Disease relevance of Electroconvulsive Therapy

• Effects of electroconvulsive therapy on mood, parkinsonism, and tardive dyskinesia in a depressed patient: ECT and dopamine systems [1].
• Repeated epileptic seizures and electroconvulsive therapy treatments produce successively less marked rises in serum HPR [2].
• We describe a case of status migrainosus precipitated by electroconvulsive therapy (ECT) that was refractory to treatment with triptan medications but which resolved with dihydroergotamine (DHE) [3].
• Propofol and electroconvulsive therapy in a patient at risk from acute intermittent porphyria [4].
• Esmolol reduces autonomic hypersensitivity and length of seizures induced by electroconvulsive therapy [5].

Psychiatry related information on Electroconvulsive Therapy

• Consistent with these findings, mood stabilizers such as lithium ion and valproic acid, which are used to treat bipolar disorder, as well as antidepressants and electroconvulsive therapy have recently been shown to activate interconnected intracellular signaling pathways that promote neurogenesis and synaptic plasticity [6].
• Serial 1-mg dexamethasone suppression tests with concurrent plasma dexamethasone assessments were conducted in 58 patients with endogenous depression treated with electroconvulsive therapy (ECT) [7].
• Influence of L-triiodothyronine on memory following repeated electroconvulsive shock in rats: implications for human electroconvulsive therapy [8].
• Dexamethasone in electroconvulsive therapy: efficacy for depression and post-ECT amnesia [9].
• The purpose of this study was to determine whether pindolol administration can induce a rapid improvement in depressive symptoms in patients receiving electroconvulsive therapy (ECT) within six ECT treatments [10].

High impact information on Electroconvulsive Therapy

• Propofol and electroconvulsive therapy [11].
• Plasma concentrations of oestrogen-stimulated neurophysin (ESN), prolactin, and growth hormone were measured before and after the first treatment in a course of electroconvulsive therapy (ECT) given to 25 psychiatric patients and during induction of anaesthesia in 9 women undergoing elective cholecystectomy [12].
• Electroconvulsive therapy and the brain: evidence for increased dopamine-mediated responses [13].
• The growth-hormone (GH) response to subcutaneous administration of the dopamine agonist, apomorphine (0.005 mg/kg), was assessed in 15 depressed patients at the beginning and at the end of a course of electroconvulsive therapy (ECT) [13].
• The Northwick Park electroconvulsive therapy trial [14].

Chemical compound and disease context of Electroconvulsive Therapy

• Patients were divided into four treatment groups based on primary mode of therapy during index admission; the groups included electroconvulsive therapy, adequate lithium carbonate, inadequate lithium carbonate, and neither treatment [15].
• Serial dexamethasone suppression tests and plasma dexamethasone levels. Effects of clinical response to electroconvulsive therapy in major depression [7].
• Eleven of the 18 depressed patients were restudied during clinical remission following either electroconvulsive therapy or treatment with amitriptyline hydrochloride [16].
• METHODS: We assessed cortical blood flow with the xenon 133 technique in depressed patients prior to a course of electroconvulsive therapy (ECT), 30 minutes before and 50 minutes after a single treatment, and during the week following ECT [17].
• Electroconvulsive therapy is still considered to be the treatment of choice for severe depression, whereas the combination of low doses of phenelzine and amitriptyline are ineffective [18].

Biological context of Electroconvulsive Therapy

• CONCLUSIONS: Electroconvulsive therapy is not likely to induce hippocampal atrophy or cell death, which would be reflected by a decrease in the N-acetylaspartate signal [19].
• Succinylcholine drug interactions during electroconvulsive therapy [20].
• Implications: Oral clonidine (0.2-0.3 mg) decreases the acute hypertensive response after electroconvulsive therapy; however, this antihypertensive effect was achieved by decreasing the blood pressure before the electrical stimulus [21].
• With recent emphasis on stabilisation of heart rate in preference to blood pressure in at-risk cardiac patients, our study suggests that, in the doses selected, esmolol is preferred to nitroglycerin to control the heart rate response to electroconvulsive therapy [22].
• Recovery from depression after electroconvulsive therapy is accompanied by evidence of increased tetrahydrobiopterin-dependent hydroxylation [23].

Anatomical context of Electroconvulsive Therapy

• In severely depressed patients before and after electroconvulsive therapy (ECT), we measured cerebrospinal fluid (CSF) NE, plasma NE, plasma epinephrine (EPI), and plasma cortisol hourly for 30 h [24].
• Effect of electroconvulsive therapy on erythrocyte adenosine triphosphatase activity in depressive illness [25].
• The comparative effects of propofol versus thiopental on middle cerebral artery blood flow velocity during electroconvulsive therapy [26].
• Treatment of endogenously depressed patients with tricyclic antidepressants, lithium salts or electroconvulsive therapy results in a decrease in the number of alpha 2 adrenoreceptors on blood platelet membranes [27].
• Management for electroconvulsive therapy of a patient with inoperable coronary artery disease and ankylosing spondylitis [28].

Gene context of Electroconvulsive Therapy

• Effects of single and repeated electroconvulsive therapy sessions on plasma ACTH, prolactin, growth hormone and cortisol concentrations [29].
• Plasma melatonin was not affected by electroconvulsive therapy, TRH-injection, L-Dopa or bromoergocryptine orally [30].
• Effects of electroconvulsive therapy on neuropsychological function and circulating levels of ACTH, cortisol, prolactin, and TSH in patients with major depressive illness [31].
• While the patient showed a marked decrease of cortisol and ACTH secretion during the DEX/CRH test within one week, a pronounced and ongoing deterioration of depressive symptoms with suicidal thoughts occurred that was resistant to antidepressant medication and had to be treated with electroconvulsive therapy [32].
• RESULTS: Electroconvulsive therapy produced a marked short-term increase in delta and theta power [33].

Analytical, diagnostic and therapeutic context of Electroconvulsive Therapy

• Also, antidepressants, mood stabilizers, electroconvulsive therapy, and GABA agonists have been shown to reverse the depression-like behavior in animal models and to be effective in unipolar and bipolar patients by increasing brain GABAergic activity [34].
• Repetitive transcranial magnetic stimulation is as effective as electroconvulsive therapy in the treatment of nondelusional major depressive disorder: an open study [35].
• The dramatic rise in pancreative polypeptide observed following electroconvulsive therapy probably results from vagal stimulation and reflects insufficient atropine premedication [36].
• The present report notes that systemic lupus erythematosus should be considered among possible causes of catatonia and shows that plasma exchange could be an efficient treatment option for such neuropsychiatric manifestations of systemic lupus erythematosus, to avoid the use of electroconvulsive therapy in young patients [37].
• Seizure duration in unilateral electroconvulsive therapy (ECT) was recorded by means of EEG in an intraindividual comparison under different alveolar O2- and CO2-concentrations [38].

References