Flunarizine‐ and cinnarizine‐induced extrapyramidal reactions

Micheli, Federico; Pardal, Manuel Fernández; Gatto, M. Lo; Torres, Marta E; Paradiso, Guillermo; Parera, Ignacio Casas; Giannaula, Rolando

doi:10.1212/wnl.37.5.881

Cited by 96 publications

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“…Drug -induced parkinsonism (DIP) is the most common cause of symptomatic parkinsonism (PK) [1][2][3] . It can be caused by any drug that inhibits dopamine metabolism [1][2][3] .…”

mentioning

confidence: 99%

“…It can be caused by any drug that inhibits dopamine metabolism [1][2][3] . Neuroleptic drugs are the best-recognized offending agents 2 .…”

mentioning

confidence: 99%

“…It can be caused by any drug that inhibits dopamine metabolism [1][2][3] . Neuroleptic drugs are the best-recognized offending agents 2 . Cinnarizine (CZ) and flunarizine (FZ) represent one of the most common causes of DIP in many countries where they are prescribed [1][2][3][4][5][6] .…”

mentioning

confidence: 99%

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Parkinsonism and other movement disorders in outpatients in chronic use of cinnarizine and flunarizine

Fabiani¹,

Pastro

Froehner

2004

Arq. Neuro-Psiquiatr.

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-The purpose of this study is to determine the prevalence and the patterns of movement disorders (MD) in outpatients submitted to the chronic use of cinnarizine (cz) or flunarizine (fz), and to establish the main risk factors for MD development. Over a period of 3 months, data were collected from outpatients who were chronic users of cz or fz in a municipal health institute. A total of 26 outpatients were included and all of them were submitted to a protocol that included DSM-4 diagnosis criteria for druginduced movement disorders, parkinsonism (PK) and depression. Parkinsonism was diagnosed in 34% of the patients, PK plus akathisia, PK plus akathisia and bucco-linguo-masticatory syndrome (BLMS), isolated BLMS and dystonia were found in 4% patients each. Patients with BLMS had the highest median age and the longest average period in which they used the drugs. The affected group, when compared to the nonaffected one, presented with higher rates of depression. This study demonstrates the existence of a direct relationship between the time of use of cz and fz, the age and the prevalence of PK and other MD. It also suggests that these drugs increase the incidence of depression.KEY WORDS: parkinsonism, drug-induced movement disorders, cinnarizine, flunarizine.Parkinsonismo e outros distúrbios do movimento em pacientes ambulatoriais sob uso crônico de cinarizina ou flunarizina RESUMO -O objetivo deste estudo foi determinar a prevalência e os padrões de distúrbios do movimento (DM) em pacientes ambulatoriais sob uso crônico de cinarizina (cz) ou flunarizina (fz), além de estabelecer os principais fatores de risco para o seu aparecimento. Durante três meses foram coletados dados de pacientes ambulatoriais em uso de cz ou fz. Todos esses pacientes foram submetidos a protocolo pré-estabelecido que incluía critérios diagnósticos do DSM-IV para distúrbios do movimento induzido por drogas e critérios para diagnostico de depressão maior. Parkinsonismo (PK) puro foi diagnosticado em 34% dos pacientes, PK com acatisia, PK com acatisia e síndrome mastigatória bucolingual (SMBL), SMBL isoladamente e distonia, foram encontrados em 4% dos pacientes. Os pacientes com SMBL apresentavam a média de idade mais avançada, o maior tempo médio de uso das drogas, configurando-se o grupo de maior risco ao aparecimento dos DM. O grupo dos pacientes com DM apresentou maior incidência de depressão quando comparados com os não afetados. O estudo demonstra uma relação direta entre o tempo de uso da droga, a idade avançada do paciente e o surgimento dos DM. Os resultados também sugerem que estas drogas aumentam a incidência de depressão. PALAVRAS-CHAVE: parkinsonismo, distúrbios do movimento induzido por drogas, cinarizina, flunarizina.

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“…Drug -induced parkinsonism (DIP) is the most common cause of symptomatic parkinsonism (PK) [1][2][3] . It can be caused by any drug that inhibits dopamine metabolism [1][2][3] .…”

mentioning

confidence: 99%

“…It can be caused by any drug that inhibits dopamine metabolism [1][2][3] . Neuroleptic drugs are the best-recognized offending agents 2 .…”

mentioning

confidence: 99%

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Parkinsonism and other movement disorders in outpatients in chronic use of cinnarizine and flunarizine

Fabiani¹,

Pastro

Froehner

2004

Arq. Neuro-Psiquiatr.

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“…Diğer taraftan, kalsiyumun dopaminerjik hücre ölümüne neden olduğu ve bunun da parkinsonizme neden olabileceği bildirilmiştir (33). Substantia nigra'daki nöronların diğer nöronlardan farklı olduğu ve otonom elektrik aktivite sağlayabildikleri, bu nedenle yüksek kalsiyum iyon girişine maruz kaldıkları ve bu bölgenin kalsiyum homeostazındaki bozukluklara hassas olduğu bilinmektedir (40). Bezerra 1993'de FCIP görülen 47 hastayı incelemiş ve sonuç olarak FCIP'ın diğer ilaçlarla indüklenen parkinsonizmlerden farklı olarak daha ileri yaşlarda ortaya çıktığını; ilacın alımı ve parkinsonizm belirtilerinin ortaya çıkışı arasında belirli bir sürenin bulunduğu-nu; durumun daha geç iyileştiğini; istirahat halinde veya postural tremorlarla kendini gösterdiğini; bu duruma büyük oranda depresyonun da eşlik ettiğini ve antikolinerjikler veya levodopa ile tedavi edilemediğini bildirmiştir.…”

Section: Kalsiyum Kanal Blokörleriunclassified

Ters ilaç reaksiyonu olarak ilaçlarla indüklenen parkinsonizm

Erkekoğlu¹

2011

mpj

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G RBugün toplumun yakla k % 0,1'inde görülen Parkinson hastal ilk defa 1817'de James Parkinson taraf ndan bildirilmi ve "titremeli felç" olarak tan mlam t r. Genellikle orta ya la beraber görülen dopaminerjik nöronlar n harabiyetinden kaynaklanan bir progresif nörodejeneratif hastal kt r. Parkinson hastal üst beyin sap böl-gesinde yer alan "substantia nigra" hücrelerinin azalmas ndan ileri gelir. Bu hücreler "dopamin" salg lar, depolar ve dopamin nörotransmitter olarak ön beyindeki "striatum" denilen bölgede sinir hücreleriyle kurulan ba lant da kullan l r. Substantia nigra hücreleri hasara u rarsa dopamin yap p depolayamazlar ve sonuç olarak striatumda dopamin eksilir. Bu hücre hasar % 80 gibi ciddi boyutta oldu unda Parkinson hastal belirtileri ortaya ç kmaya ba lar (1).Hastal kta görülen temel bozukluk tremor, kaslarda rijidite ve hareketlerin yava lamas d r. Titreme ilk olarak tek elde görülür, zamanla ayn taraftaki baca a ve kar ele geçebilir. S kl kla hastal ktan vücudun bir yar s bask n olarak etkilenir. Mimik ve jestler silinir, donuk, anlams z çehre (maske yüzü) vard r. Hasta harekete ba lamakta güçlük çeker, cildi ya lan r ve hastalar n %40' nda bunama görülür. Birincil ya da idiyopatik, ikincil ya da semptomatik parkinsonizm, Parkinson+sendromlar ve kal tsal-dejeneratif hastal klarla birliktelik gösteren grup olmak üze-re dört s n fta ele al nmaktad r. E er Parkinson hastal spontan geli iyorsa "idiyopatik Parkinson hastal ", sebebin belli oldu u durumlarda ise "ikincil (semptomatik) parkinsonizm" veya "Parkinsonien sendromlar" olarak adland r lmaktad r (2).Parkinsonizmin çok say da nedeni vard r: genetik, geçirilmi beyin enfeksiyonlar (örne in, viral ansefalit), ateroskleroz, travma, zehirlenmeler, tümörler, çe itli toksik maddelere temas (örne-in, 1-metil-4-fenil-1,2,3,6-tetrahidropiridin [MPTP], eroin) ve baz ilaçlar n kullan m (3).Bu derleme kapsam nda "ikincil (semptomatik) parkinsonizm"e neden olan ilaçlardan bahsedilecektir. Parkinson hastal n indükleyen ilaçlar

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“…Their therapeutic effectiveness re lies on their abiliy to block calcium entry through voltage sensitive calcium channels. Recently, side effects such as extrapyramidal symptoms and depression have been observed in patients, especially in elderly patients, treat ed with calcium antagonists such as flunarizine and cinnarizine (1,2). Neuroleptics such as chlorpromazine are known to elicit extrapyram idal side effects by blocking postsynaptic dopa mine D2 receptors in the striatum (3,4).…”

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confidence: 99%

Neurochemical Investigation on the Effects of a New Diphenylpiperazine Calcium Antagonist, KB-2796, on the Central Dopaminergic System of Rats.

Akira¹,

Ozaki²,

Hara³

et al. 1992

Jpn.J.Pharmacol

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-The effects of KB-2796, a new diphenylpiperazine calcium antagonist, on the striatal dopaminergic system of rats were investigated in comparison with var ious calcium antagonists and the dopamine antagonist chlorpromazine. The inhibiting effect of KB-2796 on [3H]spiperone binding to striatal membranes in vitro was weaker than those of chlorpromazine and the other diphenylpiperazine analogues, flunarizine and cinnarizine, and more potent than those of verapamil and nicardipine. Diltiazem and nifedipine were inactive. KB-2796 (30, 100 mg/kg, p.o.) had no effect on Kd and Bmax values of in vitro [3H]spiperone specific binding to striatal membranes obtained from the rat at 36 hr and 7 days after repeated administration for 18 days, whereas flu narizine (30 mg/kg, p.o.) and chlorpromazine (3 mg/kg, p.o.) increased Bmax values by 47% and 31%, respectively, at 36 hr, but not at 7 days after the final administra tion. At 1 hr after the single administration, KB-2796 (30, 100 mg/kg, p.o.) had no effect on the content of dopamine and its metabolites in the striatum, whereas flunar izine (30 mg/kg, p.o.) and chlorpromazine (3 mg/kg, p.o.) increased the level of homovanillic acid. These results indicate that flunarizine may affect dopaminergic neurotransmission by partially blocking dopamine D2 receptors, while KB-2796 has negligible in vivo effect on the dopaminergic system.

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Flunarizine‐ and cinnarizine‐induced extrapyramidal reactions

Cited by 96 publications

References 0 publications

Parkinsonism and other movement disorders in outpatients in chronic use of cinnarizine and flunarizine

Parkinsonism and other movement disorders in outpatients in chronic use of cinnarizine and flunarizine

Ters ilaç reaksiyonu olarak ilaçlarla indüklenen parkinsonizm

Neurochemical Investigation on the Effects of a New Diphenylpiperazine Calcium Antagonist, KB-2796, on the Central Dopaminergic System of Rats.

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