RSD/CRPS is a very painful condition and patients need to search out and try methods beneficial in relieving their painful condition.
Movement disorders are common in most RSD/CRPS patients, as the movement disorder is frequently ascribed to hysteria and pain. This condition is seen in complex regional pain syndrome (CRPS I/RSD) as well (CRPS I I ) ( causalgia ) where the movement disorder, due to peripheral trauma, may be in the form of Parkinsonian Tremor.
In extensive studies movement disorders in RSD/CRPS have been accompanied by tremor and dystonia. Experiments have demonstrated the importance of damage and degeneration especially in the dorsal horn of the spinal cord due to a noxious stimulus. This secondary abnormality in the central nervous system(spinal cord) may play a role in movement disorders seen in neuropathic pain syndromes. Pathological, peripheral nervous system input can also cause reorganization of other CNS structures such as the spinal cord, basal ganglia, nucleus gracilis, and thalamus. Obviously such secondary disorganization cerebral nuclei are compatible with secondary development of movement disorder accompanying peripheral nervous system damage.
Patients suffering from RSD/CRPS report a facilitation and enhancement of physiologic tremors that can begin one day to nine months after injury to peripheral nerves. Obviously the peripheral nerve damage in and of itself is in capable of starting and perpetuating tremor, dystonia ,or hypertonicity. On the other hand , the tremor is usually accompanied by certain degree of flex or spasm and tendency for dystonia. Goldman and Ahlskog, as well as Dewey and colleagues – both groups of authors from the Mayo Clinic have emphasized that post traumatic dystonia secondary to a cervical sprain is:
(i). Not psychogenic
(ii). The condition is on the basis of centrally driven post traumatic muscle spasms. Such movement disorders (tremor or dystonia) originate from a peripheral nerve injury with secondary pathologic input to CNS (especially the spinal cord). The prolonged neuropathic afferent input, in the long run, causes disturbance of plasticity in the spinal cord. The disruption of normal plasticity and inhibitory effect of the spinal cord on the neuropathic afferent input eventually results in the following phenomena.
Application of a cast causes immobilization and stimulation of the deep mechanoreceptors. These silent sleeping nociceptors become activated with rest and inactivity which, in turn, leads to pain, edema and movement disorder.
Myoclonic jerks are common forms of movement disorder in RSD/CRPS:
(i). They may be a manifestation of deafferentation and sensitization of spinal cord due to long-term afferent cytokines damage to the inhibitory granular cells in layers I and I I. As such, they develop in later stages of the disease. Any form of immobilization ( cast, wheelchair, etc .) contributes to this phenomenon.
(ii). The myoclonic jerks are seen in patients undergoing withdrawal of opioids ( rebound phenomenon).
(iii). In patients suffering from RSD/CRPS due to spinal cord injury myoclonic jerks were invariably noted. In addition, myoclonic jerks were present in RSD/CRPS patients secondary to electrical injury. This may be due to electricity going through the path of least resistance (afferentc -fibers) and secondarily originating spinal cord dysfunction.
(iv ). Myoclonic jerks are a long-te rm complication of limb amputation among patients. Myoclonic jerks are frequently mistaken for “pseudoseizures ” due to the fact that theictal events or iginating from spinal cord a re too deep to present themselves on scalp video -EEG monitoring. In more severe cases, such as electrical injury complicated by RSD/CRPS, somatosensory evoked potentia l (SSEP) test identifies the spinal cord dysfunction as the originator of this form of myelogenic seizure.
RSD tremors are usually a late development ( stage I I I) of the clinical picture of RSD . It is well known that stage III RSD is somewhat resistant to treatment. This is due to the fact that the chronic disturbance of plasticity of the CNS is due to the long-standing presence of the disease. However, nerve blocks, alpha I and alpha I I blockers (Clonidine, Hytrin, and Dibenzyline ) may be quite helpful in the management of the tremor. In our study of 82 patients with late stage RSD treated with an infusion pump, seven patients suffered from tremors. Six patients were reverting back to normal, and in one patient the tremor was markedly improved.
As noted, immobilization of the involved extremity is a major activation of the development of tremors in RSD. Removal of cast, braces and the discontinuation of using crutches or a wheelchair helps in the prevention and management of movement disorders in RSD patients.
For access to the full study: Dr. H. Hooshmand, M.D.