Protein molecules may be denatured by reorientation of the secondary and tertiary structure when non-polar groups protrude into the bubble gas and hydrophilic groups remain in the surrounding blood, which may generate a cascade of pathophysiological events with consequent production of clinical signs of decompression sickness.The physiological effects of a reduction in environmental pressure depend on the rate of bubble growth, the site, and surface activity. A sudden release of sufficient pressure in saturated tissue results in a complete disruption of cellular organelles, while a more gradual reduction in pressure may allow accumulation of a smaller number of larger bubbles, some of which may not produce clinical signs, but still cause physiological effects typical of a blood/gas interface and mechanical effects. Gas is dissolved in all tissues, but decompression sickness is only clinically recognised in the central nervous system, bone, ears, teeth, skin and lungs.Necrosis has frequently been reported in the lower cervical, thoracic, and upper lumbar regions of the spinal cord. A catastrophic pressure reduction from saturation produces explosive mechanical disruption of cells by local effervescence, while a more gradual pressure loss tends to produce discrete bubbles accumulated in the white matter, surrounded by a protein layer. Typical acute spinal decompression injury occurs in the columns of white matter. Infarcts are characterised by a region of oedema, haemorrhage and early myelin degeneration, and are typically centred on small blood vessels. The lesions are generally discrete. Oedema usually extends to the adjacent grey matter.
Habit-induced individuals generally have a history of bulimia nervosa or of intentional regurgitation (magicians and professional regurgitators, for example), which though initially self-induced, forms a subconscious habit that can continue to manifest itself outside the control of the affected individual. Trauma-induced individuals describe an emotional or physical injury (such as recent surgery, psychological distress, concussions, deaths in the family, etc. ), which preceded the onset of rumination, often by several months. Pathophysiology
Rumination syndrome is a poorly understood disorder, and a number of theories have speculated the mechanisms that cause the regurgitation, which is a unique symptom to this disorder. While no theory has gained a consensus, some are more notable and widely published than others.The most widely documented mechanism is that the ingestion of food causes gastric distention, which is followed by abdominal compression and the simultaneous relaxation of the lower esophageal sphincter (LES). This creates a common cavity between the stomach and the oropharynx that allows the partially digested material to return to the mouth. There are several offered explanations for the sudden relaxation of the LES. Among these explanations is that it is a learned voluntary relaxation, which is common in those with or having had bulimia. While this relaxation may be voluntary, the overall process of rumination is still generally involuntary. Relaxation due to intra-abdominal pressure is another proposed explanation, which would make abdominal compression the primary mechanism. The third is an adaptation of the belch reflex, which is the most commonly described mechanism.