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Biomedical subjects

K M Welch

Publications and source records attributed to K M Welch.

At least 127 records · Page 7Linked to original sources
PubMed1990

Magnetoencephalographic studies of migraine.

We report for the first time the detection by magnetoencephalography (MEG) of signals observable in migraine patients during headache, but not in controls. These signals consisted of three features: suppression of spontaneous cortical activity, long duration field changes, and large amplitude waves (LAW) of several seconds duration. LAW were also seen during the interictal period. We discuss the possible relationship of these signals to spreading depression (SD), and why the LAW have not been observed in previous studies of SD.

Adolescent↗
PubMed1990

Fluorocarbon-23 measure of cat cerebral blood flow by nuclear magnetic resonance.

We employed fluorocarbon-23 (trifluoromethane) as a nuclear magnetic resonance gaseous indicator of cerebral blood flow in seven cats. Pulsed inhalation of this indicator and switching between two coils allowed the acquisition of both an arterial input and a cerebral response function, making possible multicompartmental curve fits to cerebral uptake and clearance data. The brain:blood partition coefficient for trifluoromethane was 0.9 for both gray and white matter. Fast-compartment blood flows were normal and showed appropriate CO2 reactivity. Slow-compartment blood flows did not demonstrate CO2 reactivity, probably because cranial as well as white-matter blood flows were lumped together in the slow compartment. Although cerebral blood flow was stable during administration of 60% trifluoromethane, the compound did prove to be a mild cardiac sensitizer to epinephrine in five cats.

Animals↗
PubMed1990

Chronic cerebral intracellular alkalosis following forebrain ischemic insult in rats.

We measured cerebral intracellular pH using in vivo phosphorus-31 nuclear magnetic resonance spectroscopy during 1 week after forebrain ischemia or sham operation in eight and seven rats, respectively. Mean maximum pH was significantly higher (p less than 0.003) in the ischemic group than in the sham-operated group (7.34 +/- 0.03 and 7.19 +/- 0.02, respectively). The difference between mean maximum pH and baseline pH (7.08 +/- 0.01 in each group) was significantly greater (p less than 0.02) in the ischemic group than in the sham-operated group. In the ischemic group, alkalosis occurred primarily after 48-72 hours of recirculation. We speculate that brain tissue alkalosis occurring chronically after ischemia is associated with delayed ischemic neuronal death.

Alkalosis↗
PubMed1990

Acute toxicity of a nuclear magnetic resonance cerebral blood flow indicator in cats.

We studied trifluoromethane as a potential gaseous indicator in nuclear magnetic resonance measurements of cerebral blood flow. We considered the effects of trifluoromethane on cerebral blood flow in 17 cats and on the electroencephalogram and electrocardiogram in nine cats and compared these with the effects of the more toxic compound chlorodifluoromethane in five cats. Inhaled at 60%, trifluoromethane had no effect on cerebral blood flow, the cerebral metabolic rate for oxygen, or oxyhemoglobin content. At 70%, trifluoromethane sensitized the cats' hearts to epinephrine, but to a much lesser degree than 40% chlorodifluoromethane, and produced only moderate changes in cerebral electrical activity as measured by the electroencephalogram. We found trifluoromethane to be suitable for use in animals, but its toxicity needs to be studied further before it can be used in humans for the measurement of cerebral blood flow.

Animals↗
PubMed1990

Cerebrovascular and neurologic disease associated with antiphospholipid antibodies: 48 cases.

Lupus anticoagulants and anticardiolipin antibodies are antiphospholipid antibodies (APLAb) with related antigenic specificities and are newly recognized markers for an increased risk of thrombosis. We studied 48 patients who presented with cerebral or visual dysfunction associated with APLAb to help clarify the diagnostic, clinical, laboratory, radiologic, and pathologic features in these patients. Most patients presented with transient cerebral ischemia or cerebral infarction. Recurrent and stereotypic events were frequent. Visual disturbances resulted from amaurosis fugax, retinal arterial or venous occlusion, occipital ischemia, diplopia, and migraine-like disturbances. Three patients presented with severe atypical classic migraine. Recurrent infarcts of brain and eye were significantly associated with the presence of cigarette smoking, hyperlipidemia, and a positive antinuclear antibody. During 44.4 patient-years of prospective follow-up, the combined stroke and systemic thrombotic event rate was 0.27 events per patient-year and was 0.54 events per patient-year if TIA and death were included. Forty (83%) of the patients did not have systemic lupus erythematosus (SLE). Thrombocytopenia was present in 15 (31%) and a false-positive VDRL in 11 (23%) of the patients. Cerebral angiography was normal or revealed large-vessel occlusion or stenosis without changes suggestive of vasculitis. Patients with only transient dysfunction generally had normal radiologic studies, including angiography. Organs and arterial vessels studied pathologically revealed thrombotic occlusive disease without vasculitis. APLAb are strongly associated with an immune-mediated thrombotic tendency, generally in the absence of SLE. Other stroke risk factors may add to the risk of recurrent ischemic events in patients with APLAb.

Adult↗
PubMed1990

The concept of migraine as a state of central neuronal hyperexcitability.

This article explores the hypothesis that migraine with aura is associated with a state of central neuronal hyperexcitability. The authors propose that this central neuronal hyperexcitability involves overactivity of the excitatory amino acids, glutamate, and possibly aspartate. Stimuli that activate the migraine attack evoke neuronal depolarization, slow depolarization shifts, and spreading suppression of spontaneous neuronal activity possible by glutamate and K+ dependent mechanisms. A low brain Mg2+ and consequent reduced gating of glutamatergic receptors may provide the link between the physiologic threshold for a migraine attack and the mechanisms of the attack itself by promoting glutamate hyperactivity, neuronal hyperexcitability, and susceptibility to glutamate-dependent spreading depression.

Adult↗
PubMed1989

Evidence for the presence of red and white cells within "platelet" aggregates formed in whole-blood.

Collagen-induced platelet aggregation and secretion (ATP-release) in whole-blood and platelet-rich plasma was compared. Although the amount of ATP released was comparable in whole-blood and platelet-rich plasma, the maximum extent of aggregation was greater when platelets were studied in their natural milieu, i.e. whole-blood. A scanning electron microscopic survey of the "platelet" aggregate formed in whole-blood showed that it contained erythrocytes and leucocytes as well as aggregated platelets.

Adenosine Triphosphate↗
PubMed1989

Platelet serotonin metabolism and ultrastructure in migraine.

Biochemical and ultrastructural techniques were used to study the nature of platelet serotonin involvement in migraine. Serotonin levels were increased to a moderate degree in classic migraine, but not in common migraine. The platelet content of 5-hydroxyindoleacetic acid was equally reduced in both classic and common migraine. Platelet-dense bodies, the storage organelles for serotonin, were increased in both migraine groups, particularly in classic migraine. The results were interpreted as evidence for reduced platelet serotonin turnover combined with dense body hyposecretion in migraine sufferers. These findings are further supportive evidence for altered serotonergic function between attacks of migraine, and argue in favor of a role for serotonin in the mechanisms of a migraine attack.

Adolescent↗
PubMed1989

Stroke risk and age do not predict behavioral activation of brain blood flow.

Twenty-four neurologically normal subjects, 12 in their twenties and 12 in their sixties, were included in a protocol that studied the relationship of resting cerebral blood flow and cerebral blood flow activation by neuropsychological testing to age and stroke risk factors. Both age and a stroke risk index were predictive of a reduced resting cerebral blood flow. Despite this, cerebral blood flow activation relative to resting flow was preserved. Subclinical lesions of deep white matter are proposed to explain the apparently paradoxical result that resting cerebral blood flow is decreased by factors that damage cerebral vessels, while cerebral vascular reactivity is unimpaired.

Adult↗
PubMed1989

Antiphospholipid antibodies.

Lupus anticoagulants and anticardiolipin antibodies, known collectively as antiphospholipid antibodies, are becoming established as markers for increased risk of thrombosis, including ischemic cerebrovascular disease. In this brief review, we highlight evidence for and against a pathogenetic role of these antibodies in ischemic brain disease and comment on currently available laboratory studies to detect them. Future research on the association of antiphospholipid antibodies with neurological disease should focus on establishing the pathogenicity of these antibodies, identifying groups at high risk for recurrent ischemic cerebrovascular events, and initiating prospective multicenter natural history and treatment protocols.

Autoantibodies↗
PubMed1989

Interleaved 31P NMR with transcutaneous nerve stimulation (TNS): a method of monitoring compliance-independent skeletal muscle metabolic response to exercise.

31P NMR spectroscopy was used to monitor the metabolic response of the tibialis anterior muscle group to transcutaneous nerve stimulation of the peroneal nerve at a rate of 4 Hz for 5 min in human volunteers (n = 8). It is demonstrated that this technique can be used as a method of investigating effort-free and compensation-independent skeletal muscle exercise.

Adult↗
PubMed1989

Rubidium transport in human erythrocyte suspensions monitored by 87Rb NMR with aqueous chemical shift reagents.

Dysprosium(III) triethylenetraamine-N,N,N',N",N"',N"'-hexaacetic acid (DyTTHA3-) was used as an aqueous chemical shift reagent in conjunction with high-resolution nuclear magnetic resonance (NMR) spectroscopy to monitor 87-rubidium (87Rb+) transport in human erythrocyte suspensions. NMR spectra demonstrated two resonances which were assigned to the intra- and extracellular compartments of the erythrocyte suspension. Uptake of 87Rb+ was shown to proceed via the [Na,K]-ATPase dependent pump as evidenced by the inhibition of uptake in the presence of ouabain. The steady state intra- to extracellular concentration ratio of 87Rb was 3.00 and 1.13 in the absence and presence of ouabain, respectively. The rate of uptake of 87Rb+ in the absence and presence of ouabain was found to be 1.3 and 0.5 mmol Rb+/L erythrocytes/h at 18 mM Rb+, respectively. Data are also presented which indicate that the intracellular component of 87Rb is less than 100% NMR visible.

Biological Transport↗
PubMed1989

The effect of CO2 and non-CO2-generating buffers on cerebral acidosis after cardiac arrest: A 31P NMR study.

There is controversy regarding the use of alkalinizing agents during reperfusion after cardiac arrest. The potential deleterious effects of sodium bicarbonate (bicarb) administration, including paradoxic cerebral acidosis, have led to the search for alternative agents. Tromethamine (tris) is a non-CO2-generating buffer that has been proposed for use during cardiopulmonary resuscitation. The purpose of this experiment was to compare the ability of tris with bicarb to correct brain pH (pH B) during reperfusion after a 12-minute cardiac arrest. Adult mongrel dogs were instrumented and placed in the bore of a Bruker Biospec 1.89 tesla superconducting magnet system. Ventricular fibrillation was induced; after 12 minutes, cardiopulmonary bypass was initiated and maintained for two hours with minimum flows of 80 mL/kg/min. Bicarb (n = 5) or tris (n = 5) were administered to correct arterial pH as rapidly as possible. 31P NMR spectra were obtained at baseline and throughout ischemia and reperfusion. The pH B was determined with the inorganic phosphate relative to the phosphocreatine resonance signal shift. Profile analysis indicates a difference between groups (P less than .02) related to an initial delay in pH B correction in the tris group. By 48 minutes of reperfusion, pH B did not differ between the groups. Moreover, there was no evidence of paradoxic cerebral acidosis in the bicarb group. Although tris corrects blood pH as quickly as bicarb, it is less effective in correcting pH B. Absence of paradoxic acidosis may be caused by efficient elimination of CO2 by cardiopulmonary bypass.

Acidosis↗
PubMed1989

The metabolic effects of mild hypothermia on global cerebral ischemia and recirculation in the cat: comparison to normothermia and hyperthermia.

The metabolic effects of graded whole body hypothermia on complete global cerebral ischemia and recirculation was investigated in the cat. Hypothermia was induced to one of three levels prior to ischemia; T = 26.8 degrees +/- 0.5 degrees C (n = 4), T = 32.1 degrees +/- 0.2 degrees C (n = 5), and T = 34.6 degrees +/- 0.3 degrees C (n = 6), and maintained constant throughout 16 min of ischemia and 1.5-2 h of recirculation. Intracellular cerebral pH and relative concentrations of high-energy phosphate metabolites were continuously monitored, using in vivo 31P nuclear magnetic resonance (NMR) spectroscopy. Except for the first 4 min of ischemia, no significant differences were detected in the response of adenylate intensities and intracellular pH to ischemia and recirculation between the hypothermic groups. The three hypothermic groups were then pooled into one group, and the data compared to previously published data from a normothermic group, T = 38.4 degrees +/- 0.6 degrees C (n = 14), and a hyperthermic group, T = 40.6 degrees +/- 0.2 degrees C (n = 9), subjected to the identical ischemic and NMR measurement protocols. The hypothermic animals exhibited a statistically significant reduction of cerebral intracellular acidosis, both during ischemia and recirculation, as well as a more rapid return of adenylate intensities during recirculation, compared to the normothermic or hyperthermic groups. The data thus suggest that mild hypothermia has an ameliorative affect on brain energy metabolism and intracellular pH under conditions of complete global cerebral ischemia and recirculation.

Animals↗