Clinical significance of serum S100B levels in neurointensive care

Objective  S100B is viewed as the most promising biomarker for brain damage. It has been proposed that this marker is useful in a Neurointensive Care Unit (NICU) as a monitoring parameter. This study aims to examine the clinical usefulness of daily serum S100B measurements in this setting. Design  Prospective consecutive inclusion of patients. Patients  A total of 79 patients with confirmed or suspected head injury or cerebrovascular insults (CVIs) (based upon patient history, computed tomography (CT) and/or magnetic resonance imaging (MRI) and neurological examination including coma scoring) who required neurointensive care were included in the study. Interventions  Sampling for S100B was performed at admission and daily until patients were discharged from the NICU. S100B measurements were statistically compared to occurrence of secondary complications and outcome according to Glasgow Outcome Scale (GOS), with focus on clinical prediction. Measurements and main results  17 of 79 patients (22%) had secondary neurological complications. Mean S100B levels were found to be an independent parameter associated with these complications (P = 0.03). Mean S100B levels were higher in patients with complications compared to those without on both the complication day (P = 0.033) and the day after (P = 0.015), but not the day prior to the complication (P = 0.62). S100B did not predict secondary neurological complication. Neither mean (P = 0.182) nor peak (P = 0.370) S100B levels were associated with or predicted outcome according to dichotomised GOS. Conclusion  Daily S100B measurements are associated with secondary complications but not to outcome. However, daily S100B levels do not predict secondary complications, which limit the usefulness of this brain biomarker in this setting. This work was performed at the Neurointensive Care Unit at the department of Neurosurgery, Lund University Hospital, Lund, Sweden.     

Different circuits for different pain: patterns of functional connectivity reveal distinct networks for processing pain in self and others

The ability to empathize with the suffering of others is critical for maintaining relationships and engaging in prosocial behavior. Recently, a series of studies have demonstrated that while watching other people experience pain (other pain), participants engage the anterior insula (AI) and anterior cingulate cortex (ACC), brain regions involved in the direct experience of pain (self pain). Here we test the hypothesis that common activity in ACC and AI may reflect the operation of distinct but overlapping networks of regions that support perception of self or other pain. To address this possibility, we scanned participants using fMRI while they received noxious thermal stimulation (self pain) or watched short videos of other people sustaining painful injuries (other pain). We isolated overlapping regions for self and other pain in the ACC and AI and then used them as seed regions for two kinds of functional connectivity analyses. These analyses identified areas whose activity co-varied with ACC and AI activity during self or other pain either across time (intra-individual connectivity) or across participants (inter-individual connectivity). Both connectivity analyses identified clusters in the midbrain and periaqueductal gray with greater connectivity to the AI during self pain as opposed to other pain. The opposite pattern was found in the dorsal medial prefrontal cortex, that showed greater connectivity to the ACC and AI during other pain than during self pain using both types of analysis. Intra-individual connectivity analyses also revealed regions in the superior temporal sulcus, posterior cingulate, and precuneus that became more connected to ACC during other pain as compared to self pain. Together, these data demonstrated that regions showing similar activity during self and other pain may nonetheless be part of distinct functional networks. These networks could not have been detected in prior work that examined overlap between self and other pain in terms of average activity, but not connectivity.     

S100 proteins calprotectin and S100A12 are related to radiographic changes rather than disease activity in psoriatic arthritis with low disease activity

OBJECTIVE: To investigate serum levels of calprotectin (S100A8/S100A9) and S100A12 as markers of disease activity or distinct clinical or radiographic features in patients with psoriatic arthritis (PsA). METHODS: Serum levels of calprotectin and S100A12, erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP) were determined in 119 patients with PsA. Correlations to clinical variables were calculated, and subgroups of patients were compared. RESULTS: The correlations to clinical disease activity measures were stronger for CRP than for ESR and calprotectin. In the regression analysis, calprotectin was identified as an independently associated factor for presence of peripheral radiographic features of arthritis (OR 1.33, 95% CI 1.01-1.76). S100A12 levels were also elevated in those with peripheral radiographic features (p = 0.036), but did not correlate with clinical variables of disease activity. CONCLUSION: Calprotectin and S100A12 do not perform better than traditional biomarkers of disease activity in PsA, but were associated with presence of peripheral radiographic features in this cross-sectional study. The patients' low level of disease activity may have led to underestimation of the associations between any biomarker and disease measures.     

Placebo effects on human mu-opioid activity during pain

Placebo-induced expectancies have been shown to decrease pain in a manner reversible by opioid antagonists, but little is known about the central brain mechanisms of opioid release during placebo treatment. This study examined placebo effects in pain by using positron-emission tomography with [¹¹C]carfentanil, which measures regional μ-opioid receptor availability in vivo. Noxious thermal stimulation was applied at the same temperature for placebo and control conditions. Placebo treatment affected endogenous opioid activity in a number of predicted μ-opioid receptor-rich regions that play central roles in pain and affect, including periaqueductal gray and nearby dorsal raphe and nucleus cuneiformis, amygdala, orbitofrontal cortex, insula, rostral anterior cingulate, and lateral prefrontal cortex. These regions appeared to be subdivided into two sets, one showing placebo-induced opioid activation specific to noxious heat and the other showing placebo-induced opioid reduction during warm stimulation in anticipation of pain. These findings suggest that a mechanism of placebo analgesia is the potentiation of endogenous opioid responses to noxious stimuli. Opioid activity in many of these regions was correlated with placebo effects in reported pain. Connectivity analyses on individual differences in endogenous opioid system activity revealed that placebo treatment increased functional connectivity between the periaqueductal gray and rostral anterior cingulate, as hypothesized a priori, and also increased connectivity among a number of limbic and prefrontal regions, suggesting increased functional integration of opioid responses. Overall, the results suggest that endogenous opioid release in core affective brain regions is an integral part of the mechanism whereby expectancies regulate affective and nociceptive circuits.     

Congenital Ichthyosiform Erythroderma Superimposed with Chronic Dermatophytosis: A Report of Three Siblings

Congenital ichthyosiform erythroderma is an autosomal recessive ichthyosis characterized by severe scaling and erythroderma. We report a family of three siblings who were all born with a collodion membrane and presented with diffuse scaling and pruritus. All three children subsequently developed chronic cutaneous dermatophyte infections requiring oral antifungals. One child developed superinfection with methicillin‐resistant Staphylococcus aureus requiring antibiotics.