, Volume 47, Issue 6, pp 1010–1032 | Cite as


A Review of its Pharmacology and Therapeutic Potential in the Management of Alcohol Dependence Syndrome
  • David H. Peters
  • Diana Faulds
Drug Evaluation



Tiapride, an atypical neuroleptic agent, is a selective dopamine D2-receptor antagonist with little propensity for causing catalepsy and sedation. It shows preferential activity at receptors previously sensitised to dopamine and those located extrastriatally. Tiapride demonstrates anti-dyskinetic activity reflecting antidopaminergic actions, and also anxiolytic activity mediated by mechanisms that are poorly understood. Unlike the benzodiazepines, tiapride does not affect vigilance and has a low potential for interaction with alcohol (ethanol), and possibly for abuse.

Tiapride facilitates management of alcohol withdrawal, but its use inpatients at risk of severe reactions in acute withdrawal should be accompanied by adjunct therapy for hallucinosis and seizures. Since it may prove difficult to identify such patients and there is also a small risk of neuroleptic malignant syndrome (particularly with parenteral administration), the usefulness of tiapride in this setting is likely to be limited. Nevertheless, relativ e freedom from the complications associated with benzodiazepine therapy suggest a possible role for the drug in the treatment of individuals suitable for alcohol detoxification as outpatients.

Preliminary clinical studies in alcoholic patients following detoxification have shown that tiapride ameliorates psychological distress, improves abstinence, and reduces drinking behaviour, and in the short term facilitate s reintegration within society. These benefits were associated with reduced consumption of health care resources. However, the potential risk of tardive dyskinesia at the dosage employed (300 mg/day) requires evaluation and necessitates medical supervision.

Thus, with its lack of adverse effects on vigilance and low propensity for interaction with alcohol and possibly for abuse, tiapride will probably find particular use in the management of alcoholic patients suitable for detoxification in an outpatient setting; and, if initial findings are confirmed in large well-designed trials, in the short term (<6 months) therapy of reformed alcoholic patients under medical supervision.

Pharmacodynamic Properties

Tiapride, an atypical neuroleptic agent, is a selective adenylate cyclase-independent dopamine D2-receptor antagonist which lacks affinity for dopamine D1-receptors. It possesses only weak sedative and cataleptic effects and is particularly active at receptors previously sensitised to dopamine; this latter property is considered responsible for its antidyskinetic effects. In vivo, tiapride binds preferentially to extrastriatal dopamine receptors in the rat brain, particularly in the hippocampus. Antagonism of dopamine activity by tiapride is generally weak in normal animals, but is often much greater under conditions where the dopaminergic system is altered by pharmacological manipulation or selective tissue destruction.

The anxiolytic activity of tiapride has been demonstrated in several animal models, including those involving alcohol (ethanol) withdrawal. The mechanism(s) responsible for the anxiolytic properties of tiapride have not been fully elucidated, but it is distinct from the antidopaminergic activity of the drug.

Tiapride does not appear to cause physical or psychological dependence. It does not possess antiepileptic properties, but conversely does not lower the epileptogenic threshold. In common with other dopaminergic antagonists, tiapride causes hyperprolactinaemia, although the effects of prolonged tiapride administration on circulating prolactin levels have not been assessed.

Pharmacokinetic Properties

The pharmacokinetic profile of tiapride requires further definition, particularly in terms of pharmacodynamic-pharmacokinetic relationships. Indeed, the maximum dosage recommended by the manufacturer for the treatment of delirium during acute alcohol withdrawal (1800 mg/day) exceeds those assessed in pharmacokinetic studies by at least 5- to 6-fold.

Bioavailability of tiapride is about 75% following oral or intramuscular administration. Peak plasma tiapride concentrations are achieved within about 0.4 to 1.5 hours when given by either route, and steady-state occurs 24 to 48 hours after initiating 3 times daily administration. The drug is rapidly distributed and does not bind appreciably to plasma proteins. Tiapride is mainly eliminated by renal excretion, principally in the unchanged form. The elimination half-life is approximately 3 to 4 hours, and may increase with age and declining renal function.

Therapeutic Potential in Alcohol Dependence Syndrome

Tiapride has demonstrated clinical efficacy in patients undergoing acute alcohol withdrawal, although there are methodological deficiencies in most trials which limit their interpretation. The drug appeared to prevent development of delirium, but no conclusions could be drawn regarding its effects on hallucinosis and it is ineffective against seizures. Tiapride resolved or reduced gastrointestinal and psychological distress, most autonomic manifestations, and sleep disturbances without adversely affecting vigilance. In comparative clinical trials, the overall efficacy of tiapride was superior to that of placebo, and approached, or was comparable to that of benzodiazepines or chlormethiazole.

Tiapride has also demonstrated efficacy in preliminary investigations which assessed alcoholic patients during rehabilitation (up to 6 months following detoxification). It improved abstinence, drinking behaviour, self-esteem, psychological distress and social complications, which was reflected in reduced consumption of health care resources among patients with symptoms of depression or anxiety. No interaction between tiapride and alcohol was evident among those who resumed drinking. Furthermore, although dependence liability was not specifically assessed, there was no indication of drug abuse (in accordance with the results of animal studies).


Tiapride was generally well tolerated in clinical trials. The most frequently reported adverse events (>1%) were drowsiness, extrapyramidal syndromes, dizziness and orthostatic hypotension. Compared with the overall population that have received tiapride, alcoholic patients undergoing therapy with this drug appear less likely to experience drowsiness or extrapyramidal syndromes, but appear more prone to orthostatic hypotension (particularly those treated parenterally). Serious adverse events are reported to occur rarely (1.7 per 100 000 treatment months). There have been only 4 reports of tardive dyskinesia, and these were in elderly patients undergoing ‘long term’ therapy. For patients undergoing acute alcohol withdrawal with tiapride the most worrisome serious event appears to be malignant neuroleptic syndrome (25 case reports); it is difficult to differentiate between this and delirium. In comparative clinical trials, the tolerability of tiapride was similar to that of other established therapies for acute alcohol withdrawal, although sedation was less marked compared with diazepam. The tolerability of tiapride 300 mg/day for up to 6 months was comparable to that of placebo during rehabilitation after alcohol withdrawal.

Dosage and Administration

For the treatment of delirium or pre-delirium during alcohol withdrawal, intravenous or intramuscular tiapride 400 to 1200 mg/day given 4- to 6-hourly is recommended, increased to 1800 mg/day if required. No other dosage recommendations are available for the facilitation of alcohol withdrawal. However, recommended dosages for the treatment of agitation and aggressiveness are 200 to 300 mg/day for 1 to 2 months, or longer with medical supervision. Higher dosages are recommended for the treatment of abnormal movements (300 to 800 mg/day) and may be necessary for alleviation of tremor during alcohol withdrawal. Tiapride 300 mg/day has proved beneficial in the treatment of patients following alcohol detoxification. The dosage should be reduced in patients with renal insufficiency.


Alcohol Dependence Tardive Dyskinesia Neuroleptic Malignant Syndrome Alcohol Withdrawal Alcoholic Patient 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. Agricola R, Mazzarino M, Urani R. Treatment of acute alcohol withdrawal syndrome with carbamazepine: a double-blind comparison with tiapride. Journal of International Medical Research 10: 160–165, 1982PubMedGoogle Scholar
  2. Albertini F. Mémorisation et céphalées. Semaine des Höpitaux de Paris 54: 1257–1259, 1978PubMedGoogle Scholar
  3. Barry JM, Costall B, Kelly ME, Naylor RJ. Withdrawal syndrome following subchronic treatment with anxiolytic agents. Pharmacology Biochemistry Behavior 27: 239–245, 1987CrossRefGoogle Scholar
  4. Bischoff S, Bittiger H, Delini-Stula A, Ortmann R. Septo-hippocampal system: target for substituted benzamides? European Journal of Pharmacology 79: 225–232, 1982PubMedCrossRefGoogle Scholar
  5. Bondarenko NA, Gorantcheva J, Tyutyulkova N, Nokolova M, Valdman AV. Effects of some benzamide derivatives on stress-induced behavior and striatum dopamine receptors. Methods and Findings in Experimental and Clinical Pharmacology 10: 629–633, 1988PubMedGoogle Scholar
  6. Bourasset G. Le tiapride dans le sevrage des maladies alcooliques. Semaine des Hôpitaux de Paris 57: 1936–1937, 1981PubMedGoogle Scholar
  7. Bruno F. Buspirone in the treatment of alcoholic patients. Psychopathol-ogy 22: 49–59, 1989CrossRefGoogle Scholar
  8. Cheymol G, Mouillé P. Étude des effets anti-arythmisants de dérivés du métoclopramide. Archives Internationales de Pharmacodynamic et de Therapie 215: 150–159, 1975Google Scholar
  9. Chivers JK, Gommeren W, Jenner P, Leysen J, Marsden CD, et al. Comparison of in vivo and in vitro actions of tiapride in rodents. Abstract. British Journal of Pharmacology 79 (Suppl.): 398P, 1983Google Scholar
  10. Chivers JK, Gommeren W, Leysen JE, Jenner P, Marsden CD. Comparison of the in-vitro receptor selectivity of substituted benzamide drugs for brain neurotransmitter receptors. Journal of Pharmacy and Pharmacology 40: 415–421, 1988PubMedCrossRefGoogle Scholar
  11. Costall B, Kelly ME, Naylor RJ. The anxiolytic and anxiogenic actions of ethanol in a mouse model. Journal of Pharmacy and Pharmacology 40: 197–202, 1987CrossRefGoogle Scholar
  12. Costall B, Kelly ME, Naylor RJ. The production of assymetry and circling behaviour following unilateral, intrastriatal administration of neuroleptic agents: a comparison of abilities to antagonise striatal function. European Journal of Pharmacology 96: 79–86, 1983PubMedCrossRefGoogle Scholar
  13. Costall B, Kelly ME, Naylor RJ. Unilateral striatal dopamine denervation: reduced motor inhibitory effects of dopamine antagonists revealed in models of asymmetric and circling behaviour. Naunyn-Schmiedebergs Archives of Pharmacology 326: 29–35, 1984CrossRefGoogle Scholar
  14. Costall B, Naylor RJ. Assessment of the test procedures used to analyse neuroleptic action. Review of Pure and Applied Pharmacological Sciences 1: 3, 1980Google Scholar
  15. Costall B, Naylor RJ. Experimental studies of dopamine function in movement disorders. Neurotransmitter systems and their clinical disorders, Academic Press, London, 1977Google Scholar
  16. Costall B, Naylor RJ, Nohria V. Use of the mouse circling model to demonstrate enhanced striatal actions for oxiperomide and tiapride following denervation. British Journal of Pharmacology 66: 121P, 1979Google Scholar
  17. Costall B, Naylor RJ, Owen RT. Gabaminergic and serotonergic modulation of the antidyskinetic effects of tiapride and oxiperomide in the model using 2-(N,N-dipropyl)amino-5,6-dihydroxytetralin. European Journal of Pharmacology 49: 407–413, 1978PubMedCrossRefGoogle Scholar
  18. Costall B, Naylor RJ, Owen RT. Investigations into the nature of the peri-oral movements induced by 2-(N,N-dipropyl)amino-5,6-dihydroxytetralin. European Journal of Pharmacology 45: 357–367, 1977PubMedCrossRefGoogle Scholar
  19. Crisp AH, Ralph PC, McGuiness B, Harris G. Psychoneurotic profiles in the adult population. British Journal of Medical Psychology 51: 293–301, 1978PubMedCrossRefGoogle Scholar
  20. Crown S, Crisp AH. Crown-Crisp Experiential Index. Hodder & Stoughton, 1979Google Scholar
  21. Csernansky JG, Csernansky CA, Hollister LE. 3[H]-Sulpiride labels mesolimbic non-dopaminergic sites that bind antidepressant drugs. Ex-perientia 41: 1419–1421, 1985Google Scholar
  22. Dainelli C, Sivini G. Tiapride ed alcoolismo: valutazione dell’efficacia terapéutica in 80 casi di alcoolopatia. Clinica Terapéutica 103: 161–171, 1982PubMedGoogle Scholar
  23. DeFigueiredo R. Action du tiapride dans les manifestations aigues du sevrage alcoolique. Semaine des Hôpitaux de Paris 59: 2551–2554, 1983Google Scholar
  24. Delamaire D, Carpentier MC, Eudier F, Derouet J, Bourel M. Essai ambulatoire du tiapridal après sevrage alcoholique hospitalier. Etude randomisée de cinquante et une hépatopathies alcooliques en double insu. Semaine des Hôpitaux de Paris 62: 3109–3114, 1986Google Scholar
  25. Elliott PNC, Jenner P, Huizing G, Marsden CD, Miller R. Substituted benzamides as cerebral dopamine antagonists in rodents. Neuropharmacology 16: 333–342, 1977PubMedCrossRefGoogle Scholar
  26. Evens M. Tiapridal et sevrage éthylique. Acta Psychiatrica Bélgica 80: 149–155, 1980PubMedGoogle Scholar
  27. Fontaine J, Reuse JJ. Etude comparative de l’action de quelques benzamides substitués sur l’iléon isolé de cobaye. Archives Internationales de Pharmacodynamie et de Therapie 213: 322–327, 1975PubMedGoogle Scholar
  28. Fontaine J, Reuse JJ. Pharmacological analysis of the effects of substituted benzamides on the isolated guinea-pig ileum. Study of metoclopramide, sulpiride, bromopride, tiapride, and sultopride. Archives Internationales de Pharmacodynamie et de Therapie 235: 51–61, 1978Google Scholar
  29. Fontaine J, Reuse JJ. The effects of substituted benzamides on frog rectus abdominis. European Journal of Pharmacology 68: 55–60, 1980PubMedCrossRefGoogle Scholar
  30. Foy A. Management of alcoholism. Medical Journal of Australia 144: 689–693, 1986aPubMedGoogle Scholar
  31. Foy A. The management of alcohol withdrawal. Medical Journal of Australia 145: 24–27, 1986bPubMedGoogle Scholar
  32. Fuller RK, Branchey L, Brightwell DR, Derman RM, Emrick CD, et al. Disulfiram treatment of alcoholism: a Veterans Administration Cooperative study. Journal of the American Medical Association 256: 1449–1455, 1986PubMedCrossRefGoogle Scholar
  33. Gennari C, Nami R, Pizzuti M, D’Ascenzo G, Bianchini C. Effets du tiapride sur le taux plasmatique de béta-endorphine, prolactine et dopamine chez des patients souffrant d’algies cancéreuses. Semaine des Hôpitaux de Paris 57: 795–800, 1981PubMedGoogle Scholar
  34. Ginsberg F, Bourguignon RP, Smets Ph, Famaey JP. Tiapride versus glafenine: a double-blind comparative study in the management of rheumatic pain. Current Medical Research Opinion 8: 562–569, 1983CrossRefGoogle Scholar
  35. Goreliek DA. Serotonin uptake blockers and the treatment of alcoholism. In Galanter M (Ed.) Recent developments in alcoholism, Vol. 7, pp. 267–281, Plenum Press, New York, 1989Google Scholar
  36. Gross MM, Lewis E, Hastey J. Acute alcohol withdrawal syndrome. In Kissin B, Begleiter H (Eds) The biology of alcoholism, Vol. 3, pp. 191–263, Plenum Press, New York, 1974Google Scholar
  37. Gross MM, Lewis E, Nagarajan M. An improved quantitative system for assessing the acute alcoholic psychoses and related states (TSA and SSA). In Gross MM (Ed.) Alcohol intoxication and withdrawal: experimental studies, advances in experimental medicine and biology, Vol. 35, pp. 365–376, Plenum Press, New York, 1973Google Scholar
  38. Harro J, Vasar E, Bradwejn J. CCK in animal and human research on anxiety. Trends in Pharmacological Sciences 41: 244–249, 1993CrossRefGoogle Scholar
  39. Horton RW, Lowther S, Chivers J, Jenner P, Marsden CD, et al. The interaction of substituted benzamides with brain benzodiazepine binding sites in vitro. British Journal of Pharmacology 94: 1234–1240, 1988PubMedCrossRefGoogle Scholar
  40. Irwin M, Baird S, Smith TL, Schuckit M. Use of laboratory tests to monitor heavy drinking by alcoholic men discharged from a treatment program. American Journal of Psychiatry 145: 595–599, 1988PubMedGoogle Scholar
  41. Jenner P, Theodorou A, Marsden CD. Specific receptors for substituted benzamide drugs in brain. In Rotrosen & Stanley (Eds) The benzamides: pharmacology, neurobiology, and clinical aspects, advances in biochemical psychopharmacology, Vol. 35, pp. 109–141, Raven Press, New York, 1982Google Scholar
  42. Joshi R, Sivaganesanathan A. Tiapride versus metoclopramide: comparison after minor gynaecological surgery. European Journal of An-aesthesiology 10: 109–112, 1983Google Scholar
  43. Kebabian JW, Calne DB. Multiple receptors for dopamine. Nature 277: 93–96, 1979PubMedCrossRefGoogle Scholar
  44. Köhler C, Hall H, Magnusson O, Lewander T, Gustafsson K. Biochemical pharmacology of the atypical neuroleptic remoxipride. Acta Psychiatrica Scandinavica 82(Suppl. 358): 27–36, 1990CrossRefGoogle Scholar
  45. Kristensen CB, Rasmussen S, Dahl A, Lauritsen B, Lund K, et al. The Withdrawal Syndrome Scale for alcohol and related psychoactive drugs: Total scores as guidelines for treatment with phénobarbital. Nordic Journal of Psychiatry 40: 139–146, 1986CrossRefGoogle Scholar
  46. Laboratoires Delagrange Synthélabo, Investigator’s Brochure, September 1991Google Scholar
  47. Laboratoires Delagrange Synthélabo, tiapride prescribing information, France, 1993Google Scholar
  48. Laporte P, Bonnafoux D, Coffinet P. Conduit du sevrage. A propos du traitement de 150 alcooliques chroniques. Semaine des Hôpitaux de Paris 55: 399–402, 1979Google Scholar
  49. Laspalles F, Soultanian A. Comparative open randomized trial of tiapride and floctafenine in back pain. Semaine des Hôpitaux de Paris 56: 863–866, 1980PubMedGoogle Scholar
  50. Lepille D, Bastit PH. Essai thérapeutique dans les algies néoplasiques. Semaine des Hôpitaux de Paris 55: 791–795, 1979PubMedGoogle Scholar
  51. Lepóla U, Kokko S, Nuutila J, Gordin A. Tiapride and chlordiazepoxide in acute alcohol withdrawal. A controlled clinical trial. International Journal of Clinical Pharmacology Research 5: 321–326, 1984Google Scholar
  52. Lescut J, Verzele R, Hanon D. Intérêt du tiapride chez l’ethylique chronique. Lille Medical 17: (Suppl.): 73–77, 1979Google Scholar
  53. Lin CW, Wilk S. A comparison of the effect of substituted benzamides in radioreceptor binding assays with their effects on brain dopaminergic systems in vivo. In Rotrosen & Stanley (Eds) The benzamides: pharmacology, neurobiology, and clinical aspects, advances in biochemical psychopharmacology, Vol. 35, pp. 51–60, Raven Press, New York, 1982.Google Scholar
  54. Liskow BI, Goodwin DW. Pharmacological treatment of alcohol intoxication, withdrawal and dependence: a critical review. Journal of Studies on Alcohol 48: 356–370, 1987PubMedGoogle Scholar
  55. Litman G, Stapleton J, Oppenheim AN, Peleg N. An instrument for measuring coping behaviour in hospitalised alcoholics: implications for relapse, prevention, treatment. British Journal of Addiction 78: 269–276, 1983PubMedCrossRefGoogle Scholar
  56. Malcolm R, Anton RF, Randall CL, Johnston A, Brady K, et al. A placebo-controlled trial of buspirone in anxious inpatient alcoholics. Alcoholism — Clinical and Experimental Research 16: 1007–1013, 1992CrossRefGoogle Scholar
  57. Mayfield D, McLeod G, Hall P. The Cage questionnaire: validation of a new alcohol screening instrument. American Journal of Psychiatry 131: 1121–1123, 1974PubMedGoogle Scholar
  58. Mercier J, Scotto-di-Tella AM, Menguy A. Quelques données expérimentales sur le tiapride. Semaine des Hôpitaux de Paris 53: 84–88, 1977Google Scholar
  59. Mikawa I, Saito Y, Yokoyama O. Hemodynamics and urinary excretion of tiapride in patients with renal function disorders. [Translated into English from Japanese.] Kiso to Rinsho 18: 553–558, 1984Google Scholar
  60. Morgenstern R, Fink H. Sulpiride blocks postsynaptic dopamine receptors in the nucleus accumbens. Journal of Neural Transmission 61: 151–160, 1985PubMedCrossRefGoogle Scholar
  61. Mouillé P, Cheymol G. Effets cardiovasculaire et hémodynamiques de dérivés du métoclopramide. Archives Internationales de Pharmacodynamic et de Therapie 215: 139–149, 1975Google Scholar
  62. Murphy DJ, Shaw GK, Clarke I. Tiapride and chloraiethiazole in alcohol withdrawal: a double-blind trial. Alcohol and Alcoholism 18: 227–237, 1983Google Scholar
  63. Nandakumaran M, Challier J-C, Rey E, Richard M-O, Olive G. In vitro transfer of six benzamides in the human placenta. Developmental Pharmacology and Therapeutics 7(Suppl. 1): 60–66, 1984PubMedGoogle Scholar
  64. Naranjo CA, Ozdemir V, Bremner KE. Diagnosis and pharmacological treatment of alcoholic patients. CNS Drugs 1: ((in press)), 1994Google Scholar
  65. Nohria V, Costall B, Naylor RJ. Dopamine antagonist properties of atypical neuroleptics may be revealed following mesolimbic denervation. International Pharmacopsychiatry 16: 21–29, 1981PubMedGoogle Scholar
  66. Norman T, Chiu E, James RH, Gregory MS. Single oral dose pharmacokinetics of tiapride in patients with Huntington’s disease. European Journal of Clinical Pharmacology 32: 583–586, 1987PubMedCrossRefGoogle Scholar
  67. Parent M, Jadot M, Toussaint C. Tiapride and alcohol withdrawal symptoms. Revue Médicale de Liege 33: 672–677, 1978PubMedGoogle Scholar
  68. Pattison EM. A critique of alcoholism treatment concepts: with special reference to abstinence. Quarterly Journal of Studies on Alcohol 27: 49–71, 1966PubMedGoogle Scholar
  69. Pattison EM, Coe R, Rhodes RJ. Evaluation of alcoholism treatment. Archives of General Psychiatry 20: 478–488, 1969PubMedCrossRefGoogle Scholar
  70. Puech AJ, Simon P, Boissier JR. Benzamides and classical neuroleptics: comparison of their actions using 6 apomorphine-induced effects. European Journal of Pharmacology 50: 291–300, 1978PubMedCrossRefGoogle Scholar
  71. Renaudin C, Lemant P. Essai comparatif de l’atrium 300 et du tiapride per os dans le traitement du syndrome de sevrage alcoolique. Psychologie Médicale 13: 161–168, 1981Google Scholar
  72. Rey E, d’Athis Ph, Richard MO, de Lauture D, Olive G. Pharmacokinetics of tiapride and absolute bioavailability of three extravascular forms. International Journal of Clinical Pharmacology, Therapy and Toxicology 20: 62–67, 1982aGoogle Scholar
  73. Rey E, d’Athis Ph, Richard MO, de Lauture D, Olive G. Influence de repas sur la biodisponsibilité d’une forme orale du tiapride. Therapie 37: 651–656, 1982bPubMedGoogle Scholar
  74. Rondanelli R, Regazzi MB, Cristiani D, Ciardelli L. Cinética délia tiapride e biodisponibilità relativa di due preparad per os. Rivista Italiana di Biologia e Medicina 3: 237–244, 1983Google Scholar
  75. Roos RAC, de Haas EJM, Buruma OJS, de Wolff FA. Pharmacokinetics of tiapride in patients with tardive dyskinesia and Huntington’s disease. European Journal of Clinical Pharmacology 31: 191–194, 1986PubMedCrossRefGoogle Scholar
  76. Roufogalis BD, Thornton M, Wade DN. Specificity of the dopamine sensitive adenylate cyclase for antipsychotic antagonists. Life Sciences 19: 927–934, 1976PubMedCrossRefGoogle Scholar
  77. Sahyoun HA, Costall B, Naylor RJ. Benzamide action at α2-adrenocep-tors modifies catecholamine induced contraction and relaxation of circular smooth muscle from guinea-pig stomach. Naunyn-Schmiedebergs Archiv für Pharmakologie 319: 8–11, 1982CrossRefGoogle Scholar
  78. Satoh H, Nakanishi H, Shirakawa K, Kohjimoto Y, Kuwaki T, et al. Comparative study of tiapride and neuroleptics with anti-dopamine activity on convulsive seizure in mice. Japanese Journal of Pharmacology 43: 27–32, 1987PubMedCrossRefGoogle Scholar
  79. Scatton B, Bischoff S, Dedek J, Korf J. Regional effects of neuroleptics on dopamine metabolism and dopamine-sensitive adenylate cyclase activity. European Journal of Pharmacology 44: 287–292, 1977PubMedCrossRefGoogle Scholar
  80. Schuckit MA. Alcohol and alcoholism. In Wilson et al. (Eds) Harrison’s principles of internal medicine, 12th ed., pp. 2146–2151, McGraw-Hill, New York, 1991Google Scholar
  81. Selzer ML. The Michigan Alcohol Screening Test: the quest for a new diagnostic instrument. American Journal of Psychiatry 127: 1653–1658, 1971PubMedGoogle Scholar
  82. Shaw GK, Majumdar SK, Waller S, MacGarvie J, Dunn G. Tiapride in the long-term management of alcoholics of anxious or depressive temperament. British Journal of Psychiatry 150: 164–168, 1987PubMedCrossRefGoogle Scholar
  83. Shaw JM, Kolesar GS, Sellers EM, Kaplan HL, Sandor P. Development of optimal treatment tactics for alcohol withdrawal. I. Assessment and effectiveness of supportive care. Journal of Clinical Psychopharmacol-ogy 1: 382–389, 1981Google Scholar
  84. Skinner HA, Allen BA. Alcohol dependence syndrome: measurement and validation. Journal of Abnormal Psychology 91: 199–209, 1982PubMedCrossRefGoogle Scholar
  85. Stecchini M, Corrias G. Le traitement des subjets alcooliques par le tiapride. Semaine des Hôpitaux de Paris 58: 2724–2726, 1982PubMedGoogle Scholar
  86. Steele JW, Faulds D, Sorkin EM. Tiapride. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic potential in geriatric agitation. Drugs and Aging 3: 460–478, 1993Google Scholar
  87. Stefanini E, Clément-Cormier Y, Vernaleone F, Devoto P, Marchisio AM, et al. Sodium-dependent interaction of benzamides with dopamine receptors in rat and dog anterior pituitary glands. Neuroendocrinology 32: 103–107, 1981PubMedCrossRefGoogle Scholar
  88. Stockwell T, Murphy D, Hodgson R. The severity of alcohol dependence questionnaire: its use, reliability and validity. British Journal of Addiction 78: 145–155, 1983PubMedCrossRefGoogle Scholar
  89. Strolin-Benedetti M, Donath A, Frigerio A, Morgan KT, Laville C, et al. Absorption, élimination et métabolisme du tiapride (FLO 1347), médicament neuroleptique, chez le rat, le chien et l’homme. Annales Pharmaceutiques Françaises 36: 279–288, 1978PubMedGoogle Scholar
  90. Strolin-Benedetti M, Donath A, Malnoe A. Étude pharmacocinétique et métabolique du tiapride chez l’homme. Semaine des Hôpitaux de Paris 53: 69–71, 1977Google Scholar
  91. Tarn SW. (+)-[3H]SKF 1Q, 047, (+)-[3H]ethylketocyclazocine, μ, κ, σ and phencyclidine binding sites in guinea pig membranes. European Journal of Pharmacology 109: 33–41, 1985CrossRefGoogle Scholar
  92. Tenant Jr FS. Editorial. Disufiram will reduce medical complications but not cure alcoholism. Journal of the American Medical Association 19: 1489, 1986Google Scholar
  93. Therond JP. Un traitement des crampes musculaires essentielles. Semaine des Hôpitaux de Paris 55: 599–600, 1979PubMedGoogle Scholar
  94. Tollefson GD, Montague-Claouse J, Tollefson SL. Treatment of comorbid generalized anxiety in a recently detoxified alcoholic population with a selective serotonergic drug (buspirone). Journal of Clinical Psycho-pharmacology 12: 19–26, 1992Google Scholar
  95. Vaillant GE, Clark W, Cyrus C, Milofsky ES, Kopp J, et al. Prospective study of alcoholism treatment: eight year follow-up. American Journal of Medicine 75: 455–463, 1983PubMedCrossRefGoogle Scholar
  96. Vandel B, Bonin B, Vandel S, Blum D, Rey E, et al. Étude de l’interaction entre le tiapride et l’acohol chez l’homme. Semaine des Hôpitaux de Paris 60: 175–177, 1984PubMedGoogle Scholar
  97. Vasse M, Protais P, Costentin J, Schwartz J-C. Unexpected potentiation by discriminant benzamide derivatives of stereotyped behaviours elicited by dopamine agonists in mice. Naunyn-Schmiedebergs Archives of Pharmacology 329: 108–116, 1985CrossRefGoogle Scholar
  98. Wadworth AN, Heel RC. Remoxipride. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic potential in schizophrenia. Drugs 40: 863–879, 1990Google Scholar
  99. Whitfield CL, Thompson G, Lamb A, Spenser V, Pfeifer M, et al. Detox-ication of 1,024 alcoholic patients without psychoactive drugs. Journal of the American Medical Association 239: 1409–1410, 1978PubMedCrossRefGoogle Scholar
  100. WHO (World Health Organization). The ICD-10 classification of mental and behavioural disorders: clinical descriptions and diagnostic guidelines. Geneva, World Health Organization, 1992Google Scholar

Copyright information

© Adis International Limited 1994

Authors and Affiliations

  • David H. Peters
    • 1
  • Diana Faulds
    • 1
  1. 1.Adis International LimitedMairangi Bay, Auckland 10New Zealand

Personalised recommendations