BackgroundCommon neurological syndrome (migraine without aura) is more common among women than men. Migraine is among the top 20 causes of disability. Menstruation is known to be a powerful trigger for migraine, and so is stress, but the presentation of headache is similar in both. Also, women are more vulnerable to stress as well as migraine, and this makes a complex relationship of menstruation, stress, and migraine.ObjectiveThis study was done to understand the association of hormonal fluctuation in menstruation and stress with common migraine.Materials and methodsA cross-sectional comparative study was conducted in 40 young adult females, of whom 20 participants were cases of migraine without aura (18–35 years old), and the remaining 20 participants were age-matched controls. The study was done in Maulana Azad Medical College, New Delhi. Study participants were selected on the basis of International Headache Society (ICHD-IIA1.1) (2004) classification. Study participants with neurological disorders, chronic diseases, and disease suggestive of any hormonal disturbances were excluded. Clinically diagnosed migraine cases were asked to maintain a headache diary and to fill in the Depression Anxiety Stress Scales questionnaire. Biochemical assessment of hormonal status for thyroid-stimulating hormone, triiodothyronine, thyroxine, estrogen, follicle-stimulating hormone, luteinizing hormone, and prolactin was also done on the second day of their menstrual cycle. We used the Mann–Whitney U test to compare hormonal levels and the χ2 test to compare anxiety- or depression-related stress among the migraine and nonmigraine groups.ResultsSignificantly higher values of prolactin were observed in cases (mean ± standard deviation, 152.7 mIU/L±30.5) compared to controls (76.1 mIU/L±8.7), with a P-value <0.001. There was no statistically significant difference observed in levels of thyroid-stimulating hormone (P=0.081), estrogen (P=0.086), luteinizing hormone (P=0.091), or follicle-stimulating hormone (P=0.478). Also, anxiety with stress or depression with stress was significantly higher among the migraine group than the controls (P=0.002). Odds of any stress in migraine were higher in the migraine group than in the nonmigraine group (odds ratio 12, 95% confidence interval 2.7–53.33).ConclusionMigraine, particularly without aura, in women is mainly associated with stress-related anxiety or depression, and are more susceptible to stress in the premenstrual period.
To analyze the mechanism of the cerebral vasodilator effect of ketamine in anesthetized rabbits, we measured the internal carotid blood Sow with an electromagnetic flowmeter, the arterial pressure, intracranial pressure, end-tidal CO 2 , and the electroencephalogram. Ketamine injection (1 mg/kg) induced a significant cerebral vasodilatation that was blocked by scopolamine, a cholinergk antagonist. In contrast, the increase in cerebral blood flow after ketamine was additive to the cerebral vasodilator actions of inhaled CO } and of physostigmine infusion, two procedures that activate cholinergic mechanisms. These observations suggest that in rabbits, ketamine activates a cholinergic cerebral vasodilator system. (Stroke 1987;18:445-^49) K ETAMINE is a potent analgesic and dissociative agent used extensively for pediatric anes-, thesia, but which is not recommended for neurodiagnostic or neurosurgical procedures because of its reported tendency to increase intracranial pressure (ICP). "~3 It is generally accepted that the elevation in ICP is secondary to the cerebral vasodilatation that may accompany the alterations in brain electrical activity and possible changes in metabolism elicited by the drug. However, while the cerebral vasodilator effect of ketamine is generally supported, its cerebral metabolic effect is controversial. 13 -3 " 7 If the increase in brain metabolism is inconsistent, it is difficult to understand how this may mediate such a consistent effect as the cerebrovascular dilatation. On the contrary, this apparent poor correlation between cerebral metabolism and blood flow may result from the activation by ketamine of a nonmetabolic mechanism. We studied the cerebrovascular effects of ketamine in rabbits to analyze the possible participation of a neurogenic cholinergic mediator of vasodilatation, using a muscarinic antagonist, scopolamine, and a cholinergic agonist, physostigmine. The existence of such a mechanism has been proposed by others 89 and supported by our work on the vasodilator effect of CO 2 and halothane. 10 Materials and MethodsThe experiments were performed on 30 New Zealand white rabbits weighing 2.7-4.1 kg anesthetized inside a box with 5% halothane in air and maintained by mask until a tracheostomy was performed. The animals were then mechanically ventilated with endexpired CO 2 kept at 4%, paralyzed with pancuronium Received May 29, 1985; accepted October 20, 1986. bromide (0.2 mg/kg/hr), and maintained on 0.5-1% halothane in 35% O 2 and N 2 . Respiratory rate was maintained at 40/min and peak inspiratory pressure at 15 cm H 2 O, a combination that maximized the matching between end-tidal CO 2 and PacOj and provided excellent oxygenation, with a Pac^ always above 100 mm Hg. The femoral artery and vein were cannulated for arterial pressure monitoring and drug injection, respectively. Internal carotid blood flow (ICBF) was measured using an electromagnetic flowmeter probe placed around the common carotid artery after the laryngeal, occipital, and external carotid arteries we...
The present study examined whether (1) the cough associated with angiotensin converting enzyme inhibitor therapy is attenuated by oral intake of iron and anti-oxidants, and (2) nitric oxide (NO) has any role in this attenuation. Of the 100 patients under investigation, cough occurred in 28 of them with preponderance in females. All the 28 patients were followed up for six weeks: the first two weeks were the observation period and the remaining four weeks the experimentation period. After the observation period, 11 patients received a single oral dose of ferrous sulphate (200 mg), eight received vitamin E (200 mg, o.d.) and vitamin C (150 mg, o.d.) and nine were given placebo during the experimentation period. Cough scoring, serum NO and malondialdehyde (MDA) levels were determined during both the periods. While there were significant decreases in cough scores, NO and MDA levels between these two periods in the iron group, cough scores and MDA level decreased significantly in the anti-oxidant group. None of these parameters changed in the control group. NO level was found to be increased significantly in patients who developed cough (n = 28) compared with those who did not cough (n = 72). These results suggest that iron supplementation suppresses cough in patients on ACE-I therapy through its effect on NO generation.
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