Hostname: page-component-cd9895bd7-p9bg8 Total loading time: 0 Render date: 2024-12-23T14:17:20.617Z Has data issue: false hasContentIssue false

Obsessive compulsive disorder: Opportunities within and beyond the serotonergic domain

Published online by Cambridge University Press:  18 September 2015

Extract

Abnormality of the serotonin (5-hydroxytryptamine – 5-HT) system and particularly hypersensitivity of postsynaptic 5-HT receptors remained the leading hypothesis for the underlying pathophysiology of obsessive compulsive disorder (OCD) during the 1980s. A number of lines of evidence supported this serotonergic hypothesis, not least the treatment studies which demonstrated clearly and consistently that anti-obsessional efficacy was a function of serotonin re-uptake inhibition. Studies of markers and biological probes provided further evidence: platelet studies, for example, linked reductions in 5-HT activity with clinical response, and treatment response was correlated with decreased 5-hydroxyindolacetic acid (5-HIAA) levels within the cerebrospinal fluid of OCD patients.

Added to this was the evidence from the behavioral or physiological responses observed following serotonergic challenge with the serotonin agonists meta-chlorophenylpiperazine, a compound with high affinity for 5-HT1A-, 5-HT1D- and 5-HT2C-receptors.

Type
Research Article
Copyright
Copyright © Cambridge University Press 1997

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

Literature

1.Zohar, J, Insel, TR. Obesessive-compulsive disorder: psychobiological approaches to diagnosis, treatment and pathophysiology. Biol Psychiat 1987;22:667687.CrossRefGoogle ScholarPubMed
2.Zohar, J, Zohar-Kadouch, RC, Kindler, S. Current concepts in the pharmacological treatment of obsessive-compulsive disorder. Drugs 1992; 43: 210–8.CrossRefGoogle ScholarPubMed
3.Flament, MF, Rapoport, JL, Murphy, DL, et al.Biochemical changes during clomipramine treatment of childhood obsessive-compulsive disorder. Arch gen Psychiat 1987;44:219–25.CrossRefGoogle ScholarPubMed
4.Thoren, P, Askeng, M, Bertilsson, L, et al.Clomipramine treatment of obsessive-compulsive disorder. II. Biochemical aspects. Arch gen Psychiat;40:1085–9.Google Scholar
5.Zohar, J, Mueller, EA, Insel, TR, et al.Serotonergic responsivity in obsessive-compulsive disorder: comparison of patients and healthy controls. Arch gen Psychiat 1987;44:946–51.CrossRefGoogle ScholarPubMed
6.Zohar, J, Kindler, S. Serotonergic probes in obsessive-compulsive disorder. Int clin Psychopharmacol 1992;7:3940.CrossRefGoogle ScholarPubMed
7.Lesch, KP, Hoh, A, Disselcamp-Tietze, J, et al.5-hydroxytyptamine IA receptor receptivity in obsessive-compulsive disorder. J Am Acad Child Adolesc Psychiat 1991;29:407412.Google Scholar
8.McDougle, CJ, Goodman, WK, Leckman, JF, et al.Limited therapeutic effect of addition of buspirone in fluvoxamine refractory obsessive-compulsive disorder. Am J Psychiat 1993;150:647–9.Google ScholarPubMed
9.Bastani, B, Nash, JF, Meltzer, MY. Prolactin and cortical responses to MK-212, a serotonin agonist in obsessive-compulsive disorder. Arch gen Psychiat 1990;49:21–8.Google Scholar
10.Zohar, J. Is 5-HTID involved in obsessive-compulsive disorder? Eur Neuropsychol 1996;6 suppl:S4–5.Google Scholar
11.Marazziti, D, Hollander, E, Lensi, P, et al.Peripheral markers of serotonin and dopamine function in obsessive-compulsive disorder. Psychiat Res. 1992;42:4151.CrossRefGoogle ScholarPubMed
12.McDougle, CJ, Goodman, WK, Price, LH, et al.Neuroleptic addition in fluvoxamine-refractory obsessive compulsive disorder. Am J Psychiat 1990;147:650–4.Google ScholarPubMed
13.Leckman, JF, Goodman, WK, North, WG, et al.Elevated cerebrospinal fluid levels of oxytocin in obsessive-compulsive disorder. Arch gen Psychiat 1994;51:782–92.CrossRefGoogle ScholarPubMed
14.Altemus, M, Swedo, SE, Leonard, B, et al.Changes in cerebrospinal fluid neurochemistry during treatment of obsessive-compulsive disorder with clomipramine. Arch gen Psychiat 1994;51:794803.CrossRefGoogle ScholarPubMed
15.Pitman, RK. Animal models of compulsive behaviour. Biol Psychiat 1989;26:189198.CrossRefGoogle Scholar
16.Havlicck, V, Rezek, M, Friesen, H. Somatostatin and thyrotropin releasing hormone: central effects on sleep and motor systems. Pharmacol Biochem Behav 1976;4:455–9.CrossRefGoogle Scholar
17.Altemus, M, Piggott, T, L'Heureux, F, et al.Cerebrospinal fluid somatostatin in obsessive-compulsive disorder. Am J Psychiat 1993;15:460-4.Google Scholar
18.Swedo, SE, Leonard, H, Shapiro, MB, et al.Sydenham's chorea: physical and psychological symptoms of St. Vitus' dance. Paediatrics 1993;91:706713.Google ScholarPubMed
19.Roy, BF, Benkelfat, C, Hill, JL, et al.Serum antibody for somatostatin: 14 and prodynorphin 209-240 in patients with obsessive-compulsive disorder, schizophrenia, Alzheimer's disease, multiple sclerosis and advanced HIV infection. Biol Psychiat 1994;35: 334–44.CrossRefGoogle ScholarPubMed
20.Maes, M, Meitzer, HY, Bosmans, E. Psychoimmune investigation in obsessive-compulsive disorder: assays of plasma trasferrin, inter-leukin-2 and interleukin-6 receptor, and interleukin-lb and inter-leukin-6 concentrations. Neuropsychobiology 1994;30:5760.CrossRefGoogle Scholar
21.Weizman, R, Hermesh, H, Karp, M, et al.The platelet benzodiazepine receptor is unaltered in obsessive-compulsive disorder. Clin Neuropharmacol 1993;16:211–5.CrossRefGoogle ScholarPubMed
22.Lucey, JV, Butcher, G, Clare, AW, et al.Elevated growth hormone responses to pyridostigmine in obsessive-compulsive disorder: evidence of cholinergic supersensitivity. Am J Psychiat 1993;150: 961–2.Google ScholarPubMed
23.Catapano, F, Moneleone, P, Fuschino, A, et al.Melatonin and Cortisol secretion in patients with primary obsessive-compulsive disorder. Psychiat Res 1992;44:217–25.CrossRefGoogle ScholarPubMed