Though stuttering is manifest in its motor characteristics, the cause of stuttering may not relate purely to impairments in the motor system as stuttering frequency is increased by linguistic factors, such as syntactic complexity and length of utterance, and decreased by changes in perception, such as masking or altering auditory feedback. Using functional and diffusion imaging, we examined brain structure and function in the motor and language areas in a group of young people who stutter. During speech production, irrespective of fluency or auditory feedback, the people who stuttered showed overactivity relative to controls in the anterior insula, cerebellum and midbrain bilaterally and underactivity in the ventral premotor, Rolandic opercular and sensorimotor cortex bilaterally and Heschl's gyrus on the left. These results are consistent with a recent meta-analysis of functional imaging studies in developmental stuttering. Two additional findings emerged from our study. First, we found overactivity in the midbrain, which was at the level of the substantia nigra and extended to the pedunculopontine nucleus, red nucleus and subthalamic nucleus. This overactivity is consistent with suggestions in previous studies of abnormal function of the basal ganglia or excessive dopamine in people who stutter. Second, we found underactivity of the cortical motor and premotor areas associated with articulation and speech production. Analysis of the diffusion data revealed that the integrity of the white matter underlying the underactive areas in ventral premotor cortex was reduced in people who stutter. The white matter tracts in this area via connections with posterior superior temporal and inferior parietal cortex provide a substrate for the integration of articulatory planning and sensory feedback, and via connections with primary motor cortex, a substrate for execution of articulatory movements. Our data support the conclusion that stuttering is a disorder related primarily to disruption in the cortical and subcortical neural systems supporting the selection, initiation and execution of motor sequences necessary for fluent speech production.

The objective of this study was to identify the incidence of feeding difficulties in infants with hypoplastic left heart syndrome (HLHS) and d-transposition of the great arteries (d-TGA). Congenital heart disease is a risk factor for growth failure. The etiologies include poor caloric intake, inability to utilize calories effectively, and increased metabolic demands. The goals of our study were to (1) identify feeding difficulties in infants with HLHS and d-TGA and (2) assess their growth in the first year of life. We performed a chart review of 27 consecutive infants with HLHS and 26 with d-TGA. Descriptive statistics were generated for demographic and clinical variables within each group and are presented as means +/- standard deviations. HLHS and d-TGA groups were compared on time to achieving nutritional goals using the log rank test, on complication rate using the chi-square test, and on weight using the t-test. A significance level of 0.05 was used for all tests. Birth weight was similar for both the HLHS and d-TGA groups (3.19 +/- 0.69 vs 3.35 +/- 0.65 kg, respectively; p = 0.38). Infants with HLHS weighed less than those with d-TGA at l month (3.29 +/- 0.58 vs 3.70 +/- 0.60 kg, respectively; p = 0.021), 6 months (6.27 +/- 1.06 vs 7.31 +/- 1.02 kg, p = 0.003), and 12 months of age (8.40 +/- 1.11 vs 9.49 +/- 1.01 kg, p = 0.006). Time to achieving full caloric intake (at least 100 kcal/kg/day) for the HLHS group (24 +/- 11.9 days) was significantly longer than for the d-TGA group (12.0 +/- 11.2 days, p < 0.001). In addition, infants with HLHS had a higher incidence of feeding-related complications that those with d-TGA (48 vs 4%, respectively; p = 0.001). Compared to the d-TGA group, infants with HLHS weighed less at follow-up, took longer to reach nutritional goals, and had a much higher incidence of feeding-related complications.

Although literature suggests that providing culturally sensitive care promotes positive health outcomes for patients, undergraduate medical education currently does not provide adequate cultural competency training. At most schools, cultural competency, as a formal, integrated, and longitudinal thread within the overall curriculum, is still in its infancy. In this article, the authors summarize the current practice of cultural competency training within medical education and describe the design, implementation, and evaluation of a theoretically based, year-long cultural competency training course for second-year students at Wake Forest University School of Medicine. Evaluation of the results indicate that the course was successful in improving knowledge, attitudes, and skills related to cultural competence as well as bringing about positive changes in the medical school's approach to cultural competency training. Also discussed are the implications of the outcomes for the development of culturally competent physicians and how using appropriate theory can help achieve desired outcomes.