Memory for the intensity of past physical pain depends critically on the intensity of present pain. When their present pain intensity was high, patients with chronic headaches of myofascial origin rated their maximum, usual, and minimum levels of prior pain as being more severe than their hourly pain diaries indicated. When their present pain intensity was low, the same patients remembered all 3 levels of prior pain as being less severe than they actually had been. The results show that pain produces systematic distortions of memory similar to those associated with alterations of affect or mood, and suggest a resolution to a conspicuous conflict in the current pain literature.

Three studies are presented demonstrating the reliability of the pressure algometer as an index of myofascial trigger point sensitivity. The first study showed high reliability between and within experimenters when measuring marked trigger point locations. In study 2, significant between experimenter reliability in locating and measuring the same unmarked trigger point locations was shown, while study 3 supported the idea that trigger points are discrete points of focal tenderness within the muscle. The ability to quantify and reliably measure trigger point sensitivity opens the door to a range of clinical and research possibilities for myofascial and related musculoskeletal pain problems.

In order to determine the relationship between trigger point sensitivity and the referred symptoms of myofascial pain, VAS ratings of referred pain intensity and pressure algometer measures of myofascial trigger point sensitivity were taken pre and post treatment of the muscle containing the trigger point with passive stretch. The results in 20 subjects, experiencing unilateral or bilateral myofascial head and neck pain, showed that myofascial trigger point sensitivity decreases in response to passive stretch as assessed by the pressure algometer, and that trigger point sensitivity and intensity of referred pain are related.

The effects of transcutaneous electrical nerve stimulation (TENS) on myofascial pain and trigger point sensitivity were assessed. Four modes of TENS and a no-stimulation control were compared in a double-blind design. Stimulation, carried out for 10 min on 60 subjects (12/group), showed significant pain reductions with 100 Hz, 250 msec stimulation followed by 100 Hz, 50 msec and then pain suppressor TENS. No pain reductions were found in the 2 Hz, 250 msec TENS or the control. No significant alteration in myofascial trigger point sensitivity, assessed with the pressure algometer, was found between the groups. The results suggest that high frequency, high intensity TENS is effective in reducing myofascial pain, and that these pain reductions do not reflect changes in local trigger point sensitivity.

While these results may not generalize to acute or chronic pain patients, within the limitations of the present experimental paradigm, no support was found for TENS affecting either SNS function or acute experimental pain perception.

Huntington Disease (HD) is an autosomal dominant neurological disorder characterized by motor, psychiatric and cognitive disturbances. Recent evidence indicates that the viability and function of cerebellar Purkinje cells (PCs) are compromised in an aggressive mouse model of HD. Here we investigate whether this is also the case in the HdhQ200 knock-in mouse model of HD. Using quantitative-real time-PCR and immunofluorescence, we observed a loss of the PC marker and calcium buffer calbindin in 50 week-old symptomatic mice. Reductions were also observed in parvalbumin and glutamic acid decarboxylase protein expression, most markedly in the molecular cell layer. Stereological analysis revealed an overall reduction in the PC population in HdhQ200/Q200 mice by nearly 40%, and loose patch electrophysiology of remaining PCs indicated a reduction in firing rate in HD mice compared to control littermates. Taken together, these data demonstrate that PC survival and function are compromised in a mouse model of adult-onset HD and suggest that further experiments should investigate the contribution of PC death and dysfunction to HD-associated motor impairment.

Huntington Disease (HD) is a devastating neurological disorder characterized by progressive deterioration of psychiatric, motor, and cognitive function. Purkinje cells (PCs), the output neurons of the cerebellar cortex, have been found to be vulnerable in multiple CAG repeat disorders, but little is known about the involvement of PC dysfunction in HD. To investigate possible PC abnormalities, we performed quantitative real time PCR, western blot analysis, and immunohistochemistry experiments to explore the changes in PC markers in the R6/2 mouse model of severe HD. Interestingly, there were reductions in the transcript and protein levels of the calcium-binding proteins parvalbumin and calbindin, as well as the enzyme glutamic acid decarboxylase 67. Immunohistochemistry supported these results, with the most substantial changes occurring in the PC layer. To determine whether the reductions in PC marker expression were due to cell loss, we performed stereology on both presymptomatic and end-stage R6/2 mice. Stereological counts indicated a significant reduction in PC number by end-stage but no change in presymptomatic animals (4 weeks of age). To assess cellular function prior to cell loss and symptom onset, we measured spontaneous firing in PCs from 4-week old animals and found a striking deficit in PC firing as indicated by a 57% decrease in spike rate. Interestingly, huntingtin inclusions were not widely observed in PCs until 12 weeks of age, indicating that soluble huntingtin and/or abnormalities in other cell types may contribute to PC dysfunction. Considering the roles for PCs in motor control, these data suggest that early PC dysfunction potentially contributes to motor impairment in this model of HD.

This study questions the validity of the MPI subgroup classification algorithm. The results indicate that the K-clustering approach is more useful than the MPI in deriving meaningful patient clusters that differentially predict treatment outcome in a migraine population.