Patterns of gray matter (GM) loss were measured in 223 healthy subjects spanning eight decades. We observed significant clusters of accelerated loss in focal regions of the frontal and parietal cortices, including the dorsolateral frontal cortex, pre- and postcentral gyrus, and the inferior and superior parietal lobes. The rate of loss in these clusters was approximately twice that of the global average. By contrast, clusters of significant GM preservation were found in limbic and paralimbic structures, including the amygdala, hippocampus, thalamus, and the cingulate gyrus. In these clusters, GM loss was attenuated significantly relative to the global rate. The preservation of these structures is consistent with the functional importance of the thalamo-limbic circuits in sensory integration, arousal, emotion, and memory, and lends credence to the idea that later-maturing cortical regions are more vulnerable to age-related morphologic changes. Moreover, the limbic findings act as a frame of reference to explore further the effects of stress and learning on these structures in an evidence-based manner across age.
Background. Although cognitive behaviour therapy (CBT) is the treatment of choice for post-traumatic stress disorder (PTSD), approximately half of patients do not respond to CBT. No studies have investigated the capacity for neural responses during fear processing to predict treatment response in PTSD.Method. Functional magnetic resonance imaging (fMRI) responses of the brain were examined in individuals with PTSD (n=14). fMRI was examined in response to fearful and neutral facial expressions presented rapidly in a backwards masking paradigm adapted for a 1.5 T scanner. Patients then received eight sessions of CBT that comprised education, imaginal and in vivo exposure, and cognitive therapy. Treatment response was assessed 6 months after therapy completion.Results. Seven patients were treatment responders (defined as a reduction of 50 % of pretreatment scores) and seven were non-responders. Poor improvement after treatment was associated with greater bilateral amygdala and ventral anterior cingulate activation in response to masked fearful faces.Conclusions. Excessive fear responses in response to fear-eliciting stimuli may be a key factor in limiting responses to CBT for PTSD. This excessive amygdala response to fear may reflect difficulty in managing anxiety reactions elicited during CBT, and this factor may limit optimal response to therapy.
OBJECTIVE -To examine associations between measures of diabetes and risk of fracture in a population-based sample of older Australians.RESEARCH DESIGN AND METHODS -This was a prospective study of 3,654 subjects aged 49 years and older who were residents in the Blue Mountains, west of Sydney, Australia. At baseline, subjects were asked questions about history and treatment of diabetes, and fasting blood samples were taken. Photographs were taken of the retina and lens to grade retinopathy and cataract. Details of fractures (excluding rib and vertebral fractures) were collected by a combination of self-report and medical record searches; all fractures were radiologically confirmed.RESULTS -After 2 years of follow-up, we found that several diabetes-related factors were significantly associated (in multivariate models) with increased risk of all fractures combined, including presence of diabetic retinopathy (adjusted RR 5.4, 95% CI 2.7-10.8), diabetes duration Ն10 years (3.3, 1.3-8.2), cortical cataract involving Ն25% of the lens area (2.5, 1.3-4.7), and insulin treatment (5.9, 2.6 -13.5). The proximal humerus was the only individual fracture site associated with diabetes. Diabetic retinopathy (10.3, 2.2-48.0), diabetes duration (for Ն10 years duration; 11.4, 2.4 -54.2), and insulin treatment (18.8, 4.0 -88.7) were all associated with proximal humerus fracture.CONCLUSIONS -These data suggest a significantly increased risk of fracture associated with diabetic retinopathy, advanced cortical cataract, longer diabetes duration, and insulin treatment. However, there are some shortcomings in this study that may limit these findings.
Biological models of posttraumatic stress disorder (PTSD) suggest that patients will display heightened amygdala but decreased medial prefrontal activity during processing of fear stimuli. However, a rapid and automatic alerting mechanism for responding to nonconscious signals of fear suggests that PTSD may display heightened rather than decreased MPFC under nonconscious processing of fear stimuli. This study used functional magnetic resonance imaging to examine blood oxygenation level-dependent signal changes during nonconscious presentation (16.7 ms, masked) of fearful and neutral faces in 15 participants with PTSD and 15 age and sex-matched healthy control participants. Results indicate that PTSD participants display increased amygdala and MPFC activity during nonconscious processing of fearful faces. These data extend existing models by suggesting that the impaired MPFC activation in PTSD may be limited to conscious fear processing. Hum Brain Mapp, 2008. (c) 2007 Wiley-Liss, Inc.
This detailed clinical reference dataset will greatly facilitate diagnostic confirmation and management of patients, and has provided important insights into disease pathogenesis. Ann Neurol 2018;83:1105-1124.
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