Nimodipine versus Flunarizine in Common Migraine: A Controlled Pilot Trial

Bussone, Gennaro; Baldini, S.; D’Andrea, Giovanni; Cananzi, A.R.; Frediani, Fabio; Caresia, L.; Milone, Francesco; Boiardi, A.

doi:10.1111/j.1526-4610.1987.hed2702076.x

Cited by 23 publications

(6 citation statements)

References 7 publications

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“…In general, benefit was observed within 1-2 months after beginning of treatment (141,(145)(146)(147)(148)(149). Another randomized, controlled study of 24-weeks' duration did not report substantial benefit of nimodipine 120 mg daily in patients with common or classic migraine (142,150).…”

Section: Migrainementioning

confidence: 93%

Nimodipine and Its Use in Cerebrovascular Disease: Evidence from Recent Preclinical and Controlled Clinical Studies

Tomassoni

Lanari

Silvestrelli

et al. 2008

Clinical and Experimental Hypertension

122

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Nimodipine is a 1,4-dihydropyridine-derivative Ca(2+)-channel blocker developed approximately 30 years ago. It is highly lipophilic, crosses the blood-brain barrier, and reaches brain and cerebrospinal fluid. Early treatment with nimodipine reduces the severity of neurological deficits resulting from vasospasm in subarachnoid haemorrhage (SAH) patients. In SAH, nimodipine reduced spasm-related deficits of all severities, but no spasm-unrelated deficits. This paper has reviewed preclinical studies on the influence of nimodipine in various animal models of cerebral ischemia, with particular attention toward investigations published in the last 10 years. These studies further support the main indication of nimodipine, by clarifying some mechanisms of the anti-ischemic activity of the compound. Papers reporting a possible role of nimodipine in epileptogenesis were also examined. Clinical studies on nimodipine were grouped into subarachnoid hemorrhage, acute ischemic stroke, cerebral ischemia without stroke, dementia disorders, and migraine. Clinical investigations have shown that the drug improves neurological outcome by reducing the incidence and severity of ischemic deficits in patients with SAH from ruptured intracranial berry aneurysms regardless of their post-ictus neurological condition. No relevant effects of treatment with nimodipine were reported for acute ischemic stroke, cerebral ischemia without stroke, and migraine, except than for cluster headache. The less pronounced cardiovascular effects of nimodipine compared to other dihydropyridine-type Ca(2+)-channel blockers probably accounts for its use out of label for treating patients affected by chronic cerebral ischemia and vascular cognitive impairment. However, the blood pressure-lowering effects of nimodipine should not be minimized, as clinical studies have documented lowering blood pressure in small groups of patients, including cases of withdrawn due to pronounced hypotension induced by nimodipine administration. In the area of vascular cognitive impairment, short-term benefits of nimodipine do not justify its use as a long-term anti-dementia drug, and benefits obtained in elderly patients affected by subcortical vascular dementia require to be confirmed by other groups and in larger scale trials. In conclusion, nimodipine is a safe drug with an important place in pharmacotherapy and with the main documentation for reduction in the severity of neurological deficits resulting from vasospasm in SAH patients.

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Section: Migrainementioning

confidence: 93%

Nimodipine and Its Use in Cerebrovascular Disease: Evidence from Recent Preclinical and Controlled Clinical Studies

Tomassoni

Lanari

Silvestrelli

et al. 2008

Clinical and Experimental Hypertension

122

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“…Numerous controlled clinical studies have established that flunarizine is efficacious in migraine prophylaxis, including double-blind studies in which the drug was compared with placebo 18 and the anti-migraine drugs pizotifen, 19 ß-blockers 20 and nimodipine. 21 Our group conducted the latter study, a multicentre double-blind trial with parallel groups in which flunarizine at 10 mg/day was compared with nimodipine at 120 mg/day; the study conclusion was that flunarizine was efficacious in migraine prophylaxis. The studies cited above all used flunarize at 10 mg/day.…”

Section: Effectiveness and Safety Of Flunarizine In Migraine Therapymentioning

confidence: 99%

Flunarizine in Migraine: A Minireview

et al. 1991

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Flunarizine is a non-selective calcium antagonist. It distributes preferentially in the adipose tissue and passes the blood brain barrier. Numerous controlled clinical studies have established that flunarizine is efficacious in migraine prophylaxis, including double-blind studies in which the drug was compared with placebo or other antimigraine drugs. To avoid side effects a special schedule or administration is necessary. Flunarizine has no myogenic effect on smooth muscle cells of the vessles. It is said to be the only calcium antagonist able to protect brain cells against hypoxic damage. In addition, the considerable body of information which shows flunarizine capable of directly influencing the central nervous system, suggests that the drug's anti-migraine action may depend on its ability to influence central phenomena.

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“…The most effective CCH prophylactic today is lithium carbonate 2 but long-term use of this drug is limited by the likelihood of side effects. 3 Recently, calcium antagonists have been successfully employed to prevent migraine 4,5,6,7,8,9 and preliminary studies also indicate that verapamil in particular is an efficacious treatment for CCH 6 ; such studies in CCH have been of the open type, however, and there is a clear requirement for a double blind trial to verify or refute these initial findings. With this aim we conducted a multicentre double-blind trial comparing verapamil with the established efficacy of lithium carbonate.…”

Section: Introductionmentioning

confidence: 99%

Double Blind Comparison of Lithium and Verapamil in Cluster Headache Prophylaxis

Bussone¹,

Leone²,

Peccarisi³

et al. 1990

Headache

Self Cite

214

148

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Chronic Cluster Headache (CCH) treatment is troublesome; since there are no pain-free periods, it must be continuous. The most effective CCH prophylactic drug today is lithium carbonate but long-term use of this drug is limited by the possibility of side effects. Recently, calcium antagonists have been successfully employed to prevent migraine, and preliminary studies also indicate that verapamil in particular is an efficacious treatment for CCH. We have conducted a multicenter trial employing a double-dummy, double blind, cross-over protocol, comparing verapamil with the established efficacy of lithium carbonate, in preventing CCH attacks. Both lithium carbonate and verapamil were effective in preventing CCH but verapamil caused fewer side effects and had a shorter latency period. We did not observe any correlation between plasma levels of the two drugs and their clinical efficacy. Both the drugs tested here may exert their effect by restoring a normal inhibitory tone to the pain modulating pathways from the trigemino-vascular system, a circuit putatively implicated in CCH.

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Nimodipine versus Flunarizine in Common Migraine: A Controlled Pilot Trial

Cited by 23 publications

References 7 publications

Nimodipine and Its Use in Cerebrovascular Disease: Evidence from Recent Preclinical and Controlled Clinical Studies

Nimodipine and Its Use in Cerebrovascular Disease: Evidence from Recent Preclinical and Controlled Clinical Studies

Flunarizine in Migraine: A Minireview

Double Blind Comparison of Lithium and Verapamil in Cluster Headache Prophylaxis

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