PubMed Health⌕ Search

Biomedical subjects

S Grunfeld

Publications and source records attributed to S Grunfeld.

34 records · Page 2Linked to original sources
PubMed1990

Event-related slow potentials and associated catecholamine function in migraine.

Plasma norepinephrine and dopamine and event-related slow potentials were measured at menses and ovulation in migraine with and without aura relative to normal subjects. The results indicated that at menses, but not ovulation, plasma dopamine was increased and norepinephrine was decreased relative to normal. This catecholamine imbalance was greater in migraine without aura than in migraine with aura. Conversely, event-related slow potentials measured over the posterior cortex at ovulation but not at the menses was altered relative to normal. Early epoch negativity was reduced in migraine with aura, whereas late epoch negativity was reduced in migraine without aura. The results suggested that (a) migraine without aura may involve dynamic shifts in the function of both norepinephrine and dopamine responsive neurons; (b) pathophysiology of migraine with aura is less dependent on catecholamine imbalance (norepinephrine alone affected); (c) these pathophysiological mechanisms are most prevalent in or restricted to posterior cortical regions but may be modulated by brainstem mechanisms.

Adult↗
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

Platelet catecholamines in migraine.

We measured platelet levels of norepinephrine (NE), epinephrine (E), and dopamine (DA) in migraine patients. Platelet NE was selectively increased in common migraine. This is attributed to platelet dense body hyposecretion.

Adolescent↗
PubMed1989

Platelet activation and analysis of organelles in migraineurs.

We used transmission electron microscopy to investigate selected aspects of the platelet response (surface activation as well as aggregation) and quantify cytoplasmic organelles within the cytoplasm of platelets obtained from both healthy control women and women diagnosed as having either common or classic migraine. Comparisons between controls and migraineurs showed no differences for: (1) the number of circulating platelets, (2) degree of surface activation, (3) amount of aggregate formation or (4) percent of hyperactive platelet populations. In contrast, platelets of migraine sufferers uniformly contained a significantly greater number of dense bodies compared to control platelets. Although we did not find functional abnormalities for the platelets obtained from migraineurs, we did demonstrate that they were altered structurally.

Adult↗
PubMed1989

Platelet norepinephrine and serotonin balance in migraine.

Platelet serotonin (5 hydroxytryptamine, 5-HT) and norepinephrine (NE) were measured in common and classic migraine patients and healthy controls. Common migraine sufferers had high NE levels and a low 5-HT/NE ratio. Classic migraine patients had a high 5-HT level and a high 5-HT/NE ratio. The data suggest disparate NE and 5-HT metabolism between common and classic migraine.

Adolescent↗
PubMed1989

A plasmatic factor may cause platelet activation in acute ischemic stroke.

To study the pathogenesis of platelet activation in ischemic stroke, ionized calcium ([Cai2+]) was measured in aequorin-loaded gel-filtered platelets in the basal and stimulated state. Basal [Cai2+] was increased in stroke patients maximally 36-72 hours after onset. The increase in [Cai2+] after stimulation with thrombin, collagen, and platelet-activating factor were also greater in stroke patients, but the profiles of these [Cai2+] changes were parallel to control. Cross incubation of control platelets with plasma from stroke patients resulted in raised basal [Cai2+] and caused the release of serotonin from platelets. These results indicate that the higher platelet basal [Cai2+] in stroke patients represents a lowered threshold for activation and that this may be due to a plasmatic factor rather than a primary platelet defect.

Adult↗
PubMed1988

Baseline and activated platelet cytoplasmic ionized calcium in acute ischemic stroke. Effect of aspirin.

We measured cytoplasmic ionized calcium concentrations [( Cai2+]) in aequorin-loaded gel-filtered platelets from 38 patients with acute occlusive stroke (12 treated with aspirin, 26 untreated) and 25 healthy controls. Compared with controls, baseline [Cai2+] was higher in untreated patients (p less than 0.002), maximal 36-72 hours after the onset of neurologic dysfunction (p less than 0.0001), in those patients with as well as those without major stroke risk factors. The increase in [Cai2+] after stimulation with 0.5 and 1.0 unit/ml thrombin (p less than 0.05), 2 and 4 micrograms/ml collagen (p less than 0.02), and 0.5 and 1.0 mM platelet activating factor (p less than 0.05) were also greater in untreated patients, but the profiles of these changes were parallel to those in controls. Even though the platelets of stroke patients are more sensitive to activation, they are functionally similar to those of controls. Aspirin treatment reduced baseline [Cai2+] as well as thrombin- and collagen-induced [Cai2+] changes. Platelet activating factor-induced increase in [Cai2+] was not altered by aspirin treatment. Our results suggest that the usefulness of aspirin in stroke is limited because aspirin does not suppress platelet responsiveness to all in vivo thrombogenic stimuli. Specific platelet activating factor antagonists may prove to be useful therapeutic agents in stroke.

Acute Disease↗
PubMedDate not supplied

Platelet alpha granule secretion in cerebral ischemia: effect of short and long term low dose aspirin treatment.

The effect of short and long-term therapy with aspirin (50 mg/day) on platelet alpha granule secretion was studied in 11 healthy controls and 57 patients suffering from transient cerebral ischemic attacks (TIA) with and without accompanying diabetes and hypertension. Plasma levels of beta-thromboglobulin (beta-TG) and platelet factor 4 (PF 4) were measured as indicators of platelet alpha granule secretion. beta-TG and PF 4 levels were increased following cerebral ischemia. Aspirin treatment failed to suppress plasma levels of both proteins when measured a month and then a year after initiation of treatment. Therefore, these proteins may be poor indicators of platelet inhibition by aspirin.

Adult↗
PubMedDate not supplied

Platelet as a model to test autonomic function in migraine.

In order to evaluate the role of the sympathetic autonomic nervous system (SANS) in common migraine we measured platelet catecholamine levels in a group of patients and in control subjects after 1 and 30 min of supine rest. Common migraine patients showed, at 1 min of supine rest, higher platelet norepinephrine (NE) content in comparison with the controls. This result may reflect a decreased release of platelet dense bodies in migraineurs. The same patients showed after 30' of supine rest a hardly significant increase of platelet NE levels in contrast to the clearly significant increase found in controls. These findings support the hypothesis of sympathetic hypofunction in migraine.

Adult↗