[Challenges in pain assessment and management among individuals with intellectual and developmental disabilities : German version]. / Herausforderungen der Schmerzerfassung und -therapie bei Personen mit Intelligenzminderung und Entwicklungsstörungen : Deutsche Fassung.

INTRODUCTION: Intellectual and developmental disabilities (IDD) include conditions associated with physical, learning, language, behavioural, and/or intellectual impairment. Pain is a common and debilitating secondary condition compromising functional abilities and quality of life. OBJECTIVES: This article addresses scientific and clinical challenges in pain assessment and management in individuals with severe IDD. METHODS: This Clinical Update aligns with the 2019 IASP Global Year Against Pain in the Vulnerable and selectively reviews recurring issues as well as the best available evidence and practice. RESULTS: The past decade of pain research has involved the development of standardized assessment tools appropriate for individuals with severe IDD; however, there is little empirical evidence that pain is being better assessed or managed clinically. There is limited evidence available to inform effective pain management practices; therefore, treatment approaches are largely empiric and highly variable. This is problematic because individuals with IDD are at risk of developing drug-related side effects, and treatment approaches effective for other populations may exacerbate pain in IDD populations. Scientifically, we are especially challenged by biases in self-reported and proxy-reported pain scores, identifying valid outcome measures for treatment trials, being able to adequately power studies due to small sample sizes, and our inability to easily explore the underlying pain mechanisms due to compromised ability to self-report. CONCLUSION: Despite the critical challenges, new developments in research and knowledge translation activities in pain and IDD continue to emerge, and there are ongoing international collaborations.

Central Neuropathic Pain in Multiple Sclerosis Is Associated with Impaired Innocuous Thermal Pathways and Neuronal Hyperexcitability.

OBJECTIVE: About one-third of patients with multiple sclerosis (MS) suffers from chronic and excruciating central neuropathic pain (CNP). The mechanism underlying CNP in MS is not clear, since previous studies are scarce and their results are inconsistent. Our aim was to determine whether CNP in MS is associated with impairment of the spinothalamic-thalamocortical pathways (STTCs) and/or increased excitability of the pain system. DESIGN: The study was cross-sectional. SETTING: The study was conducted at a general hospital. PARTICIPANTS: Participants were 47 MS patients with CNP, 42 MS patients without CNP and 32 healthy controls. METHODS: Sensory testing included the measurement of temperature, pain, and touch thresholds and the thermal grill illusion for evaluating STTCs function and hyperpathia and allodynia as indicators of hyperexcitability. CNP was characterized using interviews and questionnaires. RESULTS: The CNP group had higher cold and warm thresholds (P < 0.01), as well as higher thermal grill illusion perception thresholds (P < 0.05), especially in painful body regions compared with controls, whereas touch and pain thresholds values were normal. The CNP group also had a significantly greater prevalence of hyperpathia and allodynia. Regression analysis revealed that whereas presence of CNP was associated with a higher cold threshold, CNP intensity and the number of painful body regions were associated with allodynia and hyperpathia, respectively. CONCLUSIONS: CNP in MS is characterized by a specific impairment of STTC function, the innocuous thermal pathways, and by pain hyperexcitability. Whereas CNP presence is associated with STTC impairment, its severity and extent are associated with pain hyperexcitability. Interventions that reduce excitability level may therefore mitigate CNP severity.

The effect of mindful attention training for pain modulation capacity: Exploring the mindfulness-pain link.

OBJECTIVE: Mindfulness has been shown to be beneficial for chronic pain. The underlying mechanisms of the mindfulness-pain link, however, are yet to be established. Particularly, the effects of mindfulness on pain modulation, which is shown to be dysfunctional among chronic pain patients, barely has been tested. This study investigated whether a short mindful attention training based on Langerian mindfulness mitigates reductions in pain modulation. METHOD: Systemic quantitative-somatosensory testing of conditioned pain modulation (CPM) was conducted in 60 undergraduates, who were randomly assigned to one of three groups: (1) Pain-specific mindful attention training; (2) nonspecific mindful attention training; and (3) no mindful attention training. CPM was tested before and after the intervention. RESULTS: As hypothesized, a reduction in CPM magnitude was observed only in the control group, whereas this reduction was abolished in the two mindfulness groups. CONCLUSIONS: Langerian mindfulness may mitigate pain modulation reduction as observed in chronic pain, thus shedding light on its potential advantages.

Different clinical phenotypes of persistent post-traumatic headache exhibit distinct sensory profiles.

INTRODUCTION: Persistent post-traumatic headache remains a poorly understood clinical entity. Although there are currently no accepted therapies for persistent post-traumatic headache, its clinical symptoms, which primarily resemble those of migraine or tension-type headache, often serve to guide treatment. However, evidence-based justification for this treatment approach remains lacking given the paucity of knowledge regarding the characteristics of these two major persistent post-traumatic headache phenotypes and their etiology. METHODS: We compared clinical features and quantitative sensory testing profiles between two distinct cohorts of persistent post-traumatic headache subjects that exhibited symptoms resembling either migraine (n = 15) or tension-type headache (n = 13), as well as to headache-free subjects that had suffered traumatic brain injury (n = 19), and to healthy controls (n = 10). We aimed to determine whether the two persistent post-traumatic headache subgroups could be discriminated based on additional clinical features, distinct quantitative sensory testing profiles, or the interaction of pain severity with the level of post-traumatic stress disorder. RESULTS: Persistent post-traumatic headache subjects with migraine-like symptoms reported that bright light and focused attention aggravated their pain, while stress and nervousness were reported to aggravate the headache in subjects with tension-type headache-like symptoms. Quietness was better in alleviating migraine-like persistent post-traumatic headache, while anti-inflammatory medications provided better relief in tension-type headache-like persistent post-traumatic headache. The two persistent post-traumatic headache subgroups exhibited distinct quantitative sensory testing profiles with subjects exhibiting tension-type headache-like persistent post-traumatic headache displaying a more pronounced cephalic and extracephalic thermal hypoalgesia that was accompanied by cephalic mechanical hyperalgesia. While both persistent post-traumatic headache subgroups had high levels of post-traumatic stress disorder, there was a positive correlation with pain severity in subjects with tension-type headache-like symptoms, but a negative correlation in subjects with migraine-like symptoms. CONCLUSIONS: Distinct persistent post-traumatic headache symptoms and quantitative sensory testing profiles may be linked to different etiologies, potentially involving various levels of neuropathic and inflammatory pain, and if confirmed in a larger cohort, could be used to further characterize and differentiate between persistent post-traumatic headache subgroups in studies aimed to improve treatment.

Experimental evidence for weaker endogenous inhibition of trigeminal pain than extra-trigeminal pain in healthy individuals.

Background and objectives The prevalence of pain syndromes that affect the territories innervated by the trigeminal nerve, such as headaches, is one of the highest and ranks second only to low back pain. A potential mechanism underlying this high prevalence may be a relatively weak endogenous pain modulation of trigeminal pain. Here, we sought to systematically compare endogenous pain modulation capabilities in the trigeminal region to those of extra-trigeminal regions in healthy subjects. Methods Healthy, pain free subjects (n = 17) underwent a battery of quantitative sensory testing to assess endogenous pain inhibition and pain enhancement efficiencies within and outside the trigeminal innervated region. Measurements included conditioned pain modulation (CPM), temporal summation of pain (TSP) and spatial summation of pain (SSP). Results Testing configurations that included trigeminal-innervated body regions displayed significantly weaker CPM when compared to extra-trigeminal innervated areas. SSP magnitude was smaller in the ophthalmic trigeminal innervation when compared to other body regions. TSP magnitude was not different between the different body regions tested. Conclusions Our findings point to regional differences in endogenous pain inhibition and suggest that in otherwise healthy individuals, the trigeminal innervation is subjected to a weaker inhibitory pain control than other body regions. Such weaker endogenous pain control could play, at least in part, a role in mediating the high prevalence of trigeminal-related pain syndromes, including primary headaches and TMD pain.

Increased psychological distress among individuals with spinal cord injury is associated with central neuropathic pain rather than the injury characteristics.

STUDY DESIGN: Cross-sectional study. OBJECTIVES: Central neuropathic pain (CNP) is common after spinal cord injury (SCI). The psychological impact of CNP is not clear. Previous studies reported depression and pain catastrophizing among patients with SCI and CNP; however, the lack of control groups prevented discerning whether these were attributed to CNP or to the SCI itself. The aim was to examine the psychological distress among individuals with SCI with and without CNP and controls to evaluate its impact and possible source. SETTING: Outpatient clinic of a large rehabilitation center. METHODS: Individuals with SCI and CNP (n = 27) and without CNP (n = 23), and able-bodied controls (n = 20) participated. Data collection included sociodemographics, SCI characteristics, and level of post-traumatic stress disorder (PTSD), anxiety, stress, depression, and pain catastrophizing. The sensory, affective, and cognitive dimensions of CNP were analyzed. RESULTS: Individuals with SCI and CNP exhibited elevated levels of PTSD, anxiety, stress, depression, and pain catastrophizing compared to the two control groups, which presented similar levels. The psychological variables among the CNP group correlated positively only with the affective dimension of CNP. Neither CNP nor the psychological variables correlated with SCI characteristics. CONCLUSIONS: Irrespective of CNP intensity, the affective dimension (suffering) is associated with increased psychological distress. Perhaps individual differences in the response to SCI and/or individual traits rather than the mere exposure to SCI may have a role in the emergence of CNP and psychological distress/mood dysfunction. Rehabilitation programs should prioritize stress management and prevention among individuals with SCI and CNP.

Deficient Pain Modulation in Patients with Chronic Hemiplegic Shoulder Pain.

BACKGROUND: Hemiplegic shoulder pain (HSP) following stroke significantly affects the individual's function and quality of life. The mechanism of HSP is not clearly understood; hence, it is unclear why HSP resolves spontaneously or following routine care in some patients, while in others it becomes persistent. The aim was therefore to study whether HSP is associated with deficient pain modulation. METHODS: Thirty post-stroke patients-16 with HSP and 14 without HSP-and 20 matched controls participated. Pain adaptation and conditioned pain modulation (CPM) were measured as indicators of pain modulation, in the affected (hemiplegic) and contralateral shoulder as well as in the affected shin among post-stroke patients, and in comparable body regions among controls. Post-stroke patients also underwent functional and physical evaluation of the shoulder. RESULTS: Pain adaptation was absent among HSP patients, in both the painful shoulder and the affected shin, but existed in the 2 control groups. In addition, the affected shoulder and shin among the HSP group had reduced thermal sensibility compared to the contralateral regions. CPM was similar across groups. Shoulder functional status and physical status were similar for the 2 post-stroke groups. CONCLUSIONS: The results suggest that HSP is associated with a lack of pain adaptation, characteristic not only of the painful shoulder but also of the affected side. Although we cannot determine whether lack of pain adaptation precedes the HSP or results from it, interventions that enhance descending pain inhibition may improve management and prevent HSP chronification.

Posttraumatic Stress Disorder, Orientation to Pain, and Pain Perception in Ex-Prisoners of War Who Underwent Torture.

OBJECTIVE: Studies suggest that torture survivors often experience long-term chronic pain and increased pain perception. However, it is unclear whether the actual experience of torture or rather the subsequent posttraumatic stress disorder (PTSD) explains these pain problems. Furthermore, although catastrophic and fearful orientations to pain have been suggested to play a significant role in the association between trauma and pain, the underlying mechanisms remain unclear. This study examined whether chronic pain and pain perception among torture survivors are associated with torture experience or PTSD and whether catastrophic and fearful orientations mediate or moderate these associations. METHODS: Fifty-nine ex-prisoners of war who underwent torture and 44 matched veterans participated in this study. Pain perception was evaluated by assessing pain threshold and reactivity to experimental suprathreshold noxious stimuli. Participants completed self-administered questionnaires assessing PTSD, chronic pain, pain catastrophizing, and fear of pain. RESULTS: Although chronic pain was associated with PTSD (0.44 < ß < 0.49, p < .002), increased pain perception was correlated with torture (0.33 < ß < 0.65, p < .05). Pain catastrophizing was found to mediate the association between PTSD and chronic pain (ß = 0.18 and 0.19, respectively; p < .05). Fear of pain moderated the association between torture and pain perception (ß = 0.41 and 0.42, respectively; p < .017). CONCLUSIONS: The findings suggest that chronic pain is contingent upon the psychological toll of torture, that is, PTSD. This study also indicates that PTSD exacerbates catastrophic orientation, which in turn may amplify chronic pain. Reactivity to experimental noxious stimuli was related to previous experiences of torture, which enhances perceived pain intensity when interacting with a fearful pain orientation. These findings highlight the significance of orientation to bodily experiences after trauma.

Physiological and Behavioral Responses to Calibrated Noxious Stimuli Among Individuals with Cerebral Palsy and Intellectual Disability.

Objective: As individuals with intellectual disability (ID) due to cerebral palsy (CP) are at high risk of experiencing pain, measuring their pain is crucial for adequate treatment. While verbal reports are the gold standard in pain measurements, they may not be sufficient in ID. The aim was to detect behavioral/autonomic responses that may indicate the presence and intensity of pain in individuals with CP and ID, using calibrated stimuli, here for the first time. Subjects: Thirteen adults with CP and ID (CPID), 15 healthy controls (HC), and 5 adults with CP with no ID (CPNID). Methods: Subjects received pressure stimuli of various intensities. Self-reports (using a pyramid scale), facial expressions (retrospectively analyzed with Facial Action Coding System = FACS), and autonomic function (heart rate, heart rate variability, pulse, galvanic skin response) were analyzed. Results: Self-reports and facial expressions but not the autonomic function exhibited stimulus-response relationship to pressure stimulation among all groups. The CPID group had increased pain ratings and facial expressions compared with controls. In addition, the increase in facial expressions along the increase in noxious stimulation was larger than in controls. Freezing in response to pain was frequent in CPID. Conclusions: 1) Individuals with CP and ID have increased responses to pain; 2) facial expressions and self-reports, but not autonomic variables can reliably indicate their pain intensity; 3) the pyramid scale is suitable for self-report in this population. Although facial expressions may replace verbal reports, increased facial expressions at rest among these individuals may mask pain, especially at lower intensities.

Increased Evoked Potentials and Behavioral Indices in Response to Pain Among Individuals with Intellectual Disability.

OBJECTIVE: Previous studies on the sensitivity and reactivity to pain of individuals with intellectual disability (ID) are inconsistent. The inconsistency may result from the reliance on self-reports and facial expressions of pain that are subject to internal and external biases. The aim was therefore to evaluate the reactivity to pain of individuals with ID by recording pain-evoked potentials (EPs), here for the first time, and testing their association with behavioral pain indices. SUBJECT: Forty-one healthy adults, 16 with mild-moderate ID and 25 controls. METHODS: Subjects received series of phasic heat stimuli and rated their pain on self-report scales. Changes in facial expressions and in pain EPs were recorded and analyzed offline. RESULTS: Pain self-reports, facial expressions, and the N2P2 amplitudes of the EPs exhibited stimulus-response relationship with stimulation intensity in both groups. The facial expressions and N2P2 amplitudes of individuals with ID were increased and N2P2 latency prolonged compared with controls. N2P2 amplitudes correlated with self-reports only in controls. CONCLUSIONS: Individuals with ID are hypersensitive/reactive to pain, a finding bearing clinical implications. Although pain EPs may reflect a somewhat different aspect of pain than the behavioral indices do, there is evidence to support their use to record pain in noncommunicative individuals, pending further validation.

Responses of dural mast cells in concussive and blast models of mild traumatic brain injury in mice: Potential implications for post-traumatic headache.

BACKGROUND: Chronic post-traumatic headache (PTH) is one of the most common symptoms of mild traumatic brain injury (mTBI) but its underlying mechanisms remain unknown. Inflammatory degranulation of dural mast cells (MCs) is thought to promote headache, and may play a role in PTH. Whether mTBI is associated with persistent degranulation of dural MCs is yet to be determined. METHODS: Histochemistry was used to evaluate time course changes in dural MC density and degranulation level in concussive head trauma and blast mouse models of mTBI. The effects of sumatriptan and the MC stabilizer cromolyn sodium on concussion-evoked dural MC degranulation were also investigated. RESULTS: Concussive head injury evoked persistent MC degranulation for at least 30 days. Blast trauma gave rise to a delayed MC degranulation response commencing at seven days that also persisted for at least 30 days. Neither sumatriptan nor cromolyn treatment reduced concussion-evoked persistent MC degranulation. CONCLUSIONS: mTBI evoked by closed head injury or blast exposure is associated with persistent dural MC degranulation. Such a response in mTBI patients may contribute to PTH. Amelioration of PTH by sumatriptan may not involve inhibition of dural MC degranulation. If persistent dural MC degranulation contributes to PTH, then cromolyn treatment may not be effective.

Investigating the neural processing of spatial summation of pain: the role of A-delta nociceptors.

The underlying mechanism of spatial summation (SS) of pain, an essential component in pain perception and detection, is unknown. Because of the possible differential innervations by A-delta nociceptors and pain sensitivity of hairy and glabrous skin, a comparison of the SS characteristics between the two skin types could contribute to the elucidation of its subserving system and processing. The effect of sex on SS of pain was also evaluated due to the scarcity of information on the subject. Twenty-nine healthy subjects (13 males, 16 females) received four series of heat stimuli of various intensities, in hairy and glabrous skin of the hand using large (27 mm diameter) and small (12 mm) stimulation areas, and the perceived pain intensity (PPI) was rated. A fast temperature increase rate (70°/s) was used in order to selectively activate A-delta nociceptors. The effect of skin type, stimulation intensity and sex on SS and PPI was calculated. Skin type significantly affected PPI and SS of pain; values of both variables were significantly greater in hairy compared with glabrous skin. SS of pain gradually increased concomitantly with stimulation intensity magnitude, to a point when it became saturated in both skin types. Females exhibited greater SS in glabrous skin. It would appear that AMH-II nociceptive fibers in particular subserve SS of pain. Furthermore, SS is increased under stronger stimulation intensities, probably as defense mechanism against tissue damage. Sex differences in dynamic sensory processes such as SS are revealed only under conditions where the phenomenon is subtle (as in glabrous skin).

Body awareness and pain habituation: the role of orientation towards somatic signals.

Although body awareness and pain perception are considered to be parts of the interoceptive system, the relationship between them is unclear. This study examines the association between body awareness and pain habituation, hypothesizing that this association is moderated by pain catastrophizing and mindfulness. Sixty subjects received a mildly aversive electrical stimulus for 60 s, during which they were requested to rate the amount of perceived pain. Complete habituation was indicated by abolition of pain sensation; partial habituation was indicated by a decrease in pain sensation. Individuals who demonstrated complete habituation had lower levels of pain catastrophizing and lower levels of mindfulness. As hypothesized, the association between body awareness and pain habituation was moderated by pain catastrophizing: Among low pain catastrophizers, the higher the body awareness, the stronger the tendency to exhibit complete habituation. Among high pain catastrophizers, the higher the body awareness, the greater the likelihood to present partial habituation.

Body awareness: differentiating between sensitivity to and monitoring of bodily signals.

Sensitivity to bodily signals is the tendency to be aware of bodily states and to identify subtle bodily reactions to internal and environmental conditions. Monitoring these signals is a top-down process, describing individuals' tendency to actively scan their bodies in order to detect cues for their physical condition. Two studies examined the relations between these constructs and their adaptivity among young adults. In Study 1, 180 young adults completed questionnaires assessing sensitivity, monitoring, and hypochondriac tendency. In Study 2, 205 students reported their levels of sensitivity, monitoring, pain catastrophizing, and trait anxiety. Although monitoring and sensitivity were correlated, when controlling for their shared variance, only monitoring was associated with high hypochondriac tendency and anxiety. In addition, the adaptivity of sensitivity to bodily signals was dependent on both level of monitoring of bodily signals and pain catastrophizing. That is, pain catastrophizing moderated the effect of sensitivity and monitoring on anxiety. These findings suggest that the adaptivity of sensitivity is determined by the mode of attention characterizing the individual engaged in this process.

Chronic post-traumatic headache: clinical findings and possible mechanisms.

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.

The relationship between traumatic exposure and pain perception in children: the moderating role of posttraumatic symptoms.

ABSTRACT: Adverse childhood experiences (ACEs) affect approximately half of all children worldwide. These experiences have been linked to increased pain sensitivity in adulthood and a higher likelihood of developing severe chronic pain. However, most studies have assessed the effects of ACEs retrospectively, long after they occurred, leaving room for other factors to influence the observed outcomes. We investigated, for the first time, the association between ACEs and concurrent pain perception among young children who live in a conflict zone and are consistently exposed to potentially traumatic experiences. Participants were 60 elementary school children (ages 8-11 years) living in conflict regions (n = 39) or nonconflict regions (n = 21). Posttraumatic stress symptom (PTSS) severity, traumatic exposure, pressure pain threshold (PPT), and mechanical detection threshold (MDT) were measured. Trauma-exposed children had significantly lower PPT than did controls, but MDT was similar across groups. Pressure pain threshold correlated positively with proximity to the conflict zone and inversely with traumatic exposure magnitude and PTSS severity. In addition, PTSSs moderated the relationship between repeated traumatic exposure and PPT. Children with higher PTSS severity displayed pain hypersensitivity regardless of their traumatic exposure level, whereas in children with lower PTSS severity, greater traumatic exposure correlated with pain hypersensitivity. The results suggest that ACEs among children lead to concurrent pain hypersensitivity and distress and may put them at elevated risk of chronic pain early in life. In addition, our findings emphasize the need for identifying children with various PTSS levels to provide tailored interventions and mitigate the long-term negative effects of ACEs.

Emotional burden among MS patients: associations between specific chronic pain diagnoses and psychological features.

Central neuropathic pain (CNP) and musculoskeletal pain (MSP) are often comorbid with multiple sclerosis (MS), yet data on the emotional burden entailed by this comorbidity are very limited. We studied whether MS patients with CNP exhibited greater emotional burden and pain severity than those with MSP and whether this emotional burden was attributed to the MS, the chronic pain, or both. Participants were 125 MS patients (55 with CNP; 30 with MSP; 40 MS pain-free) and 30 healthy controls (HCs). Participants completed questionnaires assessing pain interference, pain catastrophizing, depression, anxiety, stress, hypervigilance, and chronic pain. Group comparisons and a two-step cluster analysis were performed, and the association between cluster membership and clinical group membership was evaluated. Chronic pain was stronger and more widespread in the CNP group than in the MSP group. Both pain groups had higher pain interference, pain catastrophizing, and stress compared to MS pain-free and HC groups. All MS groups had greater depression levels compared to HCs, and the CNP group had the highest anxiety level. The "high psychological distress" cluster comprised mainly participants with CNP (57%), and the "minimal psychological distress" cluster comprised mainly the MS pain-free and HC groups. In conclusion, CNP seems to induce greater emotional burden and pain severity than does MSP. Whereas depression may be attributed to MS, and anxiety to CNP, enhanced pain interference, catastrophizing, and stress may be attributed to the comorbidity of MS and chronic pain. Identifying these traits among MS patients and targeting them in management programs may contribute to more effective, individually based care.

Predicting chronic pain two years following a spinal cord injury: Longitudinal study on the reciprocal role of acute pain and PTSD symptoms.

OBJECTIVES: To examine a) the development of PTSD symptoms and pain over five months post-spinal cord injury (SCI); b) the directional effects of PTSD symptoms and pain across five months post-SCI; and c) the prediction of chronic pain two-years post-SCI by PTSD symptoms and pain severity in the first five months post-SCI. STUDY DESIGN: Two-year longitudinal study. SETTING: : Individuals with an SCI admitted to the Department of Neurological Rehabilitation (N = 65). OUTCOME MEASURES: : PTSD symptoms and pain were evaluated at 1.5 months (T1), three months (T2), and five months (T3) post-SCI. Chronic pain was evaluated at 24 months post-SCI (follow-up). RESULTS: Seventy-five percent of participants reported chronic pain at follow-up. Pain severity at T1 and T2 predicted PTSD symptoms at T2 and T3, respectively. PTSD symptoms at T2 predicted pain severity at T3. Individuals with chronic pain at follow-up had reported more PTSD symptoms at T1, T2, and T3 than those without pain. A multivariate model yielded two significant indirect paths: a) PTSD symptoms at T1 predicted chronic pain severity at follow-up through PTSD symptoms at T2 and T3, and b) pain severity at T1 predicted chronic pain severity at follow-up through pain severity at T2 and T3. CONCLUSIONS: Both pain and PTSD in the acute post-SCI phase are markers for chronic pain two years later. PTSD and chronic pain exhibit a complex, reciprocal relationship across time that contributes to pain chronicity. Identifying individuals at risk and implementing interventions targeting both pain and PTSD symptoms during the acute phase may prevent their chronification.

Higher Regional Gray Matter Volume and White Matter Integrity in Individuals With Central Neuropathic Pain After Spinal Cord Injury.

Spinal cord injury (SCI) is a debilitating neurological condition that often leads to central neuropathic pain (CNP). As the fundamental mechanism of CNP is not fully established, its management is one of the most challenging problems among people with SCI. To shed more light on CNP mechanisms, the aim of this cross-sectional study was to compare the brain structure between individuals with SCI and CNP and those without CNP by examining the gray matter (GM) volume and the white matter (WM) integrity. Fifty-two individuals with SCI-28 with CNP and 24 without CNP-underwent a magnetic resonance imaging (MRI) session, including a T1-weighted scan for voxel-based morphometry, and a diffusion-weighted imaging (DWI) scan for WM integrity analysis, as measured by fractional anisotropy (FA) and mean diffusivity (MD). We found significantly higher GM volume in individuals with CNP compared with pain-free individuals in the right superior (p < 0.0014) and middle temporal gyri (p < 0.0001). Moreover, individuals with CNP exhibited higher WM integrity in the splenium of the corpus callosum (p < 0.0001) and in the posterior cingulum (p < 0.0001), compared with pain-free individuals. The results suggest that the existence of CNP following SCI is associated with GM and WM structural abnormalities in regions involved in pain intensification and spread, and which may reflect maladaptive neural plasticity in CNP.

The nature and course of sensory changes following spinal cord injury: predictive properties and implications on the mechanism of central pain.

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.