Real time ultrasound imaging shows changes in deep neck flexor activation during exercise in individuals with mechanical neck pain.

BACKGROUND: Deep neck flexor muscle atrophy and increased superficial neck muscle activation are associated with disability and pain intensity in individuals with neck pain. There is a lack of evidence to support direct assessment of deep neck flexor muscles in a non-invasive way during exercise performance to help determine the effectiveness of different neck strengthening exercises. OBJECTIVE: Compare longus colli (LC) and sternocleidomastoid (SCM) activation between individuals with and without neck pain using real time ultrasound (RTUS) during a series of craniocervical exercises. METHODS: This cross-sectional cohort study recruited 10 control and 10 neck pain participants to complete four deep neck flexor activation activities involving varying levels of craniocervical flexion. Dimensions of the LC and SCM were measured using RTUS at rest and during exercise. Independent t-tests assessed baseline differences and analysis of variance examined activation changes. RESULTS: At rest, the neck pain group had significantly smaller cross-sectional area and thickness of the LC compared to the control group (p< 0.05). During exercise, the neck pain group showed significantly larger increases in LC thickness and cross-sectional area across exercise compared to the control group, with no differences in SCM activation between groups. CONCLUSIONS: Despite atrophy, individuals with neck pain can activate their deep neck flexor muscles appropriately without activating their superficial neck flexor muscles in a supine series of craniocervical flexion exercise as measured by non-invasive ultrasound imaging.

A meta-analysis of genetic effects associated with neurodevelopmental disorders and co-occurring conditions.

A systematic understanding of the aetiology of neurodevelopmental disorders (NDDs) and their co-occurrence with other conditions during childhood and adolescence remains incomplete. In the current meta-analysis, we synthesized the literature on (1) the contribution of genetic and environmental factors to NDDs, (2) the genetic and environmental overlap between different NDDs, and (3) the co-occurrence between NDDs and disruptive, impulse control and conduct disorders (DICCs). Searches were conducted across three platforms: Web of Science, Ovid Medline and Ovid Embase. Studies were included only if 75% or more of the sample consisted of children and/or adolescents and the studies had measured the aetiology of NDDs and DICCs using single-generation family designs or genomic methods. Studies that had selected participants on the basis of unrelated diagnoses or injuries were excluded. We performed multilevel, random-effects meta-analyses on 296 independent studies, including over four million (partly overlapping) individuals. We further explored developmental trajectories and the moderating roles of gender, measurement, geography and ancestry. We found all NDDs to be substantially heritable (family-based heritability, 0.66 (s.e. = 0.03); SNP heritability, 0.19 (s.e. = 0.03)). Meta-analytic genetic correlations between NDDs were moderate (grand family-based genetic correlation, 0.36 (s.e. = 0.12); grand SNP-based genetic correlation, 0.39 (s.e. = 0.19)) but differed substantially between pairs of disorders. The genetic overlap between NDDs and DICCs was strong (grand family-based genetic correlation, 0.62 (s.e. = 0.20)). While our work provides evidence to inform and potentially guide clinical and educational diagnostic procedures and practice, it also highlights the imbalance in the research effort that has characterized developmental genetics research.

Increased excitation-inhibition balance and loss of GABAergic synapses in the serine racemase knockout model of NMDA receptor hypofunction.

There is substantial evidence that both N-methyl-D-aspartate receptor (NMDAR) hypofunction and dysfunction of GABAergic neurotransmission contribute to schizophrenia, though the relationship between these pathophysiological processes remains largely unknown. Although models using cell-type-specific genetic deletion of NMDARs have been informative, they display overly pronounced phenotypes extending beyond those of schizophrenia. Here, we used the serine racemase knockout (SRKO) mice, a model of reduced NMDAR activity rather than complete receptor elimination, to examine the link between NMDAR hypofunction and decreased GABAergic inhibition. The SRKO mice, in which there is a >90% reduction in the NMDAR coagonist d-serine, exhibit many of the neurochemical and behavioral abnormalities observed in schizophrenia. We found a significant reduction in inhibitory synapses onto CA1 pyramidal neurons in the SRKO mice. This reduction increases the excitation/inhibition balance resulting in enhanced synaptically driven neuronal excitability without changes in intrinsic excitability. Consistently, significant reductions in inhibitory synapse density in CA1 were observed by immunohistochemistry. We further show, using a single-neuron genetic deletion approach, that the loss of GABAergic synapses onto pyramidal neurons observed in the SRKO mice is driven in a cell-autonomous manner following the deletion of SR in individual CA1 pyramidal cells. These results support a model whereby NMDAR hypofunction in pyramidal cells disrupts GABAergic synapses leading to disrupted feedback inhibition and impaired neuronal synchrony.NEW & NOTEWORTHY Recently, disruption of excitation/inhibition (E/I) balance has become an area of considerable interest for psychiatric research. Here, we report a reduction in inhibition in the serine racemase knockout mouse model of schizophrenia that increases E/I balance and enhances synaptically driven neuronal excitability. This reduced inhibition was driven cell-autonomously in pyramidal cells lacking serine racemase, suggesting a novel mechanism for how chronic NMDA receptor hypofunction can disrupt information processing in schizophrenia.

Patient navigation based on predictive modeling decreases no-show rates in cancer care.

BACKGROUND: Patient adherence to appointments is key to improving outcomes in health care. "No-show" appointments contribute to suboptimal resource use. Patient navigation and telephone reminders have been shown to improve cancer care and adherence, particularly in disadvantaged populations, but may not be cost-effective if not targeted at the appropriate patients. METHODS: In 5 clinics within a large academic cancer center, patients who were considered to be likely (the top 20th percentile) to miss a scheduled appointment without contacting the clinic ahead of time ("no-shows") were identified using a predictive model and then randomized to an intervention versus a usual-care group. The intervention group received telephone calls from a bilingual patient navigator 7 days before and 1 day before the appointment. RESULTS: Over a 5-month period, of the 40,075 appointments scheduled, 4425 patient appointments were deemed to be at high risk of a "no-show" event. After the patient navigation intervention, the no-show rate in the intervention group was 10.2% (167 of 1631), compared with 17.5% in the control group (280 of 1603) (P<.001). Reaching a patient or family member was associated with a significantly lower no-show rate (5.9% and 3.0%, respectively; P<.001 and .006, respectively) compared with leaving a message (14.7%: P = .117) or no contact (no-show rate, 21.6%: P = .857). CONCLUSIONS: Telephone navigation targeted at those patients predicted to be at high risk of visit nonadherence was found to effectively and substantially improve patient adherence to cancer clinic appointments. Further studies are needed to determine the long-term impact on patient outcomes, but short-term gains in the optimization of resources can be recognized immediately.