The timing of aneurysm surgery 1985.
Explore the source record for details and available documents.
Calcium↗
Biomedical subjects
E S Flamm
Publications and source records attributed to E S Flamm.
Reductive metabolism of ascorbic acid in the central nervous system.
Rat and feline brain and feline spinal cord were examined for the presence of semidehydroascorbate reductase (EC 1.6.5.4) and dehydroascorbate reductase (EC 1.8.5.1). Semidehydroascorbate reductase (SDAR), as monitored by both ascorbyl radical-dependent nicotinamide adenine dinucleotide (NADH) oxidase activity and NADH-dependent ascorbyl radical quenching, was present in all tissues studied. Rat cerebrum exhibited the highest levels and feline spinal cord the lowest. SDAR activity was about twice as high in feline cerebral cortex as in underlying white matter, and paralleled ascorbic acid levels. Subcellular fractionation of rat cerebrum localized most SDAR in a large granular fraction. In contrast, dehydroascorbate reductase was not detectable in any of the tissues examined. The results suggest that semidehydroascorbate reductase is the major enzyme catalyzing the regeneration of reduced ascorbic acid in the central nervous system.
Animals↗
Ascorbic acid: a putative biochemical marker of irreversible neurologic functional loss following spinal cord injury.
The development of permanent paraplegia in spinal injured cats is accompanied by a large progressive decline in total ascorbic acid (AA) and a transient increase in oxidized (AAox) ascorbate. Since AA is involved in a variety of processes required for normal central nervous system (CNS) performance we suggested that such large ascorbate loss may contribute to derangements in spinal cord function following injury. We now demonstrate that methylprednisolone (15 mg/kg) and naloxone (10 mg/kg), two treatments that preserve neurologic function in this model, rapidly block deteriorating ascorbate status. Naloxone at 1 mg/kg, a treatment providing no therapeutic benefit, has no protective effect on ascorbate. The results strongly support the hypothesis that loss of ascorbate homeostasis reflects irreversible loss of neurologic function following spinal cord injury.
Animals↗
Visual recovery after transsphenoidal removal of pituitary adenomas.
We reviewed the records of 100 consecutive patients with histologically verified pituitary adenomas who underwent transsphenoidal decompression of the optic nerves and chiasm. The patients' ages ranged from 18 to 80 years, with a median of 52 years. Preoperatively, all patients had objective signs of visual acuity or field defects. Postoperatively, visual acuity was normal or improved in 79% of the eyes and the visual fields were normal or improved in 74%. The visual outcome (for both acuity and fields) was better in younger patients and those with a shorter duration of symptoms. Patients with lesser degrees of preoperative visual acuity compromise had better postoperative visual acuity outcome. However, the severity of preoperative visual field defects did not seem to predict postoperative field outcome, and even patients with severe preoperative field defects often had striking postoperative improvement. Patients who had undergone prior operation were less likely to have either visual acuity or visual field improvement after reoperation. Postoperative deterioration in visual acuity was noted in only 5 patients (6 eyes). Complications were few. There were 4 instances of cerebrospinal fluid rhinorrhea, but only 2 patients needed operative repair. There was no instance of permanent diabetes insipidus, although 17 patients developed transient diabetes insipidus. In most cases, visual improvement was sustained. The average duration of follow-up was 26 months. Three patients required a subsequent operation to correct visual loss in the immediate postoperative period, but only 1 patient has undergone late operation for recurrence of tumor. There was no operative mortality.
Adenoma↗
A phase I trial of naloxone treatment in acute spinal cord injury.
Results of a Phase I trial of the opiate antagonist naloxone for treatment of patients with acute spinal cord injury are reported. Naloxone was administered in doses ranging from 5 to 200 mg/sq m (0.14 to 5.4 mg/kg) for up to 48 hours. The patients ranged in age from 16 to 79 years (mean 37 years). Twenty patients received naloxone as a loading dose of 5 to 50 mg/sq m (0.14 to 1.43 mg/kg), followed by a maintenance dose of 20% of the loading dose given as a continuous infusion hourly for 47 hours (Group 1). Nine patients received a loading dose of 100 to 200 mg/sq m (2.7 to 5.4 mg/kg) and a maintenance dose of 75% of the initial dose hourly for 23 hours (Group 2). These higher doses (2.7 to 5.4 mg/kg) have been found to be effective in experimental spinal cord injury. Neurological examinations were performed and somatosensory evoked potentials (SEP's) were obtained as soon after admission as possible and again 1, 2, 3, and 7 days, 3 weeks, and 6 weeks to 6 months after admission. The 20 Group 1 patients who received 1.43 mg/kg or less of naloxone showed no improvement in neurological status or SEP's. All but three (15%) of these patients had a complete neurological deficit at the time of admission. Treatment was begun an average of 12.9 hours after injury. Among the nine Group 2 patients treated with 2.7 mg/kg or more, there were five patients (56%) with incomplete deficits. This group received naloxone an average of 6.6 hours after admission. Two of the five Group 2 patients with incomplete lesions showed improvement in their neurological condition and/or SEP's within 36 hours of receiving the drug. One of the four Group 2 patients with a complete lesion at the time of admission was able to localize pressure sensation in his legs 36 hours after completion of the drug infusion. Four Group 2 patients (two with complete and two with incomplete lesions) have shown improvement in their SEP's, suggesting recovery of SEP's in a dose-related fashion. Four patients experienced increased pain after administration of the loading dose and during the maintenance infusion; in only one patient was this severe enough to require discontinuation of the drug. Of the 29 patients treated with naloxone, four died within 6 weeks of admission, for a mortality rate of 13.8%.(ABSTRACT TRUNCATED AT 400 WORDS)
Adolescent↗
Methylprednisolone and neurological function 1 year after spinal cord injury. Results of the National Acute Spinal Cord Injury Study.
A multi-center double-blind randomized clinical trial was conducted by the National Acute Spinal Cord Injury Study Group to examine the efficacy of high-dose methylprednisolone (1000-mg bolus and 1000 mg daily thereafter for 10 days) compared with that of a standard dose (100-mg bolus and 100 mg daily for 10 days). No significant difference was observed in neurological recovery of motor function, pinprick response, or touch sensation 1 year after injury between the two treatment groups, after adjustment for other potentially confounding factors. Analyses that specifically took into account the patients' total steroid dose and relative weight confirmed the lack of a steroid treatment effect. The case fatality rate was 10.7% during the 1st year after injury, and this was not associated with the steroid treatment protocol or the patient's gender. Deaths did occur significantly more frequently among patients who were completely (15.3%) and partially (8.6%) plegic than among those who were paretic (2.5%, p = 0.0005), and among patients aged 50 years or older (38.6%, p = 0.0001).
Clinical Trials as Topic↗
Percutaneous transvascular treatment of giant carotid aneurysms: neuro-ophthalmologic findings.
Twelve of 17 patients with cavernous carotid aneurysms had balloon embolization directed through a percutaneous double lumen catheter for progressive pain, ophthalmoplegia, or visual loss. Functional angiography was carried out with systemic heparinization and double-lumen balloon catheters to test tolerance to carotid occlusion. Eleven were successfully treated, though two patients with initial preservation of the ipsilateral carotid artery had unplanned deflation of the balloon, necessitating re-embolization. No serious permanent neurologic complications occurred. All patients had complete resolution of pain, and nine had improvement in the extraocular eye muscle and lid function. Balloon trapping of the cavernous carotid artery, rather than placing the balloon directly into the aneurysm, resulted in involution of the aneurysm and decompression of the involved cranial nerves.
Adult↗
Labeled putrescine as a probe in brain tumors.
The polyamine metabolism of transplanted N-nitrosomethylurea-derived rat glioma was determined with radiolabeled putrescine used as a marker for malignancy. The uptake of putrescine in vivo was complete within 5 minutes and was specific for tumor tissue. The conversion of putrescine to spermine and other metabolites by the tumor was rapid, in contrast to the case for adjacent normal brain. These results suggest that putrescine labeled with carbon-11 may be used as a positron-emission tomographic tracer for the selective metabolic imaging of brain tumor and may be used in an appropriate model as a marker for tumor growth rate.
Animals↗
Effect of traumatic injury on membrane phosphatase activity in cat spinal cord.
The enzymatic activities of the spinal cord membrane phosphatases, (Na,K)ATPase, KpNPPase, 5'-nucleotidase, MgATPase, and MgpNPPase, were determined following contusion injury. Within 30 min after injury, the activities of (Na,K)ATPase, KpNPPase, and 5'-nucleotidase were suppressed at the injury site and remained suppressed for 24 h. Considerable loss of (Na,K)ATPase and KpNPPase activity was seen along the longitudinal axis of the spinal cord for the first 4 h after injury, whereas at 24 h after injury, there was almost complete restitution in the activity of those enzymes. No similar changes in activity were observed for the MgATPase, whereas the activity of the MgpNPPase progressively worsened with time at the injury site. The deduce the pathobiochemical process that accounts for the loss of spinal membrane phosphatase activity, spinal cord membranes were incubated in vitro in the presence of a superoxide anion-generating system, as well as in the presence of trypsin and lysolecithin. It was found that superoxide anions inhibited only the activity of transport phosphatase, KpNPPase, whereas trypsin inhibited the activity of both KpNPPase and MgpNPPase. No inhibition of 5'-nucleotidase was observed by superoxide anions; however, the activity of 5'-nucleotidase was enhanced by trypsin, lysolecithin, or both in concert. These results suggest that the pathobiochemical process that accounts for the loss of spinal membrane phosphatase activity that follows injury can be attributed to the concerted effects of free radical attack as well as the activation of proteolytic and lipolytic enzymes. Inactivation of spinal membrane phosphatase can occur by direct attack of these processes on the membrane or by loss of membrane material, e.g., solubilization.
Animals↗
Giant intracranial aneurysm presenting as a posterior fossa mass.
A patient with signs of brainstem compression and hydrocephalus is reported. The clinical picture suggested a posterior fossa neoplasm. Computed tomography, however, proved highly accurate in making the diagnosis of a giant, partially thrombosed vertebrobasilar aneurysm. The radiographic appearance of this entity is summarized and pathologic correlation is offered.
Basilar Artery↗
Loss of ascorbic acid from injured feline spinal cord.
Feline spinal cord contains 0.97 mM ascorbic acid, as measured by the dinitrophenylhydrazine method. Greater than 90% is maintained in the reduced form. When functioning normally, the CNS conserves its ascorbic acid with a turnover rate of 2% per h. Following contusion injury severe enough to produce paraplegia, ascorbic acid is rapidly lost from injured spinal tissue. Thus, ascorbic acid is decreased 30% by 1 h and 50% by 3 h following injury. Oxidized ascorbic acid is increased at 1, but not 3, h following impact. As a consequence of its many functions in CNS, loss of ascorbic acid may contribute to derangements in spinal cord function following injury.
Animals↗
Hemangiopericytoma of the pituitary fossa: case report.
A case of hemangiopericytoma presenting as a sellar and suprasellar mass is reported. Although this is the first report of this tumor in such a location, it appears similar to hemangiopericytomas found in other locations.
Female↗
Microsurgical removal of a balloon embolus to the internal carotid artery. Case report.
Explore the source record for details and available documents.
Arteriovenous Fistula↗
Further studies on free-radical pathology in the major central nervous system disorders: effect of very high doses of methylprednisolone on the functional outcome, morphology, and chemistry of experimental spinal cord impact injury.
The hypothesis that pathologic free-radical reactions are initiated and catalyzed in the major central nervous system (CNS) disorders has been further supported by the current acute spinal cord injury work that has demonstrated the appearance of specific, cholesterol free-radical oxidation products. The significance of these products is suggested by the fact that: (i) they increase with time after injury; (ii) their production is curtailed with a steroidal antioxidant; (iii) high antioxidant doses of the steroidal antioxidant which curtail the development of free-radical product prevent tissue degeneration and permit functional restoration. The role of pathologic free-radical reactions is also inferred from the loss of ascorbic acid, a principal CNS antioxidant, and of extractable cholesterol. These losses are also prevented by the steroidal antioxidant. This model system is among others in the CNS which offer distinctive opportunities to study, in vivo, the onset and progression of membrane damaging free-radical reactions within well-defined parameters of time, extent of tissue injury, correlation with changes in membrane enzymes, and correlation with readily measurable in vivo functions.
Animals↗
Effect of high-dose corticosteroid therapy on blood flow, evoked potentials, and extracellular calcium in experimental spinal injury.
High-dose methylprednisolone (15 to 30 mg/kg), administered 45 minutes after severe contusion injury (400 gm-cm) to cat spinal cords, rapidly reverses the typical posttraumatic ischemia that occurs in spinal injuries. White matter blood flow improves despite the systemic hypotension associated with bolus intravenous injections of such massive corticosteroid doses. In addition, this treatment facilitates extracellular calcium ionic recovery in contused spinal cords, and salvages evoked potential activity that is lost in untreated cats. These data suggest that high-dose corticosteroid treatment causes local vasodilation of spinal cord blood vessels. The consequent blood flow increase may account for the beneficial effects of high-dose corticosteroid treatment on both functional recovery and histopathological appearance of injured spinal cords.
Animals↗
Experimental spinal cord injury: treatment with naloxone.
We studied the effect of the opiate antagonist naloxone on the recovery of cats injured with a 400-g-cm impact injury to T-9. The animals were evaluated by recording somatosensory evoked potentials and performing weekly neurological examinations. Several dose schedules were followed. Six of eight cats that received an intravenous or intraperitoneal bolus of naloxone (10 mg/kg) 45 minutes after injury regained the ability to walk. Recovery occurred in only one of five animals that were treated with an infusion of naloxone, 10 mg/kg/hour, and in none of five animals given 1 mg/kg as a bolus. Because these results are not related to any observed change in blood pressure, we believe that naloxone may be achieving its effect through the preservation of spinal cord blood flow, as well as other mechanisms that have yet to be defined.
Animals↗
Early surgical management of acute spinal cord injury.
Acute surgical decompression accompanied by stabilization and fusion is a safe procedure in patients with spinal cord injury. No patient was made worse by surgery. Patients with partial preservation of function and myelographic defects, i.e., surgical candidates, made better recoveries than those with normal myelograms who were, therefore, not operated upon. These results probably signify greater intrinsic cord damage in the nonsurgical group, but confirm the safety of surgery. We doubt the value of decompression for swollen cords except where there are hematomas. The treatment of cord swelling and ischemia will depend on improved pharmacological regimens.
Adult↗
Lipid antioxidant properties of naloxone in vitro.
Explore the source record for details and available documents.
Dose-Response Relationship, Drug↗