bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cytoskeletal and extracellular matrix proteins in cerebral arteries following subarachnoid hemorrhage in monkeys
Authors: Macdonald R. Loch , Weir Bryce K. A. , Young James D. , Grace Michael G. A. 
Published: May 2009

✓ It is unclear if vasospasm after subarachnoid hemorrhage (SAH) is predominantly due to smooth-muscle contraction, proliferative vasculopathy, or other changes within the arterial wall such as fibrosis or change in smooth-muscle phenotype. In this study, immunohistochemistry was used to examine changes in extracellular and cytoskeletal proteins in cerebral arteries after SAH that might support one of these mechanisms. Following baseline cerebral angiography, bilateral SAH was created in nine monkeys. Three animals each were killed 7, 14, or 28 days after SAH. Cerebral angiography was repeated on Day 7 in all animals and immediately prior to sacrifice in animals killed on Days 14 and 28. Both middle cerebral arteries and four control basilar arteries were examined using fluorescent antibody techniques with antisera to α-actin, myosin, fibronectin, fibrinogen, vimentin, desmin, laminin, and collagens (types I, III, IV, and V).
Angiography showed that vasospasm was most severe on Day 7, present but resolving on Day 14, and completely resolved by Day 28. Microscopic study of arterial sections and blinded review of microphotographs of arterial sections by five independent observers did not reveal changes in intensity of density of staining for collagens, desmin, myosin, laminin, or α-actin in the tunica media of tunica adventitia. Fibronectin immunoreactivity increased 14 days after SAH. Seven days after SAH, occasional areas of tunica media showed immunoreactivity to fibrinogen. On Day 28, intimal thickening was observed in four of six middle cerebral arteries and this tissue demonstrated immunoreactivity to α-actin, myosin, vimentin, desmin, fibronectin, laminin, and each type of collagen. No significant increases in the number of intimal cells showing immunoreactivity to α-actin were seen and no significant changes in the hydroxyproline content of cerebral arteries developed at any time after SAH. These results suggest that rigidity and lumen narrowing of vasospasm are not due to increased arterial collagen, although other proteins in the arterial wall or an alteration in cross-linking of existing proteins could produce these changes. There is no indication that smooth-muscle contractile proteins change during vasospasm or that increases in the number of α-actin-containing myointimal cells contribute to vasospasm. The occurrence of intimal thickening and increased tunica media fibronectin after vasospasm suggests that vasospasm damages smooth muscle, possibly as a result of intense prolonged smooth-muscle contraction.
Neurovascular compression in trigeminal neuralgia: a clinical and anatomical study
Authors: Hamlyn Peter J. , King Thomas T. 
Published: May 2009

✓ Neurovascular decompression is a widely practiced tec hnique for the treatment of trigeminal neuralgia, and yet there is still debate as to whether the beneficial effect results from relieving the nerve of compression by an anatomically abnormal vessel or from the manipulation and trauma the nerve undergoes during the procedure. The development of this operation has been hampered by the lack of adequate anatomical studies in normal controls. The authors present a combined study of clinical and anatomical material employing standardized definitions of the neurovascular relationships in both groups. Detailed simulations of the operative procedure were carried out on fresh cadavers matched for age, sex, and side, and a technique of in situ blood vessel perfusion was developed that enabled the normal neurovascular arrangement to be observed post mortem at physiological pressures.
Neurovascular compression, typified by a large vessel distorting and creating a groove in the fifth cranial nerve, was found in 37 of the 41 cases of trigeminal neuralgia; recurrence of pain did not relate to the site of compression. A follow-up study was carried out for a median of 53 months (range 12 to 103 months). No distortion was found in a total of 50 normal cadaveric dissections; however, on perfusion to physiological pressures, the percentage of nerves with vessels adjacent or in simple contact increased from 16% to 40%. This study using this new technique confirms that vascular compression of the fifth cranial nerve is an anatomical abnormality specific to trigeminal neuralgia.
Interphase cytogenetics: a new tool for the study of genetic changes in brain tumors
Authors: Arnoldus Edo P. J. , Wolters Laetitia B. T. , Voormolen Joan H. C. , van Duinen Sjoerd G. , Raap Anton K. , van der Ploeg Mels , Peters A. C. Boudewijn 
Published: May 2009

✓ Interphase cytogenetics is the application of nonradioactive in situ hybridization with chromosome-specific DNA probes to interphase nuclei. In this study, interphase cytogenetics was used to investigate 66 primary brain tumors (33 gliomas, 30 meningiomas, and three medulloblastomas) for numerical chromosomal aberrations of chromosomes 1, 6, 7, 10, 11, 17, 18, X, and Y.
Of the 33 gliomas (17 astrocytomas grades II, III, and IV, five oligoastrocytomas, seven oligodendrogliomas, and four ependymal tumors), 22 were near diploid, while the remaining 11 showed a significant triploid or tetraploid component. The predominant specific aberrations in gliomas were an over-representation of chromosome 7 (13 cases) and an under-representation of chromosome 10 (16 cases), These changes were observed in grade III and grade IV astrocytomas, as well as in oligodendrogliomas. Other frequent numerical changes were a gain of chromosome 17 (six cases) and a loss of chromosome 18 (seven cases). This loss of chromosome 18 seemed relatively specific for gliomas with an oligodendroglial component (six cases). Only two of 33 gliomas displayed no genetic abnormality with the probes used. Seven patients with astrocytomas died of their brain tumor during the clinical follow-up period. Their astrocytomas did not show a different chromosomal constitution compared to the other gliomas.
For the meningiomas, the probe panel was extended with a probe specific for chromosome 22. Loss of chromosome 22 was obvious in 21 of the 30 meningiomas, and was the sole abnormality in 11 meningiomas; in the other 10, this loss was associated with other chromosomal changes. Five of these tumors with additional aberrations were recurrent or atypical meningiomas.
It is suggested that interphase cytogenetics can contribute to a better understanding of the biological behavior of these tumors and possibly result in better insights into prognosis and strategies for therapy.
Apnea testing for the determination of brain death: a modified protocol
Authors: Benzel Edward C. , Mashburn Jay P. , Conrad Steven , Modling Denise 
Published: May 2009

✓ The absence of spontaneous respirations at a PaCO2 of 60 mm Hg or above has traditionally been accepted as the respiratory criteria for the determination of brain death. The testing of patients for the presence or absence of apnea has been complicated because the rate of PaCO2 elevation may vary substantially from patient to patient, and a nonlinear relationship exists between the rate of PaCO2 increase and the duration of apnea.
In an attempt to refine the apnea test and to further elucidate the physiology of hypercapnia in humans, 11 patients who met all but the respiratory criteria for brain death were evaluated using a modification of a previously utilized apnea testing protocol. All patients were brought to a PaCO2 of 40 mm Hg or above prior to the apnea test. Baseline PaCO2 ranged from 40 to 45 mm Hg in six patients (Group I) and from 46 to 51 mm Hg in five patients (Group II). The mean rate of PaCO2 increase was 5.1 ± 1.4 mm Hg/min in Group I and 6.7 ± 3.1 mm Hg/min in Group II. No problems with cardiovascular instability or hypoxia were encountered during testing in this series. This refinement of the apnea test allows for a streamlined and safe approach to brain death detection.
Risk factors predicting operable intracranial hematomas in head injury
Authors: Gutman Michael B. , Moulton Richard J. , Sullivan Irene , Hotz Gillian , Tucker William S. , Muller Paul J. 
Published: May 2009

✓ A study was performed to examine the incidence of operable traumatic intracranial hematomas accompanying head injuries of differing degrees of severity, and to see if factors predicting operable mass lesions could be identified. Logistic analysis was used to identify independent predictors of operable traumatic intracranial hematomas.
Data were gathered prospectively on 1039 patients admitted with head injury between January, 1986, and December, 1990. Patient age, Glasgow Coma Scale (GCS) score, pupillary inequality, and injury by falling were all independent predictors of the presence of operable intracranial hematomas (p = 0.0000, 0.0000, 0.0182, and 0.0001, respectively). Injury to vehicle occupants was less likely to result in operable mass lesions (p = 0.0001) than injury by other means. The incidence of traumatic intracranial hematomas in patients over 50 years old was three to four times higher than in those under 30 years of age. Not surprisingly, the incidence of operable hematomas increased with decreasing GCS scores. However, even at a GCS score of 13 to 15, patients with other risk factors had a substantial incidence of operable mass lesions. There was a 29% incidence of operable intracranial hematomas for patients with a GCS score of 13 to 15, aged over 40 years and injured in a fall.
It is suggested that patients who are middle-aged or older, or those injured in falls, are at particular risk for traumatic intracranial hematomas even if their GCS score is high. These patients should have early definitive investigation with computerized tomography in order to identify operable hematomas and to initiate surgical treatment prior to neurological deterioration from mass effect.
Arterial hypertension and neurovascular compression at the ventrolateral medulla
Authors: Naraghi Ramin , Gaab Michael R. , Walter Gerhard F. , Kleineberg Berthold 
Published: May 2009

✓ Intraoperative observations and animal experiments suggest that neurovascular compression at the left ventrolateral medulla is a possible etiological factor in essential hypertension. In pursuing this hypothesis, the authors examined the neurovascular relations in the posterior cranial fossa of 24 patients with essential hypertension, of 10 with renal hypertension, and of 21 normotensive control patients. Artificial perfusion of the vessels and microsurgical investigations during autopsy identified the vascular relations at the brain stem and at the root entry zone of the caudal cranial nerves. There was no evidence of neurovascular compression at the ventrolateral medulla on the left side in any patient from the control group or among those with renal hypertension. Two normotensive patients had neurovascular compression at the right ventrolateral medulla by the posterior inferior cerebellar artery. In contrast, all patients with essential hypertension had definite neurovascular compression at the left ventrolateral medulla. Additional compression of the right side was seen in three of these patients. Based on the anatomical appearance, it was possible to define three distinct types of neurovascular compression at the ventrolateral medulla. Common to all three types is the compression of the medulla oblongata at its rostral part just caudal to the pontomedullary junction and lateral to the olive in the retro-olivary sulcus.
Comparative histopathological study of the microsurgically examined brain-stem specimens revealed no differences between patients with essential hypertension, those with renal hypertension, and normal controls. There was a structural integrity at the site of neurovascular compression at the ventrolateral medulla. The microanatomical findings of this study show that neurovascular relations at the ventrolateral medulla in essential hypertension give rise to pulsatile compression on the left. This supports Jannetta's hypothesis of neurovascular compression at the left ventrolateral medulla as an etiology of essential hypertension.
Occlusion of the pig superior sagittal sinus, bridging and cortical veins: multistep evolution of sinus-vein thrombosis
Authors: Fries Georg , Wallenfang Thomas , Hennen Johannes , Velthaus Markus , Heimann Axel , Schild Hans , Perneczky Axel , Kempski Oliver 
Published: May 2009

✓ Cerebral sinus-vein thrombosis may lead to severe hemodynamic changes, elevated intracranial pressure (ICP), and brain edema. It is supposed that progression of the thrombus from the sinus into bridging and cortical veins plays a key role in the development of these pathophysiological changes, but this hypothesis lacks experimental proof. The aim of this study, using a novel animal model of sinus-vein thrombosis, was to evaluate the effects of a standardized occlusion of the superior sagittal sinus and its bridging and cortical veins on hemodynamic alterations, on brain water content, and on ICP in domestic pigs.
In 10 animals, the middle third of the superior sagittal sinus was occluded with a catheter-guided balloon. Five of these pigs received an additional injection of 1 ml fibrin glue into the superior sagittal sinus anterior to the inflated balloon, leading to an obstruction of bridging and cortical veins. In five control animals the balloon was inserted but not inflated. Five pigs underwent cerebral angiography. Four hours after occlusion, the brains were frozen in liquid nitrogen, and coronal slices were examined for Evans blue dye extravasation, regional water content, and histological changes.
Occlusion of the superior sagittal sinus alone did not affect ICP or cerebral perfusion pressure (CPP). The additional injection of fibrin glue caused an obstruction of cortical and bridging veins as well as severe increases in mean (± standard deviation) ICP to 49.4 ± 14.3 mm Hg, compared with 8.3 ± 4.5 mm Hg in sham-treated controls and 7.1 ± 3.9 mm Hg in animals with occlusion of the superior sagittal sinus alone. There was also a steep fall in the mean CPP to 34.2 ± 19.6 mm Hg compared with 96.4 ± 13.8 mm Hg in the control group.
White-matter water content anterior to the occlusion site was elevated to 81.9 ± 3.7 gm/100 gm frozen weight in the fibrin group as compared to 70.7 ± 2.2 gm/100 gm in controls. Posterior to the occlusion site, water content did not differ among the three groups. Angiography demonstrated collateral flow via cortical and bridging veins in animals with occlusion of the superior sagittal sinus alone. Additional fibrin glue obstructed these collateral vessels.
The data suggest a multistep process of pathophysiological alterations in patients with sinus-vein thrombosis and may explain why these patients present with a wide variety of symptoms: minor neurological deficits or headache might indicate thrombosis of the superior sagittal sinus and/or its bridging veins. In subjects with severe symptoms, coma, and increased ICP there may be an additional involvement of tributary cortical veins. The proposed multistep process offers the rationale for heparin treatment of sinus-vein thrombosis even in patients with minor symptoms.
Transsphenoidal adenomectomy for growth hormone-secreting pituitary adenomas in acromegaly: outcome analysis and determinants of failure
Authors: Tindall George T. , Oyesiku Nelson M. , Watts Nelson B. , Clark Richard V. , Christy James H. , Adams David A. 
Published: May 2009

✓ The results of transsphenoidal adenomectomy for growth hormone (GH)-secreting pituitary adenomas in acromegaly performed over a 17-year period were analyzed retrospectively to determine which preoperative factors significantly influenced the long-term surgical outcome. These variables were then used to develop a logistic regression model to determine the probability of surgical failure.
The series consisted of 103 patients. Long-term follow-up study (mean duration 102 ± 64 months) was performed to derive outcome analysis and determinants of failure. Surgical control was defined as a long-term postoperative serum basal GH level of less than 5 µg/liter, a long-term postoperative serum somatomedin C (SM-C) level of less than 2.2 U/ml, and a favorable clinical response. Eighteen (17.5%) patients did not meet these criteria. The overall control rate by the GH criteria was 81.3% and by the SM-C criteria 76.2%.
By multivariate logistic regression analysis, tumor stage was the strongest predictor of outcome (p < 0.05). The preoperative GH level, tumor grade, and preoperative SM-C level were significant univariate predictors (p < 0.05). There were statistically significant differences in mean preoperative GH and SM-C levels (p < 0.05, t-test) and tumor stage (p < 0.05, chi-squared test) between patients whose acromegaly was controlled by surgery and those whose acromegaly was not. Furthermore, estimates were derived of the probability of surgical failure based on preoperative GH level, preoperative SM-C level, and tumor grade and stage. The authors believe these findings will enhance clinical decision-making for neurosurgeons considering transsphenoidal microsurgery in patients with acromegaly.
Noncommunicating syringomyelia following occlusion of central canal in rats
Authors: Milhorat Thomas H. , Nobandegani Fariborz , Miller John I. , Rao Chandrakant 
Published: May 2009

✓ This report describes a new and reliable technique for producing experimental noncommunicating syringomyelia. In 30 rats, 1.2 to 1.6 µl of kaolin was microinjected into the dorsal columns and central gray matter of the spinal cord at C-6. The inoculations caused transient neurological deficits in four animals and no deficits in 26 animals. Within 24 hours, kaolin and polymorphonuclear leukocytes entered the central canal and drained rostrally. The clearance of inflammatory products induced a proliferation of ependymal cells and periependymal fibrous astrocytes, which formed synechiae and obstructed the canal at the level of injection and at one or more levels up to C-1. In 22 animals followed for 48 hours or longer, the upper end of the central canal became acutely dilated and formed an ependyma-lined syrinx that enlarged to massive dimensions within 6 weeks. The rostral syrinxes did not communicate with the fourth ventricle and were not associated with hydrocephalus.
The histological findings in acute noncommunicating syringomyelia were characterized by progressive stretching and thinning of the ependyma, elongation of intracanalicular septae, and the formation of periependymal edema. After 3 weeks, there was progressive compression of the periependymal tissues associated with stretching of axons, fragmentation of myelin sheaths, and the formation of myelin droplets. These findings and the sequence in which they evolved were identical in most respects to those occurring in acute and subacute noncommunicating hydrocephalus.
Therapeutic alternatives for vein of Galen vascular malformations
Authors: Lylyk Pedro , Viñuela Fernando , Dion Jacques E. , Duckwiler Gary , Guglielmi Guido , Peacock Warwick , Martin Neil 
Published: May 2009

✓ From September, 1986, to March, 1990, the authors treated 28 children harboring a vein of Galen vascular malformation. Eleven (39.3%) of the patients were neonates, 13 (46.4%) were 1 to 2 years old, and four (14.3%) were more than 2 years old.
Fifteen patients (53.6%) presented with severe congestive heart failure, six (21.4%) had seizures, four (14.3%) had hydrocephalus, and three (10.7%) presented with intraventricular hemorrhage. Based on the Yaşargil classification of malformations, 10 lesions (35.7%) were Type I, seven (25%) were Type II, eight (28.6%) were Type III, and three (10.7%) were Type IV. In 11 patients (39.3%), a combined transfemoral, transarterial, and transvenous embolization of the vein of Galen malformation was performed. A pure transtorcular approach was utilized in eight patients (28.6%), and postembolization surgical clipping of arterial feeders was performed in two cases with intractable congestive heart failure.
Complete anatomical occlusion of the galenic malformation was achieved in 13 patients (46.4%). An immediate postembolization improvement in the patient's clinical status was obtained in 23 (82.1%) of 28 patients and a good long-term clinical outcome was seen in 17 patients (60.7%). Five deaths (17.9%) occurred in this series of 28 patients; three (10.7%) were related to a transtorcular embolization and two (7.1%) to the unchanged natural history of the disease.
A randomized controlled trial of high-dose intravenous nicardipine in aneurysmal subarachnoid hemorrhage
Authors: Haley E. Clarke , Kassell Neal F. , Torner James C. , _ _ 
Published: May 2009

✓ Because of their action as cerebral vasodilators, dihydropyridine calcium antagonists have received intense scrutiny for their potential benefit in ameliorating the devastating consequences of delayed cerebral vasospasm following aneurysmal subarachnoid hemorrhage (SAH). From October, 1987, to September, 1989, 41 North American neurosurgical centers in the Cooperative Aneurysm Study accrued 906 patients with recent (Days 0 to 7) aneurysmal SAH into a prospective randomized double-blind placebo-controlled trial of high-dose intravenous nicardipine to test whether treatment with this agent improved overall outcome. Eligible patients received 0.15 mg/kg/hr of either nicardipine or placebo by continuous infusion for up to 14 days following hemorrhage. The 449 patients randomly assigned to the nicardipine-treated group and the 457 patients assigned to the placebo-treated group were balanced with regard to prognostic factors for ischemic deficits from vasospasm and for overall outcome. Other medical and surgical interventions were used with similar frequency in both groups, except that antihypertensive agents were used less frequently in the nicardipine-treated patients (26% of the nicardipine-treated group vs. 43% of the placebo-treated group, p < 0.001), and more patients in the placebo-treated group had intentional hypervolemia, induced hypertension, and/or hemodilution administered therapeutically for symptomatic vasospasm (38% of the placebo-treated group vs. 25% of the nicardipine-treated group, p < 0.001). The incidence of symptomatic vasospasm during the treatment period was higher in the placebo-treated group (46%) than in the nicardipine-treated group (32%) (p < 0.001). Despite the reduction in symptomatic vasospasm in the nicardipine-treated group, overall outcome at 3 months was similar between the two groups. Fifty-five percent of nicardipine-treated patients were rated as having a good recovery according to the Glasgow Outcome Scale at follow-up review and 17% were dead, compared to 56% and 18%, respectively, in the placebo-treated group (not statistically significant).
These data suggest that high-dose intravenous nicardipine treatment is associated with a reduced incidence of symptomatic vasospasm in patients with recent aneurysmal SAH, but not with an improvement in overall outcome at 3 months when compared to standard management in North America. It is postulated that, while nicardipine prevents vasospasm, hypertensive/hypervolemic therapy may be effective in reversing ischemic deficits from vasospasm once they occur.