Sensory Reduction on the General Milieu of a High-Acuity Inpatient Psychiatric Unit to Prevent Use of Physical Restraints: A Successful Open Quality Improvement Trial.

BACKGROUND: Impaired sensory gating in patients with acute mental illness predisposes to overstimulation and behavioral dyscontrol. OBJECTIVE: Explore use of sensory reduction interventions on a high-acuity inpatient milieu to reduce high assault/restraint rates. DESIGN: A multidisciplinary team using failure mode and effect analysis to explore high restraint use between 4:00 p.m. and 7:00 p.m. observed patient/staff overstimulation contributed to behavioral escalations. The team implemented sensory reduction/integration improvements over a 5-month period to prevent excessive restraint use. RESULTS: Restraint rates dropped immediately following light and sound reduction interventions and by 72% at 11 months postimplementation. Mann-Whitney statistics for unpaired 6-month comparisons, 1-year pre- and postintervention showed significant reductions: Assault rates (median pre = 1.37, post = 0.18, U = 4, p = .02); Restraint rates (median pre = 0.50, post = 0.06, U = 0, p = .002). CONCLUSION: Sensory reduction during a high-stress time period on a high-acuity psychiatric unit was associated with a reduction in assaults and restraints.

Synthesis and characterization of selective dopamine D2 receptor ligands using aripiprazole as the lead compound.

A series of compounds structurally related to aripiprazole (1), an atypical antipsychotic and antidepressant used clinically for the treatment of schizophrenia, bipolar disorder, and depression, have been prepared and evaluated for affinity at D(2-like) dopamine receptors. These compounds also share structural elements with the classical D(2-like) dopamine receptor antagonists, haloperidol, N-methylspiperone, domperidone and benperidol. Two new compounds, 7-(4-(4-(2-methoxyphenyl)piperazin-1-yl)butoxy)-3,4-dihydroquinolin-2(1H)-one oxalate (6) and 7-(4-(4-(2-(2-fluoroethoxy)phenyl)piperazin-1-yl)butoxy)-3,4-dihydroquinolin-2(1H)-one oxalate (7) were found to (a) bind to the D2 receptor subtype with high affinity (K(i) values < 0.3 nM), (b) exhibit >50-fold D2 versus D3 receptor binding selectivity and (c) be partial agonists at both the D2 and D3 receptor subtype.

Lymphatic pump treatment mobilizes leukocytes from the gut associated lymphoid tissue into lymph.

BACKGROUND: Lymphatic pump techniques (LPT) are used clinically by osteopathic practitioners for the treatment of edema and infection; however, the mechanisms by which LPT enhances lymphatic circulation and provides protection during infection are not understood. Rhythmic compressions on the abdomen during LPT compress the abdominal area, including the gut-associated lymphoid tissues (GALT), which may facilitate the release of leukocytes from these tissues into the lymphatic circulation. This study is the first to document LPT-induced mobilization of leukocytes from the GALT into the lymphatic circulation. METHODS AND RESULTS: Catheters were inserted into either the thoracic or mesenteric lymph ducts of dogs. To determine if LPT enhanced the release of leukocytes from the mesenteric lymph nodes (MLN) into lymph, the MLN were fluorescently labeled in situ. Lymph was collected during 4 min pre-LPT, 4 min LPT, and 10 min following cessation of LPT. LPT significantly increased lymph flow and leukocytes in both mesenteric and thoracic duct lymph. LPT had no preferential effect on any specific leukocyte population, since neutrophil, monocyte, CD4+ T cell, CD8+ T cell, IgG+B cell, and IgA+B cell numbers were similarly increased. In addition, LPT significantly increased the mobilization of leukocytes from the MLN into lymph. Lymph flow and leukocyte counts fell following LPT treatment, indicating that the effects of LPT are transient. CONCLUSIONS: LPT mobilizes leukocytes from GALT, and these leukocytes are transported by the lymphatic circulation. This enhanced release of leukocytes from GALT may provide scientific rationale for the clinical use of LPT to improve immune function.