Unilateral transtentorial herniation

This is perhaps the best known herniation syndrome and is caused by an elevation of pressure in one supratentorial compartment of sufficient magnitude to displace the temporal lobe on the affected side over the lateral edge of the tentorium ( Fig 1). The herniation may be more marked anteriorly (uncus) or posteriorly

(hippocampal gyrus), and is usually accompanied by displacement of the ipsilateral cingulate gyrus under the falx. With the descent of the uncus through the incisural notch, the ipsilateral third nerve is compressed against the free edge of the tentorium or some other resistant structure such as the petroclinoid ligament or the superior cerebellar artery. This produces unilateral pupillary dilatation followed by other signs of oculomotor palsy.

Petroclinoid Ligament Fig

Fig. 1 Diagram of unilateral transtentorial herniation secondary to supratentorial mass lesion. The temporal lobe is herniated through the incisural notch and the midbrain is displaced laterally and downward. Note the associated herniation of the cingulate gyrus under the falx. The inset is a basal view of the brain at the level of the tentorial notch showing the relationship of the oculomotor nerve to the posterior cerebral artery and the free edge of the tentorium. (Reproduced with permission from Milhorat .(1978).)

With continuing descent of the uncus through the incisural notch, the midbrain is displaced laterally and downward. Consciousness is affected at this stage owing to compression of the ascending reticular formation, and an alteration in cardiorespiratory function may occur as a consequence of distortion of the basal diencephalon. The most common respiratory patterns associated with transtentorial herniation are Cheyne-Stokes respiration (alternating phases of hyperpnea and apnea) and central neurogenic hyperventilation. In the majority of cases the herniating temporal lobe will compress the ipsilateral cerebral peduncle, producing weakness and decorticate posturing on the opposite side of the body. However, in approximately 20 per cent of cases the contralateral cerebral peduncle is shifted laterally against the opposite edge of the tentorium, producing ipsilateral motor signs (false localizing signs) ( Crockard ef al 1992). Occasionally, large uncal herniations will occlude the ipsilateral posterior cerebral artery with subsequent infarction and swelling of the occipital lobe. This can create a vicious cycle of hemicranial hypertension which further accentuates the herniation process.

Once signs of midbrain encroachment appear, rostral-caudal deterioration proceeds rapidly. This is characterized by deepening stupor and coma, decorticate or decerebrate posturing, and profound alterations in cardiorespiratory function. Occlusion of the aqueduct of Sylvius may accelerate this process by obstructing the flow of cerebrospinal fluid (Plum and Posner.1992; Cheek. .etal 1994). Death usually results from brainstem hemorrhages (Duret hemorrhages) which characteristically develop in the central core area at any point from the diencephalon to the lower pons. Central transtentorial herniation

This is a clinically distinct syndrome which occurs more frequently in infants and children. It is seen typically in patients with acute or progressive hydrocephalus, and reflects symmetric downward displacement of both cerebral hemispheres through the tentorial incisura ( Fig..2). The early signs are due to progressive impairment of diencephalic function rather than oculomotor nerve palsy ( Or.oc.ka.rd.et...al 1992). Initially the pupils may be small or pinpoint and, if examined superficially, appear to have lost their reaction to light (Crockard.et...al 1992; Plum ...and ...Posner.1992). With progressive central transtentorial herniation, the dorsal half of the brainstem is compressed from side to side, producing a pear-shaped elongation of the midbrain and upper pons ( Bell. ..and...McCormick..1972; Crockard..et..al 1992). The resulting distortion of the quadrigeminal plate region can lead to a paralysis of upward gaze (Parinaud's syndrome), and pituitary necrosis and diabetes insipidus may occur in exceptional cases. Although the syndromes of central and unilateral transtentorial herniation are clinically distinct in the early stages, both merge into a similar picture as rostral-caudal deterioration advances.

Central Herniation

Fig. 2 Diagram of central transtentorial herniation secondary to hydrocephalus. The dorsal half of the brainstem is compressed from side to side, producing a pear-shaped deformity of the midbrain. (Reproduced with permission from Milh,oiaii19Z8))

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