Weight variations in the prophylactic therapy of primary headaches: 6-month follow-up. (1/11)

We conducted a study on 367 patients (86% female, 14% male; mean age 37+/-15 years) suffering from migraine with and without aura and chronic tension-type headache to evaluate the incidence of weight gain, an undesirable side effect observed during prophylactic therapy in primary headaches. Patients treated with amitriptyline (20 and 40 mg), pizotifen (1 mg), propranolol (80-160 mg), atenolol (50-100 mg), verapamil (160-240 mg), valproate (600 mg) and gabapentin (900-1200 mg) were evaluated after a period of 3 and 6 months. In particular, 89 patients were assessed (78% female, 22% male) at 6 months, of whom 10 were in treatment with amitriptyline 20 mg, 19 with amitriptyline 40 mg, 7 with pizotifen (1 mg), 13 with propranolol (80-160 mg), 4 with verapamil (160 mg), 10 with valproate (600 mg), 15 with atenolol (50 mg) and 11 with gabapentin (900-1200 mg). The control group consisted of 97 patients with migraine (79% female, 21% male; mean age 35+/-16 years) without indication for prophylactic therapy. Weight variations >or=1 kg were considered. After 6 months of therapy, the percentage of patients with weight gain was 86% with pizotifen (6/7; mean weight increase 4.4+/-2.5 kg), 60% with amitriptyline 20 mg (6/10; 3.1+/-1.6), 47% with amitriptyline 40 mg (9/19; 5.4+/-2.7), 25% with valproate 600 mg (2/8, 3.0+/-2.8 kg), 25% with verapamil (1/4, 2.5 kg), 20% with atenolol (3/15, 1.7+/-0.6 kg), 9% with gabapentin (1/11, 1.5 kg) and 8% with propranolol (1/13; 6 kg). We conclude that propranolol, gabapentin, atenolol, verapamil and valproate affect body weight in a modest percentage of patients at 6 months. A greater mean weight gain at 6 months was found in patients treated with pizotifen, amitriptyline, and, in one patient out of 13, with propranolol.  (+info)

Receptors for 5-hydroxytryptamine and noradrenaline in rabbit isolated ear artery and aorta. (2/11)

5-Hydroxytryptamine (5-HT) is thought to be implicated in the vascular disturbances of the external carotid artery bed associated with migraine. As part of a study of the pharmacology of some 5-HT antagonists used in the treatment of migraine we have examined the interactions of these drugs with 5-HT and noradrenaline in rabbit isolated ear artery and aortic strip. The results provide new information on the distribution of 5-HT-receptors in these preparations. In the aorta, 5-HT and noradrenaline were of similar potency in producing contractions. Methysergide produced very small contractions and was about 1000 times less potent than the other two agonists. In the ear artery noradrenaline produced monophasic vasoconstrictor responses, whereas 5-HT and methysergide produced prolonged biphasic responses. 5-HT was about 700 times less potent and methysergide about 4500 times less potent than noradrenaline. Methysergide was a better agonist in the ear artery than in the aorta. Biphasic responses to 5-HT and methysergide were also obtained in ear arteries from reserpine-treated rabbits indicating that neither agonist was acting by releasing endogenous noradrenaline. Pizotifen, cyproheptadine and phentolamine had no agonistic actions in either the aorta or ear artery. In the aorta methysergide, pizotifen and cyproheptadine were potent antagonists of 5-HT and much weaker antagonists of noradrenaline. Phentolamine possessed the opposite profile of selectivity. These results show that there are distinct receptors for 5-HT and noradrenaline in rabbit aorta. In the ear artery the pA2 values for each of the four antagonists were virtually identical against 5-HT and noradrenaline and similar to those obtained on alpha-adrenoceptors in the aorta. We conclude that 5-HT and noradrenaline act directly at alpha-receptors to produce vasoconstriction in the ear artery and that this preparation does not contain specific 5-HT receptors. This insight into the distribution of 5-HT receptors and alpha-receptors allows interpretation of the various actions of methysergide. In the aorta, methysergide was a potent antagonist at 5-HT-receptors and a weak partial agonist at alpha-receptors. In the ear artery, methysergide was a partial agonist at alpha-receptors; it was only a weak antagonist of 5-HT because this preparation does not contain specific 5-HT-receptors. The cross-reactivity demonstrated throughout these experiments indicates that 5-HT-receptors and alpha-receptors, although distinct entities, have features in common. These results are discussed in relation to the mode of action of methysergide, pizotifen and cyproheptadine in the treatment of migraine.  (+info)

P3MC: a double blind parallel group randomised placebo controlled trial of Propranolol and Pizotifen in preventing migraine in children. (3/11)

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Calcium channel antagonism by pizotifen. (4/11)

Pizotifen is a clinically effective anti-migraine agent with potent anti-serotonin and anti-histamine properties. Pizotifen is equipotent in blocking contractions of the canine basilar artery induced by serotonin, norepinephrine or calcium chloride. As a result, the primary action of pizotifen in the canine basilar artery system appears to be calcium channel blockade and not selective antagonism of serotonin or norepinephrine. Calcium channel blocking ability may be related to the clinical efficacy of pizotifen in the treatment of migraine.  (+info)

Pizotifen in deafferentation pain. (5/11)

Deafferentation pain is known usually to be resistant to both narcotic and non-narcotic analgesics. Four cases of this condition are reported here in which benefit was obtained with pizotifen, a 5-hydroxytryptamine antagonist. Further controlled clinical studies are required to verify this observation.  (+info)

Migraine. (6/11)

Recent advances in migraine therapy include the recognition of analgesic or ergotamine abuse as a cause of chronic daily migraine, the introduction of effective non-narcotic drugs such as chlorpromazine, dihydroergotamine and corticosteroids for the treatment of intractable migraine attacks, the increased number of beta-blockers now recognized as effective prophylactic agents and the introduction of calcium-channel blockers for prophylaxis. There is a sufficient variety of antimigraine drugs, and therapy should be successful for most sufferers.  (+info)

A report of acute overdosage of the anti-serotonergic drug pizotifen. (7/11)

An acute overdosage of 30 mg of pizotifen causing a pyrexial illness is reported. The clinical features suggest that the effects of overdosage are principally due to the anticholinergic activity of this drug. Resolution of symptoms occurred after 10 hours, without specific therapy.  (+info)

Inhibition of insulin secretion from the perfused pancreas of the rat by pizotifen. (8/11)

1 In the perfused rat pancreas the effects of pizotifen on insulin release induced by 20 mM glucose were studied. 2 Pizotifen (10 and 100 muM) significantly reduced the insulin release during a 25 min perfusion period to 49% and 7% of the controls. 3 The same concentrations of the structurally related agents cyproheptadine, doxepin, and chlorpromazine produced a comparable inhibition.  (+info)