Recent studies have shown that the persistence of the cavum septi pellucidi beyond the neonatal period is a marker of cerebral dysgenesis. It has been suggested that the finding of a persistent cavum vergae is also a marker of disturbed brain development. In order to investigate this hypothesis we reviewed 161 brain magnetic resonance imaging scans from normal individuals for the presence of cavum septi pellucidi or cavum vergae, or both. In the 34 prospectively obtained normal adults, there were no individuals with either a cavum septi pellucidi or cavum vergae. In the "defined" normal subjects 3 of 127 individuals (2.4%) had a cavum septi pellucidi whereas a cavum vergae was noted in 26 of 127 (20.5%). We next reviewed the neuroimaging studies of 249 children and adults evaluated for mental retardation or developmental delay. A cavum septi pellucidi was found in 38 of 249 (15.3%) and a cavum vergae in 48 of 249 (19.3%) of these patients. A cavum septi pellucidi and cavum vergae were found together in 19 of 249 (7.6%). We interpret these data as showing that the cavum septi pellucidi is rarely seen in normal individuals although the cavum vergae is seen with the same frequency in normal and retarded populations. Thus we conclude that the cavum septi pellucidi serves as a significant marker of cerebral dysfunction manifested by neurodevelopmental abnormalities while the cavum vergae alone does not identify individuals at risk for cognitive delays.

We investigated body vigilance, cardiac anxiety, and the mediating role of interoceptive fear on pain in patients with non-cardiac chest pain (NCCP; a syndrome of chest pain in the absence of identifiable organic etiology). Patients were more attentive to cardiac-congruent sensations than cardiac-incongruent sensations (e.g., gastrointestinal, cognitive dyscontrol; p's < .001). Patients with a DSM-IV Axis I anxiety or mood disorder were more body vigilant compared to patients who did not have a disorder (p's < .05). Patients with anxiety disorders were particularly vigilant to and fearful of cardiac sensations relative to patients without anxiety disorders. Latent variable path models examined the extent that interoceptive fear mediated the association between body vigilance and cardiac anxiety on chest pain. Within each model, diagnostic status, body vigilance, and cardiac anxiety were exogenous and predicted interoceptive fear that in turn predicted pain. Separate models examined body vigilance and cardiac anxiety, and both models fit the data well. Findings showed partial mediation for the body vigilance factor, and full mediation for the cardiac anxiety factor. Interoceptive fear played a mediating role in both models. The syndrome of NCCP may persist partly due to conscious hypervigilance to and fear of cardiac-congruent body sensations, particularly among anxious patients.

Chest pain can be a frightening experience that leads many to seek medical evaluation (American Heart Association, 2009). The symptom results in costly health care utilization (Kahn, 2000). Over half of patients referred for cardiac evaluations of chest pain do not obtain definitive medical explanations for their symptoms; these cases are described as non-cardiac chest pain (NCCP: Bass & Mayou, 1995). Some patients with NCCP are not reassured after being informed their chest pain is non-cardiac in origin and seek repeated medical evaluation (Tew et al., 1995). Co-morbid anxiety and mood disorders often co-exist with NCCP and are associated with health care utilization (White et al., 2008). The current study examined chest pain, general anxiety, interoceptive fear, and health care utilization in a sample of 196 chest pain patients near the time of cardiac evaluation (Time 1), and 70 of these patients one year later (Time 2). Results indicate that anxiety and interoceptive fear were significantly associated with health care utilization at Time 1, and only interoceptive fear (at Time 1) predicted health care utilization at Time 2. This study develops research in this area by examining the relation of anxiety and health care utilization longitudinally in patients with NCCP.

In this small sample, only a third of all sedentary time was attributed to viewing television. Assessing whether sedentary behavior occurs by necessity versus choice may be a factor to consider in examining its relationship to food cravings.

No abstract

Usher syndrome is a group of genetic disorders consisting of congenital sensorineural hearing loss and retinitis pigmentosa of variable onset and severity depending on the genetic type. It was suggested that the psychosis of Usher syndrome might be secondary to a metabolic degeneration involving the brain more diffusely. There have been reports of focal and diffuse atrophic changes in the supratentorial brain as well as atrophy of some of the structures of the posterior fossa. We previously performed quantitative analysis of magnetic resonance imaging studies of 19 Usher syndrome patients (12 with type I and 7 with type II) looking at the cerebellum and various cerebellar components. We found atrophy of the cerebellum in both types and sparing of cerebellar vermis lobules I-V in type II Usher syndrome patients only. We now have studied another group of 19 patients (with some overlap in the patients studied from the previous report) with Usher syndrome (8 with type I, 11 with type II). We performed quantitative volumetric measurements of various brain structures compared to age- and sex-matched controls. We found a significant decrease in intracranial volume and in size of the brain and cerebellum with a trend toward an increase in the size of the subarachnoid spaces. These data suggest that the disease process in Usher syndrome involves the entire brain and is not limited to the posterior fossa or auditory and visual systems.

Usher syndrome is a group of genetic disorders consisting of congenital sensorineural hearing loss and retinitis pigmentosa of variable onset and severity depending on the genetic type. It was suggested that the psychosis of Usher syndrome might be secondary to a metabolic degeneration involving the brain more diffusely. There have been reports of focal and diffuse atrophic changes in the supratentorial brain as well as atrophy of some of the structures of the posterior fossa. We previously performed quantitative analysis of magnetic resonance imaging studies of 19 Usher syndrome patients (12 with type I and 7 with type II) looking at the cerebellum and various cerebellar components. We found atrophy of the cerebellum in both types and sparing of cerebellar vermis lobules I-V in type II Usher syndrome patients only. We now have studied another group of 19 patients (with some overlap in the patients studied from the previous report) with Usher syndrome (8 with type I, 11 with type II). We performed quantitative volumetric measurements of various brain structures compared to age- and sex-matched controls. We found a significant decrease in intracranial volume and in size of the brain and cerebellum with a trend toward an increase in the size of the subarachnoid spaces. These data suggest that the disease process in Usher syndrome involves the entire brain and is not limited to the posterior fossa or auditory and visual systems.

Cardiac intercalated disks (ICDs) between adjacent cardiac myocytes provide mechanical attachments through adherins junctions and desmosomes mixed with gap junctions formed by connexins. ICDs are sites of electrical conduction and targets of dysrhythmic stimuli. The goal of the present study is to test the hypothesis that the ICD space is a regulated, potentially arrthythmogenic compartment that is responsive to pathological processes. We have developed a system for acquiring simultaneous electron energy-loss (EELS) and energy dispersive X-ray microscopy (EDS) for quantitative compositional imaging at nanometer resolution [1]. This approach takes advantage of the high sensitivity of the Ca-detection by EELS [2] combined with the large energy range required for detection of multiple elements through EDS. Degradation of resolution by specimen drift was circumvented by using image cross-correlation. Freeze dried sections obtained by cryo-ultramicrotomy from snap frozen guinea pig trabeculae were used for elemental mapping, with a pixel size of 5-10nm. Calcium ranging from 0 to 55 ± 1.4 mmol/kg dry wt was distributed intermittently along the ICDs. The extracellular region of E-cadherin has been shown to bind 9 Ca with a K d of 30μM. We estimate that a pure sample of E-cadherin with Ca bound to all sites would give rise to 110mmol/kg dry wt. Not surprisingly, our measurements are lower due to the inclusion of other proteins in the microvolume sampled. Furthermore, N-cadherin, the cardiac cadherin isoform, has been shown to have a lower Ca-binding affinity. The high [Ca] regions were bounded by high [P] concentrations, likely reflecting cell membrane phospholipids. High [S] was distributed on the cytoplasmic sides of the high Ca regions reflecting high S containing proteins associated with the adherins junctions. Pre-incubation of the muscles in a low Ca containing (50μM) solution lead to a loss of the periodic high [Ca] at the ICD and a swelling and separation of the ICD space likely reflecting the known Ca-dependent homotypic binding of adherins on adjacent cells. We propose that depletion of [Ca] in the very narrow ICD space could occur under pathological processes, which would impair connections and could contribute to cardiac fibrillation.Functional studies using an N-cadherin loss of function antibody made to the chicken N-cadherin EC1 region was introduced into chick trabeculae. Contractions were measured in response to electrical pacing (0.2Hz, 40ms pulse duration) using point source stimulation at one end of the muscle, alternating with wide field stimulation such that they yielded the same amount of force. Introduction of the functionally disrupting N-cadherin antibody lead to a loss of point field stimulation while retaining the magnitude of the wide field stimulation. A non-specific IgG was without affect while gap junction inhibitors (P27 peptide or 18α-glycyrrhetinic acid) lead to a loss of point field but not wide field stimulation as expected. These findings are supported by other experiments using c...