The patient should also be catheterized to test for and, if necessary, drain an over-distended bladder. A lumbar puncture can be performed after the MRI or at the time of  CT myelography. Corticosteroids are often given in high doses when symptoms begin with the hope that the degree of inflammation and swelling of the spinal cord will be lessened, but whether this is truly effective is still debated. Differential diagnosis
The differential diagnosis of acute TM includes demyelinating disorders, such as multiple sclerosis and neuromyelitis optica, infections, such as herpes zoster and herpes simplex virus, and other types of inflammatory disorders, such as systemic lupus erythematosus and neurosarcoidosis. It is important to also rule out an acute cause of compression on the spinal cord. Treatment
If treated early, some people experience complete or near complete recovery. Treatment options also vary according to the underlying cause. One treatment option includes plasmapheresis. Recovery from TM is variable between individuals and also depends on the underlying cause. Some patients begin to recover between weeks 2 and 12 following onset and may continue to improve for up to two years. Other patients may never show signs of recovery. Prognosis
The prognosis for TM depends on whether there is improvement in 3 to 6 months. Complete recovery is unlikely if no improvement occurs within this time. Incomplete recovery can still occur; however, aggressive physical therapy and rehabilitation will be very important. One-third of people with TM experience full recovery, one-third experience fair recovery but have significant neurological deficits, such as spastic gait.
Because immunological functions can modulate CNS physiology, a variety of immune processes have also been hypothesized to contribute to the initial development and maintenance of peripheral and central sensitization. Furthermore, trauma-related cytokine release, exaggerated neurogenic inflammation, sympathetic afferent coupling, adrenoreceptor pathology, glial cell activation, cortical reorganisation, and oxidative damage (e.g., by free radicals) are all factors which have been implicated in the pathophysiology of CRPS. In addition, autoantibodies are present in a wide number of CRPS patients and IgG has been recognized as one of the causes of hypersensitivity that stimulates A and C nociceptors, attributing to the inflammation.The mechanisms leading to reduced bone mineral density (up to overt osteoporosis) are still unknown. Potential explanations include a dysbalance of the activities of sympathetic and parasympathetic autonomic nervous system and mild secondary hyperparathyroidism. However, the trigger of secondary hyperparathyroidism has not yet been identified.In summary, the pathophysiology of complex regional pain syndrome has not yet been defined;  CRPS, with its variable manifestations, could be the result of multiple pathophysiological processes. Diagnosis
Diagnosis is primarily based on clinical findings. The original diagnostic criteria for CRPS adopted by the International Association for the Study of Pain (IASP) in 1994 have now been superseded in both clinical practice and research by the "Budapest Criteria" which were created in 2003 and have been found to be more sensitive and specific. They have since been adopted by the IASP.