bluuebunny/crossref_metadata_2025_split huggingface dataset:
Improved motor outcome in response to magnesium therapy received up to 24 hours after traumatic diffuse axonal brain injury in rats
Authors: Heath Deanne L. , Vink Robert 
Published: May 2009

Object. The goal of this study was to establish the therapeutic window during which delayed therapy with MgSO4 improves neurological motor outcome in rats that have suffered severe traumatic axonal brain injury.Methods. Severe brain injury was induced in male Sprague—Dawley rats by using the impact—acceleration model of severe traumatic diffuse axonal brain injury. Injured animals were subsequently treated with MgSO4 (750 µmol/kg) infused intramuscularly at 30 minutes or at 8, 12, or 24 hours after trauma and were tested for neurological motor outcome during the following week by using the rotarod test. Injured untreated (control) animals demonstrated highly significant (p < 0.001) neurological motor deficits that were sustained over the 1-week assessment period. Animals treated with MgSO4 at 30 minutes or at 8 or 12 hours postinjury demonstrated significantly improved motor outcomes compared with untreated control animals at all time points (0.001 < p < 0.05). Animals treated with MgSO4 at 24 hours had motor scores that were similar to those of untreated control animals early in the week, but demonstrated a significantly more rapid recovery in function and, by the end of the assessment period, they demonstrated significantly improved motor scores (p < 0.01). Repeated administration of MgSO4 over the 1-week observation period did not further improve outcome.Conclusions. The present results demonstrate that Mg++ plays a neuroprotective role following severe diffuse traumatic axonal brain injury. Moreover, Mg++ therapy significantly improved motor outcome when administered up to 24 hours after injury, with early treatments providing the most significant benefit. Repeated administration beyond 24 hours postinjury did not provide additional neuroprotection.
Influence of early posttraumatic hypothermia therapy on cerebral blood flow and glucose metabolism after fluid-percussion brain injury
Authors: Zhao Weizhao , Alonso Ofelia F. , Loor Judith Y. , Busto Raul , Ginsberg Myron D. 
Published: May 2009

Object. Using autoradiographic image averaging, the authors recently described prominent foci of marked glucose metabolism-greater-than-blood-flow uncoupling in the acutely traumatized rat brain. Because hypothermia is known to ameliorate injury in this and other injury models, the authors designed the present study to assess the effects of posttraumatic therapeutic hypothermia on the local cerebral metabolic rate of glucose (LCMRglu) and local cerebral blood flow (LCBF) following moderate parasagittal fluid-percussion head injury (FPI) in rats.Methods. Either cranial hypothermia (30°C) or normothermia (37°C) was induced for 3 hours in matched groups of rats immediately after FPI; LCMRglu and LCBF were assessed 3 hours after concluding these temperature manipulations.In rats subjected to FPI, regardless of whether normothermia or hypothermia ensued, LCBF was reduced relative to the sham-injury groups. In addition, when FPI was followed by hypothermia (FPI—30°C group), the subsequent LCBF was significantly lower (35–38% on average) than in FPI—37°C rats. Statistical mapping of LCBF difference imaging data revealed confluent cortical and subcortical zones of significantly reduced LCBF (largely ipsilateral to the prior injury) in FPI—30°C rats relative to the FPI—37°C group. Local glucose utilization was reduced in both hemispheres of FPI—37°C rats relative to the sham-injury group and was lower in the right (traumatized) hemisphere than in the left. However, LCMRglu values were largely unaffected by temperature manipulation in either the FPI or sham-injury groups. The LCMRglu/LCBF ratio was nearly doubled in FPI—30°C rats relative to the FPI—37°C group, in a diffuse and bihemispheric fashion. Linear regression analysis comparing LCMRglu and LCBF revealed that the FPI—37°C and FPI—30°C data sets were completely nonoverlapping, whereas the two sham-injury data sets were intermixed.Conclusions. Despite its proven neuroprotective efficacy, early posttraumatic hypothermia (30°C for 3 hours) nonetheless induces a moderate decline in cerebral perfusion without the (anticipated) improvement in cerebral glucose utilization, so that a state of mild metabolism-greater-than-blood-flow dissociation is perpetuated.
Effect of cerebral perfusion pressure on contusion volume following impact injury
Authors: Kroppenstedt Stefan-Nikolaus , Kern Michael , Thomale Ulrich-Wilhelm , Schneider Gerd-Helge , Lanksch Wolfgang Reinhardt , Unterberg Andreas Wilhelm 
Published: May 2009

Object. Although it is generally acknowledged that a sufficient cerebral perfusion pressure (CPP) is necessary for treatment of severe head injury, the optimum CPP is still a subject of debate. The purpose of this study was to investigate the effect of various levels of blood pressure and, thereby, CPP on posttraumatic contusion volume.Methods. The left hemispheres of 60 rats were subjected to controlled cortical impact injury (CCII). In one group of animals the mean arterial blood pressure (MABP) was lowered for 30 minutes to 80, 70, 60, 50, or 40 mm Hg 4 hours after contusion by using hypobaric hypotension. In another group of animals the MABP was elevated for 3 hours to 120 or 140 mm Hg 4 hours after contusion by administering dopamine. The MABP was not changed in respective control groups. Intracranial pressure (ICP) was monitored with an ICP microsensor. The rats were killed 28 hours after trauma occurred and contusion volume was assessed using hematoxylin and eosin—stained coronal slices. No significant change in contusion volume was caused by a decrease in MABP from 94 to 80 mm Hg (ICP 12 ± 1 mm Hg), but a reduction of MABP to 70 mm Hg (ICP 9 ± 1 mm Hg) significantly increased the contusion volume (p < 0.05). A further reduction of MABP led to an even more enlarged contusion volume. Although an elevation of MABP to 120 mm Hg (ICP 16 ± 2 mm Hg) did not significantly affect contusion volume, there was a significant increase in the contusion volume at 140 mm Hg MABP (p < 0.05; ICP 18 ± 1 mm Hg).Conclusions. Under these experimental conditions, CPP should be kept within 70 to 105 mm Hg to minimize posttraumatic contusion volume. A CPP of 60 mm Hg and lower as well as a CPP of 120 mm Hg and higher should be considered detrimental.
Tamoxifen radiosensitization in human glioblastoma cell lines
Authors: Donson Andrew M. , Weil Michael D. , Foreman Nicholas K. 
Published: May 2009

Object. A combined tamoxifen and radiation therapy is being used in clinical trials to treat glioblastoma multiforme (GBM). The rationale behind this therapy is that tamoxifen is a radiosensitizer. However, the evidence for this is weak. The authors, therefore, examined the effect of combined radiation—tamoxifen therapy in three GBM cell lines of human origin.Methods. The GBM cell lines were exposed to different concentrations (0.3–5 µg/ml) of tamoxifen and subsequently irradiated at varying doses (0.8–5 Gy). Tumor growth inhibition was measured using a proliferation assay. The interaction of tamoxifen and radiation therapies was quantified using the combination index method, which distinguishes whether a combined antitumor effect is synergistic, additive, or antagonistic. At high doses of tamoxifen or radiation there was significant inhibition of tumor cell proliferation. At low doses of either therapeutic agent, there was little effect. In one cell line, synergism occurred at high doses of tamoxifen and radiation. In the other two cell lines, an additive effect was observed. In only one of the three cell lines was there synergy between tamoxifen and radiation at doses that significantly inhibited tumor proliferation.Conclusions. Because synergy could not be demonstrated in all three cell lines at active dosages, the clinical combination of tamoxifen and radiation therapies may not be of benefit to all patients.
Primary cerebellar glioblastomas multiforme in children
Authors: Kulkarni Abhaya V. , Becker Laurence E. , Jay Venita , Armstrong Derek C. , Drake James M. 
Published: May 2009

✓ Primary cerebellar glioblastomas multiforme are exceedingly rare in children. The authors therefore retrospectively characterized the clinical behavior and pathological features of these tumors. A review of the database at the Hospital for Sick Children, Toronto, Canada revealed four patients with cerebellar tumors that displayed significant pleomorphism, hypercellularity, mitoses, and necrosis with pseudopalisading. The authors performed a detailed clinical, radiological, histological, and immunohistochemical analysis of the tumors in these four children (three boys and one girl; average age at presentation 7 years; range 21 months–15 years). Magnetic resonance imaging and computerized tomography most commonly revealed a large lesion with minimal edema, inhomogeneous contrast enhancement, and a discrete border. Tumor resection was subtotal in one patient and gross total in three patients. Immunostaining of the tumor cells with antisera to glial fibrillary acidic protein and vimentin was positive in varying degrees. Initial adjuvant therapy consisted of local radiation only (one patient), chemotherapy only (one patient), and radiation and chemotherapy (one patient). One patient received no adjuvant therapy. Tumor recurrence was documented in all patients: two local recurrences (at 3.5 and 7 months), one spinal recurrence (at 14 months), and one local recurrence with ventricular and spinal spread (at 8 months). Ultimately, three of the four patients developed leptomeningeal tumor spread. Patient follow up ranged from 8 to 17 months (mean 12.5 months). Three patients were dead at last follow up with a mean survival of 15 months.The prognosis for patients with cerebellar glioblastomas is extremely poor, and the tumor has a tendency for cerebrospinal fluid dissemination. The optimal management of patients harboring of these difficult-to-treat tumors, including the role of craniospinal radiation and chemotherapy, has not yet been achieved.
Obituary: Henry G. Schwartz, M.D. 1909–1998
Authors: Grubb Robert L. 
Published: May 2009

Following a long illness, Henry G. Schwartz, former editor of the Journal of Neurosurgery, died on December 24, 1998 at the age of 89 years.The author provides an annotated chronology of Dr. Schwartz's life and some highlights of his distinguished career.
The ciliospinal reflex in pentobarbital coma
Authors: Andrefsky John C. , Frank Jeffrey I. , Chyatte Douglas 
Published: May 2009

Object. This study was conducted to delineate the ciliospinal reflex (CSR), which is defined as pupillary dilation caused by a noxious stimulus to the face or head. The authors anecdotally observed that patients in a pentobarbital coma have a CSR that can mimic pathological conditions. A pentobarbital coma obscures the results of the neurological examination in patients with potentially life-threatening cerebral edema; pupil size and reactivity are the only readily monitored signs. Any condition that incorrectly suggests evolving intracranial pathological processes can lead to unnecessary clinical actions.Methods. The authors evaluated six consecutive patients in the neurointensive care unit in whom a pentobarbital coma had been induced, documenting the presence and duration of the CSR. The CSR was always bilateral and symmetrical, manifesting as enlarged (6–8 mm), seemingly nonreactive pupils continuing from 1 to 6 minutes and was usually seen after routine nursing maneuvers. The pupils appeared nonreactive to short flashes of direct light but did react if longer flashes were used.Conclusions. Recognition of the CSR can potentially lead to reduction of unnecessary transportation and complicating medical interventions in critically neurologically ill patients in whom a pentobarbital coma has been induced.
Differential effects of octreotide treatment and transsphenoidal surgery on growth hormone—binding protein levels in patients with acromegaly
Authors: Hernandez Irma , Soderlund Daniela , Espinosa-de-los-Monteros Ana Laura , Ochoa Raquel , Zarate Arturo , Mercado Moises 
Published: May 2009

Object. The high-affinity growth hormone—binding protein (GHBP) represents the extracellular portion of the growth hormone (GH) receptor, and its serum levels are a reflection of the tissue receptor status. Levels of GHBP are decreased in patients with active acromegaly, probably because of downregulation of GH receptors. However, there are no studies of patients with acromegaly in which the effects of medical (that is, administration of somatostatin analogs) and surgical therapy on GHBP levels have been compared. That is the task the authors set out to accomplish in this study.Methods. The authors studied seven patients in whom acromegaly had been recently diagnosed. They examined these patients at baseline, 2 months after octreotide treatment (subcutaneous administration of 100 µg octreotide three times per day), and 1 month after transsphenoidal surgery. Growth hormone—binding activity was measured, as well as the following biochemical markers of the somatotropic axis: GH suppression induced by oral administration of glucose, insulin-like growth factor-I (IGF-I), and insulin-like growth factor—binding protein-3 (IGFBP3). Although octreotide treatment induced a decrease in the levels of GH, IGF-I, and IGFBP3, as well as an increase in the level of GHBP, these biochemical markers did not reach normal levels. On the other hand, after transsphenoidal surgery, GHBP levels became normal, particularly in those patients in whom serum GH could be suppressed to an undetectable level after glucose loading.Conclusions. The authors conclude that persistently low GHBP levels in patients with acromegaly are normalized by successful pituitary surgery and correlate well with disease activity.
How should a subarachnoid hemorrhage grading scale be determined? A combinatorial approach based solely on the Glasgow Coma Scale
Authors: Takagi Kiyoshi , Tamura Akira , Nakagomi Tadayoshi , Nakayama Hitoshi , Gotoh Osamu , Kawai Kensuke , Taneda Mamoru , Yasui Nobuyuki , Hadeishi Hiromu , Sano Keiji 
Published: May 2009

Object. The purpose of this study was to present a combinatorial approach used to develop a subarachnoid hemorrhage (SAH) grading scale based on the patient's preoperative Glasgow Coma Scale (GCS) score.Methods. There are 4094 different combinations that can be used to compress the 13 scores of the GCS into two to 12 grades. Break points, the positions in the scale in which two adjacent scores connote a significantly different outcome, are obtained by a direct comparison of the GCS and the Glasgow Outcome Scale (GOS). Guided by the break points, the number of combinations to be considered can be limited. All possible combinations are statistically analyzed with respect to intergrade differences in outcome. Single combinations, with the maximum number of grades having maximum intergrade outcome differences for each corresponding set of adjacent grades, must be selected. The authors verified the validity of this combinatorial approach by retrospectively analyzing 1398 consecutive patients with aneurysmal SAH who underwent surgery within 7 days of the last hemorrhage episode. The patients' GCS scores were assessed just before surgery and their GOS scores were estimated 6 months post-SAH. The combinatorial approach yields only one acceptable grading scale: I (GCS Score 15); II (GCS Scores 11–14); III (GCS Scores 8–10); IV (GCS Scores 4–7); and V (GCS Score 3).Conclusions. The combinatorial approach, guided by the break points, is so simple and systematic that it can be used again in the future when revision of the grading scale becomes necessary after development of new and effective treatment modalities that improve patients' overall outcome.
Percutaneous transluminal angioplasty and stent placement for recurrent carotid artery stenosis
Authors: Lanzino Giuseppe , Mericle Robert A. , Lopes Demetrius K. , Wakhloo Ajay K. , Guterman Lee R. , Hopkins L. Nelson 
Published: May 2009

Object. Treatment consisting of percutaneous transluminal angioplasty (PTA) and stent placement has recently been proposed as an alternative to surgical reexploration in patients with recurrent carotid artery stenosis following endarterectomy. The authors retrospectively reviewed their experience after performing 25 procedures in 21 patients to assess the safety and efficacy of PTA with or without stent placement for carotid artery restenosis.Methods. The mean interval between endarterectomy and the endovascular procedures was 57 months (range 8–220 months). Seven arteries in five patients were treated by PTA alone (including bilateral procedures in one patient and repeated angioplasty in the same vessel in another). Early suboptimum results and recurrent stenosis in some of these initial cases prompted the authors to combine PTA with stent placement in the treatment of 18 arteries over the past 3 years. No major periprocedural deficits (neurological or cardiac complications) or death occurred. There was one periprocedural transient neurological event, and in one patient a pseudoaneurysm of the femoral artery (at the access site) required surgical repair. In the 16 patients who each underwent at least 6 months of follow-up review, no neurological events ipsilateral to the treated artery had occurred after a mean follow-up period of 27 months (range 6–57 months). Three of five patients who underwent PTA alone developed significant (> 50%) asymptomatic restenoses that required repeated angioplasty in one and PTA with stent placement in two patients. Significant restenosis (55%) was observed in only one of the vessels treated by combined angioplasty and stent placement.Conclusions. Endovascular PTA and stenting of recurrent carotid artery stenosis is both technically feasible and safe and has a satisfactory midterm patency. This procedure can be considered a viable alternative to surgical reexploration in patients with recurrent carotid artery stenosis.
Delayed neurological deterioration following resection of arteriovenous malformations of the brain
Authors: Morgan Michael K. , Sekhon Lali H. S. , Finfer Simon , Grinnell Verity 
Published: May 2009

Object. The aim of this study was to analyze delayed neurological deficits following surgical resection of arteriovenous malformations (AVMs).Methods. The authors report on a consecutive series of 200 patients with angiographically proven AVMs of the brain that were surgically resected between January 1989 and June 1998. The 30-day mortality rate for patients in this series was 1%, with one death caused by AVM resection and one death attributed to basilar artery aneurysm repair following successful AVM resection. The Spetzler—Martin grading system correlated well with the difficulty of surgery. No permanent incidence of morbidity resulted from resection of Grade I or II AVMs; the percentage of patients with a significant neurological deficit due to resection was 7.8% for those with Grade III lesions and 33.3% for those with Grade IV or V AVMs. However, this grading system did not accurately predict the development of delayed neurological deficits.Ten patients (5%) developed delayed neurological deficits after recovering from anesthesia and surgery. The delayed deficit was due to hemorrhage in four of the 10 patients and all four had undergone resection of AVMs measuring at least 4 cm in diameter. An increase in blood pressure during the first 8 postoperative days precipitated hemorrhage in these patients. Edema arising as a consequence of propagated venous thrombosis (two patients) was associated with extensive venous drainage networks rather than large AVM niduses. Both hemorrhagic and edematous complications can be included under the umbrella term of “arterial-capillary-venous hypertensive syndrome” to describe the common underlying pathogenesis accurately. An additional four patients developed a delayed deficit as a result of vasospasm. Vasospasm occurred when resection had involved extensive dissection of proximal anterior and middle cerebral arteries; in such cases the incidence of vasospasm was 27%.Conclusions. On the basis of their analysis of these complications, the authors recommend strict blood pressure control for patients with lesions measuring 4 cm or more in diameter (particularly those with a deep arterial supply). Thromboprophylaxis with aspirin and heparin is prescribed for patients with extensive venous drainage networks, and prophylactic nimodipine therapy and angiographic surveillance for vasospasm are suggested for patients in whom extensive dissection of proximal anterior or middle cerebral arteries has been necessary.
Role of protein tyrosine phosphorylation in erythrocyte lysate—induced intracellular free calcium concentration elevation in cerebral smooth-muscle cells
Authors: Iwabuchi Satoshi , Marton Linda S. , Zhang John H. 
Published: May 2009

Object. Tyrosine kinases play an important role in the regulation of systemic vascular smooth-muscle tone. The authors studied the involvement of protein tyrosine kinase activity in erythrocyte lysate—mediated signal transduction in cerebral smooth-muscle cells.Methods. Tyrosine kinase phosphorylation and intracellular free Ca++ ([Ca++]i) were measured in rat aortic and basilar artery smooth-muscle cells by using Western blot and fura 2-acetoxymethyl ester microfluorimetry. Erythrocyte lysate enhanced tyrosine phosphorylation in cultured rat aortic and basilar smooth-muscle cells and induced a rapid transient and a prolonged plateau phase of [Ca++]i response in rat basilar smooth-muscle cells. The tyrosine kinase inhibitors genistein and tyrphostin A51 (administered at concentrations of 30 or 100 µM) attenuated both phases of erythrocyte lysate—induced [Ca++]i elevation. Erythrocyte lysate was separated into low- (< 10 kD, which contains adenine nucleotides) and high- (> 10 kD, which contains hemoglobin) molecular-weight fractions; these fractions were tested separately in these cells. The low-molecular-weight fraction produced a similar [Ca++]i response to that of erythrocyte lysate and the high-molecular-weight fraction produced a small response. The [Ca++]i responses from both fractions were inhibited by tyrosine kinase inhibitors.Conclusions. To the authors' knowledge, this is the first report to show that tyrosine phosphorylation may be involved in erythrocyte lysate—induced signal transduction and [Ca++]i responses in cerebral smooth-muscle cells.