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The most important experiments are those that reveal gaps in our current theories and approaches. The current issue’s article by Djaldetti et al.,1 entitled “Quantitative measurement of pain sensation in patients with PD,” is this grade of clinical research gem. Their finding that parkinsonian motor symptoms and spontaneous pain are associated with large increases in sensitivity to heat pain is convincing and novel and demands that researchers in pain, motor systems, and neurodegeneration join forces to explain it.
Before this study, most of the data on parkinsonian pain were merely descriptive. Djaldetti et al. initially thought of this pain disorder as analogous to poststroke central pain. The latter syndrome is usually caused by lesions of the thalamus or spinothalamocortical pathways and is associated with elevation of heat pain and warm detection thresholds.2 To maximize the information gained about lateralization of function, Djaldetti et al. chose patients with unilateral motor symptoms and applied the widely used thermal testing methods that these authors had previously developed.3
The sensory findings were definitive but in …
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