COM
BRIEF’
Improvement BY
ZIGMOND
\IU\
IC.TlO\S
of Parkinsonism M.
LEBENSOHN,
\1.I).,
in Depressed ,NI)
RAMON
B. JENKINS.
Two patients with severe Parkinson ‘s disease were treated with electroconvulsive therapyfor a supervening depression. Not only did the symptoms of depression clear up after onlvfour treatments, hut the parkinsonian signs also showed striking and sustained improvement. This mat’ be related to ECT-induced changes in dopamine and norepinephrine metabolism. Parkinsonism does not appear to be a contraindication to ECT. On the contrary,
ECT
patients
with
complicated
mar
he the
Parkinson bs’ in tractable
treatment
‘s disease,
ofchoicefor
whether
Patients
certain
or not it is
depression.
Treated
with
ECT
MI).
fluid
was
to side
normal.
effects
Because to another (Thorazine) fluoperazine the
mild
parkinsonian
signs
were
attributed
his paranoid delusions persisted he was transferred hospital and given up to 600 mg of chlorpromazine daily, 2 mg of benztropine mesylate daily, I 0 mg of (Dexednine) each morning, and 5 mg of tn(Stelazine) twice daily. He improved rapidly dur-
dextroamphetamine ing
The
of drugs.
next
three
weeks.
The
doses
reduced,
and he was discharged 5, 1963. He continued to take daily and 200 mg ofchlorpromazine tions
were
discontinued
from
treatment
in
without
of the
drugs
were
gradually
from the hospital on February 2 mg of tnifluoperazine twice at bedtime.
March
1963,
abnormal
and
These he
was
psychiatric
medicadischarged
or neurological
signs.
Forfive MENTAL DEPRESSION OCCURS commonly in patients with Parkinson’s disease. Therapeutic response to tnicyclic antidepressant drugs is often disappointing and too slow for emergency use. Many clinicians have been reluctant to use electroconvulsive therapy to treat depression in patients with severe rigidity and bradykinesia. We recently treated two such patients suffering from severe depression and classical Parkinson’s disease with ECT. Their depression was alleviated after only four treatments; surprisingly, the objective parkinsonian signs also showed striking and sustained improvement.
stressful which
well.
he again when he
In January
developed was given
1968,
delusions 2 mg of
following of
REPORTS
treatments,
recovered
temporarily,
but
later
re-
lapsed. In April 1962 he was admitted to a psychiatric hospital where he received perphenazine (Trilafon), benztropine mesylate (Cogentin), and imipramine (Tofranil). His condition remained static, with depression and paranoid delusions predominating. In December 1962 he developed masked facies and decreased arm swing, especially on the right side. Cerebrospinal Dr. Lebensohn is Chief, Department of Psychiatry, Hospital, 5255 Loughboro Rd., NW., Washington, Jenkins is Chairman, Section of Neurology, Washington ter, Washington, D.C.
Sibley Memorial D.C. 20016. Dr. Hospital Cen-
a
reference,
years,
but
come tane).
by June
much worse Within one
1972
his rigidity
and
bradykinesia
had
pathologically
obsessed
all medications his
rigidity
with
trivial
ly able
were discontinued.
and
bradykinesia
to function.
-benztropine L-dopa because Bi
episodes
During
improved
He continued
and biperiden ofhis fragile
September
be-
despite treatment with trihexyphenidyl (Arweek he also became depressed, delusional, from
tant past. Chlorpromazine, in doses of up to 600 failed to produce the improvement that had occurred earlier. By June 28 he was so rigid that he could not
Case 1. A 62-year-old lawyer first became ill in December 1961, when he developed an acute paranoid depression precipitated by a stressful situation in his work. He was given six electroconvulsive
he remained
tnifluoperazine three times daily for one week, then twice daily for three weeks. However, his parkinsonian symptoms and signs reappeared, and medication was discontinued. Repeated examinations by neurologists over the next several years showed signs of progressive Parkinson’s disease, predominantly on the right side. Because of the asymmetry and typical clinical course of the disease, this was considered to be an independent development. The patient received no phenothiazines for the next four
and
CASE
years
legal case, disappeared
1972
the next
slightly,
to take
delusions
he was
bare-
anticholinergic
had
dis-
few months
but
(Akineton)-but psychiatric state.
his
his
mg daily, nine years move, and
agents
he was not given returned
with
such
force that he was readmitted to the psychiatric unit of Sibley Memorial Hospital. He was in a state of profound depression and psychomotor retardation. He could not rise from a chair, his
face
sonian gait
was posture.
without
sternum
masklike, He
and had
festination.
but
vere
lead-pipe
gidity
in
both
would rigidity arms,
AmJ
he
showed
difficulty He
not
fall
would
forward
of his neck and
a hint
Psychiatry
a typical He
recoil
when
had
or sideways.
and limbs, of
dystonic
speaking.
slight
tremor
on
132:3,
March
the
parkina shutTling
pushed
on
his
There
was
se-
cogwheel right
1975
side.
riHe
283
BRIEF
COMMUNICATIONS
was mentally confused and appeared to have auditory and visual hallucinations. On several occasions he was incontinent of urine. He was given four ECTs between September 28 and October 5. Each was preceded by intravenously administered sodium methohexital ( Brevital) and succinylcholine hydrochloride (Anectine), and they were well tolerated. The treatments were followed by remarkable and rapid improvement not only in his mental condition but also in his physical state. The muscular ri-
gidity
and
immobility
of his
face
almost
disappeared.
speech and gait improved greatly, particularly treatment. His delusions disappeared after the He smiled readily and walked about the ward His gait was no longer shuffling, although arm ished. He lost retropulsion to sternal push.
His
after the second third treatment. spontaneously. swing was diminThe speed with
which he initiated and performed movements was remarkably increased. His superior mental faculties were clearly unimpaired. He was discharged on October 9, 1972. He has been seen at regular intervals since discharge and has been on a regimen of 2 mg of benztropine mesylate four or five times daily, to which 100 mg of amantadine hydrochloride (Symmetrel) twice daily was later added. Since November 1972 he has resumed his full-time aCtive practice, at which he has remained highly effective. His Parkinson’s disease has been stable and there has been no recurrence of psychiatric symptoms.
Case 2. A 70-year-old businessman with a lifelong cyclothymic personality had four severe episodes of manic-dcpressive illness over a period of 25 years. He had been hospitalized and successfully treated with ECT on several occasions. His last psychiatric illness was a hypomanic episode following a prostatectomy in 1963. This was treated successfully with promazine hydrochloride (Sparine). psychotherapy, and special nursing care. ECT was not used. Promazinc therapy was discontinued in January 1964. His recovery was followed by a brief depression, which subsided in April 1964. He remained well until early 1972, when he developed bradykinesia. cogwheel rigidity, masked facies, shuffling gait, typical parkinsonian tremor, and severe retropulsion. For a while his neurological symptoms were contained by trihexyphenidyl. However, he developed progressive mental depression, primarily because of his inability to engage in many of his previous activities.
In February
1973 he became
very
rigid
and
immobile.
L-dopa (Larodopa) produced remarkable improvement at first, but in spite of increased doses his parkinsonian signs worsened and he became severely depressed. He said, “ I see no point in living. . . . I really want to die.” He was unable to sit still and had great difficulty sleeping. On admission to the psychiatric unit of Sibley Memorial Hospital on April 23, 1973, he was tremulous, anxious, agitated, and despondent. He showed shuffling gait, bradykinesia. and a typical bilateral parkinsonian tremor. He continued to receive L-dopa, the dose of which was gradually increased from 500 mg to 750 mg, four times a day. Meprobamate was given for severe agitation, and he also received I mg of benztropine mesylate three times a day. Between April 24 and April 30 he received a total of four ECTs, each preceded by intravenously administered sodium methohexital and succinylcholine. Immediately after the first ECT the extreme muscular rigidity of his limbs disappeared, only to return an hour later. The next day he showed little or no tremor and he walked without shuffling. He was in better spinits and was able to play bridge for the first time in weeks. After his second treatment he could shave himself and, apart from some
slowness
parkinsonian
284
in
movement,
signs,
even
Am J Psychiatry
showed
though
132:3,
the
no
dose
March
rigidity
or
of L-dopa
/975
any
other
remained
unchanged.
When
no longer provement
been
he was discharged
depressed in both
sustained.
The only
mg of i.-dopa
four
on May
and was walking neurological and
medication
times
2,
he
was
without difficulty. The psychiatric symptoms
1973,
imhas
he continues
to take
is 750
a day.
DISCUSSION The pressive
coincident symptoms
improvement in these
of parkinsonian patients suggests
two
mon biogenic action ofelectroconvulsive aspects of their illness. The exact ECT in depressive an electric current convulsive
illness through
seizure,
atomical
levels
terations
in
turnover
is unknown, the brain,
probably
and
the
exerts
produces
brain,
many
including
of catecholamines
levels
of
brain
son’s
disease
now
catecholamine
theory
ceived
and
clinical
- 4).
in the of
its eflects
at many
different
chemical
The
role
accepted.
endogenous
an-
aland
of
depressed of
Parkin-
Similarly,
the
depression
experimental
of a
concentration
pathogenesis
generally
on both of action of
but the passage which produces
the
( I
dopamine is
therapy mechanism
and dea corn-
support
has
(5, 6).
re-
Because
ECT improved the parkinsonian signs in these two patients, it is reasonable to ask whether it did so by increasing dopamine synthesis. This would have important implications
for
the
norepinephnine
theory
of depression.
Dopamine is the precursor of norepinephnine, and ECT may produce its antidepressant action by increasing the synthesis ofdopamine and nonepinephnine. The therapeutic effectiveness of 1.-dopa in the treatment of Parkinson’s disease is well known (7), but its role in the Patients
pathogenesis treated
with
mental
changes.
These
elation,
hypersexuality,
nations,
delusions,
of affective L-dopa have include
disorders developed
enhancement
depression, and
is
frank
less clean. a variety of of memory,
excitement,
psychosis.
halluci-
The
drug
may
cause deterioration of the mental state of schizophrenic patients (8). Paradoxically, i.-dopa has been reported to cause depression (9- 1 1) as well as to alleviate it ( I 2). Tncyclic
antidepressant
available
brain
lieving
depression
L-dopa. larly.
It might
Were
the
drugs, in
extreme
Parkinson’s
disease phase well
the extrapyramidal drug-induced
are
probably
efTective
pankinsonian
be supposed
patients a manifestation suIt of psychomotor bradykinesia, severe posture, shuffling gait, advanced We are
which
norepinephnine,
rigidity
that and
increase
agents
patients
ECT
would
bradykinesia
in re-
receiving
act
simi-
ofour
two
of Parkinson’s disease on the reretardation? The typical tremor, muscular rigidity, characteristic retropulsion, and other features of clearly
of parkinsonism. aware of the system parkinsonism
confirm effects
that of
they
were
in an
phenothiazines
and their capacity or to aggravate
on
to cause preexisting
Parkinson’s disease. However, our first patient clearly suffers from classic idiopathic Parkinson’s disease, which has been progressive and asymmetric over a number of years during which he did not receive any phenothiazines. In addition, his history revealed that at age 6 he had suffered severely from influenza during the 1918 epidemic.
BRIEF
The
question
at
all
of drug-induced
in our
second
phenothiazines Biochemical
parkinsonism
patient
since
for over
I I years.
changes
in dopamine
he
did
had
not
turnover
not
arise
taken
any
or ECT-in-
duced dopamine-receptor sensitivity may explain our patients’ improvement. More difficult to explain is the maintenance of this improvement for many months after ECT. This parallels a similar improvement in their depression and denotes the induction oflong-acting changes in the underlying mechanisms subserving movement and tone as well as mood. We hope that this report will alert clinicians who are confronted by patients with Parkinson’s disease complicated by depression to the fact that ECT is not contraindicated
and
in some
cases
may
be
the
treatment
of
choice. It remains to be seen whether ECT will be equally effective in helping parkinsonian patients without associated mental depression or those who fail to improve with L-dopa.
REFERENCES I.
Holmberg G: Rev Neurobiol
Biological aspects 5:389 412, 1963
Classification
of Suicidal
Medical
Lethality
BY
T.
AARON
of electroconvulsive
BECK.
M.D..
ROY
therapy.
Behaviors:
BECK.
,NI)
Int
in classifying
suicidal
THE
OF
BEHAVIORS
STUDY
handicapped cepts,
and
SUICIDAL
by
semantic
contradictory
‘ A complete review of suicidal behaviors
behavior.
confusion, taxonomies.’
has
been chronically amorphous con-
Many
of the literature on taxonomies was made by Beck and Greenberg
522,
1965
6. Schildkraut ii, Draskoczy PR: Effects of electroconvulsive shock on norepinephrine turnover and metabolism: basic and clinical studies, in The Psychobiology of Convulsive Therapy. Edited by Fink M, Kety 55, McGaugh I, et al. Washington, DC, VH Winston & Sons, 1974, pp 143- 170 7. Cotzias GC, Van Woent MH, Schifl’er LM: Aromatic amino acids and modification of parkinsonism. N EngI J Med 276:374-379, 1967 8. Tobias IA, Merlis 5: Levodopa and schizophrenia (hr to ed). JAMA2II:l857, 1970 9. Barbeau A: L-dopa therapy in Parkinson’s disease: a critical review of nine years’ experience. Can Med Assoc 1 191:791-800, 1969 10. Mawdsley C: Treatment of parkinsonism with laevo-dopa. Br Med J 1:331-337, 1970 II. Jenkins RB, Groh RH: Mental symptoms in parkinsonian patients treated with L-dopa. Lancet 2:177-180, 1970 12. Bunney WE, Janowsk’, DS, Goodwin FK, et al: Effect of i-dopa on depression. Lancet 1:885 886, 1969
KOVACS.
Previous studies ofattemptedsuicide have cast doubt on the value ofassessingpsychological intent. By identifying a moderating variable, name/v. the attempter’s preconceptions about the lethality ofhis act, the authors were able to solve the puzzle ofthe lo w correlations between intent andlethalitv. Suicidal intent correlate.s highly with medicallethalitv when the attempter has sufficien t kno wledge to assess proper/v the probable outcome of his attempt. The authors conclude that suicidal intent and medical lethality are useful dimensions
Engel J, Hanson LCF, Roos BE et al: Effect of electroshock on dopamine metabolism in rat brain. Psychopharmacologia 13: 140144, 1968 3. Essman WB: Neurochemical changes in ECS and ECT. Semin Psychiatry 4:67-79, 1972 4. Kety SS: Biochemical and neurochemical effects of deetroconvulsive shock, in The Psychobiology of Convulsive Therapy. Edited by Fink M, Kety 55, McGaugh I, et al. Washington. DC, VH Winston & Sons, 1974, pp 285-294 5. Schildkraut ii: The catecholamine hypothesis of affective disorders: a review ofsupporting evidence. Am J Psychiatry 122:5092.
I. Quantifying
MARIA
writers
and
have
nomenclature (I).
COMMUNICATIONS
Intent
and
P1-1.1).
lumped
completed
together group.
as Nonfatal
as unsuccessful
the
question such
“simulated tioned writer
“suicidal
suicide,” suicide.” means
nonfatal
suicide
constituted
attempts
suicides.
of suicidal as
and
these
suicide
ply terms
suicides
though
have
The
intent
a been
reported
controversy
has
a variety
“abortive
“pseudosuicide,”
It is often difficult to by a “serious suicide
sim-
surrounding
spawned
gesture,”
attempts
homogeneous
of
suicide,”
and
“sub-inten-
understand attempt”
what because
some authors confound the degree of an individual’s tent to kill himself with the medical consequences suicidal act (2-5). Other investigators, dismissing wish to die as the motive for most cases of nonfatal
a
inof his the sui-
Beck is Professor of Psychiatry, Mr. Beck is a medical student, and Dr. Kovacs is Associate in Psychiatry, University of Pennsylvania and Philadelphia General Hospital, Philadelphia, Pa. Address reprint requests to Dr. Beck at 429 Stouffer Bldg., Philadelphia General Hospital, 700 Civic Center Blvd., Philadelphia, Pa. 19104. Dr.
This study was supported stitute of Mental Health.
Am
by grant
J P.svchiatrs’
MH-I9989
/32:3,
from
March
the
/975
National
In-
285
BRIEF’
Improvement BY
ZIGMOND
\IU\
IC.TlO\S
of Parkinsonism M.
LEBENSOHN,
\1.I).,
in Depressed ,NI)
RAMON
B. JENKINS.
Two patients with severe Parkinson ‘s disease were treated with electroconvulsive therapyfor a supervening depression. Not only did the symptoms of depression clear up after onlvfour treatments, hut the parkinsonian signs also showed striking and sustained improvement. This mat’ be related to ECT-induced changes in dopamine and norepinephrine metabolism. Parkinsonism does not appear to be a contraindication to ECT. On the contrary,
ECT
patients
with
complicated
mar
he the
Parkinson bs’ in tractable
treatment
‘s disease,
ofchoicefor
whether
Patients
certain
or not it is
depression.
Treated
with
ECT
MI).
fluid
was
to side
normal.
effects
Because to another (Thorazine) fluoperazine the
mild
parkinsonian
signs
were
attributed
his paranoid delusions persisted he was transferred hospital and given up to 600 mg of chlorpromazine daily, 2 mg of benztropine mesylate daily, I 0 mg of (Dexednine) each morning, and 5 mg of tn(Stelazine) twice daily. He improved rapidly dur-
dextroamphetamine ing
The
of drugs.
next
three
weeks.
The
doses
reduced,
and he was discharged 5, 1963. He continued to take daily and 200 mg ofchlorpromazine tions
were
discontinued
from
treatment
in
without
of the
drugs
were
gradually
from the hospital on February 2 mg of tnifluoperazine twice at bedtime.
March
1963,
abnormal
and
These he
was
psychiatric
medicadischarged
or neurological
signs.
Forfive MENTAL DEPRESSION OCCURS commonly in patients with Parkinson’s disease. Therapeutic response to tnicyclic antidepressant drugs is often disappointing and too slow for emergency use. Many clinicians have been reluctant to use electroconvulsive therapy to treat depression in patients with severe rigidity and bradykinesia. We recently treated two such patients suffering from severe depression and classical Parkinson’s disease with ECT. Their depression was alleviated after only four treatments; surprisingly, the objective parkinsonian signs also showed striking and sustained improvement.
stressful which
well.
he again when he
In January
developed was given
1968,
delusions 2 mg of
following of
REPORTS
treatments,
recovered
temporarily,
but
later
re-
lapsed. In April 1962 he was admitted to a psychiatric hospital where he received perphenazine (Trilafon), benztropine mesylate (Cogentin), and imipramine (Tofranil). His condition remained static, with depression and paranoid delusions predominating. In December 1962 he developed masked facies and decreased arm swing, especially on the right side. Cerebrospinal Dr. Lebensohn is Chief, Department of Psychiatry, Hospital, 5255 Loughboro Rd., NW., Washington, Jenkins is Chairman, Section of Neurology, Washington ter, Washington, D.C.
Sibley Memorial D.C. 20016. Dr. Hospital Cen-
a
reference,
years,
but
come tane).
by June
much worse Within one
1972
his rigidity
and
bradykinesia
had
pathologically
obsessed
all medications his
rigidity
with
trivial
ly able
were discontinued.
and
bradykinesia
to function.
-benztropine L-dopa because Bi
episodes
During
improved
He continued
and biperiden ofhis fragile
September
be-
despite treatment with trihexyphenidyl (Arweek he also became depressed, delusional, from
tant past. Chlorpromazine, in doses of up to 600 failed to produce the improvement that had occurred earlier. By June 28 he was so rigid that he could not
Case 1. A 62-year-old lawyer first became ill in December 1961, when he developed an acute paranoid depression precipitated by a stressful situation in his work. He was given six electroconvulsive
he remained
tnifluoperazine three times daily for one week, then twice daily for three weeks. However, his parkinsonian symptoms and signs reappeared, and medication was discontinued. Repeated examinations by neurologists over the next several years showed signs of progressive Parkinson’s disease, predominantly on the right side. Because of the asymmetry and typical clinical course of the disease, this was considered to be an independent development. The patient received no phenothiazines for the next four
and
CASE
years
legal case, disappeared
1972
the next
slightly,
to take
delusions
he was
bare-
anticholinergic
had
dis-
few months
but
(Akineton)-but psychiatric state.
his
his
mg daily, nine years move, and
agents
he was not given returned
with
such
force that he was readmitted to the psychiatric unit of Sibley Memorial Hospital. He was in a state of profound depression and psychomotor retardation. He could not rise from a chair, his
face
sonian gait
was posture.
without
sternum
masklike, He
and had
festination.
but
vere
lead-pipe
gidity
in
both
would rigidity arms,
AmJ
he
showed
difficulty He
not
fall
would
forward
of his neck and
a hint
Psychiatry
a typical He
recoil
when
had
or sideways.
and limbs, of
dystonic
speaking.
slight
tremor
on
132:3,
March
the
parkina shutTling
pushed
on
his
There
was
se-
cogwheel right
1975
side.
riHe
283
BRIEF
COMMUNICATIONS
was mentally confused and appeared to have auditory and visual hallucinations. On several occasions he was incontinent of urine. He was given four ECTs between September 28 and October 5. Each was preceded by intravenously administered sodium methohexital ( Brevital) and succinylcholine hydrochloride (Anectine), and they were well tolerated. The treatments were followed by remarkable and rapid improvement not only in his mental condition but also in his physical state. The muscular ri-
gidity
and
immobility
of his
face
almost
disappeared.
speech and gait improved greatly, particularly treatment. His delusions disappeared after the He smiled readily and walked about the ward His gait was no longer shuffling, although arm ished. He lost retropulsion to sternal push.
His
after the second third treatment. spontaneously. swing was diminThe speed with
which he initiated and performed movements was remarkably increased. His superior mental faculties were clearly unimpaired. He was discharged on October 9, 1972. He has been seen at regular intervals since discharge and has been on a regimen of 2 mg of benztropine mesylate four or five times daily, to which 100 mg of amantadine hydrochloride (Symmetrel) twice daily was later added. Since November 1972 he has resumed his full-time aCtive practice, at which he has remained highly effective. His Parkinson’s disease has been stable and there has been no recurrence of psychiatric symptoms.
Case 2. A 70-year-old businessman with a lifelong cyclothymic personality had four severe episodes of manic-dcpressive illness over a period of 25 years. He had been hospitalized and successfully treated with ECT on several occasions. His last psychiatric illness was a hypomanic episode following a prostatectomy in 1963. This was treated successfully with promazine hydrochloride (Sparine). psychotherapy, and special nursing care. ECT was not used. Promazinc therapy was discontinued in January 1964. His recovery was followed by a brief depression, which subsided in April 1964. He remained well until early 1972, when he developed bradykinesia. cogwheel rigidity, masked facies, shuffling gait, typical parkinsonian tremor, and severe retropulsion. For a while his neurological symptoms were contained by trihexyphenidyl. However, he developed progressive mental depression, primarily because of his inability to engage in many of his previous activities.
In February
1973 he became
very
rigid
and
immobile.
L-dopa (Larodopa) produced remarkable improvement at first, but in spite of increased doses his parkinsonian signs worsened and he became severely depressed. He said, “ I see no point in living. . . . I really want to die.” He was unable to sit still and had great difficulty sleeping. On admission to the psychiatric unit of Sibley Memorial Hospital on April 23, 1973, he was tremulous, anxious, agitated, and despondent. He showed shuffling gait, bradykinesia. and a typical bilateral parkinsonian tremor. He continued to receive L-dopa, the dose of which was gradually increased from 500 mg to 750 mg, four times a day. Meprobamate was given for severe agitation, and he also received I mg of benztropine mesylate three times a day. Between April 24 and April 30 he received a total of four ECTs, each preceded by intravenously administered sodium methohexital and succinylcholine. Immediately after the first ECT the extreme muscular rigidity of his limbs disappeared, only to return an hour later. The next day he showed little or no tremor and he walked without shuffling. He was in better spinits and was able to play bridge for the first time in weeks. After his second treatment he could shave himself and, apart from some
slowness
parkinsonian
284
in
movement,
signs,
even
Am J Psychiatry
showed
though
132:3,
the
no
dose
March
rigidity
or
of L-dopa
/975
any
other
remained
unchanged.
When
no longer provement
been
he was discharged
depressed in both
sustained.
The only
mg of i.-dopa
four
on May
and was walking neurological and
medication
times
2,
he
was
without difficulty. The psychiatric symptoms
1973,
imhas
he continues
to take
is 750
a day.
DISCUSSION The pressive
coincident symptoms
improvement in these
of parkinsonian patients suggests
two
mon biogenic action ofelectroconvulsive aspects of their illness. The exact ECT in depressive an electric current convulsive
illness through
seizure,
atomical
levels
terations
in
turnover
is unknown, the brain,
probably
and
the
exerts
produces
brain,
many
including
of catecholamines
levels
of
brain
son’s
disease
now
catecholamine
theory
ceived
and
clinical
- 4).
in the of
its eflects
at many
different
chemical
The
role
accepted.
endogenous
an-
aland
of
depressed of
Parkin-
Similarly,
the
depression
experimental
of a
concentration
pathogenesis
generally
on both of action of
but the passage which produces
the
( I
dopamine is
therapy mechanism
and dea corn-
support
has
(5, 6).
re-
Because
ECT improved the parkinsonian signs in these two patients, it is reasonable to ask whether it did so by increasing dopamine synthesis. This would have important implications
for
the
norepinephnine
theory
of depression.
Dopamine is the precursor of norepinephnine, and ECT may produce its antidepressant action by increasing the synthesis ofdopamine and nonepinephnine. The therapeutic effectiveness of 1.-dopa in the treatment of Parkinson’s disease is well known (7), but its role in the Patients
pathogenesis treated
with
mental
changes.
These
elation,
hypersexuality,
nations,
delusions,
of affective L-dopa have include
disorders developed
enhancement
depression, and
is
frank
less clean. a variety of of memory,
excitement,
psychosis.
halluci-
The
drug
may
cause deterioration of the mental state of schizophrenic patients (8). Paradoxically, i.-dopa has been reported to cause depression (9- 1 1) as well as to alleviate it ( I 2). Tncyclic
antidepressant
available
brain
lieving
depression
L-dopa. larly.
It might
Were
the
drugs, in
extreme
Parkinson’s
disease phase well
the extrapyramidal drug-induced
are
probably
efTective
pankinsonian
be supposed
patients a manifestation suIt of psychomotor bradykinesia, severe posture, shuffling gait, advanced We are
which
norepinephnine,
rigidity
that and
increase
agents
patients
ECT
would
bradykinesia
in re-
receiving
act
simi-
ofour
two
of Parkinson’s disease on the reretardation? The typical tremor, muscular rigidity, characteristic retropulsion, and other features of clearly
of parkinsonism. aware of the system parkinsonism
confirm effects
that of
they
were
in an
phenothiazines
and their capacity or to aggravate
on
to cause preexisting
Parkinson’s disease. However, our first patient clearly suffers from classic idiopathic Parkinson’s disease, which has been progressive and asymmetric over a number of years during which he did not receive any phenothiazines. In addition, his history revealed that at age 6 he had suffered severely from influenza during the 1918 epidemic.
BRIEF
The
question
at
all
of drug-induced
in our
second
phenothiazines Biochemical
parkinsonism
patient
since
for over
I I years.
changes
in dopamine
he
did
had
not
turnover
not
arise
taken
any
or ECT-in-
duced dopamine-receptor sensitivity may explain our patients’ improvement. More difficult to explain is the maintenance of this improvement for many months after ECT. This parallels a similar improvement in their depression and denotes the induction oflong-acting changes in the underlying mechanisms subserving movement and tone as well as mood. We hope that this report will alert clinicians who are confronted by patients with Parkinson’s disease complicated by depression to the fact that ECT is not contraindicated
and
in some
cases
may
be
the
treatment
of
choice. It remains to be seen whether ECT will be equally effective in helping parkinsonian patients without associated mental depression or those who fail to improve with L-dopa.
REFERENCES I.
Holmberg G: Rev Neurobiol
Biological aspects 5:389 412, 1963
Classification
of Suicidal
Medical
Lethality
BY
T.
AARON
of electroconvulsive
BECK.
M.D..
ROY
therapy.
Behaviors:
BECK.
,NI)
Int
in classifying
suicidal
THE
OF
BEHAVIORS
STUDY
handicapped cepts,
and
SUICIDAL
by
semantic
contradictory
‘ A complete review of suicidal behaviors
behavior.
confusion, taxonomies.’
has
been chronically amorphous con-
Many
of the literature on taxonomies was made by Beck and Greenberg
522,
1965
6. Schildkraut ii, Draskoczy PR: Effects of electroconvulsive shock on norepinephrine turnover and metabolism: basic and clinical studies, in The Psychobiology of Convulsive Therapy. Edited by Fink M, Kety 55, McGaugh I, et al. Washington, DC, VH Winston & Sons, 1974, pp 143- 170 7. Cotzias GC, Van Woent MH, Schifl’er LM: Aromatic amino acids and modification of parkinsonism. N EngI J Med 276:374-379, 1967 8. Tobias IA, Merlis 5: Levodopa and schizophrenia (hr to ed). JAMA2II:l857, 1970 9. Barbeau A: L-dopa therapy in Parkinson’s disease: a critical review of nine years’ experience. Can Med Assoc 1 191:791-800, 1969 10. Mawdsley C: Treatment of parkinsonism with laevo-dopa. Br Med J 1:331-337, 1970 II. Jenkins RB, Groh RH: Mental symptoms in parkinsonian patients treated with L-dopa. Lancet 2:177-180, 1970 12. Bunney WE, Janowsk’, DS, Goodwin FK, et al: Effect of i-dopa on depression. Lancet 1:885 886, 1969
KOVACS.
Previous studies ofattemptedsuicide have cast doubt on the value ofassessingpsychological intent. By identifying a moderating variable, name/v. the attempter’s preconceptions about the lethality ofhis act, the authors were able to solve the puzzle ofthe lo w correlations between intent andlethalitv. Suicidal intent correlate.s highly with medicallethalitv when the attempter has sufficien t kno wledge to assess proper/v the probable outcome of his attempt. The authors conclude that suicidal intent and medical lethality are useful dimensions
Engel J, Hanson LCF, Roos BE et al: Effect of electroshock on dopamine metabolism in rat brain. Psychopharmacologia 13: 140144, 1968 3. Essman WB: Neurochemical changes in ECS and ECT. Semin Psychiatry 4:67-79, 1972 4. Kety SS: Biochemical and neurochemical effects of deetroconvulsive shock, in The Psychobiology of Convulsive Therapy. Edited by Fink M, Kety 55, McGaugh I, et al. Washington. DC, VH Winston & Sons, 1974, pp 285-294 5. Schildkraut ii: The catecholamine hypothesis of affective disorders: a review ofsupporting evidence. Am J Psychiatry 122:5092.
I. Quantifying
MARIA
writers
and
have
nomenclature (I).
COMMUNICATIONS
Intent
and
P1-1.1).
lumped
completed
together group.
as Nonfatal
as unsuccessful
the
question such
“simulated tioned writer
“suicidal
suicide,” suicide.” means
nonfatal
suicide
constituted
attempts
suicides.
of suicidal as
and
these
suicide
ply terms
suicides
though
have
The
intent
a been
reported
controversy
has
a variety
“abortive
“pseudosuicide,”
It is often difficult to by a “serious suicide
sim-
surrounding
spawned
gesture,”
attempts
homogeneous
of
suicide,”
and
“sub-inten-
understand attempt”
what because
some authors confound the degree of an individual’s tent to kill himself with the medical consequences suicidal act (2-5). Other investigators, dismissing wish to die as the motive for most cases of nonfatal
a
inof his the sui-
Beck is Professor of Psychiatry, Mr. Beck is a medical student, and Dr. Kovacs is Associate in Psychiatry, University of Pennsylvania and Philadelphia General Hospital, Philadelphia, Pa. Address reprint requests to Dr. Beck at 429 Stouffer Bldg., Philadelphia General Hospital, 700 Civic Center Blvd., Philadelphia, Pa. 19104. Dr.
This study was supported stitute of Mental Health.
Am
by grant
J P.svchiatrs’
MH-I9989
/32:3,
from
March
the
/975
National
In-
285
