Treatment of Kleine-Levin Syndrome With Intranasal Photobiomodulation and Methylene Blue.

Kleine-Levin syndrome (KLS) is a rare neuropsychiatric disorder, characterized by recurrent episodes of idiopathic hypersomnia, and cognitive and behavioral abnormalities, such as memory loss and child-like language. There is no definitive etiology for KLS; however, there are hypotheses of genetic predisposition, autoimmune mechanisms, and abnormal thalamic and hypothalamic functioning. Similarly, there is no definitive treatment for KLS as one method may be beneficial for one patient and not for another. We present a case of KLS in a patient who has no clinical improvement in symptoms with a variety of treatments. The parents of the patient agreed to attempt a trial of intranasal photobiomodulation (i-PBM) with red light, in combination with methylene blue (MB). The patient showed remission of the KLS episode following treatment with no further KLS episodes reported after treatment.

The power of meaning: the quest for an existential roadmap.

Where can we turn to find the story of our lives-an existential roadmap that explains where we have come from, why we are here, and where we are headed? Must each of us discover meaning within the context of our individual lives, or are there universal sources of meaning that we can all access? Is there any relationship between living a meaningful life and the quality of our health and well-being? And how can we find meaning in the face of adversity and suffering? Neurologist Jay Lombard, philosophers Massimo Pigliucci and Michael Ruse, and author Emily Esfahani Smith shed light on these perennial questions in conversation with Steve Paulson, executive producer and host of To the Best of Our Knowledge.

Resiliency: Natural Solutions to Stress and Anxiety.

No Abstract Available.

A Naturalistic Study of the Effectiveness of Pharmacogenetic Testing to Guide Treatment in Psychiatric Patients With Mood and Anxiety Disorders.

OBJECTIVE: To examine the effectiveness of genetic testing in a real-world setting and to assess its impact on clinician treatment decisions. METHOD: This was a naturalistic, unblinded, prospective analysis of psychiatric patients and clinicians who utilized a commercially available genetic test (between April and October of 2013), which incorporates 10 genes related to pharmacokinetics and pharmacodynamics of psychiatric medications. Each patient's genetic results were provided to participating clinicians, who completed a baseline survey including patient medications, history, and severity of illness. Clinicians were prompted to complete surveys within 1 week of receiving the genetic results and again 3 months later. Patients likewise completed assessments of depression, anxiety, medication side effects, and quality of life at baseline, 1 month, and 3 months. RESULTS: Data from 685 patients were collected. Approximately 70% and 29% of patients had primary diagnoses of either a mood or anxiety disorder, respectively. Clinician-reported data, as measured by the Clinical Global Impressions-Improvement scale, indicated that 87% of patients showed clinically measurable improvement (rated as very much improved, much improved, or minimally improved), with 62% demonstrating clinically significant improvement. When analysis was restricted to the 69% of individuals with ≥ 2 prior treatment failures, 91% showed clinically measurable improvement. Patients also reported significant decreases in depression (P < .001), anxiety (P < .001), and medication side effects (P < .001) and increases in quality of life (P < .001). CONCLUSIONS: These results suggest that a substantial proportion of individuals receiving pharmacogenetic testing showed clinically significant improvements on multiple measures of symptoms, adverse effects, and quality of life over 3 months. In the absence of a treatment-as-usual comparator, the proportion of improvement attributable to the test cannot be estimated. TRIAL REGISTRATION: ClinicalTrials.gov identifier: NCT01507155.

Pharmacogenetic-guided psychiatric intervention associated with increased adherence and cost savings.

OBJECTIVES: Pharmacogenetic testing as a means of guiding treatment decisions is beginning to see wider clinical use in psychiatry. The utility of this genetic information as it pertains to clinical decision making, treatment effectiveness, cost savings, and patient perception has not been fully characterized. STUDY DESIGN: In this retrospective study, we examined health claims data in order to assess medication adherence rates and healthcare costs for psychiatric patients. METHODS: Individuals for whom pharmacogenetic testing was ordered (cases) were contrasted with those who did not undergo such testing (controls). Cases and controls were propensity score matched in order to minimize risk of confounding in this nonrandomized study. An initial analysis of 111 cases and 222 controls examined both adherence and healthcare costs. A replication study of 116 cases and 232 controls examined adherence alone, as cost data was not available for this latter cohort. RESULTS: Overall, individuals with assay-guided treatment were significantly more medication adherent (P = 1.56 3 10­3; Cohen's d = 0.511) than patients with standard treatment and demonstrated a relative cost savings of 9.5% in outpatient costs over a 4-month follow-up period, or $562 in total savings. CONCLUSIONS: The data show the utility of pharmacogenetic testing in everyday psychiatric clinical practice, as it can lead to improved patient adherence and decreased healthcare costs.

The potential utility of pharmacogenetic testing in psychiatry.

Over the last decade, pharmacogenetics has become increasingly significant to clinical practice. Psychiatric patients, in particular, may benefit from pharmacogenetic testing as many of the psychotropic medications prescribed in practice lead to varied response rates and a wide range of side effects. The use of pharmacogenetic testing can help tailor psychotropic treatment and inform personalized treatment plans with the highest likelihood of success. Recently, many studies have been published demonstrating improved patient outcomes and decreased healthcare costs for psychiatric patients who utilize genetic testing. This review will describe evidence supporting the clinical utility of genetic testing in psychiatry, present several case studies to demonstrate use in everyday practice, and explore current patient and clinician opinions of genetic testing.

What is the role of pharmacogenetics in clinical psychiatry?

Psychiatric disorders are a leading cause of disability worldwide and despite significant pharmacologic advances, often remain difficult to diagnose correctly and treat fully. Factors which contribute to these difficulties include imprecise understanding of etiology, syndromal nature of many disorders and overlap in diagnostic criteria between conditions, medical and psychiatric comorbidity and high rates of noncompliance to treatment either due to lack of efficacy or adverse effects. In addition to genetics and known biological factors, the severity and presentation of many psychiatric conditions may be influenced by psychosocial factors, which in turn can affect treatment outcomes. Currently, the selection of medications for a given patient in psychiatry is primarily based on a trial and error process; thus, there is an urgent need to identify biomarkers that can improve diagnostic homogeneity and provide useful prognostic information. Pharmacogenetics has the potential, in combination with other approaches, to enhance both care at an individual level as well as in drug development by improving efficacy and minimizing drug-induced side effects.

Dyke-Davidoff-Masson syndrome in postcerebral malaria.

Dyke-Davidoff-Masson syndrome is a disorder involving hemiatrophy or hypoplasia of 1 cerebral hemisphere secondary to an insult in the developing brain. Often this will manifest with seizures, hemiparesis, mental retardation, and facial changes. Associated with this pathology are the radiologically evident changes, such as thickening of the calvarium, hyperpneumatization of the sinuses, and dilation of the ipsilateral lateral ventricle among others. The following is a case presentation of an 18-year-old female emigrating from Ghana who presented to the emergency department with complaints of seizures diagnosed as being caused by cerebral malaria at 13 years of age. We hypothesize that the cerebral malaria and related vascular occlusion are the causes of her acquired cerebral changes. Included are computed tomography images.

Brain injury due to ventricular shunt placement delineated by diffusion tensor imaging (DTI) tractography.

OBJECTIVE: Infection and hemorrhage are well-known complications from insertion of intracranial shunts. However, permanent injury to the brain caused by catheterization of the cerebral ventricles has rarely been reported. METHODS: We report a patient who presented at age 14 years for evaluation of a severe behavioral disorder. The patient had sustained direct injury to the corticospinal tract and limbic system during revision of a ventriculoperitoneal shunt at the age of 9 years. RESULTS: Despite persistent evidence of severe disruption of the corticospinal tract on diffusion tensor imaging at age 14 years, the patient had regained complete motor function. CONCLUSION: Recovery of motor function after serious injury to motor cortex during childhood is a dramatic example of the plasticity of the child's brain to injury. In addition, we suggest that the behavioral disorder that emerged in this patient may be related to limbic system injury suffered during the shunt revision.

Pathophysiology of Alzheimer's disease.

Tremendous progress has been made in understanding the processes of the Alzheimer's disease (AD) cascade, laying the groundwork for improvements in diagnosis and treatment. Advancement has been made in understanding the genetic basis of AD, with identification of causative genes for early-onset familial AD, and the role of the polymorphism of the APOE gene in the late-onset form of the disease. Understanding cerebral degeneration and accumulation of beta-amyloid has generated hopes for discovery of disease-modifying treatments. Progress is needed in understanding the mechanisms that link beta-amyloid accumulation and neuronal death. The next 5 years will be crucial in this respect.