Search PubMed⌕ Search

Biomedical subjects

W R Selman

Publications and source records attributed to W R Selman.

At least 55 records · Page 3Linked to original sources
PubMed1987

Radiculomeningeal vascular malformations of the spine: MR imaging.

Three patients (two men, one woman; 63-81 years old) with radiculomeningeal vascular malformations of the spine were examined using high-resolution surface coil magnetic resonance (MR) imaging at 1.5 T. The findings included previously described high-velocity signal loss within the vessels of the malformation as well as previously unreported signal-intensity changes within the cord (long T1/long T2) distal to the malformation. The MR images correlate well with previous reports of location and pathophysiology of these dural lesions.

Aged↗
PubMed1987

Large pituitary gland adenomas evaluated with magnetic resonance imaging.

Magnetic resonance imaging (MRI), computed tomographic (CT) scanning, and angiography or digital subtraction angiography (DSA) were used preoperatively to evaluate 16 surgically proven cases of sellar tumor with extrasellar extension. There were 15 pituitary tumors and 1 schwannoma. The capabilities of MRI in evaluating these tumors were compared with CT scanning and angiography. Bone destruction and tumor calcification were better detected by CT scanning than by MRI. MRI was as effective as CT scanning in detecting a cyst or variation in tumor consistency. Neither MRI nor CT scanning was capable of distinguishing specific tumor types. In every case, MRI was superior to CT scanning for delineating spatial relationships of the tumor to the 3rd ventricle, the optic apparatus, adjacent brain, and parasellar vasculature. Vessel encasement by tumor was clearly seen on MRI when there was no direct indication of this on other studies. Cavernous sinus invasion was not demonstrated by CT scanning, but was indicated by MRI in 5 cases and was surgically confirmed in 3. MRI can provide more precise spatial information on extrasellar tumor extension. Vascular encasement and cavernous sinus invasion may be determined preoperatively. Treatment expectations and operative approaches can be guided by this information. When MRI is available, it is the test of choice for the preoperative evaluation of patients with suspected large pituitary gland (sellar region) tumors. Contrast-enhanced CT scanning and angiography can be used as supplementary studies to add information inherently unique to these techniques.

Adenoma↗
PubMed1987

Visually defined zones of focal ischemia in the rat brain.

A technique to guide brain tissue sampling in experimental focal ischemia is described. This technique allows visual identification for accurate metabolic analysis of regions with variable tissue perfusion. After 2.5 hours of unilateral middle cerebral artery occlusion (MCAO) in the rat, intravenous infusion of the vital dye, neutral red (NR), identified three distinct regions: (a) an intensely stained region consisting of the entire contralateral hemisphere and the medial ipsilateral hemisphere; (b) a blanched region in the lateral ipsilateral hemisphere; and (c) a zone of intermediately stained tissue interposed between the medial and lateral ipsilateral regions. Close regional correlation between NR staining and the iodoantipyrine intensity of adjacent brain slices suggests that NR distribution is a qualitative indicator of brain perfusion. Using the NR staining pattern to guide tissue dissection for metabolite analysis of high energy phosphates (adenosine triphosphate and phosphocreatine) and glucose-related metabolites showed that the blanched region contained ischemic tissue, whereas values from the contralateral cortex resembled those of control tissue. The intermediately stained region exhibited a gradient of metabolic perturbation. Tissue near intensely stained regions resembled control tissue, and tissue near blanched regions resembled ischemic tissue. These results confirm the concept of a metabolic penumbra. When present, it occupies only the most medial area of the intermediate region at 2.5 hours after MCAO.

Adenosine Triphosphate↗
PubMed1987

Advances in neuroradiologic imaging of the pituitary gland: changing concepts.

A review of pituitary imaging is presented based on the history of neuroradiologic definition of the sellar contents as well as modern diagnostic techniques. The importance of normal pituitary and seller anatomy is stressed in an attempt to determine the limitations of defining abnormal sellar contents with the imaging techniques of computed tomography and magnetic resonance imaging. The sensitivity and specificity of these techniques are illustrated with histopathologic correlation.

Cerebrospinal Fluid↗
PubMed1986

The occurrence of dural invasion in pituitary adenomas.

This report describes 60 dural specimens from patients with pituitary adenomas treated by transsphenoidal microsurgery, and attempts to define more precisely the clinical and pathological correlation of microscopic dural invasion. Analysis of the adenomas was based on four characteristics; size, surgical invasiveness (based on the surgeon's assessment of involvement by tumor of bone, dura, or cavernous sinus), histological evidence of invasion, and immunohistochemical staining characteristics. The incidence of surgical invasiveness (24 cases, 40%) was greater than previously reported, but most important was the frequent occurrence of microscopic dural invasion (51 cases, 85%). There was a clear progression of microscopic evidence of dural invasion with increasing tumor size: 69%, 88%, and 94% of the dural specimens from microadenomas, macroadenomas, and tumors with suprasellar extension, respectively, showed microscopic dural invasion. A correlation of invasiveness with immunohistochemical classification of tumor type was not evident.

Adenoma↗
PubMed1985

Cerebrospinal fluid penetration of moxalactam in ventriculostomy patients.

The cerebrospinal fluid penetration of moxalactam was simultaneously investigated in three patients with presumed bacterial meningitis. When ratios of simultaneously drawn ventriculostomy to serum moxalactam levels of 1, 2, 3, and 4 h were examined, the penetration ratios were 7.8 +/- 2.4, 11.2 +/- 1.3, 14.2 +/- 2.5, and 15.0 +/- 4.9%, respectively. These ratios were not statistically different from the penetration of moxalactam calculated by the area under the concentration-time curve technique (8.97 +/- 1.89%).

Drug Administration Schedule↗
PubMed1984

New lumboperitoneal shunt catheter.

A new catheter is described for percutaneous lumboperitoneal shunts. The method of introduction and indications for this shunt are reviewed.

Catheterization↗
PubMed1984

Liver abscess: complication of a ventriculoperitoneal shunt.

Liver abscess is a previously unreported complication of ventriculoperitoneal shunting. We present such a case, which was diagnosed by computed tomography (CT) and managed by CT-guided percutaneous catheter drainage of the liver abscess, appropriate antibiotics, and shunt externalization.

Adult↗
PubMed1983

Ineffectiveness of DMSO in treating experimental brain ischemia.

A beneficial effect of dimethyl sulfoxide (DMSO) in the treatment of acute focal cerebral ischemia has not been proven. In the present study, two established experimental models of acute focal cerebral ischemia were treated with DMSO. Twenty adult cats lightly anesthetized with ketamine hydrochloride underwent right middle cerebral artery (MCA) occlusion for 6 hours. Ten cats were not treated and 10 cats received DMSO (2.5 g/kg i.v.) immediately after occlusion. No improvement of EEG findings, erythrocyte transit, regional cerebral blood flow (rCBF), blood-brain barrier permeability, or morphological findings were demonstrated in the DMSO-treated cats. In a second study, 15 conscious adult baboons underwent temporary left MCA occlusion (6 or 12 hours) using an implanted occluding device. Seven baboons were not treated and 8 baboons received continuous intravenous infusions of DMSO for 10 hours beginning 30 minutes after occlusion. Four of the baboons that were treated with DMSO also were treated with pentobarbital coma for 96 hours starting 4 hours after occlusion. Analysis of the neurological scores after 1 week survival indicated that treatment with DMSO alone and DMSO and pentobarbital coma did not improve the outcome. Morphological changes were similar in the 3 groups. The findings of our investigation indicate that DMSO is ineffective in treating acute focal cerebral ischemia.

Animals↗
PubMed1982

Cerebral revascularization during barbiturate coma in primates and humans.

Extracranial-intracranial arterial bypass was performed in five baboons to assess the effectiveness of the procedure in preventing acute cerebral ischemia following middle cerebral artery occlusion in our primate model. Thirty minutes following middle cerebral artery occlusion, the animals were placed in barbiturate coma while the extracranial-intracranial artery bypass was being completed. In the three animals with patent extracranial-intracranial arterial bypasses, infarction was prevented. In the two with occluded extracranial-intracranial arterial bypasses, a large infarction in the territory of the middle cerebral artery occurred. In a clinical correlate, postoperative ischemia was presumably prevented in three patients by barbiturate administration and revascularization for unanticipated intracranial vessel occlusion.

Animals↗
PubMed1982

Barbiturate coma in focal cerebral ischemia. Relationship of protection to timing of therapy.

The therapeutic application of barbiturate-induced coma was evaluated in a primate model of focal cerebral ischemia. A standardized regimen of pentobarbital was used, and the times of initiation of administration were varied following a 6-hour middle cerebral artery occlusion in baboons. Three groups of five animals were treated at 30, 120, and 240 minutes after occlusion, while one group of five animals received no barbiturate therapy. Complete protection from intracranial pressure (ICP) elevation and ischemic damage was seen only in the group treated at 30 minutes. Those treated at 120 minutes, while doing better than untreated animals, still had ICP elevation and a marked neuropathological deficit. Animals treated at 240 minutes suffered a detrimental effect, in that malignant ICP and marked ischemic damage occurred earlier than in the untreated animals. The safe "therapeutic window" for barbiturate-induced coma in this animal model does not extend beyond 2 hours. Delayed administration results in a deleterious response and not merely a lack of protection.

Animals↗
PubMed1981

Barbiturate resuscitation from focal cerebral ischemia--A review.

Barbiturate therapy has been shown to be of benefit in certain instances for focal cerebral ischemia. This therapy can, however, result in a deleterious outcome. Early institution in combination with revascularization appears to be important for successful barbiturate application. Whether combinations of agents designed to act on different mechanisms in the pathophysiology of cerebral ischemia can prolong the 'therapeutic window' of barbiturate application is an area for future investigation.

Animals↗
PubMed1981

Management of prolonged therapeutic barbiturate coma.

Barbiturate administration for protection from focal ischemia was evaluated in baboons. All animals were monitored for 96 hours in an intensive care unit during various regimens of pentobarbital administration. Intermittent bolus injections of barbiturate yielded inconsistent electroencephalographic responses and produced the most cardiovascular instability. Continuous barbiturate infusion safely allowed the greatest amount of barbiturate to be employed with the most stable electrophysiological and cardiovascular response.

Animals↗
PubMed1981

Barbiturate-induced coma therapy for focal cerebral ischemia. Effect after temporary and permanent MCA occlusion.

The authors have studied the therapeutic effect of barbiturate coma following middle cerebral artery (MCA) occlusion in primates. The relationship of the efficacy of barbiturate protection to the presence or absence of recirculation was examined. Barbiturate therapy was begun 30 minutes after MCA occlusion. The findings were as follows: 1) barbiturate-induced coma, with its attendant monitoring, was safely tolerated by primates for 96 hours; 2) 6 hours of MCA occlusion followed by recirculation resulted in a neurological deficit that was worse than the neurological deficit produced by permanent MCA occlusion; 3) barbiturate-induced coma for 96 hours, initiated 30 minutes after the onset of MCA occlusion, in the absence of reperfusion, was in fact detrimental; 4) barbiturate-induced coma for 96 hours, initiated 30 minutes after MCA occlusion, with the establishment of reperfusion at 6 hours, provided nearly complete protection from ischemic damage.

Animals↗
PubMed1980

Percutaneous lumboperitoneal shunt: review of 130 cases.

One hundred thirty consecutive cases of percutaneous lumboperitoneal shunting are reviewed. The efficacy of this procedure in the management of cerebrospinal fluid fistulas and bulging craniotomies is documented. The place of lumboperitoneal shunts in the management of communicating hydrocephalus, with particular emphasis on "normal pressure" hydrocephalus, is discussed.

Adolescent↗
PubMed1980

Chronic reversible cerebral ischemia: evaluation of a new baboon model.

The authors describe their experience with a baboon model of reversible cerebral ischemia. Middle cerebral artery occlusion was achieved by external compression with an implantable, inflatable balloon cuff in awake, unanesthetized baboons. Selective cerebral angiography confirmed consistent, reliable occlusion. Computed tomography demonstrated early density changes after ischemia, which were reversible with reperfusion. Neurological evaluation demonstrated a "recruitment response" of increasingly persistent deficit with repeated occlusion. Permanent deficits were noted after extensive angiography during periods of occlusion. This was accompanied by the dropout of small vessels in the middle cerebral artery distribution. The results of pathological examinations were consistent with the clinical examinations. No gross or microscopic changes were noted after repeated occlusions that caused deficits like those of transient ischemic attacks. Consistent infarctions were noted in animals with permanent deficits after permanent occlusion or after repeated occlusion and extensive angiography.

Animals↗