Sherree Geyer

Physically active adolescents appear to handle exercise-related pain better than inactive adolescents, a study found.

The first study to determine adolescent pain relief after high-intensity aerobic exercise concludes “greater reduction in response to a pain stimulus” may result among physically-active individuals. “

Pain Response after Maximal Aerobic Exercise in Adolescents across Weight Status

,” published recently by the American College of Sports Medicine, reports similar rates of exercise-induced hypoalgesia (EIH) among normal- and over-weight/obese adolescents.

Lead author Stacy C. Stolzman—MPT and PhD student, department of physical therapy, Marquette University, Milwaukee&mdash;and her team assessed 62 adolescents, including 29 males and 33 females, using pressure pain thresholds (PPTs) before and after quiet rest; and pain questionnaires. Accelerometers and self-reports measured physical activity and a dual-energy x-ray absorptiometry, body composition.

The study found “no differences between the fit and unfit group for the adolescent’s clinical pain and child’s or parent’s perspectives for pain catastrophizing (negative mental response to anticipated or actual pain).” Fit adolescents, who comprised 75 percent of study participants, showed lower body mass indices and shorter “sedentary bouts” than their unfit counterparts, it adds.

The study calls physical inactivity “a major contributor” to the obesity epidemic and its associated increased pain. “Unfortunately, pain is commonly overlooked as a health outcome, despite most obese youth reporting they currently feel pain,” it states.

Researchers suggest an expanded population sample with more distinct weight groups, saying “These results significantly add to the literature by providing much needed evidence in the prescription of therapeutic exercise as a pain management tool for adolescents of varying weight and fitness levels. Additional pediatric research is warranted in identifying the effect of weight status on pain perception at rest and after exercise with multiple stages of obesity and community-based versus clinically based populations,” it adds.

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Fit Teens Manage Pain Better, Study Finds

Anesthesia can cause brain injury in infants, but so far such damage it is difficult to detect. A George Washington University team says it may have found a way to do that by examining a patient's retina.

While other retrospective studies associate having anesthesia with the later appearance of cognitive and behavioral disorders in young children, this one indicates that what happens in the retina of the eye reflects what happens in the brain.

In a murine study, Richard J. Levy, MD, of the division of anesthesiology and pain medicine, Children’s National Medical Center, The George Washington University School of Medicine and Health Sciences, Washington, DC, and colleagues investigated the effects of isoflurane exposure on the retinas of mice pups.

Half of the animals were exposed to isoflurane for an hour and the other half breathed room air. 

After the exposure, they looked at the animals' retinas to see how much activated caspase-3, capase-9, and caspase-8 were present.They also looked at cytochrome c release from retinal mitochondria, and the number and types of cells undergoing apoptosis. 

in the inner nuclear layer (INL) and activated both the intrinsic and extrinsic pathways in the ganglion cell layer. Immunofluorescence demonstrated that bipolar and amacrine neurons within the INL underwent physiologic cell death in both cohorts and that amacrine cells were the likely targets of isoflurane-induced apoptosis. After injection, fluorescent-labeled annexin V was readily detected in the INL of both air-exposed and isoflurane-exposed mice and co-localized with activated caspase-3-positive cells.

They found  that isoflurane activated the intrinsic apoptosis pathway

"These findings indicate that isoflurane-induced neuronal apoptosis occurs in the developing retina and lays the groundwork for development of a noninvasive imaging technique to detect anesthesia-induced neurotoxicity in infants and children," they concluded.  

Anesthesia-Induced Neuronal Apoptosis in the Developing Retina: A Window of Opportunity

“Because the retina provides a window to the central nervous  and can be imaged noninvasively, our findings create an opportunity to explore anesthesia-induced neuronal degeneration in the developing retina as a potential surrogate for neurotoxicity in the brain. Ultimately, we may be able to develop a noninvasive imaging modality to determine whether anesthesia-induced neuronal apoptosis occurs in infants and children,” the team concludes.

Anesthesia can cause brain injury in infants, but so far such damage is difficult to immediately detect. A George Washington University team says it may have found a way to do that by examining a patient's retina.

Retina Can Reflect Anesthesia Injury in Infants

Total hip arthroplasty (THA) reduces use of analgesics, hypnotics and anxiolytics to extend the positive effects of surgery according to a Norwegian study of pre- and post-operative prescription trends in the Nov. 14 issue of 

Tone Blågestad of the department of clinical psychology, University of Bergen, Norway and lead author of “

Prescription trajectories and effect of total hip arthroplasty on the use of analgesics, hypnotics, antidepressants and anxiolytics: Results from a population of total hip arthroplasty patient

s”— used merged data from the Norwegian Prescription Database and Norwegian Arthroplasty Register to examine redeemed medications in a complete population undergoing THA between 2005 and 2011.

Divided data into eight quarters—four (Q1-Q4) before and four (Q5-Q8) after surgery&mdash; Blågestad and the team analyzed use of non-steroid anti-inflammatory drugs (NSAIDs), opioids, non-opioids and psychotropics over the two-year period.

Almost 50 percent (49.3) of the study population took at least one analgesic drug with nearly 38 percent receiving NSAIDs, 16.3 percent opioids and 12.4 percent non-opioids, they found. “Use of opioids, non-opioids and hypnotics dramatically increased from Q4 to Q5,” they wrote.

“Hypnotic use follows the same prescription trajectory as analgesics, supporting the link between pain and sleep,” the authors noted, adding that narcotics “disrupt sleep architecture and increased the need for hypnotics, post-surgically.

“Long-term (Q4 vs. Q8), surgery reduced prescriptions of analgesics, hypnotics and anxiolytics, but not anti-depressants. Overall, the study results extend the positive effects of THA to include reduced reliance on medication to alleviate symptoms,” they concluded.

Total hip arthroplasty (THA) reduces use of analgesics, hypnotics and anxiolytics to extend the positive effects of surgery according to a Norwegian study of pre- and post-operative prescription trends in the Nov. 14 issue of Pain.

Fewer Pain Meds after Hip Arthroplasty

Eliminating RGS7, a brain protein inhibitor, enhanced reward behavior, analgesic effect and withdrawal response and delayed tolerance according to “

Regulator of G-Protein Signaling 7 Regulates Reward Behavior by Controlling Opioid Signaling in the Striatum

,” published ahead of print in August in 

. Dissecting central-specific actions, lead author Laurie P. Sutton—Ph.D, The Scripps Research Institute, Jupiter, Fla.&mdash;and her team ascertained that RGS7 may regulate morphine behavior through nucleus accumbens neurons.

Morphine, part of the G-protein-coupled receptors family, mediates euphoria and analgesia through the u-opiod receptor. Methods to assess analgesia, tolerance and physical dependence included conditioned place preference and self-administration paradigms. Electrophysiology determined RGS7’s influence on morphine-induced neuronal excitability and glutamatergic synapses.

Genetic approaches to ablate G-protein signaling of RGS7, globally and in specific neuronal populations, developed an “encompassing model,” which suggests multiple synaptic mechanisms contribute to morphine-mediated reward behavior, notes the study. Dissociating circuit-specific action, gave “a better understanding of the molecular mechanism involved in diverse actions of morphine use,” it adds.

Researchers call RGS7 in striatal neurons “selectively responsible for rewarding and reinforcing behaviors to morphine without effecting analgesia, tolerance and withdrawal.” RGS7 deletion in dopaminergic neurons didn’t influence morphine reward, they say. G-protein signaling may regulate GPCR, they add.

New clues on morphine behavior hold promise for withdrawal treatment. 

Sherree Geyer

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