bluuebunny/crossref_metadata_2025_split huggingface dataset:
Management and outcome of posttraumatic syringomyelia
Authors: Sgouros Spiros , Williams Bernard 
Published: June 2009

✓ Traumatic paraplegia is the most common cause of nonhindbrain—related syringomyelia. Fifty-seven patients with a mean age of 34.3 years at presentation were treated at the Midland Centre for Neurosurgery and Neurology between 1973 and 1993. A variety of treatment strategies have been used over the years, including syringosubarachnoid and syringopleural shunts, spinal cord transection, and pedicled omental graft transposition. More recently decompressive laminectomy, subarachnoid space reconstruction and formation of surgical meningocele have been used. A total of 81 operations were performed in these patients, 69 of them at the Syringomyelia Clinic. Combinations of strategies were often chosen; the use of one strategy such as drainage did not preclude another such as transection or augmentation of the cerebrospinal fluid pathways.The overall postoperative complication rate was 12%. Problems specific to the operation type included dislodged, blocked, and infected drains (10 patients). Acute gastric dilation was seen following pedicled omental graft (one patient). At 6 years only 49% of the drains inserted still functioned. A higher than expected rate of cervical spondylotic myelopathy has been noted. Two patients developed Charcot's joints. Thirty-six patients were asked to score themselves with regard to limb function and performance of daily living activities and 30% reported improvement, particularly in arm function.Since the use of magnetic resonance imaging has become widespread, it has become apparent that decompressive laminectomy with subarachnoid space reconstruction is effective in controlling the syrinx cavity. In complete paraplegia, spinal cord transection is an effective alternative. Pedicled omental grafting was associated with poor outcome and an increased complication rate and has been abandoned.
Biomechanical characteristics of C1–2 cable fixations
Authors: Dickman Curtis A. , Crawford Neil R. , Paramore Christopher G. 
Published: June 2009

✓ The biomechanical characteristics of four different methods of C1–2 cable fixation were studied to assess the effectiveness of each technique in restoring atlantoaxial stability. Biomechanical testing was performed on the upper cervical spines of four human cadaveric specimens. Physiological range loading was applied to the atlantoaxial specimens and three-dimensional motion was analyzed with stereophotogrammetry. The load–deformation relationships and kinematics were measured, including the stiffness, the angular ranges of motion, the linear ranges of motion, and the axes of rotation.
Specimens were nondestructively tested in the intact state, after surgical destabilization, and after each of four different methods of cable fixation. Cable fixation techniques included the interspinous technique, the Brooks technique, and two variants of the Gallie technique. All specimens were tested immediately after fixation and again after the specimen was fatigued with 6000 cycles of physiological range torsional loading.
All four cable fixation methods were moderately flexible immediately; the different cable fixations allowed between 5° and 40° of rotational motion and between 0.6 and 7 mm of translational motion to occur at C1–2. The Brooks and interspinous methods controlled C1–2 motion significantly better than both of the Gallie techniques. The motion allowed by one of the Gallie techniques did not differ significantly from the motion of the unfixed destabilized specimens. All cable fixation techniques loosened after cyclic loading and demonstrated significant increases in C1–2 rotational and translational motions. The bone grafts shifted during cyclic loading, which reduced the effectiveness of the fixation.
The locations of the axes of rotation, which were unconstrained and mobile in the destabilized specimens, became altered with cable fixation. The C1–2 cables constrained motion by shifting the axes of rotation so that C-1 rotated around the fixed cable and graft site. After the specimen was fatigued, the axes of rotation became more widely dispersed but were usually still localized near the cable and graft site.
Adequate healing requires satisfactory control of C1–2 motion. Therefore, some adjunctive fixation is advocated to supplement the control of motion after C1–2 cable fixation (that is, a cervical collar, a halo brace, or rigid internal fixation with transarticular screws).
Symptomatic epidural lipomatosis secondary to obesity
Authors: Kumar Krishna , Nath Rahul K. , Nair C. P. V. , Tchang S. P. 
Published: June 2009

✓ The authors present a case of thoracic spinal cord compression secondary to epidural lipomatosis in an obese patient. This patient represents the 10th case of epidural lipomatosis secondary to simple obesity reported in the literature. The diagnosis is based on three criteria: 1) medical history and physical examination consistent with segmental spinal cord compression; 2) epidural fat thickness greater than 7 mm in the region of compression, based on magnetic resonance imaging (preferred) or computerized tomographic imaging; and 3) a height-to-weight ratio greater than 27.5 kg/m2. This specific correlation between epidural fat thickness measurement and calculation of height-to-weight ratio has not previously been reported.
Surgical decompression through a posterior laminectomy and excision of excess epidural fat resulted in immediate reversal of the patient's symptoms. Knowledge of the association of epidural lipomatomis with obesity in the absence of glucocorticoid imbalance is important in discerning what may be an underrecognized syndrome.
Clinical significance of the flow gap in carotid magnetic resonance angiography
Authors: Heiserman Joseph E. , Zabramski Joseph M. , Drayer Burton P. , Keller Paul J. 
Published: June 2009

✓ Magnetic resonance (MR) angiography offers a safe, noninvasive alternative to conventional angiography in patients with suspected carotid stenosis; however, it tends to overestimate the severity of stenosis. Loss of the MR signal with a resulting flow gap is a frequent finding in cases of high-grade stenosis. The authors undertook this study to define the range of carotid stenosis associated with a flow gap on two-dimensional time-of-flight (2DTF)-MR angiography.
Blinded evaluations were made of 102 common carotid bifurcations in 51 patients who had undergone both conventional angiography and 2DTF-MR angiography. The percent of diameter stenosis was calculated from the conventional angiogram using the method adopted by the Asymptomatic Carotid Atherosclerosis Study (ACAS) trial. An MR flow gap was noted if there was a segment of the vessel that was completely free of signal with a reappearance of the signal distally. According to conventional angiography, the minimum percentage of stenosis associated with a flow gap is 56%. Flow gaps were present in 20 of 22 arteries (sensitivity 91%) with stenosis of 60% or more and in two of the 66 arteries (specificity 97%) with less than 60% stenosis. Flow gaps were present in all arteries with stenosis of 70% or more. Complete occlusion was correctly identified in 10 of 10 cases.
These results demonstrate that the presence of a flow gap on 2DTF-MR angiography is a reliable marker of clinically significant carotid stenosis (measuring 60% or more), with sensitivity and specificity comparable to duplex carotid ultrasound. In addition, MR angiography can be used to screen the intracranial circulation for significant vascular pathology in patients being considered for carotid endarterectomy.
Moderate hypothermia in patients with severe head injury: cerebral and extracerebral effects
Authors: Metz Christoph , Holzschuh Matthias , Bein Thomas , Woertgen Christian , Frey Anton , Frey Irmgard , Taeger Kai , Brawanski Alexander 
Published: June 2009

✓ Cerebral and extracerebral effects of moderate hypothermia (core temperature 32.5°C–33.0°C) were prospectively studied in 10 patients with severe closed head injury (Glasgow Coma Scale score, < 7) in the intensive care unit of a university hospital. Hypothermia was induced by cooling the patient's body surface with water-circulating blankets. Before cooling, a conventional intracranial pressure (ICP) reduction therapy was applied, which remained unchanged throughout the study. Cerebral blood flow (CBF), cerebral metabolic rates for oxygen (CMRO2) and lactate (CMRL), and ICP were simultaneously measured prior to inducing hypothermia, after obtaining hypothermia, after 24 hours of hypothermia, and after rewarming. With respect to extracerebral effects, supplemental investigations were conducted 24 and 72 hours after rewarming. The median delay between injury and induction of hypothermia was 16 hours.
Hypothermia reduced CMRO2 by 45% (p < 0.01), whereas CBF did not change significantly. Before cooling, six patients had elevated CMRL indicating cerebral ischemia. Cooling normalized CMRL in all patients (p < 0.01). The intracranial hypertension present prior to cooling declined markedly during hypothermia (p < 0.01) without significant rebound effects after rewarming. Cardiac index decreased by 18% after hypothermia was reached (p < 0.05), recovered at 24 hours of hypothermia, and surpassed baseline values after rewarming. Platelet counts dropped continuously up to 24 hours after rewarming (p < 0.01). Plasma coagulation tests did not show significant worsening. Creatinine clearance decreased during cooling (p < 0.01) and recovered by 24 hours after rewarming. Twenty-four hours after cooling had begun, eight patients had elevated serum lipase activity (p < 0.01) and four of them acquired pancreatitis. Rewarming normalized both pancreatic alterations. Seven patients made a good recovery; one survived severely disabled; and two patients died.
Moderate hypothermia is effective in preventing secondary brain damage while reducing cerebral ischemia. However, there are potentially hazardous side effects that require additional monitoring.
Effect of the novel high-affinity glycine-site N-methyl-d-aspartate antagonist ACEA-1021 on 125I-MK-801 binding after subdural hematoma in the rat: an in vivo autoradiographic study
Authors: Di Xiao , Bullock Ross 
Published: June 2009

✓ Acute subdural hematoma (SDH) complicates 20% of severe human head injuries and causes death or severe disability in 60% of these cases, due to brain swelling and high intracranial pressure. Although the mechanisms for these phenomena are unknown, previous studies have implicated excitatory amino acid—mediated mechanisms in both humans and animal models. The authors therefore performedin vivoautoradiography using125I-MK-801, a high-affinity noncompetitiveN-methyl-d-aspartate (NMDA) receptor antagonist, as a tracer to evaluate NMDA ion channel activation spatially and temporally as a factor causing cytotoxic swelling.Acute SDH was induced in 16 anesthetized rats using 0.4 ml autologous venous blood. Fifty microcuries of125I-MK-801 was injected via an aortic arch cannula 30 minutes after onset of SDH. The effect of a new putatively neuroprotective drug, ACEA-1021, a glycine-specific binding site NMDA antagonist, on125I-MK-801 binding was tested on five animals. “Nonspecific”125I-MK-801 binding in the rat brain was assessed by pretreatment with “cold” (nonradiolabeled) MK-801 in five more animals. Four hours later the animals were sacrificed and brain sections were apposed to radiation-detecting high-sensitivity photographic film with precalibrated plastic standards for 4 weeks. A striking and highly significant 1.7- to 4.8-fold increase in125I-MK-801 binding was seen in the penumbra of viable tissue surrounding the ischemic zone beneath the acute SDH, when compared to contralateral hemisphere binding (p < 0.001). The MK-801 pretreatment markedly reduced125I-MK-801 uptake in this penumbral zone (4.73 ± 0.36 nCi/mg control vs. 2.85 ± 0.08 nCi/mg cold MK-801; p < 0.0001), indicating that the increased binding in the penumbra of the lesion was due to NMDA ion channel activation. Pretreatment with ACEA-1021 reduced125I-MK-801 uptake by 28% (3.41 ± 0.26 nCi/mg vs. 4.73 ± 0.36 nCi/mg; p < 0.05), indicating that this agent prevents opening of the NMDA ion channel and, thus, exposure of its receptor for MK-801 binding.These studies show intense foci of penumbral NMDA receptor-mediated ion channel activation after onset of SDH, which is markedly reduced by an NMDA antagonist. Such agents are thus likely to reduce cell swelling after SDH occurs.
Adverse effects of pentobarbital on cerebral venous oxygenation of comatose patients with acute traumatic brain swelling: relationship to outcome
Authors: Cruz Julio 
Published: June 2009

✓ Global cerebrovenous oxygenation was evaluated before and after intravenous administration of pentobarbital sodium for the management of refractory intracranial hypertension in 151 comatose patients who had acute traumatic brain swelling. Two groups of patients were identified: a group in which the jugular oxyhemoglobin saturation (SjO2) remained at or above 45% after pentobarbital bolus, and a group in which the SjO2 dropped below 45%. The two groups were matched by predominant findings on computerized tomography scans of the head, as well as age, postresuscitation Glasgow Coma Scale scores, levels of total hemoglobin content, SjO2, intracranial pressure (ICP), and cerebral perfusion pressure (CPP) prior to pentobarbital bolus.
Outcomes were significantly worse (p < 0.0001) in patients who developed decreases in SjO2 to levels below 45% than in those whose SjO2 remained at or above 45%, despite the fact that there were no significant differences between the two groups with regard to ICP and CPP after an intravenous bolus of pentobarbital.
Hyperemia following traumatic brain injury: relationship to intracranial hypertension and outcome
Authors: Kelly Daniel F. , Kordestani Rouzbeh K. , Martin Neil A. , Nguyen Tien , Hovda David A. , Bergsneider Marvin , McArthur David L. , Becker Donald P. 
Published: June 2009

✓ The role of posttraumatic hyperemia in the development of raised intracranial pressure (ICP) has important pathophysiological and therapeutic implications. To determine the relationship between hyperemia (cerebral blood flow (CBF) > 55 ml/100 g/minute), intracranial hypertension (ICP > 20 mm Hg), and neurological outcome, 193 simultaneous measurements of ICP and CBF (xenon-133 method) were obtained in 59 patients with moderate and severe head injury.
Hyperemia was associated with an increased incidence of simultaneous intracranial hypertension compared to nonhyperemic CBF measurements (32.2% vs. 21.6%, respectively; p < 0.059). However, in 78% of blood flow studies in which ICP was greater than 20 mm Hg, CBF was less than or equal to 55 ml/100 g/minute. At least one episode of hyperemia was documented in 34% of patients, all of whom had a Glasgow Coma Scale (GCS) score of 9 or below. In 12 individuals with hyperemia without simultaneous intracranial hypertension, ICP was greater than 20 mm Hg for an average of 11 ± 16 hours and favorable outcomes were seen in 75% of patients. In contrast, in eight individuals with hyperemia and at least one episode of hyperemia-associated intracranial hypertension, ICP was greater than 20 mm Hg for an average of 148 ± 84 hours (p < 0.001), and a favorable outcome was seen in only one patient (p < 0.001). Compared to the remainder of the cohort, patients with hyperemia-associated intracranial hypertension were distinctive in being the youngest, exhibiting the lowest GCS scores (all ≤ 6), and having the highest incidence of effaced basilar cisterns and intractable intracranial hypertension.
In the majority of individuals with hyperemia-associated intracranial hypertension, their clinical profile suggests the occurrence of a severe initial insult with resultant gross impairment of metabolic vasoreactivity and pressure autoregulation. In a minority of these patients, however, high CBF may be coupled to a hypermetabolic state, given their responsiveness to metabolic suppressive therapy. In patients with hyperemia but without intracranial hypertension, elevated CBF is also likely to be a manifestation of appropriate coupling to increased metabolic demand consistent with a generally favorable outcome. This study supports the concept that there are multiple etiologies of both elevated blood flow and intracranial hypertension after head injury.
The validity of classification for the clinical presentation of intracranial dural arteriovenous fistulas
Authors: Davies Mark A. , TerBrugge Karel , Willinsky Robert , Coyne Terry , Saleh Jamshid , Wallace M. Christopher 
Published: June 2009

✓ A number of classification schemes for intracranial dural arteriovenous fistulas (AVFs) have been published that claim to predict which lesions will present in a benign or aggressive fashion based on radiological anatomy. We have tested the validity of two proposed classification schemes for the first time in a large single-institution study.
A series of 102 intracranial dural AVFs in 98 patients assessed at a single institution was analyzed. All patients were classified according to two grading scales: the more descriptive schema of Cognard, et al. (Cognard) and that recently proposed by Borden, et al. (Borden). According to the Borden classification, 55 patients were Type I, 18 Type II, and 29 Type III. Using the Cognard classification, 40 patients were Type I, 15 Type IIA, eight Type IIB, 10 Type IIA+B, 13 Type III, 12 Type IV, and four Type V.
Intracranial hemorrhage (ICH) or nonhemorrhagic neurological deficit was considered an aggressive presenting clinical feature. A total of 16 (16%) of 102 intracranial dural AVFs presented with hemorrhage. Eleven of these hemorrhages (69%) occurred in either anterior cranial fossa or tentorial lesions. When analyzed according to the Borden classification, none (0%) of 55 Type I intracranial dural AVFs, two (11%) of 18 Type II, and 14 (48%) of 29 Type III intracranial dural AVFs presented with hemorrhage (p < 0.0001). After exclusion of visual or cranial nerve deficits that were clearly related to cavernous sinus intracranial dural AVFs, nonhemorrhagic neurological deficits were a feature of presentation in one (2%) of 55 Type I, five (28%) of 18 Type II, and nine (31%) of 29 Type III patients (p < 0.0001). When combined, an aggressive clinical presentation (ICH or nonhemorrhagic neurological deficit) was seen most commonly in intracranial dural AVFs located in the tentorium (11 (79%) of 14) and the anterior cranial fossa (three (75%) of four), but this simply reflected the number of higher grade lesions in these locations. Aggressive clinical presentation strongly correlated with Borden types: one (2%) of 55 Type I, seven (39%) of 18 Type II, and 23 (79%) of 29 Type III patients (p < 0.0001). A similar correlation with aggressive presentation was seen with the Cognard classification: none (0%) of 40 Type I, one (7%) of 15 Type IIA, three (38%) of eight Type IIB, four (40%) of 10 Type IIA+B, nine (69%) of 13 Type III, 10 (83%) of 12 Type IV, and four (100%) of four Type V (p < 0.0001).
No location is immune from harboring lesions capable of an aggressive presentation. Location itself only raises the index of suspicion for dangerous venous anatomy in some intracranial dural AVFs. The configuration of venous anatomy as reflected by both the Cognard and Borden classifications strongly predicts intracranial dural AVFs that will present with ICH or nonhemorrhagic neurological deficit.
Systemic administration of an inhibitor of endothelin-converting enzyme for attenuation of cerebral vasospasm following experimental subarachnoid hemorrhage
Authors: Caner Hakan H. , Kwan Aij-Lie , Arthur Adam , Jeng Arco Y. , Lappe Rodney W. , Kassell Neal F. , Lee Kevin S. 
Published: June 2009

✓ The potent vasoconstrictor peptide, endothelin-1 (ET-1), has been implicated in the pathophysiology of cerebral vasospasm that occurs after subarachnoid hemorrhage (SAH). This peptide is synthesized as a large prepropeptide that requires a series of modifying steps for its activation. The last of these steps involves the proteolytic conversion of a relatively inactive propeptide, Big ET-1, to its active, 21—amino acid peptide form. The enzyme responsible for converting Big ET-1 to ET-1 is a metalloprotease called endothelin-converting enzyme (ECE). In the present study the authors examined the effects of a newly developed inhibitor of ECE on responses to ET peptides in the normal basilar artery and on pathophysiological constriction in the spastic basilar artery after SAH.In the first series of experiments the authors examined normal basilar arteries in the rabbit, which were exposed transclivally and measured on-line using videomicroscopy. Intravenous administration or topical application of an active inhibitor of ECE, CGS 26303, blocked vasoconstrictor responses to topically applied Big ET-1 but not to ET-1. In contrast, topical application of a structurally related compound that does not inhibit ECE, CGS 24592, was ineffective in blocking vasoconstriction that was elicited by a topical application of Big ET-1. These findings indicate that CGS 26303 when administered systemically is capable of blocking the conversion of Big ET-1 to ET-1 in the basilar artery without affecting the ability of the vessel to respond to ET-1. In the second series of experiments the authors examined the effects of the ECE inhibitor on cerebral vasospasm after experimental SAH. Intraperitoneal administration of CGS 26303 via osmotic minipumps significantly attenuated the delayed spastic response of the basilar artery to an intracisternal injection of autologous blood.This study provides the first evidence that systemic administration of an inhibitor of ECE is capable of preventing cerebral vasospasm after SAH. The results reinforce a growing body of evidence that ETs play a critical role in the development of spastic constriction after SAH. Moreover, the findings indicate that blocking the conversion of Big ET-1 to its active ET-1 form using CGS 26303 may represent a feasible strategy for ameliorating cerebral vasospasm.