The Cushing Reflex
Progressive hypertension associated with bradycardia and diminished respiratory effort is a specific response to acute, potentially lethal rises in ICP. This response is called the Cushing reflex, and its occurrence indicates that the ICP has reached life-threatening levels. The Cushing reflex can occur whenever ICP is increased, regardless of the cause. The full triad of hypertension, bradycardia, and respiratory irregularity is seen in only one third of cases of life-threatening increased ICP.
Cerebral herniation occurs when increasing cranial volume and ICP overwhelms the natural compensatory capacities of the CNS. Increased ICP may be the result of posttraumatic brain swelling, edema formation, traumatic mass lesion expansion, or any combination of the three. When increasing ICP cannot be controlled, the intracranial contents will shift and herniate through the cranial foramen.
The most common clinically significant traumatic herniation syndrome is uncal herniation, a form of transtentorial herniation (Fig. 31-5) (Figure Not Available) . Uncal herniation is often associated with traumatic extraaxial hematomas in the lateral middle fossa or the temporal lobe. The classic signs and symptoms are caused by compression of the ipsilateral uncus of the temporal lobe on the U-shaped edge of the tentorium cerebelli as the brain is forced through the tentorial hiatus. As compression of the uncus begins, the third cranial nerve is compressed. Anisocoria and a sluggish light reflex in the dilated pupil develop on the side ipsilateral to the expanding mass lesion. This phase may last for minutes to hours, depending on how rapidly the expanding lesion is changing. As the herniation progresses, compression of the ipsilateral oculomotor nerve eventually causes ipsilateral pupillary dilatation and nonreactivity.
Initially in the uncal herniation process, the motor examination can be normal, but contralateral Babinski’s responses develop early. Contralateral hemiparesis develops as the ipsilateral peduncle is compressed against the tentorium. With continued progression of the herniation, bilateral decerebrate posturing eventually occurs; decorticate posturing is not always seen with the uncal herniation syndrome. In up to 25% of patients, the contralateral cerebral peduncle is forced against the opposite edge of the tentorial hiatus. Hemiparesis is then detected ipsilateral to the dilated pupil and the mass lesion. This is termed Kernohan’s notch syndrome and causes false localizing motor findings.
As uncal herniation progresses, direct brain stem compression causes additional alterations in the level of consciousness, respiratory pattern, and the cardiovascular system. Mental status changes may initially be quite subtle, such as agitation, restlessness, or confusion. This is soon replaced with lethargy and progression to frank coma. The patient’s respiratory pattern may initially be normal, followed by sustained hyperventilation. With continued brain stem compression, an ataxic respiratory pattern develops. The patient’s hemodynamic status may change, with rapid fluctuations in blood pressure and cardiac conduction. Herniation that is uncontrolled progresses rapidly to brain stem failure, cardiovascular collapse, and death.