Paul G. Harch, KW Van Meter, SF Gottlieb, P Staab. Jo Ellen Smith Hyperbaric Medicine Unit (JESHMU), New Orleans, LA 70131 and University of South Alabama, Mobile, AL.
Background: We describe a prospective case study of a sport SCUBA diver with Type II DCS (brain) in which HMPAO SPECT brain imaging with oxygen intervention was used in the identification of potentially recoverable brain tissue which subsequently responded to low pressure HBOT as demonstrated by improvement in neurological functions and SPECT brain images.
Case: A 49 year old sport SCUBA diver presented 28 days following a 7 day, 14 dive trip with irritability, expressive aphasia, short-term memory dysfunction, imbalance, bilateral tinnitus and hearing loss, and right-sided discoordination. Symptions persisted despite two monoplace USN Table 6 and one 2 atm abs/90 min HBOT in a 36 hour period. At this time HMPAO SPECT brain images were obtained using a Picker Prism 3000, tissue resolution of 6-10 mm, and showed right frontal, occipital, basal ganglia, temporal, cerebellar, and left temporal and frontal perfusion/metabolism deficits consistent with neurological condition which demonstrated improvement upon a single exposure to 1.5 atm abs oxygen. Scans were read qualitatively with general concordance by 2 blinded independent radiologist. MRI of the brain was obtained on a Diasonics MRI Scanner, .5 Tesla magnet TR/TE’s of 700/25, 2600/40, and 2600/80. The patient underwent 60 HBOT treatments (17 Rxs at 2.0 atm abs, 7 at 1.75 atm abs, and 35 at 1.5 atm abs). Treatment pressure began at 2 atm abs, was decreased to 1.5 p second SPECT scan, and empirically increased to 1.75 toward the end of the treatment course. During treatment the patient’s tinnitus decreased, hearing, memory, balance, right-sided coordination, aphasia, and irritability improved while the SPECT images normalized.
Conclusion: This case uniquely demonstrates the importance of SPECT brain imaging with oxygen intervention and low pressure HBOT in diagnosing the extent of Type II DCS, identifying recoverable brain tissue, treating residual deficits of Type II DCS following standard tx, and in determining the endpoint of treatment.