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At least 1,657 records · Page 92Linked to original sources
PubMed1995

Effects of early adolescent drug use on cognitive efficacy in early-late adolescence: a developmental structural model.

Despite an accumulated body of research evidence that documents the negative physical consequences of chronic alcohol and drug use, it is less clear whether the use of these same substances produces impaired cognitive abilities during the early stages of use. Early drug use may impede acquisition of critical thinking skills and hinder the learning of important cognitive strategies required for successful transition to adulthood. To better understand these relations, longitudinal latent-variable analyses were used to examine the effects of early adolescent drug use on early-late adolescent cognitive efficacy. Latent factors of polydrug use, behavioral control, and cognitive efficacy were hypothesized in early adolescence, the latter two controlling for potential spurious relations. At outcome, six constructs were hypothesized tapping polydrug use, cognitive mastery, self-reinforcement, problem-solving confidence, decision-making skills, and cognitive and affective self-management strategies. Models were psychometrically sound and accounted for large portions of variance. Early adolescent drug use had a small but significant negative effect on cognitive and affective self-management strategies. By the 12th grade, linkages between drug use and cognitive functioning were of larger magnitude than long-term influences, perhaps reinforcing the argument that deficits in cognitive skills are developmentally delayed and surface only with exacerbated or persistent drug use. Overall, specific effects of drug use adversely influenced important cognitive skills that may be critically related to functioning in both interpersonal and intrapersonal domains.

Adolescent↗
PubMed2005

Olanzapine-induced vasculitis.

INTRODUCTION: Elderly patients are particularly vulnerable to adverse drug reactions as a result of polypharmacy and metabolic changes associated with aging. We present a case of leukocytoclastic vasculitis induced by olanzapine, a medication commonly used in elderly patients. CASE SUMMARY: An 82-year-old woman was admitted to the extended-care center for short-term rehabilitation after prolonged hospitalization for a pulmonary embolism requiring mechanical ventilation. The pulmonary problem resolved, but her hospitalization and subsequent rehabilitation were complicated by agitated delirium, which was treated with olanzapine and modification of contributory factors. At the time of admission to the rehabilitation facility, the patient had been receiving warfarin for 2 weeks and olanzapine for 6 days. On the eighth day after initiation of olanzapine, erythematous skin lesions developed on dependent areas. The international normalized ratio for warfarin was within the acceptable range; however, because warfarin has been associated with subcutaneous bleeding presenting as petechiae and ecchymosis, subcutaneous enoxaparin was substituted for warfarin. The skin lesions continued to worsen over the next week and developed into palpable lesions. Biopsy of the rash revealed leukocytoclastic vasculitis. In the absence of another cause, olanzapine was discontinued and the rash improved significantly. When the agitation recurred, risperidone was initiated, but the patient experienced dizziness with this agent. Olanzapine was resumed and the skin lesions recurred. Olanzapine was then changed to quetiapine, and the skin lesions improved over the next few weeks. DISCUSSION: Olanzapine is commonly used in elderly patients to control behavioral disturbances associated with dementia, delirium, and other psychiatric disorders. Leukocytoclastic vasculitis is an infrequently reported adverse drug reaction with olanzapine. Its exact pathogenic mechanism is unknown, but both cell-mediated and humoral immunity appear to play important roles. Because drug-induced vasculitis has an identical clinical presentation and identical serologic/pathologic parameters to idiopathic forms of vasculitis, a high index of suspicion is necessary for its accurate diagnosis. CONCLUSIONS: Because adverse drug reactions are common in elderly patients taking multiple medications, physicians should be vigilant when starting new medications and should attempt to eliminate unnecessary medications. Clinicians should be aware of the potential for leukocytoclastic vasculitis in association with olanzapine.

Aged↗
PubMed2006

The conceptualization of physical restraint as a nursing-sensitive adverse outcome in acute care psychiatric treatment settings.

The occurrence of physical restraint episodes in psychiatric settings is a major public health issue because the therapeutic utility of this form of behavior control has not been substantiated empirically. The purpose of this article was to examine the extant literature to determine if evidence supports the conceptualization of a physical restraint episode as an adverse client outcome that is sensitive to the organization of nursing care in psychiatric settings. An adapted version of the Quality Health Outcomes Model (Mitchell, P. H., Ferketich, S., & Jennings, B. M. (1998). Quality Health Outcomes Model. Image Journal of Nursing Scholarship, 30, 43-46) was used as the conceptual model to guide this inquiry. The databases Cumulative Index to Nursing and Allied Health Literature, Health and Psychosocial Instruments, HealthSTAR/Ovid and Healthstar, Medline, and psychINFO were searched from 1990 to 2005. There are 101 sources in this review. Evidence strongly suggests that a physical restraint episode is an adverse outcome that is sensitive to the organization of nursing care. A systematic exploration of the specific structures and processes of the organization that affect adverse outcomes, such as physical restraint episodes, is lacking in the United States.

Hospitals, Psychiatric↗
PubMed2006

Microglia serve as a neuroimmune substrate for stress-induced potentiation of CNS pro-inflammatory cytokine responses.

Prior exposure to a stressor can potentiate CNS pro-inflammatory immune responses to a peripheral immune challenge. However, the neuroimmune substrate(s) mediating this effect has not been determined. The present investigation examined whether microglia serve as this neuroimmune substrate given that microglia are the primary immune effector cell in the CNS. The effect of inescapable shock (IS) on glial activation (MHC II, CD11b, Iba-1, and GFAP) and regulatory markers (CD200) in vivo, and microglia pro-inflammatory responses (interleukin-1beta; IL-1beta) to lipopolysaccharide (LPS) ex vivo, were assessed in rat hippocampus. IS upregulated the microglia activation marker MHC II 24h post-IS, while the astroglia marker GFAP was unaffected. IS also downregulated the neuronal glycoprotein CD200, which functions to hold microglia in a quiescent state. Moreover, IS potentiated the pro-inflammatory response to LPS ex vivo 24h post-IS in isolated hippocampal microglia. Finally, the behavioral controllability of shock was manipulated and the effect of escapable (controllable) shock was comparable to the effect of IS on hippocampal microglia responses to LPS ex vivo. The present results suggest that stress can activate microglia, thereby sensitizing the pro-inflammatory reactivity of microglia to immunogenic stimuli.

Animals↗