Under the heading of "Now for something completly different" here's an facinating abstract and "Discussion" section (footnotes omitted) from the following article, which is too large to post: "Prism Adaptation to Optical Deviation Alleviates Pathologic Pain," Neurology 2007; 68:128–133, M. Sumitani, MD; Y. Rossetti, MD; M. Shibata, MD; Y. Matsuda, MD; G. Sakaue, MD; T. Inoue, MD; T. Mashimo, MD; and S. Miyauchi, PhD [epost January 9, 2007]

It will be interesting to see whether the study can be replicated, and what the long terms effects of the treatment may be with periodic "boosters." Maybe 10 years from now many of us will be regularly going in for prism glass therapy. Who knows?

I will be happy to email anyone a copy of the article in a .pdf fromat., just sent me a pm with your email address. (Personal, non-commercial use only, please.)

Mike
--------------------------------------------------------------------------------------------------------------------------------

Abstract—Background: The human visual and somatosensory systems are interdependent. Using a visual subjective body-midline (SM) judgment task, we previously confirmed that pathologic pain and deafferentation can modify visuospatial perception, indicating that altered somatosensory experience can modify visual perception. Conversely, in the present study we investigated whether a change in visual experience can modify perception of pathologic pain. Methods: We used prism adaptation (PA) to modify subjects’ visual experience. Five patients with complex regional pain syndrome (CRPS)adapted to wedge prisms, producing a 20-degree visual displacement toward the unaffected side. Further, we used several types of prisms in a longitudinal single-case study. Wearing prismatic goggles, the subjects performed a target-pointing task once a day for 2 weeks. We evaluated pain intensity and visual SM judgment to measure the adaptive aftereffects at three time points: before PA (pre-test), immediately after the first PA exposure (IA-test), and after a 14-day sequence of PA exposure (post-test). Results: PA toward the unaffected side alleviated pathologic pain and other CRPS pathologic features, when measured at post-test. None of the IA-test results showed an analgesic effect. In the longitudinal study, sham PA and 5-degree PA did not produce any effects, and PA toward the affected side actually exacerbated the subjective pain. Conclusions: Our findings suggest that vision can influence pathologic pain, and preliminarily suggest that prism adaptation has a direction-specific and reproducible effect on not only pathologic pain but also other CRPS pathologic features. Thus, prism adaptation may be a viable cognitive treatment for CRPS. [Emphasis added.]


Discussion. We demonstrated that adaptation to 20° prismatic displacement of visual field toward the unaffected side can alleviate pathologic pain. Next, we confirmed that the amelioration of pathologic pain by 20° prism adaptation toward the unaffected side was reproducible, and that 20° prism adaptation toward the affected side tended to exacerbate pathologic pain. Since it was a longitudinal single-case study, we used two types of goggles designed to create appropriate control conditions: 1) neutral goggles as a control for the pointing procedure; and 2) 5° prisms as a control for conscious visual displacement with a relatively small adaptation to the visual displacement, as observed with the vSMJ-task. These control goggles did not significantly affect pathologic pain. Therefore, we verified that visuomotor experience altered by prism adaptation, which caused substantial aftereffects, can modify pathologic pain in a direction-specific manner. Although it is not yet clear whether the interdependency between vision and pathologic pain is specific to CRPS or general to overall pathologic pain, this finding suggests that pathologic pain and vision are interdependent, as expected by cross-modal interaction between vision and “physiologic” somatosensory functions such as proprioception and touch.

A series of reports has suggested that incongruent sensorimotor feedback loops between motor outputs and sensory inputs may generate and maintain pathologic pain disorders such as CRPS and phantom limb pain or motor abnormalities such as dystonia. Our recent finding that unilateral limb pathologic pain shifts the visual SM representation toward the affected side in patients with CRPS may support this idea, with the following possible explanation. Since visual SM representation contributes to the egocentric body reference frame, the deviation of visual SM representation can cause incorrect coding of target-objects in relation to the body. Such incorrect coding of target-objects leads to discordance between visual-motor reference (the action expected from a feedforward movement plan) and proprioceptive-motor reference (the action achieved under feedback control). Thus, the deviation of visual SM representation can provoke discordance of the visual-proprioceptive linkage, leading to incongruent sensorimotor feedback loops. From this viewpoint, because prism adaptation has the potential to realign the spatial relationship between visual-motor and proprioceptive-motor references, these sensorymotor references would be combined to retrieve visual-proprioceptive coordinative linkage by prism adaptation. The amelioration of pathologic pain might then result from such coordinative linkage by 20° prism adaptation toward the unaffected side. Furthermore, the fact that 20° prism adaptation toward the affected side exacerbated pathologic pain in the longitudinal study may be due to a greater incongruity in sensorimotor feedback loops following an extended displacement of visual SM representation. Pain amelioration thus seemed to correspond with various types of prism adaptation. Alternatively, considering the multi-factorial nature of unilateral neglect, prism adaptation could ameliorate the attentional bias that is common in unilateral neglect. In other words, prism adaptation helps to re-balance the distribution of spatial attention by activating right hemisphere cortical areas. With respect to the relationship between attention and pathologic pain, it is commonly observed that enhanced attention to the painful site exacerbates pathologic pain, suggesting the transformation of attentional processes into facilitators of pain perception. On the contrary, a previous pathologic pain study reported analgesic effects when various types of sensory stimuli and a task were used to distract attention from the pain. Taking account of these notions about spatial attention, prism adaptation might re-balance the distribution of spatial attention which had been exclusively focused on the affected site, thus alleviating pathologic pain. Although conventional treatments were applied simultaneously with the prism adaptation, it is unlikely that they contributed to the analgesic effect because these treatments remained constant throughout the study. These findings suggest that implicit visual-motor adaptation helps to re-establish congruent sensorimotor integration or re-balance the distribution of spatial attention, or both, thereby improve pathologic pain. Of clinical importance, CRPS pathologic features, including CRPS-associated motor-somatic neglect, improved along with pain amelioration by prism adaptation. Consequently, our results suggest that CRPS is accompanied not only by peripheral and somatosensory abnormalities but also by cognitive and multimodal disturbances. Moreover, our results suggest that prism adaptation may be a viable cognitive treatment for CRPS. Further randomized controlled trials would be required to determine whether the beneficial effect on CRPS is a specific consequence of prism adaptation.

There is a striking difference between patients with unilateral neglect and CRPS in the effectiveness of different beneficial directions of visual displacement generated by prisms. Rightwarddisplacing prism adaptation can alleviate unilateral neglect, whereas leftward-displacing prism adaptation can alleviate right-sided CRPS, although visual SM representations of both patients with unilateral neglect and right-sided CRPS tend to shift to the right. Thus, the beneficial directions of prismatic displacement appear to be opposite when the pathologic side is considered. This apparent contradiction might be explained in the following way: patients with unilateral neglect exhibit a deficit on the left side, and hence a deviation toward the right. The rightward shift in patients with unilateral neglect is thought to be, at least in part, expressed by a pathologic deviation of proprioceptive SM representation. Meanwhile, the pathologic pain found in CRPS appears to correlate with a pathologic deviation of visual SM representation. Interestingly, proprioceptive and visual compensatory aftereffects of prism adaptation are produced in opposite directions. Therefore, adaptation to rightward-displacing prisms results in 1) a leftward shift of the proprioceptive-motor reference followed by competition with the pathologic rightward deviation, thus reducing the left-sided deficit in unilateral neglect; and 2) a rightward shift of the visual-motor reference followed by neutralizing the pathologic leftward deviation of visual SM representation, thus retrieving the visual-proprioceptive coordinative linkage in left-sided CRPS.

In the present study, prism adaptation did not immediately affect pathologic pain. Rather, pathologic pain decreased within 1 week of daily prism exposure. Likewise, interruption of prism adaptation treatment increased pathologic pain gradually within 1 week. Supporting evidence comes from a few studies regarding the time lag between acquisition of prism adaptation and emergence of its effect: prism adaptation improved the signs of unilateral neglect immediately, but a more beneficial effect was obtained 2 hours after taking off the prismatic goggles. Even after prism adaptation treatment is stopped, the beneficial effects remain observable for a few days, and better recovery has been observed for up to 5 weeks after the treatment. Furthermore, prism adaptation is based on bottom-up mechanisms that do not require patients with unilateral neglect to be aware of their difficulty, and the cognitive effects induced by prism adaptation can influence a relatively higher-order level of visuospatial representation because the effects extend to tests that require visuomotor coordination (e.g., cancellation tests and object-reaching test) as well as tests that do not require a motor response (e.g., reading tests and room description test). Considering that such widespread adaptive aftereffects are expanded implicitly, prism adaptation is viewed as triggering or enhancing autonomous active processes involved in brain plasticity which relates to multisensory integration. Therefore, some latent period would be expected before prism adaptation reaches the maximum effect on the somatosensory-motor system. Furthermore, there is circumstantial evidence that the size and duration of prismatic adaptive aftereffects vary depending on the function being tested and the condition of the patients: a reliable improvement was observed for pressure sensitivity and proprioception (finger position sense) after prism adaptation in a single unilateral neglect case study in which the beneficial effect on proprioception was longer lasting than that on pressure sensitivity; and the prismatic aftereffect seems to be particularly long-lasting for patients with unilateral neglect as compared to normal subjects. Our results are in accord with these ideas about the size, duration, and nature of the prismatic adaptive aftereffect, which might also explain why pain symptoms had improved for all subjects at post-test, though the adaptive aftereffects on visual SM representation at post-test varied among the patients.