Mania is a mood disorder characterized by elation, hyperactivity, and flight of ideas. Manic episodes may alternate with depression in patients with a bipo-lar (formerly manic–depressive) disorder. Mania is thought to be related to excessive norepinephrine activity in the brain. Lithium which interferes with Na+ ion transport with effects on many signaling path-ways in the brain affecting neurotransmitter release, and lamotrigine, which inhibits sodium channels and modulates release of excitatory amino acids, are the drugs of choice for treating acute manic episodes and preventing their recurrence, as well as suppressing episodes of depression. Concomitant administration of an antipsychotic (haloperidol) or a benzodiazepine (lorazepam) is usually necessary during acute mania. Alternative treatments include valproic acid, carbam-azepine, and aripiprazole as well as ECT.
The mechanism of action of lithium is poorly understood. It has a narrow therapeutic range, with a desirable blood concentration between 0.8 and 1.0 mEq/L. Side effects include reversible T-wave changes, mild leukocytosis, and, on rare occasions, hypothyroidism or a vasopressin-resistant diabetes insipidus-like syndrome. Toxic blood concentra-tions produce confusion, sedation, muscle weakness, tremor, and slurred speech. Still higher concentra-tions result in widening of the QRS complex, atrio-ventricular block, hypotension, and seizures.
Although lithium is reported to decrease mini-mum alveolar concentration and prolong the dura-tion of some NMBs, clinically these effects seem to be minor. Nonetheless, this is yet another reason why neuromuscular function should be monitored when NMBs are used. Blood levels should be checked perioperatively. Sodium depletion (secondary to loop or thiazide diuretics) decreases renal excre-tion of lithium and can lead to lithium toxicity. Fluid restriction and overdiuresis should be avoided. Lithium dilution cardiac output measurements are contraindicated in patients on lithium therapy.