bluuebunny/crossref_metadata_2025_split huggingface dataset:
Prevention of cerebral vasospasm after SAH with a thromboxane synthetase inhibitor, OKY-1581
Authors: Sasaki Tomio , Wakai Susumu , Asano Takao , Takakura Kintomo , Sano Keiji 
Published: May 2009

✓ The efficacy of thromboxane synthetase inhibitor in the prevention of cerebral vasospasm after subarachnoid hemorrhage (SAH) was evaluated in a prolonged experiment using dogs. Changes in the diameter of the basilar artery were followed by angiography, and morphological changes were studied by photomicroscopy and electron microscopy. As a thromboxane synthetase inhibitor, OKY-1581 (sodium-(E)-3-(4(-3-pyridylmethyl)phenyl)-2-methylacrylate)was used. Dogs received intravenous injections of 160 mg of OKY-1581 dissolved in 2 ml of physiological saline immediately after subarachnoid blood injection. Subsequently, the animals received continuous intravenous infusion of the drug at the rate of 4 gm/50 ml/24 hours until sacrifice 4 days after induction of SAH. Control dogs received subarachnoid blood injection without treatment with OKY-1581.
Angiographic examination revealed that the late spasm was almost completely abolished by the treatment with OKY-1581. Early spasm was also prevented, but the drug's effect was less prominent than it was on the late spasm. Morphological study revealed degenerative changes in the endothelium and myonecrotic changes in the tunica media following SAH in the basilar arteries of the treated as well as the untreated dogs. However, corrugation of the internal elastic lamina was almost completely absent in the treated dogs.
The above results indicate that a disproportionate synthesis of thromboxane A2 plays an important role in the evolution of chronic cerebral vasospasm following SAH, and that drugs such as OKY-1581 that selectively inhibit thromboxane synthetase might be useful in the prevention of vasospasm.
Medulloblastoma and other primary malignant neuroectodermal tumors of the CNS
Authors: Allen Jeffrey C. , Epstein Fred 
Published: May 2009

✓ Studies to evaluate the extent of their disease were performed on 30 children with newly diagnosed malignant neuroectodermal tumors of the central nervous system, including 25 children with medulloblastomas. The studies consisted of postoperative computerized tomography scanning, cerebrospinal fluid (CSF) cytology, myelography, and bone marrow aspiration. In 11 patients (36%) one or more of these studies was positive, indicating disease dissemination (Group 1), and in 19 (64%) all four studies were negative (Group 2). The CSF cytology was positive for malignant cells in all 11 Group 1 patients; myelograms indicated subclinical filling defects in nine, and the bone marrow aspirate from two patients revealed extrinsic cells.
All patients received a conventional course of neuraxis radiation therapy as tolerated, and some also received chemotherapy. Patients with abnormal myelograms received additional radiation to areas of identifiable subarachnoid disease. The median survival time in Group 1 was 12 months, with five patients still surviving. The prognosis for Group 2 patients was considerably more favorable; only three of the 19 had died at the time of this report. Four of the six deaths in Group 1 were related to disease dissemination, the other two to chemotherapy toxicity. All three deaths in Group 2 were related to local tumor recurrence.
The mean age of Group 1 patients was 3.9 years compared to 11 years for Group 2. Of the 14 patients aged 5 years and under in both groups, nine presented with widely disseminated disease (Group 1), six of whom had a relatively short survival time. The performance of a postoperative extent-of-disease evaluation is especially important in young children with medulloblastoma. Knowledge of disease dissemination at diagnosis not only helps determine prognosis, but also assists in planning treatment. Aggressive multimodal therapy appears warranted in younger patients who present with widely disseminated disease.
Reversal of intracerebral steal by STA-MCA anastomosis
Authors: Laurent John P. , Lawner Pablo M. , O'Connor Michael 
Published: May 2009

✓ A major factor determining the severity of neurological deficits caused by cerebral ischemia is the ability of the vasculature to provide collateral circulation to the ischemic areas. By establishing a major conduit by means of extracranial-intracranial anastomosis, the increased perfusion pressure through the collateral arterioles may reduce morbidity in these patients. Twenty-seven patients were selected for superficial temporal artery to middle cerebral artery (STA-MCA) anastomosis based on clinical and angiographic evidence of lesions of the internal carotid arterial system. Cerebral blood flows (CBF's) were determined by the xenon-133 inhalation method using 16 symmetrically placed scintillator probes; two-compartment analysis was used to compute a mean flow for the compartment. An average mean flow was computed for each hemisphere, and for four regions with the lowest mean CBF in each hemisphere. The CBF was measured preoperatively and within 8 weeks postoperatively.
The average mean flow was 29 ml/100 gm/min in the symptomatic hemisphere, and 30 ml/100 gm/min in the asymptomatic hemisphere. In 11 patients, the mean flow for the symptomatic hemisphere increased by 24% postoperatively, and for the asymptomatic hemisphere by 23%. Regions with lowest CBF showed an increase of 32% in the symptomatic hemisphere, and of 35% in the asymptomatic hemisphere. The low-flow regions differed from the total hemisphere (symptomatic: p < 0.02; asymptomatic: p < 0.05). Areas of lowest blood flow preoperatively had the greatest increase in flow postoperatively. Postoperative elevation of CBF in the contralateral hemisphere is consistent with an “intracerebral steal” before surgery. The postoperative elevation of flow in the asymptomatic hemisphere is related to improved perfusion pressure in the symptomatic hemisphere.
Facial nerve preservation during surgery for removal of acoustic nerve tumors
Authors: Lye Richard H. , Dutton John , Ramsden Richard T. , Occleshaw Joseph V. , Ferguson Iain T. , Taylor Ian 
Published: May 2009

✓ A series of 33 patients with 35 acoustic nerve tumors is reviewed. Tumor size was estimated from computerized tomography (CT) scans, and its influence on anatomical and functional preservation of the facial nerve was assessed. Six tumors (one invading the petrous bone, three medium and two large tumors) were not detected on CT scans. The translabyrinthine approach was used in seven instances (one small and six medium tumors) and the suboccipital transmeatal approach for 28 tumors (seven medium and 21 large tumors). Anatomical preservation of the facial nerve was achieved in 83% of operations for tumor removal, two of which were subtotal. A further two patients underwent subtotal removal, but the facial nerve was destroyed. Large tumors carried an increased risk of damage to the facial nerve, but even in this group the nerve was preserved anatomically intact in 70% of cases. Damage to the facial nerve occurred more frequently in patients with preoperative evidence of facial weakness; however, this factor did not appear to influence functional recovery of the facial nerve, provided that the nerve was intact at the end of the operation.
A simple grading system for facial nerve function is described. Only 76% of anatomically intact facial nerves showed any evidence of function 1 month after surgery. Postoperatively, facial function improved with time. At the latest review, 45% of these patients had normal facial function or mild facial weakness (Grades I and II).
Enzymatic changes in serum and cerebrospinal fluid in neurological injury
Authors: Bakay Roy A. E. , Ward Arthur A. 
Published: May 2009

✓ Enzymatic determinations in serum and cerebrospinal fluid (CSF) of creatine phosphokinase (CPK) and its isoenzymes, lactic dehydrogenase (LDH) and its isoenzymes, and glutamic oxaloacetic transaminase (GOT) were performed on patients with closed head injury with Glasgow Coma Scale (GCS) scores of 3 to 15. The purpose of the work was to study the usefulness of these determinations as a biochemical index of brain injury. Detailed analysis of serum determinations on 139 patients demonstrated a prognostic correlation for only the CPK1 isoenzyme. The presence of the CPK1 isoenzyme correlated with the degree of head injury (as indexed by the GCS) and with the ultimate outcome. Although the presence of the CPK1 isoenzyme was a foreboding sign, it was not consistently present even with severe head injury, and its presence was not invariably associated with poor outcome. Therefore, serum enzymatic determinations have an inadequate sensitivity and specificity for use as an index of neurological trauma.
Fifty-seven patients had CSF enzymatic determinations, and each of the enzymes studied was correlated directly with GCS and with the ultimate outcome. Within the subgroup of severely head-injured patients with a GCS score of 3 to 7, only the CPK1 and LDH1 isoenzymes correlated with the degree of head trauma and outcome. The CPK1 isoenzymes were not detectable in CSF from control patients, but were invariably present following head trauma. These CPK1 isoenzymes in the CSF were particularly useful in that they appeared in the acute course and were subsequently absent unless secondary injury to the brain occurred causing additional neurological damage. Secondary injuries due to delayed hemorrhage, infarction, hypoxia, or pathological evaluations of intracranial pressure were readily detected. The LDH1 isoenzyme is present in the CSF from normal patients and does elevate with neurological trauma; these LDH1 isoenzymes appear to be elevated for a period of weeks to months following injury and thus are less useful in detecting secondary injuries. An attempt was made to investigate the effect of Decadron (dexamethasone) on these enzymatic changes, but no significant effect was identified. Also noted in this study was the presence of CPK1 isoenzymes in the CSF of patients with gunshot wounds to the head, spinal cord injuries, and herniation syndromes. It is concluded, therefore, that CPK1 isoenzymes in the CSF appear to be a specific marker for neurological trauma, and may be of value both in clinical practice and in clinical investigations.
The recurrence of intracranial meningiomas after surgical treatment
Authors: Adegbite Andrew B. , Khan Moe I. , Paine Kenneth W. E. , Tan Leonard K. 
Published: May 2009

✓ A study of 114 surgically treated patients with intracranial meningiomas was carried out to evaluate factors influencing recurrence. The date of the initial surgery extended over a 24-year period from January, 1956, to December, 1979. The patients ranged in age from 1½ years to 82 years. Seventy-one (62.3%) were females and 43 (37.7%) were males. The surgical procedure was graded according to Simpson's classification from 1 to 5 (Grade 1 = complete excision, Grade 5 = simple decompression). In this series, 33 procedures (28.9%) were Grade 1, 55 (48.2%) were Grade 2, seven (6.1%) were Grade 3, 18 (15.8%) were Grade 4, and one (0.9%) was Grade 5. There were eight (7%) postoperative deaths.
Approximately 60% of the tumors were located in the sphenoid wing (23.7%), convexity (21.1%), and parasagittally (14.9%). Histological diagnosis in 96% of the patients was transitional (42.1%), syncytial (34.2%), and fibroblastic (20.2%) meningiomas. Eight (7%) patients received postoperative radiotherapy. There was evidence of recurrence in 22 patients (19.3%). Twenty-one underwent a second surgical procedure. Using survival analysis, it was determined that 80% of the patients were free of recurrence 5 years after the initial surgery, and approximately 50% showed no recurrence 20 years after the initial surgery. Only the grade of the initial surgery had a statistically significant influence on recurrence. Sex of patients, site and histology of the tumor, and postoperative radiotherapy had no statistically significant influence on recurrence. Angioblastic and malignant meningiomas were rare (only four cases), and recurred relatively quickly.
Pharmacologically induced profound arterial hypotension in the anesthetized dog
Authors: Kassell Neal F. , Boarini David J. , Sprowell James A. , Olin Julie J. 
Published: May 2009

✓ The purpose of this study was to compare the behavioral, hematological, and biochemical effects of profound arterial hypotension induced by adenosine potentiated with dipyridamole with those of hypotension induced by trimethaphan camsylate or sodium nitroprusside. Twenty dogs were anesthetized with halothane and nitrous oxide, paralyzed with pancuronium, and ventilated to an arterial pCO2 of 40 torr. Arterial pressure and heart rate were monitored continuously. The animals were divided into four groups of five dogs each. The first group served as controls, while in the remaining groups the mean arterial pressure (MAP) was lowered to 40 mm Hg with adenosine/dipyridamole, trimethaphan, or nitroprusside for 1 hour, following which the animals were allowed to recover from the anesthetic and observed for 48 hours. Determinations of arterial blood gases and hematological and biochemical parameters were made immediately prior to and at the completion of the 1-hour hypotensive period and 48 hours later.
Reduction of MAP to 40 mm Hg was readily achieved with adenosine/dipyridamole. There was no tachyphylaxis to this drug, and arterial pressure promptly returned toward control levels without overshoot after the infusion was discontinued. In contrast, hypotension of this degree could be produced only with toxic doses of nitroprusside. Trimethaphan was more effective in producing hypotension than nitroprusside, but the dose required was extremely variable, and prolonged intervals were required for pressure to return toward normal after the agent was stopped. The control animals and those that received adenosine/dipyridamole recovered promptly from the anesthetic and were neurologically intact. The animals that received trimethaphan recovered more slowly but were neurologically normal within 12 hours. All of the animals that received nitroprusside died without recovering from the anesthesia. Aside from a mild transient metabolic acidosis and transient elevation of blood urea nitrogen and creatinine in the dogs that received adenosine/dipyridamole or trimethaphan, no specific cardiovascular, hematological, hepatic, or renal toxic effects were noted. Evidence of fatal cyanide toxicity was present in the nitroprusside group.
These data suggest that hypotension using adenosine/dipyridamole is readily induced, maintained, and reversed, and is not associated with any apparent hematological, or biochemical evidence of toxicity. Further studies leading to a clinical trial of adenosine-induced hypotension appear to be indicated.
Stem cell studies of human malignant brain tumors
Authors: Rosenblum Mark L. , Gerosa Massimo A. , Wilson Charles B. , Barger Geoffrey R. , Pertuiset Bertran F. , Tribolet Nicolas de , Dougherty Dolores V. 
Published: May 2009

✓ A stem cell assay for human malignant gliomas has been developed. Cells obtained from tumor biopsies grew into colonies composed of malignant glial cells, as documented by histochemical, immunohistochemical, and immunobiological techniques. Studies suggest that the disaggregated cells are representative of the cells within the solid tumor.
Clonogenic cells were obtained from 48 tumors and analyzed for their in vitro sensitivity to graded doses of 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU). The in vitro anti-tumor activity of BCNU at clinically achievable doses was compared to clinical response to the agent based on changes in computerized tomographic scan, radionuclide brain scan, and neurological examinations. Twenty-two patients received nitrosoureas before or after tumor specimen analysis, and were eligible for in vitro-in situ correlations. Clinical tumor sensitivity to nitrosoureas was predicted by culture results in 42% of all evaluable patients, and clinical resistance was predicted in 100%. The capability of the assay can be appreciated best for the 13 patients not treated with BCNU prior to culture; the in vitro prediction of clinical sensitivity and resistance was 71% and 100%, respectively.
Preliminary findings show that clinical tumor resistance to BCNU may result from “intrinsic” cell resistance in some patients and from inadequate delivery of drug to tumor cells in other cases. The potential utility of this method to study the reason(s) for tumor cell resistance to drugs, to screen new chemotherapeutic agents, to individualize patient treatment, and to investigate tumor biology is discussed.
Failure of prophylactically administered phenytoin to prevent late posttraumatic seizures
Authors: Young Byron , Rapp Robert P. , Norton J. A. , Haack Dennis , Tibbs Phillip A. , Bean James R. 
Published: May 2009

✓ This randomized double-blind placebo-controlled study was undertaken in a series of 179 patients to determine whether phenytoin administered soon after head injury lessens the incidence of late posttraumatic epilepsy. When delayed hypersensitivity to phenytoin developed, the patient was switched to phenobarbital. The patients were followed for 18 months to detect the occurrence of seizures and to serially measure plasma phenytoin concentrations. There was no significant difference in the percentage of patients having late seizures in the treated and placebo groups (p = 0.75). The time between injury and seizures did not significantly differ between the two groups. The results provide no support for the continued use of phenytoin in the low therapeutic range for prophylaxis against late posttraumatic seizures.
It cannot be concluded that higher phenytoin plasma concentrations and higher compliance rates than obtained in this study would not have significantly decreased the occurrence of late posttraumatic epilepsy. The finding that no patient with a phenytoin plasma concentration of 12 µg/ml or higher had a seizure raises the question of whether phenytoin in blood concentrations in higher therapeutic ranges might lessen the occurrence of posttraumatic epilepsy, and should be studied further. Posttraumatic epilepsy is a major public health problem deserving a large cooperative trial to determine if phenytoin at higher blood levels than obtained in this study, or other currently available or newly developed drugs, can prevent the occurrence of posttraumatic epilepsy.
Bleeding from cerebral arteriovenous malformations as part of their natural history
Authors: Graf Carl J. , Perret George E. , Torner James C. 
Published: May 2009

✓ The case records of 191 patients with a cerebral arteriovenous malformation (AVM) were reviewed to determine bleeding characteristics of these lesions. Possible influences of age, sex, the location and size of the AVM, type of initial hemorrhage, and condition of the patients were analyzed. Of these 191 patients, 102 had a single hemorrhage, 32 had a recurrent hemorrhage, and 57 never bled. The follow-up period for patients with an unruptured AVM was a mean of 4.8 years and a maximum of 31 years; for those with a ruptured AVM, the mean was 2 years, and the maximum 37 years.
Size of the AVM was significantly related to the risk of first hemorrhage. The average yearly risk for first hemorrhage was between 2% and 3%. Bleeding occurred most frequently in the 11- to 35-year-old age group. The risk of rebleeding increased with advancing age. Among 93 patients followed after their AVM had ruptured, the risk of rebleeding was 6% in 1 year. After the first year, the average rebleeding rate was about 2% per year up to 20 years.
Aneurysms of the posterior inferior cerebellar artery
Authors: Hudgins Rroger J. , Day Arthur L. , Quisling Ronald G. , Rhoton Albert L. , Sypert George W. , Garcia-Bengochea Francisco 
Published: May 2009

✓ The clinical and anatomical features of 21 surgically treated saccular aneurysms of the posterior inferior cerebellar artery (PICA) are analyzed. Seventeen of these lesions originated from the PICA-vertebral junction, and four arose from distal PICA branching sites. Twelve lesions arose from the left PICA, nine were right-sided, and all were small (less than 12.5 mm). Most of these aneurysms occurred in females (16 of 21) and presented as classic subarachnoid hemorrhage. The lack of specific focal deficits prevented an accurate pre-angiographic determination of aneurysm location in most instances. Clinically significant vasospasm and aneurysm multiplicity occurred with approximately equal frequency as at other locations.
The angiographic and surgical features of these lesions are determined by the course of the vertebral artery and PICA; that is, they occur at branching sites and at curves in the parent vessel, and point in the direction in which flow would have continued if the curve at the aneurysm's origin had not been present. Aneurysms at the PICA-vertebral junction usually occur at least 1 cm above the foramen magnum level, arise distal to the PICA origin in the angle between the two vessels, and are best approached by a paramedian incision with the patient in the lateral recumbent position. Isolated clipping of the aneurysm neck is essential in this instance, as trapping may compromise vital perforating arteries of the brain stem. More distal (retromedullary) PICA aneurysms are sometimes associated with another vascular anomaly (two cases in this series), and are best handled through a bilateral suboccipital craniectomy. Clipping of the neck is the preferred treatment, but trapping is usually safe, if necessary.
Effect of triiodo-L-thyronine on axonal regeneration in the rat spinal cord after acute compression injury
Authors: Tator Charles H. , Rivlin Alex S. , Lewis Anthony J. , Schmoll Beatrice 
Published: May 2009

✓ Studies were performed on the effect of triiodo-L-thyronine (T3) on clinical recovery and axonal counts in the pyramidal tract of 56 rats subjected to an acute spinal cord compression injury at T-7. The T3 was given at a daily dose of 5 µg/kg for 4 weeks to 28 rats in the treatment group. The treatment and control animals were tested weekly for clinical recovery, and cord function as determined by the inclined-plane technique. Groups of animals were killed at 4 weeks and 12 weeks, and the axons in the pyramidal tract cephalad and caudad to the injury site were counted in sections prepared with Holmes' silver stain.
There was no difference in clinical recovery between the treatment and control groups. This negative result contrasts with other studies which showed improved recovery of cord-injured animals treated with thyroid hormones. The possible explanations for this discrepancy are discussed. Similarly, there was no difference in the axon counts between the treated and control groups. Thus, T3 did not improve recovery or axonal regeneration in the pyramidal tract of rats after acute spinal cord compression injury. Between 4 and 12 weeks, there was a marked reduction in the cephalad axon counts in the pyramidal tract in both groups, indicating that approximately 50% of the axons in the pyramidal tract had undergone retrograde degeneration or dying back by 12 weeks after this degree of injury. The T3 did not affect the degree of retrograde degeneration.