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Mobile health (mHealth) apps have the potential to enhance pain management through the use of daily diaries, medication and appointment reminders, education, and facilitating communication between patients and providers. Although many pain management apps exist, the extent to which these apps utilize evidence-based behavior change techniques (BCTs) remains largely unknown, making it nearly impossible for providers to recommend apps with evidence-based strategies. The present study systematically evaluated commercially available pain management apps for evidence-based BCTs and app quality. Pain management apps were identified using the search terms "pain" and "pain management" in the App and Google Play Stores. Reviewed apps were specific to pain management, in English, for patients, and free. A total of 28 apps were coded using the taxonomy of BCTs. App quality was assessed using the Mobile App Rating Scale (MARS). Apps included 2-15 BCTs (M=7.36) and 1-8 (M=4.21) pain management specific BCTs. Prompt intention formation, instruction, behavioral-health link, consequences, feedback, and self-monitoring were the most common BCTs used in the reviewed apps. App quality from the MARS ranged from 2.27-4.54 (M=3.65) out of a possible 5 with higher scores indicating better quality. PainScale followed by Migraine Buddy demonstrated the highest number of overall and pain management BCTs as well as good quality scores. Although existing apps should be assessed through RCTs and future apps should include capabilities for electronic medical record integration, current pain management apps often use evidence-based pain management BCTs.
Learn More >After traumatic brain injury (TBI), a host of symptoms of varying severity and associated functional impairment may occur. One of the most commonly encountered and challenging to treat are the post-traumatic cephalalgias. Post-traumatic cephalalgia (PTC) or headache is often conceptualized as a single entity as currently classified using the ICHD-3. Yet, the terminology applicable to the major primary, non-traumatic, headache disorders such as migraine, tension headache, and cervicogenic headache are often used to specify the specific type of headache the patients experiences seemingly disparate from the unitary definition of post-traumatic headache adopted by ICHD-3. More complex post-traumatic presentations attributable to brain injury as well as other headache conditions are important to consider as well as other causes such as medication overuse headache and medication induced headache. Treatment of any post-traumatic cephalalgia must be optimized by understanding that there may be more than one headache pain generator, that comorbid traumatic problems may contribute to the pain presentation and that pre-existing conditions could impact both symptom complaint, clinical presentation and recovery. Any treatment for PTC must harmonize with ongoing medical and psychosocial aspects of recovery.
Learn More >Recent guidance from the US Immigration and Customs Enforcement drastically altered the lives of international students in America, especially those who are matriculating. This commentary describes how international students still face uncertainty concerning their visa statuses and their place in American society.
Learn More >Patients with classic trigeminal neuralgia (CTN) have abnormalities in white matter integrity of the corpus callosum (CC). However, in CTN patients, it is unclear whether the CC substructure region is affected to varying degrees.
Learn More >The aim of this investigation was to evaluate the effects of local anaesthesia on nerve growth factor (NGF) induced masseter hyperalgesia. Healthy participants randomly received an injection into the right masseter muscle of either isotonic saline (IS) given as a single injection (n = 15) or an injection of NGF (n = 30) followed by a second injection of lidocaine (NGF + lidocaine; n = 15) or IS (NGF + IS; n = 15) in the same muscle 48 h later. Mechanical sensitivity scores of the right and left masseter, referred sensations and jaw pain intensity and jaw function were assessed at baseline, 48 h after the first injection, 5 min after the second injection and 72 h after the first injection. NGF caused significant jaw pain evoked by chewing at 48 and 72 h after the first injection when compared to the IS group, but without significant differences between the NGF + lidocaine and NGF + IS groups. However, the mechanical sensitivity of the right masseter 5 min after the second injection in the NGF + lidocaine group was significantly lower than the second injection in the NGF + IS and was similar to the IS group. There were no significant differences for the referred sensations. Local anaesthetics may provide relevant information regarding the contribution of peripheral mechanisms in the maintenance of persistent musculoskeletal pain.
Learn More >Clinical guidelines recommend that healthcare providers assist children to understand their experience of persistent pain, with pain science education a key component of clinical management in pediatric pain clinics. Currently, no tool exists to assess a child's concept of pain. The aim of this study was to develop such a tool and to evaluate its psychometric properties.
Learn More >High risks of falls have been reported in older adults with chronic pain but chronic pain similarly affects adults of all ages. This cross-sectional study aimed to determine the prevalence of falls and associated risk factors in adults of all ages living with chronic pain.
Learn More >To demonstrate that calcitonin gene-related peptide (CGRP) induces headache exacerbation with migraine-like features in patients with persistent post-traumatic headache (PTH) attributed to mild traumatic brain injury (TBI).
Learn More >Activation of nociceptor sensory neurons by noxious stimuli both triggers pain and increases capillary permeability and blood flow to produce neurogenic inflammation, but whether nociceptors also interact with the immune system remains poorly understood. Here we report a neurotechnology for selective epineural optogenetic neuromodulation of nociceptors and demonstrate that nociceptor activation drives both protective pain behavior and inflammation. The wireless optoelectronic system consists of sub-millimeter-scale light-emitting diodes embedded in a soft, circumneural sciatic nerve implant, powered and driven by a miniaturized head-mounted control unit. Photostimulation of axons in freely moving mice that express channelrhodopsin only in nociceptors resulted in behaviors characteristic of pain, reflecting orthodromic input to the spinal cord. It also led to immune reactions in the skin in the absence of inflammation and potentiation of established inflammation, a consequence of the antidromic activation of nociceptor peripheral terminals. These results reveal a link between nociceptors and immune cells, which might have implications for the treatment of inflammation.
Learn More >As one of the thalamic midline nuclei, the thalamic paraventricular nucleus (PVT) is considered to be an important signal integration site for many descending and ascending pathways that modulate a variety of behaviors, including feeding, emotions and drug-seeking. A recent study has demonstrated that the PVT is implicated in the acute visceral pain response, but it is unclear whether the PVT plays a critical role in the central processing of chronic pain. Here, we report that the neurons in the posterior portion of the PVT (pPVT) and their downstream pathway are involved in descending nociceptive facilitation regarding the development of neuropathic pain conditions in male rats. Lesions or inhibition of pPVT neurons alleviated mechanical allodynia induced by spared nerve injury (SNI). The excitability of pPVT-central amygdala (CeA) projection neurons was significantly increased in SNI rats. Importantly, selective optogenetic activation of the pPVT-CeA pathway induced obvious mechanical hypersensitivity in naïve rats. In addition, we used rabies virus-based and cell-type-specific retrograde transsynaptic tracing techniques to define a novel neuronal circuit in which glutamatergic neurons in the vlPAG were the target of the pPVT-CeA descending facilitation pathway. Our data suggest that this pPVT-CeA-vlPAG circuit mediates central mechanisms of descending pain facilitation underlying persistent pain conditions.Studies have shown that the interactions between the posterior portion of the thalamic paraventricular nucleus (pPVT) and central amygdala (CeA) play a critical role in pain-related emotional regulation. However, most reports have associated this circuit with fear and anxiety behaviors. Here, an integrative approach of behavioral tests, electrophysiology, and immunohistochemistry was used to advance the novel concept that the pPVT-CeA pathway activation facilitates neuropathic pain processing. Using rabies virus-based and cell-type-specific retrograde transsynaptic tracing techniques, we found that glutamatergic neurons in the vlPAG were the target of the pPVT-CeA pathway. Thus, this study indicates the involvement of a pPVT-CeA-vlPAG pathway in a descending facilitatory mechanism underlying neuropathic pain.
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