Cushing reflex
[3] The Cushing reflex classically presents as an increase in systolic and pulse pressure, reduction of the heart rate (bradycardia), and irregular respiration.
In the past, physicians and nurses have relied on hemodynamic changes or bradycardia, the late phase of the reflex, to identify the ICP increase.
Once the initial stage of the Cushing reflex (bradycardia combined with hypertension) was discovered, it offered a much more reliable and swift warning sign of high ICP.
[9] It was found that hypertension and bradycardia occurred 93% of the time when cerebral perfusion pressure (CPP) dropped below 15 mmHg due to raised ICP.
[10] It has also been reported that the presence of a Cushing reflex due to an ICP increase could allow one to conclude that ischemia has occurred in the posterior cranial fossa.
In one study, it was confirmed that raised ICP due to subarachnoid hemorrhaging causes mechanical distortion of the brainstem, specifically the medulla.
Due to the mechanism of the Cushing reflex, brainstem distortion is then swiftly followed by sympathetic nervous system over activity.
[13] In addition, during typical neurosurgical procedures on patients, especially those involving neuroendoscopic techniques, frequent washing of the ventricles have been known to cause high intracranial pressure.
It has been found that if a Cushing reflex occurs, brain plateau wave changes can be erased due to disappearance of high ICP.
[citation needed] Meanwhile, baroreceptors in the aortic arch detect the increase in blood pressure and trigger a parasympathetic response via the vagus nerve.
[18] Bradycardia may also be caused by increased ICP due to direct mechanical distortion of the vagus nerve and subsequent parasympathetic response.
[21] Raised intracranial pressure can ultimately result in the shifting or crushing of brain tissue, which is detrimental to the physiological well-being of patients.
It is widely accepted that the Cushing reflex acts as a baroreflex, or homeostatic mechanism for the maintenance of blood pressure, in the cranial region.
[9] Specifically, the reflex mechanism can maintain normal cerebral blood flow and pressure under stressful situations such as ischemia or subarachnoid hemorrhages.
[9] Eventually, the ICP drops to a level range where a state of induced hypertension in the form of the Cushing reflex is no longer required.
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 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".
To begin, Cushing monitored the caliber and color of cortical vessels by fitting a glass window into the skull of the dog.
He also noted that there must exist a specific regulatory mechanism that increased blood pressure to a high enough point such that it did not create anemic conditions.
[25] Several notable figures in the medical field, including Ernst von Bergmann,[26] Henri Duret,[27] Friedrich Jolly,[28] and others experimented with intracranial pressure similarly to Cushing.
[31] It has been determined that rate of respiration is affected by the Cushing reflex, though the respiratory changes induced are still an area that needs more research.
[6] Early experiments also put animal subjects under artificial ventilation, only allowing for limited conclusions about respiration in the Cushing reflex.
[7] The use of anesthetics proposes ideas for future research, since the creation of the Cushing response has been difficult to create under basal conditions or without anesthesia.
[30] Although the Cushing reflex was primarily identified as a physiological response when blood flow has almost ceased, its activity has also been seen in fetal life.
