bluuebunny/crossref_metadata_2025 huggingface dataset:
Intraosseous glomus tumor of the spine
Authors: Robinson James C. , Kilpatrick Scott E. , Kelly David L.
Published: June 2009

✓ The authors report a case of glomus tumor originating within the lumbar spine. Glomus tumors of intraosseous origin are rare, with the only case reported in the spine arising in the sacrum. The patient presented with the solitary complaint of radiating back pain that resolved postoperatively. The histopathological and radiographic findings are reviewed. To the authors' knowledge, this represents the first case report of a glomus tumor of the spine originating above the sacrum.
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.
Traumatic interdural arachnoid cyst in the upper cervical spine
Authors: Chen Han-Jung , Chen Leung
Published: June 2009

✓ The case of an interdural arachnoid cyst of traumatic origin at the C3–5 level in an 18-year-old man was admitted to our hospital with a 1-year history of progressive weakness in left limbs and numbness below the clavicles is reported. He had had a C-2 fracture at the age of 9 years without definite neurological deficits. Magnetic resonance imaging revealed a cystic lesion in the C3–5 level. Laminectomy was performed, and an interdural cyst was found. Histological examination revealed fibrous thickening of the arachnoid membrane. A cyst located in the interdural space of upper cervical spine is extremely rare.
Use of a split dura for revascularization of ischemic hemispheres in moyamoya disease
Authors: Kashiwagi Shiro , Kato Shoichi , Yasuhara Shinko , Wakuta Yukio , Yamashita Tetsuo , Ito Haruhide
Published: June 2009

✓ A new technique of indirect revascularization using the dural arterial supply to provide donor vessels is presented together with the results of an assay performed to determine the angiogenic activity of the dura. At surgery, a portion of the dura near the branches of the middle meningeal artery was split into outer and inner layers, and the split surface of the outer layer was attached to the cortical surface. This procedure, combined a with standard encephaloduroarteriosynangiosis, was applied to 25 hemispheres in 18 patients with pediatric moyamoya disease (mean age 6 years). All of the patients were symptom free by 1.5 years after surgery. The follow-up period ranged from 1 to 12 years (mean 6.5 years). Thirteen (81%) of 16 patients were able to lead normal lives and three were mildly handicapped due to mental retardation that existed preoperatively. Postoperative superselective angiograms demonstrated effective cortical revascularization through the dural arteries as well as from the scalp arteries. A histological study of the dura in cases of moyamoya disease showed an increased number of blood vessels in the outer layer. Angiogenic activity determined by chorioallantoic membrane assay was higher in the split surface of the dura than in the internal surface of the dura (the natural interface between the dura and cortex). The split duroencephalosynangiosis described in this report is a useful addition to indirect revascularization techniques, allowing extension of the area of revascularization in the ischemic hemispheres of patients with moyamoya disease.
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.
Are peripheral neurectomies of value in the treatment of trigeminal neuralgia? An analysis of new cases and cases involving previous radiofrequency gasserian thermocoagulation
Authors: Murali Raj , Rovit Richard L.
Published: June 2009

✓ The indications, advantages, complications, and benefits of peripheral neurectomy in patients with trigeminal neuralgia were studied in detail in 40 patients treated between 1982 and 1991. Twenty-eight patients had previously received radiofrequency thermocoagulation; peripheral neurectomy was performed for pain recurrence. These patients had excellent or good pain relief for at least 5 years postsurgery. Of the 12 patients who had peripheral neurectomy as their only procedure, seven had an excellent result and five had a good result. Five of the patients had recurrence of pain after 2 years but responded well to a second neurectomy. Elderly patients who experienced pain in the first and second divisions of the trigeminal distributions were the best candidates. Peripheral neurectomy is an effective, safe procedure for elderly patients who suffer from trigeminal neuralgia and have a limited life span.
Long-term effects of continuous intrathecal opioid treatment in chronic pain of nonmalignant etiology
Authors: Winkelmüller Matthias , Winkelmüller Wolfhard
Published: June 2009

✓ In the present retrospective investigation, the long-term effects of continuous intrathecal opioid therapy via implantable infusion pump systems were examined in 120 patients with chronic, nonmalignant pain syndromes. The follow-up period was 6 months to 5.7 years (mean 3.4 years ± 1.3 standard error of the mean). Deafferentation pain and neuropathic pain showed the best long-term results, with 68% and 62% pain reduction (visual analog scale), respectively. The mean morphine dosage initially administered was 2.7 mg/day (range 0.3–12 mg/day); after an average of 3.4 years, it was 4.7 mg/day (range 0.3–12 mg/day). In a long-term observation of 28 patients who received intrathecal morphine for longer than 4 years, 18 patients (64.3%) had a constant dosage history and 10 patients (35.7%) showed an increase in morphine dosage to more than ± mg/day 1 year after dosage determination. In seven cases, a tolerance developed; in four patients the tolerance was controlled by means of “drug holidays”; but in three patients it was necessary to remove the pump systems. Explantation of the pump system occurred in 22 additional cases for other reasons. Throughout the follow-up period, 74.2% of the patients profited from the intrathecal opiate therapy; the average pain reduction after 6 months was 67.4% and, as of the last follow-up examination, it was 58.1%. Ninety-two percent of the patients were satisfied with the therapy and 81% reported an improvement in their quality of life. The authors' 6-year experience with administration of intrathecal opioid medications for nonmalignant pain should encourage the use of this method in carefully selected patients.
Giant intracranial aneurysm and fibromuscular dysplasia in an adolescent with α1-antitrypsin deficiency
Authors: Schievink Wouter I. , Puumala Michael R. , Meyer Fredric B. , Raffel Corey , Katzmann Jerry A. , Parisi Joseph E.
Published: June 2009

✓ Recent studies have suggested that a deficiency of α1-antitrypsin may be a genetic risk factor for the development of intracranial aneurysms and arterial fibromuscular dysplasia. The authors report a 16-year-old girl with a history of lung disease who suffered a cerebral hemorrhage due to the rupture of a giant intracranial aneurysm arising from the middle cerebral artery. This fusiform aneurysm was associated with fibromuscular dysplasia of the intimal type. She was found to have an unusual α1-antitrypsin deficiency (PiMP phenotype). This case provides further evidence of an underlying arteriopathy in α1-antitrypsin deficiency.
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.
Functional results after resective procedures involving the supplementary motor area
Authors: Zentner Josef , Hufnagel Andreas , Pechstein Ulrich , Wolf Helmut K. , Schramm Johannes
Published: June 2009

✓ In this article, the authors report their experience with surgically induced supplementary motor area (SMA) deficiency syndrome in a prospective clinical trial of 28 patients who underwent surgery for tumorous (19 patients) or nontumorous (nine patients) lesions. The dominant side was affected in 17 patients and the nondominant side in 11 patients. The primary presenting symptoms included seizure activity (23 patients), hemiparesis (four patients), and aphasia (one patient). Functional topographic mapping, achieved by phase reversal of somatosensory evoked potentials, allowed precise localization of the central sulcus in 25 of the 28 patients. Motor evoked potential (MEP) monitoring, which was performed successfully in 13 of 15 cases during the resective procedure, showed no significant changes in the potentials in any patient. Immediately after surgery, 25 (89%) of the 28 patients displayed additional neurological deficits (aphasia and/or hemiparesis) that depended on the extent of the SMA resection. In 12 patients the SMA was resected completely: nine of these patients demonstrated a complete and three an incomplete deficit. In 16 patients the SMA resection was incomplete: 13 of these patients displayed an incomplete deficit, whereas three had no deficit. Neurological disorders resolved completely within 3 to 42 days (mean 11 days), except for a minimal disturbance of fine motor and/or speech function in complex tasks or at high speed. Electromagnetically elicited MEPs, examined postoperatively in five patients, were initially absent but recovered with improvement of motor function. In conclusion, although the SMA is known to control important functions such as initiation of motor activity or speech, our findings show that unilateral SMA removal can be accomplished without resulting in significant permanent deficits. Functional topographic mapping and monitoring facilitate the exact delineation of the adequate resection plane along the precentral sulcus, and postoperative magnetic resonance imaging allows precise correlation of clinical and anatomical data.
The central sulcal vein: a landmark for identification of the central sulcus using functional magnetic resonance imaging
Authors: Yousry Tarek Ahmed , Schmid Urs Dieter , Schmidt Dorothea , Hagen Thomas , Jassoy Andre , Reiser Maximilian Friedrich
Published: June 2009

✓ The authors evaluated the anatomical location of the central sulcus (CS) in 24 cerebral hemispheres (eight in which tumors were located centrally, 16 in controls) using: 1) classic anatomical landmarks seen on magnetic resonance (MR) imaging (24 hemispheres); 2) functional MR imaging (24 hemispheres); and 3) intraoperative electrical stimulation mapping (eight hemispheres). On MR imaging the CS was identified with certainty in 79% of hemispheres (four of eight in patients, 15 of 16 in controls). Functional MR imaging identified a parenchymal “motor hand area” in only 83% (20 of 24 hemispheres; five of eight in patients, 15 of 16 in controls); this area was located in the precentral gyrus in 16 (80%) of 20, additionally in the postcentral gyrus in 10 (50%) of 20, and exclusively in the postcentral gyrus in four (20%) of 20. In contrast, functional MR imaging detected one to three sulcal veins presumably draining blood from the adjacent motor hand area in 100% (24 of 24) of the hemispheres studied, and anatomical MR imaging and intraoperative mapping localized these veins in the CS. It is concluded that sulcal veins lying deep within the CS: 1) drain activated blood from the adjacent pre- or postcentral cortex during performance of a motor hand task; 2) can be identified easily with functional MR imaging; and 3) are an anatomical landmark for noninvasive indentification of the CS and thus the sensorimotor strip. The detection of these veins provides a more consistent landmark than the detection of parenchymal motor areas by functional MR imaging; this technique may be used when classic anatomical landmarks fail to identify the sensorimotor strip.
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.
Toxicity studies in thymidine kinase—deficient herpes simplex virus therapy for malignant astrocytoma
Authors: Jia William W. G. , Tan Jiren , Redekop Gary J. , Goldie James H.
Published: June 2009

✓ Previous studies have shown that genetically engineered thymidine kinase (tk)—defective herpes simplex virus type 1 (HSV-1) can effectively and selectively destroy gliomas in animal models. The consequences of viral infection and tumor regression must be characterized before this therapy can be applied in human trials. To study the potential for long-term toxicity, immunocompetent rats harboring 9L gliosarcomas were injected intratumorally with a tk—defective HSV-1, KOS-SB, at titers that previously have been demonstrated to cause tumor regression. In animals surviving 3 months or longer following viral treatment, there was no evidence of persistent infection or inflammation in peritumoral brain tissue or in remote systemic organs studied with routine histological and immunocytochemical analyses. Polymerase chain reaction using primers specific for HSV-1 detected HSV-1 DNA in peritumoral tissue only in animals sacrificed within 3 months of viral injection. There was no evidence of HSV-1 DNA in systemic tissues at any time after treatment. We conclude that stereotactic intratumoral injection of tk—deficient HSV can be attempted for the treatment of brain tumors without risk of systemic infection or significant toxicity to normal brain or remote proliferating tissues.
Hydrocephalus secondary to diffuse villous hyperplasia of the choroid plexus
Authors: Britz Gavin W. , Kim D. Kyle , Loeser John D.
Published: June 2009

✓ Diffuse villous hyperplasia of the choroid plexus, which is distinct from bilateral choroid plexus papillomas, is extremely rare and is often associated with hydrocephalus due to the overproduction of cerebrospinal fluid (CSF). The authors describe an infant with hydrocephalus, diagnosed by computerized tomography scanning, who developed ascites following placement of a ventriculoperitoneal shunt and, subsequently, demonstrated excessive CSF production when the shunt was externalized. The patient was later successfully treated by placement of a ventriculoatrial shunt. Magnetic resonance imaging demonstrated diffuse villous hyperplasia of the choroid plexus as the cause of the patient's hydrocephalus. The literature on diffuse villous hyperplasia of the choroid plexus is reviewed.
Atypical monoclonal plasma cell hyperplasia: its identity and treatment
Authors: Hsiang John N. K. , Ng Ho-Keung , Poon Wai-Sang
Published: June 2009

✓ Atypical monoclonal plasma cell hyperplasia, like plasma cell granuloma, is an inflammatory pseudotumor. Both are extremely rare in the central nervous system. Atypical monoclonal plasma cell hyperplasia is a recently identified neuropathological entity described by Weidenheim, et al., in 1989. A second case of this disease entity is now reported. The histological findings that differentiate this lesion from plasma cell granuloma, plasmacytoma, and meningioma are discussed. The present case clearly demonstrates the complete resolution of the disease after a course of fractionated radiotherapy.
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.
Periodontoid calcium pyrophosphate dihydrate deposition disease: “pseudogout” mass lesions of the craniocervical junction
Authors: Zünkeler Bernhard , Schelper Robert , Menezes Arnold H.
Published: June 2009

✓ Between 1984 and 1996, seven patients with symptomatic masses located posterior to the odontoid process and containing calcium pyrophosphate dihydrate crystals were evaluated by the senior author (A.H.M.). All patients presented with distal paresthesias and myelopathy and underwent transoral-transpharyngeal resection of the anterior arch of C-1, the odontoid process, and the compressing mass. Histological examination revealed the characteristic changes of calcium pyrophosphate dihydrate (CPPD) deposition disease, with nodular deposits of birefringent rhomboid crystals. On magnetic resonance imaging, the masses appeared predominantly isointense with neural tissue on T1-weighted images and iso- to hyperintense on T2-weighted images. On computerized tomography scans, small areas of calcifications within the masses were apparent in all cases. All patients improved postoperatively, with six of seven patients requiring posterior fixation for instability as a second procedure. Calcium pyrophosphate dihydrate deposition causing periodontoid mass lesions is a distinct clinical disease entity that probably is underdiagnosed. In the authors' opinion, the diagnosis can often be established preoperatively by the distinctive neuroradiological appearance of the masses. Therefore, CPPD deposition disease should be considered in the differential diagnosis of masses of the craniocervical junction, because it is amenable to early surgical intervention. The consulting neuropathologist should be made aware of this diagnostic possibility at the time of surgery.
Atlantoaxial degenerative articular cysts
Authors: Birch Barry D. , Khandji Alexander G. , McCormick Paul C.
Published: June 2009

✓ Cysts associated with spinal joints are not a common cause of neurological symptoms. The authors report a series of five patients with cysts of the atlantodental articulation and review five additional cases from the literature. The patients ranged from 60 to 85 years of age and included three men and seven women. No patient had evidence of rheumatoid arthritis or previous trauma. The cysts caused ventral cervicomedullary compression, did not enhance on magnetic resonance imaging, and were not associated with widening of the anterior atlantodental interval or osseous degeneration of the dens. All patients improved postsurgery. Fusion was required if a transoral procedure was performed. Patients undergoing posterior decompressions were clinically and radiographically stable after operation.
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.
Expression of vascular endothelial growth factor in pediatric and adult cerebral arteriovenous malformations: an immunocytochemical study
Authors: Sonstein William J. , Kader Abraham , Michelsen W. Jost , Llena Josefina F. , Hirano Asao , Casper Diana
Published: June 2009

✓ Children and adults may differ with respect to their cerebral vasculature in both normal and pathological states. The authors have identified four pediatric patients in whom a cerebral arteriovenous malformation (AVM) recurred after surgery for removal of the AVM and in whom a normal postoperative angiogram had been obtained. This phenomenon has not been observed in adults. The propensity to regrow a cerebral AVM may reflect a less mature cerebral vasculature and a disregulated angiogenic process. Recently, attention has focused on vascular endothelial growth factor (VEGF) as a possible general mediator of angiogenesis in development and neoplasia. A retrospective immunocytochemical analysis of VEGF expression in AVM tissue was conducted to test the hypothesis that VEGF expression may be found in association with the regrowth of AVMs. The results demonstrate a high degree of astrocytic VEGF expression in four (100%) of four specimens from the initial operation in the children with recurrent AVMs as compared to one (14%) of seven nonrecurrent AVMs in the pediatric and two (25%) of eight adult specimens. All of the specimens from the first operation of the recurrent group demonstrate a clear association of cellular immunoreactivity to the abnormal blood vessels, a relationship that was not observed in the specimens from the nonrecurrent groups. These observations indicate that a humoral mechanism mediated by VEGF may play a role in AVM recurrence.
Inhibition of vascular contraction by intracisternal administration of preproendothelin-1 mRNA antisense oligoDNA in a rat experimental vasospasm model
Authors: Onoda Keisuke , Ono Shigeki , Ogihara Kotaro , Shiota Tomomi , Asari Shoji , Ohmoto Takashi , Ninomiya Yoshifumi
Published: June 2009

✓ To clarify the role of endothelin-1 (ET-1) in the etiology of hemolysate-induced contraction of vessels, the authors introduced antisense oligoDNA for preproendothelin-1 (ppET-1) messenger RNA in a rat model of vasospasm. Phosphorothioate antisense oligoDNAs for ppET-1 were injected into the cisterna magna. Fluorescein isothiocyanate-labeled phosphorothioate antisense oligoDNAs were proven by fluorescence chasing to be incorporated into the vascular wall. Striking inhibitory effects of experimental vasospasm were observed in the basilar artery (BA) in which the oligoDNAs were injected. The vascular contraction was significantly inhibited by oligoDNAs after 20 minutes of hemolysate exposure, which suggested that ET synthesis started approximately 20 minutes after hemolysate stimulation. Expression of ppET-1 in the BA in which the spasm was inhibited was markedly suppressed at the transcription level. The results indicate that ET-1 may play an important role in hemolysate-induced vasoconstriction in rats. In addition, the antisense approach in the cerebrospinal fluid might be a useful tool for preventing cerebral vasospasm.
Cerebral blood flow and vasoresponsivity within and around cerebral contusions
Authors: McLaughlin Mark R. , Marion Donald W.
Published: June 2009

✓ There is increasing evidence that regional ischemia plays a major role in secondary brain injury. Although the cortex underlying subdural hematomas seems particularly vulnerable to ischemia, little is known about the adequacy of cerebral blood flow (CBF) or the vasoresponsivity within the vascular bed of contusions. The authors used the xenon-enhanced computerized tomography (CT) CBF technique to define the CBF and vasoresponsivity of contusions, pericontusional parenchyma, and the remainder of the brain 24 to 48 hours after severe closed head injury in 10 patients: six patients with one contusion and four with two contusions, defined as mixed or high-density lesions on CT scanning. The CBF within the contusions (29.3 ± 16.4 ml/100 g/minute, mean ± standard deviation) was significantly lower than both that found in the adjacent 1-cm perimeter of normal-appearing tissue (42.5 ± 15.8 ml/100 g/minute) and the mean global CBF (52.5 ± 17.5 ml/100 g/minute) (p < 0.004, repeated-measures analysis of variance). A subset of seven patients (10 contusions) also underwent a second Xe-CT CBF study during mild hyperventilation (a PaCO of 24–32 mm Hg). In only two of these 10 contusions was vasoresponsivity less than 1% (range 0%–7.6%); in the rim of normal-appearing pericontusional tissue, it was 0.4% to 9.1%. The authors conclude that CBF within intracerebral contusions is highly variable and is often above 18 ml/100 g/minute, the reported threshold for irreversible ischemia. Intracontusional CBF is significantly reduced relative to surrounding brain parenchyma, and CO2 vasoresponsivity is usually present. In the contusion and the surrounding parenchyma, vasoresponsivity may be nearly three times normal, suggesting hypersensitivity to hyperventilation therapy. Given this possible hypersensitivity and relative hypoperfusion within and around cerebral contusions, these lesions are particularly vulnerable to secondary injury such as that which may be caused by hypotension or aggressive hyperventilation.
A model of diffuse traumatic brain injury in the immature rat
Authors: Adelson P. David , Robichaud Paul , Hamilton Ronald L. , Kochanek Patrick M.
Published: June 2009

✓ Diffuse cerebral swelling after severe traumatic brain injury (TBI) develops more commonly in children than adults; however, models of diffuse brain injury in immature animals are lacking. The authors developed a new model of diffuse severe TBI in immature rats by modifying a recently described closed head injury model for adult rats. A total of 105 Sprague—Dawley immature rats (17 days old; average weight 38.5 ± 5.46 g) were subjected to head impact using variable weights (0 g (sham), 75 g, 100 g, or 125 g) delivered from a height of 2 m onto a metal disk cemented to the intact cranium. Mortality, physiological and neurological parameters (from early reflex recovery to escape), and early histopathological changes were assessed. During the acute period after severe injury (SI) (100 g delivered from a height of 2 m; 50 rats), apnea was frequently observed and the mortality rate was 38%. Neurological recovery was complete in the sham-injured animals (11 rats) by 4.1 ± 0.23 minutes (mean ± standard error of the mean), but was delayed in both moderately injured (MI) (75 g/2 m; 11 rats) (14.97 ± 3.99 minutes) and SI (20.57 ± 1.31 minutes (p < 0.05)) rats. In the first 24 hours, the sham-injured animals were more active than the injured ones as reflected by a greater net weight gain: 2.9 ± 1.0 g, 1.2 ± 1.6 g, and −0.6 ± 2.1 g in sham-injured, MI, and SI animals, respectively. Immediately after injury, transient hypertension (lasting < 15 seconds) was followed by hypotension (lasting < 3 minutes) and loss of temperature regulation. Both injuries also induced apnea (0.75 ± 0.7 minutes and 1.27 ± 0.53 minutes in MI and SI groups, respectively), which either resolved or deteriorated to death. Intubation and assisted ventilation in animals with SI for 9.57 ± 3.27 minutes in the peritrauma period eliminated mortality (p < 0.05, intubated vs. nonintubated). Histologically, after SI, there was diffuse edema throughout the corpus callosum below the region of injury and in the thalami. Other injuries included neuronal death in the deep nuclei, bilateral disruption of CA3, diffuse subarachnoid hemorrhage, and, in some, ventriculomegaly. Following a diffuse TBI in immature rats, SI produced a mortality rate, neurological deficit, and histological changes similar to those previously reported for an injury resulting from a 450-g weight dropped from 2 m in adult rats. A graded insult was achieved by maintaining the height of the weight drop but varying the weights. Weight loss, acute physiological instability, and acute neurological deficits were also indicative of an SI. Mortality was eliminated when ventilatory support was used during the peritrauma period. This model should be useful in studying the response of the immature rat to diffuse severe TBI.
Role of endothelin in pial artery vasoconstriction and altered responses to vasopressin after brain injury
Authors: Armstead William M.
Published: June 2009

✓ Pial artery constriction following fluid-percussion injury to the brain is associated with elevated cerebrospinal fluid (CSF) vasopressin concentration in newborn pigs. It has also been observed that fluid-percussion injury reverses the function of vasopressin from that of a dilator to a constrictor. Endothelin-1 (ET-1), a purported mediator of cerebral vasospasm, can be released by several stimuli, including vasopressin. The present study was designed to investigate the role of ET-1 in pial artery constriction and in the reversal of vasopressin from a dilator to a constrictor, which is observed after fluid-percussion injury. Brain injury of moderate severity (1.9–2.3 atm) was produced in anesthetized newborn pigs that had been equipped with a closed cranial window. Endothelin-1 elicited pial dilation at low concentrations and vasoconstriction at higher concentrations. Fluid-percussion injury reversed the process of dilation to that of constriction at the low ET-1 concentration and potentiated this constriction at high ET-1 concentrations (10% ± 1%, −8% ± 1%, and −15% ± 1% vs. −6% ± 1%, −17% ± 1%, and −26% ± 2% for 10−12, 10−10, 10−8M ET-1 before and after fluid-percussion injury, respectively). Vasopressin modestly increased CSF ET-1 concentration before fluid-percussion injury. Fluid-percussion injury markedly increased CSF ET-1 concentration and the ability of vasopressin to release ET-1 (20 ± 2, 26 ± 3, and 40 ± 4 pg/ml vs. 93 ± 6, 141 ± 9, and 247 ± 31 pg/ml for control, 40 pg/ml vasopressin, and 400 pg/ml vasopressin before and after fluid-percussion injury, respectively). An ET-1 antagonist, BQ 123 (10−6M) blunted pial artery constriction following fluid-percussion injury (146 ± 5 µm−127 ± 6 µm vs. 144 ± 5 µm−136 ± 4 µm). The BQ 123 also blocked the reversal of vasopressin's function from that of a dilator to a constrictor after fluid-percussion injury (8% ± 1%, 21% ± 3%, and −5% ± 1%, −14% ± 2% vs. 8% ± 1%, 21% ± 2% and 4% ± 1%, 2% ± 1% for 40 and 4000 pg/ml vasopressin before and after fluid-percussion injury in the absence and presence of BQ 123, respectively). The BQ 123 blocked the constrictor component to ET-1, whereas it had no effect on the dilator component. These data show that ET-1 contributes to pial constriction after fluid-percussion injury. These data also indicate that vasopressin-induced release of ET-1 contributes to the reversal of vasopressin from a dilator to a constrictor following fluid-percussion injury. Furthermore, these data indicate that elevated CSF vasopressin and ET-1 interact in a positive feedback manner to promote pial artery constriction following fluid-percussion injury.
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.
Cerebral protection by intermittent reperfusion during temporary focal ischemia in the rat
Authors: David Carlos A. , Prado Ricardo , Dietrich W. Dalton
Published: June 2009

✓ Temporary arterial occlusion has been routinely used as an adjunct in intracranial aneurysm surgery. This has commonly been performed using a protocol of multiple short periods of occlusion alternating with periods of restoration of normal circulation. Recently, the logical basis of this method has come under scrutiny. There is extensive experimental evidence to suggest that repetitive, brief periods of global ischemia may cause more severe cerebral injury than an equivalent single period of global ischemia. Only recently has this issue begun to be addressed with regard to focal ischemia. Hence, despite the common use of temporary clipping, little experimental data are available regarding the ischemic consequences of temporary arterial occlusion with periods of reperfusion versus uninterrupted temporary occlusion.

To investigate this issue, a protocol of occlusion/reperfusion that simulates the temporal profile that occurs during surgery was performed in a rat model of focal ischemia. Sixteen anesthetized Sprague—Dawley rats were divided into two groups. The animals in Group I underwent 60 minutes of uninterrupted middle cerebral artery occlusion and the animals in Group II were subjected to six separate 10-minute occlusion periods with 5 minutes of reperfusion between occlusions. Histopathological analysis was performed 72 hours postischemia. Group I had significantly increased mean infarction volumes (50.0 ± 12.1 mm3) compared to Group II (8.7 ± 3.1 mm3) (p = 0.008). Injuries in Group I occurred in both the cortex and striatum, whereas Group II showed only striatal injuries. Furthermore, the extent of the injuries in Group II was less severe, characterized by ischemic neuronal injury rather than frank infarction.

The results indicate that intermittent reperfusion is neuroprotective during temporary focal ischemia and support the hypothesis that intermittent reperfusion is beneficial if temporary clipping is required during aneurysm repair.