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Cited by 73Bipolar Disorder and TreatmentTreatment of Major DepressionNeuroscience and Neuropharmacology Research

The DOI matches its Crossref record; 202 of the 207 references it cites were found in a registry or an index.

Antidepressant withdrawal-induced activation (hypomania and mania): Mechanism and theoretical significance

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Dilsaver, Steven C., Greden, John F.·1984·Brain Research Reviews
DOI 10.1016/0165-0173(84)90028-6
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Abstract

Electrocortical and behavioral arousal are separate phenomena subserved by different neural substrata operating in parallel. A comprehensive theory of 'activation' must take into account the relationships between the electrical and behavioral activating systems. In pathological or experimentally induced states paradoxes, resolvable by a theory positing functional interaction between these systems, arise. EEG arousal is directly mediated, in both the waking and sleeping state, by cholinergic mechanisms. Antidepressant withdrawal precipitates cholinergic overdrive; this would account for the apparent disturbances of REM sleep occurring when antidepressants are stopped. Generally, cholinergic overdrive would produce behavioral inhibition but in particular instances it triggers marked psychomotor arousal by mobilizing a 'limbic activating system'. The existence of a monoaminergic 'limbic activating system', system 'A', with the properties attributed to it in this paper, is supported by both clinical and laboratory observations. System 'A' theory provides a parsimonious means of adequately explaining many phenomena. This theory also has in its favor explanatory power and scope. The Cholinergic-Monoaminergic Interaction Theory of antidepressant withdrawal induced activation and of rapidly-cycling manic-depressive illness maintains that system 'A' and a cholinergic inhibitory system interact dynamically, and that excessive monoaminergic function can precipitate excessive cholinergic function and a dearth of monoaminergic function (due to autoregulation) and hence depression. Likewise, excessive cholinergic function is posited to activate monoaminergic systems and hence to secondarily cause behavioral activation. Rapidly-cycling manic-depressive patients, according to the model, develop alternating cholinergic and monoaminergic overdrive states because the homeostatic mechanisms which should serve to maintain, within normal limits, the composite of cholinergic inhibitory and monoaminergic activating influences are defective. Consequently, rather than reaching a reasonable balance compatible with adaptive function there is oscillation between extremes. Each oscillatory movement is actually a move towards the 'golden mean' and is induced by deviation from this ideal but the defective homeostatic mechanisms promote ' perpetual ' overshooting. Lithium and ECT may be useful in the treatment of rapidly-cycling patients as both treatments may down-regulate muscarinic receptors, and otherwise modify cholinergic and monoaminergic systems in ways promoting homeostasis.(ABSTRACT TRUNCATED AT 400 WORDS)

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Research works printed but not linked: 11

  1. Bremer, 1949, Acetylcholine et cortex cerebral, Arch. Int. Physiol., 57, 106
  2. Dilsaver, S. C., Leckrone, J. G. and Greden, J. F., An ‘anticholinesterase-like’ syndrome precipitated by psychotropic withdrawal in a chronic abuser of marijuana, Psychosomatics, in press.
  3. Doerr, 1983, Physostigmine-induced escape from dexamethasone in normal subjects, Biol. Psychiatry, 18, 261
  4. Fabre, 1978, A double-blind placebocontrolled study of bupropion hydrochloride (Wellbutrin) in the treatment of depressed inpatients, Curr. Ther. Res., 23, 392
  5. Gershon, E. S., Nurnberger, J. I., Nadi, S. N., Sitaram, N. and Gillin, J. C., A muscarinic hypothesis of genetic vulnerability to affective disorders, in press.
  6. Grob, 1947, The administration of diisopropylfluorophosphate (DFP) to man, John's Hopkins Hasp. Bull., 81, 257
  7. Kumbarachi, 1980, Effects of Δ9tetrahydrocannibinol on excitable membranes and neuromuscular transmission, Molec. Pharmacol., 17, 344
  8. Layman, 1971, Some actions of Δ1tetrahydrocannabinol and cannabinoid at cholinergic functions, Brit. J. Pharmacol., 41, 379P
  9. Maziere, 1981, Positron tomography, A new method for in vivo brain studies of benzodiazepine receptors in animal and in man, Advanc. Biochem. Psychopharmacol., 26, 283
  10. McVicar, 1977, Abuse of antiparkinson drug by psychiatric patients, Amer. J. Psychiatry, 138, 809
  11. Risch, 1982, β-endorphin hypersecretion in depression: possible cholinergic mechanisms, Biol. Psychiatry, 17, 1071

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Metadata

Authors
Dilsaver, S. C., & Greden, J. F.
Affiliations
  • Michigan Medicine (US)
  • University of Michigan (US)
Corresponding author
Dilsaver, Steven C.
Venue
Brain Research Reviews
Publisher
Elsevier BV
Published
1984-03
Volume
7
Issue
1
Pages
29-48
ISSN
0165-0173 (ISSN-L)
DOI
10.1016/0165-0173(84)90028-6
OpenAlex
W2417584883
Cited by
73
References
207
Citations by year
2021: 1 · 2020: 1 · 2019: 2 · 2018: 1 · 2015: 2 · 2014: 1 · 2013: 1 · 2012: 1
FWCI
2.08
Type
journal article
Language
en
Open access
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Brain Research Reviews (publishedVersion)
  • PubMed (publishedVersion)
  • Deep Blue (University of Michigan) (submittedVersion)
Topics
  • Health Sciences › Medicine › Psychiatry and Mental health › Bipolar Disorder and Treatment
  • Health Sciences › Medicine › Pharmacology (medical) › Treatment of Major Depression
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Keywords
antidepressant discontinuation, hypomania, mania, behavioral arousal, EEG arousal, muscarinic receptors, lithium, electroconvulsive therapy, homeostatic mechanisms, depression, bipolar disorder
MeSH terms
Adrenergic Fibers, Animals, Antidepressive Agents, Arousal, Behavior, Animal, Bipolar Disorder, Brain, Cholinergic Fibers, Electroencephalography, Evoked Potentials, Humans, Sleep Stages, Substance Withdrawal Syndrome, Receptors, Neurotransmitter, Neurotransmitter Agents

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