Central herniation

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)

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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

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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

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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

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The progression of symptoms indicates irreversible ischemia and therefore intervention must occur before the midbrain stage to prevent permanent deficits from central herniation

Clinical characteristics differentiating uncal from central herniation

● decreased consciousness occurs early in central herniation, late in uncal herniation

● uncal herniation syndrome rarely gives rise to decorticate posturing