverse effect of hypothermia regardless of admission temperature due to medical complications. Patients who were hypothermic on admission, ageor = 45 years (n = 81), and assigned to hypothermia had a significantly lower percentage of poor outcomes than those assigned to normothermia (hypothermia, 52%; normothermia, 76%; p = 0.02). Factors associated with hypothermia on admission were increased age, prehospital hypotension, smaller size, positive blood alcohol, larger volume of pre-hospital fluids, slightly higher injury severity, and winter enrollment The treatment effect was found in all of the four centers, which randomized the majority (80%) of the patients. It is unclear whether the improved outcome when hypothermia is maintained is a beneficial effect of very early hypothermia induction or an adverse effect of permitting the patients to rewarm passively.

AIM: To study the risks and benefits of intracerebroventricular (ICV) opiate pumps for the management of benign head and face pain. METHODS: SSix patients with refractory trigeminal neuralgia and/or cluster headaches were evaluated for implantation of an ICV opiate infusion pump using either ICV injections through an Ommaya reservoir or external ventricular drain. Four patients received morphine ICV pumps and two patientS received a hydromorphone pump. Of the Four patients with morphine ICV pumps, one patient had the medication changed to hydromorphone. Preoperative and post-operative visual analog scores (VAS) were obtained. Patients were evaluated post-operatively for a minimum of 3 mo and the pump dosage was adjusted at each outpatient clinic visit according to the patient’s pain level. RESULTS: All 6 patients had an intracerebroventricular opiate injection trial period, using either an Ommaya reservoir or an external ventricular drain. There was an average VAS improvement of 75.8%. During the trial period, no complications were observed. Pump implantation was performed an average of 3.7 wk (range 1-7) after the trial injections. After implantation, an average of 20.7 ± 8.3 dose adjustments were made over 3-56 mo after surgery to achieve maximal pain relief. At the most recent follow-up (26.2 mo, range 3-56), VAS scores significantly improved from an average of 7.8 ± 0.5 (range 6-10) to 2.8 ± 0.7 (range 0-5) at the final dose (mean improvement 5.0 ± 1.0, P < 0.001). All patients required a stepwise increase in opiate infusion rates to achieve maximal benefit. The most common complications were nausea and drowsiness, both of which resolved with pump adjustments. On average, infusion pumps were replaced every 4-5 years. CONCLUSION: These results suggest that ICV delivery of opiates may potentially be a viable treatment option for patients with intractable pain from trigeminal neuralgia or cluster headache.

Superior sagittal sinus (SSS) thrombosis has high morbidity and mortality, and urgent recanalization is critical for severe cases. Standard endovascular techniques for thrombolysis and thrombectomy use retrograde venous access, an approach that may be unsuccessful in cases with extensive firm clot burden involving the dural sinuses distal to the SSS. An anterior open transcranial approach to the SSS for catheter sheath placement to facilitate antegrade mechanical thrombectomy and thrombolysis of the SSS and more distal sinuses has not been previously described. Here we describe a case in which multiple unsuccessful attempts at retrograde endovascular access were attempted. Thus, a burr hole over the anterior SSS was performed for daily endovascular antegrade procedures using the Angiojet rheolytic catheter device and chemical thrombolysis. Near-complete recanalization of the SSS was achieved with venous outflow via dilated left transverse and left sigmoid sinuses, along with significant collateral flow in multiple cerebral veins.

Traumatic brain injury (TBI) is a leading cause of injury, hospitalization, and death among pediatric patients. Admission CT scans play an important role in classifying TBI and directing clinical care, but little is known about the differences in CT findings between pediatric and adult patients. The aim of this study was to determine if radiographic differences exist between adult and pediatric TBI.The authors retrospectively analyzed TBI registry data from 1206 consecutive patients with nonpenetrating TBI treated at a Level 1 adult and pediatric trauma center over a 30-month period.The distribution of sex, race, and Glasgow Coma Scale (GCS) score was not significantly different between the adult and pediatric populations; however, the distribution of CT findings was significantly different. Pediatric patients with TBI were more likely to have skull fractures (OR 3.21, p0.01) and epidural hematomas (OR 1.96, p0.01). Pediatric TBI was less likely to be associated with contusion, subdural hematoma, subarachnoid hemorrhage, or compression of the basal cisterns (p0.05). Rotterdam CT scores were significantly lower in the pediatric population (2.3 vs 2.6, p0.001).There are significant differences in the CT findings in pediatric versus adult TBI, despite statistical similarities with regard to clinical severity of injury as measured by the GCS. These differences may be due to anatomical characteristics, the biomechanics of injury, and/or differences in injury mechanisms between pediatric and adult patients. The unique characteristics of pediatric TBI warrant consideration when formulating a clinical trial design or predicting functional outcome using prognostic models developed from adult TBI data.

Object. Abnormal accumulation of intracellular calcium following traumatic brain injury (TBI) is thought to contribute to a cascade of cellular events that lead to neuropathological conditions. Therefore, the possibility that specific calcium channel antagonists might exert neuroprotective effects in TBI has been of interest. The focus of this study was to examine whether Ziconotide produces such neuroprotective effects.Methods. The authors report that the acceleration—deceleration model of TBI developed by Marmarou, et al., induces a long-lasting deficit of neuromotor and behavioral function. The voltage-sensitive calcium channel blocker Ziconotide (also known as SNX-111 and CI-1009) exerts neuroprotective effects in this model of diffuse brain injury (DBI) in rats. The dose and time of injection of Ziconotide chosen for the present study was based on the authors' previous biochemical studies of mitochondria. Rats were trained in a series of motor and memory tasks, following which they were subjected to DBI using the Marmarou, et al., model. At 3, 5, and 24 hours, all rats were injected with 2 mg/kg Ziconotide for a total cumulative dose of 6 mg/kg Ziconotide. Control brain-injured animals were injected with an equal volume of saline vehicle at each of these time points. The rats were tested for motor and cognitive performance at 1, 3, 7, 14, 21, 28, 35, and 42 days postinjury. Saline-treated rats displayed severe motor and cognitive deficits after DBI. Compared with saline-treated control animals, rats treated with Ziconotide displayed better motor performance during inclined plane, beam balance, and beam walk tests; improved memory while in the radial arm maze; and improved learning while in the Morris water maze.Conclusions. These results demonstrated that the acceleration—deceleration model, which had been developed by Marmarou, et al., induces severe motor and cognitive deficits. We also demonstrated that Ziconotide exhibits substantial neuroprotective activity in this model of TBI. Improvement was observed in both motor and cognitive tasks, even though treatment was not initiated until 3 hours after injury. These findings support the development of neuronal N-type calcium channel antagonists as useful therapeutic agents in the treatment of TBI.

Despite medical and technological advances in neurosurgical intensive care, severe traumatic brain injury still carries a poor prognosis. Invasive monitoring of cerebral oxygenation has recently been proposed as a means for the detection and prevention of cerebral ischemia in comatose patients; however, it has not proven to influence the patient’s outcome after severe brain injury. Eight recent reports selected from the literature are reviewed, and the authors’ own clinical experience is presented in order to define the indications, usefulness, limitations, and potential complications of the available methodology for the invasive monitoring of cerebral interstitial oxygen saturation.

Complex Regional Pain Syndrome (CRPS) is the new name for entities formerly known mostly as Reflex Sympathetic Dystrophy and Causalgia. Treatment of CRPS with either the calcium channel blocker nifedipine or the alpha-sympathetic blocker phenoxybenzamine was assessed in 59 patients, 12 with early stages of CRPS, 47 with chronic stage CRPS. In the early stage CRPS patients, 3 of 5 were cured with nifedipine and 8 of 9 (2 of whom had earlier received nifedipine) with phenoxybenzamine, for a cure rate of 92% (11 out of 12). In the chronic stage CRPS patients, 10 of 30 were cured with nifedipine; phenoxybenzamine cured 7 of 17 patients when administered as a first choice and another 2 of 7 patients who received nifedipine earlier, for a total late stage success rate of 40% (19 out of 47). The most common side effects necessitating discontinuing the drug were headaches for nifedipine and orthostatic dizziness, nausea and diarrhoea for phenoxybenzamine. All male patients on phenoxybenzamine experienced impotence, but this did not lead to discontinuing this agent and immediately disappeared after stopping the drug. These results once again stress the importance of early recognition of CRPS, and treatment with either of these drugs could be considered as a first choice for early CRPS, especially because in this series this treatment was not combined with physical therapy making it very cost-effective. In the chronic stage of CRPS, treatment with these drugs was much less successful (40%), even though it was always combined with physical therapy, but it can still be considered, either as a first choice or when other types of treatment have failed.

SummaryBackgroundOn the basis of mixed results from previous trials, we assessed whether therapeutic hypothermia for 48–72 h with slow rewarming improved mortality in children after brain injury.MethodsIn this phase 3, multicenter, multinational, randomised controlled trial, we included patients with severe traumatic brain injury who were younger than 18 years and could be enrolled within 6 h of injury. We used a computer-generated randomisation sequence to randomly allocate patients (1:1; stratified by site and age [

PURPOSE Second insults following traumatic brain injury (TBI), such as ischemia and hypoxia, significantly worsen outcome in patients and in experimental models of TBI. Following TBI there is a pathological increase in intracellular calcium, triggering cellular mechanisms of dysfunction and death. N-type specific voltage gated calcium channel (VGCC) blockers reduce cell death in both in vitro mechanical strain injury (MSI) and in vivo models of TBI, but they have not been previously explored in a model of TBI followed by a second insult. METHODS In the following studies, cortical neurons and astrocytes experienced MSI followed by incubation in 20% CO2. Cultures were treated with the N-type VGCC blocker, ω-conopeptide SNX-185 (1 μM), 5-minutes post-injury and intracellular calcium accumulation was assessed at 3, 6 and 24 h. Neuronal viability was assessed 24 h after MSI. RESULTS Increasing incubator CO2 to 20% significantly increased calcium accumulation and cell death regardless of MSI severity. Treatment with 1 μM of SNX-185 significantly reduced the accumulation of calcium 3 hours following injury and increased the number of viable neurons 24 h post-injury and incubation in 20% CO2. CONCLUSIONS In vitro models provide a critical tool for identifying roles of cell specific mechanisms involved in neuronal dysfunction and death following injury. These data demonstrate the potential of N-type VGCC blockers in reducing the damaging effects of TBI and second insults.

To describe the clinical presentations and outcomes of children with intraventricular hemorrhages (IVHs) after blunt head trauma (BHT).Subanalysis of a large, prospective, observational cohort study performed from June 1, 2004, through September 31, 2006.Twenty-five emergency departments participating in the Pediatric Emergency Care Applied Research Network. Patients Children presenting with IVH after BHT. Exposure Blunt head trauma.Clinical presentations and outcomes, including the Pediatric Overall Performance Category (POPC) and Pediatric Cerebral Performance Category (PCPC) scores at hospital discharge.Of 15 907 patients evaluated with computed tomography, 1156 (7.3%) had intracranial injuries. Forty-three of the 1156 (3.7%; 95% CI, 2.7%-5.0%) had nonisolated IVHs (ie, with intracranial injuries on computed tomography), and 10 of 1156 (0.9%; 95% CI, 0.4%-1.6%) had isolated IVHs. Only 4 of 43 (9.3%) of those with nonisolated IVHs had Glasgow Coma Scale (GCS) scores of 14 to 15, and all 10 (100.0%) with isolated IVHs had GCS scores of 15. No patients with isolated IVHs required neurosurgery or died. One patient had moderate overall disability (by the POPC score), and no patient had moderate or severe disability at discharge (by the PCPC score). Of the 43 patients with nonisolated IVHs, however, 16 (37.2%) died and 18 (41.9%) required neurosurgery. In 27 patients (62.8%), injuries ranged from moderate overall disability to brain death by the POPC score.Children with nonisolated IVHs after BHT typically present with GCS scores of less than 14, frequently require neurosurgery, and have high mortality rates. In contrast, those with isolated IVHs typically present with normal mental status and are at low risk for acute adverse events and poor outcomes.