The ocular tilt reaction (OTR) comprises  skew deviation, head tilt and ocular torsion involving structures of the inner ear responsible for maintenance of balance of the body i.e. the semi-circular canals (SCC), utricle and saccule. Each anterior semi-circular canals has excitatory projections to the ipsilateral superior rectus muscle and its yoke i.e., the contralateral inferior oblique while simultaneously inhibiting the ipsilateral inferior rectus muscle and its yoke i.e. the contralateral superior oblique. Also, each posterior semi-circular canals has excitatory projections to the ipsilateral superior oblique and its yoke i.e. the contralateral inferior rectus, while simultaneously inhibiting the ipsilateral inferior oblique and its yoke i.e. the contralateral superior rectus. A head tilt causes stimulation of both anterior semi-circular canals and the posterior semi-circular canals resulting in excitation of ipsilateral intorters (superior oblique and superior rectus) and contralateral extorters (inferior oblique and inferior rectus) while their antagonists are simultaneously inhibited. The otoliths (utricle and saccule) probably follow a similar pathway. Normally, a body tilt (along with the initial head tilt) to the right causes a shift of the subjective visual vertical (SVV) to the left resulting in reflex, compensatory orientation of the head to left to realign the SVV to the true vertical. The initial head tilt to right will cause stimulation of the right utricle resulting in excitory signals to pass to the SR and SO (right eye), and IO and IR (left eye). Simultaneously, inhibitory signals pass to their antagonists.
Once the abdominal wall can no longer expand, any further fluid leaking into the tissue results in fairly rapid rises in the pressure within the closed space. Initially this increase in pressure does not cause organ failure but does prevent organs from working properly – this is called intra-abdominal hypertension and is defined as a pressure over 12 mmHg in adults. ACS is defined by a sustained IAP(intra-abdominal pressure) above 20 mmHg with new-onset or progressive organ failure. Severe organ dysfunctionent syndrome. These pressure measurements are relative. Small children get into trouble and develop compartment syndromes at much lower pressures while young previously healthy athletic individuals may tolerate an abdominal pressure of 20 mmHg very well. The underlying cause of the disease process is capillary permeability caused by the systemic inflammatory response syndrome (SIRS) that occurs in every critically ill patient. SIRS leads to leakage of fluid out of the capillary beds into the interstitial space in the entire body with a profound amount of this fluid leaking into the gut wall, mesentery and retroperitoneal tissue. Abdominal compartment syndrome follows a destructive pathway similar to compartment syndrome of the extremities. When increased compression occurs in such a hollow space, organs will begin to collapse under the pressure. As the pressure increases and reaches a point where the abdomen can no longer be distended it starts to affect the cardiovascular and pulmonary systems. When abdominal compartment syndrome reaches this point without surgery and help of a silo the patient will most likely die.