Davin K. Quinn

Neuropsychiatric Effects of Prescription Drug Abuse

Prescription drugs have become a major category of abused substances, and there is evidence that the prevalence of prescription drug abuse may soon overtake that of illicit drugs. Study of prescription drugs has been hampered by vague terminology, since prescription drugs are only separated from other drugs of abuse by social and legal constructs. Reviewed herein is published literature on the abuse of four major categories of abused prescription drugs: sedative-hypnotics, stimulants, anabolic steroids, and anticholinergics. The review emphasizes evidence regarding the effects of these drugs on neural systems. Other abused prescription drugs that fall outside of the major categories are also briefly addressed.

A Review of Longitudinal Electroconvulsive Therapy Neuroimaging Investigations

Electroconvulsive therapy (ECT) is the most effective treatment for a depressive episode but the mechanism of action and neural correlates of response are poorly understood. Different theories have suggested that anticonvulsant properties or neurotrophic effects are related to the unique mechanism of action of ECT. This review assessed longitudinal imaging investigations (both structural and functional) associated with ECT response published from 2002 to August 2013. We identified 26 investigations that used a variety of different imaging modalities and data analysis methods. Despite these methodological differences, we summarized the major findings of each investigation and identified common patterns that exist across multiple investigations. The ECT response is associated with decreased frontal perfusion, metabolism, and functional connectivity and increased volume and neuronal chemical metabolites. The general collective of longitudinal neuroimaging investigations support both the anticonvulsant and the neurotrophic effects of ECT. We propose a conceptual framework that integrates these seemingly contradictory hypotheses.

Linezolid and serotonin syndrome.

Have you ever wondered if problems might arise when a patient taking an antidepressant needs linezolid for treatment of methicillin-resistant Staphylococcus aureus (MRSA) or vancomycin-resistant Enterococcus (VRE) infection? Have you wondered what complications might follow such coadministration? Have you been apprehensive when deciding whether a washout interval is needed before or after use of linezolid and a serotonergic antidepressant? If so, then the following questions and answers should stimulate discussion and provide much needed information.

Post-MI Psychiatric Syndromes: Six Unanswered Questions

&NA; Depression, anxiety, and other psychological variables following acute myocardial infarction (MI) have been the subject of intense study over the last two decades. Through selective literature review and editorial commentary, we address six vital, unanswered questions concerning these psychological variables and their impact on coronary outcome. The picture that emerges is complex. Despite all that has been learned about the nature, consequences, and management of post‐MI depression and related disorders, there remain many open issues. First, the prevalence, phenomenology, medical impact, and method of diagnosis of post‐MI depression and other psychiatric syndromes remain unclear. In addition, at least four pathophysiologic mechanisms have been proposed to explain the link between depression and cardiac disease, but evidence of causation remains elusive. There have been increasingly well‐designed treatment studies of post‐MI depression, but the optimal agents and timing of treatment have yet to be defined. Finally, few recent studies of post‐MI anxiety have been conducted. To make further progress, large, multicenter trials that use optimized screening tools, obtain data at several time points, consider multiple psychosocial variables, and correct carefully for medical/cardiac severity are required.

The spectrum of mild traumatic brain injury: A review

Objective: This review provides an in-depth overview of diagnostic schema and risk factors influencing recovery during the acute, subacute (operationally defined as up to 3 months postinjury), and chronic injury phases across the full spectrum of individuals (e.g., athletes to neurosurgery patients) with mild traumatic brain injury (mTBI). Particular emphasis is placed on the complex differential diagnoses for patients with prolonged postconcussive symptoms. Methods: Select literature review and synthesis. Results: In spite of an increase in public awareness surrounding the acute and potential long-term effects of mTBI, the medical field remains fragmented both in terms of the diagnostic (different criteria proffered by multiple medical organizations) and prognostic factors that influence patient care. Conclusions: Given the lack of objective biomarkers and the spectrum of different disorders that likely encompass mTBI, clinicians are encouraged to adopt a probabilistic, rather than definitive, diagnostic and prognostic framework. The relevance of accurately diagnosing and managing the different manifestations of mTBI becomes clear when one considers the overall incidence of the disorder (42 million people each year worldwide), and the different treatment implications for patients with a true neurodegenerative disorder (e.g., chronic traumatic encephalopathy; rare) vs potentially treatable conditions (e.g., depression or posttraumatic headache; frequent).

Rationale and design of A Trial of Sertraline vs. Cognitive Behavioral Therapy for End-stage Renal Disease Patients with Depression (ASCEND)

Major Depressive Disorder (MDD) is highly prevalent in patients with End Stage Renal Disease (ESRD) treated with maintenance hemodialysis (HD). Despite the high prevalence and robust data demonstrating an independent association between depression and poor clinical and patient-reported outcomes, MDD is under-treated when identified in such patients. This may in part be due to the paucity of evidence confirming the safety and efficacy of treatments for depression in this population. It is also unclear whether HD patients are interested in receiving treatment for depression. ASCEND (Clinical Trials Identifier Number NCT02358343), A Trial of Sertraline vs. Cognitive Behavioral Therapy (CBT) for End-stage Renal Disease Patients with Depression, was designed as a multi-center, 12-week, open-label, randomized, controlled trial of prevalent HD patients with comorbid MDD or dysthymia. It will compare (1) a single Engagement Interview vs. a control visit for the probability of initiating treatment for comorbid depression in up to 400 patients; and (2) individual chair-side CBT vs. flexible-dose treatment with a selective serotonin reuptake inhibitor, sertraline, for improvement of depressive symptoms in 180 of the up to 400 patients. The evolution of depressive symptoms will also be examined in a prospective longitudinal cohort of 90 HD patients who choose not to be treated for depression. We discuss the rationale and design of ASCEND, the first large-scale randomized controlled trial evaluating efficacy of non-pharmacologic vs. pharmacologic treatment of depression in HD patients for patient-centered outcomes.

Metoclopramide and Homicidal Ideation: A Case Report and Literature Review

BACKGROUND Metoclopramide is an anti-emetic and gastrointestinal pro-motility agent associated with well-known neuropsychiatric adverse effects, such as dyskinesia, akathisia, and depression. It has never been reported to be associated with homicidal ideation. OBJECTIVE The authors review the literature on metoclopramide-induced adverse neuropsychiatric reactions and the mechanisms by which these may occur. METHODS The authors present a case report of a patient who developed anxiety, agitation, suicidal and homicidal ideation following brief exposure to metoclopramide. RESULTS The adverse effects of agitation and homicidal ideation were temporally related to the starting and stopping of metoclopramide. The patient subsequently developed agitation without homicidal ideation when given a serotonergic antidepressant a week later, suggesting that serotonin handling may have played a significant role in causing the patients symptoms. CONCLUSIONS Although metoclopramide is well-known for its side effects related to dopamine blockade, its action at 5-HT₃ and 5-HT₄ receptors may also be clinically significant in the genesis of neuropsychiatric side effects, especially related to mood and behavior.

Ertapenem-Induced Delirium: A Case Report and Literature Review

Antibiotics are associated with a broad spectrum of neurologic and psychiatric side effects, ranging from central nervous systemdysfunction to peripheral neuropathies and neuromuscular paralysis. More than 70% of intensive care unit patients receive at least one antibiotic during their hospitalization and antimicrobial agents are credited with causing more adverse events than any other single class of drugs. They may often go unrecognized as contributors to a patients presentation, particularly if the initial symptoms are solely psychiatric. Although certain antibiotics such as antimalarials are well known to cause psychiatric symptoms, the neuropsychiatric effects of other less commonly used agents may go unrecognized. Wepresent a case of apatient inwhomhallucinations, altered mental status, and myoclonus developed after being treated with ertapenem for cellulitis and myositis.

Catatonia After Cerebral Hypoxia: Do the Usual Treatments Apply?

BACKGROUND Neurologic deterioration occurring days to weeks after a cerebral hypoxic event accompanied by diffuse white matter demyelination is called delayed posthypoxic leukoencephalopathy (DPHL). Manifestations of DPHL are diverse and include dementia, gait disturbance, incontinence, pyramidal tract signs, parkinsonism, chorea, mood and thought disorders, akinetic mutism, and rarely catatonia. METHODS We report a case of malignant catatonia in a patient diagnosed with DPHL that was refractory to electroconvulsive therapy (ECT) and review the literature on catatonia in DPHL. RESULTS The patient was a 56-year-old woman with schizoaffective disorder who was admitted with catatonia 2 weeks after hospitalization for drug overdose and respiratory failure. Her catatonic symptoms did not respond to treatment of lorazepam, amantadine, methylphenidate, or 10 sessions of bilateral ECT at maximum energy. Repeat magnetic resonance imaging revealed extensive periventricular white matter lesions not present on admission scans, and she was diagnosed with DPHL. DISCUSSION No treatment for DPHL has been proven to be widely effective. Hyperbaric oxygen treatments may reduce the rate of development, and symptom improvement has been reported with stimulants and other psychotropic agents. Review of literature reveals rare success with GABAergic agents for catatonia after cerebral hypoxia and no cases successfully treated with ECT. There are 7 case reports of neurologic decompensation during ECT treatment after a cerebral hypoxic event. CONCLUSION Caution is advised when considering ECT for catatonia when delayed sequelae of cerebral hypoxia are on the differential diagnosis, as there is a dearth of evidence to support this treatment approach.

Cotard's Syndrome with Catatonia: A Case Presentation and Discussion

Cotard’s syndrome (named after its founder Dr. Jules Cotard, 1840–1889) or delire des negations is generally defined to be a nihilistic delusion that one is dead or paradoxically immortal, has lost his/her soul, is without functional body systems, is rotting internally, or is without limbs. Although rare, the syndrome is most often seen with psychiatric disorders, including depression with psychosis, schizophrenia, and bipolar disorder. It may also occur in various neurologic conditions, including neurosyphilis, multiple sclerosis, cerebrovascular disease, migraine, and traumatic brain injury. Catatonia is a syndrome that may accompany Cotard’s syndrome in these disorders but literature supporting this association is sparse. This case report expands on the existing knowledge base by presenting the case of a 68-year-old male who presented with Cotard’s syndrome and subsequently developed catatonia, both of which responded to benzodiazepine therapy.