BACKGROUND
Symptoms of spinal cord decompression sickness (DCS) occur almost immediately after emerging from the water. It is recommended that recompression treatment be performed soon to decrease the bubble size and avoid further tissue injury. Unfortunately, there may be significant time delay from surfacing to recompression. The recompression therapy of which the hyperbaric treatment is effective is unclear. The purpose of this study was first to evaluate the effect of delayed hyperbaric treatment, initiated more than 30 hours after surfacing for DCS and second, to evaluate the different treatment protocols. METHODS: Sixty-eight injured divers presenting symptoms of spinal cord DCS were retrospectively included from the Seoul Medical Center. Diving information, time interval between symptom onset, and hyperbaric treatment were studied. The initial severity of spinal cord DCS was rated with the Boussuges severity score and muscle power examination and the presence of sequelae was evaluated at two weeks. Initial recompression treatment at 2.8–4 ATA (atmospheres absolute) with 100% oxygen breathing or deeper recompression was conducted. RESULTS: There were no significant differences between each group in age, diving experience, depth of dive, bottom time of dive, and Boussuges's score. With respect to treatment results, for the delayed treatment divers, good recovery was achieved in 47.1% of the divers. When treatment started early, good recovery was achieved in 58.8% of the divers. Hyperbaric treatment using the U.S. Navy Table 6a protocol trended toward a better clinical outcome, statistically significant (p=0.04) compared to the U.S. Navy Table 6. CONCLUSIONS: The prognosis was as good as the early treatment when the recompression therapy was delayed in patients with spinal decompression sickness. Hyperbaric oxygen treatment was better in the U.S. Navy Table 6a than the U.S. Navy Table 6 in patients with spinal decompression sickness.

Background
Decompression sickness may involve the central nervous system, and the most common site is spinal cord. This study was conducted to determine the relationship between magnetic resonance (MR) imaging findings of spinal damage and clinical findings in acute decompression sickness.
Methods
We conducted a retrospective review of 12 patients (male=10, female=2) who presented with spinal cord symptoms. We investigated their clinical features, neurological findings and radiologic findings.
Results
The depth and bottom time of the dive were 34.5 meters (range 22-56) and 22.7 minutes (range 10-55) respectively. Most divers ascended within appropriate time frame as shown by the decompression tables. The most frequent initial symptoms were lower limbs weakness (n=12), followed by sensory disturbances (n=10) and bladder dysfunction (n=5). The chief radiologic abnormalities were continuous (n=3), or non-continuous (n=5) high signal intensity on T2-weighted images at posterior paramedian portion of the spinal cord, mainly thoracic level. There were no abnormal findings in remaining 4 patients and they showed good prognosis. All patients were treated with hyperbaric oxygen therapy and some received high dose dexamethasone. On discharge, 5 patients had made a full recovery, 7 had some residual neurological sequelae, and most patients except one regained normal bladder function.
Conclusions
Spinal cord decompression sickness is a neurological emergency. Early recognition and treatment may minimize neurological damage. Initial normal finding in MR imaging was a good redictor for prognosis in spinal decompression sickness.

Various immunotherapeutic modalities have been used based on the autoimmune pathogenic mechanisms of myasthenia gravis (MG). Cell-mediated immunity as well as auto-antibodies may play a role in the remission and relapse of MG. We recently experienced two patients with MG who showed spontaneous remission fter inadvertent severe leukopenia. These findings suggest that the cell-mediated immune process is important in the treatment of MG, and selective suppression of leukocyte may induce remission in the patients with intractable MG.