Electroconvulsive therapy

Current Opinion in Psychiatry

Volumn 9, Issue 1, 1996, Pages 35-39

  Prudic, Joan ^a   Sackeim, Harold A ^b  

^a NEW YORK STATE PSYCHIATRIC INSTITUTE   (United States)

^b Columbia University ^*  (United States)

Author keywords

[No Author keywords available]

Indexed keywords

BIOCHEMISTRY; BRAIN; COMPARATIVE STUDY; DOSE RESPONSE; ELECTROCONVULSIVE THERAPY; HEART DISEASE; HUMAN; PHYSIOLOGY; RETROGRADE AMNESIA; REVIEW; RISK FACTOR; SEIZURE; STIMULUS; UNITED KINGDOM; UNITED STATES;

EID: 0030038947     PISSN: 09517367     EISSN: None     Source Type: Journal    
DOI: 10.1097/00001504-199601000-00007     Document Type: Review

References (27)

1. Thompson JW, Weiner RD, Myers CP: Use of ECT in the United States in 1975, 1980, and 1986. Am J Psychiatry 1994, 151:1657-1661. Data from the National Institute of Mental Health Sample Survey Program for 1975, 1980, and 1986, which included samples of inpatients in public and private general hospitals, and private, state, and county psychiatric hospitals, were analyzed. Use of ECT and clinical and demographic features of patients for whom ECT was prescribed are presented.
2. Kornhuber J, Weller M Patient selection and remission rates with the current practice of electroconvulsive therapy in Germany. Convulsive Ther 1995, 11:104-109.
3. Pike AL, Otegui J, Save G, Fernandez M: ECT: changing in Uruguay. Convulsive Ther 1995, 11:58-60.
4. Herman RC, Corwart RA, Hoover CW, Brody J: Variation in ECT use in the United States. Am J Psychiatry 1995, 152:869-875.
5. Lerer B, Shapira B, Calev A, Tubi N, Drexler H, Kindler S, Lidsky D, Schwartz JE: Antidepressant and cognitive effects of twice- versus three-times-weekly ECT. Am J Psychiatry 1995, 152:564-570. Fifty-two depressed patients were randomized to twice compared with three times weekly ECT and measured for response and cognitive side effects. Clinical response was similar in both groups at 1 week and 1 month, rates of response were faster in the three times weekly group and cognitive side effects were more prominent in that group as well.
6. Sackeim HA, Decina P, Kanzler M, Kerr B, Malitz S: Effects of electrode placement on the efficacy of titrated, low-dose ECT. Am J Psychiatry 1987, 144:1449-1455.
7. Sackeim HA, Prudic J, Devanand DP, Kiersky JE, Firzsimons L, Moody BJ, McElhiney MC, Coleman EA, Settembrino JM: Effects of stimulus intensity and electrode placement on the efficacy and cognitive effects of electroconvulsive therapy. N Engl J Med 1993, 328:839-846.
8. Weiner RD, Fink M, Hammersley D, Moench L, Sackeim HA, Small I, American Psychiatric Association: The practice of ECT: recommendation for treatment, training and privileging. Washington, DC: American Psychiatric Press; 1990.
9. Enns M, Karvelas L: Electrical dose titration for electroconvulsive therapy: a comparison with dose prediction methods. Convulsive Ther 1995, 11:86-93. Three methods for selecting electrical stimulus dosage, empirical titration, age-based dosing, and a formula based on age, sex, and electrode placement, were compared. The titration method resulted in lower variability in dosing relative to actual seizure threshold than the formula-based methods.
10. Simpson KH, Halsall PJ, Carr CME, Stewart KG: Seizure duration after methohexitone or propofol for induction of anaesthesia for electroconvulsive therapy (ECT). Br J Anaesth 1987, 59:1323-1324.
11. Maisch E, Gratz I, Mani S, Backup C, Levy S, Allen E: Efficacy of electroconvulsive therapy after propofol and methohexital anesthesia. Convulsive Ther 1994, 10:212-219. The authors randomly assigned 58 patients to either propofol or methohexital anesthesia. Although seizure duration was shortened with propofol, response rates and number of treatments were comparable in the two groups.
12. Fear CF, Littlejohns CS, Rouse E, McQuail P: Propofol anaesthesia in electroconvulsive therapy reduced seizure duration may not be relevant Br J Psychiatry 1994, 165:506-509. The investigators randomly assigned 20 patients to either propofol or methohexitone anesthesia in a prospective, double-blind study. Seizure durations were shorter in the propofol group but no differences in clinical response occurred.
13. Rice EH, Sombrotto LB, Markowitz JC, Leon AC: Cardiovascular morbidity in high-risk patients during ECT. Am J Psychiatry 1994, 151:1637-1641. The authors, using a case-control method, assessed the risk associated with ECT for patients with pre-existing cardiovascular disease by examining the medical complications in patients over 50 years of age undergoing ECT during a 1 -year period. Although the at-risk group had more minor complications during treatment, the two groups did not differ in the rate of major complications. No patient died or developed permanent cardiac morbidity.
14. Gerring JP, Shields HM: The identification and management of patients with a high risk for cardiac arrhythmias during modified ECT. J Clin Psychiatry 1982, 34:140-143.
15. Castelli I, Steiner LA, Kaufmann MA, Alfillé PH, Schouten R, Welch CA, Drop LJ: Comparative effects of esmolol and labetalol to attenuate hyperdynamic states after electroconvulsive therapy. Anesth Analg 1995, 80:557-561. In a randomized, within-patient study, the authors compared esmolol, 1.3 or 4.4 mg/kg, labelolol, 0.13 or 0.44 mg/kg, and no beta-blockers in a group considered at risk for complications of hyperdynamic states. No adverse effects, including changes in ST segments, were observed in any treatment group, including placebo treatment, even though patients at risk had been chosen for the study.
16. Sobin C, Sackeim HA, Prudic J, Devanand DP, Moody BJ, McElhiney MC: Predictors of retrograde amnesia following ECT. Am J Psychiatry 1995, 152:995-1001. Seventy-one depressed patients who had been randomly assigned to four ECT conditions underwent measures of cognitive side effects. The study found that global cognitive status before ECT, as measured by the modified Mini-Mental State Examination, and the duration of postictal disorientation were strong predictors of the magnitude of retrograde amnesia for autobiographical memory immediately and 2 months after ECT. These relationships were maintained regardless of the technical parameters used in the administration of ECT.
17. Khan A, Mirolo MH, Claypoole K, Bhang J, Copx G, Horita A, Tucker G: Effects of low-dose TRH on cognitive deficits in the ECT postictal state. Am J Psychiatry 1994, 151:1694-1696.
18. Stern RA, Whealin JM, Mason GA, Noonan LR, Silva SG, Arruda JE, Prange AJ: Influence of L-tri-iodothyronine on memory following repeated electroconvulsive shock in rats: Implications for human electroconvulsive therapy. Biol Psychiatry 1995, 37:198-201.
19. Devanand DP, Dwork AJ, Hutchinson ER, Bolwig TG, Sackeim HA: Does ECT alter brain structure? Am J Psychiatry 1994, 151:957-970 The evidence from neuropathological investigations regarding the possibility of alteration of brain structure by ECT was reviewed. Prospective computed tomography, magnetic resonance imaging studies, human postmortem studies, animal electroshock studies, using conditions comparable to ECT in patients and appropriate controls, blind ratings, and fixation techniques showed no evidence of any ECT or ECS-induced structural changes or neuronal cell loss. Other studies found that the passage of electricity, thermal effects, and the transient disruption of blood-brain barrier during ECS did not result in structural brain damage.
20. Coffey CE: The role of structural brain imaging in ECT. Psychopharmacol Bull 1994, 30:477-484.
21. Hofmann P, Gangadhar BN, Probst C, Koinig G, Hatzinger R: TSH response to TRH and ECT. J Affective Disord 1994, 32:127-131.
22. Clark CP, Alexopoulos GS, Kaplan J: Prolactin release and clinical response to electroconvulsive therapy in depressed geriatric impatients: a preliminary report Convulsive Ther 1995, 11:24-31.
23. Smith J, Williams K, Birkett S, Nicholson H, Glue P, Nutt DJ: Neuroendocrine and clinical effects of electroconvulsive therapy and their relationship to treatment outcome. Psychol Med 1994, 24:547-555.
24. Devanand DP, Shapira B, Petty F, Kramer G, Ritzsimons L, Lerer B, Sackeim HA: Effects of electroconvulsive therapy on plasma GABA. Convulsive Ther 1995, 11:3-13. This group presents the first evidence from two studies regarding the behavior of plasma GABA in patients undergoing ECT. The authors found that plasma GABA was reduced for about 1 h after ECT, and that patients with the highest baseline levels of GABA before and after the ECT course were the most likely to respond to treatment.
25. Malaspina D, Devanand DP, Krueger RB, Prudic J, Sackeim HA: The significance of clinical EEG abnormalities in depressed patients treated with ECT. Convulsive Ther 1994, 10:259-266.
26. Nobler MS, Sackeim HA, Prohovnik I, Moeller JR, Mukherjee S, Schnur DB, Prudic J, Devanand DP: Regional cerebral blood flow in mood disorders, III: treatment and clinical response. Arch Gen Psychiatry 1994, 51:884-897. Depressed and manic patients responding to ECT showed decreases in global and topographic cerebral blood flow in both the acute period and 1 week after the ECT course was completed. For depressed patients, acute decreases were greatest in frontal and anterior temporal areas, and patients with the greatest decreases, particularly in the anterior posterior gradient, were the most likely to be ECT responders. The pattern of cerebral blood flow change was affected by electrode placement, with bilateral ECT resulting in symmetrical decreases, whereas unilateral ECT produced decreases restricted largely to the right hemisphere.
27. 2 relaxation times and their relationship to cognitive side effects: a pilot study. Psychiatry Res 1994, 54:177-184.