Electroconvulsive Therapy in Late-Life · PDF fileChapter 13 Electroconvulsive Therapy in...
Transcript of Electroconvulsive Therapy in Late-Life · PDF fileChapter 13 Electroconvulsive Therapy in...
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
Part IV / Affective Disorders388
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
Chapter 13 / Electroconvulsive Therapy in Late-Life Depression 389
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)
Part IV / Affective Disorders390
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)
Chapter 13 / Electroconvulsive Therapy in Late-Life Depression 391
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)
Part IV / Affective Disorders392
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
Chapter 13 / Electroconvulsive Therapy in Late-Life Depression 393
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)
Part IV / Affective Disorders394
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.
Chapter 13 / Electroconvulsive Therapy in Late-Life Depression 395
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
Part IV / Affective Disorders396
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-
Chapter 13 / Electroconvulsive Therapy in Late-Life Depression 397
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-
Part IV / Affective Disorders398
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
Chapter 13 / Electroconvulsive Therapy in Late-Life Depression 399
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-
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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-
Chapter 13 / Electroconvulsive Therapy in Late-Life Depression 401
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
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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
Chapter 13 / Electroconvulsive Therapy in Late-Life Depression 403
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
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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
Chapter 13 / Electroconvulsive Therapy in Late-Life Depression 405
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.
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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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