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The Universal Field Hypothesis of Catatonia and Neuroleptic Malignant Syndrome

Published online by Cambridge University Press:  07 November 2014

Brendan T. Carroll
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Abstract

Catatonia and neuroleptic malignant syndrome (NMS) are uncommon disorders that can be life-threatening. Many researchers consider them as clinically divergent entities; however, they share similar and overlapping literature on causative agents, phenomenology, and treatment response. This hypothesis considers both disorders as a single entity that result from variable combinations of the following: 1) γ-aminobutyric acid (GABA) hypoactivity at the GABAA receptor; 2) dopamine hypoactivity at the D2 receptor; 3) serotonin hyperactivity at the 5-HT1A receptor and hypoactivity at the 5-HT2A receptor; and 4) glutamate hypoactivity at the N-methyl-D-aspartate (NDMA) receptor. In this paper, evidence to support this hypothesis is limited to retrospective human studies of catatonia and NMS. The four components of the hypothesis are: 1) GABAA agonists have been shown to alleviate catatonia and NMS; 2) D2 antagonism is proportional to the relative likelihood of NMS and catatonia; 3) 5-HT1A agonism with 5-HT2A antagonism is implicated in catatonia and NMS; 4) NMDA receptor antagonists, such as phencyclidine and ketamine, reduce glutamate transmission. This hypothesis proposes that it is the interaction of these systems that prediposes, initiates, and maintains the twin syndromes of catatonia and NMS.

Type
Feature Articles
Information
CNS Spectrums , Volume 5 , Issue 7: Mechanisms and Presentations of Catatonia , July 2000 , pp. 26 - 33
Copyright
Copyright © Cambridge University Press 2000

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References

REFERENCES

1.Kahlbaum, KL, Levij, Y, Pridon, T, trans. Catatonia. Baltimore, MD: Johns Hopkins University Press; 1973.Google Scholar
2.Braunig, P, Kruger, S, Kahlbaum, KL. 1828–1899 (Images in Psychiatry) Am J Psychiatry. 1999;156:989.Google Scholar
3.Kraepelin, E. Dementia Praecox and Paraphrenia. RM, Barclay, trans. Edinburgh: E.&S. Livingstone; 1919:132.Google Scholar
4.Blueler, E. Dementia Praecox or the Group of Schizophrenias. Zinkin, J, trans. New York, NY: International Universities Press; 1950:301.Google Scholar
5.Leonhard, K. The Classification of Endogenous Psychoses. 5th edition. R, Berman, trans. New York, NY:Irvington; 1979.Google Scholar
6.Jong de, H, Baruk, H. La catatonie experimentale par la bulbocapnine: etude phsiologique et clinique. Paris, France: Masson; 1930.Google Scholar
7.Gjessing, R. Disturbances of somatic function in catatonia with a periodic course and their compensation. J Ment Sci. 1938;84:608–621.CrossRefGoogle Scholar
8.Blumer, D. Catatonia and the neuroleptics: psychobiologic significance of remote and recent findings. Comp Psychiatry. 1997;38:193–201.CrossRefGoogle ScholarPubMed
9.Friedman, JH. Stereotypy and Catatonia in Parkinson's disease and movement disorders. 3rd edition. Jankovic, J, Tolosa, E, eds. Philadelphia, PA: Williams and Wilkins; 1998.Google Scholar
10.Cairns, H. Disturbances of consciousness with lesions of the brain-stem and diencephalon. Brain. 1952;75:8–146.CrossRefGoogle ScholarPubMed
11.Gelenberg, AJ. The catatonic syndrome. Lancet. 1976;1:1339–1341.CrossRefGoogle ScholarPubMed
12.Mahendra, B. Where have all the catatonics gone? Psychol Med. 1981;11:669–67l.CrossRefGoogle ScholarPubMed
13.Chesselet, MF, Delfs, JM. Basal ganglia and movement disorders: an update. Trends Neurosci. 1996;19:417–422.CrossRefGoogle ScholarPubMed
14.Caroff, SN. The neuroleptic malignant syndrome. J Clin Psychiatry 1980;41:79–83.Google ScholarPubMed
15.Rosebush, PI, Hildebrand, AM, Furlong, BG, et al.Catatonic syndrome in a general psychiatric inpatient population: frequency, clinical presentation, and response to lorazepam. J Clin Psychiatry. 1990;51:357–362.Google Scholar
16.Bush, G, Fink, M, Petrides, Get al.Catatonia II. Treatment with Lorazepam and Electroconvulsive Therapy. Acta Psychiatr Scand. 1996;93:137–143.CrossRefGoogle ScholarPubMed
17.Ungvari, GS, Leung, CM, Wong, MK, et al.Benzodiazepines in the treatment of catatonic syndromes. Acta Psychaitr Scand. 1994;89:285–288.CrossRefGoogle Scholar
18.Rosebush, PI, Mazurek, MF. Catatonia: Reawakening to a forgotten disorder. Movement Disorders. 1999;14:395–397.3.0.CO;2-L>CrossRefGoogle ScholarPubMed
19.Lauterbach, EC. Catatonia-like events after valproic acid with risperidone and sertraline. Neuropsychiatry, Neuropsychology and Behavioral Neurology 1998;11:157–163.Google ScholarPubMed
20.Rogers, DM. Motor Disorder in Psychiatry: Towards a Neurological Psychiatry. West Sussex, England: John Wiley & Sons; 1992.Google Scholar
21.Wahner, A. Das maligne neurolepticsche Syndrome (MNS)-Diagnose, Therapie und Pathogenese. In: Braunig, P, ed. Differenzierung katatoner und neuroleptikainduzierter Bewegungsstorungen. Stutgard: Georg Thime Verlag; 1995:131–135.Google Scholar
22.Lohr, JB, Wisniewski, AA. Catatonia. In: Movement Disorders: A Neuropsychiatric Approach. New York, NY: The Guilford Press; 1987:201–207.Google Scholar
23.Fink, M. Neuroleptic malignant syndrome and catatonia: one entity or two? Biol Psych. 1996;39:1–4.CrossRefGoogle ScholarPubMed
24.Carroll, BT, Taylor, RE. The nondichotomy between lethal catatonia and neuroleptic malignant syndrome. J Clin Psychopharmacology. 1997;17:235–238.CrossRefGoogle ScholarPubMed
25.Koch, M, Changragiri, S, Rizvi, S, et al.Catatonic signs in neuroleptic malignant syndrome. Comp Psych. 2000;41(1):73–75.CrossRefGoogle ScholarPubMed
26.White, DAC. Catatonia and the neuroleptic malignant syndrome. Br J Psychiatry. 1992;161:558–560.CrossRefGoogle ScholarPubMed
27.White, DAC. 17 Catatonic Patients Diagnosed as Neuroleptic Malignant Syndrome. CNS Spectrums. 2000;7:xx–xx.Google Scholar
28.Carroll, BT, Anfinson, TJ, Kennedy, JC, et al.Catatonic disorder due to general medical conditions. J Neuropsych Clin Neurosci. 1994;6:122–133.Google ScholarPubMed
29.Salam, SA, Kilzieh, N. Lorazepam treatment of psychogenic catatonia: an update. J Clin Psychiatry. 1988;49(suppl):16–21.Google ScholarPubMed
30.Rosebush, PI, Mazurek, MF. A consideration of the mechanisms by which lorazepam might treat catatonia. J Clin Psychiatry. 1991;52:187–188.Google Scholar
31.Wetzel, H, Heuser, I, Benkert, O. Stupor and affective status: alleviation of the psychotmotor disturbances by lorazepam and recurrence of symptoms after Ro 15–1788. J Nerv Ment Dis. 1987;175:240–242.CrossRefGoogle Scholar
32.Rosebush, PI, Mazurek, MF. Catatonia after benzodiazepine withdrawal. J Clin Psychopharmacol. 1996;16:315–319.CrossRefGoogle ScholarPubMed
33.Ungvari, GS, Chiu, HFK, Chow, LY, et al.Lorazepam for chronic catatonia: a randomized, double-blind, placebo controlled crossover study. Psychopharmacology. 1999;142:393–398.CrossRefGoogle Scholar
34.Carroll, BT. The GABAA versus GABAB hypothesis of catatonia. (letter) Movement Disorders 1999;14:702.3.0.CO;2-N>CrossRefGoogle ScholarPubMed
35.Mastain, B, Rascle, C, Thomas, P, et al.Zolpidem in catatonic syndrome: from a pharmacological test to a pathophysiological hypothesis. Movement Disorders. 1998;13(supl. 2):46.Google Scholar
36.Parmar, MS. Akinetic mutism after baclofen. Ann Int Med. 1991;115:499–500.CrossRefGoogle ScholarPubMed
37.Daniele, A., Albanese, A, Gainotti, G, et al.Zolpidem in Parkinson's disease. Lancet. 1997;349:1222–1223.CrossRefGoogle ScholarPubMed
38.Daniele, A, Moro, E, Bentivoglio, AR. Zolpidem in progressive supranuclear palsy (letter). NEMJ. 1999;341:543–544.CrossRefGoogle Scholar
39.Francis, A, Changragiri, S, Rizvi, S, et al.Lorazepam treatment of neuroleptic malignant syndrome. Am J Psychiatry. In press.Google Scholar
40.Ereshefsky, L. The future of antipsychotic drug therapy: current atypical agents and beyond. Abstract in: Bender, KJ, ed. New antipsychotics enhance function while improving symptoms. Psychiatric Times. 1999;Nov (suppl):1–4.Google Scholar
41.Burnet, PWJ, Eastwood, SL, Harrison, PJ. (3H) WAY-100635 for 5-HT1A receptor autoradiography in human brain: a comparison with (3H)-OH-DPAT and demonstration of increased binding in the frontal cortex in schizophrenia. Neurochemistry International. 1997;30:565–574.CrossRefGoogle Scholar
42.Burnet, PWJ, Eastwood, SL, Harrison, PJ. 5-HT1A and 5-HT2A receptor mRNAs abd binding site densities are differentially altered in schizophrenia. Neuropsychopharm. 1996;15:442–455.CrossRefGoogle Scholar
43.Prinssen, EP, Kleven, MS, Koek, W. The cataleptogenic effects of the neuroleptic nemonapride are attenuated by its 5-HT1A receptor agonist properties. Eur J Pharmacol. 1998;356:189–192.CrossRefGoogle ScholarPubMed
44.Assi'e, MB, Cosi, C, Koek, W. 5-HT1A receptor agonist properties of the antipsychotic, nemonapride: comparison with bromerguride and clozapine. Eur J Pharmacol 1997;334:141–147.CrossRefGoogle Scholar
45.Olney, JW, Farber, NB. Glutamate receptor dysfunction and schizophrenia. Arch Gen Psychiatry. 1995;52:998–1007.CrossRefGoogle ScholarPubMed
46.McCarron, MM, Schulze, BW, Thompson, GA, et al.Acute phencyclidine intoxication: clinical patterns, complications, and treatment. Ann Emerg Med. 1981;10:290–297.CrossRefGoogle ScholarPubMed
47.Javitt, DC, Zukin, SR. Recent advances in the phencyclidine model of schizophrenia. Am J Psychiatry. 1991;148:1301–1308.Google ScholarPubMed
48.Lees, KR. Cerestat and other NMDA antagonists in ischemic stroke. Neurology. 1997;49(suppl):66–69.CrossRefGoogle ScholarPubMed
49.Northoff, G, Eckert, J, Fritze, J. Glutamanergic dysfunction in catatonia? Successful treatment of three acute akinetic catatonic patients with NMDA antagonist amantidine. Neurol Neurosurg Psychiatry. 1997;62:404–406.CrossRefGoogle Scholar
50.Merello, M, Nouzeilles, MI, Cammarota, A, et al.Effect of mematine (NMDA antagonist) in Parkinson's disease: a double-blind cross-over randomized study. Clin Neuropharmacol. 1999;22:273–276.Google Scholar
51.Lazarus, A, Mann, SC, Caroff, SN. The neuroleptic malignant syndrome and related conditions. Washington, DC: American Psychiatric Association Press; 1989.Google Scholar