Despite one-quarter of patients with primary hyperparathyroidism (PHPT) experiencing psychiatric symptoms, there remains a dearth of literature regarding the diagnosis and further management of psychiatric sequelae in PHPT. We aim to review the literature pertaining to the epidemiology, disease presentation, pathophysiology, diagnostics, and therapeutics regarding psychiatric sequelae of PHPT with an emphasis on clinical pearls for practicing psychiatrists. A literature search was conducted using the US National Library of Medicine's PubMed resource using the following keywords in various combinations: primary hyperparathyroidism, neuropsychiatric, calcium, psychosis, mania, depression, catatonia, delirium, parathyroidectomy, and psychotropic medication. We discuss in depth all aspects of the diagnosis and management of psychiatric sequela in PHPT. We have also identified epidemiological trends, discussed the most common clinical presentations, and postulated possible mechanisms for psychiatric symptoms in PHPT. Psychiatrists should maintain diagnostic suspicion for PHPT in older adult female patients presenting with new-onset psychiatric illness. Several mechanisms involving the following may explain the variety of psychiatric symptoms in PHPT: tyrosine hydroxylase, parathyroid hormone, interleukin-6, monoamine oxidase, calcium, and the sodium-potassium adenosine triphosphatase transporter. We recommend psychiatrists take a symptom-oriented approach to management. Treating a patient's psychosis, mania, depression, catatonia, delirium, or eating disorder pathology via conventional therapeutics seems like a rational approach despite the underlying medical etiology. Only parathyroidectomy has been proven to be definitive in the complete amelioration of psychiatric symptoms.

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In this report, we describe a case of atypical neuroleptic malignant syndrome (NMS) presenting with an isolated lesion in the splenium of the corpus callosum (ILSCC). There is a paucity of information regarding this topic within the literature and only 7 previous case reports have been published at the time of writing. To our knowledge, this case report is also the first to describe an atypical NMS variant in the context of an ILSCC. In this report, we describe the important considerations in formulating differential diagnosis for ILSCC and are the first report to propose a possible pathophysiological mechanism relating ILSCC with NMS.

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