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In the first phase of central herniation, the diencephalon and the medial parts of both temporal lobes are forced through a notch in the tentorium cerebelli.
Caused by diffuse brain edema as seen in patients with severe traumatic brain injury
CT Scan shows effacement of the perimesencephalic cisterns and loss of gray-white matter differentiation.
Early diencephalic stage (reversible)
Decreasing level of consciousness with difflculty concentating, agitation and drowsiness
Pupils are small (1-3 mm) but reactive
Pupils dilate briskly in response to a pinch of the skin on the neck (ciliospinal reflex)
Oculocephalic reflexes are intact (Doll’s eyes)
Plantar responses are flexor
Respirations contain deep sighs, yawns and occasional pauses then progress to Cheyne -Stokes
Late diencephalic stage
Patient becomes more difficult to arouse
Localizing motor responses to pain disappear and decorticate posturing appears with eventual progression to decerebrate posturing
Progressive diencephalic impairment is thought to be the result of stretching of the small penetrating vessels of the posterior cerebral and communicating arteries which supply the hypothalamus and thalamus
As herniation progresses to the midbrain stage signs of oculomotor failure appear The pupils become irregular and then fixed at midposition Oculocephalic movements become more difficult to elicit Extensor posturing appears spontaneously Motor tone is increased and plantar responses are extensor
The progression of symptoms indicates irreversible ischemia and therefore intervention must occur before the midbrain stage to prevent permanent deficits from central herniation
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