Nonconvulsive status epilepticus and Creutzfeldt-Jakob-like EEG changes in a case of lithium toxicity
1Department of Neurology, M.S. Ramaiah Medical College, New BEL Road, Mathikere, Bangalore -560054, India.
We report a case of a 63-year-old lady with bipolar affective disorder on lithium who was brought to our emergency center in a comatose state. Neurologically, the patient was comatose and had generalized hypotonia and hyporeflexia. Lithium toxicity was considered. Laboratory examinations revealed leukocytosis, normal blood sugar, blood level of lithium was 4.7 mEq/L and she had renal dysfunction. Cerebrospinal fluid examination and cranial computerized tomography were unremarkable. Blood lithium level was 4.7 mEq/L. Hemodialysis was initiated. However, in spite of dialysis and decreasing lithium levels, the patient remained unconscious. A possibility of nonconvulsive status epilepticus was considered; hence, EEG was advised. The EEG demonstrated bihemispheric slowing (4- to 5-Hz theta range) with bilateral periodic triphasic waves of 1- to 2-Hz frequency, similar to the EEG changes seen in Creutzfeldt-Jakob disease. She was started on lorazepam. Her sensorium improved gradually, which correlated with the decline in blood lithium levels. A normal background alpha rhythm on EEG was ensured prior to discharge. At discharge, clinically, she had recovered completely, with no apparent neurological deficit or cognitive impairment. This case highlights the importance of therapeutic drug-level monitoring of lithium, especially where toxicity is suspected, and the important role electroencephalography plays in diagnosing NCSE and its management.
We report a case of a 63-year-old lady with bipolar affective disorder on lithium who was brought to our emergency center in a comatose state. Neurologically, the patient was comatose and had generalized hypotonia and hyporeflexia. Lithium toxicity was considered. Laboratory examinations revealed leukocytosis, normal blood sugar, blood level of lithium was 4.7 mEq/L and she had renal dysfunction. Cerebrospinal fluid examination and cranial computerized tomography were unremarkable. Blood lithium level was 4.7 mEq/L. Hemodialysis was initiated. However, in spite of dialysis and decreasing lithium levels, the patient remained unconscious. A possibility of nonconvulsive status epilepticus was considered; hence, EEG was advised. The EEG demonstrated bihemispheric slowing (4- to 5-Hz theta range) with bilateral periodic triphasic waves of 1- to 2-Hz frequency, similar to the EEG changes seen in Creutzfeldt-Jakob disease. She was started on lorazepam. Her sensorium improved gradually, which correlated with the decline in blood lithium levels. A normal background alpha rhythm on EEG was ensured prior to discharge. At discharge, clinically, she had recovered completely, with no apparent neurological deficit or cognitive impairment. This case highlights the importance of therapeutic drug-level monitoring of lithium, especially where toxicity is suspected, and the important role electroencephalography plays in diagnosing NCSE and its management.
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