They may also show the underlying cause and the extent to which the disease has progressed. Treatment
Several methods of treatment are available, mainly consisting of careful drug therapy and surgery. Glucocorticoids (such as prednisone or methylprednisolone) decrease the inflammatory response to tumor invasion and edema surrounding the tumor. Glucocorticoids are most helpful if the tumor is steroid-responsive, such as lymphomas. In addition, diuretics (such as furosemide) are used to reduce venous return to the heart which relieves the increased pressure.In an acute setting, endovascular stenting by an interventional radiologist may provide relief of symptoms in as little as 12–24 hours with minimal risks.Should a patient require assistance with respiration whether it be by bag/valve/mask, bilevel positive airway pressure (BiPAP), continuous positive airway pressure (CPAP) or mechanical ventilation, extreme care should be taken. Increased airway pressure will tend to further compress an already compromised SVC and reduce venous return and in turn cardiac output and cerebral and coronary blood flow. Spontaneous respiration should be allowed during endotracheal intubation until sedation allows placement of an ET tube and reduced airway pressures should be employed when possible. Prognosis
Symptoms are usually relieved with radiation therapy within one month of treatment. However, even with treatment, 99% of patients die within two and a half years. This relates to the cancerous causes of SVC found in 90% of cases. The average age of disease onset is 54 years. See also
Pembertons sign

References
Further reading
Wilson LD, Detterbeck FC, Yahalom J (May 2007). "Clinical practice. Superior vena cava syndrome with malignant causes". N Engl J Med.
When feeling motion but not seeing it (for example, in the cabin of a ship with no portholes), the inner ear transmits to the brain that it senses motion, but the eyes tell the brain that everything is still. As a result of the incongruity, the brain concludes that the individual is hallucinating and further concludes that the hallucination is due to poison ingestion. The brain responds by inducing vomiting, to clear the supposed toxin. Treismans indirect argument has recently been questioned via an alternative direct evolutionary hypothesis, as well as modified and extended via a direct poison hypothesis. The direct evolutionary hypothesis essentially argues that there are plausible means by which ancient real or apparent motion could have contributed directly to the evolution of aversive reactions, without the need for the co-opting of a poison response as posited by Treisman. Nevertheless, the direct poison hypothesis argues that there still are plausible ways in which the bodys poison response system may have played a role in shaping the evolution of some of the signature symptoms that characterize motion sickness. Nystagmus hypothesis
Yet another theory, known as the nystagmus hypothesis, has been proposed based on stimulation of the vagus nerve resulting from the stretching or traction of extra-ocular muscles co-occurring with eye movements caused by vestibular stimulation. There are three critical aspects to the theory: first is the close linkage between activity in the vestibular system, i.e., semicircular canals and otolith organs, and a change in tonus among various of each eyes six extra-ocular muscles.