Lithium-Induced Hypercalcemia Presenting as Catatonia in a Patient With Schizoaffective Disorder.

Catatonia, a relatively rare and less explored consequence of lithium-induced hypercalcemia, represents a notable yet understudied side effect. Lithium is utilized in the management of acute mania and as a maintenance therapy for bipolar disorder. However, the specific catatonic presentation resulting from hypercalcemia remains poorly understood. Here, we present a case study involving a 55-year-old male with a history of schizoaffective disorder, bipolar type, who had been receiving lithium therapy. The patient presented with catatonia and altered mental status. Manifesting as mutism, rigidity, immobility, and staring, these symptoms were subsequently attributed to hyperparathyroidism-induced hypercalcemia. Markedly elevated levels of both calcium and parathyroid hormone (PTH) were detected in the patient's laboratory results. The patient's lithium therapy was promptly discontinued. Serum calcium and PTH levels began to decrease gradually and returned to normal limits over 29 days. The patient returned to his baseline level of functionality. There was a notable improvement in his mental status and his ability to communicate using simple sentences. This case underscores the significance of recognizing uncommon clinical presentations of hypercalcemia in patients undergoing chronic lithium therapy. Given the broad range of neuropsychiatric manifestations associated with hypercalcemia, it is crucial to enhance our understanding of this phenomenon and develop the capacity to differentiate it from primary psychiatric disturbances.

On Neuropsychiatric Manifestations of Basal Ganglia Injury: A Report of Three Cases and Literature Review.

The basal ganglia have been considered to primarily play a role in motor processing. A growing body of theoretical and clinical evidence shows that in addition to the motor functions the basal ganglia play a key role in perceptual and visual disturbances. This role may be evident in patients with basal ganglia pathology and subsequent manifestation of symptoms that include cognitive, perceptual, and affective disturbances. We present three cases with basal ganglia pathology that demonstrate affective and psychotic symptoms. Two of the cases presented with late onset psychotic disturbances suggesting likely neurological etiologies. The third case presented with treatment refractory psychosis and symptoms that are rare for a diagnosis of schizophrenia. The role of incidental bilateral basal ganglia calcifications in all the cases is discussed. A review of current literature highlighting various neuropsychiatric manifestations of basal ganglia pathologies in various patients with psychiatric symptoms is presented.

The Pathophysiology and Management of Coprophagia: A Report of Two Cases and Literature Review.

Coprophagia is a rare and distressing disorder characterized by symptoms of compulsive consumption of feces. Several attempts have been made in literature to explore the pathophysiology, management, and outcomes of this disorder. However, critical questions remain, related to characterizing effective management, features of associated comorbidities, time to recovery of symptoms, sustainability of recovery, and the determinants of outcomes. Unfortunately, there is a dearth of available literature addressing these questions. We present two cases of patients with coprophagia in seeking to address these questions. Common symptoms of thought content disorder related to coprophagic behavior are noted in both cases. A shorter time to resolution of coprophagia is noted in one of the patients compared to previously reported studies. Recent and pertinent literature was reviewed and the implications for diagnosis and management of coprophagia are discussed.