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Biomedical subjects

K Rajamani

Publications and source records attributed to K Rajamani.

8 recordsLinked to original sources

Infection and risk of ischemic stroke: differences among stroke subtypes.

BACKGROUND AND PURPOSE: Although prior studies have demonstrated that 25% to 35% of stroke patients have had a recent infection, the role of infection as a risk factor remains unclear. Our aim was to characterize the effect of infectious/inflammatory syndromes on stroke risk. METHODS: Case-control and crossover analyses of 233 cases and 363 controls aged 21 to 89 years were performed. Cases were patients hospitalized with a first ischemic stroke at a Los Angeles, California, medical center. Controls were outpatients in the hypertension, diabetes, and general medical clinics. All subjects were administered a neurological examination, an infection/inflammation (I/I) examination, and an interview to elicit recent I/I history at baseline (within several days of stroke onset) and again approximately 2 months later. Three physicians classified subjects by the presence or absence of I/I within 1 month of the index dates, based on findings of the I/I examination, the interview report, and laboratory results. RESULTS: Infections, either total or specific, were not found more frequently in cases than controls. However, patients with a recent respiratory tract infection suffered more often from large-vessel atherothromboembolic or cardioembolic stroke than did patients without infection (48% vs 24%, P=0.07). The age- and sex-adjusted relative risk estimate for these subtypes was 1.75 (95% CI, 0.86 to 3.55). The risk was notably high for those without stroke risk factors: 4.15 (95% CI, 1.22 to 14.1) for normotensives, 2.71 (95% CI, 1.04 to 7.06) for nondiabetics, and 1.74 (95% CI, 0.74 to 4.07) for nonsmokers. Patients with a recent respiratory infection also had a more severe neurological deficit on admission than those without infection (P=0.05). CONCLUSIONS: Our results suggest that respiratory tract infection may act as a trigger and increase the risk of large-vessel and/or cardioembolic ischemic stroke, especially in those without vascular risk factors.

Adult↗

Prejunctional actions of methylenedioxymethamphetamine in vas deferens from wild-type and alpha(2A/D)-adrenoceptor knockout mice.

Methylenedioxymethamphetamine (MDMA, 'ecstasy') has major agonist actions at prejunctional alpha(2A/D)-adrenoceptors in the rat. We wished to establish whether MDMA has potency at more than one subtype of alpha(2)-adrenoceptor, in line with affinity in ligand-binding studies. We have investigated the effects of MDMA in vas deferens from wild-type and from knockout mice lacking the alpha(2A/D)-adrenoceptor. The potency of the alpha(2)-adrenoceptor agonist xylazine at inhibiting stimulation-evoked contractions to a single stimulus in the presence of cocaine was significantly reduced in knockout (pD(2) of 8.27+/-0.07, -log M, n=4) as compared with wild-type mice (8.69+/-0.08, n=4, P<0.05), whereas potency of MDMA was unchanged (5.39+/-0.06, n=4 versus 5.38+/-0.06, n=6). Similar differences between xylazine and MDMA were seen for responses to stimulation at 10 Hz for 4 s. In studies of mouse atria pre-incubated with (3)H-noradrenaline, the stimulation-evoked release of tritium was inhibited to a similar extent by MDMA (10 microM) in tissues from wild-type and knockout mice. The prejunctional alpha(2A/D)-adrenoceptor is reported to be replaced by the alpha(2C)-adrenoceptor in this knockout mouse, so that we have evidence that suggests that MDMA has similar potencies at both subtypes in functional studies.

Adrenergic Agents↗

Transcranial Doppler in stroke.

Transcranial Doppler (TCD) has been extensively used in various clinical situations, and in the last two decades has established its role in the management of patients with cerebrovascular disease and stroke. Based on the Doppler principle, it uses ultrasound waves to insonate the blood vessels supplying the brain to obtain hemodynamic information. Anatomic abnormalities of vascular occlusion, stenosis and spasm can be indirectly derived. Intracranial arterial disease is an important cause of ischemic stroke and TCD can detect these with a fair amount of sensitivity and specificity. In hemodynamically significant extracranial internal carotid artery disease, TCD shows significant abnormalities in flow dynamics of the anterior circulation and abnormalities of cerebral vasomotor reactivity. A distinct advantage of TCD is the ability to monitor blood flow in a blood vessel over prolonged periods of time, which has shown microembolic signals in acute ischemic stroke, carotid artery disease, atrial fibrillation and during angiography. In acute ischemic stroke, TCD can be used to elucidate stroke mechanisms, plan and monitor treatment, and determine prognosis. In an era when stroke is increasingly being recognized as an emergency requiring immediate treatment, TCD may be capable of providing rapid information about the hemodynamic status of the cerebral circulation, within the time frame of the rather small 'therapeutic window'. TCD predicts vasospasm with a high degree of sensitivity and specificity and because of its non-invasive nature repeated assessments can be performed after subarachnoid hemorrhage.

Brain Ischemia↗

Stroke precipitated by moderate blood pressure reduction.

Rapid lowering of blood pressure can precipitate or worsen ischemic strokes. This usually has been observed in the setting of profoundly lowered pressure and hypotension. We report on six patients in whom ischemic neurologic injury ensued or worsened after moderate reduction of blood pressure by pharmacological treatment. The 6 patients suffered new or worsened ischemic neurologic deficits after receiving oral or intravenous antihypertensive medications, mostly after relatively small doses. Mean arterial blood pressure in these patients was decreased by 25 +/- 7.7%, or 37 +/- 16 mm Hg (mean +/- SD) without resultant hypotension. These cases emphasize the potential hazards of moderate blood pressure reduction by antihypertensive medications in the setting of an acute ischemic stroke or transient ischemic attack (TIA), as well as rapidly treated hypertension even in those who have not yet manifested ischemic symptoms.

Adult↗

Effect of glycemic control on the overnight dexamethasone suppression test in patients with diabetes mellitus.

Because many of the clinical features associated with Cushing's syndrome are frequently found in patients with diabetes mellitus, diabetic patients are often evaluated for Cushing's syndrome. The initial test for Cushing's syndrome is the 1 mg overnight dexamethasone suppression test (DST), but its value as a screening test in diabetic subjects, especially those with poor glycemic control, has been questioned. To address this issue, an overnight DST was administered to 100 subjects with diabetes. Only 7 patients failed to suppress their plasma cortisol to less than 140 nmol/L (5.0 micrograms/dL), achieving a specificity of 93%. There was no relation between acute glycemic control (as measured by the mean of 4 serum glucose values obtained before receiving dexamethasone) or chronic glycemic control (as measured by glycohemoglobin) and false positive responses to the 1 mg overnight DST. The mean of the measures of acute glycemic control of the 7 subjects who had false positive results, 14.4 +/- 2.8 mmol/L, was not significantly different than that of the 93 subjects with normal responses, 13.2 +/- 3.3 mmol/L. Similarly, the mean glycohemoglobin of the subjects with false positive results, 12.8 +/- 2.4%, was not significantly different than that of the subjects with normal responses, 12.9 +/- 2.5%. There was no correlation between plasma cortisol after dexamethasone and glycohemoglobin (r = 0.05), and only a weak correlation with the mean serum glucose (r = 0.21). We conclude that the 1 mg overnight DST is a valid screening test for Cushing's syndrome in patients with diabetes, regardless of glycemic control.

Adult↗

Normeperidine-induced seizures in hereditary coproporphyria.

Seizures are common in acute exacerbations of hepatic porphyria, even though the etiology is not identified in most cases. We have reported a case of normeperidine-induced seizures in a patient with hereditary coproporphyria. Although meperidine is commonly used for pain control during acute attacks in these patients, this report suggests that meperidine is not a good analgesic choice in porphyria. Normeperidine-induced seizures in patients with porphyria may be treated by withdrawal of meperidine therapy and selective use of anticonvulsants.

Adult↗