PCN reports : psychiatry and clinical neurosciences · 2026
A case of acute lithium encephalopathy associated with elevated myelin basic protein levels in cerebrospinal fluid.
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Yokoyama Teruo, Hashimoto Takuya, Moriyama Yasushi, Yoshino Aihide
Аннотация
BACKGROUND: Acute lithium intoxication can cause severe central nervous system (CNS) manifestations, sometimes leading to long-term sequelae known as the syndrome of irreversible lithium-effectuated neurotoxicity (SILENT). However, its underlying pathophysiology remains unclear. We report a case of acute lithium encephalopathy presenting with elevated myelin basic protein (MBP) levels in the cerebrospinal fluid (CSF), offering insights into its pathogenesis.
CASE PRESENTATION: A 50-year-old man with schizophrenia developed coma following acute lithium intoxication. Two days prior to symptom onset, his serum lithium concentration had reached a toxic level of 3.95 mEq/L, prompting immediate drug discontinuation. Electroencephalography (EEG) demonstrated generalized rhythmic delta activity (GRDA) with triphasic morphology, characteristic of lithium encephalopathy, but not fulfilling the criteria for non-convulsive status epilepticus. A lumbar puncture on Day 6 revealed an elevated CSF MBP level of 141 pg/mL (normal, <102 pg/mL) without pleocytosis or an elevated IgG index. Although his serum lithium concentration dropped below 0.1 mEq/L by Day 8, his altered mental status was prolonged. His consciousness gradually improved from Day 10, but neurological deficits including dysarthria, gait instability, and intention tremor persisted until Day 40 before fully resolving.
CONCLUSION: The elevated CSF MBP level suggests that toxic lithium exposure may induce CNS demyelination. While the clinical symptoms were reversible in this patient, such a mechanism may underpin the prolonged or permanent neurological deficits seen in SILENT.
CASE PRESENTATION: A 50-year-old man with schizophrenia developed coma following acute lithium intoxication. Two days prior to symptom onset, his serum lithium concentration had reached a toxic level of 3.95 mEq/L, prompting immediate drug discontinuation. Electroencephalography (EEG) demonstrated generalized rhythmic delta activity (GRDA) with triphasic morphology, characteristic of lithium encephalopathy, but not fulfilling the criteria for non-convulsive status epilepticus. A lumbar puncture on Day 6 revealed an elevated CSF MBP level of 141 pg/mL (normal, <102 pg/mL) without pleocytosis or an elevated IgG index. Although his serum lithium concentration dropped below 0.1 mEq/L by Day 8, his altered mental status was prolonged. His consciousness gradually improved from Day 10, but neurological deficits including dysarthria, gait instability, and intention tremor persisted until Day 40 before fully resolving.
CONCLUSION: The elevated CSF MBP level suggests that toxic lithium exposure may induce CNS demyelination. While the clinical symptoms were reversible in this patient, such a mechanism may underpin the prolonged or permanent neurological deficits seen in SILENT.