The authors reviewed 29 cases of spinal tuberculosis treated from 1973 to 1993 with an average follow-up time of 7.4 years. Clinical findings included back pain, paraparesis, kyphosis, fever, sensory disturbance, and bowel and bladder dysfunction. Twenty-two patients (76%) presented with neurological deficit; 12 (41%) were initially misdiagnosed. Sixteen patients (55%) had predominant vertebral body involvement; nine had marked bone collapse with neurological compromise. Eleven individuals (39%) had intraspinal granulomatous tissue causing neurological dysfunction in the absence of bone destruction, and two (7%) had intramedullary tuberculomas. All patients received antituberculous medications: 13 were initially treated with bracing alone, eight underwent laminectomy and debridement of extra- or intradural granulomatous tissue, and eight underwent anterior, posterior, or combined fusion procedures. No patient with neurological deficit recovered or stabilized with nonoperative management. Thirteen patients were readmitted with progression of inadequately treated osteomyelitis; 12 (92%) of these required new or more radical fusion procedures. Anterior fusion failure was associated with marked preoperative kyphosis and multilevel disease requiring a graft that spanned more than two disc spaces. Courses of antibiotic medications shorter than 6 months were invariably associated with disease recurrence. It was concluded that 1) patients should receive at least 12 months of appropriate antituberculous therapy; 2) individuals with neurological deficit should undergo surgical decompression; 3) laminectomy and debridement are adequate for intraspinal granulomatous tissue in the absence of significant bone destruction; 4) when vertebral body involvement has produced wedging and kyphosis, aggressive debridement and fusion are indicated to prevent delayed instability and progression of disease.

Hyperbaric O2 has a more robust posttreatment effect than NBH on oxidative cerebral metabolism related to its ability to produce a brain tissue PO2 > or = 200 mm Hg. However, it appears that O2 treatment for severe TBI is not an all or nothing phenomenon but represents a graduated effect. No signs of pulmonary or cerebral O2 toxicity were present.

The authors enrolled 168 patients with closed-head trauma into a prospective trial to evaluate the effect of hyperbaric oxygen in the treatment of brain injury. Patients were included if they had a total Glasgow Coma Scale (GCS) score of 9 or less for at least 6 hours. After the GCS score was established and consent obtained, the patient was randomly assigned, stratified by GCS score and age, to either a treatment or a control group. Hyperbaric oxygen was administered to the treatment group in a monoplace chamber every 8 hours for 1 hour at 1.5 atm absolute; this treatment course continued for 2 weeks or until the patient was either brain dead or awake. An average of 21 treatments per patient was given. Outcome was assessed by blinded independent examiners. The entire group of 168 patients was followed for 12 months, with two patients lost to follow-up study. The mortality rate was 17% for the 84 hyperbaric oxygen-treated patients and 32% for the 82 control patients (chi-squared test, 1 df, p = 0.037). Among the 80 patients with an initial GCS score of 4, 5, or 6, the mortality rate was 17% for the hyperbaric oxygen-treated group and 42% for the controls (chi-squared test, 1 df, p = 0.04). Analysis of the 87 patients with peak intracranial pressures (ICP) greater than 20 mm Hg revealed a 21% mortality rate for the hyperbaric oxygen-treated patients, as opposed to 48% for the control group (chi-squared test, 1 df, p = 0.02). Myringotomy to reduce pain during hyperbaric oxygen treatment helped to reduce ICP. Analysis of the outcome of survivors reveals that hyperbaric oxygen treatment did not increase the number of patients in the favorable outcome categories (good recovery and moderate disability). The possibility that a different hyperbaric oxygen treatment paradigm or the addition of other agents, such as a 21-aminosteroid, may improve quality of survival is being explored.

T he enormous negative social and economic impact of TBI throughout the world cannot be overemphasized. The major issue is premature death and disability both in civilian and military populations. Conservative estimates of the prevalence of long-term disability due to TBI in the United States are well over 3 million people. The economic toll of TBI exceeds $60 billion per year. 18 Our previous investigations of HBO 2 Object. Preclinical and clinical investigations indicate that the positive effect of hyperbaric oxygen (HBO 2 ) for severe traumatic brain injury (TBI) occurs after rather than during treatment. The brain appears better able to use baseline O 2 levels following HBO 2 treatments. In this study, the authors evaluate the combination of HBO 2 and normobaric hyperoxia (NBH) as a single treatment.Methods. Forty-two patients who sustained severe TBI (mean Glasgow Coma Scale [GCS] score 5.7) were prospectively randomized within 24 hours of injury to either: 1) combined HBO 2 /NBH (60 minutes of HBO 2 at 1.5 atmospheres absolute [ATA] followed by NBH, 3 hours of 100% fraction of inspired oxygen [FiO 2 ] at 1.0 ATA) or 2) control, standard care. Treatments occurred once every 24 hours for 3 consecutive days. Intracranial pressure, surrogate markers for cerebral metabolism, and O 2 toxicity were monitored. Clinical outcome was assessed at 6 months using the sliding dichotomized Glasgow Outcome Scale (GOS) score. Mixedeffects linear modeling was used to statistically test differences between the treatment and control groups. Functional outcome and mortality rates were compared using chi-square tests.Results. There were no significant differences in demographic characteristics between the 2 groups. In comparison with values in the control group, brain tissue partial pressure of O 2 (PO 2 ) levels were significantly increased during and following combined HBO 2 /NBH treatments in both the noninjured and pericontusional brain (p < 0.0001). Microdialysate lactate/pyruvate ratios were significantly decreased in the noninjured brain in the combined HBO 2 /NBH group as compared with controls (p < 0.0078). The combined HBO 2 /NBH group's intracranial pressure values were significantly lower than those of the control group during treatment, and the improvement continued until the next treatment session (p < 0.0006). The combined HBO 2 /NBH group's levels of microdialysate glycerol were significantly lower than those of the control group in both noninjured and pericontusional brain (p < 0.001). The combined HBO 2 /NBH group's level of CSF F2-isoprostane was decreased at 6 hours after treatment as compared with that of controls, but the difference did not quite reach statistical significance (p = 0.0692). There was an absolute 26% reduction in mortality for the combined HBO 2 /NBH group (p = 0.048) and an absolute 36% improvement in favorable outcome using the sliding dichotomized GOS (p = 0.024) as compared with the control group.Conclusions. In this Phase II clinical trial, in comparison with standard care (control t...