Prognosis Baik Prognosis buruk

Onset lambat Onset muda

Onset Akut Tidak ada factor-faktor pencetus yang
jelas
Gejala-gejala gangguan Mood (terutama
gangguan depresi)
Riwayat buruk dari kehidupan social,
seksual dan pekerjaan sebelum
mengalami gangguan
Sudah Menikah Single, bercerai atau yang single karena
ditinggal meninggal oleh pasangan
Sistem dukungan yang baik Riwayat keluarga dengan skizofrenia
Gejala-gejala positif Sistem dukungan yang buruk
Faktor-faktor pencetus yang jelas Gejala negatif
Tanda-tanda dan gejala-gejala
neurological
Riwayat trauma perinatal
Tidak ada remisi dalam 3 tahun
Sering menjadi relaps
Riwayat dari
Riwayat kehidupan social, seksual dan
lingkungan pekerjaan yang baik sebelum
mengalami gangguan
Perilaku menyendiri atau autisme
Riwayat keluarga dengan gangguan
mood
Onset yang tersembunyi (kronik)

Perlu diketahui bahwa salah satu penyebab utama kegagalan terapi dan seringnya
kekambuhan, adalah bahwa penderita tidak disiplin mengkonsumsi obat dengan
teratur rutin setiap harinya. Penderita mengeluh bosan, jenuh, dan merasa tidak
sembuh-sembuh dari penyakitnya, atau merasa dirinya sudah sembuh serta banyak
lupa, yang akibatnya penderita tidak mengkonsumsi obat dan pada gilirannya
penyakitnya kambuh. Oleh karena itu diperlukan peran keluarga untuk selalu
memonitor pemakaian obat psikofarmaka pada penderita, jangan dikurangi atau
dihentikan sebelum berkonsultasi dengan dokter.


Clinical Guidelines
Patients and their famili es are often apprehensi ve
about ECT; therefore, cli ni cians must expl ai n both
benefi cial and adverse effects and alternati ve
treatment approaches. The i nformed-consent process
shoul d be documented i n the patients' medi cal records
and shoul d incl ude a di scussion of the di sorder, its
natural course, and the option of recei vi ng no
treatment. Pri nted literature and vi deotapes about ECT
may be useful i n attempti ng to obtai n a trul y i nformed
consent. The use of i nvol untary ECT i s rare today and
shoul d be reserved for pati ents who urgently need
treatment and who have a legally appoi nted guardian
who has agreed to its use. Cli ni cians must know l ocal ,
state, and federal l aws about the use of ECT.

Electrical Stimulus
The el ectrical stimul us must be suffici entl y strong to
reach the seizure threshol d (the level of i ntensity
needed to produce a seizure). The el ectri cal sti mul us
is gi ven i n cycl es, and each cycl e contains a positive
and a negati ve wave. Ol d machines use a si ne wave;
however, this type of machi ne i s now consi dered
obsol ete because of the ineffi ci ency of that wave
shape. When a si ne wave i s del ivered, the el ectrical
sti mulus i n the si ne wave before the seizure threshol d
is reached and after the seizure i s act ivated i s
unnecessary and excessive. Modern ECT machi nes use
a bri ef pul se waveform that admi ni sters the el ectri cal
sti mulus usually in 1 to 2 mil liseconds at a rate of 30
to 100 pul ses a second. Machi nes that use an
ultrabrief pul se (0.5 milli seconds) are not as effective
as bri ef pulse machi nes.
Establi shi ng a patient's seizure threshol d is not
strai ghtforward. A 40 ti mes vari abili ty i n seizure
threshol ds occurs among pati ents. In additi on, duri ng
the course of ECT treatment, a pati ent' s seizure
threshol d may i ncrease 25 to 200 percent. The seizure
threshol d is al so hi gher i n men than i n women and
hi gher i n ol der than i n younger adults. A common
technique is to i nitiate treatment at an el ectri cal
sti mulus that i s thought to be below the sei zure
threshol d for a parti cular pati ent and then to i ncrease
thi s i ntensity by 100 percent for unil ateral placement
and by 50 percent for bilateral placement until the
seizure threshol d i s reached. A debate i n the literature
concerns whether a mi ni mally suprathreshol d dose, a
moderately suprathreshold dose (one and a half times
the threshol d), or a hi gh suprathreshol d dose (three
times the threshol d) i s preferabl e. The debate about
sti mulus i ntensi ty resembl es the debate about
el ectrode pl acement. Essentiall y, the data support the
concl usion that doses of three times the threshold are
the most rapi dl y effecti ve and that minimal
suprathreshol d doses are associated with the fewest
and least severe cogniti ve adverse effects.
Induced Seizures
A bri ef muscul ar contraction, usual l y strongest in a
pati ent's jaw and facial muscl es, i s seen concurrentl y
with the flow of sti mul us current, regardl ess of
whether a seizure occurs. The first behavioral sign of
the seizure i s often a plantar extension, whi ch l asts 10
to 20 seconds and marks the toni c phase. Thi s phase
is followed by rhythmi c (i .e., cl oni c) contractions that
decrease i n frequency and fi nall y di sappear. The toni c
phase i s marked by hi gh-frequency, sharp EEG acti vity
on whi ch a hi gher frequency muscle artifact may be
superi mposed. Duri ng the cloni c phase, bursts of
polyspi ke acti vity occur si multaneously with the
muscul ar contractions but usual ly persi st for at least a
few seconds after the cloni c movements stop.
Monitoring Seizures
A physi cian must have an objective measure that a
bilateral general ized seizure has occurred after the
sti mulation. The physi ci an shoul d be abl e to observe
either some evi dence of tonic-cloni c movements or
el ectrophysiological evi dence of seizure activity from
the EEG or el ectromyogram (EMG). Sei zures with
unilateral ECT are asymmetri cal , with higher i ctal EEG
amplitudes over the stimul ated hemisphere than over
the nonsti mulated hemisphere. Occasi onally, unilateral
seizures are i nduced; for thi s reason, at l east a si ngl e
pai r of EEG electrodes shoul d be pl aced over the
contralateral hemi sphere when usi ng unilateral ECT.
For a seizure to be effecti ve i n the course of ECT, it
shoul d last at least 25 seconds.
Failure to Induce Seizures
If a particul ar stimul us fail s to cause a seizure of
suffici ent durati on, up to four attempts at sei zure
induction can be tri ed duri ng a course of treatment.
The onset of sei zure acti vity i s sometimes del ayed as
long as 20 to 40 seconds after the sti mul us
admi ni stration. If a sti mul us fai ls to result i n a
seizure, the contact between the el ectrodes and the
ski n shoul d be checked, and the intensi ty of the
sti mulus shoul d be i ncreased by 25 to 100 percent.
The cli ni cian can al so change the anestheti c agent to
mi nimize i ncreases i n the seizure threshol d caused by
the anestheti c. Additional procedures to lower the
seizure threshol d i ncl ude hyperventil ation and
admi ni stration of 500 to 2,000 mg IV of caffei ne
sodi um benzoate 5 to 10 mi nutes before the stimul us.
Prolonged and Tardive Seizures
Prolonged seizures (seizures lasti ng more than 180
seconds) and status epil epti cus can be termi nated
either with addi tional doses of the barbiturate
anestheti c agent or with IV diazepam (Vali um) (5 to
10 mg). Management of such complications shoul d be
accompani ed by intubation, because the oral ai rway i s
insuffici ent to maintai n adequate ventilation over an
extended apnei c period. Tardi ve seizuresthat is,
additional seizures appeari ng some ti me after the ECT
treatmentmay develop i n patients with preexisti ng
seizure disorders. Rarel y, ECT preci pitates the
development of an epi lepti c di sorder i n pati ents. Such
situations shoul d be managed clini call y as if they were
pure epil epti c di sorders.
Number and Spacing of Treatments
El ectroconvul si ve therapy treatments are usual ly
admi ni stered two to three ti mes a week; twi ce-weekl y
treatments are associated with less memory
impai rment than thri ce-weekl y treatments. In general,
the course of treatment of major depressive di sorder
can take 6 to 12 treatments (al though up to 20
sessions are possible); the treatment of mani c
epi sodes can take 8 to 20 treatments; the treatment
of schi zophreni a can take more than 15 treatments;
and the treatment of catatonia and deli ri um can take
as few as 1 to 4 treatments. Treatment shoul d
conti nue until the patient achi eves what i s consi dered
the maxi mal therapeuti c response. Further treatment
does not yi el d any therapeuti c benefit, but increases
the severity and duration of the adverse effects. The
poi nt of maxi mal improvement i s usuall y thought to
occur when a patient fail s to conti nue to improve after
two consecutive treatments. If a pati ent i s not
improvi ng after 6 to 10 sessions, bil ateral placement
and high-densi ty treatment (three ti mes the sei zure
threshol d) shoul d be attempted before ECT i s
abandoned.
Multiple Monitored Electroconvulsive
Therapy
Multi ple monitored ECT (MMECT) i nvolves givi ng
multi pl e ECT sti muli during a si ngl e session, most
commonl y two bilateral sti muli withi n 2 mi nutes. Thi s
approach may be warranted i n severely ill patients and
in those at especiall y hi gh ri sk from the anestheti c
procedures. MMECT i s associated
P.1123

with the most frequent occurrences of serious
cognitive adverse effects.
Maintenance Treatment
A short-term course of ECT i nduces a remi ssi on i n
symptoms but does not, of itsel f, prevent a relapse.
Post-ECT mai ntenance treatment shoul d al ways be
considered. Mai ntenance therapy i s generally
pharmacologi cal , but maintenance ECT treatments
(weekly, bi weekly, or monthl y) have been reported to
be effective relapse prevention treatments, al though
data from l arge studies are lacking. Indications for
mai ntenance ECT treatments can i ncl ude rapi d relapse
after i nitial ECT, severe symptoms, psychotic
symptoms, and the i nabi lity to tolerate medi cati ons. If
ECT was used because a pati ent was unresponsive to a
speci fi c medication, then, following ECT, the patient
shoul d be gi ven a trial of a di fferent medi cati on.
Failure of Electroconvulsive Therapy
Trial
Patients who fai l to i mprove after a tri al of ECT shoul d
agai n be treated with the pharmacologi cal agents that
fail ed i n the past. Although the data are pri mari ly
anecdotal , many reports i ndi cate that pati ents who
had previousl y failed to i mprove whil e taki ng an
anti depressant drug do i mprove whil e taking the same
drug after recei ving a course of ECT treatments, even
if the ECT seemed to be a therapeutic fail ure.
Nonethel ess, wi th the i ncreased availabili ty of drugs
that act at di verse receptor sites, it is l ess often
necessary to return to a drug that has fail ed than it
was formerly.
Adverse Effects
Contraindications
El ectroconvul si ve therapy has no absol ute
contrai ndications, only situations i n which a patient i s
at i ncreased ri sk and has an i ncreased need for close
monitoring. Pregnancy i s not a contrai ndication for
ECT, and fetal monitoring i s generally consi dered
unnecessary unl ess the pregnancy is hi gh risk or
compl icated. Patients with space-occupyi ng central
nervous system lesions are at i ncreased ri sk for
edema and brai n herniation after ECT. If the l esion i s
small , however, pretreatment wi th dexamethasone
(Decadron) i s gi ven, and hypertension i s controlled
duri ng the sei zure, and the ri sk of serious
compl ications can be mi nimi zed for these pati ents.
Patients who have i ncreased i ntracerebral pressure or
are at ri sk for cerebral bleedi ng (e.g., t hose with
cerebrovascular di seases and aneurysms) are at ri sk
duri ng ECT because of the i ncreased cerebral bl ood
flow duri ng the seizure. This ri sk can be lessened,
although not eli mi nated, by control of the pati ent' s
blood pressure duri ng the treatment. Pati ents with
recent myocardi al i nfarctions are another hi gh-risk
group, although the ri sk i s greatly di mi nished 2 weeks
after the myocardi al i nfarction and is even further
reduced 3 months after the i nfarcti on. Pati ents with
hypertension shoul d be stabilized on their
anti hypertensive medi cations before ECT is
admi ni stered. Propranolol (Inderal ) and subli ngual
nitroglyceri n can al so be used to protect such patients
duri ng treatment.
Mortality
The mortali ty rate with ECT i s about 0.002 percent per
treatment and 0.01 percent for each pati ent. These
numbers compare favorabl y with the ri sks associated
with general anesthesi a and chi ldbirth. ECT death i s
usuall y from cardiovascul ar compli cations and i s most
likel y to occur i n pati ents whose cardiac status is
already compromi sed.
Central Nervous System Effects
Common adverse effects associ ated with ECT are
headache, confusion, and deli ri um shortly after the
seizure whil e the patient i s coming out of anesthesia.
Marked confusion may occur i n up to 10 percent of
pati ents withi n 30 mi nutes of the seizure and can be
treated with barbiturates and benzodi azepi nes.
Deliri um is usually most pronounced after the fi rst few
treatments and in pati ents who recei ve bilateral ECT
or who have coexisti ng neurological disorders. The
deliri um characteristi cally cl ears wi thi n days or a few
weeks at the longest.
Memory
The greatest concern about ECT is the association
between ECT and memory loss. About 75 percent of all
pati ents gi ven ECT say that the memory i mpairment i s
the worst adverse effect. Although memory
impai rment duri ng a course of treatment i s almost the
rule, follow-up data i ndi cate that al most all patients
are back to thei r cognitive baselines after 6 months.
Some pati ents, however, compl ain of persi stent
memory difficul ties. For exampl e, a pati ent may not
remember the events leadi ng up to the hospitalization
and ECT, and such autobiographical memori es may
never be recall ed. The degree of cognitive i mpairment
duri ng treatment and the ti me i t takes to return to
baseli ne are rel ated, i n part, to the amount of
el ectri cal sti mul ation used duri ng treatment. Memory
impai rment is most often reported by pati ents who
have experi enced little i mprovement with ECT. Despite
the memory i mpairment, which usuall y resol ves, no
evi dence i ndi cates brai n damage caused by ECT. Thi s
subject has been the focus of several brai n-i magi ng
studies, usi ng a vari ety of modalities; virtually all
concl uded that permanent brai n damage i s not an
adverse effect of ECT. Neurol ogi sts and epil eptologi sts
generally agree that sei zures that last less than 30
mi nutes do not cause permanent neuronal damage.
Other Adverse Effects of
Electroconvulsive Therapy
Fractures often accompani ed treatments i n the earl y
days of ECT. With routi ne use of muscl e rel axants,
fractures of long bones or vertebrae shoul d not occur.
Some pati ents, however, may break teeth or
experi ence back pai n because of contractions during
the procedure. Muscl e soreness can occur in some
indivi duals, but it often results from the effects of
muscl e depol ari zation by succi nylcholi ne and i s most
likel y to be particularly troubl esome after the fi rst
session i n a seri es. Thi s soreness can be treated wi th
mil d anal gesi cs, incl udi ng nonsteroidal anti -
infl ammatory drugs (NSAIDs). A si gnificant mi nority of
pati ents experi ence nausea, vomiti ng, and headaches
followi ng an ECT treatment. Nausea and vomiti ng can
be prevented by treatment with anti emeti cs at the
time of ECT (e.g., metocl opramide [Reglan], 10 mg IV,
or prochlorperazine [Compazi ne], 10 mg IV;
ondansetron [Zofran]
P.1124

is an acceptabl e alternative if adverse effects precl ude
use of dopami ne receptor antagoni sts).
El ectroconvul si ve therapy can be associ ated with
headaches, although thi s effect is usually readi ly
manageabl e. Headaches often respond to NSAIDs
given i n the ECT recovery period. In patients with
severe headaches, pretreatment with ketorolac
(Toradol ) (30 to 60 mg IV), an NSAID approved for
bri ef parenteral use, can be hel pful . Acetami nophen
(Tylenol ), tramadol (Ultram), propoxyphene (Darvon),
and more potent anal gesia provided by opi oids can be
used i ndivi duall y or i n various combi nations (e.g.,
pretreatment wi th ketorol ac and postseizure
management wi th acetaminophen-propoxyphene) to
manage more i ntractabl e headache. ECT can i nduce
mi grai nous headache and rel ated symptoms;
sumatri ptan (Imitrex) (6 mg SC or 25 mg orall y) may
be a useful addi tion to the agents descri bed above.
Ergot compounds can exacerbate cardiovascular
changes observed duri ng ECT and probably shoul d not
be a component of ECT pretreatment.













Premedications, Anesthetics, and
Muscle Relaxants
Patients shoul d not be gi ven anythi ng orally for 6
hours before treatment. Just before the procedure, the
pati ent's mouth shoul d be checked for dentures and
other forei gn objects, and an intravenous (IV) l ine
shoul d be established. A bite bl ock i s i nserted i n the
mouth just before the treatment is admi nistered to
protect the pati ent' s teeth and tongue duri ng the
seizure. Except for the bri ef i nterval of electri cal
sti mulation, 100 percent oxygen is admi nistered at a
rate of 5 L a mi nute duri ng the procedure until
spontaneous respi ration returns. Emergency
equi pment for establi shi ng an airway shoul d be
immedi ately availabl e i n case it is needed.
Muscarinic Anticholinergic Drugs
Muscari ni c anticholi nergi c drugs are admi nistered
before ECT to mini mize oral and respiratory secretions
and to block bradycardias and asystol es, unl ess the
resti ng heart rate i s above 90 beats a mi nute. Some
ECT centers have stopped the routi ne use of
anti choli nergics as premedi cati ons, although their use
is still i ndicated for pati ents taking -adrenergi c
receptor antagoni sts and those with ventri cular
ectopic beats. The most commonly used drug i s
atropi ne, whi ch can be admi nistered 0.3 to 0.6 mg
intramuscul arl y (IM) or subcutaneously (SC) 30 to 60
mi nutes before the anestheti c or 0.4 to 1.0 mg IV 2 or
3 mi nutes before the anestheti c. An option i s to use
glycopyrrolate (Robi nul) (0.2 to 0.4 mg IM, IV, or SC),
whi ch i s l ess li kely to cross the bloodbrain barrier
and less likely to cause cogniti ve dysfuncti on and
nausea, although it i s thought to have l ess
cardiovascul ar protecti ve acti vi ty than does atropi ne.
Anesthesia
Admi ni stration of ECT requires general anesthesia and
oxygenati on. The depth of anesthesia shoul d be as
light as possi bl e, not only to mi ni mize adverse effects
but also to avoi d el evati ng the seizure threshol d
associated with many anestheti cs. Methohexital
(Brevital) (0.75 to 1.0 mg/kg IV bol us) is the most
commonl y used anestheti c because of its shorter
duration of acti on and lower association with posti ctal
arrhythmias than thiopental (Pentothal ) (usual dose 2
to 3 mg/kg IV), although thi s difference i n cardiac
effects is not universall y accepted. Four other
anestheti c alternati ves are etomi date (Ami date),
ketami ne (Ketal ar), al fentanil (Alfenta), and propofol
(Di privan). Etomi date (0.15 to 0.3 mg/kg IV) i s
sometimes used because it does not i ncrease the
seizure threshol d; thi s effect i s parti cularly useful for
el derl y pati ents because the sei zure threshol d
increases with age. Ketami ne (6 to 10 mg/kg IM) i s
sometimes used because it does not i ncrease the
seizure threshol d, although its use i s li mited by the
frequent associ ation of psychotic symptoms with
emergence from anesthesia with thi s drug. Al fentanil
(2 to 9 mg/kg IV)
P.1121

is someti mes coadmi ni stered wi th barbiturates to
allow the use of low doses of the barbiturate
anestheti cs and, thus, reduce the seizure threshol d
less than usual, although its use can be associ ated
with an i ncreased i nci dence of nausea. Propofol (0.5
to 3.5 mg/kg IV) i s l ess useful because of its strong
anti convulsant properti es.
Muscle Relaxants
After the onset of the anestheti c effect, usually wi thi n
a minute, a muscl e relaxant i s admi nistered to
mi nimize the ri sk of bone fractures and other i njuri es
resulti ng from motor acti vity during the seizure. The
goal i s to produce profound rel axation of the muscl es,
not necessari ly to paralyze them, unl ess the patient
has a hi story of osteoporosis or spi nal i njury or has a
pacemaker and, therefore, i s at ri sk for i njury related
to motor activi ty duri ng the sei zure. Succi nyl choline,
an ultrafast-acti ng depolarizi ng blocki ng agent, has
gai ned virtually universal acceptance for the purpose.
Succi nyl choli ne is usuall y admi nistered in a dose of
0.5 to 1 mg/kg as an IV bol us or dri p. Because
succi nylchol ine i s a depolarizi ng agent, its action i s
marked by the presence of muscle fasci cul ations,
whi ch move i n a rostrocaudal progression. The
di sappearance of these movements i n the feet or the
absence of muscl e contractions after peri pheral nerve
sti mulation indi cates maxi mal muscl e relaxati on. In
some pati ents, tubocurari ne (3 mg IV) i s administered
to prevent myoclonus and i ncreases i n potassi um and
muscl e enzymes; these reactions can be a probl em i n
pati ents with muscul oskeletal or cardiac di sease. To
monitor the duration of the convul sion, a blood
pressure cuff may be i nflated at the ankl e to a
pressure i n excess of the systolic pressure before
infusion of the muscl e relaxant, to allow observation
of rel ativel y i nnocuous seizure acti vity i n the foot
muscl es.
If a pati ent has a known history of
pseudocholi nesterase defi ci ency, atracuri um
(Tracrium) (0.5 to 1 mg/kg IV) or curare can be used
instead of succi nyl choli ne. In such a pati ent, the
metaboli sm of succinyl choli ne i s di srupted, and
prolonged apnea may necessitate emergency ai rway
management. In general , however, because of the
short hal f-life of succi nyl choli ne, the duration of apnea
after its admi ni stration i s generall y shorter than the
delay i n regai ni ng consciousness caused by the
anestheti c and the posti ctal state.