A PET study of the neural systems of stuttering

The cause of stuttering is unknown. Failure to develop left-hemispheric dominance for speech is a long-standing theory although others implicated the motor system more broadly, often postulating hyperactivity of the right (language nondominant) cerebral hemisphere. As knowledge of motor circuitry has advanced, theories of stuttering have become more anatomically specific, postulating hyperactivity of premotor cortex, either directly or through connectivity with the thalamus and basal ganglia. Alternative theories target the auditory and speech production systems. By contrasting stuttering with fluent speech using positron emission tomography combined with chorus reading to induce fluency, we found support for each of these hypotheses. Stuttering induced widespread overactivations of the motor system in both cerebrum and cerebellum, with right cerebral dominance. Stuttered reading lacked left-lateralized activations of the auditory system, which are thought to support the self-monitoring of speech, and selectively deactivated a frontal-temporal system implicated in speech production. Induced fluency decreased or eliminated the overactivity in most motor areas, and largely reversed the auditory-system underactivations and the deactivation of the speech production system. Thus stuttering is a disorder affecting the multiple neural systems used for speaking.     

Assessment of baroreceptor-cardiac reflex sensitivity using time domain analysis in patients with IDDM and the relation to left ventricular mass index

Autonomic dysfunction in insulin-dependent diabetic (IDDM) patients has been associated with abnormalities of left ventricular function and an increased risk of sudden death. A group of 30 patients with IDDM and 30 age, sex and blood pressure matched control subjects underwent traditional tests of autonomic function. In addition, baroreceptor-cardiac reflex sensitivity (BRS) was assessed using time domain (sequence) analysis of systolic blood pressure and pulse interval data recorded non-invasively using the Finapres beat-to-beat blood pressure recording system. 'Up BRS' sequences-increases in systolic blood pressure associated with lengthening of R-R interval, and 'down BRS' sequences-decreases in systolic blood pressure associated with shortening of R-R interval were identified and BRS calculated from the regression of systolic blood pressure on R-R interval for all sequences. We also assessed heart rate variability using power spectral analysis and, after expressing components of the spectrum in normalised units, assessed sympathovagal balance from the ratio of low to high frequency powers. IDDM subjects underwent 2-D echocardiography to assess left ventricular mass index. Standard tests of autonomic function revealed no differences between IDDM patients and control subjects, but dramatic reductions in baroreceptor-cardiac reflex sensitivity were detected in IDDM patients. 'Up BRS' when supine was 11.2 +/- 1.5 ms/mmHg (mean +/- SEM) compared with 20.4 +/- 1.95 in control subjects (p < 0.003) and when standing was 4.1 +/- 1.9 vs 7.6 +/- 2.7 ms/mmHg (p < 0.001). Down BRS when supine was 11.5 +/- 1.2 vs 22 +/- 2.6 (p < 0.001) and standing was 4.4 +/- 1.9 vs 7.3 +/- 2.5 ms/mmHg (p < 0.003). There were significant relations between impairment of the baroreflex and duration of diabetes (p < 0.001) and poor glycaemic control (p < 0.001). From a fast Fourier transformation of supine heart rate data and using a band width of 0.05-0.15 Hz as low-frequency and 0.2-0.35 Hz as high frequency total spectral power of R-R interval variability was significantly reduced in the IDDM group for both low-frequency (473 +/- 62.8 vs 746.6 +/- 77.6 ms2 p = 0.002) and high frequency bands 125.2 +/- 12.9 vs 459.3 +/- 89.8 ms2 p < 0.0001. When the absolute powers were expressed in normalised units the ratio of low frequency to high frequency power (a measure of sympathovagal balance) was significantly increased in the IDDM group (2.9 +/- 0.53 vs 4.6 +/- 0.55, p < 0.002 supine: 3.8 +/- 0.49 vs 6.6 +/- 0.55, p < 0.001 standing). Thus, time domain analysis of baroreceptor-cardiac reflex sensitivity detects autonomic dysfunction more frequently in IDDM patients than conventional tests. Impaired BRS is associated with an increased left ventricular mass index and this abnormality may have a role in the increased incidence of sudden death seen in young IDDM patients.     

Reduced dosage of genes encoding ribosomal protein S18 suppresses a mitochondrial initiation codon mutation in Saccharomyces cerevisiae

A yeast mitochondrial translation initiation codon mutation affecting the gene for cytochrome oxidase subunit III (COX3) was partially suppressed by a spontaneous nuclear mutation. The suppressor mutation also caused cold-sensitive fermentative growth on glucose medium. Suppression and cold sensitivity resulted from inactivation of the gene product of RPS18A, one of two unlinked genes that code the essential cytoplasmic small subunit ribosomal protein termed S18 in yeast. The two S18 genes differ only by 21 silent substitutions in their exons; both are interrupted by a single intron after the 15th codon. Yeast S18 is homologous to the human S11 (70% identical) and the Escherichia coli S17 (35% identical) ribosomal proteins. This highly conserved family of ribosomal proteins has been implicated in maintenance of translational accuracy and is essential for assembly of the small ribosomal subunit. Characterization of the original rps18a-1 missense mutant and rps18a delta and rps18b delta null mutants revealed that levels of suppression, cold sensitivity and paromomycin sensitivity all varied directly with a limitation of small ribosomal subunits. The rps18a-1 mutant was most affected, followed by rps18a delta then rps18b delta. Mitochondrial mutations that decreased COX3 expression without altering the initiation codon were not suppressed. This allele specificity implicates mitochondrial translation in the mechanism of suppression. We could not detect an epitope-tagged variant of S18 in mitochondria. Thus, it appears that suppression of the mitochondrial translation initiation defect is caused indirectly by reduced levels of cytoplasmic small ribosomal subunits, leading to changes in either cytoplasmic translational accuracy or the relative levels of cytoplasmic translation products.     

Is the Promissory Note of Personality as Vulnerability to Depression in Default? Reply to Zuroff, Mongrain, and Santor (2004).

In contrast to D. C. Zuroff, M. Mongrain, and D. A. Santor (2004), the current authors find the promissory note of dependency-sociotropy (DEP-SOC) and self-criticism-autonomy (SC-AUT) as a model of risk for depression to be in default. The authors propose reorganizing what has been cast as unitary effort into 3 distinct endeavors: a psychoanalytic clinical theory, development of a refined empirical model of risk for clinical depression, and research examining the effects of DEP-SOC and SC-AUT on interpersonal relationships in nonclinical samples. The authors identify some issues that need to be accommodated regardless of whether the assessment of Zuroff et al. (2004) or their own is accepted. DEP-SOC and SC-AUT are best construed as correlated, continuous dimensions. Future work also needs to accommodate depression as chronic recurrent condition, advances in developmental psychopathology, and more stringent criteria for positing a risk factor for clinical disorder. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Characterisation of plasticity-induced closure--crack flank contact force versus plastic enclave

This paper presents some results from a totally new and powerful fusion between automated, digital photoelastic techniques and mathematical analysis of a crack experiencing closure. In essence, real-time photoelastic stress field data is acquired and fitted to a Muskhelishvili complex potential model of a loaded crack experiencing closure. The fit entails optimisation of multiple variables via a memetic algorithm, which combines a genetic algorithm and a local search. From observations made in this work, it is proposed that the plastic enclave around a crack tip will shield the crack from the full influence of the applied stress field. Furthermore, the effects of this ‘back stress’ are overcome by the applied tensile load in a way that, often, cannot be readily correlated with crack contact length, wake contact force, or with compliance.     

Two studies of the long-term follow-up of minimal therapist contact treatments of vascular and tension headache.

Tension and vascular headache patients, initially treated with biofeedback and/or relaxation training in either a minimal therapist contact protocol (3 visits) or an intensive individual protocol (10 or 16 visits) were followed-up prospectively for 2 years. In the first study, for the first 6 months of follow-up, half of all patients continued to keep headache diaries and were seen monthly and the other half had only minimal contact. The results at 1-year follow-up, based on 4 weeks of daily headache diaries, revealed equally good maintenance from both treatment protocols and from both follow-up conditions. In Study 2, we found that patients remained improved over pretreatment baseline levels at the 2-year follow-up regardless of initial treatment intensity. Approximately three quarters of vascular patients who were initially improved at posttreatment remained improved at 2 years. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Exposure plus response-prevention treatment of bulimia nervosa.

A controlled study evaluating the effectiveness of exposure plus response-prevention treatment of bulimia nervosa was conducted in a sample of 47 women. This was a four-group comparison involving three treatment conditions and a waiting-list control group. The three treatment conditions were (a) exposure plus response prevention conducted in a single setting (clinic), (b) exposure plus response prevention conducted in multiple settings (clinic, patients' homes, and restaurants), and (c) cognitive–behavioral therapy without exposure plus response prevention. All treatment was provided to groups of 3 patients at a time. Outcome was evaluated at posttreatment and at a 6-month follow-up. The three treatment groups improved significantly on most outcome measures, whereas the waiting-list control group showed little change. At follow-up, there was a slightly better outcome on vomiting behavior and amount of food consumed in one of the test meals for the exposure plus response-prevention groups relative to the no-exposure group. However, on all other measures, the degree of improvement from pretreatment to follow-up was the same for all three treatment groups. (PsycINFO Database Record (c) 2010 APA, all rights reserved)