Central representation of the RIII flexion reflex associated with overt motor reaction: an fMRI study.

Recent neuroimaging studies precised the functions of the brain regions included in the so-called "pain-matrix". They isolated brain structures mediating attentional, emotional, anticipatory, cognitive, and discriminative aspects of pain perception. Surprisingly, little attention was devoted to isolate the cerebral network associated with the motor response to pain. In this study, we used fMRI to measure BOLD signal changes in nine volunteers while they received low- (L-) and high- (H-) intensity painful electrical shocks on the (left) lower limb. High-intensity stimulation was associated with a significantly stronger pain sensation and with a pronounced motor (withdrawal) reflex. BOLD responses common to L- and H-stimulation intensities were found in the right prefrontal and right posterior parietal cortices. These did not correlate with subjective pain ratings and probably mediate attentional processes unrelated to pain intensity and withdrawal. In contrast, signal changes in insula, left SII cortices and right amygdala did correlate with pain ratings and are therefore likely to encode for pain intensity. High-intensity shocks selectively recruited a motor network, including vermis, MI, SI, and paracentral cortices bilaterally, right premotor, right SII and posterior cingulate cortices. These responses, assessed for the first time in a functional imaging study, emphazised on the presence of a motor component in what has been described as the pain-matrix. They should be considered as a motor component of pain-related processes activated in case of intense pain.

Cardiac output during exercise in paraplegic subjects.

The purpose of this study was to measure the cardiac output using the CO2 rebreathing method during submaximal and maximal arm cranking exercise in six male paraplegic subjects with a high level of spinal cord injury (HP). They were compared with eight able bodied subjects (AB) who were not trained in arm exercise. Maximal O2 consumption (VO2max) was lower in HP (1.11.min, SD 0.1; 17.5 ml.min-1.kg-1, SD 4) than in AB (2.5 l.min-1, SD 0.6; 36.7 ml.min-1.kg, SD 10.7). Maximal cardiac output was similar in the groups (HP, 14 l.min-1, SD 2.6; AB, 16.8 l.min-1, SD 4). The same result was obtained for maximal heart rate (fc,max) (HP, 175 beats.min-1, SD 18; AB, 187 beats.min-1, SD 16) and the maximal stroke volume (HP, 82 ml, SD 13; AB, 91 ml, SD 27). The slopes of the relationship fc/VO2 were higher in HP than AB (P less than 0.025) but when expressed as a %VO2max there were no differences. The results suggest a major alteration of oxygen transport capacity to active muscle mass in paraplegics due to changes in vasomotor regulation below the level of the lesion.

Aerobic performance capacity in paraplegic subjects.

To determine adaptation to prolonged exercise in paraplegics, maximal O2 uptake (VO2max) and lactate threshold (LT) were evaluated during an arm cranking exercise in nine patients (P) and nine able-bodied (AB) subjects. Mean VO2max averaged 25.1 and 31.6 ml X min-1 X kg-1 in P and AB groups respectively. VO2max in P was found to be directly related to the level of spinal injury: the higher the lesion the lower the uptake. Lactate threshold expressed as a percentage of VO2max was higher in P (59%) than in AB (43%), and close to that observed in arm-trained athletes. Since training has less effect on VO2max in paraplegics than in able-bodied subjects, attributable to a deficiency in the circulatory adaptation of paraplegics to exercise, the observed differences between AB and P in lactate threshold and submaximal exercise indicate that the possible effect of training in paraplegics is located at the level of intracellular chemistry, with a diminution in glycogenolysis (higher LT) and a higher rate of lipid utilization (lower RQ).