The authors describe a modification of the encephalo-duro-arterio-synangiosis (EDAS) surgical technique for patients with moyamoya syndrome in which the arachnoid is widely opened over the exposed brain and the donor superficial temporal artery adventitia is sutured directly to the pia with 10–O nylon suture (‘pial synangiosis’). The procedure has been performed in 34 patients over a 10-year period, with follow-up arteriograms 1 year following the procedure demonstrating markedly enhanced middle cerebral artery flow through the surgical site. Operative morbidity has been limited to two postoperative strokes, both in patients who were neurologically unstable preoperatively; and the clinical stability of the operated patients has thus far been excellent.
Objective-Oxidative stress contributes to secondary damage after traumatic brain injury (TBI). Hypothermia decreases endogenous antioxidant consumption and lipid peroxidation after experimental cerebral injury. Our objective was to determine the effect of therapeutic hypothermia on oxidative damage after severe TBI in infants and children randomized to moderate hypothermia vs normothermia.Design-Prospective randomized controlled study. Setting-Pediatric ICU of Pittsburgh Children's Hospital Patients-The study included 28 patientsMeasurements and main results-We compared the effects of hypothermia (32-33°C) vs normothermia in patients treated in a single center involved in a multi-center randomized controlled trial of hypothermia in severe pediatric TBI (GCS score ≤ 8). The patients randomized to hypothermia (n=13) were cooled to target temperature within ∼6h-24h for 48h and then re-warmed. Antioxidant status was assessed by measurements of total antioxidant reserve [AOR] and glutathione. Protein oxidation and lipid peroxidation were assessed by measurements of protein-thiols and F 2 -isoprostane, respectively in ventricular CSF samples (n=76) obtained on day1-3 after injury. The association between GCS score, age, gender, treatment, temperature, time after injury, and CSF AOR, glutathione, protein-thiol, F2-isoprostane levels were assessed by bivariate and multiple regression models. Corresponding Demographic and clinical characteristics were similar between the two treatment groups. Mechanism of injury included both accidental injury and nonaccidental injury. Multiple regression models revealed preservation of CSF antioxidant reserve by hypothermia (p = 0.001). Similarly, a multiple regression model showed that glutathione levels were inversely associated with patient temperature at the time of sampling (p = 0.002). F2-isoprostane levels peaked on day 1 after injury and were progressively decreased thereafter. Although F2-isoprostane levels were ∼3-fold lower in patients randomized to hypothermia vs. normothermia, this difference was not statistically significant.Conclusion-To our knowledge this is the first study demonstrating that hypothermia attenuates oxidative stress after severe TBI in infants and children. Our data also support the concept that CSF represents a valuable tool for monitoring treatment effects on oxidative stress after TBI.
In our series of 33 children who underwent temporal and extended temporal lobe resections because of seizures, the average age at surgery was 7 years, 11 months. Sixteen cases (48%) were diagnosed as having tumors: low-grade astrocytoma (6), hamartoma (5), and ganglioglioma/neuroma (5). Other pathologic diagnoses included one or more cytoarchitectural abnormalities and/or reactive changes. Due to a more aggressive and early radiologic and electrophysiologic investigation of children with seizures, a resectable focus, e.g. neoplasm or structural abnormality, was found in a much younger age group of patients than previously reported. In children who had intractable seizures but normal radiologic studies, positron emission tomography was of great value in localizing the seizure focus. In a group of children with infantile spasms, seizures were controlled following the identification and resection of a focal lesion. Prompt detection and precise localization of lesions in the temporal lobe in the pediatric population may lead to surgical management and seizure control.
Children often suffer sustained cognitive dysfunction after severe diffuse traumatic brain injury (TBI). To study the effects of diffuse injury in the immature brain, we developed a model of severe diffuse impact (DI) acceleration TBI in immature rats and previously described the early motor and cognitive dysfunction posttrauma. In the present study, we investigated the long-term functional ability after DI (150 gm/2 m) compared to sham in the immature (PND 17) rat. Beam balance and inclined plane latencies were measured daily for 10 days after injury to assess gross vestibulomotor function. The Morris water maze (MWM) paradigm was evaluated monthly up to 3 months after DI and sham injuries. Reduced latencies on the balance beam and inclined plane were observed in DI rats (p < 0.05 vs. sham [n = 10 per group]) at 24 h and persisted for 10 days postinjury. DI produced sustained MWM performance deficits (p < 0.05 vs. sham) as indicated by the greater latencies to find the hidden platform remarkably through 90 days after injury. Lastly, the brain and body weights of the injured animals were less than sham (p < 0.05) after 3 months. We conclude that a diffuse TBI in the immature rat: (a) created a consistent, marked, but reversible motor deficit up to 10 days following injury; (b) produced a long-term, sustained performance deficit in the MWM up to 3 months posttrauma; and (c) affected body and brain weight gain in the developing rat through 3 months after injury. This TBI model should be useful for the testing of novel therapies and their effect on long-term outcome and development in the immature rat.
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