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Biomedical subjects

H J Gelmers

Publications and source records attributed to H J Gelmers.

At least 19 recordsLinked to original sources
PubMed1990

Effect of nimodipine on acute ischemic stroke. Pooled results from five randomized trials.

In a review of pooled data from five double-blind, placebo-controlled studies of nimodipine in acute ischemic stroke, we compared the effect of 120 mg nimodipine given orally with that of placebo. In the five studies, 871 patients were followed, and 781 adhered to entry and inclusion criteria. End points were mortality and outcome at the end of the treatment period (21 or 28 days). Outcome was assessed with Mathew's scale and the physician's clinical judgement. The treatment and control groups were well matched with respect to demographic data, risk factors, and baseline Mathew scores. In the treatment group, 34 patients (7.9%) died during the treatment period, whereas 54 (12.3%) in the control group died, corresponding with a mortality reduction of 36%. Significantly less neurologic impairment at the end of the treatment period was documented under nimodipine treatment, and this impairment improved more in patients with moderate-to-severe stroke (baseline Mathew score less than 66) if administration of nimodipine occurred within 12 hours after stroke onset or if the patient was more than 65 years old. The overall incidence of adverse reactions was relatively modest, and these were of minor severity; only a few appeared to have more than a remote relation to the study medication.

Aged↗
PubMed1988

A controlled trial of nimodipine in acute ischemic stroke.

Recent investigations suggest that increased cellular calcium concentrations may be implicated in neuronal death after ischemia. To determine whether treatment with a calcium-channel blocker would improve survival and neurologic outcome in acute ischemic stroke, we enrolled 186 patients in a prospective, double-blind, randomized, placebo-controlled trial of nimodipine (30 mg every six hours), begun within 24 hours of the onset of symptoms of an acute ischemic stroke. During the four-week treatment period, mortality from all causes was significantly reduced with nimodipine as compared with placebo (8 deaths [8.6 percent] vs. 19 [20.4 percent]). The improvement in survival was restricted to men. During the follow-up period of six months, an additional eight patients in each group died. A significantly better neurologic outcome, as assessed by the Mathew scale of neurologic deficit, was also observed in the nimodipine group. The improvement in neurologic status was greatest in patients with a moderate to severe deficit at base line. There were no important side effects except for one episode of reversible azotemia that may have been related to treatment with nimodipine. Our data suggest that patients with acute ischemic stroke may benefit from early treatment with nimodipine, but this therapeutic effect appears to be limited to men.

Aged↗
PubMed1988

Assessment of interobserver variability in a Dutch multicenter study on acute ischemic stroke.

Quantitative assessment of patient data is a pertinent part of controlled clinical studies. When several centers are involved, the degree of agreement between different observers becomes important. Therefore, in addition to developing a multicenter study on acute ischemic stroke, we have estimated the interobserver agreement expressed in terms of kappa statistics. Twelve patients suffering from neurologic deficits due to acute ischemic stroke were examined by four investigators, and the results were assessed using the Mathew scale. Considerable interobserver variability was found. Agreement on items based on subjective information from the patient was low, and it is also possible that this information changes with time. It is advised that in the development of assessment scales, items with low interobserver agreement should be avoided.

Acute Disease↗
PubMed1987

Effect of calcium antagonists on the cerebral circulation.

Current research suggests that cerebral ischemia induces a cascade of pathophysiologic reactions. A massive influx of calcium into the neuron constitutes the "final common pathway," resulting in catabolism and cell necrosis due to calcium overload. Treatment with calcium antagonists may offer a means of arresting and possibly preventing the destruction of cerebral tissue in patients with stroke. One such drug, nimodipine, selectively inhibits spasm of isolated cerebral arteries induced by either depolarization or receptor stimulation. In vivo experiments have shown that nimodipine prevents the postischemic impairment of cerebral blood flow that may be a major contributor to neuronal damage. After encouraging although not conclusive results of a single-blind pilot study, a double-blind, placebo-controlled, multicenter clinical investigation of nimodipine was undertaken. Some benefit was strongly suggested in patients with acute ischemic stroke who were treated with 120 mg of nimodipine, begun within 24 hours after the onset of the event, combined with "standard" treatment (i.e., hemodilution using low molecular dextran). Calcium antagonists such as nimodipine may be useful in the treatment of stroke due to acute cerebral ischemia.

Animals↗
PubMed1985

Calcium-channel blockers in the treatment of migraine.

According to classic theory, a migraine attack is initiated by cerebrovascular spasm followed by extracranial vasodilatation. Results of recent studies support this theory and suggest that cerebral blood flow during the initial phase of migraine symptoms is, in fact, decreased and this decrease probably leads to ischemia and hypoxia. Cellular hypoxia, in turn, can cause an increase in the flow of calcium from the extracellular fluid to the intracellular space, resulting in calcium overload and cellular dysfunction. Because calcium-channel blockers selectively inhibit the intracellular influx of calcium ions, investigators have begun evaluating the efficacy of these agents for migraine prophylaxis. Nimodipine, a calcium-channel blocker that exhibits selective effects on cerebral vessels, seems to offer protection against the cerebral ischemia and hypoxia presumed to be operative during migraine attacks. In a double-blind, placebo-controlled study, nimodipine decreased the frequency and duration of migraine attacks by at least half in 69% of patients treated with this agent. Comparable reductions in migraine frequency and duration were attained in 58, 51, 41 and 52% of patients treated with methysergide maleate, pizotifen, clonidine hydrochloride and propranolol, respectively. The piperazine derivative flunarizine also has calcium-channel blocking properties. This agent prevents vasospasm in cerebral arteries and protects against cerebral hypoxia. Results of double-blind studies of migraine prophylaxis with flunarizine demonstrate the beneficial effects of this agent, particularly in younger patients. Flunarizine proved to be superior to pizotifen in decreasing the severity of migraine attacks and comparable to pizotifen in decreasing their frequency.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcium Channel Blockers↗
PubMed1985

Calcium-channel blockers: effects on cerebral blood flow and potential uses for acute stroke.

Current research suggests that ischemia induces a massive shift of calcium from the extracellular fluid to the intracellular space. This is associated with a precipitous decrease in the concentration of adenosine triphosphate, the energy source required to drive the ion pumps of the calcium channels that maintain intracellular calcium homeostasis. The result is a further increase in free intracellular calcium, leading to calcium overload and thus to cell catabolism and cell necrosis. Treatment with calcium-channel blockers may therefore offer a new approach to arresting and, possibly, preventing destruction of cerebral tissue in stroke victims. Animal studies using nimodipine, a calcium antagonist with marked vasodilator effects, have shown that this agent prevents both spasm of the isolated rabbit basilar artery, produced either by depolarization or by receptor stimulation, and postischemic impairment of cerebral blood flow (CBF), which may be a major contributor to neuronal damage. In patients with acute ischemic stroke, intravenous nimodipine therapy caused a dose-dependent increase in hemispheric CBF. These data prompted us to conduct a prospective, single-blind, randomized trial of 60 patients to determine whether nimodipine treatment would reduce neurologic deficits in patients with acute ischemic stroke. The 29 treated patients were given standard dextran therapy supplemented with daily 120 mg doses of nimodipine, and the 31 control subjects received dextran therapy alone. Mathew scale neurologic scores indicated decreased consciousness and impaired cerebral function in both treated and control groups; however, cerebral deficits were significantly smaller in patients who received nimodipine.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1984

Exacerbation of systemic lupus erythematosus, aseptic meningitis and acute mental symptoms, following metrizamide lumbar myelography.

A clinical constellation of exacerbation of systemic lupus erythematosus (SLE), together with aseptic meningitis, and acute mental symptoms occurred following lumbar myelography with metrizamide. Exacerbation of SLE has not been previously described following myelography with any contrast agent. Meningeal reactions and acute mental symptoms have been reported earlier, but this clinical constellation is new.

Delirium↗
PubMed1984

The effects of nimodipine on the clinical course of patients with acute ischemic stroke.

60 patients with acute ischemic stroke were enrolled in a prospective single-blind, randomized trial to determine whether treatment with the calcium antagonist nimodipine would reduce their neurological deficit. All patients received a standard treatment. In addition, 29 received a daily dose of 120 mg nimodipine orally as 3 divided doses (treatment group). Evaluation of therapy was assessed with a neurological scoring system ( Mathew scale). Comparison of the Mathew sum scores in the standard group with those of the nimodipine group (analysis of variance) revealed a highly significant difference (P less than 0.0001) in favour of nimodipine during the 4 week period of treatment. Based on the individual items of the Mathew scale, the level of consciousness and disability were significantly improved under the nimodipine-therapy. Side effects were of minor importance and of no clinical relevance.

Acute Disease↗
PubMed1983

Tapia's syndrome after thoracotomy.

Tapia's syndrome, a unilateral paralysis of the muscles of the tongue associated with palsy of the ipsilateral vocal cord, was observed in two patients within a short time of each other, after they had undergone thoracotomy. It can be understood as an extremely localized lesion just at the crossing of the vagal and hypoglossal nerves. Pressure neuropathy of both nerves due to inflation of the cuff within the larynx is an accepted cause. An alternative explanation is that stretch, caused by downward traction of the esophagus, is transferred to both nerves, those being closely connected in many places, and ultimately causing damage to them.

Adult↗
PubMed1983

The role of calcium and the significance of calciumantagonists in some neurological and neurosurgical diseases.

Calcium is an important intracellular 'second messenger' in the activation of contractile proteins in vascular smooth muscle cells. Intracellular calcium accumulation probably has a major pathological effect in the occurrence of ischemic cell damage. Calcium antagonists are a heterogenous group of substances with one property in common, that is they interfere with the transmembrane movement of calcium. Their therapeutic usefulness in cerebral vasospasms, migraine and cerebral ischemia is reviewed.

Calcium↗
PubMed1983

Non-paralytic motor disturbances and speech disorders: the role of the supplementary motor area.

A right-handed patient with a lesion demonstrated by CT to involve the right medial frontal cortex is described. He exhibited a strong contralateral grasp reflex, motor perseveration and the presence of purposeful movements that appeared to be dissociated from conscious volition. In addition, there was a disorder of speech consisting of a lack of spontaneous speech production, with preserved ability to imitate. It is suggested that these disorders are due to damage to the supplementary motor area.

Aged↗
PubMed1982

Relation of false localizing signs and remote hyperaemia in patients with intracranial mass lesions.

Seventeen patients with intracranial mass lesions underwent rCBF measurements with the xenon-133 carotid injection technique. In 11 patients remote areas of hyperaemia were found. There was a relation between location of the remote hyperaemia and the site of the mass lesion. In 10 of 11 patients with remote hyperaemia autoregulation was focally lost, and in 5 of 7 patients there was focal impairment of arterial pCO2-reactivity. In 8 of 11 patients with remote hyperaemia false localizing signs were found, related to the hyperaemic areas. It is suggested that the remote hyperaemic areas may be the result of brain bulk shifting due to the mass lesion and represent the initial stage of brain herniation.

Adult↗
PubMed1982

Effect of nimodipine (Bay e 9736) on postischaemic cerebrovascular reactivity, as revealed by measuring regional cerebral blood flow (rCBF).

Regional cerebral blood flow (rCBF) was measured, using the xenon-133 intracarotid injection technique in 10 patients with an acute ischaemic stroke, involving the cerebral cortex, before and after intravenous injection of a single dose of nimodipine (Bay e 9736). After nimodipine application in all patients a dose dependent increase of hemispheric blood flow was observed. In the regional pattern the stroke area showed, after nimodipine in 9 patients relatively similar changes in blood flow as the hemispheric flow did. In three of these patients the increase reached such a level, that the presence was concluded of an inverse steal phenomenon. The intracerebral steal phenomenon was not observed. As a side effect in one patient a mild fall in blood pressure and sinusbradycardia was observed, of short duration.

Brain Ischemia↗