Originally Posted by Annie Poo

Welcome,

If your CRPS is caused by a defined nerve injury, then it's CRPS type II (which I have, resulting from venipuncture nerve injury).

Following are abstracts of two recent research articles dealing with treatment of neuropathic pain with Botox:

(1) Ranoux et al, 2008, Annals of Neurology, "Botulinum toxin type A induces direct analgesic effects in chronic neuropathic pain"

OBJECTIVE: Botulinum toxin type A (BTX-A) has been reported to have analgesic effects independent of its action on muscle tone, possibly by acting on neurogenic inflammation. Such a mechanism may be involved in peripheral neuropathic pain. METHODS: A possible direct analgesic effect of BTX-A pain processing was investigated in 29 patients with focal painful neuropathies and mechanical allodynia using a randomized, double-blind, placebo-controlled design. Patients received a one-time intradermal administration of BTX-A (20-190 units) into the painful area. Outcome measures, evaluated at baseline, then at 4, 12, and 24 weeks, included average spontaneous pain intensity, quantified testing of thermal and mechanical perception and pain, allodynia to brushing (area, intensity), neuropathic symptoms, clinical global impression, and quality of life. RESULTS: BTX-A treatment, relative to placebo, was associated with persistent effects on spontaneous pain intensity from 2 weeks after the injection to 14 weeks. These effects correlated with the preservation of thermal sensation at baseline (p < 0.05). BTX also improved allodynia to brush and decreased pain thresholds to cold, without affecting perception thresholds. There were sustained improvements in the proportion of responders (number needed to treat for 50% pain relief: 3.03 at 12 weeks), neuropathic symptoms, and general activity. Most patients reported pain during the injections, but there were no further local or systemic side effects. INTERPRETATION: These results indicate for the first time that BTX-A may induce direct analgesic effects in patients with chronic neuropathic pain independent of its effects on muscle tone and suggest novel indications for BTX-A in analgesia.

(2) Yuan et al, 2009, Neurology, "Botulinum toxin for diabetic neuropathic pain"

BACKGROUND: Diabetic neuropathy is a common complication in diabetes, with patients typically experiencing diverse sensory symptoms including dysesthesias in the feet and usually accompanied by sleep disturbance. There is still no comprehensive understanding of the underlying biologic processes responsible for diabetic neuropathic pain. Thus, the current symptomatic therapy remains unsatisfactory. Recent experimental evidence suggests that botulinum toxin type A (BoNT/A) may not only inhibit the release of acetylcholine at the neuromuscular junctions, but also modulate afferent sensory fiber firing, thereby relieving neuropathic pain. METHODS: A double-blind crossover trial of intradermal BoNT/A for diabetic neuropathic pain in 18 patients was conducted to evaluate the effectiveness. RESULTS: We find significant reduction in visual analog scale (VAS) of pain by 0.83 +/- 1.11 at 1 week, 2.22 +/- 2.24 at 4 weeks, 2.33 +/- 2.56 at 8 weeks, and 2.53 +/- 2.48 at 12 weeks after injection in the BoNT/A group, as compared to the respective findings for a placebo group of 0.39 +/- 1.18, -0.11 +/- 2.04, 0.42 +/- 1.62, and 0.53 +/- 1.57 at the same timepoints (p < 0.05). Within the BoNT/A group, 44.4% of the participants experienced a reduction of VAS >/=3 within 3 months after injection, whereas there was no similar response in the placebo group. At the 4-week postinjection stage, improvement in sleep quality was measured using the Chinese version of the Pittsburgh Sleep Quality Index. CONCLUSIONS: This pilot study found that botulinum toxin type A significantly reduced diabetic neuropathic pain and transiently improved sleep quality. Further large-scaled study is warranted.

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Botox is the commercial preparation of Botulinum toxin type A produced now by Allergan Pharmaceuticals. Although well-known for cosmetic uses, Botox is also used for the treatment of various severe spastic muscle disorders, and has been for a long time. Botulinum toxins bind to neurons at neuromuscular junctions and block the release of neurotransmitters, effectively paralyzing muscles. Basically, it binds to nerves in a specific manner, preventing them from telling muscles to move. It's also the toxin responsible for the foodborne disease botulism, which results in an overall paralysis, and potentially death. However, if injected in small amounts into a target muscle, the toxin will paralyze that muscle. This can be advantageous for dystonias and other spastic muscle disorders where muscles move uncontrollably.

Potential medical uses of botulinum toxin in the future are numerous, and treatment of neuropathic pain by the toxin is fascinating. I'm assuming there are numerous additional funded projects in the works.

Ironically, I've worked in a research lab with botulinum toxins for many many years. Because it's so potent, I'm immunized against types A-E, and thus treatment of my CRPS by Botox would be useless. Guess I'm destined to have a lot of wrinkles as well when I get older.

It's a fascinating toxin.