He explained in detail the pathophysiology involved, “When the ligament fibers do not regain their normal tensile strength following strain, the fibers stretch under normal tension and permit excessive tension-stimulation of the non-stretchable sensory nerve fibrils, which are abundant within the fibro-osseous attachments. This is the original of noxious barrages of sensory afferent and antidromic impulses which cause pain and bone dystrophy (decalcification). Tension stimulation on afferent sensory nerves within the weak fibro-osseous attachments of ligament to bone is the origin of barrages of afferent impulses transmitted to the spinal cord and to the brain where they are interpreted as pain and referred pain. While from the same origin, barrages of antidromic impulses pass directly and by axon reflex to bone blood vessels and cause a neurovascular disturbance of bone metabolism that results in direct decalcification, which further weakens the ligamentous attachment to bone. From the afferent stimulation in the spinal cord, there are noxious barrages of efferent impulses that cause muscle spasm, while other efferent and sympathetic impulses pass from the same and adjacent cord segments and cause a reflex neurovascular decalcification of large areas of bone. This weakens the attachment of all ligaments and tendons in the decalcified areas and completes a vicious circle of ligament relaxation and decalcification.”250 (See Figure 15.)
| Figure 15. Pathophysiologic schemata connecting ligament weakness to bone decalcification.250 |
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The decalcification or weakening of bone is one of the hallmark features of chronic CRPS.251-253 Dr. Hackett showed that Prolotherapy not only could resolve the localized ligament pain, but also the autonomic nervous system phenomenon of referral pain, vasomotor changes, and bone dystrophy.254-257 The resolution of disorders involving the autonomic nervous system including reflex sympathetic with Prolotherapy has subsequently been reported.258-260
COMPLEX REGIONAL PAIN SYNDROME CASE REPORT
R.A., a 27 year-old female college student sustained a severe injury to her left foot after twisting her left ankle while out walking in the fall of 2002. X-rays revealed a metatarsal fracture in November, 2002. Initial treatment involved primarily rest and several prolonged sessions of immobilization involving the patient wearing a walking boot. She was also prescribed NSAIDs, narcotics, and received several spinal blocks because of the intense pain. She remained on these treatments for two years after the initial injury but only saw her pain increase to the point where she could not put pressure on the left foot, and was unable to walk without a crutch. She said she could not wear a sock, slept with her foot outside the covers, and even the water from a shower caused intense pain. Her studies suffered, and she needed higher and higher doses of narcotics and anti-depressant medications just to get through the day. She saw around 20 specialists during a two year span including orthopedists, podiatrists, psychiatrist pain specialist and various therapists. In December 2004, an MRI revealed a torn tendon in the foot which was surgically repaired. Unfortunately, surgery did not help her symptoms. The severe pain and swelling in the foot and ankle increased and persisted. Treatment at this time included several rounds of steroid and trigger point injections, immobilization, more NSAIDs, immobility and physical therapy without success. In 2005, she was diagnosed with reflex sympathetic dystrophy (CRPS).
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