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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.

Attempted and completed self-enucleation, or removal of one's own eyes, is a rare but devastating form of self-mutilation behavior. It is often associated with psychiatric disorders, particularly schizophrenia, substance induced psychosis, and bipolar disorder. We report a case of a patient with a history of bipolar disorder who gouged his eyes bilaterally as an attempt to self-enucleate himself. On presentation, the patient was manic with both psychotic features of hyperreligous delusions and command auditory hallucinations of God telling him to take his eyes out. On presentation, the patient had no light perception vision in both eyes and his exam displayed severe proptosis, extensive conjunctival lacerations, and visibly avulsed extraocular muscles on the right side. An emergency computed tomography scan of the orbits revealed small and irregular globes, air within the orbits, and intraocular hemorrhage. He was taken to the operating room for surgical repair of his injuries. Attempted and completed self-enucleation is most commonly associated with schizophrenia and substance induced psychosis, but can also present in patients with bipolar disorder. Other less commonly associated disorders include obsessive-compulsive disorder, depression, mental retardation, neurosyphilis, Lesch-Nyhan syndrome, and structural brain lesions.

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.

Violence is elevated in older adolescents and adults with schizophrenia; however, little is known about younger children. This report focuses on rates of violence in younger children with schizophrenic-spectrum illnesses. A retrospective review of structured diagnostic interviews from a case series of 81 children, ages 4-15 years of age, with childhood onset of schizophrenic-spectrum illness is reported. Seventy-two percent of children had a history of violent behavior, including 25 children (31%) with a history of severe violence. Of those with a history of violence, 60% had a least one episode of violence that did not appear to be in response to an external stimulus (internally driven violence). There was no significant impact of age or gender. For many children, these internally driven violent episodes were rare and unpredictable, but severe. Similar to what is found in adolescents and adults, violence is common in children with schizophrenic-spectrum illnesses. General violence prevention strategies combined with early identification and treatment of childhood psychotic illnesses may decrease the morbidity associated with childhood psychotic violence.

22q11.2 deletion syndrome (22q11DS) is a risk factor for psychiatric illnesses, including schizophrenia and anxiety. Small studies have shown that several neuroleptic medications are effective in treating psychosis in this population, but are also associated with an increased risk of adverse effects - particularly, seizures. In this case, we discuss a 34-year-old patient presenting with late onset schizophrenia, which ultimately led to her diagnosis of 22q11DS. Subsequent management of the patient's psychosis with asenapine was complicated by concurrent anxiety and panic disorder; thus, we examine the role of anxiolytic therapy in conjunction with antipsychotics in this patient population.

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.

Noninvasive brain stimulation (NIBS) such a transcranial magnetic stimulation, intermittent theta burst stimulation, transcranial direct current stimulation and electroconvulsive therapy have emerged as an efficacious and well-tolerated therapy for treatment-resistant psychiatric disorders. While novel NIBS techniques are an exciting addition to the current repertoire of neuropsychiatric therapies, their success is somewhat limited by the wide range of treatment responses seen among treated patients.

In this study, the authors will review the studies on relevant genetic polymorphisms and discuss the role of RNA genotyping in personalizing NIBS.

Genome studies have revealed several genetic polymorphisms that may contribute for the heterogeneity of treatment response to NIBS where the presence of certain single nucleotide polymorphisms (SNPs) are associated with responders versus nonresponders.

Historically, mental illnesses have been arguably some of the most challenging disorders to study and to treat because of the degree of biological variability across affected individuals, the role of genetic and epigenetic modifications, the diversity of clinical symptomatology and presentations and the interplay with environmental factors. In lieu of these challenges, there has been a push for personalized medicine in psychiatry that aims to optimize treatment response based on one’s unique characteristics.

The purpose of this paper is to illustrate delirium as a possible consequence of the application of symptom-triggered therapy for alcohol withdrawal and to explore alternative treatment modalities. In the management of alcohol withdrawal syndrome, symptom-triggered therapy directs nursing staff to regularly assess patients using standardized instruments, such as the Clinical Institute for Withdrawal Assessment of Alcohol, Revised (CIWA-Ar), and administer benzodiazepines at symptom severity thresholds. Symptom-triggered therapy has been shown to lower total benzodiazepine dosage and treatment duration relative to fixed dosage tapers (Daeppen et al., 2002). However, CIWA-Ar has important limitations. Because of its reliance on patient reporting, it is inappropriate for nonverbal patients, non-English speakers (in the absence of readily available translators) and patients in confusional states including delirium and psychosis. Importantly, it also relies on the appropriate selection of patients and considering alternate etiologies for signs and symptoms also associated with alcohol withdrawal.

The authors report a case of a 47-year-old male admitted for cardiac arrest because of benzodiazepine and alcohol overdose who developed worsening delirium on CIWA-Ar protocol.

While symptom-triggered therapy through instruments such as the CIWA-Ar protocol has shown to lower total benzodiazepine dosage and treatment duration in patients in alcohol withdrawal, over-reliance on such tools may also lead providers to overlook other causes of delirium.

This case illustrates the necessity for providers to consider using other available assessment and treatment options including objective alcohol withdrawal scales, fixed benzodiazepine dosage tapers and even antiepileptic medications in select patients.

Clozapine is often considered the gold standard for the treatment of schizophrenia. Clinical guidelines suggest a gradual titration over 2 weeks to reduce the risks of adverse events such as seizures, hypotension, agranulocytosis, and myocarditis. The slow titration often delays time to therapeutic response. This raises the question of whether, in some patients, it may be safe to use a more rapid clozapine titration. The following case illustrates the potential risks associated with the use of multiple antipsychotics and rapid cloza-pine titration. We present the case of a young man with schizophrenia who developed life threatening neuroleptic malignant syndrome (NMS) during rapid clozapine titration and treatment with multiple antipsychotics. We were unable to find another case in the literature of NMS associated with rapid clozapine titration. This case is meant to urge clinicians to carefully evaluate the risks and benefits of rapid clozapine titration, and to encourage researchers to further evaluate the safety of rapid clozapine titration. Rapid clozapine titration has implications for decreasing health care costs associated with prolonged hospitalizations, and decreasing the emotional suffering associated with uncontrolled symptoms of psychosis. Clozapine is considered the most effective antipsychotic available thus efforts should focus on developing strategies that would allow for safest and most efficient use of clozapine to encourage its utilization for treatment resistance schizophrenia.