Biomedical subjects

R A Ratcheson

Publications and source records attributed to R A Ratcheson.

At least 19 recordsLinked to original sources

PubMed2001

Functional evaluation of arteriovenous malformations.

Detailed knowledge of the angioarchitecture of arteriovenous malformations (AVMs) is necessary in determining the optimal timing and method of treatment of these challenging lesions. Many techniques are available for studying the functionality of surrounding cortical structures of AVMs. These include the use of positron emission tomography, functional magnetic resonance imaging, magnetoencephalography, and direct provocative testing of cortical function. The use of these methods to determine flow dynamics and tissue perfusion is also reviewed. These techniques are discussed in the present study, and their judicious utilization will enhance the safety of AVM therapy.

Amobarbital↗

PubMed1998

Cost and outcomes analysis.

Cerebral aneurysms and their treatment have numerous consequences for patients and society, including loss of life, permanent neurologic deficits, decreased functioning in daily life, vast expenditures of health care resources, and loss of economic productivity. By the use of administrative, clinical, functional, and economic data, outcomes research increases neuro-surgeons' understanding of aneurysmal disease, and consequently, our ability to provide more effective interventions.

Activities of Daily Living↗

PubMed1997

Mortality rates, hospital length of stay, and the cost of treating subarachnoid hemorrhage in older patients: institutional and geographical differences.

The risk of disability and death and the cost of medical care are particularly high for patients with aneurysmal subarachnoid hemorrhage (SAH) who are 65 years of age or older. A retrospective analysis of 47,408 Medicare patients treated over an 8-year period was performed to determine whether a relationship exists between the mortality rate and surgical volume for older patients with SAH. The mortality rate, length of stay in the hospital, and cost of treatment for patients with SAH in California and New York state were also compared. The mortality rate was 14.3% for patients with SAH who were 65 years old or older and who were treated surgically in hospitals in which an average of five or more craniotomies were performed per year; in hospitals averaging between one and five craniotomies annually the mortality rate was 18.4%; and in those averaging less than one such operation per year the rate was 20.5% (trend p = 0.01). There was no difference in the mortality rate for patients in California versus the rate for those in New York. Surgically and medically treated patients, respectively, left the hospital an average of 6.7 and 5.1 days sooner in California than in New York. The unadjusted average reimbursement from Medicare to hospitals for surgically treated patients averaged $1468 more in New York than in California (p < 0.0001), but was equivalent for medically treated patients in the two states. The mortality rate in older patients who are treated surgically for SAH may be inversely correlated with the annual number of craniotomies performed for SAH in patients 65 years of age or older at a given institution. Hospital stays for patients with SAH are significantly shorter in California than in New York.

Aged↗

PubMed1997

Brain attack. The emergent management of hypertensive hemorrhage.

Intracerebral hemorrhage (ICH) accounts for one half of stroke-related deaths, with hypertensive hemorrhage being the primary etiology. The evolution of minimally invasive devices for removal of ICHs, and the earlier delivery of patients for medical attention may have a great impact on the management of hypertensive hemorrhage.

Case Management↗

PubMed1996

Temporary vessel occlusion during intracranial aneurysm repair.

Any method that decreases the risk of intraoperative rupture should improve outcome if complications associated with its use do not negate positive effect. If application time is limited and a form of cerebral protection and appropriate monitoring of cerebral function are used, temporary clip application may meet these requirements. The efficacy of temporary occlusion as an adjunct to aneurysm clipping may be limited by technical considerations with respect to regional anatomy, aneurysm size, and aneurysm consistency. In areas of limited access, positioning proximal clips may not be feasible. The use of endovascular techniques of balloon occlusion may provide proximal control in these situations (9, 106). The decision to use total circulatory arrest and profound hypothermia, as opposed to temporary clip application, remains largely a matter of the surgeon's judgment. The role of proximal parent vessel ligation must also be considered in the decision-making process regarding the treatment of giant or technically difficult aneurysms (114). Further refinements in cerebral monitoring that can accurately reflect intracellular processes in all territories affected by the application of temporary clips or balloon occlusion and development of more effective forms of cerebral protection may permit safer use of this technique. An adequately controlled clinical trial of temporary occlusion with or without putative "cerebral protection" is needed to confirm the efficacy of this technique.

Animals↗

PubMed1995

Case Western Reserve University and University Hospitals of Cleveland: a neurosurgical chronicle.

There is a strong tradition of neurosurgery in Cleveland. This article traces the origin of Case Western Reserve University School of Medicine and University Hospitals of Cleveland and examines the evolution of neurological surgery at these institutions. It looks at the strong Cushing influence on the process, by both Harvey Cushing and his family. The contributions of such luminaries as George Crile, Elliott Cutler, Claude Beck, and Frank Nulsen are described.

History, 19th Century↗

PubMed1995

Cerebral arterial aneurysm formation and rupture in 20,767 elderly patients: hypertension and other risk factors.

Cerebral arterial aneurysms are common in the general population and their rupture is a catastrophic event. Considerable uncertainty remains concerning the conditions that predispose individuals to aneurysm formation or rupture. The role of systemic hypertension in aneurysm formation and rupture has been especially controversial. Demographic variables have rarely been addressed because of the small sample sizes in previous studies. The authors describe the demographics and prevalence of hypertension in 20,767 Medicare patients with an unruptured aneurysm and compared these to a random sample of the hospitalized Medicare population. The prevalence of hypertension in patients with unruptured aneurysms was 43.2% compared with 34.4% in the random sample. Patients who survived their initial hospitalization were separated into two groups: those with an unruptured cerebral aneurysm as the primary diagnosis and those with an unruptured cerebral aneurysm as a secondary diagnosis. Follow-up data for 18,119 patients were examined to determine the risk of subarachnoid hemorrhage (SAH) associated with age, gender, race, hypertension, insulin-dependent diabetes mellitus, and surgical treatment. For patients with an unruptured cerebral aneurysm as the primary diagnosis, hypertension was found to be a significant risk factor for future SAH (risk ratio: 1.46, 95% confidence interval (CI): 1.01-2.11), whereas surgical treatment (risk ratio: 0.29, 95% CI: 0.09-0.97) had a significant protective effect. Advancing age had a small but significant protective effect in both groups. Elderly patients identified with unruptured aneurysms are more likely to have coexisting hypertension than the general hospitalized population. In elderly patients hospitalized with an unruptured cerebral aneurysm as their primary diagnosis, hypertension is a risk factor for subsequent SAH, whereas surgical treatment is a protective factor against SAH.

Age Factors↗

PubMed1994

Temporary vessel occlusion in spontaneously hypertensive and normotensive rats. Effect of single and multiple episodes on tissue metabolism and volume of infarction.

Temporary occlusion of an intracranial artery is frequently necessary in the surgical management of intracranial aneurysms, arteriovenous malformations, and tumors. While the risks of vessel damage associated with clip application have been lessened by improved design, the threat of ischemic damage remains. It is unclear whether multiple, brief periods of clip application are more or less safe than a single period of occlusion, and whether the underlying cerebrovascular status influences the outcome from either method. The effect of each of these paradigms (single: 1-hour occlusion; multiple: three 20-minute episodes separated by 10 minutes of reperfusion) on histopathological outcome was assessed in a middle cerebral artery (MCA) occlusion model using both normotensive and spontaneously hypertensive rats. The mean volume of infarction (+/- standard error of the mean) was not different between the single-ischemic (49.4 +/- 17.3 cu mm) and the multiple-ischemic (42.9 +/- 12.9 cu mm) episode groups of normotensive rats, whereas in the spontaneously hypertensive rats a significant difference existed between the volume of infarction for the single-occlusion group (126.7 +/- 18.7 cu mm) and the multiple-occlusion group (162.4 +/- 15.5 cu mm) (p < 0.05). The metabolic data obtained from spontaneously hypertensive animals did not provide an explanation for the larger infarction in that there were no significant differences between the single- and multiple-occlusion groups with respect to tissue glucose, adenosine triphosphate, or lactate levels. The results suggest that intermittent reperfusion may have different effects depending not only on the degree and duration of ischemia and reperfusion, but also on the underlying cerebrovascular status.

Adenosine Triphosphate↗

PubMed1994

Early reversal of acidosis and metabolic recovery following ischemia.

Tissue acidosis is believed to be a key element in ischemic injury of neural tissue. The goal of this study was to determine whether persisting postischemic acidosis or the extent of acidosis would affect metabolic recovery following an ischemic event. Intracellular pH (pHi), adenosine triphosphate, phosphocreatine, and lactate levels were measured in the cerebral cortex during the early stages of reperfusion, following either 5 or 10 minutes of global ischemia in both normo- and hyperglycemic gerbils. A total of 130 gerbils were injected with a solution containing 1.5 ml Neutral Red (1%) (+/- 2.5 gm/kg glucose); 30 minutes later, the gerbils were placed under halothane anesthesia, and the carotid arteries were occluded for either 5 or 10 minutes. The brains were frozen in liquid nitrogen at 0, 15, 30, 60, and 120 seconds after reperfusion; they were sectioned and the block face was photographed to determine the pHi by using Neutral Red histophotometry. At the conclusion of the ischemia, the pHi in all groups had decreased significantly from a control value of 7.05 +/- 0.03) (mean +/- standard error of the mean). In normoglycemic brains, the pHi values fell to 6.71 +/- 0.04 and 6.68 +/- 0.11 after 5 and 10 minutes of ischemia, respectively. Hyperglycemic brains were more acidotic; values fell to 6.57 +/- 0.10 and 6.52 +/- 0.24 after 5 and 10 minutes of ischemia, respectively. Lactate levels were approximately fivefold greater than those of control tissue in normoglycemic brains, while lactate levels in hyperglycemic brains were increased eightfold. The adenosine triphosphate and phosphocreatine levels were depleted at the end of ischemia in all groups. After 2 minutes of reflow activity, the pHi levels in both normo- and hyperglycemic brains were restored to those of control values in the '5-minute ischemic group, while the pHi levels remained significantly depressed in the 10-minute ischemic group. Restoration of high-energy phosphates was similar in normoglycemic brains regardless of ischemic duration, recovering to only 20% of the restoration obtained in control tissue at 2 minutes. In hyperglycemic brains, however, there was complete recovery of high-energy phosphates by 2 minutes of reflow activity following 5 minutes of ischemia. Extending the ischemic period to 10 minutes in hyperglycemic brains slowed the rate of metabolic recovery to that observed in normoglycemic brains. The results indicate that the reflow period permits the rapid restoration of pHi levels substantially before the normalization of primary energetic compounds.(ABSTRACT TRUNCATED AT 400 WORDS)

Acidosis↗

PubMed1992

Glutamate-induced energetic stress in hippocampal slices: evidence against NMDA and glutamate uptake as mediators.

The introduction of exogenous glutamate to normally respiring hippocampal slices produced substantial reductions in ATP, phosphocreatine (PCr) and intracellular pH (pHi) when the concentration exceeded 1 mM. These changes were not prevented by addition of MK-801 (an NMDA receptor antagonist), nor were they mimicked by NMDA or high potassium. In addition, the glutamate-induced metabolic alterations were not prevented by addition of aspartate-b-hydroxymate or sodium substitution by choline, both of which should inhibit high-affinity sodium-dependent glutamate uptake. These results suggest that glutamate alone can produce marked energetic stress in neural tissue, even when glucose and oxygen are maintained at control levels; and that the energetic stress does not appear to be specifically mediated by NMDA-induced depolarization, or by high-affinity uptake of glutamate.

Animals↗

PubMed1992

[Effect of metabolic stress on the release of glutamic acid and GABA in the brain tissue of Mongolian hamsters].

The concentrations of glutamic acid and GABA were determined in the brain tissue in gerbils under conditions simulating "metabolic stress", that is ischaemia, aglycaemia and anoxia. The material for the determinations was taken from fragments of the hippocampus incubated under these conditions in artificial cerebrospinal fluid, and the concentrations of these neurotransmitters were determined by histochemical methods in vitro. The release of glutamic acid and GABA into the extracellular space increased with longer duration of the incubation in a linear fashion in all experimental groups and was most pronounced in ischaemia. In case of calcium absence in the extracellular space inhibition was observed of the release of these neurotransmitters which suggested an important role of bivalent cations in the regulation of the studied process, especially under control conditions. During anoxia and ischaemia a considerable part of the release of glutamic acid and GABA seems to be calcium-independent which may suggest presence of additional sources of release of the amino acid neurotransmitters, apart from their release from the direct pool. It is possible that these sources are activated during metabolic stress involving nerve cells.

Animals↗

PubMed1992

[Metabolic effects of experimental thermal damage of the brain in rats--cold lesion].

Experimental thermal brain injury leads to significant reduction of glucose utilization in the damaged hemisphere particularly evident in the cortex 3 days after the injury. The rate of development of these changes is not parallel with the observed damage to the blood-brain barrier, coexistent brain oedema and slight disturbances of cerebral blood flow. In a series of experiments it was possible to demonstrate significant accumulation of glucose, high-energy phosphate compounds and their metabolites in the areas of the brain near the damaged part. The authors think that this is an evidence of reduced glucose uptake by the brain resulting from reduced energy needs of the damaged brain tissue despite sufficient supply of energy-yielding substances. Since cerebral metabolism and functions are in close interrelationship reduced glucose metabolism in the damaged tissue leads to reduced activity of the cortex, which contributes to transient (or permanent) functional neurological deficits observed after cranio-cerebral trauma in humans. The knowledge and understanding of these processes regulating the development of local depression of cerebral metabolic processes may help in better results of treatment in such cases.

Adenosine Triphosphate↗

PubMed1991

Rapid metabolic failure in spontaneously hypertensive rats after middle cerebral artery ligation.

The metabolic characteristics of the penumbral region were examined in spontaneously hypertensive rats one hour after permanent middle cerebral artery occlusion. The effect of hyperglycemia on this region was examined by providing a glucose load prior to occlusion. The depressed concentrations of adenosine triphosphate and elevated levels of lactate in the penumbral region were similar to those found in the ischemic focus. The purported neuroprotective effect of hyperglycemia in the penumbral region was not reflected in an increased high-energy phosphate level in the penumbral region. The rapid deterioration of the metabolic status of this region in this strain of rat suggests that the increased consistency of infarction may come at the expense of the penumbral region, and thus this model may not be well suited for the study of metabolic changes and perhaps even therapeutic intervention.

Adenosine Triphosphate↗

PubMed1991

Effects of focal cortical freezing lesion on regional energy metabolism.

Freezing lesions have been shown to cause a depression in glucose use, particularly in cortical areas of the brain ipsilateral to the lesion, and this effect was interpreted to be caused by a depressed functional activity in these regions. The metabolic status of the affected areas has not been previously examined and could be a factor in the observed changes in local CMRglc. In frozen-cut and dried sections taken from brains 3 days after freeze lesioning, discrete pieces of the median and lateral parietal cortex, striatum, hippocampus, and hypothalamus were dissected and analyzed for ATP, P-creatine, glucose, and lactate. CMRglc measurements were also made in the same animals. The concentrations of the four metabolites were significantly increased in the lesioned hemisphere, with the most predominant effects observed in the cortical areas that exhibited the greatest depression in CMRglc. The enriched metabolite profile, particularly in the cortical areas, is consistent with the hypothesis that decreased glucose use in the traumatized brain is caused by diminished need rather than by decreased supply of energy. Because the lumped constant in the operational equation of the deoxyglucose method for determination of CMRglc is a function of brain glucose content and decreases gradually in hyperglycemia, the degree of metabolic depression in cortical areas of lesioned hemisphere probably have been somewhat overestimated in this and previous publications. However, provisionally recalculated local CMRglc in the lesioned hemisphere remain significantly lower than in the contralateral hemisphere and in the normal brain.

Adenosine Triphosphate↗

PubMed1990

The evolution of focal ischemic damage: a metabolic analysis.

Focal cerebral ischemia in the rat was induced by left middle cerebral artery occlusion. The area of ischemia was determined by infusion of a qualitative perfusion indicator, neutral red. The temporal evolution of alterations in regional energy metabolism was assessed by direct microquantitative histochemical analysis of high-energy phosphates, glucose, glycogen, and lactate content of the tissue. Perfusion analyses demonstrated a perifocal region of diminished, but not absent perfusion up to 6 hr after occlusion. By 24 hr, there was an abrupt demarcation between perfused and nonperfused regions. Profound metabolic alterations were seen as early as 20 min after occlusion. Although there was an area of intermediate metabolic derangement in the more medial portions of the lateral ipsilateral cortex up to 6 hr, by 24 hr there was an abrupt transition from normal to abnormal cortex. No evidence of metabolic recovery was seen in this model of permanent occlusion.

Adenosine Triphosphate↗

PubMed1990

Lactate compartmentation in hippocampal slices: evidence for a transporter.

Lactic acid accumulation has been implicated in the evolution of brain damage after ischemia. Since compartmentation of lactate may play a role in acid-base balance, lactate release from gerbil hippocampal slices was examined during a number of metabolic stresses including elevated [K+]e, ischemia, anoxia, and aglycemia. Slices were preincubated for 1 hr in artificial cerebrospinal fluid (ACSF) equilibrated with 95% O2/5% CO2 (pH 7.4 at 37 degrees C) and then transferred to tubes containing 300 microliters of test medium. The rate of lactate release in control slices was 9.64 nmol/min/mg protein and increased 2.6- and 3.2-fold in the presence of 60 mM potassium and anoxia, whereas the rate of lactate release was decreased by 50 and 25% during ischemia and aglycemia. Lactate release was temperature dependent and was only minimally influenced by removing Ca2+ or by adding 5 mM d-lactate to the ACSF. In contrast, pyruvate inhibited lactate release with an apparent Ki of 2.4 mM. The results suggest that lactate can be released from cells via a saturable and stereospecific lactate transporter with an apparent Km of 10.7 mM and Vmax of 43.7 nmol/mg protein/min. Such a relatively high-capacity transporter system can rapidly equilibrate brain lactate but is probably not involved in regulating intracellular acid-base balance.

Adenosine Triphosphate↗

PubMed1990

Impairment of metabolic recovery with increasing periods of middle cerebral artery occlusion in rats.

We examined the consequences of reflow on metabolic recovery following increasing periods of focal ischemia. The middle cerebral artery of 21 Sprague-Dawley rats was occluded with a snare ligature for 1, 2, or 6 hours followed by 5, 4, or 0 hours of reflow, respectively (seven rats in each group). All animals were injected with neutral red for visual confirmation that the affected regions were reperfused. The brains were frozen in situ, and the concentrations of adenosine triphosphate, phosphocreatine, glycogen, and lactate were determined in those areas corresponding to the normally perfused medial ipsilateral cortex, the perifocal region, and the ischemic focus. Values for the 6 hours' occlusion with no reflow group served as a control to demonstrate restoration of metabolite concentrations. In both groups with reflow, the levels of high-energy phosphates were greater than control, but this effect of reflow was primarily significant for the group with 1 hour's occlusion (p less than 0.05). The levels of glycogen and lactate provided additional evidence that the extent of metabolite restoration was graded; following 2 hours of occlusion, metabolite recovery was compromised (p less than 0.05). Our data strongly support the concept that the window of opportunity for effective treatment of focal ischemia by reperfusion is narrow (of short duration).

Adenosine Triphosphate↗

PubMed1989

Preservation of hearing in the surgical removal of cerebellopontine angle tumors.

It is claimed that postsurgical hearing preservation is possible in about 5 to 8 per cent of cases of acoustic neuroma. Even with small tumors, hearing preservation can be accomplished in about half of the patients who are fortunate to have anatomic integrity of facial and cochlear nerves, as well as intact inner ear blood supply at the end of the surgical procedure. Monitoring of seventh and eighth nerve function through evoked potentials may be important. On the other hand, even if evoked potentials are preserved during surgery with wave V latency and amplitude similar to preoperative recording, hearing may still be completely lost during the immediate postoperative period. There is no predictable pattern that assures postoperative preservation of hearing. In Case 2, the seventh and eighth nerves as well as the inner ear blood supply were carefully dissected and anatomically and electrophysiologically preserved during the intraoperative period. At the end of the surgical procedure, the evoked potentials were the same as preoperatively. Nevertheless, the patient ended up with no detectable hearing postoperatively. We feel that the suboccipital-retrosigmoid transcanal approach can be safely used for the removal of cerebellopontine angle tumors of all sizes. We believe the argument that "only the translabyrinthine approach can accomplish total tumor removal" is not valid. No complications have been attributed by having the patient in the semisitting position. Older patients, who cannot tolerate the semisitting position, are operated on while in the park bench position. Planned subtotal removal of a CPA tumor is done with the patient in the supine position (transmastoid-retrolabyrinthine or retrosigmoid). The relationship between the otologic surgeon and neurosurgeon is very important. The surgical approach used should be selected on the basis of the combined experience of the surgical team. Finally, an attempt should be made to preserve facial nerve function and hearing in all suitable patients. The postoperative course using the suboccipital-retrosigmoid approach is usually benign, and the patients are discharged from the hospital between 7 and 10 days following surgery. The translabyrinthine approach, in our opinion, should be reserved for smaller lesions in patients with anacusis or with residual hearing that is not worth saving.

Adult↗