Pain and related suffering reduce attention toward others

Background

It has been proposed that the expression of pain-related suffering may lead to an enhanced focus on oneself and reduced attention toward the external world. This study aimed at investigating whether experimentally induced painrelated suffering may lead persons to withdraw into themselves, causing a reduced focus on external stimuli as reflected by impaired performance in a facial recognition task and heightened perception of internal stimuli measured by interoceptive awareness.

Methods

Thirty-two participants had to recognize different emotional facial expressions (neutral, sad, angry, happy), or neutral geometrical figures under conditions of no pain, low, and high prolonged pain intensities. Interoceptive accuracy was measured using a heartbeat-detection task prior to and following the pain protocol.

Results

Males but not females were slower to recognize facial expressions under the condition of high painful stimulation compared to the condition of no pain. In both, male and female participants, the difficulty in recognizing another person's emotions from a facial expression was directly related to the level of suffering and unpleasantness experienced during pain. Interoceptive accuracy was higher after the pain experiment. However, neither the initial interoceptive accuracy nor the change were significantly related to the pain ratings.

Conclusions

Our results suggest that long-lasting and intense painful stimuli, which induce suffering, lead to attentional shifts leading to withdrawal from others. These findings contribute to a better understanding of the social dynamics of pain and pain-related suffering.     

Intracystic Gadolinium‐Enhanced MRI in the Evaluation of Residual Giant‐Cystic Craniopharyngiomas in Children: Report of Four Cases

Residual giant‐cystic craniopharyngiomas are amenable to intracavitary bleomycin treatment. Radiologic identification of potential cyst leaks is of paramount for treatment decisions. This report describes our experience in the use of intracystic Gadolinium (Gd)‐enhanced MR imaging to determine potential communications between the tumoral cysts and other intra‐axial spaces in 4 pediatric patients with residual giant‐cystic craniopharyngiomas in whom intracavitary bleomycin treatment was planned after the injection of .1‐.2 mL of gadopentetate dimeglumine (Gd‐DTPA). In three cases no leaks were found. In one case, whose previous water‐soluble iodinated contrast‐enhanced CT cystography was negative for leaks, intracystic Gd‐enhanced MR showed intraventricular Gd enhancement. We conclude that MR imaging after intracystic administration of Gd‐based contrast paramagnetic agents is useful in the detection of potential leaks in cases of giant residual craniopharyngiomas.     

Sensory stimulus‐sensitive drop attacks and basal ganglia calcification: new findings in a patient with FOLR1 deficiency

Loss‐of‐function mutations in the FOLR1 gene (MIM *136430), encoding the folate receptor alpha, impair cerebral folate transport and lead to a progressive neurometabolic disorder. We report on a 5‐year‐old boy with progressive ataxia, from the age of 2 years and 6 months, with myoclonic jerks, regression, and impressive myoclonic tonic spasms with drop attacks, which were partially provoked by touching his face or washing his hands. Delayed myelination and cerebellar atrophy on cranial MRI were important clues to the diagnosis of cerebral folate transport deficiency, which was confirmed by homozygosity for the known nonsense mutation p.R204X in the FOLR1 gene. Computed tomography taken after head injury revealed bilateral calcifications in the basal ganglia as a novel finding in a patient with FOLR1 mutation. [Published with video sequences]     

The longitudinal and interactive effects of HIV status,stimulant use,and host genotype upon neurocognitive functioning

Both human immunodeficiency virus (HIV)-1 infection and illicit stimulant use can adversely impact neurocognitive functioning, and these effects can be additive. However, significant variability exists such that as-of-yet unidentified exogenous and endogenous factors affect one’s risk for neurocognitive impairment. Literature on both HIV and stimulant use indicates that host genetic variants in immunologic and dopamine-related genes are one such factor. In this study, the individual and interactive effects of HIV status, stimulant use, and genotype upon neurocognitive functioning were examined longitudinally over a 10-year period. Nine hundred fifty-two Caucasian HIV+ and HIV? cases from the Multicenter AIDS Cohort Study were included. All cases had at least two comprehensive neurocognitive evaluations between 1985 and 1995. Pre-highly active antiretroviral therapy (HAART) data were examined in order to avoid the confounding effect of variable drug regimens. Linear mixed models were used, with neurocognitive domain scores as the outcome variables. No four-way interactions were found, indicating that HIV and stimulant use do not interact over time to affect neurocognitive functioning as a function of genotype. Multiple three-way interactions were found that involved genotype and HIV status. All immunologically related genes found to interact with HIV status affected neurocognitive functioning in the expected direction; however, only C-C chemokine ligand 2 (CCL2) and CCL3 affected HIV+ individuals specifically. Dopamine-related genetic variants generally affected HIV-negative individuals only. Neurocognitive functioning among HIV+ individuals who also used stimulants was not significantly different from those who did not use stimulants. The findings support the role of immunologically related genetic differences in CCL2 and CCL3 in neurocognitive functioning among HIV+ individuals; however, their impact is minor. Being consistent with findings from another cohort, dopamine (DA)-related genetic differences do not appear to impact the longitudinal neurocognitive functioning of HIV+ individuals.     

Founder effect and ancestral origin of the spinocerebellar ataxia type 7 (SCA7) mutation in Mexican families

Spinocerebellar ataxia type 7 (SCA7) is an autosomal dominant disease characterized by progressive cerebellar ataxia and macular degeneration causing progressive blindness. It accounts for 1 to 11.6 % of spinocerebellar ataxias (SCAs) cases worldwide and for 7.4 % of SCA7 cases in Mexico. We identified a cluster of SCA7 families who resided in a circumscribed area of Veracruz and investigated whether the high incidence of the disease in this region was due to a founder effect. A total of 181 individuals from 20 families were studied. Four microsatellite markers and one SNP flanking the ATNX7 gene were genotyped and the ancestral origin and local ancestry analysis of the SCA7 mutation were evaluated. Ninety individuals from 19 families had the SCA7 mutation; all were found to share a common haplotype, suggesting that the mutation in these families originated from a common ancestor. Ancestral origin and local ancestry analysis of SCA7 showed that the chromosomal segment containing the mutation was of European origin. We here present evidence strongly suggesting that the high frequency of SCA7 in Veracruz is due to a founder effect and that the mutation is most likely of European origin with greatest resemblance to the Finnish population.     

Combined PTSD and depressive symptoms interact with post-deployment social support to predict suicidal ideation in Operation Enduring Freedom and Operation Iraqi Freedom veterans

Rates of suicide are alarmingly high in military and veteran samples. Suicide rates are particularly elevated among those with post-traumatic stress disorder (PTSD) and depression, which share overlapping symptoms and frequently co-occur. Identifying and confirming factors that reduce, suicide risk among veterans with PTSD and depression is imperative. The proposed study evaluated, whether post-deployment social support moderated the influence of PTSD–depression symptoms on, suicidal ideation among Veterans returning from Iraq and Afghanistan using state of the art clinical, diagnostic interviews and self-report measures. Operations Enduring and Iraqi Freedom (OEF/OIF) Veterans (n=145) were invited to, participate in a study evaluating returning Veterans? experiences. As predicted, PTSD–depression, symptoms had almost no effect on suicidal ideation (SI) when post-deployment social support was high; however, when, post-deployment social support was low, PTSD–depression symptoms were positively associated with, SI. Thus, social support may be an important factor for clinicians to assess in the context of PTSD and, depressive symptoms. Future research is needed to prospectively examine the inter-relationship, between PTSD/depression and social support on suicidal risk, as well as whether interventions to, improve social support result in decreased suicidality.     

Longitudinal features of stir bright signal in FSHD1

Introduction: Magnetic resonance imaging of muscle shows short tau‐inversion recovery (STIR) brightness in autosomal dominant facioscapulohumeral muscular dystrophy (FSHD1) suggestive of active inflammation/injury. We measured the longitudinal stability/progression of this potential disease biomarker. Methods: Nine subjects underwent calf MRI imaging over 2 years. Two radiologists evaluated qualitative muscle changes. Results: In 3/9 subjects, calf muscles demonstrated moderate/severe STIR hyperintensity at Time 1 that had progressed to fatty replacement 2 years later (Time 2). In the remaining subjects, moderate/severe muscle STIR abnormalities, when present, were consistent between exams. Mild STIR+ elevations had roughly similar patterns between exams. Conclusions: Moderate/severe STIR hyperintensities often foreshadow fatty replacement over a 2‐year interval. Whether longer time courses are required to observe muscle degeneration and fatty replacement in some subjects remains to be explored. Muscle Nerve 49 : 257–260, 2014     

MRI findings of intracranial anomalies associated with cephalocele—a case series

Introduction

Cephalocele is a relatively rare cranial dysraphism characterised by herniation of intracranial structures through the skull. Surgical management is primarily necessary where a risk of infection through communication of the lesion with the intracranial space exists, a risk of rupture, or for cosmetic purposes. Cephalocele is often associated with venous anomalies such as vertical embryonic positioning of the straight sinus, splitting of the superior sagittal sinus, vein of Galen elongation, along with tenting of the tentorium [Morioka et al. Childs Nerv Syst 25:309–315, 2009]

Patients

Here, we report four cases of cephalocele with pre-operative MRI imaging retrospectively studied, demonstrating associated venous anomalies. Three of these patients went on to have uncomplicated, corrective surgery, while one was managed conservatively.

Results

All four cases demonstrated the main venous drainage going through a persistent falcine sinus to drain into the superior sagittal sinus. Upward tenting of the tentorium was observed in three cases (cases 1, 3 and 4). Two of our cases demonstrated other venous anomalies frequently reported in the literature, namely splitting of the superior sagittal sinus and absence of the transverse sinus (case 1) and communication of the cephalocele with the superior sagittal sinus and absence of the straight sinus (case 2).

Conclusion

The association between cephalocele and venous anomalies suggests that pre-operative MRI should be mandatory for a full evaluation of a suspicious midline cranial lesion in order to evaluate the safety of corrective surgery.     

How Tough Is Brittle Bone? Investigating Osteogenesis Imperfecta in Mouse Bone

The multiscale hierarchical structure of bone is naturally optimized to resist fractures. In osteogenesis imperfecta, or brittle bone disease, genetic mutations affect the quality and/or quantity of collagen, dramatically increasing bone fracture risk. Here we reveal how the collagen defect results in bone fragility in a mouse model of osteogenesis imperfecta (oim), which has homotrimeric α1(I) collagen. At the molecular level, we attribute the loss in toughness to a decrease in the stabilizing enzymatic cross‐links and an increase in nonenzymatic cross‐links, which may break prematurely, inhibiting plasticity. At the tissue level, high vascular canal density reduces the stable crack growth, and extensive woven bone limits the crack‐deflection toughening during crack growth. This demonstrates how modifications at the bone molecular level have ramifications at larger length scales affecting the overall mechanical integrity of the bone; thus, treatment strategies have to address multiscale properties in order to regain bone toughness. In this regard, findings from the heterozygous oim bone, where defective as well as normal collagen are present, suggest that increasing the quantity of healthy collagen in these bones helps to recover toughness at the multiple length scales. © 2014 American Society for Bone and Mineral Research.