In contrast to MS, PD is typically a disorder of the middle-aged and elderly. Some secondary causes of par-kinsonism may present earlier. Pain in PD has been the subject of a recent review article.25
Parkinsonism provides a useful second model of a neurologic disorder in which chronic pain is both common and underestimated.26'27 The etiology very probably involves both genetic and environmental factors; various toxic environmental chemicals have been implicated in the disease, as well as familial clustering of cases consistent with autosomal dominant inheritance. Concerning the pathology, degeneration of dopaminergic neurons of the substantia nigra is the hallmark of the idiopathic disease. The prevalence in the USA is in the order of
0.4.percent overall, increasing to 1 percent in individuals over age 55.
Parkinsonian syndromes classically present with a triad of features:
1. bradykinesia - slowness of spontaneous movement;
3. tremor - typically at rest.
Of this triad of components, it is usually the first two which are associated with pain.
PD is now hardly ever seen in its unmodified form in advanced cases as treatment with L-dopa and other dopa-minergic drugs is more or less universal in developed countries. While L-dopa therapy has dramatic therapeutic benefit early on, its continued use ultimately typically gives rise to a state of clinical fluctuation between bradykinesia/ rigidity and dyskinesia ("on-off" phenomenon). In this state, the parkinsonian patient may exhibit pain associated with both hyperkinetic and hypokinetic disorder.
Although pain has long been recognized in PD, there were few data on which to base estimates of its prevalence until the important paper by Snider et al. in 1976.28 On the basis of this study, the prevalence is probably in the order of 40-50 percent (similar to
MS), although the authors quote a lower figure on the basis of excluding burning sensations and also muscular pains clearly resulting directly from increased tone. A later study by Goetz et al.29 closely mirrors these findings; however, Snider et al. attribute much of the limb pain to central mechanisms, whereas Goetz's paper places more emphasis on nociceptive pain attributable to the effects of the disease on muscle tone, movement, and posture.
Although Snider et al. cite a lack of correlation between muscle hypertonia and pain as evidence of a central cause for the pain, it is usually worse on the side with most motor dysfunction, and the character of the pain suggests a musculotendinous origin. In advanced treated cases with an "on-off" pattern, pain may be a feature of both the "on" and the "off" phase. Sufferers typically complain of a constant aching, cramp-like discomfort of the muscles while "off," and "muscle-strain" pain while "on."
However, some pains cannot be explained on this basis and seem likely to be neuropathic in nature, such as the reports of oral/genital pain.30'31 A fairly recent study suggests that in approximately 8 percent of parkinsonian patients with pain, the pain is neuropathic.27 A small proportion of patients with PD have sensory symptoms (including pain) which precede any clinically apparent motor effects of the disease. Burning pain is often, though not invariably, related to L-dopa therapy.
There is evidence that the prevalence of pain in multiple system atrophy, the most common cause of secondary parkinsonism, is similar to that of PD.32
Quinn et al.33 have proposed a classification of pain in Parkinson's disease largely based on its relation to medication, although this sheds no light on putative pain mechanisms.
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