The Clinical journal of pain
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To outline the modes of action of topiramate and to examine the theoretical reasons as to why topiramate may alleviate neuropathic pain. Results of animal and human studies in the use of topiramate for treating pain are reviewed, together with case studies describing situations where topiramate was effective when other treatments have failed. ⋯ Topiramate acts on neuronal transmission in at least five ways: by modulating voltage-gated sodium ion channels, potentiating gamma-aminobutyric acid inhibition, blocking excitatory glutamate neurotransmission, modulating voltage-gated calcium ion channels, and by inhibiting carbonic anhydrase. This review suggests that there are good theoretical reasons for a trial of topiramate in patients with neuropathic pain where conventional medical treatments have failed. Although not currently licensed for treating pain, topiramate should be considered before invasive methods of pain relief are contemplated. Most of the side effects of topiramate are dose dependent, but by starting medication with a low dose (=25 mg/d) that is gradually titrated upward, tolerance is much more easily achieved.
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Comparative Study
Factors associated with willingness to try different pain treatments for pain after a spinal cord injury.
To develop and establish the psychometric properties of a pain treatment willingness scale and identify factors associated with willingness to try specific pain treatments for spinal cord injury (SCI)-related pain. ⋯ Willingness to use a specific pain treatment may be a key factor mediating the behavior of using that specific treatment. Assessment of patient attitudes toward various treatments options, particularly regarding opioid medications, is warranted to optimize treatment adherence. Once the factors that determine these attitudes are identified, interventions to increase willingness to use nonpharmacological or opioid treatments can be designed and evaluated.
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(CRPS I [formerly called reflex sympathetic dystrophy]) is a syndrome with pain and signs of autonomic dysfunction after trauma or immobilization; the pathophysiologic mechanisms of CRPS I, however, remain unknown. ⋯ This case supports the hypothesis that immobilization is one of the major contributing factors for CRPS I.