Adolescent mental health: Challenges with maternal noncompliance

The leading cause of suicide ideation, attempts, and completion in adolescents is persistent and unresolved parental conflict. National statistics show extremely high rates of childhood neglect and abuse are perpetrated most often by single mothers. Psychiatric disorders arising from maternal–child dysfunction are well-documented. However, resources to prevent offspring victimization are lacking. Here, we report maternal neglect of a 15-year-old male brought to the psychiatric emergency room for suicidal ideation. An inpatient treatment plan including pharmacotherapy, family therapy and psychological testing was initiated. The patient’s mother failed to attend clinic appointments or family therapy sessions. Clinician attempts to engage the mother in the treatment plan was met with verbal assaults, aggression, and threatening behavior. The patient decompensated in relation to the mother’s actions. Child Protective Services were contacted and a follow-up assessment with the patient and mother is pending. Psychiatric treatment of the mother may be a necessary intervention and prevention regimen for both the adolescent and the mother. Without consistent Child Protective Services oversight, medical and psychosocial follow-up, the prognosis and quality of life for this adolescent is considered very poor. Stringent mental health law and institutional policies are needed to adequately intercede and protect adolescents with mental illness

A case of mistaken identity: alcohol withdrawal, schizophrenia, or central pontine myelinolysis?

Demyelination is a hallmark of central pontine myelinolysis (CPM). Neuropsychiatric manifestations of this condition include weakness, quadriplegia, pseudobulbar palsy, mood changes, psychosis, and cognitive disturbances. These psychiatric symptoms are also associated with schizophrenia and alcohol withdrawal. Thus, it is clinically relevant to differentiate between CPM, schizophrenia, and alcohol withdrawal as the treatment and prognostic outcomes for each diagnosis are distinct. We present a series of events that led to a misdiagnosis of a patient admitted to the medical emergency center presenting with confusion, psychomotor agitation, and delirium who was first diagnosed with schizophrenia and alcohol withdrawal by emergency medical physicians and later discovered by the psychiatric consult team to have CPM. With a thorough psychiatric evaluation, a review of the laboratory results first showing mild hyponatremia (127 mmol/L), subsequent hypernatremia (154 mmol/L), and magnetic resonance brain imaging, psychiatrists concluded that CPM was the primary diagnosis underlying the observed neuropsychopathology. This patient has mild impairments in mood, cognition, and motor skills that remain 12 months after her emergency-center admission. This case report reminds emergency clinicians that abnormal sodium metabolism can have long-term and devastating psychopathological and neurological consequences. Differentiating between CPM, schizophrenia, and alcohol withdrawal using neuroimaging techniques and preventing the risks for CPM using slow sodium correction are paramount

PINK1 knockout rats show premotor cognitive deficits measured through a complex maze

Cognitive decline in Parkinson’s disease (PD) is a critical premotor sign that may occur in approximately 40% of PD patients up to 10 years prior to clinical recognition and diagnosis. Delineating the mechanisms and specific behavioral signs of cognitive decline associated with PD prior to motor impairment is a critical unmet need. Rodent PD models that have an impairment in a cognitive phenotype for a time period sufficiently long enough prior to motor decline can be useful to establish viable candidate mechanisms. Arguably, the methods used to evaluate cognitive decline in rodent models should emulate methods used in the assessment of humans to optimize translation. Premotor cognitive decline in human PD can potentially be examined in the genetically altered PINK1−/− rat model, which exhibits a protracted onset of motor decline in most studies. To increase translation to cognitive assessment in human PD, we used a modified non-water multiple T-maze, which assesses attention, cognitive flexibility, and working memory similarly to the Trail Making Test (TMT) in humans. Similar to the deficiencies revealed in TMT test outcomes in human PD, 4-month-old PINK1−/− rats made more errors and took longer to complete the maze, despite a hyperkinetic phenotype, compared to wild-type rats. Thus, we have identified a potential methodological tool with cross-species translation to evaluate executive functioning in an established PD rat model

The Role of Charity Care and Primary Care Physician Assignment on ED Use in Homeless Patients

AbstractObjectiveHomeless patients are a vulnerable population with a higher incidence of using the emergency department (ED) for noncrisis care. Multiple charity programs target their outreach toward improving the health of homeless patients, but few data are available on the effectiveness of reducing ED recidivism. The aim of this study is to determine whether inappropriate ED use for nonemergency care may be reduced by providing charity insurance and assigning homeless patients to a primary care physician (PCP) in an outpatient clinic setting.MethodsA retrospective medical records review of homeless patients presenting to the ED and receiving treatment between July 2013 and June 2014 was completed. Appropriate vs inappropriate use of the ED was determined using the New York University ED Algorithm. The association between patients with charity care coverage, PCP assignment status, and appropriate vs inappropriate ED use was analyzed and compared.ResultsFollowing New York University ED Algorithm standards, 76% of all ED visits were deemed inappropriate with approximately 77% of homeless patients receiving charity care and 74% of patients with no insurance seeking noncrisis health care in the ED (P=.112). About 50% of inappropriate ED visits and 43.84% of appropriate ED visits occurred in patients with a PCP assignment (P=.019).ConclusionsBoth charity care homeless patients and those without insurance coverage tend to use the ED for noncrisis care resulting in high rates of inappropriate ED use. Simply providing charity care and/or PCP assignment does not seem to sufficiently reduce inappropriate ED use in homeless patients

Aging-related limit of exercise efficacy on motor decline

<div><p>Identifying lifestyle strategies and allied neurobiological mechanisms that reduce aging-related motor impairment is imperative, given the accelerating number of retirees and increased life expectancy. A physically active lifestyle prior to old age can reduce risk of debilitating motor decline. However, if exercise is initiated after motor decline has begun in the lifespan, it is unknown if aging itself may impose a limit on exercise efficacy to decelerate further aging-related motor decline. In Brown-Norway/Fischer 344 F₁ hybrid (BNF) rats, locomotor activity begins to decrease in middle age (12–18 months). One mechanism of aging-related motor decline may be decreased expression of GDNF family receptor, GFRα-1, which is decreased in substantia nigra (SN) between 12 and 30 months old. Moderate exercise, beginning at 18 months old, increases nigral GFRα-1 and tyrosine hydroxylase (TH) expression within 2 months. In aged rats, replenishing aging-related loss of GFRα-1 in SN increases TH in SN alone and locomotor activity. A moderate exercise regimen was initiated in sedentary male BNF rats in a longitudinal study to evaluate if exercise could attenuate aging-related motor decline when initiated at two different ages in the latter half of the lifespan (18 or 24 months old). Motor decline was reversed in the 18-, but not 24-month-old, cohort. However, exercise efficacy in the 18-month-old group was reduced as the rats reached 27 months old. GFRα-1 expression was not increased in either cohort. These studies suggest exercise can decelerate motor decline when begun in the latter half of the lifespan, but its efficacy may be limited by age of initiation. Decreased plasticity of GFRα-1 expression following exercise may limit its efficacy to reverse motor decline.</p></div

Impact of 8 months of exercise on aging-related decline in locomotor activity from 18–27 months old.

<p><b>A. Movement number.</b> The increase in movement number from the exercise regimen at 24 months of age was not observed in the subsequent 2 rounds, but a trend toward increased locomotor activity was seen at when the rats reached 27 months of age 2 way Repeated Measures ANOVA results for all 8 rounds of exercise showed highly significant interaction (F_(8,144) = 2.76, <i>p</i><0.01) between aging effects (F_(8,144) = 23.30, <i>p</i><0.0001) and exercise. (round by round outcome; round 5 (t = 2.44, *<i>p</i> = 0.016), round 6 (t = 1.19, ns), round 7 (t = 1.16, ns), round 8 (t = 1.75, ns). <b>B.</b> Linear regression analysis of aging-related decreases in locomotor activity (combined movement number and horizontal activity results) against baseline in non-exercise vs exercise groups out to 27 months of age. There was significant deviation from zero in the non-exercise group (x) (F_(1,14) = 52.91, <i>p</i><0.0001; R² = 0.791) and in the exercise group (◊) (F_(1,14) = 9.71, <i>p</i> = 0.007; R² = 0.410). There was a significant difference in the slope of aging-related decline in movement frequency between the non-exercise (-4.95 ±0.68) and exercise groups (-2.60 ± 0.83), (F_(1,28) = 4.78, <i>p</i><0.05).</p