Electroconvulsive Therapy in Late-Life · PDF fileChapter 13 Electroconvulsive Therapy in Late-Life Depression Harold A. Sackeim Electroconvulsive therapy (ECT) plays a significant

Chapter 13Electroconvulsive Therapy inLate-Life Depression

Harold A. Sackeim

Electroconvulsive therapy (ECT) plays asignificant role in the treatment of late-life depression and other psychiatric con-ditions in the elderly. Compared to phar-macologic treatments, ECT is adminis-tered to an especially high proportion ofelderly patients. For example, a survey ofpractice in California between 1977 and1983 indicates that the probability of re-ceiving ECT increases markedly with pa-tient age (Figure 1). Of 1.12 persons per10,000 in the general adult populationtreated with ECT, 3.86 per 10,000 areaged 65 years or older;1 treatment withECT was constant over this period and thehigh percentage of elderly patients isnoteworthy. A national survey of inpatientpsychiatric facilities conducted by the Na-tional Institute of Mental Health (NIMH)also indicates that patients aged 61 andolder comprise the largest age group toreceive ECT in 1975 to 1980.2 In the mid-1970s when use of ECT in the UnitedStates had declined, ECT treatment of in-patients aged 61 and over remained con-stant.2 Use increased again during the1980s; in 1986 the national estimate wasthat 15.6% of inpatients aged 65 or olderwith mood disorders received ECT, com-pared with only 3.4% of younger inpa-tients with mood disorders.3

Data from the most comprehensive na-tional study of factors associated with in-patient use of ECT, published in 1998, es-timated that nearly 10% of a sample of

nearly 25,000 depressed inpatients re-ceived ECT during their hospital stay.4

(Figure 2) Factors most strongly predict-ing ECT use were age, race, insurance sta-tus, and median income of the patient’shome zip code. Older patients, Cauca-sians, and those with private insurance liv-ing in affluent areas were most likely tobe treated with ECT. Diagnosis ratherthan age, however, is the primary indica-tion for the use of ECT. The vast majorityof patients treated with ECT in the UnitedStates were experiencing an episode ofmajor depression, either unipolar or bipo-lar. The NIMH national diagnostic surveyconducted in 1986 reveals that 84% of pa-tients who receive ECT are diagnosed witha major mood disorder.3 The primary fac-tors leading to consideration of ECT,regardless of age, are (1) a history of inad-equate response or intolerance to anti-depressant medication or (2) a history ofgood ECT response during prior depres-sive episodes.5–7 ECT is administered lessfrequently for schizophrenia8 and mania.9

Among patients of all ages, ECT ismore effective and more likely to producesymptom remission than antidepressantmedication.10–15 The extent to which ECTis used early or late in the course of antide-pressant treatment varies markedly fromcountry to country and, within the UnitedStates, varies considerably among locali-ties and practitioners.16,17 ECT is particu-larly beneficial when elderly depressed pa-tients are also medically ill, psychotic, orsuicidal. Thus, ECT is most frequently ad-ministered to geriatric patients when anti-

Part IV / Affective Disorders386

Figure 13.1. Patients treated withECT in California, by age group andyear; data for 1993 were unavail-able.

depressant medications are too risky, haveproven ineffective, or when ensuring arapid or full clinical response is particu-larly important.

Indications for ECT

ECT is indicated for the acute treatmentof depression as well as for maintenancetreatment and prevention of relapse. Clin-ical outcome of ECT is more predictablein patients exhibiting particular charac-teristics of major depression. As with phar-

Figure 13.2. Rate of ECT utilization in a sam-ple representative of inpatients in the US in1993 with a diagnosis of recurrent, majordepression. (From Olfson, et al. 1998.)4

macologic treatment, duration of the de-pressive episode consistently correlateswith a positive ECT response: patients (ofall ages) with longer duration of illnessrespond less well.18–24 This relation be-tween duration of illness and treatmentresponse may reflect the impact of depres-sion in CNS functioning. Duration of adepressed state correlates with the extentof hippocampal atrophy associated withchronic depression. Because the hippo-campus has an established role in regulat-ing the hypothalamic–pituitary—adrenal

Chapter 13 / Electroconvulsive Therapy in Late-Life Depression 387

(HPA) axis, the atrophic effects of depres-sion may lead to increased vulnerabilityto stress and prolongation of the episode.Patients with hippocampal atrophy areespecially resistant to antidepressantmedications, particularly tricyclics. Poorresponse to antidepressants, in turn,predicts/correlates with inferior short-term response to ECT18,25–27 as well as toother somatic treatments.28,29 ECT islikely to be of greatest value when it is ad-ministered early in the course of a depres-sive episode and not as a last resort afterall other treatments have failed.

Maintenance ECT, with treatmentsspaced over weekly to monthly intervals,is increasingly used for relapse preven-tion.30–32 Unfortunately, continuation ormaintenance ECT is commonly employedonly after pharmacologic methods of re-lapse prevention have failed following suc-cessful ECT. At present, the vast majorityof patients who respond to ECT are thentreated with antidepressant medicationsdespite evidence that failed medicationregimens during the acute depressive epi-sode are ineffective in preventing relapsefollowing ECT.24,26,30,33,34

Efficacy

Overall, research observations and clini-cal experience indicate that ECT is partic-ularly useful in the treatment of late-lifedepression. Prior to the introduction ofECT, elderly depressed individuals oftenexhibited chronic depression or died ofintercurrent medical illnesses in psychiat-ric institutions.35 A number of studies con-trast the clinical outcome of depressed pa-tients who received inadequate or nosomatic treatment to that of patients whoreceived ECT (Figure 3) While none ofthis work involves prospective, random-as-signment designs, the findings are largelyuniform. Contemporary ECT adminis-tered to elderly patients results in de-creased chronicity, decreased morbidity,and possible decreased rates of mor-tality.36–39

Studies comparing ECT to other formsof antidepressant treatment15,40 are rela-tively sparse. A metaanalysis of early com-parative-age patient samples11 reportsthat the average response rate to ECT is20% higher when compared to tricyclicantidepressants (TCAs) and 45% higherwhen compared to monoamine oxidaseinhibitors (MAOIs), although by modernstandards, the pharmacologic treatmentsused were often suboptimal.18,33,41,42 Nostudy has ever found a pharmacologic reg-imen to be superior in antidepressant ef-fects when compared to ECT. Rather,ECT consistently has had either equal orsuperior efficacy. In both young and el-derly populations, ECT is superior to astandard antidepressant,15 although theaddition of lithium to an antidepressantresults in more rapid onset of improve-ment compared to ECT in patients withtreatment-resistant depression.40,43,44

Other differences between ECT andantidepressant treatments concern speedand quality of clinical response as well asresidual symptoms. Residual symptom-atology resulting from incomplete re-sponse to antidepressant medications maybecome chronic or lead to relapse.45 Be-cause remission is more likely followingECT, there is less chance of recurrence ofchronic residual depressive symptoms.

Whether ECT reduces depressivesymptoms more quickly than antidepres-sants in the elderly has not been ade-quately tested. Nonetheless, evidence sug-gests that no pharmacologic strategyresults in as rapid symptomatic improve-ment as ECT.10,12,13 Significant clinicalimprovement is usually seen within thefirst few treatments, with maximal gainsseen by 3 weeks. This rapid improvementis less common with antidepressant medi-cations.

Aging and Efficacy

The response rate to ECT is higher amongolder patients,46–49 and a positive associa-tion is seen between patient age and de-gree of clinical improvement following


Figure 13.3. Examples of waveforms used in ECT. Top left: sine wave. Top right: chopped, recti-fied sine wave. Bottom left: brief pulse, square wave. Bottom right: ultra-brief pulse, square wave.(From Sackeim HA, Long J, Luber B, et al. Physical properties and quantification of the ECTstimulus: I. Basic principles. Convuls Ther 1994;10:93–123).

ECT.46–49 Table 13.1 provides a selectivesummary of studies addressing the rela-tion between patient age and ECT out-come. Older individuals, however, mayhave a diminished response to unilateral,as opposed to bilateral, ECT50,51 and mayrequire longer courses of treatment toachieve the same level of remission asyounger patients.52,53 ECT may also be ef-fective in the very oldest depressed pa-tients.54–57

Predictors of Response

Two factors correlate with response toECT in the elderly: intensity of the electri-cal stimulus, and the patient’s diagnosis.

The extent to which the intensity of theelectroconvulsive stimulus exceeds the in-dividual patient’s seizure threshold deter-mines the efficacy of right unilateral ECTand speed of response regardless of elec-trode placement.58–62 Age is one of themore reliable predictors of seizure thresh-old62–64: the oldest patients generally havethe highest thresholds, shortest seizureduration, and lowest EEG seizure ampli-tude.60,65,66

In addition to stimulus intensity, evi-dence shows that among depressed pa-tients, those with psychotic or delusionaldepression respond especially well toECT.25,30,67–72 Although not definitively


Tabl

e 13

.1.

Rel

atio

n B

etw

een

Pat

ient

Age

and

EC

T O

utco

me:

Sel

ecte

d S

tudi

es

Stud

y*P

atie

nts

Stud

y D

esig

nE

CT

Tre

atm

ent

Res

ults

/Com

men

ts

Pru

dic

et a

l.34

7 pa

tient

s w

ith m

ajor

Pros

pect

ive,

nat

ural

istic

stu

dy o

fM

odifi

ed E

CT

giv

en 3

tim

es/w

eek;

Age

, tre

ated

as

a co

ntin

uous

var

iabl

e,(2

004)

depr

essi

on tr

eate

d at

7E

CT

pra

ctic

es a

nd o

utco

mes

indi

vers

e el

ectr

ode

plac

emen

t and

not r

elat

ed to

sym

ptom

impr

ovem

ent

hosp

itals

in th

e N

ew Y

ork

com

mun

ity s

ettin

gs; e

valu

atio

nsdo

sing

pra

ctic

esor

cat

egor

ical

clin

ical

out

com

esm

etro

polit

an a

rea

befo

re, i

mm

edia

tely

aft

er, a

ndm

onth

ly fo

r 6

mon

ths

follo

win

g E

CT

O’C

onno

r25

3 pa

tient

s w

ith m

ajor

Pros

pect

ive

natu

ralis

tic a

cute

Mod

ified

EC

T g

iven

3 ti

mes

/wee

k;L

ower

rem

issi

on (

70%

) in

you

nges

t age

et a

l.de

pres

sion

, tre

ated

ope

nly

phas

e st

udy

follo

wed

by

doub

le-

patie

nts

titra

ted

at fi

rst s

essi

ongr

oup

than

eith

er o

lder

adu

lts(2

001)

with

titr

ated

(50

% a

bove

blin

d co

ntin

uatio

n tr

ial

and

trea

ted

afte

rwar

d w

ith(8

9.8%

) or

eld

erly

(90

%);

whe

nse

izur

e th

resh

old)

com

pari

ng n

ortr

ipty

hlin

e an

dsu

prat

hres

hold

inte

nsity

50%

thes

e di

men

sion

s w

ere

trea

ted

asbi

late

ral E

CT

lithi

um w

ith c

ontin

uatio

n E

CT

;ab

ove

thre

shol

dco

ntin

uous

var

iabl

es, a

ge w

as a

lso

acut

e re

spon

se to

EC

Tre

late

d to

out

com

e.co

ntra

sted

in 3

pat

ient

gro

ups:

youn

g ad

ult (

!45

yea

rs),

old

erad

ult (

46 to

64

year

s) a

ndel

derl

y (6

5 ye

ars

and

olde

r)

Sack

eim

et a

l.80

inpa

tient

s w

ith m

ajor

Dou

ble-

blin

d, p

rosp

ectiv

e st

udy

Mod

ified

EC

T g

iven

3 ti

mes

/wee

k;H

igh

dosa

ge r

ight

uni

late

ral E

CT

(200

0)de

pres

sion

ran

dom

ized

of e

ffec

ts o

f ele

ctri

cal d

osag

epa

tient

s ra

ndom

ized

to 3

form

s(6

" th

resh

old)

and

bila

tera

l EC

Tto

4 g

roup

s (r

ight

and

elec

trod

e pl

acem

ent;

of r

ight

uni

late

ral E

CT

(1.

5, 2

.5,

(2.5

"th

resh

old)

equ

al in

eff

icac

yun

ilate

ral a

t 1.5

, 2.5

, or

patie

nts

eval

uate

d be

fore

EC

Tor

6 "

seiz

ure

thre

shol

d) o

ran

d su

peri

or to

low

er d

osag

e ri

ght

6 tim

es s

eizu

rean

d re

gula

rly

duri

ng a

nd a

fter

bila

tera

l EC

T (

2.5

"ST

)un

ilate

ral E

CT

; no

age-

rela

ted

effe

cts

thre

shol

d or

bila

tera

ltr

eatm

ent c

ours

eE

CT

at 2

.5 ti

mes

sei

zure

thre

shol

d); f

ree

of a

llm

edic

atio

ns e

xcep

tlo

raze

pam

(up

to 3

mg/

day

PRN

)(c

ontin

ued)


Tabl

e 13

.1.

(con

tinue

d).

Stud

y*P

atie

nts

Stud

y D

esig

nE

CT

Tre

atm

ent

Res

ults

/Com

men

ts

Tew

et a

l.26

8 pa

tient

s w

ith m

ajor

Pros

pect

ive

natu

ralis

tic a

cute

pha

seM

odifi

ed E

CT

giv

en 3

tim

es/w

eek;

Mor

e ph

ysic

al il

lnes

s an

d co

gniti

ve(1

999)

depr

essi

on, t

reat

ed o

penl

yst

udy

follo

wed

by

doub

le-b

lind

patie

nts

titra

ted

at fi

rst s

essi

onim

pair

men

t in

both

old

er a

ge g

roup

sw

ith s

upra

thre

shol

dco

ntin

uatio

n ph

arm

acot

hera

pyan

d tr

eate

d w

ith s

upra

thre

shol

dth

an in

adu

lt gr

oup.

Bot

h ol

der

unila

tera

l or

bila

tera

l EC

T;

tria

l; ac

ute

resp

onse

to E

CT

inte

nsity

sel

ecte

d by

trea

ting

grou

ps h

ad s

hort

er d

epre

ssiv

efr

ee o

f all

med

icat

ions

cont

rast

ed in

3 p

atie

nt g

roup

s:ps

ychi

atri

step

isod

es a

nd w

ere

less

like

ly to

be

exce

pt lo

raze

pam

adul

t (59

yea

rs a

nd y

oung

er),

med

icat

ion

resi

stan

t. T

he a

dult

(up

to 3

mg/

day

PRN

)yo

ung-

old

(60

to 7

4 ye

ars)

and

patie

nts

had

a lo

wer

rat

e of

EC

Tol

d-ol

d (7

5 ye

ars

and

olde

r)re

spon

se (

54%

) th

an th

e yo

ung-

old

patie

nts

(73%

), w

hile

the

old-

old

patie

nts

had

an in

term

edia

te r

ate

ofre

spon

se (

67%

).

Sack

eim

et a

l.96

inpa

tient

s w

ith m

ajor

Dou

ble-

blin

d, p

rosp

ectiv

e st

udy

ofM

odifi

ed E

CT

giv

en 3

tim

es/w

eek;

Ele

ctri

cal d

osag

e de

term

ined

uni

late

ral

(199

3)de

pres

sion

ran

dom

ized

effe

cts

of e

lect

rica

l dos

age

and

patie

nts

titra

ted

at fi

rst s

essi

onE

CT

eff

icac

y an

d sp

eed

of r

espo

nse

to 4

gro

ups

(uni

late

ral o

rel

ectr

ode

plac

emen

t; pa

tient

san

d tr

eate

d ei

ther

at j

ust a

bove

for

unila

tera

l and

bila

tera

l EC

T; n

obi

late

ral E

CT

at l

ow- o

rev

alua

ted

befo

re E

CT

and

thre

shol

d or

at 2

.5 ti

mes

initi

alag

e-re

late

d ef

fect

s se

en.

high

-stim

ulus

inte

nsity

);re

gula

rly

duri

ng a

nd a

fter

seiz

ure

thre

shol

dfr

ee o

f all

med

icat

ions

trea

tmen

t cou

rse

exce

pt lo

raze

pam

(up

to3

mg/

day

PRN

); a

gera

nge,

22–

80; m

ean,

56.

4

Bla

ck e

t al.

423

depr

esse

d in

patie

nts

Ret

rosp

ectiv

e ch

art r

evie

w u

sing

Mod

ified

EC

T g

iven

3 ti

mes

/wee

k;Pa

tient

s ra

ted

as r

ecov

ered

(n

#29

5)(1

993)

betw

een

1970

and

198

1m

ultip

le lo

gist

ic r

egre

ssio

n to

bila

tera

l, un

ilate

ral,

mix

edol

der

than

thos

e ra

ted

asid

entif

y re

spon

se p

redi

ctor

sco

urse

s in

clud

edun

reco

vere

d (n

#12

8)


Sack

eim

et a

l.52

inpa

tient

s w

ith m

ajor

Dou

ble-

blin

d, p

rosp

ectiv

e st

udy

Bila

tera

l or

righ

t uni

late

ral

Low

-dos

age

righ

t uni

late

ral E

CT

(198

7a, b

)de

pres

sion

ran

dom

ized

com

pari

ng lo

w-d

ose,

titr

ated

mod

ified

EC

T 3

tim

es/w

eek;

inef

fect

ive;

reg

ardl

ess

of E

CT

to u

nila

tera

l or

bila

tera

lbi

late

ral a

nd u

nila

tera

l EC

T;

patie

nts

titra

ted

and

trea

ted

atm

odal

ity, a

ge u

nrel

ated

to c

linic

alE

CT

; pat

ient

s fr

ee o

f all

patie

nts

eval

uate

d be

fore

EC

Tju

st a

bove

thre

shol

dou

tcom

em

edic

atio

ns e

xcep

tan

d fo

llow

ing

trea

tmen

ts 1

, 3, 5

,lo

raze

pam

(up

to 3

6 an

d ev

ery

trea

tmen

t the

reaf

ter

mg/

day

PRN

); a

ge r

ange

,25

–83;

mea

n, 6

1.3

Cor

yell

&31

pat

ient

s w

ith u

nipo

lar

Pros

pect

ive

stud

y of

EC

T r

espo

nse

Mos

t tre

atm

ents

uni

late

ral;

mos

tA

ge in

depe

nden

tly a

ssoc

iate

d w

ithZi

mm

erm

ande

pres

sion

sel

ecte

dpr

edic

tors

; rat

ings

mad

e on

patie

nts

had

at le

ast 6

outc

ome

on m

ore

than

1 o

f 3(1

984)

pros

pect

ivel

yH

AM

- D a

t wee

kly

inte

rval

s by

trea

tmen

ts; p

atie

nts

with

few

erou

tcom

e m

easu

res;

sup

erio

r ou

tcom

ebl

ind

rate

rsth

an 4

trea

tmen

ts e

xclu

ded

in o

lder

pat

ient

s

Ric

h et

al.

Dat

a fr

om 2

gro

ups

ofPr

ospe

ctiv

e st

udy

of r

espo

nse

rate

toM

odifi

ed E

CT

giv

en 3

tim

es/w

eek;

Age

ass

ocia

ted

with

long

er ti

me

to(1

984)

patie

nts

pool

ed: 6

6 w

ithco

nven

tiona

l EC

T b

y id

entif

ying

righ

t uni

late

ral E

CT

use

d $

80%

achi

eve

resp

onse

; stu

dy fl

awed

by

use

maj

or d

epre

ssiv

epo

int o

f max

imal

impr

ovem

ent;

of p

atie

nts;

mea

n no

. of

of d

iffer

ent r

atin

g sc

ales

and

epis

ode

or o

rgan

icpa

tient

s ra

ted

on H

AM

-D b

efor

etr

eatm

ents

for

each

of 2

gro

ups

diff

eren

t EC

T d

evic

es fo

r 2

grou

psaf

fect

ive

synd

rom

e;fir

st E

CT

and

at 3

6–48

hou

rs a

fter

8.6

and

8.3

antid

epre

ssan

tea

ch tr

eatm

ent

med

icat

ions

eith

erst

oppe

d pr

ior

to E

CT

or h

eld

cons

tant

Fras

er &

29 d

epre

ssed

(Fe

igne

rPr

ospe

ctiv

e, d

oubl

e-bl

ind,

Mod

ified

EC

T w

ith tw

ice-

wee

kly

No

age

diff

eren

ce b

etw

een

good

and

Gla

sscr

iteri

a) e

lder

ly (

64–8

6ra

ndom

ized

stu

dy; p

ostic

tal

trea

tmen

t unt

il pa

tient

wel

l or

mod

erat

e ou

tcom

e gr

oups

(198

0)ye

ars)

ran

dom

ized

tore

cove

ry ti

mes

, mem

ory

chan

ges,

EC

T s

topp

edun

ilate

ral o

r bi

late

ral E

CT

and

clin

ical

impr

ovem

ent

asse

ssed

by

HA

M-D

Hes

he e

t al.

51 p

atie

nts

with

end

ogen

ous

Pros

pect

ive

blin

d ev

alua

tions

bef

ore

Eith

er m

odifi

ed u

nila

tera

l (av

erag

eIn

pat

ient

s ov

er 6

0, s

igni

fican

tly b

ette

r(1

978)

depr

essi

on r

ando

miz

ed to

EC

T, a

t end

of E

CT

, and

3 m

onth

s9.

2 tr

eatm

ents

) or

bila

tera

l EC

Tth

erap

eutic

eff

ect f

rom

bila

tera

l tha

nun

ilate

ral o

r bi

late

ral E

CT

afte

r fin

al tr

eatm

ent

(ave

rage

8.5

trea

tmen

ts),

twic

eun

ilate

ral t

reat

men

t; re

gard

less

of

wee

kly,

num

ber

of tr

eatm

ents

mod

ality

, sat

isfa

ctor

y re

sults

in 7

5%de

cide

d by

trea

ting

clin

icia

nof

pat

ient

s $60

yea

rs a

nd 9

6% o

fpa

tient

s !60

yea

rs–a

sig

nific

ant

diff

eren

ce(c

ontin

ued)


Tabl

e 13

.1.

(con

tinue

d).

Stud

y*P

atie

nts

Stud

y D

esig

nE

CT

Tre

atm

ent

Res

ults

/Com

men

ts

Her

ring

ton

43 c

onse

cutiv

e se

vere

lyPa

tient

s ra

ted

on d

ay b

efor

eE

CT

giv

en tw

ice

wee

kly

for

tota

l of

Age

unr

elat

ed to

out

com

eet

al.

depr

esse

d pa

tient

s (a

ged

trea

tmen

t and

wee

kly

ther

eaft

er6–

8 tr

eatm

ents

(197

4)25

–69)

ran

dom

ized

to E

CT

for

4 w

eeks

or l-

tryp

toph

an (

up to

8g/

day)

; 40

patie

nts

incl

uded

in e

ffic

acy

anal

ysis

Strö

mgr

en10

0 pa

tient

s w

ith e

ndog

enou

sPr

ospe

ctiv

e, d

oubl

e-bl

ind

stud

yM

inim

um o

f 6 tr

eatm

ents

giv

en;

Of 5

3 pa

tient

s ag

ed 1

9–44

, 17

wer

e(1

974)

unip

olar

or

bipo

lar

cont

rast

ing

unila

tera

l and

dura

tion

of c

urre

ntre

sist

ant;

7 of

47

aged

45–

65 w

ere

depr

essi

on; a

ged

19–6

5;bi

late

ral E

CT

indi

vidu

aliz

ed; a

vera

ge o

f 9re

sist

ant–

a si

gnifi

cant

diff

eren

cepa

tient

s dr

ug-fr

ee e

xcep

ttr

eatm

ents

giv

en to

you

nger

effic

acy

supe

rior

in o

lder

pat

ient

s fo

rfo

r hy

pnot

ics

and

mild

patie

nts,

8.7

to o

lder

pat

ient

sbo

th b

ilate

ral a

nd u

nila

tera

l EC

Tse

dativ

es

Fols

tein

et a

l.11

8 co

nsec

utiv

e pa

tient

s w

hoR

etro

spec

tive

char

t rev

iew

: pro

gres

sN

atur

e an

d du

ratio

n of

EC

T n

otIm

prov

emen

t rel

ated

to o

lder

age

and

(197

3)re

ceiv

ed E

CT

; dia

gnos

es o

fno

tes

at ti

me

of d

isch

arge

rat

ed a

sde

scri

bed

shor

ter

hosp

ital s

tay;

no

sign

ifica

nce

schi

zoph

reni

a, n

euro

ticto

whe

ther

or

not p

atie

nt im

prov

edte

sts

prov

ided

; mea

n ag

e of

impr

oved

reac

tions

, and

aff

ectiv

epa

tient

s (n

#86

) 50

, com

pare

d w

ithdi

sord

ers

31 in

patie

nts

rate

d no

t im

prov

ed(n

#32

)

Men

dels

53 c

onse

cutiv

e in

patie

nts

Pros

pect

ive

stud

y: p

atie

nts

rate

d w

ith4–

11 tr

eatm

ents

(m

ean

6.4)

with

Supe

rior

out

com

e in

pat

ient

s ov

er 5

0 at

(196

5a,

eval

uate

d pr

e-E

CT

and

1H

AM

-D; e

valu

ator

s no

t blin

d to

mod

ified

EC

T3-

mon

th fo

llow

-up

but n

ot a

t19

65b)

and

3 m

onth

s po

st- E

CT

;tr

eatm

ent h

isto

ry1-

mon

th fo

llow

-up

age

21–7

6, m

ean

48.8

Car

ney

et a

l.12

9 de

pres

sed

inpa

tient

sPr

ospe

ctiv

e st

udy

to e

stab

lish

Patie

nts

rece

ived

3 o

r m

ore

Bet

ter

resp

onse

in e

ndog

enou

s(1

965)

pred

ictiv

e fa

ctor

s; p

atie

nts

scor

edtr

eatm

ents

depr

essi

ves

at 3

and

6 m

onth

s (p

erfo

r pr

esen

ce o

r ab

senc

e of

35

fact

or a

naly

sis)

; in

patie

nts

over

40,

feat

ures

, fol

low

ed u

p at

3 a

nd 6

type

of d

epre

ssio

n no

t ass

ocia

ted

mon

ths

post

-EC

T; o

utco

me

with

out

com

ecr

iteri

a de

fined


Nys

trom

2 se

ries

of p

atie

nts:

254

inPr

ospe

ctiv

e, b

lind

eval

uatio

n;M

odifi

ed b

ilate

ral E

CT

at 2

Lun

d se

ries

: pos

itive

ass

ocia

tion

(196

4)G

othe

nbur

g se

ries

, 188

outc

ome

crite

ria

spec

ified

trea

tmen

ts/w

eek

initi

ally

;be

twee

n ag

e an

d de

gree

of

in L

und;

mos

t cas

esav

erag

e nu

mbe

r in

Lun

d se

ries

impr

ovem

ent i

n fe

mal

es; G

othe

nber

gde

pres

sed

but o

ther

6.9,

4.4

in G

othe

nber

gse

ries

: age

!25

yea

rs n

egat

ivel

ydi

agno

ses

incl

uded

rela

ted

to o

utco

me

Gre

enbl

att

128

patie

nts

rand

omiz

edPr

ospe

ctiv

e st

udy

com

pare

d E

CT

and

EC

T m

odifi

ed b

y su

ccin

ylch

olin

eM

edic

atio

ns a

nd E

CT

equ

ally

eff

ectiv

eet

al.

to 4

trea

tmen

t gro

ups;

antid

epre

ssan

t med

icat

ions

;gi

ven

3/w

eekl

y fo

r 3

wee

ksin

you

nges

t age

gro

up; E

CT

(196

2)di

agno

sis

of s

chiz

ophr

enia

,ex

plic

it ou

tcom

e cr

iteri

a us

edm

inim

um, m

ore

at d

iscr

etio

n of

sign

ifica

ntly

mor

e ef

fect

ive

than

psyc

hone

urot

ic a

ndps

ychi

atri

stm

edic

atio

ns in

old

est a

ge g

roup

psyc

hotic

dep

ress

ive

reac

tions

, inv

olut

iona

lps

ycho

sis;

28

rece

ived

EC

T;

age

16–7

0, m

ean

46

Ott

oson

44 (

18 m

ales

, 26

fem

ales

) w

ithPr

ospe

ctiv

e st

udy

with

blin

d ra

ters

;M

odifi

ed b

ilate

ral E

CT

with

Age

not

sig

nific

antly

rel

ated

to e

ffic

acy;

(196

0)en

doge

nous

dep

ress

ion;

effic

acy

eval

uate

d by

out

com

e 1

inte

rval

s be

twee

n fir

st 3

ther

apeu

tic r

espo

nse

late

r in

old

erag

e 36

–70,

mea

n 55

.8w

eek

afte

r 4t

h tr

eatm

ent,

1 w

eek

trea

tmen

ts o

f 2–4

day

s an

dpa

tient

saf

ter

end

of E

CT

cou

rse,

and

tota

lbe

twee

n fo

llow

ing

trea

tmen

ts o

fnu

mbe

r of

trea

tmen

ts r

equi

red

3–7

days

; dos

e ad

just

ed u

pwar

dfo

r ag

e; p

atie

nts

divi

ded

into

2gr

oups

: one

rec

eive

d st

imul

usgr

ossl

y ab

ove

thre

shol

d, o

nem

oder

atel

y ab

ove

thre

shol

d

Ham

ilton

&49

hos

pita

lized

mal

e pa

tient

sPa

tient

s as

sess

ed p

rosp

ectiv

ely

and

1U

sual

cou

rse

6 tr

eatm

ents

,A

ge u

nrel

ated

to O

utco

me

Whi

tew

ith s

ever

e de

pres

sion

; age

mon

th a

fter

end

of E

CT

max

imum

10;

14

patie

nts

had

(196

0)ra

nge

21–6

9, m

ean

51.7

seco

nd c

ours

e

Rob

erts

50 p

atie

nts,

wom

en 4

1–60

Pros

pect

ive

stud

y of

pre

dict

ors

ofT

wic

e w

eekl

y m

odifi

ed E

CT

unt

ilSy

mpt

om s

core

s at

1 m

onth

: sig

nific

ant

(195

9a,b

)ye

ars

EC

T r

espo

nse;

pat

ient

s sc

ored

on

max

imum

ben

efit;

ave

rage

din

vers

e co

rrel

atio

n w

ith a

ge (

olde

rcl

inic

al fe

atur

es p

rior

to E

CT

and

betw

een

7 an

d 8

trea

tmen

tsw

omen

mor

e im

prov

ed);

no

pres

ence

or

abse

nce

of s

ympt

oms

corr

elat

ion

at 3

mon

ths

at 1

and

3 m

onth

s po

st-E

CT

(con

tinue

d)


Tabl

e 13

.1.

(con

tinue

d).

Stud

y*P

atie

nts

Stud

y D

esig

nE

CT

Tre

atm

ent

Res

ults

/Com

men

ts

Her

zber

g22

7 ca

ses

sele

cted

from

all

Ret

rosp

ectiv

e ch

art r

evie

w o

f pat

ient

sN

atur

e an

d du

ratio

n of

EC

T n

otSu

peri

or o

utco

me

or s

usta

ined

(195

4)pa

tient

s w

ho h

ad r

ecei

ved

rate

d fo

r in

itial

res

pons

e to

EC

T,

desc

ribe

dim

prov

emen

t in

patie

nts

in 4

thE

CT

; dia

gnos

es o

fco

ntin

ued

resp

onse

, no

rela

pse

deca

de c

ompa

red

with

pat

ient

s in

schi

zoph

reni

a, m

anic

afte

r di

scha

rge

othe

r ag

e gr

oups

depr

essi

ve p

sych

oses

,in

volu

tiona

l mel

anch

olia

Hob

son

150

patie

nts

at M

auds

ley

Pros

pect

ive

stud

y to

iden

tify

Nat

ure

and

num

ber

of E

CT

Age

unr

elat

ed to

out

com

e; s

ever

al(1

953)

Hos

pita

l; no

dia

gnos

ticpr

edic

tors

of E

CT

res

pons

e;tr

eatm

ents

not

des

crib

edot

her

pred

icto

rs id

entif

ied

crite

ria

used

, but

alm

ost

patie

nts

cate

gori

zed

as e

ither

free

all c

ases

wer

e de

pres

sed;

of s

ympt

oms

or s

till h

avin

g12

7 in

clud

ed in

ana

lyse

sm

arke

d sy

mpt

oms

afte

r E

CT

Ric

kles

&20

0 pr

ivat

e pa

tient

s tr

eate

dR

etro

spec

tive

stud

y of

why

pat

ient

sU

sual

cou

rse

10–1

2 tr

eatm

ents

;A

utho

rs fe

lt th

at E

CT

faile

d if

patie

ntP

olan

with

EC

T; d

iver

sefa

iled

EC

T; t

reat

men

t con

side

red

patie

nts

with

sch

izop

hren

ia a

lso

was

men

opau

sal o

r po

stm

enop

ausa

l;(1

948)

diag

nost

ic c

ateg

orie

sfa

iled

whe

n im

prov

emen

t not

rece

ived

24–

40 s

ubco

ma

insu

linst

atis

tics

not p

rese

nted

incl

uded

sch

izop

hren

iam

aint

aine

d fo

r at

leas

t 1 y

ear

shoc

ks

Gol

d &

121

cons

ecut

ive

mal

ePr

ospe

ctiv

e st

udy

of o

utco

me

Typ

e an

d nu

mbe

r of

trea

tmen

tsSu

peri

or c

linic

al o

utco

me

in o

lder

age

Chi

arel

lopa

tient

s, 1

03 d

iagn

osed

as

pred

icto

rs a

nd o

utco

me;

pat

ient

sno

t des

crib

edgr

oups

(194

4)sc

hizo

phre

nic;

age

ran

gepl

aced

in 1

of 4

cat

egor

ies

from

15–6

0m

uch

impr

oved

to n

o ch

ange

* C

ompl

ete

refe

renc

e ci

tatio

ns a

t end

of c

hapt

er.


established, it is also probable that, amongpatients who receive ECT, the elderly havea lower rate of comorbid Axis II pathology(e.g., personality disorders), which fur-ther contributes to a superior ECT re-sponse rate.24,73

ECT Treatment of PsychoticDepression

ECT is a primary treatment for patientswith psychotic depression due to the se-verity of the disorder, the high rate of re-sponse to ECT, and relative poor rate ofresponse to antidepressant monother-apy.5,30 In mixed-age samples, approxi-mately 30 to 40% of depressed patientswho receive ECT present with psychoticdepression.27,67 This rate is likely higheramong the elderly, who are more likelyto present with psychotic depression thanyounger patients.74,75

Between 20 and 45% of hospitalized el-derly depressed patients present with psy-chotic depression.76–78 Typically, the el-derly patient with psychotic features hassevere depressive illness, although theoverall severity of late-life depression doesnot invariably indicate psychosis. Identify-ing psychotic features in elderly depressedpatients is essential because these individ-uals are at considerably high risk for sui-cide.21,79,80

Psychotic depression is often underrec-ognized, particularly in the elderly. A tell-tale sign of psychotic depression is foundin the elderly patient who denies beingdepressed despite psychomotor retarda-tion, anorexia, markedly diminished so-cial interactions, or other symptoms ofdepression. Further complicating identifi-cation of psychotic depression is the needto distinguish between overvalued ideas(‘‘near-delusional states’’) and true delu-sions. Delusions are significantly morecommon than hallucinations in the geria-tric patient with psychosis. In the elderlypatient, greater difficulty also occurs indistinguishing between hypochondriasisand somatic delusions because of thecommon preoccupation with health inolder people. Mood-incongruent delu-

sions or hallucinations, whose content isinconsistent with depressive themes, are aconsistent feature of psychotic depres-sion. Some elderly patients, however,deny delusions, making diagnosis of psy-chotic depression more difficult. Sincemood-incongruent features may be morecommon among younger depressed pa-tients and/or those with bipolar depres-sion, the presence of mood-incongruentpsychotic features in an elderly patientshould trigger consideration of possiblebipolarity or an organic affective disorder.

Evidence that the manifestations of psy-chotic depression tend to be consistentfrom episode to episode suggests a trait-like quality.81–83 Furthermore, psychoticdepression appears to be inherited, withrelatives sharing the same psychotic con-tent.84,85 Psychotic depression is more fre-quent in bipolar compared to unipolardepression.75 However psychotic depres-sion that appears as a first episode afterage 50 is frequently unipolar in course.Compared with unipolar depression, theelderly bipolar patient with psychoticdepression more frequently experiencespsychomotor retardation and sleep dis-turbance.

Particularly difficult to treat, late-onsetpsychotic depression is not only subjectto a relapsing course; it may lead to laterdevelopment of dementia.82,86 Distin-guishing between delusions of dementiaas opposed to psychotic depression maybe problematic. In contrast to the delu-sions of psychotic depression, the patientwith an organic psychotic affective disor-der usually has delusions that are lesssystematized and less congruent with de-pressive themes whereas the delusionsaccompanying psychotic depression areusually highly organized and reflect un-realistic or bizarre ideas about somatic ill-ness, nihilism, persecution, guilt, or jeal-ousy. However, the elderly patient withpsychotic depression is particularly sub-ject to gross global cognitive deteriora-tion (‘‘pseudodementia’’), which reverseswith successful treatment of the mood dis-order.87 Evidence also suggests that such


patients later develop a dementing ill-ness.88

Elderly patients with psychotic depres-sion respond less positively to pharmaco-logic treatment (particularly monother-apy) but more positively to ECT thannonpsychotic patients.89 Specific delu-sions, in addition to vegetative or melan-cholic symptoms, predict favorable re-sponse,19,70,90–93 as may psychomotordisturbance.67,94 In elderly patients withpsychotic depression, observation of earlyresolution of delusions, appetite andsleep disruption, with later improvementin subjective mood and feelings of self-worth is common. Certain delusional ele-ments (bizarreness, effect on behavior,strength of delusional conviction, insightinto delusional thoughts) may take longerto improve, with gradual recession duringthe course of ECT.

Traditionally, bilateral ECT has beenthe standard treatment for elderly pa-

Figure 13.4. Initial seizure threshold as a function of age for 245 patients treated with rightunilateral ECT (From Boylon LS, Haskett RF, Mulsant BH, et al. Determinants of seizure thresholdin ECT: benzodiazepine use, anesthetic dosage, and other factors. J ECT 2000;16:3–18). The lineat the diagonal represents the dosage patients would receive based on age-based dosing, e.g.,50% of device output for 50-year-old. The lower line is the fit of the regression of age on seizurethreshold. While there is a significant relationship (r ! 0.19 for raw values), there is markedvariability. Dosing based solely on age provides a poor approximation of dosing needs and resultsin the greatest over-dosing in the oldest age patients.

tients with psychotic depression. How-ever, recent experience suggests thathigh-dosage right unilateral ECT is at leastas effective as bilateral ECT, with less long-term amnesia, which usually accompaniesbilateral electrode placement. In the caseof right unilateral ECT, high dosage is de-fined as treatment at least 6 times the sei-zure threshold. In the case of bilateralECT, high dosage is defined as 2.5 timesthe seizure threshold (Figure 4).

The average number of ECT treat-ments given to patients of all ages in theUnited States in previous years for majordepression was approximately 6; at pres-ent, the average is approximately 8 to 9(possibly indicating increasing ECT treat-ment resistance) and the use of lower-in-tensity stimulation. Some depressed pa-tients only begin to show clinical benefitafter an extended ECT course, i.e., 10 to12 treatments. Other elderly depressedpatients with psychosis who do not im-


prove after a standard course of bilateralECT may subsequently show rapid im-provement with extended treatment. Forthe elderly patient with psychotic depres-sion who shows slow or insufficientresponse to ECT, the addition of a neuro-leptic, especially the newer second-gener-ation antipsychotic drugs clozapine andrisperidone, may augment treatment re-sponse.95–99

Medical Complications andRelative Contraindications

Rates of medical complications among el-derly patients during the course of ECTrange from 0 to 77% for one or more com-plications.20,46,54,57,100–114 This wide vari-ability reflects different definitions of‘‘complication’’ as well as differences inthe medical status of patient samples.Nonetheless, ECT-related medical com-plications are considerably more likely inthe elderly, particularly in the oldest agesubgroups, especially among patients withreexisting medical conditions.

ECT and Medical Illness Risks

The rate of ECT-associated mortality isvery low among patients of all ages (esti-mated as about 1 per 10,000 mixed-agedpatients treated), which is comparable tomortality rates from general anesthesia inminor surgery.5,48,115 ECT may be a safertherapeutic treatment than the older TCAmedications, particularly for the frail el-derly.5,47,116 Although there are no ab-solute medical contraindications forECT,5,117 risks for the elderly increasewith the following conditions:

• space-occupying cerebral lesion• recent intracerebral hemorrhage• increased intracranial pressure• recent myocardial infarction with insta-

ble cardiac function• unstable vascular aneurysm or malfor-

mation• pheochromocytoma

Cardiovascular Illness

Cardiovascular complications are theleading cause of mortality and significantmorbidity with ECT, especially for geria-tric patients.5,100,118 The peripheral he-modynamic and cerebrovascular changesduring and following the brief seizure aretypically well tolerated, even in the frailelderly, despite their intensity. Prophylac-tic use of beta-adrenergic blocking agents,such as labetalol or esmolol, lessen the hy-pertensive and tachycardic effects of sei-zure induction.119–124 Other agents thatare similarly used include nitrates125, hy-dralazine126,127 calcium channel block-ers,128–132 diazoxide,133 and ganglionicblockers (e.g., trimethaphan).134 In re-cent years, a growing number of centersroutinely use propofol as the anesthesia-induction agent, rather than methohexi-tal or thiopental, partly because propofolresults in less severe hemodynamicchanges.135–147

Conservative clinical practice shouldguide the use of pharmacologic modifica-tions of standard ECT in elderly patients.In 2001, an APA Task Force Report onECT5 recommended fully blocking thehemodynamic changes that accompanyseizure induction for all treatments in pa-tients who are unequivocally at increasedrisk for complications. In patients with un-stable hypertension or cardiac conditionsfor whom ECT is not being considered anemergency treatment, clinicians shouldattempt to stabilize the medical conditionbefore beginning ECT and closely moni-tor cardiovascular changes during initialtreatments. If sustained hypertensionand/or significant arrhythmia occur fol-lowing seizure induction, prophylacticmedication may be used for subsequenttreatments.100

Cognitive Side Effects

Serious short- and long-term cognitive im-pairment is the primary side effect of ECTin the elderly, which argues against ag-gressive use in this population.5,148,149

Prior to treatment, elderly depressed pa-


tients often exhibit deficits in acquiringinformation, which is mostly related todisturbances in attention and concentra-tion as indicated by tests of immediate re-call or recognition-of-item lists.150–153

Clinically, depressed elderly patientscomplain of pronounced problems withattention and concentration. ECT causesa new deficit in consolidation or retentionso that newly learned information is rap-idly forgotten154 due to interrupted func-tion of the medial temporal lobe.155–161

During and following a course of ECT, el-derly patients may also display retrogradeamnesia (memory for events in the past,prior to receiving ECT). Deficits in the re-call or recognition of both personal andgeneral information are usually greatestfor events that occurred closest to thetreatment.162–165 Both anterograde andretrograde amnesia are most marked forexplicit or declarative memory, whereasno effect is expected on implicit or proce-dural memory.166–168

Patients vary considerably both in theseverity of postictal cognitive changes andin speed of recovery. Specific postictal def-icits may reflect a more intense form ofthe amnesia observed following the ECTcourse. For example, the disorientationwith regard to identity, place, and timeseen in the postictal state has been viewedas a form of rapidly shrinking retrogradeamnesia (Figure 5).169,170 Elderly patientsoften ‘‘age’’ with progressive recoveryfrom disorientation. When first asked hisor her age, the 80-year old patient fre-quently answers to being 20 years old; withrepeated questioning, the correct age iseventually given, reflecting a remarkablyrapid resolution of retrograde amnesia.Similarly, patients often revert to theirmother tongue on awakening and onlygradually return to English. Thus the se-verity of postictal disorientation predictsthe degree of amnesia following termina-tion of ECT.169 Cognitive improvementafter a course of ECT follows a sequen-tial temporal pattern. Organic mental syn-dromes typically resolve within 2 to 10days post-ECT.171

Figure 13.5. Relationship between the dura-tion of acute postictal disorientation and retro-grade amnesia for autobiographical informa-tion during the week following the ECTcourse. (From Sobin, et al. 1995, Reference169.)

Recovery of cognitive function follow-ing a single ECT treatment is rapid, al-though in the immediate postictal periodfollowing ECT patients may manifest tran-sient neurologic abnormalities, altera-tions of consciousness (disorientation,attentional dysfunction), sensorimotorabnormalities, and disturbance in thehigher cognitive functions, particularlylearning and memory.148 Within severaldays following the course of ECT treat-ments, the cognitive functioning of anelderly patient slows or is typicallyunchanged. Occasionally immediatememory improves: change in clinical stateis the critical predictor of the degreeof subsequent improvements in cogni-tion.27,59,151,154 Following a typical courseof ECT, patients of all ages often manifesta marked disturbance in their ability toretain information, reflecting ECT effectson impaired anterograde learning (theforming of new memories).148 As thetreatment series progresses, recovery ofcognition in the elderly patient is oftenincomplete by the time of the next treat-ment,20,110,170—173 causing progressivecognitive deterioration, and, in some


elderly patients, an organic mental syn-drome characterized by marked disorien-tation.170,174 The development of a severeorganic mental syndrome often results ininterruption or premature termination ofECT since patients, relatives, and clini-cians are unwilling to risk further deterio-ration of mental status functioning.175

Within days of ECT termination, el-derly depressed patients often manifestsuperior cognitive performance relativeto their pretreatment baseline. Intelli-gence test scores for all age groups, in-cluding the elderly, may even be highershortly after ECT relative to scores in theuntreated depressed state.148,176 Morethan a week or two following the end ofthe ECT course, differences in the cogni-tive effects of bilateral and right unilateralelectrode placements are difficult to dis-cern in domains other than retrogradeamnesia.27,59,148,164,165 Early evidence ofimproved cognition following ECT ismanifested in patients’ activities. After afew treatments with ECT, elderly individu-als may begin to read books, attend groupmeetings, and become capable of follow-ing complex instructions. However, de-spite this improvement in attention andconcentration, elderly patients still maynot retain information after a brief timeperiod. This anterograde amnesia typi-cally resolves within a few weeks of ECTtermination.59,148 It is doubtful that ECTalone ever causes a persistent deficit in an-terograde amnesia.59,177 Not infrequently,elderly inpatients will repeatedly requestinformation about a pass for the weekendor an expected visit from a relativewhereas memory for more remote eventsis intact. Patients may have difficulty re-calling events that occurred during treat-ment, and months or, in rare instances,years prior to the ECT course.178

Retrograde amnesia gradually disap-pears so that over time more distant mem-ories, seemingly ‘‘forgotten’’ immediatelyfollowing the treatment course, subse-quently return.163,165,177,179 However, insome patients amnestic effects of ECT per-sist,27,163,165 most likely due to a combina-tion of retrograde and anterograde ef-

fects. Patients vary considerably in the de-gree of cognitive impairment, regardlessof how ECT is administered.

Individual Correlates of CognitiveDysfunction

Two key clinical questions arise regardingECT-induced cognitive impairment: (1),are there signs during the ECT course thatpredict which patients will develop moresevere and/or persistent short- and long-term cognitive deficits and (2), can weidentify the patients most at risk for severeand/or persistent amnesia prior to thestart of ECT?

Over the 70-year history of convulsivetherapy, numerous investigations of thetechnical factors that influence the de-gree of cognitive side effects have beenconducted. Surprisingly, only in the lastfew years has investigation focused on thepatient factors that predict the variabilityin these deficits. Some patients will taketwice or three times as long to reorientand be capable of leaving the recoveryroom; others will develop an organic men-tal syndrome, a continuous confusionalstate.170,171 Although rapid improvementin global cognitive status immediately fol-lowing termination of ECT will occur, pa-tients with prolonged postictal disorienta-tion are likely to develop the most severeand persistent retrograde amnesia.

A range of retrospective studies indi-cates that patient age and medical statusare also predictors of the developmentof persistent confusion during the ECTcourse.20,57,103,110,111,113,175,180 Older pa-tients and those with compromised medi-cal status are most at risk for prolongedconfusion during the course of ECT.Older depressed patients experiencemore severe anterograde and retrogradeamnesia immediately following the end ofECT relative to younger patients, withsome differences persisting at one-monthfollow-up.181 Elderly patients with preex-isting cognitive impairment, even outsidethe context of frank neurologic disease,are at risk for more prolonged retrogradeamnesia and require appropriate modifi-cation of ECT technique to lessen cogni-


tive deficit (see Table 13.2). Global cogni-tive impairment seen in the depressedstate also increases vulnerability for theamnestic effects of seizure induction. Forexample, elderly pseudodemented pa-tients87 often show dramatic improve-ment in global cognitive status during andfollowing ECT but are at increased riskfor more prolonged and deeper amnesia.Consequently, baseline cognitive impair-ment in the elderly depressed patient maydenote a subgroup whose memory func-tion is more fragile and likely to be af-fected by ECT.

Technical Administration

A variety of technical factors associatedwith ECT administration determine thedegree and persistence of the cognitiveside effects. These include the nature ofelectrical waveform, anatomic positioningof stimulating electrodes (electrodeplacement), electrical stimulus intensity,spacing or frequency of treatments, totalnumber of treatments, duration of sei-zures, type and dosage of anestheticagent, adequacy of oxygenation, and useof concomitant medications.5,148 Table13.2 summarizes the steps that can betaken to minimize cognitive side effects byaltering ECT technique.

In recent years, sine wave stimulationhas been replaced by standard brief-pulsestimulus, which dramatically reduces theacute cognitive side effects of ECT. (seeFigure 6) Another recent modification,ultrabrief pulse stimulation, reduces ad-verse cognitive effects.182–185 Ultrabriefpulse (0.3 ms) right unilateral ECT ad-ministered at 6 times initial seizure thresh-old is comparable in efficacy to standardpulse width (1.5 ms), bilateral (2.5 " ST),or right unilateral (6 " ST) ECT. In con-trast, ultrabrief pulse (2.5 " ST) bilateralECT lacks efficacy and has markedly infe-rior therapeutic effects than right unilat-eral ECT. Because ultrabrief right unilat-eral ECT (0.3 ms and 6 " ST) is highlyeffective and has a profoundly reducedside-effect profile, it is likely to becomewidely adopted as the ‘‘standard’’ ECTtreatment.

Electrode Placement and CognitiveDysfunction

Over the past 30 years, one of the mostcontroversial aspects of ECT administra-tion has been the anatomic positioning ofstimulating electrodes, specifically the useof bilateral and right unilateral ECT. Thisdebate has centered on possible differ-ences in efficacy as well as experience sug-gesting that bilateral ECT accentuateslong-term amnesia.48,149,186,187 That bilat-eral ECT results in more profound acuteand short-term cognitive impairmentrather than right unilateral ECT is widelyrecognized.148 In the immediate postictalperiod, the duration of disorientation willbe considerably longer after bilateral rela-tive to right unilateral ECT position-ing.59,169,170,188 During treatment and inthe days following ECT termination, bilat-eral ECT will result in greater retrogradeamnesia for personal and general in-formation.59,163–165 Anterograde amne-sia—verbal memory in particular—willalso be greater following bilateralECT.59,151,165,189 Compared to depressedpatients treated with medications, pa-tients treated with right unilateral ECT donot show greater retrograde amnesia forautobiographical information 6 monthsafter the ECT course.165

Bilateral ECT is usually reserved forpsychiatric or medical emergency or formedically high-risk patients for whom thenumber of treatments must be mini-mized. When bilateral ECT is adminis-tered, a switch to right unilateral ECTshould be considered for patients exhibit-ing substantial clinical progress but unac-ceptable cognitive side effects. When rightunilateral ECT is ineffective, increasedstimulus dosage should be considered be-fore a switch back to bilateral ECT.

Stimulus Dosing and SeizureThreshold

Three factors reliably predict seizurethreshold: electrode placement, gender,and age.60–62,190–192 In males relative tofemales, and in older patients, seizurethreshold is higher with bilateral place-


Table 13.2. Treatment Technique Factors and Severity of CognitiveSide Effects

Treatment Effects on Cognitive Methods to ReduceFactor Parameters Cognitive Side Effects Referencesa

Stimulus Sine wave stimulation Use square wave, brief pulse Weiner et al. (1986)waveform grossly increases stimulation Daniel & Crovitz (1983a)

cognitive side effects Valentine et al. (1968)

Electrode Standard bilateral Switch to right unilateral McElhiney et al. (1995)placement (bifrontotemporal) ECT Sackeim et al.

ECT results in more (2000, 1993, 1996)widespread, severe, Weiner et al. (1986)and persistent cognitive Daniel & Crovitz (1983b)side effects

Stimulus Grossly suprathreshold Adjust stimulus intensity Sobin et al. (1995)dosage stimulus intensity to needs of individual Sackeim et al. (1993)

increases acute and patients by dosage Sackeim et al. (1986)short-term cognitive titration Squire & Zouzounisside effects (1986)

Number of Progressive cognitive Limit treatments to Calev et al. (1991)treatments decline with high- number necessary to Sackeim et al. (1986)

intensity treatments achieve maximal clinical Daniel & Crovitz (1983a)(sine wave, bilateral, or gains Fraser & Glass (1978,grossly suprathreshold) 1980)

Frequency More frequent treatments Decrease frequency of ECT Lerer et al. (1995)of treatments (3–5 per week) result McAllister et al. (1987)

in greater cognitivedeficits

Oxygenation Poor oxygenation can Pulse oximetry to monitor APA (2001, 1990)result in hypoxia and oxygen saturation and Holmberg (1953)increased cognitive administer 100% 02 priordeficits to seizure induction

Concomitant High anesthetic dose Reduce anesthetic dose to Mukherjee (1993)medications may increase cognitive produce light level of APA (2001, 1990)

effects, which some anesthesia; decrease or Small & Milstein (1990)psychotropics can discontinue psychotropic Miller et al. (1985)augment dosage; discontinue

lithium prior to ECT

Adapted from American Psychiatric Association Task Force on ECT. The practice of ECT: recommendationsfor treatment, training, and privileging. Washington, D.C.: American Psychiatric Press, 2001, with permission.a Complete reference citations at end of chapter.

ment than with right unilateral electrodeplacement. However, the combined pre-dictive power of these features is insuffi-cient to base choice of electrical dosageon a formula.5,192,193 Regardless of dosagechoice, patients with the highest seizurethresholds are predominantly elderlymales, especially those with cardiac dis-ease.194 The use of ultrabrief stimulation

may partially redress this issue. Since thisform of stimulation is considerably moreefficient, seizure thresholds are much re-duced, allowing greater effective rangefor dosing relative to threshold.

The efficacy of right unilateral ECT isespecially sensitive to electrical dosage.When stimulus intensity is near the sei-zure threshold, right unilateral ECT lacks


Figure 13.6. Score on the Squire SubjectiveMemory Questionnaire before and after thetreatment course in ECT responders andnonresponders. Scores of ‘0’ indicate nochange in memory relative to before the epi-sode of depression. (From Coleman EA,Sackeim HA, Prudic J, et al. Subjective mem-ory complaints before and after convulsivetherapy. Biol Psychiatry 1996;39:346–356).

therapeutic properties.58,59 Since ad-vanced age correlates with higher seizurethreshold, older patients are less likely tobenefit from standard electrical dos-age.60,62,190,191,195 The efficacy of rightunilateral ECT improves with escalationof intensity of electrical stimulation rela-tive to seizure threshold.27,59 At markedlysuprathreshold dosing (e.g., 6 times theinitial seizure threshold), right unilateralECT achieves an efficacy that is equivalentto that of robust forms of bilateral ECT(e.g., 2.5 times the initial seizure thresh-old).27,59 Even at grossly suprathresholdstimulus intensities, right unilateral ECTretains significant advantages with respectto cognitive parameters.27 The high sensi-tivity of geriatric patients to the cognitiveside effects of bilateral ECT suggests thatsuprathreshold forms of right unilateralECT should be routine in this population.Indeed, given the marked cognitive bene-fits of ultrabrief stimulation, optimal treat-ment might involve dose-titrated, ul-trabrief stimulation, using markedlysuprathreshold right unilateral ECT.

Efficacy, speed of response, and cogni-tive side effects of ECT depend on the de-gree to which the ECT stimulus exceedsthe seizure threshold. Suprathresholddosing will improve the efficacy of rightunilateral ECT, enhance speed of clinicalimprovement with right unilateral and bi-lateral ECT, and will result in more severeacute and short-term cognitive impair-ment.59,169,188,196

Number and Schedule of Treatments

Cognitive effects of ECT are proportionalto the frequency with which treatment isadministered as well as to the total num-ber of treatments given.197–199 This is par-ticularly true when the most intense formof ECT, suprathreshold, bilateral treat-ment is used. The most common schedulein the United States involves 3 treatmentsper week, whereas in England, 2 treat-ments per week is more common. TheU.S. schedule results in more rapid im-provement but increased short-termcognitive impairment.198,200,201 Elderlypatients may be more sensitive to the


frequency and number of treat-ments.20,110,172,188,202 Some clinicians re-duce the frequency of treatment to twiceweekly in elderly patients who show pro-gressive clinical improvement but exces-sive cognitive deficit.

Concomitant Medications andCognitive Effects

Evidence suggests that the dose of anes-thetic agent may contribute to the severityof cognitive impairment during the post-ictal recovery period.203 Not surprisingly,excessive anesthetic dose may result inprolonged postictal disorientation. Forthis reason, older patients should receivelower doses of anesthetic agents thanyounger patients. This is particularly im-portant since the dose of the anestheticmay also alter seizure duration and inten-sity.60,204

A small dose of a muscarinic anticho-linergic agent (0.4–0.8 mg atropine or0.2–0.4 mg glycopyrrolate) is commonlyadministered intravenously in ECT, justprior to the anesthetic agent. The anticho-linergic agent serves to block vagal out-flow and limit the bradycardia producedby the ECT stimulus. This is especially nec-essary whenever the possibility of subcon-vulsive stimulation exists, or when patientsare administered a !-blocker.100 Atropineis preferred to glycopyrrolate since pro-tection against bradycardia is less certainwith glycopyrrolate. In addition, inci-dence of postictal nausea is also higherwith glycopyrrate,205,206 and glycopyrro-late holds no advantage with respect tocognitive effects during ECT.205–211

In sensitive elderly patients, a variety ofpsychotropic agents may intensify the ad-verse cognitive effects of ECT. Lithiumcarbonate, for example, causes acute con-fusion during ECT in approximately 1 in15 patients; more rarely, status epilepticusoccurs.212–216 Lithium should be discon-tinued prior to the start of an ECT series,or it can be withheld the night and morn-ing before an ECT treatment. In the el-derly, concurrent use of benzodiazepines,neuroleptics, or other sedating psycho-

tropic agents may increase cognitive sideeffects. Benzodiazepines and anticonvul-sant medications may also interfere withefficacy by raising seizure threshold.217,218

ECT for Depressed Patients withNeurologic Disorders

Increasingly, ECT is used to treat psychiat-ric manifestations in a variety of patientpopulations with frank neurologic illness,including Parkinson’s disease,219–225

poststroke depression,226–228 and to alesser extent, dementing disorders.229,230

Across a variety of neurologic disorders,ECT is effective in the treatment of pri-mary or secondary mood disorders. In thecase of Parkinson’s disease, ECT fre-quently exerts beneficial effects on as-pects of the movement disorder and hasbeen used as a primary treatment for theneurologic condition. Duration of the an-tiparkinsonian effects is, however, unpre-dictable; some patients lose benefit withindays, while others maintain improvementin the movement disorder for months orlonger.231 The role of continuation ormaintenance ECT in sustaining improve-ment in the movement disorder is largelyundocumented, although clinical experi-ence indicates that such long-term treat-ment can be highly effective. Patients withParkinson’s disease who receive ECT maybe at increased risk for prolonged confu-sion or delirium.232,233 ECT is also effec-tive in treating poststroke depression andmajor depression in the context of de-menting illness,229,230 although there isrisk of increased severe cognitive side ef-fects.

CLINICAL VIGNETTES

Case 13.1

Ms. A., a 71-year-old married retired school-teacher, was seen in consultation regarding aserious chronic depression. Over the course ofher adult life, she had suffered many suchdepressions that were always characterized byextreme anergia, anhedonia, and a sense of


pointlessness. Ms. A. was never psychotic andnever suicidal, but her diminished energy wouldoften reach such severe proportions that shewas unable to get out of bed for long periodsduring the day. She maintained her weight byforcing herself to eat, but no longer enjoyed thepreparation or taste of food or, indeed, any-thing else. What was most striking to her was hersubjective loss of interest in her grandchildren.Untreated, these depressive periods could lastup to one year. Typically, however, althoughMs. A. would begin to feel some symptomaticrelief after a few months, a chronic pessimismand dysphoria persisted even in the absenceof serious depressive symptoms (doubledepression).

Over the course of her life, Ms. A. had beentreated with at least one antidepressant fromeach class of medication and had respondedat least once to each. She had successful trialsof imipramine, fluoxetine, venlafaxine; her re-sponse to monotherapy with nefazodone, mir-tazapine, and bupropion was nontherapeutic.She never took an MAO inhibitor and never hadlithium augmentation.

At the time she presented for evaluation, Ms.A. was in a state of profound melancholic,nonpsychotic depression. Out of desperation,she requested a consultation regarding ECTand agreed to a course of treatment. She ini-tially received 2 bilateral treatments, and thenwas given 4 more treatments applied to the uni-lateral nondominant hemisphere on a thrice-weekly basis. Ms. A.’s response was rapid anddramatic. After the first 2 treatments, she nolonger remained in bed and began actively toparticipate in family life. By the sixth treatmentshe proclaimed herself to be ‘‘back to nor-mal.’’ Based on evidence regarding high ratesof relapse following ECT, Ms. A. was placed ona low dose of lithium carbonate (600 mg; bloodlevel 0.4) for maintenance. She remaineddepression-free at one-year followup.

This case illustrates the importance of consider-ing this most useful antidepressant treatmenteven for older patients who have had chronicdepression over the course of a lifetime. Hertreatment also illustrates the usefulness of post-ECT lithium maintenance to prevent relapse. Al-though Ms. A. experienced impairment of re-cent recall for the period during and prior tothe ECT, she reported that this memory loss wasa small price to pay for the dramatic improve-ment in her mood. Like other older patientswhose depression has responded to ECT, shealso indicated that the quality of the responseto treatment was better than that from chemi-cal antidepressants. She stated that her moodand thinking felt ‘‘clearer’’ following the ECT

during the memory loss. This is consistent withobservations of clinicians experienced with useof ECT who have noted that some patients’ re-sponse to ECT does seem to produce a betterremission than chemical antidepressants,which may produce only a response or a partialresponse.

Case 13.2

Mr. B., a 76-year-old widowed attorney, devel-oped a classical syndrome of severe majordepression with melancholia. His first symptomsof depression appeared at the age of 73 afterpartial retirement from his law firm. Treatmentwith desipramine 85 mg daily (blood level of140 ng/mL) led to dry mouth and mild urinaryhesitancy; intravenous pyelogram revealed nosignificant residual urine. After approximately 4weeks on desipramine, Mr. B.’s symptoms ofdepression remitted, although a feeling of‘‘mild uneasiness’’ remained. He was able toreturn to work for a few hours a week and re-sumed most of his social activities. Approxi-mately 3 months after the initial response, Mr.B.’s ‘‘uneasiness’’ intensified and became par-ticularly prominent in the morning. Finally, de-pressed mood and feelings of hopelessness aswell as insomnia and appetite loss developedover a period of 2 months despite mainte-nance therapy with desipramine together withsupportive psychotherapy.

Severe exacerbation of his depressive symp-toms followed some changes in Mr. B.’s law firm.Desipramine dosage was raised to a bloodlevel of 182 ng/mL; later, thyroid augmentationwas attempted with triiodothyronine (up to 50mg daily) for 2 weeks. Because no change inhis mental status occurred, triiodothyronine wasdiscontinued, and lithium augmentation wasattempted, with dosage gradually increasedto 600 mg daily (blood level of 0.75 mEg/L). De-pressive symptoms were ameliorated approxi-mately 3 weeks after the introduction of lithium,but he developed tremor and unstable gaitthat required reducing the dosage to 300 mgdaily (blood level of 0.44 mEg/L). Mr. B. re-mained partially symptomatic with mildly anx-ious and depressed mood, particularly in themorning, with early morning awakening andcomplaints of poor concentration.

Approximately 2 months after the improvementinduced by lithium, Mr. B.’s depression wors-ened severely; suicidal ideation developed,and he was hospitalized in a geriatric psychiatryunit. Psychotropic drugs were discontinued,and 10 unilateral ECTs were administered, re-sulting in complete remission of his depression.Sertraline, 50 mg daily, was started immediately


after the last ECT and increased to 75 mg 5 dayslater. This drug was chosen because the tri-cyclic antidepressant desipramine had failedto maintain Mr. B.’s remission. However, 3 weeksafter the last ECT, Mr. B. began again to experi-ence depressed mood, early morning awaken-ing, and suicidal ideation. Sertraline was dis-continued a week later, and three additionalunilateral ECT treatments were administered,with excellent response. Although therapy withMAOIs was considered, maintenance ECT waschosen because his rapid development of sui-cidal ideation and lack of supervision after dis-charge placed him at risk. Compliance withMAO diet was also a concern, especially duringthe period after ECT when his memory was im-paired. Maintenance ECT was given every 2weeks during the first 2 months and thenmonthly. Nine months after completion of theinitial ECT trial, Mr. B. was still asymptomatic.

Some depressed geriatric patients respond wellto antidepressant treatment but cannot sustainremission despite continuation therapy withantidepressant drugs. Mr. B.’s major depressionwith onset in late life responded favorably todesipramine, desipramine combined with lith-ium, and a trial of ECT at various times. How-ever, approximately 1 to 3 months after initialimprovement, his depression returned, necessi-tating additional antidepressant treatment. Pa-tients like Mr. B. often are difficult to treat, par-ticularly if they cannot tolerate particularantidepressants or therapies. ECT is usually ef-fective in such cases and should be consid-ered, especially when the patient becomes dis-heartened by the repeated failures. Therollercoaster of hope and disappointment,coupled with the pessimism of the depressivesyndrome, may cause the patient to give upand facilitate development of suicidal idea-tion.

Maintenance ECT needs further investigation.Many patients, however, remain in remissionfrom depression while receiving ECT every 4 to6 weeks. ECT appears to be a reasonable op-tion for patients with severe depression who failto remain in remission while on an adequatedosage of a heterocyclic antidepressant, a se-rotonin-reuptake inhibitor, or an MAOI. Only de-pressed patients who are able to tolerate andrespond to a trial of ECT should be consideredfor maintenance ECT.

Case 13.3

Mrs. C., a 76-year-old widow, was diagnosedwith Alzheimer’s disease. Although her demen-tia was moderate, she was still able to functionin her own home with a 24-hour companion.

After a fall, Mrs. C. sprained her right ankle, andher mobility decreased for 2 to 3 weeks. Duringthis time, she became apathetic, lost interest intelevision or socialization, and developed in-somnia and appetite loss. After a diagnosis ofdepression, imipramine was begun, with dos-age increased by 25 mg every other day up to75 mg daily. After 6 days on imipramine 75 mg,Mrs. C. developed agitation, confusion, inabil-ity to sustain her attention, and incoherentspeech. Her symptoms were significantly worseat night; she appeared frightened and keptsaying that her neighbors were coming to ‘‘puther away.’’ Her face was flushed, her skin dry,and her pulse was 120 beats per minute.

Mrs. C. was admitted to an acute psychiatricunit with a diagnosis of anticholinergic delirium.Imipramine was discontinued, a course of hy-dration was begun, her vital signs were moni-tored closely, and her pulse decreased to 95beats per minute within 24 hours. Three dayslater, her confusion and agitation lessened, butthe symptoms of depression were even moreapparent. She gradually developed severepsychomotor retardation and began refusingto eat or drink. Treatment with desipramine, 10mg daily, began and was increased by 10 mgevery 3 days. A week later, Mrs. C. requiredtube feeding. At 40 mg of desipramine daily,her pulse rate ranged between 100 and 110beats per minute. At this point, desipramine wasdiscontinued, and 5 days later unilateral ECTwas begun. ECT was administered twice aweek, and after a total of eight treatments, Mrs.C.’s depression was in complete remission.

Elderly patients are sensitive to the anticholiner-gic effect of heterocyclic antidepressants. De-lirium, persistent sinus tachycardia, or urinary re-tention often lead to discontinuation of thesedrugs. When the diagnosis of anticholinergicdelirium is in doubt, physostigmine 1 mg dilutedin 10 mL of normal saline should be adminis-tered intravenously over 5 to 7 minutes. Themental status of patients with anticholinergicdelirium improves almost immediately. How-ever, physostigmine should be avoided for veryold patients or those with cardiac disease be-cause it may cause sinus brachycardia or tran-sient sinus arrest. Patients with bronchial asthmamay develop bronchospasm after administra-tion of physostigmine.

ECT is the treatment of choice in a rapidly wors-ening depressed elderly patient. Although ECT-induced memory dysfunction may be more se-vere and prolonged in demented than innondemented patients, there is no evidencethat ECT worsens the course of dementia.


Acknowledgment. Preparation of this chap-ter was supported in part by grantsMH35636, MH47739, MH55646,MH55716, MH59069, MH60884, andMH61609 and an award from the Na-tional Alliance for Research in Schizo-phrenia and Depression.

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188. Sackeim HA, Portnoy S, Neeley P, et al. Cogni-tive consequences of low–dosage electrocon-vulsive therapy. Ann N Y Acad Sci 1986;462:326–340.

189. Daniel W, Crovitz H. Acute memory impair-ment following electroconvulsive therapy. 2.Effects of electrode placement. Acta PsychiatrScand 1983;67:57–68.

190. Coffey CE, Lucke J, Weiner RD, et al. Seizurethreshold in electroconvulsive therapy: I. Ini-tial seizure threshold. Biol Psychiatry 1995;37:713–720.

191. Enns M, Karvelas L. Electrical dose titration forelectroconvulsive therapy: a comparison withdose prediction methods. Convuls Ther 1995;11:86–93.

192. Colenda CC, McCall WV. A statistical modelpredicting the seizure threshold for right uni-lateral ECT in 106 patients. Convuls Ther 1996;12:3–12.

193. Sackeim HA. Comments on the ‘half–age’method of stimulus dosing. Convuls Ther 1997;13:37–43.

194. Lisanby SH, Devanand DP, Nobler MS, et al.Exceptionally high seizure threshold: ECT de-vice limitations. Convuls Ther 1996;12:156–164.

195. Coffey CE, Lucke J, Weiner RD, et al. Seizurethreshold in electroconvulsive therapy (ECT)II. The anticonvulsant effect of ECT. Biol Psy-chiatry 1995;37:777–788.

196. Squire L, Zouzounis J. ECT and memory: briefpulse versus sine wave. Am J Psychiatry 1986;143:596–601.

197. McAllister D, Perri M, Jordan R, et al. Effectsof ECT given two vs. three times weekly. Psychia-try Res 1987;21:63–69.

198. Lerer B, Shapira B, Calev A, et al. Antidepres-sant and cognitive effects of twice–versusthree–times–weekly ECT. Am J Psychiatry 1995;152:564–570.

199. Sackeim HA, Prudic J, Olfson M, Fuller RB.Short– and long–term cognitive effects of elec-troconvulsive therapy in community settings.Submitted.

200. Lerer B, Shapira B. Optimum frequency ofelectroconvulsive therapy: Implications forpractice and research [editorial]. ConvulsiveTher 1986;2:141–144.

201. Shapira B, Calev A, Lerer B. Optimal use ofelectroconvulsive therapy: choosing a treat-ment schedule. Psychiatr Clin North Am 1991;14:935–946.

202. Calev A, Nigal D, Shapira B, et al. Early andlong–term effects of electroconvulsive therapyand depression on memory and other cogni-tive functions. J Nerv Ment Dis 1991;179:526–533.

203. Miller A, Faber R, Hatch J, Alexander H. Fac-tors affecting amnesia, seizure duration, andefficacy in ECT. Am J Psychiatry 1985;142:692–696.

204. Krueger RB, Fama JM, Devanand DP, et al.Does ECT permanently alter seizure threshold?Biol Psychiatry 1993;33:272–276.

205. Kramer B, Allen R, Friedman B. Atropine andglycopyrrolate as ECT preanesthesia. J Clin Psy-chiatry 1986;47:199–200.

206. Swartz CM, Saheba NC. Comparison of atro-pine with glycopyrrolate for use in ECT. Con-vulsive Ther 1989;5:56–60.

207. Greenan J, Dewar M, Jones C. Intravenous gly-copyrrolate and atropine at induction of anaes-thesia: a comparison. J R Soc Med 1983;76:369–371.

208. Kellway B, Simpson K, Smith R, Halsall P. Ef-fects of atropine and glycopyrrolate on cogni-tive function following anaethesia and electro-convulsive therapy. Int Clin Psychopharm 1986;1:296–302.

209. Simpson KH, Smith RJ, Davies LF. Comparisonof the effects of atropine and glycopyrrolate oncognitive function following general anaesthe-sia. Br J Anaesth 1987;59:966–969.

210. Sommer BR, Satlin A, Friedman L, Cole JO.Glycopyrrolate versus atropine in post–ECTamnesia in the elderly. J Geriatr Psychiatry Neurol1989;2:18–21.

211. Kramer BA. Anticholinergics and ECT. Convul-sive Ther 1993;9:293–300.

212. Small JG, Kellams JJ, Milstein V, Small IF. Com-plications with electroconvulsive treatmentcombined with lithium. Biol Psychiatry 1980;15:103–112.

213. Weiner RD, Volow MR, Gianturco DT, CavenarJOJ. Seizures terminable and interminable withECT. Am J Psychiatry 1980;137:1416–1418.


214. Milstein V, Small JG. Problems with lithiumcombined with ECT [letter]. Am J Psychiatry1988;145:1178.

215. Small JG, Milstein V. Lithium interactions: lith-ium and electroconvulsive therapy. J Clin Psy-chopharmacol 1990;10:346–350.

216. Mukherjee S. Combined ECT and lithium ther-apy. Convulsive Ther 1993;9:274–284.

217. Pettinati HM, Stephens SM, Willis KM, RobinSE. Evidence for less improvement in depres-sion in patients taking benzodiazepines duringunilateral ECT. Am J Psychiatry 1990;147:1029–1035.

218. Greenberg RM, Pettinati HM. Benzodiazepinesand electroconvulsive therapy. Convulsive Ther1993;9:262–273.

219. Andersen K, Balldin J, Gottfries C, et al. Adouble–blind evaluation of electroconvulsivetherapy in Parkinson’s disease with ‘‘on–off’’phenomena. Acta Neurol Scand 1987;76:191–199.

220. Balldin J, Eden S, Granerus A, et al. Electrocon-vulsive therapy in Parkinson’s syndrome with‘‘on–off’’ phenomena. J Neural Transm 1980;47:11–21.

221. Fromm G. Observations on the effect of elec-troshock treatment on patients with parkinson-ism. Bull Tulane Med Faculty 1959;18:71–73.

222. Asnis G. Parkinson’s disease, depression, andECT: a review and case study. Am J Psychiatry1977;134:191–195.

223. Douyon R, Serby M, Klutchko B, Rotrosen J.ECT and Parkinson’s disease revisited: a ‘‘natu-ralistic’’ study. Am J Psychiatry 1989;146:1451–1455.

224. Faber R, Trimble MR. Electroconvulsive ther-apy in Parkinson’s disease and other move-ment disorders. Mov Disord 1991;6:293–303.

225. Kellner CH, Beale MD, Pritchett JT, et al. Elec-troconvulsive therapy and Parkinson’s disease:the case for further study. Psychopharmacol Bull1994;30:495–500.

226. Murray G, Shea V, Conn D. Electroconvulsivetherapy for poststroke depression. J Clin Psy-chiatry 1986;47:258–260.

227. Hsiao JK, Messenheimer JA, Evans DL. ECTand neurological disorders. Convulsive Ther1987;3:121–136.

228. Gustafson Y, Nilsson I, Mattsson M, et al. Epide-miology and treatment of post–stroke depres-sion. Drugs Aging 1995;7:298–309.

229. Price TR, McAllister TW. Safety and efficacy ofECT in depressed patients with dementia: Areview of clinical experience. Convulsive Ther1989;5:61–74.

230. Nelson JP, Rosenberg DR. ECT treatment ofdemented elderly patients with major depres-sion: A retrospective study of efficacy andsafety. Convulsive Ther 1991;7:157–165.

231. Pridmore S, Pollard C. Electroconvulsive ther-apy in Parkinson’s disease: 30 month follow upJ Neurol Neurosurg Psychiatry 1996;60:693.

232. Figiel GS, Hassen MA, Zorumski C, et al.ECT–induced delirium in depressed patientswith Parkinson’s disease. J Neuropsychiatry ClinNeurosci 1991;3:405–411.

233. Oh JJ, Rummans TA, O’Connor MK, AhlskogJE. Cognitive impairment after ECT in patients

with Parkinson’s disease and psychiatric illness[letter]. Am J Psychiatry 1992;149:271.

Table 13.1 References

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Carney MWP, Roth M, Garside RF. The diagnosis ofdepressive syndromes and the prediction of ECTresponse. Br J Psychiatry 1965;111:659–674.

Coryell W, Zimmerman M. Outcome following ECTfor primary unipolar depression: a test of newlyproposed response predictors. Am J Psychiatry1984;141:862–867.

Folstein M, Folstein S, McHugh PR. Clinical predic-tors of improvement after electroconvulsive ther-apy of patients with schizophrenia, neurotic reac-tions, and affective disorders. Biol Psychiatry 1973;7:147–152.

Fraser RM, Glass IB. Unilateral and bilateral ECT inelderly patients. A comparative study. Acta Psychi-atr Scand 1980;62:13–31.

Gold L, Chiarello CJ. Prognostic value of clinicalfindings in cases treated with electroshock. J NervMent Dis 1944;100:577–583.

Greenblatt M, Grosser GH, Wechsler H. A compara-tive study of selected antidepressant medicationsand EST. Am J Psychiatry 1962;119:144–153.

Hamilton M, White J. Factors related to outcome ofdepression treated with ECT. J Ment Sci 1960;106:1030–1040.

Herrington RN, Bruce A, Johnstone EC. Compara-tive trial of L–tryptophan and E.C.T. in severedepressive illness. Lancet 1974;2:731–734.

Herzberg F. Prognostic variables for electro–shocktherapy. J Gen Psychol 1954;50:79–86.

Heshe J, Roder E, Theilgaard A. Unilateral and bilat-eral ECT. A psychiatric and psychological studyof therapeutic effect and side effects. Acta Psychi-atr Scand Suppl 1978;275:1–180.

Hobson RF. Prognostic factors in ECT. J Neurol Neuro-surg Psychiatry 1953;16:275–281.

Mendels J. Electroconvulsive therapy and depres-sion. I. The prognostic significance of clinical fac-tors. Br J Psychiatry 1965a;111:675–681.

Mendels J. Electroconvulsive therapy and depres-sion. II. Significance of endogenous and reactivesyndromes. Br J Psychiatry 1965b;111:682–686.

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Sackeim HA, Decina P, Prohovnik I, Malitz S. Seizurethreshold in electroconvulsive therapy. Effects ofsex, age, electrode placement, and number oftreatments. Arch Gen Psychiatry 1987b;44:355–360.

Sackeim HA, Prudic J, Devanand DP, et al. Effectsof stimulus intensity and electrode placement onthe efficacy and cognitive effects of electrocon-vulsive therapy. N Engl J Med. 1993;328:839–846.

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Stromgren LS. Unilateral versus bilateral electrocon-vulsive therapy. Investigations into the therapeu-tic effect in endogenous depression. Acta Psychi-atr Scand Suppl 1973;240:8–65.

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American Psychiatric Association. The Practice of ECT:Recommendations for Treatment, Training and Privi-leging. Second Edition. Washington, D.C.: Ameri-can Psychiatric Press, 2001.

Calev A, Nigal D, Shapira B, et al. Early andlong–term effects of electroconvulsive therapyand depression on memory and other cognitivefunctions. J Nerv Ment Dis 1991;179:526–533.

Daniel WF, Crovitz HF. Acute memory impairmentfollowing electroconvulsive therapy. 2. Effects ofelectrode placement. Acta Psychiatr Scand 1983b;67:57–68.

Fraser RM, Glass IB. Recovery from ECT in elderlypatients. Br J Psychiatry 1978;133:524–528.

Fraser RM, Glass IB. Unilateral and bilateral ECT inelderly patients. A comparative study. Acta Psychi-atr Scand 1980;62:13–31.

Holmberg G. The influence of oxygen administra-tion on electrically induced convulsions in man.Acta Psychiatr Neurol Scand 1953;28:365–386.

Lerer B, Shapira B, Calev A, et al. Antidepressantand cognitive effects of twice–versus three–times–weekly ECT. Am J Psychiatry 1995;152:564–570.

McAllister DA, Perri MG, Jordan RC, et al. Effectsof ECT given two vs. three times weekly. PsychiatryRes 1987;21:63–69.

McElhiney MC, Moody BJ, Steif BL, et al. Autobio-graphical memory and mood: Effects of electro-convulsive therapy. Neuropsychology 1995;9:501–517.

Miller AL, Faber RA, Hatch JP, Alexander HE. Fac-tors affecting amnesia, seizure duration, and effi-cacy in ECT. Am J Psychiatry 1985;142:692–696.

Mukherjee S. Combined ECT and lithium therapy.Convulsive Ther 1993;9:274–284.

Sackeim HA, Luber B, Moeller JR, et al. Electrophysi-ological correlates of the adverse cognitive effectsof electroconvulsive therapy. J ECT 2000;16:110–120.

Sackeim HA, Prudic J, Devanand DP, et al. Effectsof stimulus intensity and electrode placement onthe efficacy and cognitive effects of electrocon-vulsive therapy. N Engl J Med. 1993;328:839–846.

Sackeim HA, Portnoy S, Neeley P. Cognitive conse-quences of low–dosage electroconvulsive ther-apy. Ann N Y Acad Sci 1986;462:326–340.

Small JG, Milstein V. Lithium interactions: lithiumand electroconvulsive therapy. J Clin Psychophar-macol 1990;10:346–350.

Sobin C, Sackeim HA, Prudic J, et al. Predictors ofretrograde amnesia following ECT. Am J Psychia-try 1995;152:995–1001.

Squire L, Zouzounis J. ECT and memory: brief pulseversus sine wave. Am J Psychiatry 1986;143:596–601.

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Supplemental Readings

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Anesthesia

Boey WK, Lai FO. Comparison of propofol and thio-pentone as anaesthetic agents for electroconvul-sive therapy. Anaesthesia 1990;45:623–628.

Bone ME, Wilkins CJ, Lew JK. A comparison of pro-pofol and methohexitone as anaesthetic agentsfor electroconvulsive therapy. Eur J Anaesthesiol1988;5:279–286.

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Ciraulo D, Lind L, Salzman C, et al. Sodium nitro-prusside treatment of ECT–induced bloodpressure elevations. Am J Psychiatry 1978;135:1105–1106.

Dwyer R, McCaughey W, Lavery J, et al. Comparisonof propofol and methohexitone as anaestheticagents for electroconvulsive therapy. Anaesthesia1988;43:459–462.

Gaines GY 3d, Rees DI. Electroconvulsive therapyand anesthetic considerations. Anesth Analg 1986;65:1345–1356.

Greenan J, Dewar M, Jones CJ. Intravenous glycopyr-rolate and atropine at induction of anaesthesia:a comparison. J R Soc Med 1983;76:369–371.

Ilivicky H, Caroff SN, Simone AF. Etomidate duringECT for elderly seizure–resistant patients. Am JPsychiatry 1995;152:957–958.

Kellway B, Simpson K, Smith R, Halsall P. Effects ofatropine and glycopyrrolate on cognitive func-tion following anaethesia and electroconvulsivetherapy. Int Clin Psychopharm 1986;1:296–302.

Kraus RP, Remick RA. Diazoxide in the managementof severe hypertension after electroconvulsivetherapy. Am J Psychiatry 1982;139:504–505.

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Concomitant Pharmacology

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Milstein V, Small JG. Problems with lithium com-bined with ECT. Am J Psychiatry 1988;145:1178.

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Small JG, Kellams JJ, Milstein V, Small IF. Complica-tions with electroconvulsive treatment combinedwith lithium. Biol Psychiatry 1980;15:103–112.


Small JG, Milstein V. Lithium interactions: lithiumand electroconvulsive therapy. J Clin Psychophar-macol 1990;10:346–350.

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Efficacy and ECT Technique

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Frances A, Weiner RD, Coffey CE. ECT for an elderlyman with psychotic depression and concurrentdementia. Hosp Community Psychiatry 1989;40:237–238,242.

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O’Shea B, Lynch T, Falvey J, O’Mahoney G. Electro-convulsive therapy and cognitive improvementin a very elderly depressed patient. Br J Psychiatry1987;150:255–257.


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Perera TD, Luber B, Nobler MS, et al. Seizureexpression during electroconvulsive therapy: re-lationships with clinical outcome and cognitiveside effects. Neuropsychopharmacology 2004;29:813–825.

Petrides G, Fink M. Choosing a dosing strategy forelectrical stimulation in ECT [letter; comment].J Clin Psychiatry 1996;57:487–488.

Petrides G, Fink M. The ‘half–age’ stimulation strat-egy for ECT dosing. Convuls Ther 1996;12:138–146.

Pettinati HM, Nilsen SM. Increased incidence ofmissed seizures during ECT in the elderly male.Convulsive Ther 1987;3:26–30.

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Roemer RA, Dubin WR, Jaffe R, et al. An efficacystudy of single–versus double–seizure inductionwith ECT in major depression. J Clin Psychiatry1990;51:473–478.

Sackeim HA, Long J, Luber B, et al. Physical proper-ties and quantification of the ECT stimulus: I.Basic principles. Convuls Ther 1994;10:93–123.

Sackeim HA, Rush AJ. Melancholia and response toECT. Am J Psychiatry 1995;152:1242–1243.

Sackeim HA. Are ECT devices underpowered? Con-vulsive Ther 1991;7:233–236.

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Mechanisms of Action

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D’Costa A, Breese CR, Boyd RL, et al. Attenuationof Fos–like immunoreactivity induced by a singleelectroconvulsive shock in brains of aging mice.Brain Res 1991;567:204–211.

Devanand DP, Dwork AJ, Hutchinson ER, et al. DoesECT alter brain structure? Am J Psychiatry 1994;151:957–970.

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Mann JJ, Manevitz AZ, Chen JS, et al. Acute effectsof single and repeated electroconvulsive therapyon plasma catecholamines and blood pressure inmajor depressive disorder. Psychiatry Res 1990;34:127–137.

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Mileusnıc R, Veskov R, Rakıc L. The effect of electro-convulsive shock on brain tubulin during devel-opment and aging. Life Sci 1986;38:1171–1178.

Nobler MS, Sackeim HA, Prohovnik I, et al. Regionalcerebral blood flow in mood disorders, III. Treat-ment and clinical response. Arch Gen Psychiatry1994;51:884–897.

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Medical and Neurological Conditions

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Medical Complications and CognitiveEffects

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Coffey CE, Weiner RD, McCall WV, Heinz ER. Elec-troconvulsive therapy in multiple sclerosis: amagnetic resonance imaging study of the brain.Convulsive Ther 1987;3:137–144.

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Decina P, Malitz S, Sackeim H, et al. Cardiac arrestduring ECT modified by beta–adrenergic block-ade. Am J Psychiatry 1984;141:298–300.

Devanand DP, Briscoe KM, Sackeim HA, Prudic J.Clinical features and predictors of postictal ex-citement. Convulsive Ther 1989;5:140–146.

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Perera TD, Luber B, Nobler MS, et al. Seizureexpression during electroconvulsive therapy: re-lationships with clinical outcome and cognitiveside effects. Neuropsychopharmacology 2004;29:813–825

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Pettinati HM, Bonner KM. Cognitive functioning indepressed geriatric patients with a history ofECT. Am J Psychiatry 1984;141:49–52.

Pettinati HM, Tamburello TA, Ruetsch CR, KaplanFN. Patient attitudes toward electroconvulsivetherapy. Psychopharmacol Bull 1994;30:471–475.

Prudic J, Fitzsimons L, Nobler MS, Sackeim HA. Nal-oxone in the prevention of the adverse cognitiveeffects of ECT: a within–subject, placebo con-trolled study. Neuropsychopharmacology 1999;21:285–293.

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Sackeim HA. Acute cognitive side effects of ECT.Psychopharmacol Bull 1986;22:482–484.

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Post–ECT Treatment

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Electroconvulsive Therapy in Late-Life · PDF fileChapter 13 Electroconvulsive Therapy in Late-Life Depression Harold A. Sackeim Electroconvulsive therapy (ECT) plays a significant