These waves are characterized by acute rises of the ICP, and are accompanied by a decrease of the cerebral perfusion pressure. It has been found that if a Cushing reflex occurs, brain plateau wave changes can be erased due to disappearance of high ICP. Mechanism
The Cushing reflex is complex and seemingly paradoxical. The reflex begins when some event causes increased intracranial pressure (ICP). Since cerebrospinal fluid is located in an area surrounded by the skull, increased ICP consequently increases the pressure in the fluid itself. The pressure in the cerebral spinal fluid eventually rises to the point that it meets and gradually exceeds the mean arterial blood pressure (MAP). When the ICP exceeds the MAP, arterioles located in the brains cerebrum become compressed. Compression then results in diminished blood supply to the brain, a condition known as cerebral ischemia.During the increase in ICP, both the sympathetic nervous system and the parasympathetic nervous system are activated. In the first stage of the reflex, sympathetic nervous system stimulation is much greater than parasympathetic stimulation. The sympathetic response activates alpha-1 adrenergic receptors, causing constriction of the bodys arteries. This constriction raises the total resistance of blood flow, elevating blood pressure to high levels, which is known as hypertension. The bodys induced hypertension is an attempt to restore blood flow to the ischemic brain. The sympathetic stimulation also increases the rate of heart contractions and cardiac output. Increased heart rate is also known as tachycardia.
Cushings triad
Cushings triad is a clinical triad variably defined as having:

Irregular, decreased respirations (caused by impaired brainstem function)
Bradycardia
Systolic hypertension (widening pulse pressure)

History
Cushings reflex is named after Harvey Williams Cushing (1869–1939), an American neurosurgeon. Cushing began his research in Bern, Switzerland studying abroad with Emil Theodor Kocher. A month into his trip, Cushing received a formal proposition from Emil Theodor Kocher to begin testing how compression of the brain affected blood vessels. Cushing also enlisted the aid of Hugo Kronecker, a known blood pressure researcher. Utilizing Kroeneckers assistance and resources, Cushing began his research. Cushing left Bern in 1901 to work in Turin, Italy with Angelo Mosso, a previous student of Kroenecker. He continued to work on the same research project, while also simultaneously improving his methods of recording coincidence of blood pressure and ICP. In June 1901 Cushing published his first paper through Johns Hopkins Hospital Bulletin entitled "Concerning a definite regulatory mechanism of the vasomotor centre which controls blood pressure during cerebral compression". Between 1901 and 1903, Cushing published five papers pertaining to his research on the vasopressor response. These papers were published in German and English, and one was authored by Emil Theodor Kocher. Experimental setup and results
Cushing began experimenting once he obtained approval from Kocher. His experimental setup was a modified version of  Leonard Hills model to similarly test the effects of brain pressure on sinus pressure, cerebrospinal fluid pressure, arterial and venous blood pressure. Like Hill, Cushing used dogs for his experiments.