Complex Regional Pain Syndromes type 1 and 2 represent regional pain disorders not limited to the site of injury, with the following features:

1. Pain greater than might be expected from the original injury
2. Altered blood flow, localized edema, skin and hair changes
3. The pain itself may be burning or electrical in nature and is usually non-dermatomal due to hyperalgesia. Allodynia is often present.

The distinction between CRPS 1 and CRPS 2 is made by the specific neural mechanism of injury. CRPS 1 patients have the involvement of the Sympathetic Nervous System, while CRPS 2 patients have involvement of a specific injured Nerve. Both syndromes exhibit pain beyond the distribution of the original injury.

Sometimes both conditions are present and it is impossible to distinguish between CRPS1 and CRPS 2. The mechanism at play is one of local nerve injury with subsequent sympathetic coupling.

On an anatomical basis, severed axons and damaged axons form new sprouts known as microneuromas. These are hyperexcitable and within minutes to days after injury begin ectopic firing. Intact collateral nerves also develop ectopia and this spreads the area of pain. Normally non-painful touch fibers join in the excessive stimulation, initially creating paresthesias, but with central sensitization, allodynia develops and spreads to non-dermatomal sites.

At the same time it appears that there are several processes occurring in the sympathetic axis. One involves central sympathetic coupling with Wide Dynamic Range (WDR) Neurons in the Dorsal Horn serving to link the Dorsal Horn Nuclei with Sympathetic Nuclei. Increased activity of Sympathetic Efferents only tells part of the story. There is also an increase in Catecholamine sensitivity at the site of the injury. Additionally the sustained pain from the sensitization of Dorsal Root Ganglion Cells may trigger increased release of epinephrine systemically and in the local area of injury.

When both of these processes occur together there is increased pain from the nerve injury and another increase in pain from the sympathetic augmentation. The other problem is that sympathetic pain conditions do best with mobilization of the painful area, which is distant from the sustaining sympathetic coupling. On the other hand nerve injury does not yield to physical manipulation and may in fact worsen. This complicates and confounds ultimate rehabilitation.

Treatment for this condition should focus on medication and block management of pain, then physical therapy that takes into account aggravation of peripheral nerves. If the therapy causes ongoing aggravation, it should be stopped.

Pain control with anticonvulsants (Gabapentin, Carbemazepine, Lamotrigine, Topramax), Tricyclic Analgesics (Nortriptyline, Desipramine, Amitriptyline), Long Acting Opioids (MS Contin, Oramorph, Kadian, OxyContin, Duragesic, Methadone), Alpha 1 Blockers (Phenoxybenzamine, Terazocin), Alpha 2 agonists (Clonidine), Sodium Channel Blockers (LIdocaine, Mexilletine, Amantadine, Ketamine) and Calcium Channel Blockers (Verapamil, Ditelizem, Niphedipine) may help individually or in combination. Local Sympathetic Blocks of specific regional ganglia may be very helpful, especially if the condition is caught in the acute phase. These may be done without steriods and are often tried as a series of blocks every day or every other day. At times a constant infusion with a catheter may be necessary. Selective nerve root blocks, Neuroma blocks and epidural blocks may be helpful. Spinal Cord Stimulators can be highly effective. Intrathecal pumps are useful in delivering opioids in combination with Sodium Channel Blockers (Bupivacaine), Antispasmodics (Baclofen), or Alpha 2 agonists (Clonidine).