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Peduncluar hallucinosis is a rare neurological disorder characterized by visual hallucinations, often described to be vivid and dream-like. While the exact pathophysiology has yet to be elucidated, most cases to date have suggested an etiology stemming from lesions to the thalamus or midbrain. Here presented is a case of a 54-year-old female with peduncular hallucinosis secondary to a pontine cavernoma hemorrhage in the setting of essential hypertension. The patient's vivid visual and auditory hallucinations aligned temporally with the lesion's discovery and resolved after pharmaceutical treatment. This case represents a rare form of peduncular hallucinosis secondary to a pontine cavernoma hemorrhage leading to vasospasm in the arteries feeding the brainstem.

Haloperidol is a first-generation antipsychotic butyrophenone that is lipophilic, readily absorbed, and extensively metabolized in the liver. The occurrence of elevated liver enzymes with haloperidol is reported to be 2.4% with cases generally occurring in the setting of chronic use. In this case, we present a patient who developed elevated liver enzymes 1-2 days after starting haloperidol treatment on two separate occasions and in the context of negative hepatic viral and autoimmune serology. Liver enzymes consistently had alanine transaminase > aspartate transaminase and peaked at 288 U/L prior to discontinuation of the medication. The patient was taken off haloperidol after serology resulted and clozapine regimen started. He was able to tolerate clozapine well with recovery of his transaminitis and psychiatric stabilization.

Since the development of antipsychotic drugs in the 1950s, a variety of studies and case reports have been published that suggest an association between exposure to typical antipsychotics and venous thromboembolisms (VTE). Therefore, when starting treatment with antipsychotics, especially low-potency typical antipsychotics and clozapine, health-care providers must account for the patient’s existing VTE risk factors.

In this case report, the authors describe the development of a pulmonary embolism associated with use of chlorpromazine in the treatment of an acute manic episode in a 51-year-old female patient with bipolar disorder type 1.

The patient was brought to the emergency room by the police on a legal hold for bizarre behaviors at a bus stop, which included incessantly yelling at bystanders. The patient was found to have disorganized thoughts, poor sleep, rapid speech, labile mood, distractibility, auditory hallucinations and grandiose delusions. During the course of her stay, the patient received extensive IM chlorpromazine for extreme agitation, in addition to chlorpromazine 200 mg IM Q8H, which was later decreased to chlorpromazine 100 mg chlorpromazine IM/PO Q8H. On day 4 of the treatment, the patient experienced difficulty breathing, hypoxia and tachycardia and was found to have bilateral expiratory wheezes. CT angiography showed sub-segmental pulmonary embolus and the patient was transferred to MICU service. The patient was then intubated and started on heparin by the medical team. Over the course of the next day, her respiratory distress resolved and the patient was extubated.

It is possible that chlorpromazine may indeed increase VTEs, and there are various physiological postulations regarding the mechanism of action. However, multiple confounding variables existed in the authors’ report, including venous stasis and the use of restraints, tobacco and valproic acid. Each of these variables has been shown to increase VTE occurrence. Further controlled studies are necessary to identify the true relationship between antipsychotics and VTEs.