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Biological Psychiatry, Vol. 14, No. 6, 1979

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The Natural History of Acute Organic Mental

- 9 7± Syndrome After Bilateral Electroconvulsive Therapy

W. K. Summers,' Eli Robins,2 and Theodore Reich2/

Received October20, 1978; revisedApril 6, 1979

Thirty-a, ie patients undergoing bilateral electroconvulsive therapy IfCr1 were a

Jolla wed prospectively for the development of' acute organic mental syndromeA0M57; 15 patients 48.4% developed A OMS during Ii'CT For these 15 patients, the average nunber of ECTs before development of A OMS was 5S withai'erage duration of' A 0415 being 20.1 days. comparison of these 15 patients tothe 16 patients who did not develop A OMSfor diagnoses, demographic data, preWi' laboratocy data, and medications, differed only in exposure to psychoactive

iiiedications and prior presence ofmajor medical illness.

INTRODUCTION

Memory deficits and confusional states are said to be characteristic side

effects of electroconvulsive therapy Harper and Wiens, 1975; 1-Iarwitz, 1974.

5 Nevertheless, there are few published data on the frequency and duration of

mild organic mentaj syndrome after electroconvulsive therapy ECT. It is as

surned that such confusional states are caused by the electroconvulsive therapy.

Other possible causes of postelectroconvulsive therapy confusion, such as meta

bolic or drug-induced confusional states, have not been excluded.

This study reports on the incidence, duration, and associated risk of acute

organic mental syndrome in patients receiving ECT.

Supported in part by U.S. Public Health Service grant MH 1-4677.

JñbiefMtj of-SóutheUS Callforn1jSdflOoI'ofMed1cIñe, Los Angeles, California.Washington University School of Medicine, St. Louis, Missouri.

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906 Summers1 Robins, and Reich Acute Organic Mental Syndrome After Bilateral ECT 907

METHOD

Thirty-one randomly selected patients undergoing bitemporal electrocon

vulsive shock treatments at Renard Hospital 1St. Louis, Missouri agreed to parti

cipate in this study. All subjects were older than 16 years and before treatment

were medically screened with an electrocardiogram, spine radiographs, complete

blood count, serum electrolyte, blood urea nitrogen, and serum glucose, calcium,

phosphorus. glutamic-oxaloacetic transaminase, lactic dehydrogenase, biliruhin,

alkaline phosphatase. and creatine phosphokinase. All 3 1 subjects were inter

viewed before initiation of ECT and a minimum of four times after initiation of

therapy. The initial interview consisted of a routine medical history and a stan

dardized research questionnaire based on psychiatric diagnostic criteria of Feigh

ncr et at. 1172. By the diagnostic method of Feighner et at, it is possible for

the same individual to have more than one psychiatric diagnosis Robins et at,

1177. Standardized evaluation of orientation, recent meniory, and remote

memory was done initially and on each follow-up visit. The method used was

that of Irving er at 1Q70. Memory testing of all subjects was done 30 36 hr

alter every second ECT second. fourth, sixth, etc. and the last ECT. Subjects

who developed confusion were tested daily until the acute organic mental

syndrome AOMS cleared or the patient was discharged 0froni the hospital.

Charts were reviewed for observations of confusion, disorientation, or other

svmptonis of organic niental syndrome. Exposure to psychoactive drugs was

estimated h' nìeans of drug risk number DRN calculation. The DRN method

is described in detail elsewhere Summers, lQ7M. Essentially, the higher the

DRN number, the greater the exposure to drugs known to induce or enhance

anticholinergic onianic mental syndromes.

The terms post-ECT confusion and AOMS are used interchangeably in

this paper. Acute oreanic mental syndrome was defined in this study by the pre

sence of either of the following: i Acute deterioration of intellectual function

inc as measured liv "names learning" and remote memory test Irving et at.

l10 I: or ii Acute loss of orientation to time greater than 3 days error, place.

or person. The term "lelirium" was reserved for patients who met criteria for

AUNtS and had two of the following: delusions, hallucinations, depersonaliza

Don. rapid fluctuation of affect, or bizarre psychomotor activity.

ECT procedure was bifrontal with seizure precipitated by a Reiter MOLAt

11 electroshock device. A 60-cycle a-c flow set at "low" milliamperage at 105

125 V for 1 .0 2.0 sec between bifrontal electrodes was usually adequate to ii

duce a grand ma! seizure. Pre-ECT medications were: atropine, 1 .0 mg subcuta

neously 30-oU mm before treatment; methohexital, 0.3 mg/lb iv; and sue

elm Icholine. 0.2 mg/lb iv PiUs, 1972. Only three subjects received pretreat

ment oveen. Duration of seizures were 15--3D sec.

Table 1. Characteristics or Postetectroconvulsive Therapy Confusion°

Mean Range

days days

ICTo onset 5.5 ± 1.3 1-19Iay of onset 1 .5 ± 2.2 1-33Day of termination 30.5 t 2.4 19-44Duration 20.1 ± 3.2 5-43

Data front 1 3 subjects with no evidenceof organic mental syndrome prior toEC F.

RESULTS

Of 31 subjects completing the study, 15 48.4 developed AOMS. Nouhject met criteria for delirium. Two subjects had mild chronic organic mentalsyndrome and affective disorder before ECT. Both developed acute organicmental syndrome which had a duration of 45+ and 65+ days after the first ECT.Characteristics of AOMS in 13 subjects with no previous history of memoryimpairment are given in Table 1.

There were no significant differences between the 16 comparison subjectsand the 15 AOMS subjects for age, sex, or race. Table II gives data on factors previously associated with organic mental syndromes. Comparison between AOMSPatients and comparison patients for preelectroconvulsive therapy laboratoryvalues shosved no significant differences. The psychiatric diagnoses prior to treatment are given in Table 111.

Exposure to psychoactive drugs is given in Fig. 1. AOMS subjects receivedtimore exposure to psychoactive agents than comparison subjects during the course

Table 11. Risk Factors Associated with Acute Organic Mental Syndrome

N Age years pjoa PDI FroliC ECTI!

AOMS 15 47.0 t 12.4 9C 9 8 9.7 ± 0.9Comparison 16 36.5 ± 7i 3" 9 9 8.8 + 0.3

alMl = Presence of significant medical illness in past.= Previous major surgery.

C Foul = Family history of psychiatric disease.dECT = Mean number of clectroconvulsive treatments given. Fur age andFD, 1.96 SE is given.

Ctefers to p -c 0.05.

908 Summers, Robins, and Reich Acute Organic Mental Syndrome After Bilateral ECT 909

Table Ill. Psychiatric Diagnosis of Comparison and Poswlcctro

convulsive Therapy Confusion Subjects OMSa

Diagnosis ,O1S Comparison

Voipolar affective disorder primary 6 4Unipolar affective disorder secondary 5 4Bipolar affective disorder primary

Bipolar affective disorder secondary

3

1

2

2Antisocial personality 0 2tIriquet's syndrome 1

Anxiew neurosis ii 3Ohsessive-compulsive neurosis 1

Alcohol abuse 1Drug abuse 1 1

Schizophrenia 1 0Schizophrenia affective 1

Chronic organic mental syndrome tUndiagnosed 1 2

ap > 0.05 not significant or all diagnoses.16 AOMS subjects had 2 diatnoscs. 5 coot parison sohjects had 2dianoses. I comparison subject tad 3 diagnoses.

` Post-ECT confusion in these two suhlccis tas markcdly pnlonL'cdsee te'.t.

ot' ECT. This difference reached significance of p <0.05 on days 5, 7, 14, 16,

18, and 1 after the initiation of ECT.

DISCUSSION

Shortly after Cerletti and Bini 1938 described electroconvulsive therapy,

the problem of memory deficit was recognized Sherman et at, 1941; Stain

hmook. P46: Huston and Strother, 1948; Stone, 1947: Wilcox, 1949. initially,

memory deficit was felt to be a necessary side effect of electroconvulsive therapy

I3rengelniann. l59. Korin et at 1956, Cronholm and Ottosson 1961, and

Ottosson 1004: l62: 1967 demonstrated that memory deficit after ECT was

not necessary for clinical improvement. Since the recognition of electroconvul

sive therapy induced memory deficit as a side effect, and since the advent of

unilateral ECT. there have been many studies and reviews of post-ECT memory

deficits Crnnholm and Molander, 1957; Cronholm and Blomquist, 1959;

Fink. 1977: Halliday er at, 1970; Domnbush, 1972;Squire, 1974,1975; Dornbush

and Williams. 1974: Squire and Chace, 1975; Harper and Weins, l975;Reichert

it at, IC6: Squire er at, 1975, 1976; Small Ct at, 1977; D'Elia and Raottna,it77 Squire and Stater. 1978; Frankel et at, 1978. Few of these studies are

pertinent to these data, as they concern only the single symptom of memory

Jeficit. and man of these studies concern only effects immediately after ECT.

I he symptom of memory disturbance is an integral part of AOMS, hut it is pus-

6

15

14

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2

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9zgo

7

6

5

4

3

2

50%

240%CI

30%

U

0%

0P2 3 4 5 6 7 8 9011231456710192021days

Fig. 1. Exposure to psychoactive drugs estimated by drug risk numberDRN catculation.

sible to have mild memory disturbance without the presence of clinical AOMS.This paper concerns the clinical syndrome of acute organic mental syndrome.

There are only two studies addressing AOMS after ECT Kalinowsky andfloch, 1946; Stainbrook, 1946. Both using less precise methods note that theAUMS clears within "2 weeks." if one assumes that post-ECT confusion represents an extension of the process causing minimal memory deficits, crude comparison with the literature is possible. The frequency of no discernible memorydeficit after ECT has been reported to be 12.6-27.0% Bidder et at, 1970;Brunsehwig a' at, 1971. In this study, 51.6% of subjects did not meet criteriafor AUMS. The average onset of ECT-related AOMS reported here was 5.5 ± 1 .3With a mean duration of 20.1 ± 3.1 days. Brunschwig ct at 1971 tested memoryfunction 36 hr after ECT and found an average onset of memory deficit afterthe fourth ECT. Follow-up studies of memory deficits are consistent with theduration of AOMS observed here Strain et at, 1968; Bidder a' at, 1970; Squire,

I I I I I i__j_0P2 3 4 5 67 8 90 I2341567 15192021

_......._t____i I I - I I I

910 Summers, Robins, and Reich

and `hace, 1Q75: Squire eta!., 1976. Squire and associates demonstrated mem

on deficits 12 days after completion of ECT, hut not at 6-9 month follow-up

Squire. 1975; Squire ci a!.. 1976. Strain cia!. 1968 and Brunschwig et a!.

I7 1 noted a trend of improvement in recent memory between the last ECT

and 10 days of follow-up. Follow-up of these patients at 30 days and 1 year

showed memory to be better than pre-ECT testing Bidder ci at, 1970.

The etiology of post-ECT confusion is elusive. llolmberg 1Q53 postu

lated anoxia as a cause in unmodified ECT. Ottosson 1960 proposed that ex

cessive electrical current was causal. Others have proposed psychologic phobic

reactions as causal J. Vortis. personal communication. It is known that other

forms of AOMS are associated with drug toxicity, increasing age, preexisting

chomic organic mental syndromes, and prior major medical problems Summers

and Reich, IQ7Q.

In this studs', there were no apparent significant differences in environ

mental factors. demographic data. number of treatments, and pre-ECT laboratory

studies. There was definite association between prior medical illness and pro

hahle association with prior chronic organic mental syndromes.

The finding of higher drug exposure in AOMS subjects is of theoretical

and possibly practical interest - Drachman 1977 has postulated that memory

is a function of central nervous systeni cholinergic neur&ns and that acute mciii

or' loss represents dysfunction of these neurons or an anticholinergic state. The

DRN data sould support this theory, because high DRN values reflect increased

exposure to anticliolinergic drugs Summers. 1978. It seems unlikely that anti

cholinergic drugs alone are responsible for the AOMS seen in this study. The

DRN values noted here are considerably less than that noted in other types of

AUNIS Summers. 1Q78: Summers and Reich, 1979. Further, convulsive ther

apy alone is knos n to cause AOMS. Anticholinergic drugs, then, may only he

contributory to AOMS after ECT.

If Drachmans hypothesis is correct, ECT itself should exert an anti

cholinergic effect. The effect of ECT on neurotransmitters has been reviewed

by Essnian 1Q73. In this review, there is evidence that 111 induces rupture

or increased permeability of presynaptic vesicles containing hound acetylcholine.

The liberated acetylcholine is reflected by elevation of extracellular acetyl

choline after ECT. Because of reduced availability of "bound" intracellular

acetylcholine. ECT may cause a synaptic acetylcholine deficit. If this hypothesis

Es correct. anticholinesterase drugs may improve or reverse AOMS after Ed.

Further. the incidence of AOMS after EdT could be reduced by minimizing

psychiactive drug exposure during EdT.

Acute Organic Mentat Syndrome Alter Bilateral ECT911

Brengelniann, J. C. 1959. The Effect ofRepeated Electros/jock on Learning in Depress/peg,Springer-Verlag, Berlin.Vronschwig, L., Strain. .1. J., and Bidder, T. U. 1971. Issues in the assessment of post-ECTmemory changes. Ps;'chiat. 119: 73.`erletti, U and Bini, L. 1938. L'elettroshock. Arc/i. Ge,:. Neuro!. Psychiat. Psyehoanai.19: 266.ronholns B., and Bioniquist, C. 1959. Memory disturbances after electroconvulsivetherapy: 2. conditions one week after a series of treatments. Acre Frye/i/at. Scand.34: 18.

ronliol in, B., and Molander, L. I 957. Memory distorhances after etectroconvulsive tIterapy: 1. conditions six hours after electroshock treatment. .4cta Ps;'c/,lot. Scand.32: 280. -

`ronhohn, B., and Ottosson, 1. 0. 196t, Memory fonctions in endogenous depressionbefore and after electroconvulsive therapy. Arch. Ge,,. Psych/at. 5: 193.1'Elia, U., anti Roatma, A. Il 977. Memory impairment after convulsive therapy. Arc/s.Psyc/ilat. Nen'cnkr. 223: 219.lt,rnbush, 14. L. 1972. Memory and indoced ECT convulsions, Set,,. Psj'chjat. 4: 47,Dornbush, U. L., and Williams, M. 1974;, Memory and ECT', in Psychobiology ofconi'ulslit' Therapy, link, M,, Kety, S., McUaoglt, J. eds.t, V. 1-1. Winston & Sons. Washington, D.C., p. 199.traLiinian, D. A. 1977. Memory and cognitive fonction in man: does the cliolinergic system have a specitic role? Neurology 27: 783.I -.Ioan, W. B. 1 973. Neuroc/jep/,-1 of cerebral Electroshock, Spectrum Publications,i'loshing, New York.I eighner, J. P., Robins, E., Goze, S. B., Voodroff, U. A., Winokur, U., and Munoz, 11.1972. Diagnostic criteria tor use in psychiatric research. ire/s. Ge:,. Ps'chiat.26: 57.link-, M. 1977. Myths of "shock therapy." Am. J. Psych/at, 134: 991.Irankel, F. ii., Bidder, T. U., Fink, M. et at teds.. 1 978. America,, Psychiatric Association Task Force Report 14: Electroco,,puigjt'e Therapy, APA, Washington, D.C.lialliday, A. M,, Davison, K., Browne, M. V. ci a!. 1970. A comparison of the effects ondepression and memory of bilateral ECT and onilateral ECT to dominant and nondominent hemispheres. Br. J, Ps chiat. 127: 430.Ilarper, U. U., and Wiens, A. N. 1975. Eleetroconvoisive therapy and memoryj. Nen'ousAJenta/Discase 161: 245.Ilarsviti, T. D. 1974. Eteetroconvolsive therapy: A review. co:npr. Psych/at. IS: 303.1 liii:: he rg, U. 1 953. The tac tor ot hypoxemia in electroshock therapy. A ,,,. J, Ps,j'c/siat.110: 115.houston, P. F., and Strother, C. U. 1948. The effect of electric shock on mental efficiency.An,.J. Psych/at. 104: 707.Irving, U., Robinson, U. A., and McAdain, W. t1970;. The validity of some cognitive testsin diagnosis of dementia. Brit. J. Psychiat. 11 7:149.Kalinowsky L. 13., and I-loch, P. H. 1946. Shock Treat,nenrs, Urone and Stratton, NewYork.Korin, H., Fink, M., and Kwalwasser, S. 1956. Relation of changes in memory and learningto improvement in electroshock. Con/in. Neurol. 16: 88.Ottosson, J. 0. 1960. Experimental studies of memory impairment after electroconvulsivetherapy: The role of the electrical stimulus intensity and modification by lidocaineof seizure discharge. Acta Psych/at. Scant!, 145: 103.ttttosson, 1. 0. 1962, Electroconvulsive therapy: Electrostimolatory or convulsive therapy?J. Neuropsychiat. 3: 216.

trtoss 1. 0. 1967. Memory distorbance after ECT: A major or minor side effect. fi-oc.First hit. co:ig. Acad. Psychosoinat. Mcd, 134: 161.j Pots, F. N. 1972. Medical aspects of ECT. Sent. Psych/at. 4: 27.keicher, H., Benjamin, J., Meufeldt, A. H., and Marjerrison, U. 1976. Bilateral and non-dominant unilateral ECT. Part 11: Development of prograde effects, can. Psych/ar.Assoc,J, 21: 79.

REFERENCES

Biddcr. T. C'.. Strain, J. J., and Brunschwig, L. 19701. Bilateral and unilateral ECT: Foliofl

op siody and critique. ,ini. J. Psych/at. 1 27: 737.

912 Summers, Robins, and Reich I Biological Psj'c/ziatry, VoL 14, No. 6, 1979

Robins, IL, Gentry, K. A., and Munoz. R. A. 1977. A contrast of the three more common

illnesses with ten less common in a study and 1 8-month follow-up of 314 psychiatric

emcrgcncy room patients. .4mb. Gen. Pryc/ziat. 34: 259.

Sherman, 1., Mergenen, 1., and Levitin, D. 1941. The effect at convulsive treatment on

memory. Am. J. Psychiat. 98: 401.

Small, J. 3., Small, V., Milstein, V., and Dian, D. A. 1977. Effects of ACTFI U-ID on ECT

induced memory dysfunctions. Acta Psychiar. Scand. 55: 241.

Squire, L. R. 1974. Amnesia for remote events following electroconvulsive therapy. Rehat

Riol. 12: 119.

Squire, L. R. 1975. A stable impairment of remote memory following electroconvulsive

therapy ..Veuropsychologia 13: 51.

Squire, L. R., and Chace, P. SI. 1975. Memory functions six to nine months after electro

convulsive therapy. .`lrc/i. Gen. Psyelziar. 32: 1557.

Squire, L. K., and Slater. P.C. 1978. Bilateral and unilaleral ECT: effects on verbal and

non-verbal memory. Am. J. Psychiat. 135: 1316.

Squire. L. K., Slitter, P. C., and Chace. P. ft 1975. Retrograde amnesia: temporal gradient

in very long-term memory following electroconvulsive therapy. Science 187: 77.

Squire, L. R., Slater, P. C., and Chace, P. NI. 1976. Reactivation of recent or remote

mentory before electroconvulsive therapy does not produce retrograde amnesia. Be-

hat. Riot 18: 335.

Stainhrook. E. J. 19461. Shock therapy: psychologic theory and research. Prychol. Bolt

43: 21.

Stone. C. 1'. 19471. Losses and gains in cognitive functions as related to electroconvulsive

shocks. J. .4bnormal Soc. Psycho?. 42: 206.

Strain, J. 3.. Bronschwig. L.. Dully. 3. P., and Bidder, T. 3. 1968. Comparison of thera

peutic effects and memory changes with bilateral and unilateral EçT. Am. J. Pst'chiat.

125: 294.

Summers. V. K. t t9St. A clinical method of estimating risk of drug-induced delirium. Life

Sct 22: 1511.

Summers. W. K.. and Reich. T. 1979. Delirium after cataract surgery: review and two

cases. A in .1. Pss'chiat. 1 36.

Wilcox. K. W. fl949L Oranie Shock syndrome. .llich. Acaci. Sct 35: 357.

ii119

Potentials

`S

I `isual evoked brain potentials 6'VIfP trepeated stimuli ofseveral interstisnulus

intervals 1Sf were recorded from youitg adults it'itlz Dost'n `s syndrome DS.

The folio `wing results were obt/tined: i A n"45'I effect previously observed in norfuels: VEP amplitudes increa/ed wit/i increasin 151; some 151 effect on latency

was also observed; ii VEIJ amplitudes of Dsubjects were larger than VEP

amplitudes of normals; iii!VEP peak latencies fDS subjects were longer than

VEPpeak latencies obtainec/froin normals; iv 151 h'bQ a more pronounced effectop VEP amplitudes ofDLS7 than ii orinal sub/ects. Thes'çresults are discussed Wit/i

respect to CNS differencfrs and issues of attention and'sQfonnation processing.

INTRODUCTION

A number of studies have demonstrated a relationship htween evoked

potentials EP and stimulus presentation rate or tts complimentary terstimulus

interval JSI. This effect recovery function, IS! effect has been ftoted in hu

mans for the early components eg., Shagass, 1977 and long-1aten compo

tents of the EP, and for ISIs of less than 1 sec e.g., Surwilo, 1977 anU greaterI S

Supported in part by'U.S. Public Health Service grant #927 from Maternal and Child Health

Service; and grants #HD-00345, HD-04612, and HD-05615 from NICHD; and the Mental

Retardation Program, Neuropsychiatric Institute, UCLA; and the Department of Psychi

atry, University of Minnesota.

Department at Ppita Box 95 Ma u BIdL University of Minnesota MinneapoltsMinnesota.

lealtIi Training Center, Los Angeles, California.Departm of Psychiatry, University of California, Los Angeles, California.

913

tiniulusEffects of Re of Repetiti

Presentation o"n the V

of Young AduIwith

A. M. Yellin,t A. K. Lodwig,

Rm'ceit'cd February 5, 1979: revised

0006-3223/79/1200-0913 $03.00/i © 1979 Society of Biological Psychiatry