syndrome: Report of two further cases. Ann Genet 17:87, 1974.
13. Penrose LS: Dermatoglyphic patterns in a case of trisomy 8. Lancet 1:957, 1972.
14. Kucherlapati RS, Nichols EA, Creagan RP, et al: Assign-ment of the gene for glutathione reductase to human chromosome 8 by somatic cell hybridiza-tion. Read before the American Society of Human Genetics, Portland, Oregon, October 1974. 15. Bass HN, Crandall BF: Trisomy 8-an identifiable
syndrome. Read before the American Society of
Human Genetics, Portland, Oregon, October 1974.
ACKNOWLEDGMENT
We are most indebted to Susan Lewis, Ph.D., psychologist, Vanderbilt Child Psychiatric Division, for the child’s psycho-motor evaluation.
Epileptiform
Activity
in the
Electroencephalogram
Induced
by
Lithium
Carbonate
Lithium
salts
have
been
used
in the
prophylaxis
of
manic-depressive
disease
in
adults,’2
in
the
treatment
of
episodic
behavior
disturbances
in
children,34
and
recently
in
the
treatment
of
thyrotoxicosis. Side effects of therapy with
lithium
salts
have
been
frequent
at
toxic
blood
levels
(>
1.5
mEq/liter)
but
rare
at
therapeutic
blood
levels
(0.8
to
1.5
mEq/liter).6
This report describes the development of
paroxysmal
electroencephalographic
abnormali-ties
in
a
child
under
treatment
with
lithium
carbonate
for
a behavior
disturbance.
Such
parox-ysmal activity has not been described previously
during
lithium
carbonate
therapy.
CASE REPORT
This white boy was the 2,920-gm product of a normal pregnancy, labor, and repeat Cesarean section delivery in a 39-year-old gravida 2 woman. Growth and development were normal with walking at 1 1 months and speaking three-word sentences at 2 years. At the age of 6#{189}years he was hospitalized for presumed encephalitis after a three-week history of peculiar fidgeting mannerisms, excessive activity,
and staggering gait. He was unable to sit still, he talked continuously with a marked dysarthria, and he was severely ataxic. Admission lumbar puncture revealed clear and color-less cerebrospinal fluid containing 154 mononuclear cells per
cubic millimeter with a protein level of 37 mg/dl; bacterial
7
Is
v’V
iii’
V\
J’’ .
FIG. 2. EEC performed after three days of lithium carbonate therapy (blood lithium level 0.6 mEq/liter).
FIG. 3. EEC performed after ten days of lithium carbonate therapy (blood lithium level 1.2 mEq/liter).
832
EPILEPTIFORM
ACTIVITY
by guest on September 8, 2020
www.aappublications.org/news
I
2372
3
5
5
\5\’”M
. ,.Ftc. 4. EEC performed one month after discontinuing lithium carbonate (patient receiving diphenylhydantoin, haloperidol, and chlordiazepoxide).
cultures were negative. A second lumbar puncture ten days later contained 10 mononuclear cells per cubic millimeter with a protein level of 39 mg/dl.
After the hospitalization his parents noted a marked change in his behavior. He was extremely hyperactive and destructive, had a short attention span, and was disruptive in school. At the age of 6 years 7 months he was referred to the St. Louis Children’s Hospital. An electroencephalogram at that time showed no abnormality in both awake and drowsy states. His behavior was modified with various conibinations of tranquilizers (chlorpromazine, thioridazine, chlordiaze-poxide, and haloperidol) and antidepressants (amitriptyline and imipramine); however, he continued to have episodic moodiness, belligerance, hyperactivity, push of speech, irrit-ability, and sleep disturbance. He had no clinical seizure activity and received no anticonvulsant medication. There
was no family history of epilepsy. At the age of 12#{189}years he developed a marked change in behavior over a six-week period with greatly increased hyperactivity, intrusiveness, distractability, push of speech (including frequent use of vulgarities), flight of ideas, delusions that he was “Bruce
Lee” and “Evel Knievel,” and marked agitation. He was hospitalized after threatening on several occasions to kill his parents. At the time of admission his only current medication
(
chlordiazepoxide) was discontinued. Examination on adm is-sion was unremarkable except for his hyperactivity, marked hostility, intrusiveness, and continuous vulgar speech. On thefifth hospital day an EEC was normal (Fig. 1). He was then begun on lithium carbonate in an attempt to control his abnormal behavior. After three days of lithium carbonate therapy (blood lithium level was 0.6 mEq/liter) he had a single spike-wave complex noted on his EEC (Fig. 2). After ten days of lithium carbonate therapy he showed no clinical improvement in his behavior. An EEC on the tenth day
(blood lithium level was 1.2 mEq/liter) showed frequent bursts of high-voltage diffuse spikes and poly-spike wave
complexes (Fig. 3). He had no clinical seizures, but the lithium carbonate was discontinued and he was treated with a combination of diphenylhydantoin, haloperidol, and chlor-diazepoxide. After one month his behavior improved dra-matically and a repeat EEC was again normal (Fig. 4).
DISCUSSION
During
the
latter
part
of
the
19th
century
an
increased
anticonvulsant
effect
was
attributed
to
lithium
bromide
over
other
bromide
salts.7
Recently,
Carrere
and
Pochard5
used
lithium
citrate
as
a
supplement
to
barbiturates
in
the
treatment
of
psychomotor
epilepsy.
However,
convulsions were a frequent consequence of the use
of
lithium
chloride
as
a
salt
substitute
in
patients
with
congestive
heart
failure.”
With
the
introduction
of
lithium
carbonate
as
the
treat-ment
of
choice
in
mania,
convulsions
were
re-ported
frequently
with
blood
lithium
levels
exceeding
2.0
mEq/liter’#{176}
and
occasionally
with
therapeutic
blood
levels.”
EEGs
performed
after
these seizures showed only diffuse slowing.
accentua-834
EPILEPTIFORM
ACTIVITY
tion
of
focal
abnormalities
in
the
EEGs
of
psychiatric
patients
with
therapeutic
blood
lithium
levels.
In contrast,
Erwin
et al.’7recently
described
the
normalization
of paroxysmal
EEGs
and
reduction
of
seizure
frequency
in
chronic
epileptic
patients
given
lithium
carbonate.
With
therapeutic
blood
lithium
levels
our
patient
developed
paroxysmal
spike-slow
wave
bursts on his EEG. The EEG returned to normal
after
cessation
of
the
lithium
carbonate.
An
imderlying
abnormality
(possibly
secondary
to the
episode
of
encephalitis)
may
have
been
accen-tuated
by
the
lithium
carbonate
therapy.
A
similar
effect
of
lithium
salts
might
explain
the
seizures
reported
in patients
receiving
only
ther-apeutic
doses.
Lithium
salts
have
been
used
infrequently
in children
and
are
not
approved
by
the
US
Food
and
Drug
Administration
for
use
in
patients
under
age
12 years.
Lithium
salts
should
only be used
with
caution,
and
certainly
serial
EEGs
are
indicated
in order
to detect
developing
epileptiform
discharges
prior
to
the
onset
of
clinical
seizures.
St. Louis, Missouri
ROGER A. BRUMBACK,
M.D.
WARREN A. WEINBERG,
M.D.
BARBARA L. HERJANIC,
M.D.
Departments
of Pediatrics,
Neurology,
and
Psychiatry,
St.
Louis
Children’s
Hospital
This work was supported in part by grant No. NINDS Ti NS5633-07 from the National Institutes of Health (Dr. Brumback) and by a grant from the Allen P. and Josephine B. Creen Foundation, Mexico, Missouri.
ADDRESS FOR REPRINTS: (W.A.W.) Department of Neurology, University of Texas Health Science Center,
5323 Harry Hines Boulevard, Dallas, Texas 75235.
REFERENCES
1. Levy BS: A practicum for the use of lithium salts in affective psychoses. JAMA 206: 1045, 1968.
2. Prien 1W, Klett CJ, Caffey EM: Lithium prophylaxis in recurrent affective illness. Am
J
Psychiatry 131:198, 1974.3. Gram LF, Rafaelsen OJ: Lithium treatment of psychotic
children and adolescents. Acta Psychiatr Scand 48:253, 1972.
4. Feinstein SC, Wolpert EA: Juvenile manic-depressive illness: Clinical and therapeutic considerations.
J
Am Acad Clin Psychiatry 12:123, 1973.
5. Lazarus JH, Addison CM, Richards AR, Owen GM:
Treatment of thyrotoxicosis with lithium carbonate. Lancet 2:1160, 1974.
6. Gershon 5: Lithium in mania. Clin Pharmacol Ther 11:168, 1970.
7. Mitchell SW: On the use of bromide of lithium. Am
J
Med Sci 60:443, 1870.
8. Carrere MJ, Pochard M: Le citrate de lithium dans le
traitement des syndromes d’excitation
psychomo-trice. Ann Med Psychol ii2:566, 1954.
9. Corcoran AC, Taylor RD. Page I: Lithium poisoning
from
the
use of salt substitutes. JAMA 139:685, 1949.10. Schou M, Amdisen A, Trap-Jensen
J:
Lithium poisoning. AmJ
Psychiatry 125:520, 1968.ii. Demers R, Lukesh R, Pnchard
J:
Convulsion duringlithium therapy. Lancet 2:315, 1970.
12. 1W TM, Akpinar S: Lithium effect on human
electroen-cephalogram. Clin Electroencephalogr 2:89, 1971. 13. Johnson C, Maccario M, Cershon 5, Korein
J:
Theeffects
of
lithium on electroencephalogram, behav-ior and serum electrolytes.J
Nerv Ment Dis151:273, 1970.
14. Small JG, Milstein V, Perez HG, et al: EEG and
neurophysiological studies of lithium in normal volunteers. Biol Psychiatry 5:65, 1972.
15. Barratt ES, Creson DL, Russell C: The effects of lithium salts on brain activity in the cat. Am
J
Psychiatry125:530, 1968.
16. Mayfield D, Brown RG: The clinical laboratory and
electroencephalographic effects of lithium.
J
Psychiatr Res 4:207, 1966.
17. Erwin CW, Gerber CJ, Morrison SD, James JF: Lithium carbonate and convulsive disorders. Arch Gen Psychiatry 28:646, 1973.
ACKNOWLEDGMENT
Drs. A. L. Prensky and P. R. Dodge critically reviewed this
work.
GENERIC
AND BRAND
NAMES
Lithium carbonate-.-Lithane, Eskalith, Lithotabs.
