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PubMed1963

METHYSERGIDE (SANSERT) IN THE PREVENTION OF MIGRAINE: A CLINICAL TRIAL.

Methysergide was used as a regular medication to prevent migraine in a series of 87 patients with frequently recurring severe attacks of three types, common, classical and cluster migraine, in a study conducted during a 30-month period. Results were classified as excellent, good, fair and nil. The total reporting excellent and good results was 50.6%. In a few patients the drug appeared to lose effectiveness in long-term treatment. Other investigators have described more favourable results, notably Friedman, who reported improvement in common migraine in 79% of patients and in cluster migraine in 90% of patients. Side effects were noted in 34.2% of patients and led to discontinuing the trial in 10.4%; these promptly subsided when the drug was withdrawn. Methysergide appears to be a useful additional agent for prevention of severe, frequently recurring migraine of common and cluster type. In this small series it had little effect on headaches of combined tension and vascular type.

Biomedical Research↗

PubMed1979

Lower extremity arterial insufficiency after long-term methysergide maleate therapy. Its evaluation with Doppler ultrasonic velocity detector.

Iatrogenic ergotism is the primary source of ergot intoxication. The patient whose case is reviewed had migraine headaches and received methysergide maleate for 13 years. She had, in July 1977, severe claudication of the lower extremities. Measurements of the peripheral arterial circulation were made using the Doppler ultrasonic velocity detector. The extent of disease and subsequent reversal were documented using arteriographic examination. Initial measurements showed the patient was able to walk for one minute and 34 seconds on a treadmill (2 mph, 10% grade) before stopping because of claudication. Symptoms cleared after drug withdrawal and repeated testing produced no claudication. The calculated index (posterior tibial/arm pressure) increased from a mean of 0.22 to 0.74 during the eight-month period following discontinuance of methysergide therapy with no recurrence of migraine headaches. A review of the literature is also presented.

Constriction, Pathologic↗

PubMed1985

Control of suckling and feeding by methysergide in weaning albino rats: a determination of Y-maze preferences.

To assess the effects of serotonergic receptor blockade on the weaning process, 20-, 25-, and 30-day-old albino rat pups were injected with methysergide and were permitted to choose between suckling and feeding in a Y maze. At every age, progressively larger doses of methysergide enhanced pup preferences for the suckling goal, increased the frequency of suckling when in the suckling goal, and decreased the frequency of feeding when in the feeding goal. These results, with the support of other findings, suggest that the weaning process may be, in part, the result of emerging or changing serotonergic neurological mechanisms.

Age Factors↗

PubMed1997

Evaluation of the anti-oedematous effects of some H1-receptor antagonists and methysergide in rats.

A combined method was used for a comparative study of some H1 and H2 antagonists and methysergide. In male rats of the Wistar strain weighing 130 +/- 5 g, oedema was induced in the hind paw by the subplantar injection of zymosan, and simultaneously in the ear by the application of croton oil to the inner surface of the ear. Intraperitoneally orally administered H1 antagonists (dimethindene, clemastine, cyproheptadine, astemizole, cetirizine, loratadine and terfenadine) inhibited the oedema to a statistically significant extent, in a dose-dependent manner. Outstanding inhibition was observed after simultaneous administration of the antiserotonin methysergide with dimethindene, clemastine, loratadine or cetirizine.

Animals↗

PubMed1984

Methysergide decreases prolactin release after FK 33-824 [Tyr-D-Ala-Gly-MePhe-Met(o)-ol], a potent analogue of methionine enkephalin. A study in man.

This study investigated the mechanisms which may underly the prolactin (PRL) stimulating effects of FK 33-824, a potent enkephalin analogue. FK 33-824 (1 mg) was infused in healthy volunteers before and after pretreatment with 3 mg methysergide, a serotonin receptor blocker. All subjects showed a release of PRL after FK 33-824, which was significantly diminished after pretreatment with methysergide.

Adult↗

PubMed1991

Treatment of progressive supranuclear palsy with methysergide. A clinical study.

We present a clinical study of a patient aged 69 years with a clinical history of severe difficulty in walking and voluntary conjugate eye movement reduction in sideways glance and absence in vertical gaze. These symptoms led to diagnosis of Parkinson disease and treatment with L-Dopa + anticholinergics drugs. The treatment with antiparkinsonian drugs was suspended and no change in his clinical condition resulted. Methysergide therapy was initiated and the patient's response was monitored by video recording. On the basis of our experience and the data reported in the literature we believe that methysergide therapy affords some relief of symptoms in patients suffering from PSP.

Aged↗

PubMed1981

The effects of aspirin and methysergide, singly and in combination, on systemic haemodynamic responses to pulmonary embolism.

Pretreatment of anaesthetized rabbits with aspirin (A), 250 mg.kg-1, methysergide (M) 3 mg.kg-1 or a combination of both (A + M) was done before pulmonary embolism with a 1.0 ml autologous blood clot and compared with no pretreatment (C). Experiments were done until 10 survivors were present in each group. Mortality rate in controls (C) was 55 per cent (death in less than 30 minutes) compared to zero in (A) and (A + M) and nine per cent in (M). Arterial blood pressure fell to 60 per cent of pre-embolism values two minutes after embolism in (C) but had returned to 85 per cent of pre-embolism values after 60 minutes. This compares with a drop to 82 per cent at two minutes and 83 per cent at 60 minutes in (A), a drop to 70 per cent at two minutes and 90 per cent at 60 minutes in (M) and a very small drop to 92 per cent at two minutes which was unchanged at 60 minutes in (A + M). Right ventricular pressure increased by 75 per cent after two minutes compared to pre-embolism values in (C) and was still elevated by 37 per cent after 60 minutes. This compares with increases at two minutes and 60 minutes respectively of 58 and 23 per cent in (A), 65 and 35 per cent in (M) and 55 and 18 per cent in (A + M). Heart rate did not show any significant changes in any of the groups after embolism. These results show a dramatic reduction in mortality from pulmonary embolism with aspirin or methysergide pretreatment, which is associated with significant attenuation of the hypotensive response seen in controls. These agents may act by inhibiting the actions of a release of prostaglandins and serotonin. The additive effects of the combination used suggests that both mediators may play a role in the haemodynamic responses to pulmonary embolism.

Animals↗

PubMed1978

The effect of TRH on the release of TSH, PRL and GH in man under basal conditions and following methysergide.

Pretreatment with methysergide, a blocker of serotoninergic receptors, significantly reduced the TSH response to TRH in six male volunteers. The TRH-induced PRL release was also slightly decreased, while plasma GH levels were not significantly modified by TRH either during the control period or after methysergide. These results indicate that alterations of central nervous system monoaminergic pathways may modify the hypophysiotropic effects of TRH.

Adult↗

PubMed1981

Effects of methysergide and naloxone on analgesia induced by the peripheral electric stimulation in mice.

We investigated the antinociceptive effects produced by peripheral electric stimulation (PES) in mice and the influence of administration of L-5-hydroxytryptophan (5-HTP), methysergide and naloxone on the antinociceptive effect of the PES. Administration of 5-HTP enhanced antinociceptive effects induced by PES, while methysergide and naloxone abolished this antinociception. The mechanisms of analgesia produced by PES involve both endogenous opiate systems and central serotonergic mechanisms.

5-Hydroxytryptophan↗

PubMed1984

Antagonism of stimulation-produced antinociception by intrathecal administration of methysergide or phentolamine.

This study examined whether the antinociception produced by electrical stimulation of medullary raphe nuclei is mediated by activation of monoaminergic neurons projecting to the spinal cord. Ninety-four sites distributed about the midline of the medulla were stimulated and their ability to produce antinociception was determined using two different analgesiometric tests. Stimulation of sites in the nuclei raphe pallidus and raphe obscurus did not produce antinociception, but rather, produced tremor and, on occasion, extensor rigidity. In contrast, stimulation at sites located in the nucleus raphe magnus and the adjacent nucleus reticularis paragigantocellularis produced antinociception, as indicated by increased tail flick latencies and decreased responsiveness to noxious pinch applied to the extremities. Intrathecal administration of saline prior to electrical stimulation of these sites did not attenuate either the elevation of tail flick latencies or the decreased responsiveness to pinch. However, intrathecal administration of 30 micrograms of either methysergide or phentolamine prior to stimulation at these same sites significantly attenuated the increase in tail flick latency and restored responsiveness to pinch. Naloxone (1 mg/kg, s.c.) did not attenuate the stimulation-produced antinociception evoked from any of these sites. These data support the postulate that the antinociceptive effect of electrical stimulation of the nucleus raphe magnus and the nucleus reticularis paragigantocellularis is mediated by activation of serotonergic and noradrenergic neurons projecting to the spinal cord. The inability of either methysergide or phentolamine alone to completely antagonize the elevation of tail flick latency further suggests that the serotonergic and noradrenergic bulbospinal systems are coactivated by electrical stimulation of these sites.

Animals↗

PubMed1983

The effect of somatostatin on self-stimulation behavior in atropine- and methysergide-pretreated rats.

The effect of somatostatin on lateral hypothalamic self-stimulation was investigated in atropine- and methysergide-pretreated rats. Somatostatin markedly decreased the self-stimulation rate of the animals. Atropine in a dose which had no action on self-stimulation partly antagonized the effect of somatostatin. Methysergide potentiated the somatostatin-induced depression of self-stimulation behavior. These results suggest that the central cholinergic and serotoninergic systems may play a role in the somatostatin-induced inhibition of self-stimulation.

Animals↗

PubMed1983

Hyponeophagia in the Roman rat strains: effects of 5-methoxy-N,N-dimethyltryptamine, diazepam, methysergide and the stereoisomers of propranolol.

The effects of 5-MeODMT (2.5 mg/kg), diazepam (1 mg/kg), methysergide and the stereoisomers of propranolol (6 mg/kg) on hyponeophagia were studied in both sexes of the Roman strains of rats, selectively bred for acquisition of a two-way conditioned avoidance response. Diazepam, methysergide and 1-propranolol increased feeding in a novel environment whilst 5-MeODMT decreased it and d-propranolol was inactive. Several strain differences in drug responsiveness occurred, the Roman Low Avoidance subjects being most sensitive to all drugs tested as well as being most neophobic. A sex difference in 5-MeODMT sensitivity was also found, female rats of the Roman High and Control Avoidance strains being more sensitive than males. The findings are discussed in connection with differences in arousal and biochemical parameters between these strains.

Animals↗

PubMed1992

Inhibition of mesencephalic morphine analgesia by methysergide in the medial ventral medulla of rats.

The neural substrates of endogenous supraspinal opioid pain inhibition are mediated in part by connections between the midbrain periaqueductal gray (PAG) and the ventral-medial medulla, including the nucleus raphe magnus (NRM) and nucleus reticularis gigantocellularis (NRGC). To ascertain whether a serotonergic synapse participated in this pathway, the present study determined whether microinjections of methysergide into the NRM or NRGC would alter analgesia elicited by morphine microinjections into the PAG. Morphine (2.5 micrograms) in the PAG and immediately adjacent areas produced significant analgesia on the tail-flick and jump tests in rats. Pretreatment with the serotonin receptor antagonist methysergide (0.5-5 micrograms) in either the NRM or NRGC significantly reduced morphine analgesia elicited from the PAG by 69% on the tail-flick and by 50% on the jump tests without altering basal nociceptive thresholds. Medullary placements ventral or lateral to the NRM/NRGC failed to support this antagonistic effect. These data indicate that a ventro-medial medullary serotonergic synapse participates in the transmission of opioid pain-inhibitory signals from the PAG.

Animals↗

PubMed1989

Ventilatory response to sustained hypoxia: effect of methysergide and verapamil.

The biphasic nature of the ventilatory response to sustained (30 min) hypoxia may be explained by the central accumulation of a neurochemical with net inhibitory effect or, alternatively, peripheral chemoreceptor adaptation. To determine the role of serotonin (a putative central neuroinhibitor) and calcium ions (a putative peripheral neurotransmitter) in this response we measured VI and breathing pattern during 30 min of sustained isocapnic hypoxia in 11 normal adults 1 h after the double blind administration of either 2 mg methysergide (serotonin antagonist), 80 mg verapamil (calcium channel blocker), or placebo. Each subject was studied once a day for three days. After placebo the mean VI peaked at 12.5 +/- 3.4 L/min (176% of resting room air VI). VI then declined to a mean of 9.8 +/- 2.3 L/min (138% of room air VI) during 25 min of constant hypoxia. VI during hypoxia was always greater than VI during room air breathing (p less than 0.01), and peak VI during hypoxia was greater than final VI during hypoxia (p less than 0.05). The hypoxic response was not significantly affected by either pharmaceutical. At their maximal safe dosage in humans, methysergide and verapamil suggest no role for serotonin and calcium ions. Not excluded is the possibility that drug levels were inadequate to effect meaningful blockade.

Adult↗

PubMed1977

Self-stimulation of the subfornical organ and lateral hypothalamus: differential effects of atropine and methysergide.

The effects of cholinergic blockade of neurons by atropine or serotonergic blockade by methysergide was investigated in rats responding for brain-stimulation reward. Bipolar stimulating electrodes were placed either in the subfornical organ (SFO) or the lateral hypothalamus (LH). Atropine sulphate and methysergide significantly suppressed self-stimulation of the SFO but not of the LH, suggesting that cholinergic and serotonergic neurons are involved in brain-stimulation reward associated with this site.

Amphetamine↗

PubMed1984

The effects of dl-cathinone, d-amphetamine and cocaine on avoidance responding in rats and their interactions with haloperidol and methysergide.

The effects of dl-cathinone (dl-CAT), d-amphetamine (d-A), and cocaine (COC) on conditioned shock avoidance responding and their interactions with haloperidol and methysergide on this behavior were studied in male Wistar rats. All three stimulants produced significant increases in intertrial interval (ITI) responding and in the number of avoidance responses and a decrease in avoidance latencies. These actions were antagonized by pretreatment with haloperidol (0.07 and 0.15 mg/kg, IP). Pretreatment with methysergide (1.0 and 2.0 mg/kg, IP) increased the effects of all three stimulants on ITI responding, but not on the other two parameters. These results suggest that the effects of these stimulants on avoidance responding may be mediated by dopaminergic systems. In addition, these stimulant-induced changes on ITI responding probably also involve actions on serotonergic systems.

Alkaloids↗

PubMed1993

MDL 72222, ketanserin, and methysergide pretreatments fail to alter breaking points on a progressive ratio schedule reinforced by intravenous cocaine.

The effects of three serotonin [5-hydroxytryptamine (5-HT)] receptor antagonists on cocaine self-administration behavior were investigated. Specifically, the effects of MDL 72222 (a specific 5-HT3 receptor antagonist), ketanserin (a specific 5HT2 receptor antagonist), and methysergide (an aselective 5-HT1/5-HT2 receptor antagonist) on the breaking points reached by rats on a progressive ratio schedule for cocaine reinforcement were examined. Pretreatments with MDL 72222 (7.5-1,920 micrograms/kg, SC), ketanserin (0.4-6.4 mg/kg, IP), and methysergide (2.5-20 mg/kg, IP) failed to alter breaking points from baseline values. Although tested at twice the highest doses previously reported to have significant behavioral effects, the three 5-HT receptor antagonists were without effect. These data suggest that relatively specific blockade of 5-HT receptor subtypes does not influence the reinforcing effects of cocaine.

Animals↗

PubMed1984

Antagonism of 5-hydroxytryptamine-evoked excitation in the superficial dorsal horn of the cat spinal cord by methysergide.

Ionophoretically applied methysergide was tested on 9 units excited by 5-hydroxytryptamine (5-HT) recorded in the superficial dorsal horn of cat spinal cord. In all cases, methysergide produced a prolonged and repeatable antagonism of the excitatory action of 5-HT, but it had no effect on glutamate-evoked activity or on that caused by adequate stimulation of the receptive field. This result supports the proposal that excitation by 5-HT is a direct synaptic effect, and not a 'non-specific' action.

Animals↗