Facial Expression Overrides Lumbopelvic Kinematics for Clinical Judgements about Low Back Pain Intensity.

Background. Through real-time behavioral observation systems, pain behaviors are commonly used by clinicians to estimate pain intensity in patients with low back pain. However, little is known about how clinicians rely on pain-related behaviors to make their judgment. According to the Information Integration Theory (IIT) framework, this study aimed at investigating how clinicians value and integrate information from lumbopelvic kinematics (LK), a protective pain behavior, and facial expression intensity (FEI), a communicative pain behavior, to estimate pain in patients with chronic low back pain (cLBP). Methods. Twenty-one experienced clinicians and twenty-one novice clinicians were asked to estimate back pain intensity from a virtual character performing a trunk flexion-extension task. Results. Results revealed that both populations relied on facial expression and that only half of the participants in each group integrated FEI and LK to estimate cLBP intensity. Among participants who integrated the two pain behaviors, averaging rule predominated among others. Results showed that experienced clinicians relied equally on FEI and LK to estimate pain, whereas novice clinicians mostly relied on FEI. Discussion. The use of additive rule of integration does not appear to be systematic when assessing others' pain. When assessing pain intensity, communicative and protective pain behaviors may have different relevance.

Perceptual weighting of pain behaviours of others, not information integration, varies with expertise.

BACKGROUND: Being able to estimate effort pain in patients is important for health care providers working in physical rehabilitation services. Previous studies have shown that clinicians and physiotherapists underestimate patients' pain. METHODS: The present study examined how two sources of visual information, namely body kinematics (movement speed and postural constraints) and facial expressions are integrated in order to estimate effort pain magnitude experienced by a paraplegic person performing a sitting pivot transfer. In addition, the effect of familiarity with paraplegia on judgment was assessed by comparing performance among physiotherapists, paraplegic patients and unfamiliar participants. Functional measurement was used to determine the psychophysical law of visual information integration carried by pain behaviours (guarding and facial expression). RESULTS: Results indicate that guarding behaviour (specified by movement speed) carried important information for perceived effort pain independently of familiarity. In contrast, facial expression of pain was relevant only to unfamiliar and physiotherapist participants and not to paraplegic participants. Even if physiotherapists underestimated effort pain as compared to the other groups, they relied more strongly on facial expression, than other participants, in their estimation of effort pain expressed by a paraplegic patient. CONCLUSIONS: These results bring further insights into understanding physiotherapists' perception of patients' pain. In order to improve their ability to adapt the difficulty of the rehabilitation sessions, they should learn to raise their global level of pain magnitude estimation (for example, by performing themselves the body movement) instead of overweighting facial pain expression signals.

14-3-3-regulated Ca(2+)-dependent protein kinase CPK3 is required for sphingolipid-induced cell death in Arabidopsis.

In eukaryotic cells, sphingoid long chain bases (LCBs) such as sphingosine or phytosphingosine (PHS) behave as second messengers involved in various processes including programmed cell death (PCD). In plants, induction of PCD by LCBs has now been described, but the signalling pathway is still enigmatic. Using Arabidopsis, we identify new key steps in this pathway. We demonstrate that PHS induces activation of the calcium-dependent kinase CPK3, which phosphorylates its binding partners, the 14-3-3 proteins. This phosphorylation leads to the disruption of the complex and to CPK3 degradation. Using cpk3 knockout lines, we demonstrate that CPK3 is a positive regulator of LCB-mediated PCD. These findings establish 14-3-3-regulated CPK3 as a key component of the LCB pathway leading to PCD in plants.