Synopsis Pain is a common complaint among clients seeking physical therapy services, yet interpretation of associated sensory changes can be difficult for the clinician. Musculoskeletal injury typically results in nociceptive pain due to noxious stimuli of the damaged muscle or joint tissues. However, with progression from acute to chronic stages, altered nociceptive processing can give rise to an array of sensory findings. Specifically, patients with chronic joint injury may present with signs and symptoms typically associated with neuropathic injury, due to changes in nociceptive processing. Clinical presentation may include expansion of hyperalgesia into adjacent and remote areas, allodynia, dysesthesias, and perceptual deficits. Quantitative sensory testing (QST) may provide an objective method of examining sensation and, thereby, of recognizing potential changes in the nociceptive pathways. The purpose of this paper is to provide an overview of altered nociceptive processing and somatosensory changes that may occur following a musculoskeletal injury without associated neural injury. Recommendations are made on clinical uses of quantitative sensory testing in orthopaedic physical therapy practice, and supporting clinical and laboratory evidence are presented. Examples related to joint injury are discussed, specifically, osteoarthritis of the knee and low back pain. Quantitative sensory testing may be a useful clinical tool to aid clinical decision making and for determination of prognosis. J Orthop Sports Phys Ther 2010;40(12):818–825. doi:10.2519/jospt.2010.3314

Pain is a major cause of impaired mobility in elderly patients with chronic osteoarthritis (OA) of the knee. Central sensitization and impaired nociceptive inhibitory mechanisms have both been identified as contributing factors to heightened pain in this patient population. While central sensitization has been shown to produce enhanced pain responses and spread of pain to adjacent and remote body regions, conditioned pain modulation has also been shown to be adversely affected, and may be characteristic of those patients with chronic pain. Alterations of quantitative sensory testing measures have been demonstrated in patients with knee OA, and may serve as a clinical means of staging chronic musculoskeletal pain, including assessment of hyperalgesia and hypoesthesia. In addition, pain and altered somatosensation commonly associated with OA may be correlated with functional deficits.

The Mexican artist Frida Kahlo (1907-1954) is one of the most celebrated artists of the 20th century. Although famous for her colorful self-portraits and associations with celebrities Diego Rivera and Leon Trotsky, less known is the fact that she had lifelong chronic pain. Frida Kahlo developed poliomyelitis at age 6 years, was in a horrific trolley car accident in her teens, and would eventually endure numerous failed spinal surgeries and, ultimately, limb amputation. She endured several physical, emotional, and psychological traumas in her lifetime, yet through her art, she was able to transcend a life of pain and disability. Of her work, her self-portraits are conspicuous in their capacity to convey her life experience, much of which was imbued with chronic pain. Signs and symptoms of chronic neuropathic pain and central sensitization of nociceptive pathways are evident when analyzing her paintings and medical history. This article uses a narrative approach to describe how events in the life of this artist contributed to her chronic pain. The purpose of this article is to discuss Frida Kahlo's medical history and her art from a modern pain sciences perspective, and perhaps to increase our understanding of the pain experience from the patient's perspective.