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Myoclonic seizures with lithium
1184
BIOL
PSYCHIATRY
1987:22:1184-1190
Myoclonic
Seizures with Lithium
Steven C. Julius and Richard
Myoclonus
has been infrequently
associated
electroencephalographic
P. Brenner
observed (EEG)
in patients receiving changes
lithium therapy,
and
have not been well described.
We
report two women, ages 3.5 and 48, who, after the initiation of lithium carbonate therapy, had several generalized
tonic-clonic
seizures followed
by myoclonic
seizures.
In both,
myoclonus was associated with repetitive sharp waves on the EEG. Although the epileptogenicity of lithium remains controversial,
the occurrence
ciated with lithium treatment suggests a proconvulsant
of myoclonic
seizures asso-
efSect of lithium in susceptible
individuals.
Introduction Generalized tonic-clonic seizures have been reported in patients treated with lithium carbonate, both with toxic (Schou et al. 1968; Wharton 1969; Spring 1979; Ghadirian and Lehmann 1980) as well as therapeutic serum levels (Wharton 1969; Baldessarini and Stephens 1970; Demers et al. 1970; Massey and Folger 1984). Electroencephalographic (EEG) changes, including epileptiform abnormalities, have also been noted (Brumback et al. 1975; Strayhom and Nash 1977; Spatz et al. 1978; Spring 1979; Rosen and Stevens 1983; Massey and Folger 1984). Myoclonus, however, has infrequently been observed with lithium therapy (Spatz et al. 1978; Warick 1979; Bauer 1982; Rosen and Stevens 1983), and associated EEG changes have not been well described. We report two patients who developed myoclonus with concomitant EEG discharges after receiving lithium.
Case
1 A 35year-old mildly mentally retarded woman with no prior history of seizures was admitted to Western Psychiatric Institute and Clinic for evaluation of temper outbursts and behavioral problems. She had a history of aggressive outbursts and paranoid delusions for which she had been treated with thioridazine and trazodone hydrochloride. During the preceding 4 weeks, the frequency and severity of these outbursts had increased. On examination, she was alert and oriented. Except for mild cognitive impairment, neurological examination was otherwise unrevealing. A complete blood count (CBC), electrolytes, creatinine, and thyroid function tests were normal. A waking EEG showed
From the Departments Pittsburgh, PA.
of Neurology
(S.C.J.,R.P.B.)
and Psychiatry
Address reprint requests to Dr. Richard 15213.
P. Brenner.
Presented in part at the annual meeting
of the American
Received
@> 1987 Society
November
of Biological
15, 1986; revised January 26.
Psychiatry
(R.P.B.),
EEG Laboratory-3rd EEG
Society,
University
Floor. Orlando,
WPIC,
of Pittsburgh 381
FL, October
I O’Hara
School of Medictne. Street. Pittsburgh,
PA
1985.
1987.
OCKI6-3223/87!$03
SO
Myoclonic Seizures with Lithium
BIOL PSYCHIATRY 1987:22:1184-1190
1185
moderate diffuse abnormalities (increased theta and delta activity), which were most marked posteriorly. A computerized tomographic (CT) scan, with and without contrast, was normal. After 3 weeks of hospitalization on no medication and minimal improvement in her behavior, lithium carbonate (1200 mg/day) was begun. Five days later, she became tremulous, with periods of hyperactivity. Her serum lithium level was elevated at 1.57 meq/liter (therapeutic 0.5-1.5 meq/liter), and the lithium dose was decreased to 900 mgi day. Two days later, the serum lithium level was 1.37 meq/liter. Four days after reducing the lithium dosage, her level had decreased to 0.94 meq/liter. However, later that day, she had four generalized tonic-clonic seizures within a period of 2 hours, which were terminated with intravenous benzodiazepines. Postictally, she was somnolent and mildly dysarthric, without focal findings. Her serum lithium level was 0.77 meqiliter, and serum electrolytes, blood urea nitrogen (BUN), creatinine, calcium, magnesium, and liver function tests were unremarkable. Cerebrospinal fluid (CSF) examination was normal. Her lithium was discontinued and phenytoin was begun. Within several hours, she was alert and responding appropriately to questioning. An EEG 3 days later showed nearly continuous repetitive sharp waves, maximal at the midline vertex electrode (Cz). Intermittently throughout the tracing she had myoclonus of the right foot, which had not been previously noted. The movement occurred only with the midline discharges (Figure l), although the majority of the discharges were not associated with movements. On the following day, the myoclonus had ceased, and an EEG showed infrequent midline sharp waves. Midline epileptiform abnormalities were not present on subsequent EEGs (6 days and 3 weeks later), and she has remained seizure free for 18 months on no anticonvulsant medications.
Case 2 A 48-year-old woman was admitted to a state psychiatric hospital because of manic behavior of 3 weeks duration. She had a history of generalized seizures related to alcohol withdrawal 2 months prior to admission, as well as postpartum seizures 30 years earlier. On admission, lithium carbonate (1800 mg/day) was begun. However, after 3 days, she developed diarrhea and her lithium dose was decreased to 1200 mg/day. Four days later, she was lethargic, and her serum lithium level was elevated at 2.15 meq/liter. Her lithium was withheld, but the following day (8 days after admission) she became tremulous and had 3 generalized tonic-clonic seizures. She was transferred to the University of New Mexico Hospital for further evaluation and treatment. On examination, she was lethargic but arousable to verbal stimuli, afebrile and with normal vital signs. Repetitive myoclonic jerks of all extremities were present, occurring independently or synchronously. Deep-tendon reflexes were hyperactive and symmetrical, and plantar responses were extensor. General medical and neurological examinations were otherwise unremarkable. Laboratory studies revealed an admission serum lithium level of 0.95 meq/liter. A repeat level 10 hr later was 0.70 meq/liter. CBC, serum electrolytes, BUN, creatinine, calcium, and liver and thyroid function tests were normal. A serum thiamine level, also obtained on admission, was reported subsequently as normal. A CT scan without contrast was normal, and CSF analysis was unremarkable. She was given thiamine and started on phenytoin, 300 mg/day, after receiving a loading
1186
BIOL PSYCHIATRY 1987:22:1184-l 190
S.C. Julius and R,P. Brenner
Figure I. EEG in Case 1 shows repetitive sharp waves maximal at the midline vertex (CL) associated with myoclonic movements of the right foot, which are monitored in the bottom channel.
dose of 1000 mg. An EEG was performed 2 days after admission at which time her serum lithium level was 0.15 meq/liter. Clinically, she was confused, but followed simple commands. Throughout the tracing, she had continuous repetitive myoclonic jerks of the feet and less often of the legs, which were associated with bisynchronous sharply contoured waves in the frontal-central regions (Figure 2A). These discharges were usually maximal at the midline efectrodes (Fz,Cz). Over the next few days, her confusion resolved, and the frequency and intensity of the myoclonic jerks lessened. An EEG 9 days after admission showed intermittent repetitive sharp waves, maximal at the midline vertex (Cz), often associated with myoclonic jerks of the legs (Figure 2B). The myoclonic jerks ceased, and she was returned to the state hospital for further treatment. She remained hospitalized for an additional 6 weeks, during which time she was again treated with lithium, at a lower dose of 900 mglday. No further seizure activity or myoclonus was observed during that period. She has been lost to follow-up.
Myoclonic Seizures with Lithium
P3-PZ
BIOL PSYCHIATRY 1987;22:11841190
1187
mn
t_ FOOT _p~,~,---‘c’
,,,.. ’
,.i ^ ,^1 - ‘, / I” ,’
,* “44’_,-J~ ,] ,g
7~p;,-i-~ 1Eeij50 vv
Figure 2. (A) Initial EEG of Case 2. Myoclonic movements of the left foot (channel 17) associated with repetitive frontal-central sharp waves (seen best in channels 13 and 16). (B) Repeat EEG 7 days later shows repetitive sham waves, maximal at Cz. Myoclonic jerks of the right leg are monitored in channel 16.
Discussion Our cases demonstrate uncommon clinical and electroencephalographic abnormalities associated with lithium carbonate therapy. Myoclonus has infrequently been described with lithium toxicity (Spatz et al. 1978; Warick 1979; Bauer 1982; Rosen and Stevens 1983). Spatz et al. (1978) observed myoclonus in a 61-year-old women with toxic serum levels. Warick (1979) reported a 36-year-old man with lithium poisoning who suffered two tonic-clonic seizures and subsequent generalized myoclonic jerks. Rosen and Stevens (1983) described “action myoclonus” in a 47-year-old woman following a lithium ov-
1188
BIOL PSYCHIATRY 1987~22~1184-1190
S.C. Julius and R.P. Brenner
F3-FZ mFZ-F4 %
erdose. Stimulus-sensitive myoclonic jerks have also been reported (Bauer 1982). In none of these cases was the myoclonus clearly epileptic. Myoclonus is a nonspecific term describing quick muscle jerks arising from dysfunction of the central nervous system (Hallett 1985). Such movements can occur in normal subjects (physiological myoclonus) or may be present in a wide variety of CNS disturbances (Fahn et al. 1986). Myoclonus can be either epileptic or nonepileptic in origin. Epileptic myoclonus is a muscle jerk produced by an abnormal discharge from neurons of the motor system (Hallett 1985). Our patients exhibited my~lonic movements p~mariIy involving the lower extremities or feet foliowing lithium carbonate therapy and occurring after several generalized tonic-clonic seizures. in both, repetitive EEG discharges (sharp waves) were associated with the myoclonus, thus demonstrating the epileptic nature of these movements.
Myoclonic Seizures with Lithium
1189
BIOL PSYCHIATRY 1987;22:I184-1190
The epileptogenicity of lithium remains unce~ain. Lithium trea~ent has been reported to induce seizures in nonepileptics (Schou et al. 1968; Wharton 1969; Baldessarini and Stephens 1970; Demers et al. 1970; Spring 1979; Ghadirian and Lehmann 1980; Massey and Folger 1984), as well as increasing seizure frequency in patients with seizure disorders (Jus et al. 1973; Moore 1981). Others (Gershon 1968; Erwin et al. 1973), however, have reported the converse, finding a decrease in seizure frequency in epileptics receiving lithium. Furthermore, although lithium has been shown in rats to significantly decrease the effectiveness of several anticonvulsants (Kadzielawa 1979), recent work with hippocampal kindled rats suggest that with acute administration, lithium is neither a potent proconvulsant nor an anticonvulsant (Clifford et al. 1985). Both of our cases had complicating features that make extrapolation of their clinical course to the general population problematic. In Case I, the patient was miidly mentally retarded and had a moderately abnormal baseline EEG. The second patient had a history of alcohol withdrawal seizures, as well as postpartum seizures. Thus, the role of lithium in inducing myoclonic seizures cannot be proven conclusively. Nevertheless, the occurrence of epileptic myoclonus in both patients following lithium therapy, with subsequent resolution off lithium, suggests some contributing effect of the drug toward the activation of seizures in susceptible individuals.
References Baldessarini RJ, Stephens JH f 1970): Lithium carbonate for affective disorders. Arch Gen Psychiutr?, 22:72-77. Bauer G (1982): EEG, drug effects, and central nervous system poisoning. In Neidermeyer E, Lopes de Silva F (eds), Elecrroencephalography: Basic Principles, Clinical Applications and Related Fields. Baltimore: Urban & Schwarzenberg, pp 479-489. Brumback RA, Weinberg WA, Herjanic BL (1975): Epileptiform logram induced by lithium carbonate. Pediatrics 56:831-834.
activity in the electroencepha-
Clifford DB, Podolsky A, Zorumski CF (1985): Acute effects of tithium on hipp~ampaf seizures. EpiIepsia 26:689-692.
kindled
Demers R, Lukesh R, Prichard J (1970): Convulsion during lithium therapy (letter). Lancer ii:3 15-3 16. Erwin CW, Gerber CJ, Morrison SD, James JF, Goldsboro convulsive disorders. Arch Gen Psychiatry 2tk646-648.
NC (1973): Lithium carbonate
and
Fahn S, Marsden CD, Van Woert MH (1986): Definition and classification of myocfonus. In Fahn S, Marsden C, and Van Woert M (eds), Advances in Neurology, Vat. 43: My~c~o~~s. New York: Raven Press, pp 1-S. Gershon S (1968): Use of lithium salts in psychiatric
disorders.
Dis Nerv Syst 29:5 l-55.
Ghadirian AM, Lehmann HE (1980): Neurological side effects of lithium: Organic brain syndrome, seizures, extrapyramidal side effects, and EEG changes. Compr Psychiatp 21:327-335. Hallett M (1985): Myoclonus:
Relation to epilepsy.
Epilepsia 26 (suppl 1):S67-77.
Jus A. Villeneuve A, Gautier J, Pires A, Cote JM, Jus K, Villeneuve R, Perron D (1973): Influence of lithium carbonate on patients with temporal epilepsy. Can Psych&r Assoc .I l&77-78. Kadzielawa K (1979): Inhibition of the action of anticonvulsants Biochem Behav 10:917-921.
by lithium treatment.
Massey EW, Folger WN (1984): Seizures activated by therapeutic Sou?h Med f 77: 1173-I 175.
Pharmacol
levels of lithium carbonate.
Moore DP (1981): A case of petit ma1 epilepsy aggravated by lithium. Arn~P~chjff~~ 138:690~91, Rosen RB, Stevens R (1983): Action myoclonus
in Iithium toxicity. Ann Neurol i3:22 l-222.
1190
S.C. Julius and R.P. Brenner
BIOL PSYCHIATRY 1987;22:1184-1190
Schou M, Amdisen A, Trap-Jensen
J (1968): Lithium poisoning.
Am J Psychiatry
Spatz R, Kugler J, Greil W, Lorenzi E (1978): Das Elektroenzephalogramm Intoxikation. Nervenarzt 49539-542. Spring GK (1979): EEG observations 136:1099-1100. Strayhom
in confirming
JM, Nash JL (1977): Severe neurotoxicity
neurotoxicity
bei der LithiumAm J Psychiurry
(letter).
despite “therapeutic”
125:520-527.
serum lithium levels.
Dis Nerv Syst 38: 107-I 11.
Warick LH (1979): Lithium poisoning: sequelae. West J Med 130:259-263.
Report of a case with neurologic,
cardiac and hepatic
Wharton RN (1969): Grand ma1 seizures with lithium treatment. Am J Psychiutv
125: 152.
BIOL
PSYCHIATRY
1987:22:1184-1190
Myoclonic
Seizures with Lithium
Steven C. Julius and Richard
Myoclonus
has been infrequently
associated
electroencephalographic
P. Brenner
observed (EEG)
in patients receiving changes
lithium therapy,
and
have not been well described.
We
report two women, ages 3.5 and 48, who, after the initiation of lithium carbonate therapy, had several generalized
tonic-clonic
seizures followed
by myoclonic
seizures.
In both,
myoclonus was associated with repetitive sharp waves on the EEG. Although the epileptogenicity of lithium remains controversial,
the occurrence
ciated with lithium treatment suggests a proconvulsant
of myoclonic
seizures asso-
efSect of lithium in susceptible
individuals.
Introduction Generalized tonic-clonic seizures have been reported in patients treated with lithium carbonate, both with toxic (Schou et al. 1968; Wharton 1969; Spring 1979; Ghadirian and Lehmann 1980) as well as therapeutic serum levels (Wharton 1969; Baldessarini and Stephens 1970; Demers et al. 1970; Massey and Folger 1984). Electroencephalographic (EEG) changes, including epileptiform abnormalities, have also been noted (Brumback et al. 1975; Strayhom and Nash 1977; Spatz et al. 1978; Spring 1979; Rosen and Stevens 1983; Massey and Folger 1984). Myoclonus, however, has infrequently been observed with lithium therapy (Spatz et al. 1978; Warick 1979; Bauer 1982; Rosen and Stevens 1983), and associated EEG changes have not been well described. We report two patients who developed myoclonus with concomitant EEG discharges after receiving lithium.
Case
1 A 35year-old mildly mentally retarded woman with no prior history of seizures was admitted to Western Psychiatric Institute and Clinic for evaluation of temper outbursts and behavioral problems. She had a history of aggressive outbursts and paranoid delusions for which she had been treated with thioridazine and trazodone hydrochloride. During the preceding 4 weeks, the frequency and severity of these outbursts had increased. On examination, she was alert and oriented. Except for mild cognitive impairment, neurological examination was otherwise unrevealing. A complete blood count (CBC), electrolytes, creatinine, and thyroid function tests were normal. A waking EEG showed
From the Departments Pittsburgh, PA.
of Neurology
(S.C.J.,R.P.B.)
and Psychiatry
Address reprint requests to Dr. Richard 15213.
P. Brenner.
Presented in part at the annual meeting
of the American
Received
@> 1987 Society
November
of Biological
15, 1986; revised January 26.
Psychiatry
(R.P.B.),
EEG Laboratory-3rd EEG
Society,
University
Floor. Orlando,
WPIC,
of Pittsburgh 381
FL, October
I O’Hara
School of Medictne. Street. Pittsburgh,
PA
1985.
1987.
OCKI6-3223/87!$03
SO
Myoclonic Seizures with Lithium
BIOL PSYCHIATRY 1987:22:1184-1190
1185
moderate diffuse abnormalities (increased theta and delta activity), which were most marked posteriorly. A computerized tomographic (CT) scan, with and without contrast, was normal. After 3 weeks of hospitalization on no medication and minimal improvement in her behavior, lithium carbonate (1200 mg/day) was begun. Five days later, she became tremulous, with periods of hyperactivity. Her serum lithium level was elevated at 1.57 meq/liter (therapeutic 0.5-1.5 meq/liter), and the lithium dose was decreased to 900 mgi day. Two days later, the serum lithium level was 1.37 meq/liter. Four days after reducing the lithium dosage, her level had decreased to 0.94 meq/liter. However, later that day, she had four generalized tonic-clonic seizures within a period of 2 hours, which were terminated with intravenous benzodiazepines. Postictally, she was somnolent and mildly dysarthric, without focal findings. Her serum lithium level was 0.77 meqiliter, and serum electrolytes, blood urea nitrogen (BUN), creatinine, calcium, magnesium, and liver function tests were unremarkable. Cerebrospinal fluid (CSF) examination was normal. Her lithium was discontinued and phenytoin was begun. Within several hours, she was alert and responding appropriately to questioning. An EEG 3 days later showed nearly continuous repetitive sharp waves, maximal at the midline vertex electrode (Cz). Intermittently throughout the tracing she had myoclonus of the right foot, which had not been previously noted. The movement occurred only with the midline discharges (Figure l), although the majority of the discharges were not associated with movements. On the following day, the myoclonus had ceased, and an EEG showed infrequent midline sharp waves. Midline epileptiform abnormalities were not present on subsequent EEGs (6 days and 3 weeks later), and she has remained seizure free for 18 months on no anticonvulsant medications.
Case 2 A 48-year-old woman was admitted to a state psychiatric hospital because of manic behavior of 3 weeks duration. She had a history of generalized seizures related to alcohol withdrawal 2 months prior to admission, as well as postpartum seizures 30 years earlier. On admission, lithium carbonate (1800 mg/day) was begun. However, after 3 days, she developed diarrhea and her lithium dose was decreased to 1200 mg/day. Four days later, she was lethargic, and her serum lithium level was elevated at 2.15 meq/liter. Her lithium was withheld, but the following day (8 days after admission) she became tremulous and had 3 generalized tonic-clonic seizures. She was transferred to the University of New Mexico Hospital for further evaluation and treatment. On examination, she was lethargic but arousable to verbal stimuli, afebrile and with normal vital signs. Repetitive myoclonic jerks of all extremities were present, occurring independently or synchronously. Deep-tendon reflexes were hyperactive and symmetrical, and plantar responses were extensor. General medical and neurological examinations were otherwise unremarkable. Laboratory studies revealed an admission serum lithium level of 0.95 meq/liter. A repeat level 10 hr later was 0.70 meq/liter. CBC, serum electrolytes, BUN, creatinine, calcium, and liver and thyroid function tests were normal. A serum thiamine level, also obtained on admission, was reported subsequently as normal. A CT scan without contrast was normal, and CSF analysis was unremarkable. She was given thiamine and started on phenytoin, 300 mg/day, after receiving a loading
1186
BIOL PSYCHIATRY 1987:22:1184-l 190
S.C. Julius and R,P. Brenner
Figure I. EEG in Case 1 shows repetitive sharp waves maximal at the midline vertex (CL) associated with myoclonic movements of the right foot, which are monitored in the bottom channel.
dose of 1000 mg. An EEG was performed 2 days after admission at which time her serum lithium level was 0.15 meq/liter. Clinically, she was confused, but followed simple commands. Throughout the tracing, she had continuous repetitive myoclonic jerks of the feet and less often of the legs, which were associated with bisynchronous sharply contoured waves in the frontal-central regions (Figure 2A). These discharges were usually maximal at the midline efectrodes (Fz,Cz). Over the next few days, her confusion resolved, and the frequency and intensity of the myoclonic jerks lessened. An EEG 9 days after admission showed intermittent repetitive sharp waves, maximal at the midline vertex (Cz), often associated with myoclonic jerks of the legs (Figure 2B). The myoclonic jerks ceased, and she was returned to the state hospital for further treatment. She remained hospitalized for an additional 6 weeks, during which time she was again treated with lithium, at a lower dose of 900 mglday. No further seizure activity or myoclonus was observed during that period. She has been lost to follow-up.
Myoclonic Seizures with Lithium
P3-PZ
BIOL PSYCHIATRY 1987;22:11841190
1187
mn
t_ FOOT _p~,~,---‘c’
,,,.. ’
,.i ^ ,^1 - ‘, / I” ,’
,* “44’_,-J~ ,] ,g
7~p;,-i-~ 1Eeij50 vv
Figure 2. (A) Initial EEG of Case 2. Myoclonic movements of the left foot (channel 17) associated with repetitive frontal-central sharp waves (seen best in channels 13 and 16). (B) Repeat EEG 7 days later shows repetitive sham waves, maximal at Cz. Myoclonic jerks of the right leg are monitored in channel 16.
Discussion Our cases demonstrate uncommon clinical and electroencephalographic abnormalities associated with lithium carbonate therapy. Myoclonus has infrequently been described with lithium toxicity (Spatz et al. 1978; Warick 1979; Bauer 1982; Rosen and Stevens 1983). Spatz et al. (1978) observed myoclonus in a 61-year-old women with toxic serum levels. Warick (1979) reported a 36-year-old man with lithium poisoning who suffered two tonic-clonic seizures and subsequent generalized myoclonic jerks. Rosen and Stevens (1983) described “action myoclonus” in a 47-year-old woman following a lithium ov-
1188
BIOL PSYCHIATRY 1987~22~1184-1190
S.C. Julius and R.P. Brenner
F3-FZ mFZ-F4 %
erdose. Stimulus-sensitive myoclonic jerks have also been reported (Bauer 1982). In none of these cases was the myoclonus clearly epileptic. Myoclonus is a nonspecific term describing quick muscle jerks arising from dysfunction of the central nervous system (Hallett 1985). Such movements can occur in normal subjects (physiological myoclonus) or may be present in a wide variety of CNS disturbances (Fahn et al. 1986). Myoclonus can be either epileptic or nonepileptic in origin. Epileptic myoclonus is a muscle jerk produced by an abnormal discharge from neurons of the motor system (Hallett 1985). Our patients exhibited my~lonic movements p~mariIy involving the lower extremities or feet foliowing lithium carbonate therapy and occurring after several generalized tonic-clonic seizures. in both, repetitive EEG discharges (sharp waves) were associated with the myoclonus, thus demonstrating the epileptic nature of these movements.
Myoclonic Seizures with Lithium
1189
BIOL PSYCHIATRY 1987;22:I184-1190
The epileptogenicity of lithium remains unce~ain. Lithium trea~ent has been reported to induce seizures in nonepileptics (Schou et al. 1968; Wharton 1969; Baldessarini and Stephens 1970; Demers et al. 1970; Spring 1979; Ghadirian and Lehmann 1980; Massey and Folger 1984), as well as increasing seizure frequency in patients with seizure disorders (Jus et al. 1973; Moore 1981). Others (Gershon 1968; Erwin et al. 1973), however, have reported the converse, finding a decrease in seizure frequency in epileptics receiving lithium. Furthermore, although lithium has been shown in rats to significantly decrease the effectiveness of several anticonvulsants (Kadzielawa 1979), recent work with hippocampal kindled rats suggest that with acute administration, lithium is neither a potent proconvulsant nor an anticonvulsant (Clifford et al. 1985). Both of our cases had complicating features that make extrapolation of their clinical course to the general population problematic. In Case I, the patient was miidly mentally retarded and had a moderately abnormal baseline EEG. The second patient had a history of alcohol withdrawal seizures, as well as postpartum seizures. Thus, the role of lithium in inducing myoclonic seizures cannot be proven conclusively. Nevertheless, the occurrence of epileptic myoclonus in both patients following lithium therapy, with subsequent resolution off lithium, suggests some contributing effect of the drug toward the activation of seizures in susceptible individuals.
References Baldessarini RJ, Stephens JH f 1970): Lithium carbonate for affective disorders. Arch Gen Psychiutr?, 22:72-77. Bauer G (1982): EEG, drug effects, and central nervous system poisoning. In Neidermeyer E, Lopes de Silva F (eds), Elecrroencephalography: Basic Principles, Clinical Applications and Related Fields. Baltimore: Urban & Schwarzenberg, pp 479-489. Brumback RA, Weinberg WA, Herjanic BL (1975): Epileptiform logram induced by lithium carbonate. Pediatrics 56:831-834.
activity in the electroencepha-
Clifford DB, Podolsky A, Zorumski CF (1985): Acute effects of tithium on hipp~ampaf seizures. EpiIepsia 26:689-692.
kindled
Demers R, Lukesh R, Prichard J (1970): Convulsion during lithium therapy (letter). Lancer ii:3 15-3 16. Erwin CW, Gerber CJ, Morrison SD, James JF, Goldsboro convulsive disorders. Arch Gen Psychiatry 2tk646-648.
NC (1973): Lithium carbonate
and
Fahn S, Marsden CD, Van Woert MH (1986): Definition and classification of myocfonus. In Fahn S, Marsden C, and Van Woert M (eds), Advances in Neurology, Vat. 43: My~c~o~~s. New York: Raven Press, pp 1-S. Gershon S (1968): Use of lithium salts in psychiatric
disorders.
Dis Nerv Syst 29:5 l-55.
Ghadirian AM, Lehmann HE (1980): Neurological side effects of lithium: Organic brain syndrome, seizures, extrapyramidal side effects, and EEG changes. Compr Psychiatp 21:327-335. Hallett M (1985): Myoclonus:
Relation to epilepsy.
Epilepsia 26 (suppl 1):S67-77.
Jus A. Villeneuve A, Gautier J, Pires A, Cote JM, Jus K, Villeneuve R, Perron D (1973): Influence of lithium carbonate on patients with temporal epilepsy. Can Psych&r Assoc .I l&77-78. Kadzielawa K (1979): Inhibition of the action of anticonvulsants Biochem Behav 10:917-921.
by lithium treatment.
Massey EW, Folger WN (1984): Seizures activated by therapeutic Sou?h Med f 77: 1173-I 175.
Pharmacol
levels of lithium carbonate.
Moore DP (1981): A case of petit ma1 epilepsy aggravated by lithium. Arn~P~chjff~~ 138:690~91, Rosen RB, Stevens R (1983): Action myoclonus
in Iithium toxicity. Ann Neurol i3:22 l-222.
1190
S.C. Julius and R.P. Brenner
BIOL PSYCHIATRY 1987;22:1184-1190
Schou M, Amdisen A, Trap-Jensen
J (1968): Lithium poisoning.
Am J Psychiatry
Spatz R, Kugler J, Greil W, Lorenzi E (1978): Das Elektroenzephalogramm Intoxikation. Nervenarzt 49539-542. Spring GK (1979): EEG observations 136:1099-1100. Strayhom
in confirming
JM, Nash JL (1977): Severe neurotoxicity
neurotoxicity
bei der LithiumAm J Psychiurry
(letter).
despite “therapeutic”
125:520-527.
serum lithium levels.
Dis Nerv Syst 38: 107-I 11.
Warick LH (1979): Lithium poisoning: sequelae. West J Med 130:259-263.
Report of a case with neurologic,
cardiac and hepatic
Wharton RN (1969): Grand ma1 seizures with lithium treatment. Am J Psychiutv
125: 152.