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Electroconvulsive stimulation

Intriguingly, antidepressant agents (including electroconvulsive stimulation, ECS) have common cellular effects leading to enhanced expression of neuroprotective proteins that bolster neinonal survival and regulate synaptic cormectivity. [Pg.70]

Perhaps counterintuitively, there is evidence that electroconvulsive stimulation has... [Pg.82]

Effechve concentration in 10% of the population Effechve concentration in 90% of the populahon Electroconvulsive stimulation Exploratory data analysis... [Pg.176]

Repetitive TMS, unlike electroconvulsive therapy (ECT), uses sub-convulsive stimuli to treat depression. Compared to ECT, TMS has a potential to target specific brain regions and to stimulate brain areas thought to be primarily involved in depression while sparing areas like the hippocampus, thereby reducing the probability of cognitive side effects. However, the therapeutic efficacy of TMS as a treatment for depression is, unlike ECT, modest. Most TMS studies use high-frequency, fast stimulation (> 10 Hz) over the left dorsolateral prefrontal cortex, an area which has been... [Pg.36]

A second part consists of two chapters covering other somatic interventions, including complementary, alternative, and naturopathic medicine approaches (such as St. John s wort), as well as more aggressive treatments less commonly used in children and adolescents, such as electroconvulsive therapy (ECT) and transcranial magnetic stimulation (TMS). [Pg.251]

Grunhaus, L., Dannon, P.N., and Schreiber, S. (2000) Repetitive trans-craneal magnetic stimulation is as effective as electroconvulsive therapy in the treatment of nondelusional major depressive disorder an open study. Biol Psychiatry 47 314-324. [Pg.481]

Ebstein R, Belmaker R, Grunhaus L, et al Lithium inhibition of adrenaline-stimulated adenylate cyclase in humans. Nature 259 411-413, 1976 Ebstein RP, Hermoni M, Belmaker RH The effect of lithium on noradrenahne-in-duced cyclic AMP accumulation in rat brain inhibition after chronic treatment and absence of supersensitivity. J Pharmacol Exp Ther 213 161-167, 1980 Ebstein RP, Lerer B, Shlaufman M, et al The effect of repeated electroconvulsive shock treatment and chronic lithium feeding on the release of norepinephrine from rat cortical vesicular preparations. Cell Mol Neurobiol 3 191-201, 1983 Ebstein RP, Moscovich D, Zeevi S, et al Effect of lithium in vitro and after chronic treatment on human platelet adenylate cyclase activity prosreceptor modification or second messenger signal amplification. Psychiatry Res 21 221-228, 1987 Eccleston D, Cole AJ Calcium-channel blockade and depressive illness. Br J Psychiatry 156 889-891, 1990... [Pg.630]

Beedle D, Krasuski J, Janicak PG. Advances in somatic therapies electroconvulsive therapy, repetitive transcranial magnetic stimulation, and bright light therapy. In Janicak PG, Davis JM, Preskorn SH, et al., eds. Principies and practice of psychopharmacotherapy update. 2nd ed. Vol 2. Baltimore Williams Wilkins, 1998. [Pg.159]

Another source of evidence supporting the neurotrophic hypothesis of depression comes from studies of the direct effects of BDNF on emotional regulation. Direct infusion of BDNF into the midbrain, hippocampus, and lateral ventricles of rodents has an antidepressant-like effect in animal models. Moreover, all known classes of antidepressants are associated with an increase in BDNF levels in animal models with chronic (but not acute) administration. This increase in BDNF levels is consistently associated with increased neurogenesis in the hippocampus in these animal models. Other interventions thought to be effective in the treatment of major depression, including electroconvulsive therapy, also appear to robustly stimulate BDNF levels and hippocampus neurogenesis in animal models. [Pg.649]

Prolactin concentrations are very rarely altered during treatment with tricyclic antidepressants, but this is more likely to occur and to produce galactorrhea or amenorrhea with clomipramine and amoxapine and when there are other contributory factors that may stimulate prolactin secretion, such as stress or electroconvulsive therapy (1139). [Pg.652]

Szuba MP, O Reardon JP, Evans DL. Physiological effects of electroconvulsive therapy and transcranial magnetic stimulation in major depression. Dep Anx 2000 12 170-177. [Pg.148]

Considerable attention has been paid to the ultimate postsynaptic effects of increased neurotransmitters in the synapses. In tests of postsynaptic effects, cAMP concentrations have consistently decreased rather than increased, in spite of the presumably longer duration of action of the transmitters. In addition, the number of postsynaptic -adrenoceptors has shown a measurable decrease that follows the same delayed time course as clinical improvement in patients. Thus, the initial increase in neurotransmitter seen with some antidepressants appears to produce, over time, a compensatory decrease in receptor activity, ie, down-regulation of receptors. Decreases in norepinephrine-stimulated cAMP and in B-adrenoceptor binding have been conclusively shown for selective norepinephrine uptake inhibitors, those with mixed action on norepinephrine and serotonin, monoamine oxidase inhibitors, and even electroconvulsive therapy. Such changes do not consistently occur after the selective serotonin uptake inhibitors, 2 receptor antagonists, and mixed serotonin antagonists. [Pg.678]

Lamberg, L. (2007). Interest surging in electroconvulsive and other brain stimulation therapies. JAMA, 298, 1147-1149. [Pg.500]

Reddy TS, Bazan NG. Arachidonic acid, stearic acid, and diacylglycerol accumulation correlates with the loss of phosphatidylinositol 4,5-bisphosphate in cerebrum 2 seconds after electroconvulsive shock complete reversion of changes 5 minutes after stimulation. J Neurosci Res 1987 18 449 55. [Pg.143]

Hasey G. Transcranial magnetic stimulation in the treatment of mood disorder A review and comparison with electroconvulsive therapy. Can J Psychiatry 2001 46 720-727. [Pg.1283]

To date, two types of major depression have been postulated. The first is often referred to as endogenous or melancholic depression. In this type of major depression, symptoms of depressed mood are related directly to internal biologic factors such as neurotransmitter dysfunction (Kaplan Sadock, 1990 Tierney et al., 1997). Electroconvulsive therapy (ECT), referred to historically as shock treatments, is often considered an endogenous treatment. Here, direct (biologic) stimulation of the neurotransmission process is the treatment strategy. Similar to ECT, antidepressant medications also are successful in lifting endogenous depression, with the major difference that they affect the neurochemical pathways chemically rather than electrically (Maxmen Ward, 1995). [Pg.79]


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See also in sourсe #XX -- [ Pg.62 ]




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