CLINICAL
AND
Cardiac
Arrhythmia
BY
DINESH
RESEARCH
and
MEHTA,
Am
REPORTS
M.D.,
SHOBANA
MEHTA,
M.D.,
JAMES
,
was
Report
A 21-year-old admitted
behavioral
unmarried to the center
alteration.
ic, talkative, he had lost
mood,
pressured
notions of psychiatrists,
entered
hospital history
his and
of ideation,
owning
was good, expansive
and grandiose to his attending He felt Jesus had
a large restaurant,
at work.
or drugabuse.
and
He had no history
His
sister
bad
had
of
emo-
tional problems that reportedly started in a similar manner. Her condition was diagnosed as secondary to Cushing’s disease,
and
were
also endocninologic.
the
parents
felt
that
their
son’s
emotional
problems
Results ofthe patient’s initial physical examination by two physicians were within normal limits except for mild cellulitis associated with an ingrowing toenail. The patient was
diagnosed
as manic
and was considered
didate for rapid neuroleptization tient initially refused the drug,
wrong
with
cian’s
Desk
him.
itored ceived
hourly by a specially 10 mg of haloperidol
an appropriate
can-
with haloperidol. The pastating that there was nothing
Later,
after demanding to see the Physihe agreed to take haloperidol by mouth. He received 90 mg of halopenidol the first day, 60 mg the next day, and 10 mg on the third day. During this intensive drug treatment, the patient’s vital signs were monReference,
assigned on the third
denly became hypotensive (blood He was pale, sweating, and had a minute, with an extrasystole every mild
parkinsonian
symptoms.
nurse. After he reday the patient sudpressure of 80/60 mm Hg). pulse rate of 100 beats per
other
He
denied
beat. any
He also had chest
comfort, but an ECG confirmed numerous multifocal, mature ventricular beats. The patient was transferred
Received
May
3, 1979; accepted
June
PETIT,
coronary itoning.
AND
care
In the coronary
caine,
1979
care unit, the patient denied no cardiac murmurs or evidence
any chest of cardiac
was
continuous
given
an intravenous
75 mg, and then a lidocaine
havior in the able and the normal beats.
he was returned coronary extrasystoles
care
investigations
bolus
of lido-
drip at the rate of 1 mg/kg
body weight per minute, with the ing to the frequency of extrasystoles. started on procainamide, 500 mg
of observation
M.D.
mon-
He
for
SHRINER,
cardiovascular
rate
being altered The next day
accordhe was
every 4 hours. After 3 days to the center because his be-
unit had
was considered unmanagedecreased to one every
showed
results
within
10
normal
complete blood counts (including differential count), serologic test for syphilis, urinalysis with toxicologic studies, serum electrolytes and blood gases, fasting chemogram, serum lactic dehydrogenase isoenzymes, serum transaminases, serum creatine phosphokinase isoenzymes, serum cortisol, thyroid studies (T3, T4, T7), X rays of the chest and skull, and a subsequent brain scan. In view of the persistence of extrasystoles (1 every 10 beats), the patient was observed without neuroleptic medication. On days 7 and 8, he was given diazepam and amobarbitol sodium p.r.n. , without much improvement in manic symptoms. On day 9 he was started on thiothixene, 30 mg/ day in divided doses, because of his increased psychomotor activity, sleeplessness, and irritability. Over the next 2 days the dosage was reduced to 5 mg/day, and his manic symptoms subsided. On day 13, the ECG was normal and mild parkinsonism was evident.
dis-
preto a
Discussion
This manic patient had no personal or family history of heart disease and the results of several preemployment physical examinations, as well as two physical examinations before initiation of haloperidol thenapy, had been normal. The etiology of his arrhythmia remains unclear, and the association with halopenidol may be entirely fortuitous. However, haloperidol was the only drug the patient was taking when he developed the arrhythmia. Rapid neunoleptization is being used increasingly to treat acutely disturbed psychotic patients. We think that intensive medical monitoring of such patients is indicated so that any adverse cardiovascular events can be diagnosed early and treated appropriately. In the case described here, routinely used anti-arrhythmic drugs effectively controlled the patient’s annthythmia. ,
1, 1979.
0002-953X179/l
WILLIAM
unit
pain and showed decompensation.
REFERENCES
Drs. Dinesh and Shobana Mehta and Dr. Petit are Psychiatrists, Katherine Hamilton Mental Health Center, 620 Eighth Ave., Terre Haute, md. 47804, where Dr. Shriner is Director. Address reprint requests to Dr. Shriner.
1468
M.D.,
The following
with his sexual prowess. The patient’s prewas said to have been quiet, gentle, and and he did as he was told by his parents
mania,
November
limits:
energet-
appetite showed
sums of money and the police.
about
employee of sudden
hyperactive,
although irritable
and his supervisors
depression,
(111 kg) a 2-week
flight
large center,
his life, talked
at home
and was
speech,
donating the
was preoccupied morbid personality nonargumentative,
obese with
He had become
sleepless, 9. 1 kg. He
/36:11,
Haloperidol
Several recent reports (1 2) have suggested that halopenidol is effective and safe in the treatment of acutely disturbed psychotic patients. Cardiovascular side effects associated with haloperidol therapy, when observed, have been benign (1-3). However, serious cardiovascular problems and even death have been neported with other psychotropic drugs (4). In view of the rarity of severe arrhythmia associated with the use ofhaloperidol, we would like to report the case ofa manic patient who developed this side effect. Case
J Psychiatry
1/1468/02/$00.35
1. Donlon -r, Hopkin J, Tupin JP: Overview: of the rapid neuroleptization method with dol. Am J Psychiatry 136:273-278, 1979 © 1979
American
Psychiatric
Association
efficacy injectable
and safety haloperi-
Am
J Psychiatry
136:11,
November
CLINICAL
1979
1977 4. Fowler NO, changes and tropic drugs.
2. Ayd Fi Jr: Haloperidol: twenty years’ clinical experience. J Clin Psychiatry 39:807-814, 1978 3. Sweet CP Jr. Shader RI: Cardiac side effects and sudden death in hospitalized psychiatric patients. Dis Nerv Syst 38:69-72,
Nocturnal BY
Head
MIRIAM
Banging
R. FREIDIN,
as a Sleep
M.D.,
Disorder:
A Case
J. JANKOWSKI,
JOSEPH
M.D.,
Head banging continues to be a poorly understood phenomenon. It has been viewed as the result of maternal deprivation on as an expression of frustration (15). We will describe a 2-year-old boy who engaged in head banging during sleep. The clinical investigation of this case included all night sleep EEGs and two trials of psychoactive medication. Case
Report
Bill was
referred at the because of nighttime
cian
months
previously.
panied
by
body
age of 27 months head banging that
The
head
rocking,
banging,
began
by his pediatrihad started 17
which
after
the
was accom-
child
had
been
any improvement. these episodes he was in a trance-like state, appearing disoriented and lacking recall for the episodes. He did not awaken during the severe head banging
and
did
not
seem
Bill was the product and his developmental lives years.
with No
parents. There
four older siblings, aged 8-21 problems were reported by the
no history
disturbance
except
his job of 25 years, Bill’s walking
been
and
of emotional Bill’s
father,
had become
who
irritable
had
in other recently
tantrum
During
head bangers
psychiatric charming
Jan.
29,
during
interviews,
and
1979;
revised
no evidence
May
of
sleep-
brother
had
childhood. including
showed
lost
and depressed.
mother had experienced a few episodes as a child and both his father and older
Bill was
Received 1979.
and delivery, He currently
his parents and other behavioral
was members
family
to be in pain.
of a normal pregnancy milestones were normal.
10, 1979;
play
sessions,
of psychiatric
accepted
June
19,
The authors are with New England Medical Center Hospital, 171 Harrison Ave. , Boston, Mass. 02111, where Dr. Freidin is Staff Child Psychiatrist, Child Psychiatry Inpatient Service; Dr. Jankowski is Director of Ambulatory Services and Community Child Psychiatry; and Dr. Singer is StaffPediatric Neurologist. Dr. Freidin is also Assistant Clinical Professor, Tufts University School of Modicine, where Dr. Jankowski is Associate Clinical Professor of Psychiatry and Dr. Singer is Assistant Professor of Pediatrics (Neurology). 0002-953X/79/
1 1/1469/02/$00.35
© 1979
D. SINGER,
M.D.
Merrill Palmer testing he level, with no signs oforganic
functioned impairment.
at
a
Bill’s mother was parent. However,
his father appeared depressed and considered Bill’s symptoms a ploy to gain special attention. Results of neurologic examination were within normal limits. Three EEGs were performed. The first, a sleep-deprived daytime EEG, showed normal, age-appropriate patterns.
Two 8-hour nighttime sleep tracings were then obtained. During the first one, approximately 90 minutes after Bill fell asleep rocking
he demonstrated during sleep Diazepam was started
doses
taking
WILLIAM
Both parents were interviewed, and found to be a very calm and experienced
in the wall. His parents’ attempts him into their bed did not lead to When Bill was awakened during
by
REPORTS
McCall D, Chou T, et al: Electrocardiographic cardiac arrhythmias in patients receiving psychoAm J Cardiol 37:223-230, 1976
disturbance. On normal cognitive
creased
him
RESEARCH
Report
AND
asleep for 2 hours; it never occurred during wakefulness or during his daytime naps. By the time Bill was 18 to 24 months old, the head banging and body rocking had become so severe that his crib had to be nailed to the floor. Eventually he broke the headboard of his bed and knocked a hole to placate
AND
this
,
to 8 mg h.s. over
medication,
Bill’s
head banging, moaning, and body stages I and 2, unrelated to REM. at a dose of 2 mg h.s. which was in-
a second
rocking
was
head banging. the behavior
less
a 2-week sleep
intense
period.
EEG
at this
tracing
time
He was free of head banging then
recurred
ofdiazepam.
The
After
and
persisted
medication
was
and despite
to it.
old, continues
head banging
obtained.
there
was
no
for 4 weeks,
discontinued
after he stopped responding One month after diazepam
30 days of
was
but
increasing I week
was discontinued, imipramine was instituted at a dose of 75 mg h.s. The head banging ceased for 6 weeks but then recurred. After the trials ofdiazepam and imipramine, we gave Bill a brief trial of phenytoin, which was unsuccessful. One year after the discontinuation of all medications, Bill, now 4 years at pretreatment
to experience levels
and body rocking
of intensity.
Discussion
Multiple etiologies of head banging have been advanced in the literature, but none has been substantiated by experimental evidence. Such etiologies include undenstimulation and maternal neglect (I 2), erotic gratification (3), and excessive physical restraint (4). Previous theories were consolidated by dividing head banging into two types, autoerotic and tantrum (6). Autoerotic head banging begins between 6 and 12 months of age and continues well into latency on even adolescence. Some of these children have severe ego disturbances; others have no developmental difficulties. Tantrum head banging begins when the child is able to walk and is related to difficulties in accepting and dealing with frustration. The case we have described does not fit into any of the above categories. This patient’s nocturnal head banging was automatic and stereotypic and was asso,
American
Psychiatric
Association
1469
AND
Cardiac
Arrhythmia
BY
DINESH
RESEARCH
and
MEHTA,
Am
REPORTS
M.D.,
SHOBANA
MEHTA,
M.D.,
JAMES
,
was
Report
A 21-year-old admitted
behavioral
unmarried to the center
alteration.
ic, talkative, he had lost
mood,
pressured
notions of psychiatrists,
entered
hospital history
his and
of ideation,
owning
was good, expansive
and grandiose to his attending He felt Jesus had
a large restaurant,
at work.
or drugabuse.
and
He had no history
His
sister
bad
had
of
emo-
tional problems that reportedly started in a similar manner. Her condition was diagnosed as secondary to Cushing’s disease,
and
were
also endocninologic.
the
parents
felt
that
their
son’s
emotional
problems
Results ofthe patient’s initial physical examination by two physicians were within normal limits except for mild cellulitis associated with an ingrowing toenail. The patient was
diagnosed
as manic
and was considered
didate for rapid neuroleptization tient initially refused the drug,
wrong
with
cian’s
Desk
him.
itored ceived
hourly by a specially 10 mg of haloperidol
an appropriate
can-
with haloperidol. The pastating that there was nothing
Later,
after demanding to see the Physihe agreed to take haloperidol by mouth. He received 90 mg of halopenidol the first day, 60 mg the next day, and 10 mg on the third day. During this intensive drug treatment, the patient’s vital signs were monReference,
assigned on the third
denly became hypotensive (blood He was pale, sweating, and had a minute, with an extrasystole every mild
parkinsonian
symptoms.
nurse. After he reday the patient sudpressure of 80/60 mm Hg). pulse rate of 100 beats per
other
He
denied
beat. any
He also had chest
comfort, but an ECG confirmed numerous multifocal, mature ventricular beats. The patient was transferred
Received
May
3, 1979; accepted
June
PETIT,
coronary itoning.
AND
care
In the coronary
caine,
1979
care unit, the patient denied no cardiac murmurs or evidence
any chest of cardiac
was
continuous
given
an intravenous
75 mg, and then a lidocaine
havior in the able and the normal beats.
he was returned coronary extrasystoles
care
investigations
bolus
of lido-
drip at the rate of 1 mg/kg
body weight per minute, with the ing to the frequency of extrasystoles. started on procainamide, 500 mg
of observation
M.D.
mon-
He
for
SHRINER,
cardiovascular
rate
being altered The next day
accordhe was
every 4 hours. After 3 days to the center because his be-
unit had
was considered unmanagedecreased to one every
showed
results
within
10
normal
complete blood counts (including differential count), serologic test for syphilis, urinalysis with toxicologic studies, serum electrolytes and blood gases, fasting chemogram, serum lactic dehydrogenase isoenzymes, serum transaminases, serum creatine phosphokinase isoenzymes, serum cortisol, thyroid studies (T3, T4, T7), X rays of the chest and skull, and a subsequent brain scan. In view of the persistence of extrasystoles (1 every 10 beats), the patient was observed without neuroleptic medication. On days 7 and 8, he was given diazepam and amobarbitol sodium p.r.n. , without much improvement in manic symptoms. On day 9 he was started on thiothixene, 30 mg/ day in divided doses, because of his increased psychomotor activity, sleeplessness, and irritability. Over the next 2 days the dosage was reduced to 5 mg/day, and his manic symptoms subsided. On day 13, the ECG was normal and mild parkinsonism was evident.
dis-
preto a
Discussion
This manic patient had no personal or family history of heart disease and the results of several preemployment physical examinations, as well as two physical examinations before initiation of haloperidol thenapy, had been normal. The etiology of his arrhythmia remains unclear, and the association with halopenidol may be entirely fortuitous. However, haloperidol was the only drug the patient was taking when he developed the arrhythmia. Rapid neunoleptization is being used increasingly to treat acutely disturbed psychotic patients. We think that intensive medical monitoring of such patients is indicated so that any adverse cardiovascular events can be diagnosed early and treated appropriately. In the case described here, routinely used anti-arrhythmic drugs effectively controlled the patient’s annthythmia. ,
1, 1979.
0002-953X179/l
WILLIAM
unit
pain and showed decompensation.
REFERENCES
Drs. Dinesh and Shobana Mehta and Dr. Petit are Psychiatrists, Katherine Hamilton Mental Health Center, 620 Eighth Ave., Terre Haute, md. 47804, where Dr. Shriner is Director. Address reprint requests to Dr. Shriner.
1468
M.D.,
The following
with his sexual prowess. The patient’s prewas said to have been quiet, gentle, and and he did as he was told by his parents
mania,
November
limits:
energet-
appetite showed
sums of money and the police.
about
employee of sudden
hyperactive,
although irritable
and his supervisors
depression,
(111 kg) a 2-week
flight
large center,
his life, talked
at home
and was
speech,
donating the
was preoccupied morbid personality nonargumentative,
obese with
He had become
sleepless, 9. 1 kg. He
/36:11,
Haloperidol
Several recent reports (1 2) have suggested that halopenidol is effective and safe in the treatment of acutely disturbed psychotic patients. Cardiovascular side effects associated with haloperidol therapy, when observed, have been benign (1-3). However, serious cardiovascular problems and even death have been neported with other psychotropic drugs (4). In view of the rarity of severe arrhythmia associated with the use ofhaloperidol, we would like to report the case ofa manic patient who developed this side effect. Case
J Psychiatry
1/1468/02/$00.35
1. Donlon -r, Hopkin J, Tupin JP: Overview: of the rapid neuroleptization method with dol. Am J Psychiatry 136:273-278, 1979 © 1979
American
Psychiatric
Association
efficacy injectable
and safety haloperi-
Am
J Psychiatry
136:11,
November
CLINICAL
1979
1977 4. Fowler NO, changes and tropic drugs.
2. Ayd Fi Jr: Haloperidol: twenty years’ clinical experience. J Clin Psychiatry 39:807-814, 1978 3. Sweet CP Jr. Shader RI: Cardiac side effects and sudden death in hospitalized psychiatric patients. Dis Nerv Syst 38:69-72,
Nocturnal BY
Head
MIRIAM
Banging
R. FREIDIN,
as a Sleep
M.D.,
Disorder:
A Case
J. JANKOWSKI,
JOSEPH
M.D.,
Head banging continues to be a poorly understood phenomenon. It has been viewed as the result of maternal deprivation on as an expression of frustration (15). We will describe a 2-year-old boy who engaged in head banging during sleep. The clinical investigation of this case included all night sleep EEGs and two trials of psychoactive medication. Case
Report
Bill was
referred at the because of nighttime
cian
months
previously.
panied
by
body
age of 27 months head banging that
The
head
rocking,
banging,
began
by his pediatrihad started 17
which
after
the
was accom-
child
had
been
any improvement. these episodes he was in a trance-like state, appearing disoriented and lacking recall for the episodes. He did not awaken during the severe head banging
and
did
not
seem
Bill was the product and his developmental lives years.
with No
parents. There
four older siblings, aged 8-21 problems were reported by the
no history
disturbance
except
his job of 25 years, Bill’s walking
been
and
of emotional Bill’s
father,
had become
who
irritable
had
in other recently
tantrum
During
head bangers
psychiatric charming
Jan.
29,
during
interviews,
and
1979;
revised
no evidence
May
of
sleep-
brother
had
childhood. including
showed
lost
and depressed.
mother had experienced a few episodes as a child and both his father and older
Bill was
Received 1979.
and delivery, He currently
his parents and other behavioral
was members
family
to be in pain.
of a normal pregnancy milestones were normal.
10, 1979;
play
sessions,
of psychiatric
accepted
June
19,
The authors are with New England Medical Center Hospital, 171 Harrison Ave. , Boston, Mass. 02111, where Dr. Freidin is Staff Child Psychiatrist, Child Psychiatry Inpatient Service; Dr. Jankowski is Director of Ambulatory Services and Community Child Psychiatry; and Dr. Singer is StaffPediatric Neurologist. Dr. Freidin is also Assistant Clinical Professor, Tufts University School of Modicine, where Dr. Jankowski is Associate Clinical Professor of Psychiatry and Dr. Singer is Assistant Professor of Pediatrics (Neurology). 0002-953X/79/
1 1/1469/02/$00.35
© 1979
D. SINGER,
M.D.
Merrill Palmer testing he level, with no signs oforganic
functioned impairment.
at
a
Bill’s mother was parent. However,
his father appeared depressed and considered Bill’s symptoms a ploy to gain special attention. Results of neurologic examination were within normal limits. Three EEGs were performed. The first, a sleep-deprived daytime EEG, showed normal, age-appropriate patterns.
Two 8-hour nighttime sleep tracings were then obtained. During the first one, approximately 90 minutes after Bill fell asleep rocking
he demonstrated during sleep Diazepam was started
doses
taking
WILLIAM
Both parents were interviewed, and found to be a very calm and experienced
in the wall. His parents’ attempts him into their bed did not lead to When Bill was awakened during
by
REPORTS
McCall D, Chou T, et al: Electrocardiographic cardiac arrhythmias in patients receiving psychoAm J Cardiol 37:223-230, 1976
disturbance. On normal cognitive
creased
him
RESEARCH
Report
AND
asleep for 2 hours; it never occurred during wakefulness or during his daytime naps. By the time Bill was 18 to 24 months old, the head banging and body rocking had become so severe that his crib had to be nailed to the floor. Eventually he broke the headboard of his bed and knocked a hole to placate
AND
this
,
to 8 mg h.s. over
medication,
Bill’s
head banging, moaning, and body stages I and 2, unrelated to REM. at a dose of 2 mg h.s. which was in-
a second
rocking
was
head banging. the behavior
less
a 2-week sleep
intense
period.
EEG
at this
tracing
time
He was free of head banging then
recurred
ofdiazepam.
The
After
and
persisted
medication
was
and despite
to it.
old, continues
head banging
obtained.
there
was
no
for 4 weeks,
discontinued
after he stopped responding One month after diazepam
30 days of
was
but
increasing I week
was discontinued, imipramine was instituted at a dose of 75 mg h.s. The head banging ceased for 6 weeks but then recurred. After the trials ofdiazepam and imipramine, we gave Bill a brief trial of phenytoin, which was unsuccessful. One year after the discontinuation of all medications, Bill, now 4 years at pretreatment
to experience levels
and body rocking
of intensity.
Discussion
Multiple etiologies of head banging have been advanced in the literature, but none has been substantiated by experimental evidence. Such etiologies include undenstimulation and maternal neglect (I 2), erotic gratification (3), and excessive physical restraint (4). Previous theories were consolidated by dividing head banging into two types, autoerotic and tantrum (6). Autoerotic head banging begins between 6 and 12 months of age and continues well into latency on even adolescence. Some of these children have severe ego disturbances; others have no developmental difficulties. Tantrum head banging begins when the child is able to walk and is related to difficulties in accepting and dealing with frustration. The case we have described does not fit into any of the above categories. This patient’s nocturnal head banging was automatic and stereotypic and was asso,
American
Psychiatric
Association
1469
