electro convulsive therapy apa

8/12/2019 Electro Convulsive Therapy APA

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askorce portsThisis the fourteenthin aseriesofreports approved by the BoardofTrusteof the American Psychiatric Association to give wider dissemination to thfindings ofAPA's ma ny com missions, committees, and task forces that acalled upontoevaluatethestate ofthe art in aproblem areaofcurrent concetotheprofession,torelateddisciplines, and to thepublic.The findings, opinions,andconclusionsof the report do not necessarirepresent the view s of theofficers, trustees, or all mem bers of the AssociatioEach report, however, does represent thethoughtfuljudgmen t andfindings


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THE AUTHORS andTASK FORCE MEMBERS

FredH.Frankel, M.B.Ch.B., D.P.M. ChairpersonDepartment of Psychiatry, Beth Israel Hospital and Harvard MedicaSchool,Boston,Mass.T. George Bidder, M.D.Department ofPsychiatry,UCLASchoolofM edicineand SepulvedVA Hospital, Los Angeles, Calif.MaxFink, M.D.Department ofPsych iatryandBehavioral Science, SchoolofMedicin


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ACKNOWLEDGEMENTSThe Task Force gratefullyacknowledges the advice, assistance, consultation andcontributionsof the following:

GregoryAsnis,M.D.H.RichardBeresford,M.D.David Boehm, B.A.RosmaryKrispinsky Cheesman, R.N.N.Jeanne Cooper, L.P.N.JaneE. EdgertonTheodore W.Lorei, M.S.W.DorisT.Pearsall, M.A.Psychotherapy Institute and Continuing Education Program


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INTRODUCTION

This report on Electroconvulsive Therapy contains few simple solutions. We will be pleased if it helps to lead to a rational perspective.Anexamination of the published literature since the early 1940reveals the mixed reception accorded ECT since its introduction i1938. Attitudes surrounding it capture the essence of the strugglbetweenthe rival philosophical approaches toemotional andmentaillness,namely the psychological, the biological, and the social.Webelieve that what follows in this report affirms that the lawordhas yet to be written on the etiology and treatment of psychiatri


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(h) comparable treatments with flurothyl;(i) associated cerebral and behavioral events; j) induced seizures andconvulsive shockinanimals.(2) Report its conclusions regarding the benefits of ECT irelationto the risksinvolved.(3) Describethe indicationsfor its use and the contraindications(4) Makerecommendations regarding:

(a) general clinical considerations;(b) pretreatment investigationsandprecautions;(c) the use ofanesthesiaandrelated measurestoreduce thdangersoftreatment;(d) techniques with reference to apparatus, schedules oadministration including those of multiple and singltreatments, appropriate numbers oftreatments, locatio


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ELECTROCONVULSIVE THERAPeffectiveness; thesedata were toprovide the context withiwhich to consider the questions raised in the mandate;(3) an open forum for the discussion of ECT at the annumeeting in 1976. As not more than 20% of the membershiwould bepolledin thenational survey,anopportunitywas be provided formembers generally toreport on their viewand experience to the members of the Task Force if they swished. Announcements in Psychiatric News extended ainvitationto themembershiptoarrangefor anappointed timat which they could address the Task Force. Twenty foindividuals had anopportunitytocommunicate personallythiswaywiththecommittee. Invitations were extended tofew highly experienced clinicians to share their views witus,aswellas to twocolleagues inneurology knowntoholstrongviews against the use ofECT.A few ofthese peop


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TaskForce Report14social,ethical andlegal aspectsofECT;trainingandeducation;areas requiring further study;recommendations.The recommendations are presented at the conclusion of th

report. Those interested primarilyinthat sectioncanproceed directltoit,referringto thesupportive dataof theindividual chaptersasthesee fit. Others might prefer to become acquainted first with threasoning in the sequence of the chapters. The recommendationhavebeen carefully considered indetail by all the membersof thTask Force. Our wish to avoid restrictions on clinical practice wamorethan balancedby ourrecognitionof the fact thatatthis time iourhistory where the profession fails toprovide its own guidelinethey will be created by others who may be less well-equipped to d


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CHAPTER IA SURVEY OF THE AMERICANPSYCH IATRIC

ASSOCIATION M E M B E R S H I P O N T H E U S E O FELECTROCONVULSIVE TH ERAPY

In the process of developing its position on ECT, the Task Force fthat it would be useful to obtain systematically solicited input frothe membership of the American Psychiatric Association (APA) rgarding their attitudes toward and experiences with this treatmemodality.


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TaskForce Report14exclusive of Members-in-Training (residents), Inactive and Corrsponding Members and Fellows, and Honorary and DistinguisheFellows. Some response was received to 3,049 (76%) ofthese quetionnaires.Inadditiontopartially completedandlate questionnaireresponses were received saying that membershaddied, weretoo ill tpractice, had had norecent experience with ECT, etc. Questionnairdatafor2,973 members (74.1%of thetarget sample) were punchedodata processing cards and are included in the analysis reported hereJudgedby theusualexperienceinmail survey research, the responsrate must be considered excellent despite the length of the questionnaire.Twofollowupmailings ofthequestionnaire were madetothoswhohad not already responded.Questionnaire

A fixed alternative questionnaire of 140items on 12pages w


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ELECTROCONVULSIVE THERAPY

"Granting thatthe question is agross over-simplification, whicof the following best characterizes your attitude toward the use oECT"Obtained response

1.Totally opposedto its use 2%2. Generally opposed,butO.K.as alastre-sortin a few selected instances 22%3. Noreally strong feeling,but tend to be

moreopposed than favorable 8%4. Ambivalent; undecided 1%5. Noreally strongfeeling, but tend to be

more favorable than opposed 6%6. Generally favorable for appropriatepatients 54%


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Non-Userson all the attitude items listed above, in each case in thdirection that wouldbe expected. Thus, forexample, Users agreelessoftenthan did Non-Users that "ECT should be used only when aelsehas failed."

Techniques of AdministrationThequestionnaire contained items dealing withthe use ofanethesia, muscle-relaxant drugs, type of machine, current used, anseveral other technique-related issues. Of the Users, 95%reportegenerally usinga short acting anesthetic drugbefore administerin

ECT; 60% of these reported having had formal training in sucadministration. Sixteen percent reported never usingthe servicesoananesthesiologistornurse anesthetist, while59%always used suc


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nance ECT. However, the number of patients being continued oECT wasrelatively small, averagingout to 6% of all ECT patients streated. W hen the average was recomputed excluding those who dinot use maintenance ECT, it rose to 16%.That is, for those psychiatristswho reported usin g ma intenance ECT at all, they reported usinitfor16% oftheirtotalECTp atient load.Themost common scheduleformaintenanceE CTwere onceamon th (41%)and nofixed schedul(38%).Opinions aboutthecombineduse of ECT andpsychoactive drug(antipsychoticagentsand tricyclic antidepressant drugs) were distributed as follows:

Psychoactivemedication. . .Shouldalmost always be stopped 8%


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sion onAccreditationof Hospitals and that, on the average,72% ECT treatments were paid for by insurance companies.Selectionof PatientsReasons for Use

It is difficult to write good items about, or for that matter frespondentsto explicitly formulatetheirreasonsfor the use ofECThis caveat notwithstanding, it will be seen that useful informatiwas obtained regarding stated reasons for ECT use. The followiquestionset wasposed separatelyforschizophrenic patients, patienwith major depressive illness, and patients with minor depressiillness.Theresponse categories andaverage percentages fo rthethrdiagnostic groups wereas follows:


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Medication in large dailydosages (atleast 1000 mgofchlorpromazine, 300 mgof imipramine or theirequivalent) wastried andfound ineffective 167 309 64

Medication in smaller dos-ages wastried and foundineffective 68 104 29Patientwasallergictomedi-cation and/or medication


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fellinto eachof 11categoriesofpathology. These categories, rankeby the average percentages, wereas follows:Majordepressive illness 77%Schizophrenia 17%Minordepressive illness 5%Manicexcitement 3%Unremittinghypochondriasis


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Schizo- Major Minorphrenia Depression DepressionExcellent response 24% 62% 32%Goodresponse 42% 37% 29%Fair response 31% 13% 24%Poorresponse 13% 6% 7%Verypoor response 1% 1%


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CHAPTER IIEFFICACYOF ECT

IN AFFECTIVE DISORD ERSAND SCHIZOPHRENIA

IntroductionFollowingits introduction in the late1930sbyCerlettiand Bini, ECsoon became a standard somatic therapy for severe psychiatric i


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respond to drugs will specifically respond to ECT(2,11,12),althouga specific ECT response in schizophrenia is not so clear.Manystudihave compared the efficacy of drugs and ECT in depression anschizophrenia,andthese willbe reviewed. However,noclear agrement hasbeen reached concerning when in the course of therapECT should be employed or if and when it should be preferred tdrugs. In this discussion, the evidence forefficacy of ECT in majaffective diseaseandschizophrenia willbereviewed, withanemphsison the role of ECT in and its pertinence to contemporary antidpressant and antipsychotic treatment.

Efficacy ofECT:Affective IllnessIn addition to the basic question of antidepressant efficacy, oth


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performed in the 1960s all demonstrated the efficacy of ECT (2, 1113-21). Actually,inmanyofthese, ECT waspresented as the antidepressant standard against which the drugs were to be measured. Aexample of this approach is the work ofGreenblatt, et al (2),whcompared an MAO inhibitor (phenelzine), a tricyclic antidepressan(imipramine), and ECT in matched groups of manic-depressiveschizophrenics (schizoaffective type), involutional psychotic reactions,andpsychoneurotic reactions. Overall,ECT wasshownto besuperior antidepressant treatment for depressed patients diagnosed amanic-depressive and involutionally psychotic. Standard rating scalewere employed in this study within a blind research design angenerally adequatedosagesofmedication (200mg. per day ofimipramine;45 mg. per day ofphenelzine) were used. ECT wasfoundbe effective in 78% of the more severely depressed sample in thstudy, compared to 59% effectiveness of tricyclic drugs. Signs an


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equal to antidepressants, and, in most cases is a more effectivtreatment (14-18). Some comparison studies do showno differencbetweenthe twotreatments (19-21).It issomewhatdifficult toassestwo of these studies by McDonald and Wittenborn because thsamplesaresmall.In the third studybyKristiansen interpretation imade difficult because the drug groupwasanalyzed prospectivelywhereas the ECTgroup data were gathered by aretrospective chareview method.Atthis point, it might appear that ECT is abettertreatment and could be argued that it should be used as preferential treatment. Yetoverthe past 15 years it has become clearthatthe tricyclic drugs alshave proven efficacy in severe depression. Recent reviews, suchathatby MorrisandBeck (8), concludethatthe tricyclicsare effectivin 66% ofdepressions. Drugs have advantagesinthat theyareeasietoprescribe,are lesscontroversial,and are more readilyacceptedb


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In summarizingthecomparison studies,ECT emergesas avereffective antidepressant treatment.It issometimesdifficult todecidwhether ECT or antidepressant medication is the bestinitial treament forsevere depressive illness sincetheantidepressants have alsshown clear efficacy for many similar patients. However, theresome evidence that certain depressed patients will respond onlytECT and not toantidepressant drugs.II. Outcome Studies

Anotherapproach to the definitionofefficacy of ECT is by tstudyof thecourseofpatients treated with this therapy. Early clinicstudies of ECT outcome conducted in the 1940s and 1950s (27-3were generally "open" trials (lacking matched control groups anblind evaluationsofprogressandoutcome)andtherefore anecdotaloat times, frankly impressionistic. During this early period patie


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found to suggest that ECT alters the long-term course or naturahistory ofaffective illness. Like the antidepressant medications, ieffects appear limited to areductionofsymptomsof the illness (15However it mightbe argued that work such as that by Avery anWinokur (32) does suggest alteration of the natural course of thaffective illness since more ECT-treated patients survived.Whereas exacerbations of depressive episodes diminish durinlongerterm administrationoftricyclics (40)andperhaps lithium (41the efficacy ofmaintenance ECT has not been supported by controlled studies although it may perhaps have some usefulness ipatients who do not tolerate even small amountsofdrugs. Maintenance studies comparing ECT to tricyclics and combinations o

tricyclics and antipsychotics are needed, especially in groups opatientssuchas theelderlywho do notappeartotolerate medicationwell. There is some evidence that adjunctive use ofmedication


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ifested "euphoria and hypomania" were more often evaluated arecovered or improved. Conversely, patients who were "introspective, impassive, non-stereotyped, native-born, better educatedyounger" and who manifested"somatization, paranoid withdrawaandpanic" tendedto beratedasunimproved,orworse.Therelevancto contemporary antidepressant practice of this type of study, peformed priorto the introduction ofantidepressants, isunclear. Thitemsdifferentiatingrespondersmayalsobeforecastersofresponsetdrugs.The descriptive studies are closely related to a series of prediction ofresponse studiesperformed over the past 20 years. Varioumethods have been described for prediction of response to EC(44-48). These calculate a "prediction index" based on presenclinical state and life history. Reported success in predictintreatment-responsive patients varied from 60-85% in these studie


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bilateral ECT appeared to be equivalent in efficacy. Follow-studies from one to 12monthstoevaluate the stability ofantidepresantefficacyshowed unilateralECT aseffective asbilateral ECT(555,58, 61,65).D'Elia and Raotma also reported that patients subjectively rported the same feeling of improvement with unilateral ECT bilateralECT andtheyconfirmed anearlier findingof Stromgren(6that severe depressions respond as well with unilateral as witbilateral ECT. These researchers also commented on some populmisconceptionswhichmayhave contributedto the ideaofunilaterECTbeinglesseffective than bilateral ECT, including submaximseizures (missed seizuresdue to inadequate stimulationandfailuretheseizure activitytospread acrossthecentrencephalicregion). Theconcluded that non-dominant unilateral ECT has the same antidepressant effect asbilateral ECT; and that in endogenous depressio


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intheaverage patient, theTask Force recognizes thatthe individupsychiatristis in themost advantageous positiontodecidewhichis thbest modeof ECTadministrationfor anyparticular individual patienOurreport simply attemptstobringtogetherthevariousfactorswhicneedto be considered inmaking this complex decision.V. Additional Clinical Considerations and SummaryAlthoughsome research suggests that patients treated adequatewith tricyclicsmay dojustaswellonstandard clinical ratingsasECTtreated patients (26), it may also be true that severely depressepatients demonstrating endogenous featuresdo notalways respondeven high dosesoftricyclics(2,11-13).Asignificant numberofthesedrespondto ECT(11,49).Sincetheonsetof thetricyclic antidepressaeffectmaytakeaslongasthree weekstooccur,patientswho areseveresuicidal, debilitated, agitated, orhomicidalmayalsoqualify ascand


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selection criteria were unclear, and samples were probably biasedFor instance, the series of reports by Baker, et al (71-73), whiccompared ECT with chlorpromazine, used patients from urbanhighly mobile, low socioeconomic backgrounds and specified thachlorpromazine was not useful fo rthis population because patienoftendemonstrated poor medication compliance following hospitalzation. Long-acting phenothiazines may be more useful with sucpatients (74), but no recent studies were found which comparelonger-term follow-upof matched groups treated with either ECT olong-acting phenothiazines.In the early1960s,a number of reports appeared which demonstrated no significant difference between ECT and antipsychotdrugs (75-77). Several reviewsatthis timefoundlittleproofofbeneffrom ECT in schizophrenia and heavily criticized statistical andesignissues inprevious studies(78, 79).


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attitude was also found amongthe psychiatrists who answered thquestionnairedistributedby this Task Force. As can beseenfrom thfindings of the questionnaire (see Chapter I), most United Statepsychiatrists use ECT for schizophrenic patients only when thehave failed torespondtoother treatment modalities.Yet some evidence exists showing that ECT may be a vereffectivetreatmentinsomeformsofschizophrenia. MurilloandExnehave reported the use of"regressive"ECT in agroupofchronico"process" schizophrenics with apparently good results (84). Thestudied schizophrenic patients treatedwith an average of 26.3 treaments and compared outcome with a matched group treated witantipsychoticdrugsand psychotherapy.On allmeasuresofoutcomincluding self-report, psychological tests (MMPI and Self FocuSentence Completion), relatives' reports as measured by the KaAdjustmentScale,andreferring therapists' reportsasmeasuredby th


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features, ifpresent, in these patients usingthefirst-rank symptomsSchneider (88, 89). Theyfoundthat schizophrenia features alone wepoor predictors ofoutcomein their patients, while eventhe presenofonly one affective feature was abetterforecasterofimprovemethanaschizophrenic diagnosis. Almostallschizophrenic patientswhimprovedhadaffective featuresandrespondedtoapproximately eigtreatments; the authors mention that many of the patients werediagnosedasschizo-affectiveemphasizingtheaffectivenatureof tdisorder.In regard to the efficacy of unilateral ECT in schizophrenseveral studies have been reported but the data are insufficientpresent to allow objective review (57, 90, 91). A recent study bReichert, et al,(57) concluded that both bilateral andunilateral ECwere very effective in the relief of global pathology and specifsymptomsassociated with schizophrenia. However, their samplew


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ELECTROCONVULSIVE THERAPY5. CostelloCG Christensen SJ,Bobey M,etal:The relationship of illneand non-illness variables to the administration of ECT. Can PsychiatrAssocJ 17: 325-326, 19726. JonesJE:Non-ECT. World Medicine9: 24, 19747. Frankel F: Task force report on ECT in Massachusetts. MassachusetJournalofMental Health3:2, 19738. Morris JB,Beck AT: The efficacy ofantidepressantdrugs: Areviewresearch 1958-1972.ArchGen Psychiatry30:667-674, 19749. Klein DF, Davis JM: Diagnosis and Treatment of Psychiatric DisorderBaltimore,WilliamsandWilkins, 1969, pp 187-29810. May PRA: Treatment of Schizophrenia. NewYork, Science House, 196811. Medical Research Council: Clinical trial of the treatment of depressivillness.Br Med J5439:881-886, 196512. Glassman A, Kantor SJ, Shostak M: Depression, delusions, and druresponse. Am J Psychiatry 132: 716-719, 197513. Wilson1C, VernonJT, Guin T, et al: A controlled study of treatments odepression.JNeuropsychiat4:331-337, 196314. BratfosO,HaugJO:Electroconvulsive therapyand antidepressant drug


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TaskForce Report14hospitalized endogenousandneurotic depressives. ArchGenPsychiat33: 1093-1102, 197627. BennetAE: Anevaluationof the shock therapies. DisNerv Syst6:20-2194528. HustonPE, LocherLM:Involutionalpsychosis: Course when untreatandwhen treated with ECT. Arch NeuroandPsychiat59:385-394,19429. Fishbein IL:Involutional melancholiaandconvulsive treatment. AmPsychiatry,106: 128-135, 194930. Bond ED: Results on treatment in psychoses. Am J Psychiatry 11881-883, 195431. KaragullaS:Evaluationof ECT ascompared with conservative methooftreatment in depressive states.JMentSci96:1060-1091, 195032. Avery D, Winokur G: Mortality in depressed patients treated wielectroconvulsivetherapy andantidepressants. ArchGenPsychiatry31029-1037, 197633. Sainz A: Clarification of the action of successful treatments in tdepressions.DisNerv Syst20:53-57, 195934. OttossonJO: ECT ofendogenous depression: Ananalysisoftheinfluen


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ELECTROCONVULSIVE THERAPY49. MandelMR,WelchCA,MieskeM, etal:Prediction ofresponse to ECin tricyclic-intolerant or tricyclic-resistant depressed patients. McLeaHospital J 2: 203-209, 197750. Bielski RJ,Friedel RO: Prediction of tricyclic antidepressant responsArchGen Psychiatry 33: 1479-1489, 197651. Pacella BL,Impastato DJ: Focal stimulation therapy. Am J Psychiat110: 576-578, 195452. Lancaster NP,SteinertRR, Frost I: Unilateral electro-convulsive therapJMent Sci 104: 221-227, 195853. Cohen BD, Penick SB,Tarter RE: Antidepressant effect of unilaterECT. ArchGenPsychiatry 31(5): 673-677, 197454. d'Elia G: Unilateral electroconvulsive therapy. Acta Psychiat Scan(Suppl)215, 197055. HallidayAM,DavisonK,BrowneMW , et al: Acomparisonof the effecon depression and memory of bilateral ECT and unilateral ECT to thdominant and non-dominant hemispheres. Br J Psychiatry114:997-101196856. Sutherland EM, Oliver JE , KnightD: EEG, memoryand confusion


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Task Force Report 14Thepurposeofthis chapteris toreviewtheliteratureof ECT usand efficacy in treating mentally ill patients other than those dianosed asschizophreniaoraffective disorder.

Reports andEstimates of ECT Use in NonpsychotiDisorders(SeeTables I-VIat the end ofthis chapter)APArecentlypolledasampleofmembers thoughtto berepresetativeof the whole group.As can be seeninTableI, themajoritythose respondingto the questionnaire (2973of4000 polled) thoug

thatECT isprobablynotappropriate ortotally inappropriate for use mental illnesses other thanaffectivedisorderorschizophrenia. Onlysmallnumber, 29 to 136(answer range depends upon the questio


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ELECTROCONVULSIVE THERAPneurosis. Tien'ssmaller Michigan survey (10) noted muchthe sampattern.A fewprivate practitioners withanatypical approachto ECtheory and therapy, as typifiedby Friedman (11), used ECT on variety ofneuroses, especially theobsessive compulsiveor phobtypes.Asurveyof ECT use inDenmark(April1972toMarch 1973) (1revealedthat18.8percentofdepartmentsofpsychiatry surveyedusECTforobsessive compulsive neuroses,depressiveneuroses, and thsymptomaticpsychoses.Areview ofToronto, Canada, hospitals duing 1969 to 1973 (13) reported 28 per cent of patients receivinECT had neurotic depressions. The authors believed, but did nodemonstrate,that patients with neurotic depressions wereoftengiveECTbecause ofsuicidal attempts.Fromthese incomplete data,itappears thatECT is and hasbeefairly widely used in the practice of psychiatry for patients wit


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TaskForce Report14the major tranquilizers and lithium. For these reasons, only the coideasofmostof thepapersareextractedand anypositive results mubereviewed with great care (16,17, 18,19).A. ECT inPatients with Organic Brain Disorders

This section is important because of therapeutic andtheoreticimplications. It is also even more controversial than other portions othis report. A short introduction is in order. Firstly, because of thdisputes about ECT causing an organic brain disorder, many wouconsider itstrange to use it for the treatmentof anorganic brain diorder (20, 21, 22). However, as Cunningham (23) has pointed ouit is the considered opinion of some psychiatrists that ECT han important place in the treatment of the more seriously diturbed patients suffering from psychiatric disorder, a category thcertainly includes the organic brain disorders. Secondly, althoug


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ELECTROCONVULSIVE THERAPYphetamine psychosis (40), barbiturate intoxication (34), delirium dutotetraethyl lead (41), cannabis (42, 43), and LSDpsychosis (44,446). Muller's paper (46) surveyed the use of ECT in LSDpsychosinoting particularly thatthethree caseshereporteddid notrespondtmore conventional drug therapy or to psychotherapy. Muller folowed each of these three cases for a year. One interesting report itheFrench literature (47) toldof thedevelopmentof astuporous stawith delirium and hallucinations, probably induced by a monoaminoxidase inhibitor drug given for the treatment of depression, thpatient recovering with ECT.Epilepsy has also been treated with ECT. In an early woCaplan (48) noted that psychotic patients undergoingECT who haepilepsy often seemed to have fewer seizures while they werreceivingECT.Wolffs work(49)was in asimilar vein.Mostclinicianfeel that ECT on the whole tends to decrease spontaneous seizure


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TaskForceReport 14disorder and the degree of physical integrity of the human body. It ihard to describe this interaction or to understand or predict tharticulated effects, among other factors, ofdynamics, physical illnesexternal circumstances,andpsychiatric treatment. Blachly (55) commented on this in his paper comparing ECT with cardioversionCarlsson (56),in arecentacademic lecture,noted thatthedrugs usetoalter moodandbehavior alsomaychange such bodilyfunctionsaheart rate, itsregularity,andliverandkidney action.Another facet ofthis articulation wasexpressed by Goldfarb(5whoheldtheopinion that breast cancer,inparticular,wasassociatewith grief subsequent to alossorfrustration. Forthis reason,heuseECT on three women with breast cancer. All three experiencepositive cancerocidal effects although in one case they were shorlived.Hethought that further investigations were warranted.In lupus erythematosus, Guze (58) reviewed 101consecutiv


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TaskForceReport14interfere with immunosuppressivedrugs. These affectivepsychosedid not tend to recurafterthe ECT induced remission.The papers in this section are uncontrolled and often retrospetive. In the main they are case reports and any positive results must bconservativelyevaluated. The short section on interaction with physcalillnessisincluded tostressthegreat clinical complexities encountered and the knowledge and judgment required to make serioumedical decisions when few hard data are available. Mention is madofthepractical problems that arisein thetreatmentof thementallyiwhen both mind and body require care.C. ECT forPatients with Neuroses

Practicing psychiatrists have used ECT for years in the depresion, hysterical, phobic, and compulsive neuroses. To a smallextent, they have used it in the anxiety neuroses. In the main,


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ELECTROCONVULSIVE THERAPYSome reports gave more positive results. Grief reactions, espciallyunresolved, were reported as responding well to ECT (95, 997,98,99). Edwards (33) reported dramatic successin the treatmentsevere hysteria with ECT. Hisnote also reviewed the literatureansuggested a method of treatment. In 1966, Sargent, etal(100) reporteunusuallygood resultsin thetreatmentofchronic tension states usinantidepressantdrugs, narcosis,andECT. Seventy-three patients werstudied for five monthstothree years. Thirty-seven received drugand ECT; and 36drugs, ECT, and continuous narcosis. Forty-ninwere symptomfree at follow-up. The ECTnarcosis grouphadonlthree referredforleucotomy comparedto 15 for the other group. Hwasnot at that time able to explain his unexpected results.Folstein, et al (101) reviewed the charts of 118 patients whreceived ECT. Patients withafamilyhistoryof mooddisorders, suicidor symptomsofhopelessness, worthlessness orguilt improved aft


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ELECTROCONVULSIVE THERAPYdiffering types of schizophrenic diagnoses. Eight received electroshock therapy, while five received electroshock therapy plus insulincoma.Thenumberoftreatments variedfrom two to 16. Theagesothepatients werefromsevento 14.They, too,did notbelieveECT hasignificantor long lasting value. On the other hand they thought did noharm.Arajarvi, et al (117) reported astudy ofpsychoses in childhoowith one case of childhood schizophrenia receiving electroshock. Thlong-termresults were equivocal. Thisworkreviewedall the childreseen between 1952 and 1960 at the neurological and psychiatrclinics of the UniversityofHelsinki.In the American literature, the most prolific writer has beeLauretta Bender (110, 111, 112). For many years she followed hschizophrenic children for a longitudinal view of personality dvelopment.Shestatedthat inschizophrenic childrenthe use of EC


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Task Force Report14ECT or ECT combined with drugs might help to end the proceearly.The existence of a catatonic state with hyperpyrexia is one verspecific indication forECT.Thecondition isconsidered one ofhigrapid mortalitybutalmost instantly reversible withECT(118). Raine(119) advocates stricter rulesfordiagnosis,EKGstudies(anincreasetheQTinterval), and the use of i.v. cortisone and phenothiazines, combined with ECT. Recently Shader (120), too, suggested the useofECtocalm violent schizophrenics.C. ECT in Patients with Psychoses other than Thought Disorders Affective Disorders

On the borderline of schizophrenia and depressive disorder athe problems ofschizo-affective disorders, thecycloid psychoses,the schizophreniform, psychogenic, or atypical psychoses. Many


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ELECTROCONVULSIVE THERAPYimpairingofmemoryand its range extended diagnostically. Blachand Gowing (128), with an updated, specially designed low energmachine, have evolved the multiple monitored mode of treatmenThey think this technique reduces the time required fortreatmendiminishes theusual side effects,andenhancesthetherapeutic effecOthers (129) have not always replicated the results. For similreasons,Weaver,etal(130) have workedinthis area too, designingaexperimental ECT machine. They and others are studying in a controlled methodeffects ofcurrent intensityasrelated tomemory losOthers, such as Reiter and Freidmen, recommended that thReiter stimulating machine be used with various types of unidrectional currents and considerable alterations in the placementsoelectrodes. It is their opinion that almost any diagnostic groupopatients can be treatedwith this machine, generally after failureodrugs and psychotherapies. For the most part the subconvulsiv


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Task Force Report14thanthe affective disordersor theschizophrenias. Thisconflictexisin the context of the larger problem of what is the risk-benefequation of ECT. Some ask, "Even if the risk-benefit equatiobalances in the direction ofhelpforthe patient, should ECT be useat all?" Further, how can ECT be used in non-affective or noschizophrenic conditions on such slim indications when we have noanswered to satisfaction the issue of amnesia and the topic of iformed consent?It hasbeen estimatedfromavailable data that15 to 30 percentpatients treated in this country with ECT are not diagnosed adepressed orschizophrenic. The APAsurvey doesnot support thestimateand indicates thatone to five per centofcase loads receiingECT are diagnosed neurotic. It appears that the use of ECT private hospitals may be declining, probably due to social pressureand the development of new treatments. Both Aden and Blach


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ELECTROCONVULSIVE THERAPYFor adults in life threatening situations, especially fulminatincatatonia, ECT can be considered invaluable. But again not apsychiatrists agree and controlled studies are lacking. Data for thuse of ECT in the schizo-affective psychosesare notcompellingbbetterthan formany areasandcomefromdiverse sources.It is notpossibletoconsiderECT usewithout studyinghow it used. Different currents, machines, electrode placements, modifictions, and ancillary treatments are thought to effect the outcomeotreatment. It ishoped that more controlled studies suchasthoseoAbrams and Taylor (133), d'Elia and Raotma (134). Lewis anMcKinney(132), Weaver,et al (130),andothers will cast more lighonthematter.The weight of the research data in the published literaturleaves little room fordoubt that ECT is an effective and valuabtreatment insome types ofaffective disordersandprobably effectiv

TABLE I


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APA SurveyPsychiatrists'Opinions

Indicationsfor ECT

ResponseRatingTotally

Appropriate1ProbablyAppropriate2 Ambivalent3

Probably No tAppropriate4TotallyInappropriate5

OpposedtoE CT6INDICATION

MinorDepressive DisorderDrug and Alcohol AbusePersonality DisordersSexual DysfunctionAnorexiaNervosaIntractable PainUnremitting HypochondriasisToxicDementiaOther

N

292429712922292291629122922915432

MEDIANRESPONSES(1-6)4.764.784.854.904.084.194.104.782.70

(SeeApp.II, Questions 20-31)


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TABLE

APASurveyOn the Use of ECT inNon-psychotic DisordersPer Cent of CaseLoadReceivingECT

Diagnosis Mean Median N-RespondersMinorDepressive Illness 5.485 0.196 458DrugandAlcohol AbusersTreated 0.298 0.015 383Personality Disorders Treated 0.159 0.012 384SexualD ysfunctions Treated 0.021 0.005 383AnorexiaNervosaTreated 0.315 0.033 391Intractable Pain Treated 0.338 0.032 385


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ELECTROCONVULSIVE THERAPTABLEVI

APASurveyMinorDepressiveDisorder

Responseof 50% or More ofCasesTreated

EXCELLENTGOODFAIRPOORVERYPOOR

Mean PerCentof Cases32.429.023.67.40.13

IV1415141211


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Task Force Report1413. Eastwood MR, Peacocke JE: Diagnosis and evaluation of ECT. Ca

PsychiatrAssocJ 21:55-59, 197614. AdenGC:Effects ofrestrictive legislationofelectroconvulsive therapata freestanding psychiatric hospital. Dis Nerv Syst38:230-233, 19715. Blachly P: Frequency ofadministration of ECT in a private hospitaConvulsiveTher Bull 1(4):34, October, 197616. Pickering G: Clinical trial of the treatment ofdepressive illness, repotothe medical research councilby itsclinical psychiatry committee. BMedJ 1:881-886, 196517. MayPRA,TumaAH,YaleC, etal: Schizophrenia a fo llowup studyresults of treatment, II. Hospital stay over two to five years. Arch GePsychiatry33:481-486, 197618. Prien RF:Lithiumprophylaxisacritical review. Compr Psychiatry1357-363, 197419. PrienRF,Caffey EM Jr, Klett CJ: Acomparisonoflithium carbonate anchlorpromazine in the treatment of mania. Arch Gen Psychiatry 26146-153, 197220. Kaplan LA,Freund JD: Electroshock therapy in patients with seve


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ELECTROCONVULSIVE THERAPY36. Salzman C: Electroconvulsive therapy. In Manual of Psychiatr

Therapeutics, Practical Psychopharmacologyand Psychiatry.EditedbShader RI. Boston,Little Brown &Co., 197637. Roberts AH: The value of EOT in delirium. Br J Psychiatry 109:653-65196338. Dudley WHC Jr, Williams JG: Electroconvulsive therapy in deliriumtremens.ComprPsychiatry 13(4):357-360, 197239. CampbellJD:Bromide intoxication: reportof 36cases. SouthMed J 42967-973, 194940. McDonaldRL:latrogenicamphetamine psychosis.Am JPsychiatry 121200-1201, 196441. BoydPR,WalkerG,Henderson IN: The treatment oftetraethylbloopoisoning. Lancet 1:181, 195742. George HR: Two psychotic episodes associated with cannabis, BrAddict65:119-121, 1970

43. ThacoreVR:Bhang psychosis.Br JPsychiatry 123: 225-229, 197344. Hatrick J, Dewhurst K: Delayed psychoses due to LSD. Lancet 2742-744, 1970


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TaskForce Report1460. Hollender MH, Steckler PP: Multiple sclerosis and schizophrenia:

case report. PsychiatryMed 3:251-257, 197261. SavitskyN,KarlinerW :Electroshocktherapyandmultiple sclerosis.NJMed 51:788, 195162. Hart FD : Historyof the treatment ofrheumatoid arthritis.Br Med J 763-765, 197663. Fisher AL: Areport on the use ofelectrotherapy in the treatmentchronic neuromuscular conditions of undetermined etiologyPsychosom Med 7: 36-42, 196664. Bradley JJ: Severe localized pain associated with depressive syndromBrJ Psychiatry 109: 741-745, 196365. Editorial: Shocksforpain.Br Med J 1:161, 195966. KrantzL :Intractable pain of aphantom limb with toxicomania dramatcally cured by four electroshock treatments. ConcoursMed (Paris)74215, 1956

67. MandelMR:Electroconvulsive therapy forchronic pain associated widepression. Am J Psychiatry 132: 632-636, 197568. Pisetsky JE : Disappearance of painful phantom limbs after electr


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TaskForce Report14105. DarlingHF:Shock treatmentinpsychopathic personality.JNervMe

Dis 101: 247-250, 1945106. SachsLJ,TiteuskyJ: ECT and thehomosexual aspectofschizophreniapsychodynamic consideration.JHillside Hosp 16(3-4):205-218, 196107. Thompson GN:Electroshock and other therapeutic considerations isexualpsychopathy.JNerv MentDis 109:531-539, 1949108. Heuyer G: La Pratique de 1'electrochoc chez 1'enfant. Zeitschrift fuKinder-Psychiatric13-14:60-64, 1946-48109. Hift E, Hift ST, Spiel W: Ergebnisse der schockbehandlungen bkindlichen schizophrenien. Schweizer Archiv. Fur Neuro log iNeurochirugie,und Psychiatric86:256-272, 1960110. BenderL: Childhood schizophrenia: areview.J Hillside Hosp 15-1610-22, 1966-67111. BenderL:Twenty yearsofclinical researchonschizophrenic childrewith special reference to those under sixyears ofage. In Emotion

Problems ofEarly Childhood. Edited by Caplan G, New York,BasBooks,1955,pp503-515112. BenderL:Presidentialaddress:atwenty-five year viewoftherapeut


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ELECTROCONVULSIVE THERAPY129. AbramsR:Multiple ECT: What havewe learned? InPsychobiologyo

Convulsive Therapy. Edited by Fink M, Kety S, McGaugh J, et aWashington,DC, VHWinston&Sons, 1974,pp79-83130. WeaverL,Ravaris C,RushS, et al:Stimulus parameters inelectroconvulsive shock.JPsychiatrRes 10:271-281, 1974131. OttossonJO: Experimental studiesof the modeofaction ofelectroconvulsive therapy: introduction. Acta Psychiatr Scand (Suppl145)35:5-61960132. Lewis JK ,McKinney WT: The effects of electrically induced convusionson thebehaviorofnormalandabnormal rhesus monkeys.DisNerSyst37:687-693, 1976133. AbramsR,Taylor MA:Diencephalic stimulationand the effects of ECinendogenous depression. Br JPsychiatry 129: 482-486, 1976134. d'Elia G, Raotma H: Is unilateral ECT less effective than bilateraECT?Br J Psychiatry 126: 83-89, 1975


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#$%&'()%#*+)*+#,*'--.%-)/+%0-'*1%


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CHAPTER IVADVERSEEFFECTSOF ECT

Section I. Memoryand ECTSection II. CNSSequelae ofECT:Risks ofTherapy andTheirProphylaxisSection III. ECT: Possible NeurologicalSide-Effects

Section I. Memory and ECT


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TaskForce Report 14grade and retrograde. Amnesia occurs for the events prior to eacseizureand animpairmentin theabilitytocommitneweventstolontermmemoryisevident followingeach seizure. This impairmentilearning new material diminishes gradually following each seizur(15)and iscumulative with successive treatments.Several general reviews of the amnesic effects of ECT aavailable (16, 17, 18). This review will summarize the current evdence regardingthe natureandextentofmemory impairment. Firstheanterograde amnesiceffects ofbilateral ECTwillbecomparedtthe effects ofright unilateral ECT. Second, retrograde effects of EConremote memory willbe reviewed. Third, the effects ofextendetreatments of ECT onmemory willbe summarized. Fourth, recenfindings involving the reinstatement procedure will be describedResultswith this procedure in animal studies suggested that learnematerialnotordinarilyaffected byelectroconvulsiveshock(ECS)ma


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possible. Delayed recall was tested on a second occasion 16 to 1hours later. Patients with identified dysfunctionof the left temporlobeareknowntoperformmore poorlyonthis test than patients witsimilar dysfunction of the frontal, parietal, orright temporal region(24). To assess nonverbal memory, patients were asked to copycomplexgeometric design (25, 26). Sixteento 19hours later, withouforewarning, they were asked tocopy itfrom memory. Patients witright temporal lesions are known to be deficient on this memory taskwhereas patients with left temporal lesions exhibit no impairmen(27).Tests were administeredone to twodays beforeECT andagaiwith equivalent forms six to 10hoursafter the fifth treatment of thseries.Figure1indicates that patients abouttobeginacourse of bilaterorunilateralECTwere nearlyidenticalindelayed recallof thestorand in delayed reproduction of the geometric figure. After ECT



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TaskForce Report 14unilateral ECT (p > .3). Scoresof the bilateralandunilateral groupwere significantly different (p


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TaskForceReport14occurred many years previously. Second, they indicate that bilateraECTproduces greater retrograde amnesia than right unilateral ECTRightunilateralECTcausednomeasurable lossofmemoryforremotevents;bycontrast,followingastandard courseofbilateral ECT,aimpairment in memoryfor remote events persisted for at least twweeks.Retrogradeamnesia for remote events: Information abouautobiographical material

The formal tests described above provide information about teffect of ECT on the abilitytorecognize public events that occurrefrom one to 16years priorto treatment. There have alsobeensominvestigations of the effect of ECT on the ability to recall autobigraphicalmaterial.In 1950, Janis (32) reported the resultsof astud


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Task Force Report 14Memory loss in patients receiving extended ECT

Mostmodern studiesof ECT andmemory loss concern patienreceivingaconventional courseofeightto 12treatments. Accordinglsuch studies do not speak topossiblelong-term effects on memory an extended course of ECT (e.g., more than 50 treatments). Thrstudies have been reported thatdoassess m em ory capacityand othcognitivefunctions in patients who have received an extended courofECT (34,35, 36). These studies are retrospective investigationspatients who have in previous years received a total of more than 5treatments. Suchpatientswere comparedtootherpatientsmatchedclosely aspossiblyforage, sex,andpsychiatric diagnosis.The resuindicated that those patients who hadreceived ECTperform ed woronavarietyofm emory tests andother cognitive tests thanthecontrgroup. However, these patients were either chronic schizophren


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aredisturbingandthat occur frequently ;sixfeltthat theyhad minmemory problems that occur frequently ; and three indicated ththeyhad only anoccasional minor problem .Unfortunately,the discrepancy between subjective and objectivmeasures ofmemoryfunction cannotbeconclusively resolved. Threpossible explanationsofthis discrepancy willbe considered here.(1The possibility cannot be ruled out that failures of recall persist aftECT that are not detected byconventional memory tests. (2) Thpossibility also cannotbe ruled out that patients receiving bilaterECT were different from patients receiving unilateral ECT insomwaythat favoredthe development ofmem ory complaints. Forexample, patients receiving bilateralECTm ight have initiallybeenmodepressed than patients receiving unilateral ECT, or they mighinitially have had different expectations about memory impairmenThus, it should not be concluded that bilateral ECT will cau

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cognitive function, but a definitive conclusion is not yepossible;4. the activation ofpreviouslylearnedmaterialjustprior to ECTdoesnotcause amnesiaforthat material;

5. new learning capacity substantially recovers by six to ninmonths after the completion of bilateral or right unilateraECT, but persistingmemorycomplaints arecommon in individualswho receivebilateraltreatment;6. memory for events that occurred long prior to ECT substantiallyrecoversby six toninemonthsafter ECT; memoryfoevents thatoccurreddayspriorto ECT may be permanentlylost

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nesia. Edited by Whitty CWM, Zangwill OL. New York, AppletoCentury-Crofts, 1966, pp 109-13315. Squire LR, Miller PL: Diminution in anterograde amnesia followielectroconvulsivetherapy.Br JPsychiatry 125: 490-495, 197416. Harper RG,WiensAN: Electroconvulsive therapy and memory.J NeMentDis 161: 245-254, 197517. DornbushR:Memoryand induced ECTconvulsions.SeminPsychia4:47-54, 1972

18.Dornbush RL, Williams M: Memory and ECT. In PsychobiologyConvulsive Therapy. Edited by Fink M, Kety S, McGaugh J, etWashingtonDC, VHWinston&Sons, 1974, pp 199-20719. SchneiderAM,ShermanW :Amnesia:Afunctionof the temporal relatiof footshock toelectroconvulsive shock. Science 159: 219-221, 196820. Misanin JR , Miller RE, Lewis DJ: Retrograde amnesia producedelectroconvulsive shockafterreactivationof aconsolidated memory traScience 160: 554-555, 196821. Lewis DJ, Bregman NJ, Mahan JJ Jr: Cue-dependent amnesia in tK-maze.JCompPhysiolPsychol81:243-247, 1972



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36. Teuber H-L, Corkin S, Twitchell TE: A study ofeingulotomy in maReport submitted to the National Commission for the ProtectionHuman SubjectsofBiomedicalandBehavioral Research37. Squire LR, Slater PC, Chace PM: Reactivation of recent or remomemory before electroconvulsive therapy does not produce retrogradamnesia. BehavBiol 17:31-41, 197638. Squire LR, Chace PM: Memory functions six to nine months aftelectroconvulsive therapy. ArchGenPsychiatry32:1557-1564, 1975


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Section II. CNS (Central Nervous System) Sequelae oECT:Risksof Therapy and their ProphylaxisIntroduction

Epilepsy is afrightening illness forwhich robust therapies agenerally prescribed. In the neurological literature, the negativeffects of seizures are emphasized and concern is great to preventhem. In folk-lore, seizures aremarksofill-omenandepilepticsaroften segregated.Yet inclinical psychiatry seizuresare induced under controlleconditionsfortheireffects onbehavior. Sincethe mid-1930s, variou



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Canthese be reduced ormodified?Theevaluationof ECT iscomplicatedbyhistoricalfactors. In thearlydecades, treatments were given without sedation, patients beinbroughtto thetreatment room, placed on apallet, protected againthe convulsions by two to four aides, and treated. Missed seizureoccurred andpatients experiencedthe panicandpain of unmodifie

electric currents or subconvulsive pentylenetetrazol (MetrazolTreatment todayismodified byspecial electrode placements, muscrelaxants,sedatives, anesthesia,andhyperoxygenationsothat misseseizures, panic, fracture, and death are exceedingly rare. Thesmodificationshavebeengradually introduced overfourdecades.Asbecame known thatthecerebral seizureisnecessaryfor the therapetic response and that neither the motor convulsions,nor fear, nmemory loss wasessential, treatments weremodified and the use

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impairment are also related to changes in current characteristiduring ECT. An example is less memory impairment when briepulsed stimuliare used to induce a seizure (15)or when threshocurrents areused (16).Inelectrical inductions,thelocationof theelectrodeshas adireeffecton the typeandextentofmemory loss. Conventional electroplacement isbitemporal with currents concentrated in the anteritemporallobesand thebrain stem. Seizuresmayalsobe inducedcurrents through electrodes on one side of the head, (unilaterplacement); and these may be placed over the dominant or thnon-dominanthemisphere.The clinical efficacy oftreatments usiunilateral electrodes isapproximately equalto the efficacy ofbilaterplacements,but theeffects onmemoryareless(17,18,19,andSecti1,this Chapter). Further,the impactonmemory tasksdiffers depening on whether electrodes are placed over the dominant or th



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(25) implanted electrodes aimed at the center of the amygdaloicomplex, and stimulated male rats with 45,1-second,400/x-Amper60-Herz stimulations, three times a day,fivedays a week. They theintubatedthe animals andadministered large amountsofalcoholfo45 intubations. When alcohol administration ceased, the withdrawsymptoms ofhyperreactivity,clonus,andbody jerks were intensifieSimilar observations were made using repeated administrations opentylenetetrazoland sub-convulsive amygdaloid stimulations. Fromthese data they hazard warnings that similar increased sensitivitytseizures may occur in patients receiving ECT.

Inherent in the definition of kindling is a lowering of the cerebrthreshold sothataseizuremay be elicited by low, incidental stimulThis explanation is inconsistent, however, with the observations bBrockman,et al(27)and Green (28)who found that the thresholdfothe currents necessary to elicit a seizure in ECT rises during th

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phrenic patients three times daily to induce an organic psychosis in process termed "regressive ECT." Glueck noted regression to bcomplete when a patient manifested memory loss, confusion, diorientation, lackofverbal spontaneity, slurringofspeechtodysarthrormuteness, and apathy. In this special form of ECT the psychotistate is reversible, the long term clinical benefits to schizophrenibeing equal to or better than those following drug therapy (31).detaileddescriptionof the recovery process from a severe dementdue to frequent ECT has been reported by Regenstein, Murawski, anEngel(32). They noted that with cessationof ECT mental functionand behavior recovered over a period of more than one year.Amodificationofregressive ECT wassuggested byBlachlyanGowing (33)inwhich multiple seizures(up tosix) wereinduced dailunder conditions of hyperoxygenation. It is not clear why this methodtermed MMECT (Multiple Monitored ECT)bythese authors, rarel



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(a) Human brain tissueThe assessmentof the pathology of ECT iscomplicated by thtime between ECT and the time of death. In some studies, tissues arexaminedafterseizures which are clearly proximal to thedeath;whiinothers, ECT is a distant event which may or may not be related tthe pathologic examination. With this caveat, brain tissues have beereported to show increased gliosis (40); diffuse degeneration (41petechial hemorrhagesin thebrain stem with fatembolism (42);anmorecommonly edema and subarachnoid hemorrhage (43, 44,45Will,et al(46)found thebrainof apatient whodied 15minutes aftthetwelfthECT to be edematousand toshow neuronal damage anincreased lipofuscin pigmentation. Madow(47) reported one caseintraventricular hemorrhage and three who died of cardiovasculdisease in four autopsies ofpatients whodied after ECT.These cases raise the question as to the basis for death in ECT


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cerebral activity. Characteristic patterns havebeen defined and related to the diagnosis of epilepsy, organic confusional states, ancerebral impairmentdue totrauma,masslesions,andcerebrovasculadeficiency.These conditionsarecharacterizedbydiffuse high voltagslow waves of two to six Hz in runs and bursts and in focaasymmetric, orsymmetric patterns (64, 65).FollowingECT,EEG slow wave activity increases, appearingibursts and runs, more prominent in the frontal and temporal lead(66). Fast frequencies decrease and disappear (67).The degree oslowing,the increase in amplitudes, the duration of burst activity, antheir persistence after the last treatment are directly related to thnumberand the frequency of seizure inductions and to the timeorecording in relation to a seizure. Following the last seizure, the slowwaves rapidly disappear, amplitudes decrease, and the mean frequency increases.Within fourweeks ofthelast treatment,the EEG

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weeks after the last seizure. Few studies relate the changes in thesmeasures to therapeutic outcome, although the language measurewere the focus of one novel hypothesis of the action of ECTWeinstein,etal(37)foundthatfollowingamobarbital, speech patternof neurological patients exhibited the language of denial and prdicted that the organic mental state elicited by ECT was conducive tthe expression of explicit and implicit verbaldenialananosognosfor the illness. Kahn, et al (38) and Kahn and Fink (77)found thdenial language patterns did increase during ECT, that the denilanguage was related topretreatmentpersonality and diagnosis, anthat denialearlyintreatmentwasprognosticofgoodclinicaloutcomThe changes in perception and language, like the changes in memorcapacity, may be additional signs of the organic mental syndromwhichm ay beuncorrelated totherapeutic outcome. (1).


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(hypothalamic)symptoms. Theseareusually accompaniedbychanginmemory,perception,andlanguage.The recognized adverse effects of ECT on the CNS includusuallytransient memory loss,arare confusional state,andextremerarely, death. Fear prior to each treatment and a mild headachfollowingit arealso sometimes associated with ECT.Thetherapeutic processfordepression liesinbiochemical evenwhich accompanyorresult from seizures,and not in theconvulsiomemory loss or other neurologic sequelae. Modifications of thtreatment process which maintain therapeutic activity and reducside-effects are sedation, anesthesia, muscle relaxation, selectivelectrode placementsandelectric currents,andhyperoxygenation.References forSection II



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16. Fink M,KahnRL, Green M:Experimental studies of the electroshocprocess.Dis NervSyst19:113-118, 195817.d'Elia G: Unilateral electroconvulsive therapy. Acta Psychiatr Scan(Suppl)215: 1-98, 197018.d'Elia G: Unilateral electroconvulsive therapy. In Psychobiology oConvulsive Therapy. Edited by Fink M, Kety S, McGaugh J, et aWashington DC, VHWinston&Sons Inc., 1974, pp 21-3419.d'EliaG,RaotmaH: Isunilateral ECTlesseffectivethan bilateral ECTBrJPsychiatry 126:83-89, 197520. SmallJG ,SmallIF:Clinical results: Indoklonvs.ECT.SeminPsychiatr4: 13-26,197221. Pacella BL,BarreraSE: Spontaneous convulsionsfollowingconvulsivshocktherapy. Am JPsychiatry 101: 783-788, 194522. Blumenthal IJ: Spontaneous seizures and related electroencephalographic findingsfollowingshock therapy.JNerv MentDis122:581-58195523. KarlinerW: Epileptic states following electroshock therapy. J HillsidHosp5: 1-9, 1956

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38. KahnRL, Fink M, Weinstein EA: Relation of amobarbitaltestto clinicimprovement in electroshock. Arch Neurol Psychiat (Chic) 76: 23-2195639. Psychiatrist, Practicing: The experience ofelectroconvulsivetherapy. BJ Psychiatry111:365-367, 196540. Ebaugh FG, Barnacle CH, Neuberger KT: Fatalities following electrconvulsive therapy: Report of two cases, with autopsy. Arch NeuroPsychiatry49:107-117, 194341. Gralnick A:Fatalities associated with electric shock treatment of psychoses: Reportof twocases, with autopsy observationsin one ofthem.ArcNeurolPsychiatry51: 397-402, 194442. Meyer A, Teare L: Cerebral fat embolism after electrical convulsiotherapy.Br Med J 2: 42-44, 194543. Alpers BJ, Hughes J: Changes in the brain after electrically induceconvulsion incats. Arch Neuro l Psychiatry47:385-398, 194244. Larsen EF, Vraa-Jensen G: Ischaemic changes in the brain followinelectroshock therapy . Acta Psychiatr Neurol Scand28:75-80, 195345. LibanE,HalpernL,RozanskiJ:Vascular changesin thebrainin afatali

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60. BarreraSE,Lewis NDC ,PacellaBI,etal: Brain changes associated wielectrically induced seizures. Trans Am NeurolAssoc 31, 194261. Globus JH, van Harreveld A,W iersma GAG: The influence of electrcurrent application on the structure of the brain of dogs. J NeuropathoExp Neurol2:263-276, 194362. Lidbeck WL: Pathologic changes in the brain after electric shock: aexperimental studyondogs.JNeuropatholExp Neurol3: 81, 194463. NeubergerKT,WhiteheadRW,RutledgeEK, et al:Pathologic changesthe brains of dogs given repeated electric shocks. Am J Med Sci 20381-387, 194264. Hill D, Parr G (Eds.): Electroencephalography. New York, Macmilla196365. Strauss H, Ostow M, Greenstein L: Diagnostic ElectroencephalographNew York,Grune & Stratton, 195266. Fink M , Kahn RL: Relation of EEG delta activity to behav ioral responsinelectroshock: quantitative serial studies. A rch Neurol Psychiatr (Chi78:516-525, 195767. Hoagland H, Malamud W, Kaufman 1C, et al: Changes in electroe

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81. FoulonL: Electrochocbilateral ouunilateral? Unerevue critique de llitterature.ActaPsychiatrBelg73:356-378, 197382. Carney MWP,Sheffield B: Electroconvulsive therapy and the diecephalon.Lancet1:1505-1507, 197383. Weaver L, Ravaris C, Rush S, et al: Stimulus parameters in electroconvulsive shock.JPsychiatrRes 10:271-281, 197484. Stromgren LS, Juul-Jensen P: EEG in unilateral and bilaterelectroconvulsivetherapy. Acta Psychiatr Scand51:340-360, 1975


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Section III. ECT: Possible Neurological Side-effectsThis briefcomm entarywill concentrateon how electroconvulsivtherapy (ECT)might injure the brain. Because relevant studies arinconclusive, itlargely begs theprior question ofwhether modifieECT does in fact produce neurological damage. While a transienamnestic-confusional state followsmost induced seizures, thereis nfirmconsensus about ECT's long-termeffects oncognitive functionRarely,acuteandneurologically disabling strokes occur (1),but thesare not the focus of recent controversy about the alleged adverseffects ofECT.Current practiceis to useparalytic agentsand ventilatoryassis

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Jugular venous lactate rose slightly late in the seizure but levelscreatine phosphokinase remained stable. These data imply that duing induced seizures cerebral metabolic demands did not outstrcerebraloxygen delivery.Patients whoexperienced spontaneous seizures less than threhoursbefore evaluation hadonlyatransient mild metabolic acidosand asmall riseinlactatelevels incerebrospinal fluid(CSF) (5).Thrisein CSFlactatepersisted forseveral hoursorevena fewdays, bthiswas not associated with impaired consciousnessor other abnomal neurological findings. In other words, a single spontaneoseizure, unmodified by paralytic drugs or ventilatory support, prduced onlyminor chemical evidence ofbrain hypoxiaand noclinicresidua. While even aslight degree ofbrain hypoxia duringaspotaneous seizure might injure some particularly susceptible neuro(e.g. those in the hippocampus), this hypothesis lacks satisfacto



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changes were not observed in all the animals, and tended to occuonly during the phase of seizure when hyperpyrexia, hypotensiohypoxemia, acidosis, and occasionally hypoglycemia were presenThese studiesareconsistent withfindingsinsmaller animals suggesingthat permanent disruption ofcerebral energy metabolism occuonlyafter aprolonged seriesofrepetitiveseizures (10-12).Thereis nconvincing experimental evidence that a single, brief, generalizeseizure in aventilated subject causes ischemic cell change ormothan atransient disruptionofcerebral energy metabolism.Even ifprolonged apnea orrespiratory obstruction are avertethecirculatory accompaniments of ageneralizedseizure couldleadbrain ischemia. While cerebral blood flow ordinarily rises substatially during seizures (13), this compensatory adjustment may noccur if cardiac output is impaired. In addition to clinical anexperimental reports ofsometimes fatal cardiac dysrhythmias follow

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in neurons (20). But the kindling model, which involves use ointracerebral electrodes, bears so little relationship to modified ECthat its relevance to the issueofcognitive changeafterECT is dubiousSummary

While the respiratory depression, heightened cerebral energrequirements, and dramatic cardiovascular changes that accompanevenamodified generalized seizure could producea gapbetween thbrain's need for oxygen and the delivery of this essential fuel, npublished study has established that such a gap develops. Indeebothclinicalandexperimental studiesindicatedthatwhereadequaoxygenation is provided, brain tissue hypoxia does not occur durininduced seizures. Mechanisms of neurological injury other thaischemia-hypoxia are even less easy to envision. Nevertheless, seems proper to continue to investigate the question of whethe


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CHAPTER VECT: METHODSOFADMINISTRATION

IntroductionThis chapterdealswiththeprocedure bywhichECT isadministereIt presents information about the physiological and neurophamacological events which are known to occur when a seizure anconvulsion are evoked by an electrical stimulus. The adverse rsponses associated withthe seizureandwiththe drugs employed


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Depth recordings indicate that the seizure process is initiatein the central partof the brain and spreads centrifugally to thcortices (4). Thisis ofclinical importanceinviewof theempiricaobservationthat the therapeutic effectof the seizure isdependenuponinvolvementof amajorportion,orevenof the entire brainin theseizure process.The occurrenceof atonic clonic musclresponse is indicative of the strengthof the electrical stimulubeing adequate togenerate seizure activityofsufficient intensitto spread from the point of initiation,deep in the brain, to thmotorcorticeson its surface.

Preconvulsivepattern Immediatepostconvulsive pattern



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induced seizures has been complicated by the occurrencevaryingdegreesofhypoxia.These studies have indicated thatthconvulsionisassociated with marked reductioninbrainATP anphosphocreatine aswellaswithanaccumulationoflactate. Thlatter findingis interpreted as signifying that brain metabolishas shifted to an anaerobic pattern as a result of the markeincrease in activity which exceeds the abilityof the increasecerebral blood flow tosupplyoxygen in sufficient quantity.The work of Plum and his co-workers (5, 8) markedsignificantadvance since they studiedthechanges occurring wianelectrically-induced seizureinanimals which were adequateventilated with oxygen-enriched mixturessothat hypoxemia anhypercarboxemia were prevented. They found that, in anethetized and paralyzed animals adequately ventilated witoxygen-enriched mixtures,no significant brain hypoxia occu

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electrically-induced convulsions (9, 10, 11). However, theschangesare ofcomparatively short duration.Morepersistent changes havebeenreported.After aseriesconvulsions, an increase in brain monoamine oxidase activipersistsforseveral weeksafter the last convulsion (12, 13).Inragiven once-daily, electrically-induced seizures for a week, icreased tyrosinehydroxylation persistsfor aweek following tfinalconvulsion(14). The same investigator observed a sustaineincrease in brain tryptophane concentration which occurrewithout significant changes in thesynthesis, turnover,oruptakof5-hydroxytryptophane.

2. Peripheral Effects Of An Electrically-Induced SeizureManyof the effects of an electrically-induced seizure occurri


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itstherapeutic effectiveness insurgically adrenalectomized indviduals(22). f) Pituitary effects

Elevations in blood concentration of several pituitary homones in the period immediately following an electricallyinducedseizure have been documented. These elevationscan bviewed as possible consequences of the "peripheralization"oseizure activity through the pituitary gland.Thefollowingpituitary hormones have been measured in thblood following anelectrically-induced convulsion:

(i) adrenocorticotrophic hormone (corticotropin, ACTHAn eight-fold increase inplasma ACTH concentration occurfollowingsingleormultiple convulsive treatmentsinpatienwhowereventilatedwith 100% oxygen,anesthetizedwith

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thiopental, and succinylcholine (29). Age, concomitapsychotropic drug administration, duration of the seizurnumber of treatments, and therapeutic response did ninterfere withthisprolactin responseAdverse Responses Associated With ECT

The followingdiscussion will deal withaselect groupofadverreactions which occur during the treatment and immediate postreatment periods. Adverse responses occurring in these two periocan be conveniently divided into those which are related to thelectrically-induced seizure and those associated with the drucommonly used in the treatment. This separation is not absolutseveral adverse reactions have their genesis in both the drugs and tseizure.



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Cardiac arrest appearsto be aleading,if not the major,causofdeaths occurring withtheadministrationofconvulsive therap(35, 36,37).Rather than trying to arrive at some precise value for thincidence ofcardiac dysrhythmias with ECT, itwould appear tbemoreuseful toemphasizetheimportanceandconsequencesothis as apotentially serious adverse reactionwhich can complcatethetreatmentevenofindividualsnotjudgedto be guardecardiovascular risks (20,34, 37, 38, 39, 40, 41, 42,43).Of equal importance with arecognition of the potential focardiacdysrhythmiagenic complicationsin ECT is anunderstanding of themechanisms wherebytheseparticular adverse effects argenerated. This understandingis ofparticular value since itmakepossible prophylactic strategies, anticipation and early recogntion of these adverse responses and, most important, effectiv

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ringpriortoparalysis,ismanifeston the S-ANodeathe bradycardia which the drug characteristicallproduces priorto itsparalytic action. This bradycardia, which is likely to be especially severe withsuccessive doses of succinylcholine, can be effectively reduced orprevented by adequate dosesoscopolamine oratropine (45, 46).(ii) those producing localized or generalized ventriculamyocardial irritabilitycoronary artery diseaseor insufficiencyThis may produce relative or absolute ischemia of themyocardium. Relative ischemia isproduced when coronarperfusion is not adequate to keep pace with the increasemetabolic needs of hyperdynamic myocardial activity (e.g


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(b) Intravenous AnestheticsTheseare almost always ultra-short-acting barbituratessuchathiopental (Pentothal) and methohexital (Brevital). The use o

intravenousanestheticsisassociated withall theformidable riskofgeneral anesthesia.It isparticularly importanttoappreciate thfact that light levels of anesthesia produced with low dosesoanesthetic agents are particularly likely to be accompanied bsuch complications aslaryngospasm.Littledoses do not necessailybeget littletroubles

Twoadditional adverse responses tointravenous anestheticare rare but serious. The first of these is accidental intra-arteriinjectionof the barbiturate with subsequent tissue necrosisansevere deformity of the hand (50,51, 52).The second is rapidly-developing hyper-sensitivity reaction. Anaphylactic reactions tothiopental arewell-documented (53, 54).They have als



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which impair the hydrolytic activity of plasma pseudocholinesterase(s): drug inhibition and genetic factors.

drug inhibitionA number of potent blockers of plasma pseudo

cholinesterases (i.e. anticholinesterases) are currentlemployed in medicine in the therapy of myasthenigravis (neostigmine, pyridostigmine [Mestinonamebonium [Mytelase]) and in the treatment oglaucoma (diisopropyl fluorophosphate [DFP], [Isoflurophate], tetraethylpyrophosphate [TEPP], echothiopate [Phospholine], bisneostigmine [DemecariumHumorsol]). In addition, a number of insecticides arpotentanticholinesterases (e.g. parathion, malathion).The duration ofanticholinesterase action varies greatly

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who are homozygousfor this type, amountsof thdrug considerably in excess of the usual 0.5-1.mg/kg can be given withoutappreciableprolongation of its paralytic action.(b) atypical form

This type isessentially devoidofhydrolyticaction on succinylcholine when it isadministered itheusual therapeutic doses. Aboutoneindividuali3,200 is homozygousfor this form of the enzymeadministration of even minute doses of succinycholine (e.g. 2-4mg) to these patients can result irespiratory insufficiency or apnea lasting 15 minuteorlonger (59).


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TaskForceReport14(ii) hyperkalemic response to succinylcholine


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Potassiumliberation occursaspartof thenormal actionosuccinylcholine. However, under certain conditions this release is somarked thatitproduces hyperkalemiasufficient tevoke cardiac dysrhythmiasandeven cardiac arrest (64, 65Succinylcholine-induced hyperkalemia becomes a seriouproblemwhenthedrugisadministeredtopatients 14-21 dayafter massive thermal body burns, direct muscle traumupper motor neurone lesions (associated with multiplsclerosis,spastic paralysisfrombraininjury)and tothosewhhave been immobilized forlong periods oftime. This exaggerated response to succinylcholinemaypersist for up to simonths after an injury. It is not rare to consider the use oECT inpatientswhohaveone oftheseconditions predispoing to the development of succinylcholine-induced hype

ELECTROCONVULSIVE THERAPYtrists who,despiteevidenceto thecontrary, remain convincedthat th


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treatment works solely through this aversive action which, in effecterrorizesthe patient intoa flight intohealth."However, there is some objective support for the observeemotionalstress associated with ECT. Thus studies have shown thatheplasma non-esterifiedfattyacid concentrations become markedlelevatedin theperiod immediately priorto atreatmentincomparisowith concentrationsondays whenno ECT isgiven (68). Elevationsinon-esterified fatty acids are considered to result from increaseplasma concentrations of catecholamines evoked by fear and stres(69).Despite the paucity of objective data, it is desirable to try describe someof the specific fears which appear to be important ipatients receiving ECT. First, though,aword shouldbesaid aboutthrelationship of these fears to the memory dysfunction which

TaskForce Report143. concern thattheelectrical current will damage, or is injurin


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thebrainand themind.The confusionandmemory deficits,atheyareobserved in other individuals orexperienced by thpatient, frequently heighten this concern.4. fear that while under the influenceof the anesthetic normbehavioral controls willbelostandthat unacceptable behavioandutterances will occur;5. concern andanxiety about being helpless and passive;6. feelings associated with the inadequacy of anesthesia whicresults in patients being conscious, or semi-conscious, bparalyzed andunabletoreact.While these fantasies, fears, andconcerns areprimarily thosethepatientwho isbeing treated, theyarealso sharedtosome degre

by the family andeven by the staff. These feelings can sabotage th

ELECTROCONVULSIVE THERAPYtive criteria formaking this determination are described in th


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section which follows.

Suggested ProcedureForAdministering ECTThe following is a detailed description of one of the severmethods available foradministeringECT in anacceptablemanner.

is included because the Task Force anticipates that this report wiserveaneducational purpose and, therefore, thatadetailed accountoone type of treatment procedure will be helpful for illustrativpurposes.Itmustbeemphasized thattheprocedure described belowis bone ofseveral acceptable methods which are used by experiencepsychiatrists for administering ECT. Procedures which differ in on

Task Force Report14(viii) metaraminol (Aramine)- 1%solution- 10 ml vial;


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(ix) methylprednisolone (Solu-Medrol)- 125 and 1000 mg/vi(x) sodium bicarbonate - 7.5% solution = 44.6 mEq. - ml (emergency syringe);(xi) L-norepinephrine (Levophed) - 2mg/ml- 4 ml ampuls.(b) Equipment to be available for immediate use:

(i) suction-tested forproper function;(ii) needles;(iii) infusion sets;(iv) electrocardiograph;(v) defibrillator. Whiletherare caseofcardiac arrest occurriwith ECT can usuallybe managed by ablow to the prcordium, the adjunctive use of a defibrillator may o

casionallybe necessary. This apparatus shouldbe reaso

ELECTROCONVULSIVE THERAPand solutions which may be required in the event ofadverse re


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sponses.8. After determining the pulse rate, increments of 0.25 mmethscopolamine or 0.5 mg of atropine are injected IV untildiscernible increase inheart rate occurs (e.g. rate increasesby10%The anticholinergic drug can be given subcutaneously45 minutepriorto thetreatmentbutthis procedure makesitdifficulttotitrate thdosesothat adequate cardiac cholinergic block willbe produced.Some patients receiving ECT will be receiving agents (e.gantipsychotic drugs, tricyclic antidepressants, antiparkinson compounds) which singly, or in combination, will have significant aticholinergic actions asmanifestby atachycardia. It may be judgethat additional anticholinergic medication is not required in thespatients (46).A quaternary (charged) anticholinergic agent (e.g. scopolamin


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ELECTROCONVULSIVETHERAP


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Figure2 Bilateral orBitemporal Electrode Placement

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(d) An attendant places onehand oneach thigh near the kne


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This support will preventthepatient from fallingoffthetreamentcartin theevent thatavigorousandessentially unmodfiedconvulsion occurs unexpectedly.16. The electrical stimulusisthen administered inaccordance witthedirectionsfor themachine being employed.TheTask Forceis noadvocating the use of any particular ECT stimulus units pending thavailabilityof theFDA's evaluationofthese devices.17. The therapeutic adequacyof the seizureisdeterminedby one obothof the following:(a) occurrence of acharacteristic major seizure pattern on thelectrocorticographtracing or oscilloscope image if this type omonitoringisbeing used;(b) occurrence of a tonic muscular contraction in anextremity


21. When spontaneous respiratory muscle activity commences, th


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anesthetic facemask should stillbeheld inplace untiltherehasbeeenough muscle recovery from the succinylcholine to permit thestablishment of anadequate tidal volume. This servestwopurposethe movements of the anesthetic bag are a measure of the tidvolume,andinadequateventilatorymovementscan be supplementebysqueezingthebag.22. With the establishment of anormaltidalvolumethe anesthetfacemaskisremovedand thepatientcan bemovedfrom thecarttobed. The positioning of the patient depends on whether or nprotective pharyngeal reflexes have returned as indicated by thpresence ofswallowing and the capacity to phonate. When reflexarenotvigorously present it isadvisable toplace the patient in thsemi-prone position. In moving the unconsciousorsemi-consciopatient, care should be taken not to twist the neck and to avo

Task Force Report 14References


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1. Holmberg G: Biological aspects of electroconvulsive therapy. Int ReNeurobiol5:389-412, 19632. Fink M (Ed) : Convulsive therapy. Sem in Psychiatry 4:1-79, 19723. Fink M, Kety SS, McGaugh J, et al: Psychobiology of ConvulsivTherapy, Washington D.C., V.H. Winston & Sons, 19744. Bickford RG , Rom e HP: The electroencephalogram recorded durinseizures produced by electroshock. Electroencephalogr CliNeurophysiol1:369, 19495. Plum F, Posn er JB, Troy B: Cerebral metabolic and circulatory responseto induced co nvu ls ions in animals . Arch Neurol 18:1-13, 1966.Lovett-DoustJW,BarchhaR, Lee RSY,et al:Acuteeffects of ECT on thcerebralcirculation inman.EuropNeurol 12:47-62, 19747. Lovett-DoustJW ,RaschkaLB:Enduring effects ofmodified ECT on thcerebral circulation inman. Psychiatr Clin8:293-303, 19758. Plum F, HowseDC, Duffy TE: Metabolic effects ofseizures. A ssocRNervMentalDis53:141-157, 1974

ELECTROCONVULSIVE THERAP21. ElithornA,BridgesPK,HodgezJR: Adrenocortical responsiveness du


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ing courses of electro-convulsive therapy. Br J Psychiatry 115:575-58196922. BidderTG: Unpublished observations23. Allen JP, Denney D, Kendall JW, etal:Corticotropin release during ECinman.Am JPsychiatry131:1225-1228, 197424. Ylikorkala O, Kauppila A, Haapalahti J, et al: The effect of electrconvulsion therapy on the circulating concentrations of pituitary homones, cortisol and cyclic adenosine monophosphate. Clin Endocrin5:571-574, 197625. Ryan RJ, Sanson DW, Faiman CH, et al: Effects of convulsive eletroshock on serum concentrations of follicle-stimulating hormonlutenizinghormone,thyroid stimulatinghormoneandgrowth hormoneman.J Clin Endocrinol Metab30:51-58, 197026. ScholchDS:Influenceofphysical stressandexerciseongrowth hormonand insulin secretion in man. J Lab Clin Med 69:256-269, 1967

27. Yalow RS,Varsano-AharonN,Echemendia E, et al: HGH andACT


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ELECTROCONVULSIVE THERAP68. Ruxin RL, Bidder TG, Agle DP: The influence of autonomic arousal, oblood clotting time in patients receiving electroconvulsive treatment.


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Psychosom Res 16:185-192, 197269. Stone WN, Gleser GC, Gottschalk LA, et al: Stimulus,affect and plasmfree fattyacid. Psychosom Med31:331-341, 196970. Bidder TG: Un published observations71. Longo VC: Behavioral and electroencephalographic effects of atropinand related compounds. Pharmacol Rev18:965-996, 1966


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ELECTRO CO N V U LSI V E THERAPAlmost all who had not improved did soduring this second cours


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indicating that the twotreatments differed in efficacy(5).With the addition ofcurare and later succinylcholine (Anectinto the treatment, the effects of the convulsion the motoreffects omusclesand limbswereseparated from the cerebral seizure. Clincally ECT modified by succinylcholine and barbiturate is approxmatelyequivalent tounmodifiedECT inefficacy,although somefinunmodified seizures to be slightly better. This observation wa

unexplained until the EEC was recorded during the seizures.Noevery administrationofelectric currentor flurothyl isaccompaniedbacerebral seizure, even when motor responses resembling clonicotonic phases are observed. It isparticularly difficult to be sure ofcerebral seizure when succinylcholine masks themotor convulsio(7). These observations led Blachly to suggest ECT or flurothtreatmentsshould be underEECcontrol,i.e.,withmonitoring of th

TaskForceReport 14moreto theoccurrenceofseizuresandtheir duration thanto themod


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of induction (18).Ifthese observationsaretrue,wewould expect thatthetreatmemethod providingthe least discomfortandriskto the patient shoupersist inclinical practice.Metrazol often elicited fear reactions anincomplete seizures,and it wasreplaced by electrical inductionsathese werefoundto be saferandeasiertoadminister.The difficultyoa safe induction and a higher incidence of missed seizures wiflurothyleventuallyled to its discontinuation.InECT,thetypeofcurrentisless important thanitsintensity (i.the relationship to seizure threshold). Studies of square wave, undirectional, andpulsed-wavecurrents find little relation between curent characteristics and outcome, provided the current used is sufcienttoinduce acerebral seizure (18).The location of the ECT electrodes affects memoryand orient

ELECTROCONVULSIVE THERAPmechanism (25), the degree of authoritarianism on the CaliforniaScale (26), and the organization of the Rorschach protocol (27) hav


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each been relatedto thetype of behavioral outcomeand to theamouoftreatmentneededtoachieveit.4. Vegetative changes as in sleep appetite weight mense

libido and mood accompany the behavioral changes induced brepeated seizures.The depressive psychoses are characterized by impairment of thphysiological functions associated with the activity of thhypothalamus and these impairments improve earlyin the courseo

ECT (2, 4,23).The efficacy of ECT may be predictedby the degreand persistence of the changes in appetite and sleep and theimpairment seems to accompany or precede relapse. The relatiobetween these physiologic functions and improvement seems mo

TaskForceReport14are reversible intime usually measured in weeks; while the clinicaand psycho-pathologicchanges may be more persistent although thes


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also are reversible.Physiologic effects ofseizuresasincreased slow wave activitythe EEG, redundancy in speech, changes in language patterns, anperformance in memory and psy

electro convulsive therapy apa

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