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.

Although the prevalence rate of chronic post-traumatic headache (CPTHA) after mild traumatic brain injury (TBI) reaches up to 95%, its mechanism is unknown, and little is known about the characteristics of the pain system in this condition. Our aim was to investigate the capabilities of two pain modulatory systems among individuals with CPTHA and study their association with CPTHA, here for the first time. Forty-six subjects participated; 16 with TBI and CPTHA, 12 with TBI without CPTHA, and 18 healthy controls. Testing included the measurement of heat-pain (HPT) and pressure-pain (PPT) thresholds in the forehead and forearm, pain adaptation to tonic noxious heat, and conditioned pain modulation (CPM).The participants completed a post-traumatic stress disorder (PTSD) questionnaire. The two TBI groups did not differ in the TBI and background characteristics. However, TBI patients with CPTHA had significantly higher HPT and lower PPT in the cranium and higher PTSD symptomatology than TBI patients without CPTHA and healthy controls. Adaptation to pain and CPM were diminished in the CPTHA group compared with the two control groups. The intensity of CPTHA correlated negatively with cranial PPT, magnitude of pain adaptation, and CPM. CPTHA intensity correlated positively with PTSD symptomatology. CPTHA appears to be characterized by cranial hyperalgesia and dysfunctional pain modulation capabilities, which are associated with CPTHA magnitude. It is concluded that damage to pain modulatory systems along with chronic cranial sensitization underlies the development of CPTHA. PTSD may reinforce CPTHA and vice versa. Clinical implications are discussed.

The commonly held view, mainly based on behavioral observations, is that individuals with mental retardation (MR) have a decreased sensitivity to pain. However, the sensitivity to noxious stimuli was not systematically measured in these individuals. For this purpose we developed an experimental protocol with which we trained individuals with mild MR (unspecified MR and Down's syndrome) in heat-pain threshold (HPT) measurement on the hand, and then performed the measurement using both the method of limits (MLI) which relies on reaction time (RT) and the method of levels (MLE) which is RT-free. This allowed for an indirect assessment of the RT and conduction velocity (CV) of these individuals. We found that HPT in individuals with unspecified MR (41.23+/-1.86 degrees C) and Down's syndrome (40.96+/-2.93 degrees C) was significantly lower than that of controls (42.86+/-2.42 degrees C) when measured with the MLE (P < 0.05). With the MLI no significant differences in HPT were found between the groups. However, the RT and CV values of individuals with unspecified MR and Down's syndrome were significantly lower compared to controls (e.g. mean RT of 1.86 and 2.55 compared to 1.2 s, respectively, P < 0.01). From this work it would appear that individuals with MR are not only pain-sensitive, but also more sensitive to heat-pain than normal. It is suggested that computerized quantitative testing of pain threshold is feasible in individuals with MR preferably by using RT-free methods (e.g. the MLE) due to the low RT and CV values exhibited by them.

To study whether the sensitivity to noxious and innocuous heat varies across the body. Heat-pain threshold and warm sensation threshold were measured in 20 patients, using the Method of Limits (MLI) and the Method of Levels (MLE) in 5 regions: the chest, forearm, mid thigh, and the dorsal surface of the hand and foot. With the Method of Limits, heat-pain threshold increased gradually from the lowest level in the chest (mean 42°C) to peak level in the foot (44.5°C, P < 0.001). With the Method of Levels, heat-pain threshold did not differ between body regions. Warm sensation thresholds measured with both Method of Limits and the Method of Levels was higher in the chest (36.2°C) and foot (36.8°C) compared to the other regions (mean of 35.3°C, P < 0.01). The correlation between heat-pain threshold and warm sensation threshold was low to moderate, depending on the tested region. Differences in heat-pain threshold and warm sensation threshold between the methods were highest in the legs and smallest in the chest. The correlation between the Method of Limits and Method of Levels was moderate for heat-pain threshold (0.57) and good for warm sensation threshold (0.71). The sensitivity to noxious heat is uniform across the body when measured with a reaction-time-free method (Method of Levels), but is greater in proximal than in distal regions, when measured with a reaction-time-dependent method (Method of Limits). Regardless of measuring method, the sensitivity to innocuous heat is not uniform across the body. It is concluded that the Method of Levels is preferred when heat-pain threshold is to be compared between body regions. For heat-pain threshold, within-patient comparisons can be made between each pair of regions tested. However, for warm sensation threshold, within-patient comparisons should be conducted between contralateral symmetrical regions.

Anecdotes on the ability of individuals to continue to function under stressful conditions despite injuries causing excruciating pain suggest that acute stress may induce analgesia. However, studies exploring the effect of acute experimental stress on pain perception show inconsistent results, possibly due to methodological differences. Our aim was to systematically study the effect of acute stress on pain perception using static and dynamic, state-of-the-art pain measurements. Participants were 29 healthy men who underwent the measurement of heat-pain threshold, heat-pain intolerance, temporal summation of pain, and conditioned pain modulation (CPM). Testing was conducted before and during exposure to the Montreal Imaging Stress Task (MIST), inducing acute psychosocial stress. Stress levels were evaluated using perceived ratings of stress and anxiety, autonomic variables, and salivary cortisol. The MIST induced a significant stress reaction. Although pain threshold and pain intolerance were unaffected by stress, an increase in temporal summation of pain and a decrease in CPM were observed. These changes were significantly more robust among individuals with stronger reaction to stress ("high responders"), with a significant correlation between the perception of stress and the performance in the pain measurements. We conclude that acute psychosocial stress seems not to affect the sensitivity to pain, however, it significantly reduces the ability to modulate pain in a dose-response manner. Considering the diverse effects of stress in this and other studies, it appears that the type of stress and the magnitude of its appraisal determine its interactions with the pain system.