012) between the LS (n = 16) and CON (n = 22) groups. Increase in iliopsoas muscle tightness in the kicking leg was a predictive risk factor of developing extension-based lumbar pain after adjusting for developmental age and body mass index (odds ratio, 1.54; 95% confidence interval, 1.05-2.27).

Development of extension-based lumbar pain from an asymptomatic stress reaction of the pedicle among adolescent male soccer players was associated with increased iliopsoas muscle tightness of the kicking leg relative to that of the supporting leg.
Development of extension-based lumbar pain from an asymptomatic stress reaction of the pedicle among adolescent male soccer players was associated with increased iliopsoas muscle tightness of the kicking leg relative to that of the supporting leg.
Major depressive disorder (MDD) is characterized by impaired cortical-subcortical functional connectivity. Apathy adds to functional impairment, but its cerebral basis in MDD remains unknown. Our objective was to describe impairments in functional connectivity during emotional processing in MDD (with varying levels of congruency and attention), and to determine their correlation with apathy.

We used the Variable Attention Affective Task during functional MRI, followed by diffusion-weighted MRI, to assess 55 right-handed women (30 with MDD and 25 healthy controls) between September 2012 and February 2015. We estimated functional connectivity using generalized psychophysiologic interaction and anatomic connectivity with tract-based spatial statistics. We measured apathy using the Apathy Evaluation Scale.

We found decreased functional connectivity between the left amygdala and the left anterior cingulate cortex (ACC) during negative stimuli in participants with MDD (t54 = 4.2; p = 0.035, family-wise error ve disorders, but possible different mechanisms.
We found that MDD was associated with impairments in cortical-subcortical functional connectivity during negative stimuli that might alter the recruitment of networks engaged in attention. Apathy-related features suggested networks similar to those observed in degenerative disorders, but possible different mechanisms.
Fear extinction alone does not erase the original fear memory. Interventions that enhance extinction can be beneficial for the treatment of fear-related disorders. Repetitive transcranial magnetic stimulation has been shown to improve memory performance. The present study examined the effects of intermittent theta-burst stimulation (iTBS) on fear extinction and the return of fear memory in humans.

Ninety-one young healthy volunteers underwent 3 experiments using a randomized controlled experimental design. Participants first acquired fear conditioning, after which they received 30 Hz iTBS before and after extinction training. SR-0813 The iTBS was applied to 1 of 2 targets the left dorsolateral prefrontal cortex (dlPFC) and the vertex (control). Fear responses were measured 24 hours later and 1 month later.

During the spontaneous recovery and reinstatement tests, iTBS of the left dlPFC before and after extinction significantly reduced fear response, whereas iTBS of the vertex had no effect on fear memory performance. This combined approach had a relatively long-lasting effect (i.e., at least 1 month).

We did not explore the effect of iTBS of the dlPFC on the expression of fear without extinction training. The neural mechanisms of iTBS with fear extinction to inhibit the fear response are unclear. Our results are preliminary and should be interpreted with caution.

The present results showed that 30 Hz iTBS of the left dlPFC enhanced retention of fear extinction. Our study introduces a new intervention for fear memory and suggests that the left dlPFC may be a treatment target for fear-related disorders.
The present results showed that 30 Hz iTBS of the left dlPFC enhanced retention of fear extinction. Our study introduces a new intervention for fear memory and suggests that the left dlPFC may be a treatment target for fear-related disorders.
Cocaine use has been associated with vascular pathologies, including cerebral white matter hyperintensities. Street cocaine is most often adulterated with levamisole, an anthelminthic drug that may also be associated with vascular toxicity. However, whether levamisole exposure from cocaine consumption further accelerates the development of white matter lesions remains unknown.

We investigated the association of cocaine and levamisole exposure with white matter hyperintensities in 35 chronic cocaine users and 34 healthy controls. We measured cocaine and levamisole concentrations in hair samples, which reflected exposure up to 6 months previously. We assessed the number and total surface area of the white matter hyperintensities using structural MRI (FLAIR sequence). Using generalized linear models, we analyzed the contributions of cocaine and levamisole to the number and area of white matter hyperintensities, accounting for several confounding factors.

Analysis using generalized linear models revealed that cocaine users had more white matter hyperintensities in terms of total surface area, but not in terms of number. Further generalized linear models that included cocaine and levamisole hair concentrations (instead of group) as predictors indicated that levamisole exposure was strongly associated with more and larger white matter hyperintensities, suggesting that the elevated white matter hyperintensities in cocaine users were driven mainly by levamisole exposure. Finally, white matter hyperintensities in levamisole-exposed cocaine users were located primarily in the periventricular and juxtacortical white matter.

The sample size was moderate, and blood pressure was not systematically assessed.

As an adulterant of cocaine, levamisole appears to increase the risk of white matter injury.
As an adulterant of cocaine, levamisole appears to increase the risk of white matter injury.
Neurobiological measures have been associated with delinquent behaviour, but little is known about the predictive power of these measures for criminal recidivism and whether they have incremental value over and above demographic and behavioural measures. This study examined whether selected measures of autonomic functioning, functional neuroimaging and electroencephalography predict overall and serious recidivism in a sample of 127 delinquent young adults.

We assessed demographics; education and intelligence; previous delinquency and drug use; behavioural traits, including aggression and psychopathy; and neurobiological measures, including heart rate, heart rate variability, functional brain activity during an inhibition task and 2 electroencephalographic measures of error-processing. We tested longitudinal associations with recidivism using Cox proportional hazard models and predictive power using C-indexes.

Past offences, long-term cannabis use and reactive aggression were strongly associated with recidivism, as were resting heart rate and error-processing.SR-0813