- Email: [email protected]
Bromocriptine in neuroleptic resistance
BIOL PSYCHIATRY 1981;22:522-524
Correspondence
References CadeJFJ (1949): Lithium salts in the treatment of psychotic excitement. Med J Aust 36349. Drabkin JE (ed) (1950): Caelius Aureliunus. On Acute Diseases and on Chronic Diseases. Chicago: University of Chicago Press, pp 535-559. Garrod AB (1859): The Nature and Treatment of Gout and Rheumatic Gout. London: Walton and Maberly, pp 43w. Garrod AB (1863): The Nature and Treatmenr of Gout and Rheumatic Gout. London: Walton and Maberly, pp 419-428. Garod AB (1876): A Treatise on Gout and Rheumatic Gout, 3rd ed. London: Longmans, pp 364-394. Hammond WA (1871): A Treatise on Diseases of the Nervous System. New York: D. Appleton and Company. Hansen HE, Amdisen A (1978): Lithium intoxication. (Report of 23 cases and review of 100 cases from the literature.) Q J Med 47:123-144.
Johnson FN (1984): The History of Lithium Therapy. London: MacMillan. Lange C (1886): Om periodiske Depressionstilstande og deres Patogenese. Copenhagen: Jacob Lunds Forlag. Lange C (18%): Periodische Depressionszustiinde
und ihre Pathogenesis auf dem Boden der harnsauren Diathese.
Hamburg: Verlag von Leopold Voss. Lange F (1894): De vigtigste Sindssygdomsgrupper i kort Omrids. (The most important groups of mental disorders in short outline.) Copenhagen: Gyldendanske Boghandels Forlag. Parkinson J (1805): Observations on the Nature and Cure of Gout; on the Nodes of the Joints; and on the Influence of Certain Articles of Diet, in Gout, Rheumatism, and Gravel. London: H.D. Symonds, Paternoster Row;
Murray, Fleet Street; Arch, Cornhill; and Cox, St. Thomas Street, Borough. Yeragani VK, Gershon S (1986): Letter: Hammond and lithium: Historical update. Biol Psychiatry 21:1101-l 102.
Response To the Editor: Dr. Amdisen’s reponse to our letter further illustrates the evolution of lithium treatment in medicine and psychiatry. The focus of our article was mainly on Hammond’s use of lithium bromide for mania as early as in 1871. We agree with Dr. Amdisen that 60 grains of lithium bromide is equivalent to about 45 mm01 of lithium, and we very much regret this mistake. However, we consider that 3.6 g of lithium bromide every 2-3 hr a day or a maximum of 6 doses (21.6 g/day) can potentially produce bromide toxicity (Greensher et al. 1983).
Bromocriptine in Neuroleptic Resistance To the Editor: We read with interest the paper by Gattaz and Kiillisch (1986) on the use of bromocriptine in the treatment of neuroleptic-resistant schizophrenia. As they suggest, neuroleptics are currently the treatment of choice in schizophrenia, and any newer effective adjunctive treatments for therapy-resistant patients would represent a much-needed addition to our psychopharmacological armamentarium.
523
V. K. Yeragani S. Gershon
Department of Psychiatry Wayne State University 951 E. Lafayette Ave Detroit, MI 48207
Reference Greensher J, Mofenson HC, Coraccio T (1983): Bromide. In Haddad LM, Winchester JF (eds), Clinical Management of Poisoning and Drug Overdose. Philadelphia: W.B. Saunders, pp 685486.
The case report they outlined suggested that bromocriptine may be such a useful adjunct. We are, however, concerned about the possibility of inducing dopamine autoreceptor subsensitivity, which would, of course, result in enhancement of dopaminergic functioning. Some authors (Baudray et al. 1977; Schwartz et al. 1978) have suggested that the presynaptic autoreceptor may be more susceptible to a drug-induced alteration by an agonist than the postsynaptic DA receptor. This phenomenon has been postulated as being responsible for the induction of a chronic paranoid psychosis by amphetamine use
524
BIOL PSYCHIATRY 1987:22:522-524
Correspondence
and may have accounted for the apparent tolerance to N-propylnorapomorphine observed in a recent study (Tamminga et al. 1986). We would be interested in learning from the authors if the decision to discontinue the bromocriptine after 4 weeks was based purely on the clinical situation or on concern about the possibility of DA autoreceptor subsensitivity occurring. It is conceivable that with the correct dosage and dosage scheduling, autoreceptor subsensitivity can be prevented. However, until this has been established, caution is required when using dopamine agonists in order to prevent a psychiatric syndrome similar to tardive dyskinesia. Husseini
K. Ma@
References Baudray A, Costentin J, Marcais M, et al. (1977): Decreased responsiveness to low doses of apomorphine after dopamine agonists and the possible involvement of hyposensitivity of dopamine autoreceptors. Neurosci Left 4:203-207.
Gattaz WF, KBllisch M (1986): Bromocriptine ment of neuroleptic-resistant chiatry 2 15 19-52 1.
schizophrenia.
in the treatBiol Psy-
Schwartz J, Costentin J, Martres MP, et al (1978): Modulation of receptor mechanisms in the CNS: Hyper and hyposensitivity 17:665-685.
Neuropharmacolog~
to catecholamines.
Tamminga CA, Gotts MD, Thaker GK, et al (1986): Dopamine agonist treatment of schizophrenia with N-propylnorapomorphine. Arch Gen Psychintry 43:398-402.
Mark Lander
Department of Psychiatry University of Manitoba Winnipeg, Manitoba R3E OW3 Canada
Response To the Editor: The concern of Drs. Manji and Lander about the possibility of inducing DA autoreceptor subsensitivity after chronic bromocriptine treatment seems to be justified by the report on a patient with hyperprolactinemia treated with bromocriptine (2.5 mg/day over 10 months) who became psychotic after abrupt discontinuation of the drug (Shukla et al. 1985). However, this appears to occur relatively seldom if we consider the wide use of bromocriptine in this clinical condition. The development of changes in DA receptor sensitivity in animals following treatment of DA agonists seems to be dose-dependent. Kamata and Rebec ( 1983) found a decrease in the sensitivity of DA autoreceptors following long-term treatment with 2 daily 5 mg/kg ( +)-amphetamine, whereas treatment with lower doses (1 mglkg) resulted in enhanced sensitivity to the drug. This suggests that the use of DA agonists in low doses (and in short-term therapy) is less likely to induce autoreceptor subsensitivity.
Nevertheless, I agree fully with the recommendation of Drs. Manji and Lander to use caution with DA agonists in the treatment of schizophrenia until we know more about their chronic effects. For this reason, we discontinued bromocriptine in our patient as soon as his clinical improvement had stabilized. Since the publication of our report, my collegue and coauthor, Dr. Manfred Kiillisch, died unexpectedly to my great personal regret. Wagner F. Gattaz
Central Institute of Mental Health 6800 Mannheim 1 Fed. Rep. Germany
References Kamata K, Rebec GV (1983): Dopaminergic and neostriatal neurons: Dose-dependent changes in sensitivity to anphetamine following long-term macology 2211377-1382.
treatment.
Neurophor-
Shukla S, Turner WJ, Newman G (1985): Bromocriptinerelated psychosis and treatment. BioI Psychiatr?; 20:32&328.
Correspondence
References CadeJFJ (1949): Lithium salts in the treatment of psychotic excitement. Med J Aust 36349. Drabkin JE (ed) (1950): Caelius Aureliunus. On Acute Diseases and on Chronic Diseases. Chicago: University of Chicago Press, pp 535-559. Garrod AB (1859): The Nature and Treatment of Gout and Rheumatic Gout. London: Walton and Maberly, pp 43w. Garrod AB (1863): The Nature and Treatmenr of Gout and Rheumatic Gout. London: Walton and Maberly, pp 419-428. Garod AB (1876): A Treatise on Gout and Rheumatic Gout, 3rd ed. London: Longmans, pp 364-394. Hammond WA (1871): A Treatise on Diseases of the Nervous System. New York: D. Appleton and Company. Hansen HE, Amdisen A (1978): Lithium intoxication. (Report of 23 cases and review of 100 cases from the literature.) Q J Med 47:123-144.
Johnson FN (1984): The History of Lithium Therapy. London: MacMillan. Lange C (1886): Om periodiske Depressionstilstande og deres Patogenese. Copenhagen: Jacob Lunds Forlag. Lange C (18%): Periodische Depressionszustiinde
und ihre Pathogenesis auf dem Boden der harnsauren Diathese.
Hamburg: Verlag von Leopold Voss. Lange F (1894): De vigtigste Sindssygdomsgrupper i kort Omrids. (The most important groups of mental disorders in short outline.) Copenhagen: Gyldendanske Boghandels Forlag. Parkinson J (1805): Observations on the Nature and Cure of Gout; on the Nodes of the Joints; and on the Influence of Certain Articles of Diet, in Gout, Rheumatism, and Gravel. London: H.D. Symonds, Paternoster Row;
Murray, Fleet Street; Arch, Cornhill; and Cox, St. Thomas Street, Borough. Yeragani VK, Gershon S (1986): Letter: Hammond and lithium: Historical update. Biol Psychiatry 21:1101-l 102.
Response To the Editor: Dr. Amdisen’s reponse to our letter further illustrates the evolution of lithium treatment in medicine and psychiatry. The focus of our article was mainly on Hammond’s use of lithium bromide for mania as early as in 1871. We agree with Dr. Amdisen that 60 grains of lithium bromide is equivalent to about 45 mm01 of lithium, and we very much regret this mistake. However, we consider that 3.6 g of lithium bromide every 2-3 hr a day or a maximum of 6 doses (21.6 g/day) can potentially produce bromide toxicity (Greensher et al. 1983).
Bromocriptine in Neuroleptic Resistance To the Editor: We read with interest the paper by Gattaz and Kiillisch (1986) on the use of bromocriptine in the treatment of neuroleptic-resistant schizophrenia. As they suggest, neuroleptics are currently the treatment of choice in schizophrenia, and any newer effective adjunctive treatments for therapy-resistant patients would represent a much-needed addition to our psychopharmacological armamentarium.
523
V. K. Yeragani S. Gershon
Department of Psychiatry Wayne State University 951 E. Lafayette Ave Detroit, MI 48207
Reference Greensher J, Mofenson HC, Coraccio T (1983): Bromide. In Haddad LM, Winchester JF (eds), Clinical Management of Poisoning and Drug Overdose. Philadelphia: W.B. Saunders, pp 685486.
The case report they outlined suggested that bromocriptine may be such a useful adjunct. We are, however, concerned about the possibility of inducing dopamine autoreceptor subsensitivity, which would, of course, result in enhancement of dopaminergic functioning. Some authors (Baudray et al. 1977; Schwartz et al. 1978) have suggested that the presynaptic autoreceptor may be more susceptible to a drug-induced alteration by an agonist than the postsynaptic DA receptor. This phenomenon has been postulated as being responsible for the induction of a chronic paranoid psychosis by amphetamine use
524
BIOL PSYCHIATRY 1987:22:522-524
Correspondence
and may have accounted for the apparent tolerance to N-propylnorapomorphine observed in a recent study (Tamminga et al. 1986). We would be interested in learning from the authors if the decision to discontinue the bromocriptine after 4 weeks was based purely on the clinical situation or on concern about the possibility of DA autoreceptor subsensitivity occurring. It is conceivable that with the correct dosage and dosage scheduling, autoreceptor subsensitivity can be prevented. However, until this has been established, caution is required when using dopamine agonists in order to prevent a psychiatric syndrome similar to tardive dyskinesia. Husseini
K. Ma@
References Baudray A, Costentin J, Marcais M, et al. (1977): Decreased responsiveness to low doses of apomorphine after dopamine agonists and the possible involvement of hyposensitivity of dopamine autoreceptors. Neurosci Left 4:203-207.
Gattaz WF, KBllisch M (1986): Bromocriptine ment of neuroleptic-resistant chiatry 2 15 19-52 1.
schizophrenia.
in the treatBiol Psy-
Schwartz J, Costentin J, Martres MP, et al (1978): Modulation of receptor mechanisms in the CNS: Hyper and hyposensitivity 17:665-685.
Neuropharmacolog~
to catecholamines.
Tamminga CA, Gotts MD, Thaker GK, et al (1986): Dopamine agonist treatment of schizophrenia with N-propylnorapomorphine. Arch Gen Psychintry 43:398-402.
Mark Lander
Department of Psychiatry University of Manitoba Winnipeg, Manitoba R3E OW3 Canada
Response To the Editor: The concern of Drs. Manji and Lander about the possibility of inducing DA autoreceptor subsensitivity after chronic bromocriptine treatment seems to be justified by the report on a patient with hyperprolactinemia treated with bromocriptine (2.5 mg/day over 10 months) who became psychotic after abrupt discontinuation of the drug (Shukla et al. 1985). However, this appears to occur relatively seldom if we consider the wide use of bromocriptine in this clinical condition. The development of changes in DA receptor sensitivity in animals following treatment of DA agonists seems to be dose-dependent. Kamata and Rebec ( 1983) found a decrease in the sensitivity of DA autoreceptors following long-term treatment with 2 daily 5 mg/kg ( +)-amphetamine, whereas treatment with lower doses (1 mglkg) resulted in enhanced sensitivity to the drug. This suggests that the use of DA agonists in low doses (and in short-term therapy) is less likely to induce autoreceptor subsensitivity.
Nevertheless, I agree fully with the recommendation of Drs. Manji and Lander to use caution with DA agonists in the treatment of schizophrenia until we know more about their chronic effects. For this reason, we discontinued bromocriptine in our patient as soon as his clinical improvement had stabilized. Since the publication of our report, my collegue and coauthor, Dr. Manfred Kiillisch, died unexpectedly to my great personal regret. Wagner F. Gattaz
Central Institute of Mental Health 6800 Mannheim 1 Fed. Rep. Germany
References Kamata K, Rebec GV (1983): Dopaminergic and neostriatal neurons: Dose-dependent changes in sensitivity to anphetamine following long-term macology 2211377-1382.
treatment.
Neurophor-
Shukla S, Turner WJ, Newman G (1985): Bromocriptinerelated psychosis and treatment. BioI Psychiatr?; 20:32&328.