Is Pain in the Uninjured Arm Associated With Unhelpful Thoughts and Distress Regarding Symptoms During Recovery From Upper-Extremity Injury?

PURPOSE: During recovery from upper-extremity injury, patients sometimes express concerns regarding pain associated with increased use of the uninjured limb. Concerns about discomfort associated with increased use may represent a manifestation of unhelpful thoughts such as catastrophic thinking or kinesiophobia. We asked the following questions: (1) Among people recovering from an isolated unilateral upper-extremity injury, is pain intensity in the uninjured arm associated with unhelpful thoughts and feelings of distress regarding symptoms, accounting for other factors? (2) Is pain intensity in the injured extremity, magnitude of capability, or accommodation of pain associated with unhelpful thoughts and feelings of distress regarding symptoms? METHODS: In this cross-sectional study of new or returning patients presenting to a musculoskeletal specialist for care for an upper-extremity injury, the patients completed scales that were used to measure the following: pain intensity in the uninjured arm, pain intensity in the injured arm, upper-extremity-specific magnitude of capability, symptoms of depression, symptoms of health anxiety, catastrophic thinking, and accommodation of pain. Multivariable analysis was used to evaluate factors associated with pain intensity in the uninjured arm, pain intensity in the injured arm, magnitude of capability, and pain accommodation, controlling for other demographic and injury-related factors. RESULTS: Greater pain intensity in both uninjured and injured arms was independently associated with greater unhelpful thinking regarding symptoms. A greater magnitude of capability and pain accommodation were independently associated with less unhelpful thinking regarding symptoms. CONCLUSIONS: Given that greater pain intensity in the uninjured upper extremity is associated with greater unhelpful thinking, clinicians can be attuned to patient concerns about contralateral pain. Clinicians can facilitate recovery from upper-extremity injury by evaluating the uninjured limb as well as identifying and ameliorating unhelpful thinking regarding symptoms. TYPE OF STUDY/LEVEL OF EVIDENCE: Prognostic II.

Asprosin is a centrally acting orexigenic hormone.

Asprosin is a recently discovered fasting-induced hormone that promotes hepatic glucose production. Here we demonstrate that asprosin in the circulation crosses the blood-brain barrier and directly activates orexigenic AgRP+ neurons via a cAMP-dependent pathway. This signaling results in inhibition of downstream anorexigenic proopiomelanocortin (POMC)-positive neurons in a GABA-dependent manner, which then leads to appetite stimulation and a drive to accumulate adiposity and body weight. In humans, a genetic deficiency in asprosin causes a syndrome characterized by low appetite and extreme leanness; this is phenocopied by mice carrying similar mutations and can be fully rescued by asprosin. Furthermore, we found that obese humans and mice had pathologically elevated concentrations of circulating asprosin, and neutralization of asprosin in the blood with a monoclonal antibody reduced appetite and body weight in obese mice, in addition to improving their glycemic profile. Thus, in addition to performing a glucogenic function, asprosin is a centrally acting orexigenic hormone that is a potential therapeutic target in the treatment of both obesity and diabetes.

Asprosin, a Fasting-Induced Glucogenic Protein Hormone.

Hepatic glucose release into the circulation is vital for brain function and survival during periods of fasting and is modulated by an array of hormones that precisely regulate plasma glucose levels. We have identified a fasting-induced protein hormone that modulates hepatic glucose release. It is the C-terminal cleavage product of profibrillin, and we name it Asprosin. Asprosin is secreted by white adipose, circulates at nanomolar levels, and is recruited to the liver, where it activates the G protein-cAMP-PKA pathway, resulting in rapid glucose release into the circulation. Humans and mice with insulin resistance show pathologically elevated plasma asprosin, and its loss of function via immunologic or genetic means has a profound glucose- and insulin-lowering effect secondary to reduced hepatic glucose release. Asprosin represents a glucogenic protein hormone, and therapeutically targeting it may be beneficial in type II diabetes and metabolic syndrome.