Subject(s)
Diving , Decompression Sickness/diagnosis , Decompression Sickness/etiology , Decompression Sickness/therapy , Diagnosis, Differential , Diving/history , First Aid , History, 17th Century , History, 19th Century , History, 20th Century , History, Ancient , Humans , Immersion , Physical Exertion , Physical Fitness , Pressure , RecurrenceSubject(s)
Cerebrospinal Fluid Shunts , Decompression Sickness/etiology , Diving/adverse effects , Bias , Humans , Research DesignSubject(s)
Coronary Circulation , Decompression Sickness/etiology , Diving/adverse effects , Heart Atria , Humans , Risk FactorsSubject(s)
Carbon Monoxide Poisoning/therapy , Hyperbaric Oxygenation , Ethics, Medical , Humans , United KingdomABSTRACT
Decompression sickness (DCS) is usually categorised as type I (mild; peripheral pain, non-neurological) or type II (serious; neurological). Type II is regarded as predominantly a spinal cord disease with infrequent cerebral involvement. Cerebral perfusion was studied by injection of 99Tcm-hexamethylpropyleneamine oxime and single photon emission tomography in 28 divers with confirmed incidents of DCS and cerebral arterial gas embolism (CAGE). Cerebral perfusion deficits were present in all 23 cases of type II DCS and in all 4 cases of CAGE. No deficits were present in the single case of type I DCS. Type II DCS should be recognised as a diffuse, multifocal, central nervous system disease.
Subject(s)
Cerebrovascular Circulation , Decompression Sickness/diagnostic imaging , Intracranial Embolism and Thrombosis/diagnostic imaging , Movement Disorders/etiology , Organometallic Compounds , Oximes , Tomography, Emission-Computed , Adolescent , Adult , Decompression Sickness/etiology , Diving/adverse effects , Female , Functional Laterality , Humans , Intracranial Embolism and Thrombosis/etiology , Male , Middle Aged , Technetium Tc 99m Exametazime , Time FactorsABSTRACT
Somatosensory evoked potentials (SEP) were used in an animal model to measure spinal cord electrophysiological function. Animals were submitted to a dive profile resulting in spinal cord decompression sickness (DCS). The animals were treated after a delay allowing the lesion to consolidate. Serial measurements of SEP documented the onset, duration, and outcome of treatment. Physiological data were recorded throughout each experiment. Group A (n = 10) was recompressed to 60 fsw (feet of sea water) breathing 100% oxygen (2.8 ATA) and Group B (n = 8) was treated at 66 fsw breathing 66% oxygen (2.0 ATA). No differences were found between groups in the severity, surface interval before treatment, or the maximum effect of treatment. The maximum effect of treatment was seen by 25 min of treatment. Animals were regrouped into responders and nonresponders. The latter displayed a more rapid onset, a more severe insult, and more adverse physiological effects than the responders. The possibility of a different etiology was considered together with the failure to differentiate between the treatment groups. It was concluded that treatment B was safer but the problems of introducing a new therapeutic table outweighed the safety advantage.
Subject(s)
Decompression Sickness/therapy , Decompression , Evoked Potentials, Somatosensory , Hyperbaric Oxygenation , Spinal Cord Injuries/therapy , Animals , Decompression Sickness/complications , Decompression Sickness/physiopathology , Dogs , Male , Spinal Cord/physiopathology , Spinal Cord Injuries/etiology , Spinal Cord Injuries/physiopathologyABSTRACT
Pathological examination of spinal cords from animals subjected to experimental decompression sickness (DCS) was undertaken in an attempt to explain the disparate response to treatment observed. Eight experimental animals, four undived control animals, and two dived but untreated animals were perfusion fixed, and the spinal cords were removed. Light microscopy of toluidine blue stained, ultrathin sections from dived animals demonstrated a distinctive widened myelin sheath showing a banded pattern of myelin disruption. This pattern was confirmed by electron microscopy and showed the separation to be between abutting double layers of myelin. Artifactual changes were also present in dived and undived animals. These previously unreported changes may be caused by DCS. They are compatible with the major mechanisms proposed in the pathophysiology of spinal cord DCS and may also account for the response to treatment seen in our experimental animals. It is suggested that these findings may also explain the response to treatment seen in patients, together with the formation of late lesions described in the spinal cords of long-term survivors of DCS.
