ABSTRACT
Psychiatric manifestations of primary hyperparathyroidism are mediated by hypercalcemia. To date, most evidence indicates that hypercalcemia and increased cerebrospinal-fluid calcium levels produce depression symptoms. Presented here is a case report of a 52-year-old woman in a manic state. She had no psychiatric history but had substantially elevated parathyroid hormone levels and hypercalcemia. On the basis of emerging evidence that calcium channel-blockers effectively treat mania, the authors propose that elevated calcium levels may act through multiple mechanisms or on various regions of the brain to produce a spectrum of psychiatric symptoms that should now include mania as a possibility.
Subject(s)
Adenoma/diagnosis , Bipolar Disorder/complications , Hyperparathyroidism/complications , Parathyroid Neoplasms/diagnosis , Abdominal Pain/complications , Adenoma/complications , Anemia, Iron-Deficiency/complications , Anemia, Iron-Deficiency/therapy , Antipsychotic Agents/administration & dosage , Aripiprazole , Benzodiazepines/administration & dosage , Bipolar Disorder/diagnosis , Bipolar Disorder/psychology , Blood Transfusion , Calcium/blood , Diagnosis, Differential , Female , Hematocrit/methods , Hemoglobins , Humans , Hypercalcemia/complications , Hypercalcemia/psychology , Hyperparathyroidism/psychology , Middle Aged , Nausea/complications , Olanzapine , Parathyroid Hormone/analysis , Parathyroid Neoplasms/complications , Piperazines/administration & dosage , Psychomotor Agitation/complications , Psychomotor Agitation/psychology , Quinolones/administration & dosage , Stomach Ulcer/complications , Weight LossABSTRACT
Ten patients treated with electroconvulsive therapy (ECT) for depressive illness received anesthesia with either etomidate or ketamine. Three patients received both etomidate and ketamine anesthesia for ECT during separate episodes of depression. Patients anesthetized with ketamine for ECT had significantly less impairment of short-term memory function than did patients who received ECT with etomidate anesthesia. All patients who received both anesthetics for ECT during 2 different episodes had less memory loss during ECT with ketamine than with etomidate. These results show the importance of studying the effects of all anesthetic agents used during ECT on cognitive functions. The results imply that the effect of ECT on memory may be largely caused by effects mediated by glutamate at N-methyl-d-aspartate receptors and suggest that N-methyl-d-aspartate antagonists may offer protection from memory dysfunction during ECT.
