Decriminalizing mental illness: specialized policing responses.

De-institutionalization of mental health patients has evolved, over nearly 3 generations now, to a status quo of mental health patients experiencing myriad contacts with first-responders, primarily police, in lieu of care. The current institutions in which these patients rotate through are psychiatric emergency units, emergency rooms, jails, and prisons. Although more police are now specially trained to respond to calls that involve mental health patients, the criminalization of persons with mental illness has been steadily increasing over the past several decades. There have also been deaths. The Crisis Intervention Team (CIT) model fosters mental health acumen among first responders, and facilitates collaboration among first responders, mental health professionals, and mental health patients and their families. Here, we review some modern, large city configurations of CIT, the co-responder model, the mitigating effects of critically situated community-based programs, as well as barriers to the success of joint efforts to better address this pressing problem.

A gamma-secretase inhibitor and quinacrine reduce prions and prevent dendritic degeneration in murine brains.

In prion-infected mice, both the Notch-1 intracellular domain transcription factor (NICD) and the disease-causing prion protein (PrP(Sc)) increase in the brain preceding dendritic atrophy and loss. Because the drug LY411575 inhibits the gamma-secretase-catalyzed cleavage of Notch-1 that produces NICD, we asked whether this gamma-secretase inhibitor (GSI) might prevent dendritic degeneration in mice with scrapie. At 50 d postinoculation with Rocky Mountain Laboratory (RML) prions, mice were given GSI orally for 43-60 d. Because we did not expect GSI to produce a reduction of PrP(Sc) levels in brain, we added quinacrine (Qa) to the treatment regimen. Qa inhibits PrP(Sc) formation in cultured cells. The combination of GSI and Qa reduced PrP(Sc) by approximately 95% in the neocortex and hippocampus but only approximately 50% in the thalamus at the site of prion inoculation. The GSI plus Qa combination prevented dendritic atrophy and loss, but GSI alone did not. Even though GSI reduced NICD levels to a greater extent than GSI plus Qa, it was unable to prevent dendritic degeneration. Whether a balance between NICD and dendrite growth-stimulating factors was achieved with GSI plus Qa but not GSI alone remains to be determined. Although the combination of GSI and Qa diminished PrP(Sc) in the brains of RML-infected mice, GSI toxicity prevented us from being able to assess the effect the GSI plus Qa combination on incubation times. Whether less toxic GSIs can be used in place of LY411575 to prolong survival remains to be determined.

The relationship between paraspinal EMG and chronic low back pain.

Two models of the relationship between paraspinal EMG and low back pain have been proposed. Specific predictions arising from these are listed and the literature relating to them reviewed. Recent research on patterns of EMG rather than absolute levels is also discussed. It is concluded that there is no consistent evidence that low back pain patients have elevated paraspinal EMG, or that its reduction is likely to be an active ingredient in biofeedback therapy. Research on paraspinal EMG patterns is still preliminary, and therefore treatment based on their modification is experimental.

A continuing medical education initiative for canadian primary care physicians: the driving and dementia toolkit: a pre- and postevaluation of knowledge, confidence gained, and satisfaction.

This study examined the effect of the Driving and Dementia Toolkit on physician knowledge and confidence gained and the anticipated change in patient assessment and evaluated the extent to which physicians found the material to be useful. Before receiving the driving toolkit, 301 randomly selected primary care physicians received a copy of the pretest questionnaire; 145 responded and met the eligibility criteria. This group was then sent the toolkit, a satisfaction a survey, and a posttest questionnaire. Physicians were faxed the questionnaires (with up to three reminders) and telephoned if necessary. Changes in pre- and posttest results were analyzed using the McNemar test and Wilcoxon signed rank test nonparametric procedures included in SPSS, Version 10.0, and paired-samples t test. Pre- and posttest data were available and could be matched for 86 physicians (59.3%) response. Knowledge and confidence increased significantly (P

Early frontotemporal dementia targets neurons unique to apes and humans.

OBJECTIVE: Frontotemporal dementia (FTD) is a neurodegenerative disease that erodes uniquely human aspects of social behavior and emotion. The illness features a characteristic pattern of early injury to anterior cingulate and frontoinsular cortex. These regions, though often considered ancient in phylogeny, are the exclusive homes to the von Economo neuron (VEN), a large bipolar projection neuron found only in great apes and humans. Despite progress toward understanding the genetic and molecular bases of FTD, no class of selectively vulnerable neurons has been identified. METHODS: Using unbiased stereology, we quantified anterior cingulate VENs and neighboring Layer 5 neurons in FTD (n = 7), Alzheimer's disease (n = 5), and age-matched nonneurological control subjects (n = 7). Neuronal morphology and immunohistochemical staining patterns provided further information about VEN susceptibility. RESULTS: FTD was associated with early, severe, and selective VEN losses, including a 74% reduction in VENs per section compared with control subjects. VEN dropout was not attributable to general neuronal loss and was seen across FTD pathological subtypes. Surviving VENs were often dysmorphic, with pathological tau protein accumulation in Pick's disease. In contrast, patients with Alzheimer's disease showed normal VEN counts and morphology despite extensive local neurofibrillary pathology. INTERPRETATION: VEN loss links FTD to its signature regional pattern. The findings suggest a new framework for understanding how evolution may have rendered the human brain vulnerable to specific forms of degenerative illness.