Hostname: page-component-586b7cd67f-vdxz6 Total loading time: 0 Render date: 2024-12-03T00:38:35.411Z Has data issue: false hasContentIssue false
  • English
  • Français

Possible Potentiation of Haloperidol Neurotoxicity in Acute Hyperthyroidism

Published online by Cambridge University Press:  29 January 2018

C. Raymond Lake  and
William E. Fann
C. Raymond Lake
Affiliation:
Department of Psychiatry, Duke University Medical Center, Durham, North Carolina 27710, and Veterans Administration Hospital, Durham, North Carolina 27705, U.S.A.
William E. Fann
Affiliation:
Psychiatry and Pharmacology, Duke University Medical Center, Durham, North Carolina 27710, U.S.A.
Get access Rights & Permissions [Opens in a new window]

Extract

Altered thyroid states may influence the effects of psychotropic drugs. Prange (1963a) reported a case in which moderate factitious hyperthyroidism and Imipramine treatment seemed to interact to produce paroxysmal auricular tachycardia. Later, this author and his colleagues described increased lethality in imipramine in hyperthyroid mice (Prange et al., 1962) and decreased lethality in hypothyroid mice (Prange et al, 1963b). Similar effects have been found for phenothiazines (Ashford et al., 1968). More recently it has been shown that a variety of physiological and behavioural effects of phenothiazines are amplified in hyperthyroid mice (Park et al., 1973). Furthermore, Selye and Szabo (1972) found that thyroxine sensitized the rat to the toxic effects of haloperidol.

Type
Research Article
Information
The British Journal of Psychiatry , Volume 123 , Issue 576 , November 1973 , pp. 523 - 525
Copyright
Copyright © Royal College of Psychiatrists, 1973 

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

Ashford, A., and Ross, J. A. (1968). Brit. med. J., 2: 217.Google Scholar
Black, J. W., Crowther, A. F., Shanks, R. G., Smith, I. H., and Dornhorst, A. C. (1961). Lancet, i, 1080–1086.Google Scholar
Canary, J. J., Schaaf, M., Duffy, B. J. Jr., and Kyle, L. H. (1957) New Eng. J. Med., 257, 435–442.CrossRefGoogle Scholar
de Wied, D. (1967). Pharmacol. Rev., 19, 251.Google Scholar
Emlen, W., Segal, D. S., and Mandell, A. J. (1972). Science, 175, 79–82.Google Scholar
Gillette, J. R. (1963). Prog. Drug. Res., 6, 13–73.Google Scholar
Park, S., Happy, J. M., and Prange, A. J. Jr. (1973). Europ. J. Pharmacol. In press.Google Scholar
Prange, A. J. Jr. (1963a). Amer. J. Psychiat., 119, 994–995 Google Scholar
Prange, A. J. Jr., and LIPTON, M. A. (1962). Nature, 196, 588–589.Google Scholar
Prange, A. J. Jr., and Love, G. N. (1963b). Nature, 197, 1212–1213.Google Scholar
Prange, A. J. Jr., Wilson, I. C, Lipton, M. A., Rabon, A. M., McClane, T. K., and Knox, A. E. (1970). Psychosoma tics 11, 442–444.Google Scholar
Selye, H., and Szabo, S. (1972). Psychopharmacologia, 24, 430–434 Google Scholar
Shanks, R. G., Hadden, D. R., Lowe, D. C, McDevitt, D. G., and Montgomery, D. A. D. (1969). Lancet, i, 993–995.Google Scholar
Sinha, J. N., Srmal, R. C, Jaju, B. P. et al. (1967). Arch. int. Pharmacol. 165, 160–165.Google Scholar
Strang, R. R. (1965). J. Neurol., Neurosurg. and Psychiat., 28, 404–406.Google Scholar
Submit a response

eLetters

No eLetters have been published for this article.