Study design: Discussion of issues and development of consensus. Objective: Present the background, purpose, development process, format and definitions of the International Spinal Cord Injury Pain (ISCIP) Classification. Methods: An international group of spinal cord injury (SCI) and pain experts deliberated over 2 days, and then via e-mail communication developed a consensus classification of pain after SCI. The classification was reviewed by members of several professional organizations and their feedback was incorporated. The classification then underwent validation by an international group of clinicians with minimal exposure to the classification, using case study vignettes. Based upon the results of this study, further revisions were made to the ISCIP Classification. Results: An overall structure and terminology has been developed and partially validated as a merger of and improvement on previously published SCI pain classifications, combined with basic definitions proposed by the International Association for the Study of Pain and pain characteristics described in published empiric studies of pain. The classification is designed to be comprehensive and to include pains that are directly related to the SCI pathology as well as pains that are common after SCI but are not necessarily mechanistically related to the SCI itself. Conclusions:The format and definitions presented should help experienced and non-experienced clinicians as well as clinical researchers classify pain after SCI.

Triathletes and ironman triathletes engage in an extremely intense sport that involves hours of considerable pain, as well as physical and psychological stress, every day. The basic pain modulation properties of these athletes has not been established and therefore it is not clear whether they present with unique features that enable them to engage in such efforts. The aim was to investigate the existence of possible alterations in pain perception and modulation of triathletes, as well as possible underlying factors. Participants were 19 triathletes and 17 non-athletes who underwent measurement of pain threshold, pain tolerance, suprathreshold perceived pain intensity, temporal summation of pain, and conditioned pain modulation (CPM). Participants also completed the fear of pain and the pain catastrophizing questionnaires, and rated the amount of perceived stress. Triathletes exhibited higher pain tolerance (P<.0001), lower pain ratings (P<.001), and lower fear of pain values (P<.05) than controls. The magnitude of CPM was significantly greater in triathletes (P<.05), and negatively correlated with fear of pain (P<.05) and with perceived mental stress during training and competition (P<.05). The results suggest that triathletes exhibit greater pain tolerance and more efficient pain modulation than controls, which may underlie their perseverance in extreme physical efforts and pain during training/competitions. This capability may be enhanced or mediated by psychological factors, enabling better coping with fear of pain and mental stress.

Post-traumatic stress disorder (PTSD) often co-occurs with chronic pain. Neither the underlying mechanism of this comorbidity nor the nature of pain perception among subjects with PTSD is well defined. This study is the first systematic and quantitative evaluation of pain perception and chronic pain in subjects with PTSD. The study group consisted of 32 outpatients with combat- and terror-related PTSD, 29 outpatients with anxiety disorder and 20 healthy controls. Quantitative somatosensory testing included the measurement of warm, cold, light touch and heat-pain thresholds and responses to acute suprathreshold heat and mechanical stimuli. Chronic pain was characterized, and levels of PTSD and anxiety symptomatology were assessed by self-report questionnaires. Subjects with PTSD exhibited higher rates of chronic pain, more intense chronic pain and more painful body regions compared with the other two groups. PTSD severity correlated with chronic pain severity. Thresholds of subjects with PTSD were significantly higher than those of subjects with anxiety and healthy controls, but they perceived suprathreshold stimuli as being much more intense than the other two groups. These results suggest that subjects with PTSD exhibit an intense and widespread chronic pain and a unique sensory profile of hyposensitivity to pain accompanied by hyper-reactivity to suprathreshold noxious stimuli. These features may be attributed to the manner with which PTSD subjects emotionally interpret and respond to painful stimuli. Alternatively, but not mutually exclusive, the findings may reflect altered sensory processing among these subjects.

Central pain below the injury level after spinal cord injury is excruciating, chronic and resistive to treatment. Animal studies suggest that pretreatment may prevent central pain, but to date there are no measures to predict its development. Our aim was to monitor changes in the sensory profile below the lesion prior to the development of below-level central pain in order to search for a parameter that could predict its risk and to further explore its pathophysiology. Thirty patients with spinal cord injury and 27 healthy controls underwent measurement of warm, cold, heat-pain and touch thresholds as well as graphaesthesia, allodynia, hyperpathia and wind-up pain in intact region and in the shin and feet (below level). Patients were tested at 2-4 weeks, 1-2.5 months and 2.5-6 months after the injury or until central pain had developed. At the end of the follow-up, 46% of patients developed below-level central pain. During the testing periods, individuals who eventually developed central pain had higher thermal thresholds than those who did not and displayed high rates of abnormal sensations (allodynia and hyperpathia), which gradually increased with time until central pain developed. Logistic regressions revealed that the best predictor for the risk of below-level central pain was allodynia in the foot in the second testing session with a 77% probability (90.9% confidence). The results suggest that neuronal hyperexcitability, which may develop consequent to damage to spinothalamic tracts, precedes central pain. Furthermore, it appears that below-level central pain develops after a substantial build-up of hyperexcitability. To the best of our knowledge, this is the first systematic report establishing that neuronal hyperexcitability precedes central pain. Predicting the risk for central pain can be utilized to initiate early treatment in order to prevent its development.

Chronic post-traumatic headache (CPTHA), the most frequent complaint after traumatic brain injury (TBI), dramatically affects quality of life and function. Despite its high prevalence and persistence, the mechanism of CPTHA is poorly understood. This literature review aimed to analyze the results of studies assessing the characteristics and sensory profile of CPTHA in order to shed light on its possible underlying mechanisms. The search for English language articles published between 1960 and 2013 was conducted in MEDLINE, CINAHL, and PubMed. Studies assessing clinical features of headache after TBI as well as studies conducting quantitative somatosensory testing (QST) in individuals with CPTHA and in individuals suffering from other types of pain were included. Studies on animal models of pain following damage to peripheral tissues and to the peripheral and central nervous system were also included. The clinical features of CPTHA resembled those of primary headache, especially tension-type and migraine headache. Positive and negative signs were prevalent among individuals with CPTHA, in both the head and in other body regions, suggesting the presence of local (cranial) mechanical hypersensitivity, together with generalized thermal hypoesthesia and hypoalgesia. Evidence of dysfunctional pain modulation was also observed. Chronic post-traumatic headache can result from damage to intra- and pericranial tissues that caused chronic sensitization of these tissues. Alternatively, although not mutually exclusive, CPTHA might possibly be a form of central pain due to damage to brain structures involved in pain processing. These, other possibilities, as well as risk factors for CPTHA are discussed at length.