The Kinetics of Transtentorial Brain Herniation: Kernohan-Woltman Notch Phenomenon Revisited.

purpose of reviewTo critically review recent literature in understanding the pathological consequences of transtentorial brain herniation resulting from unilateral expanding supratentorial mass lesions. RECENT

findingsModern neuroimaging assists in understanding the consequences of transtentorial brain herniation with the development of the Kernohan-Woltman notch phenomenon. MRI studies in post-operative patients undergoing craniotomy and removal of expanding unilateral hemispheric mass lesions (usually an extradural or subdural hematoma) have shown striking findings in the contralateral crus cerebri suggestive of damage as a result of impact against the free margin of the opposite tentorium as suggested by Kernohan and Woltman nearly a century back in autopsy studies. MR changes include T1 hypointensity, T2 and fluid-attenuated inversion recovery (FLAIR) hyperintensity, DW1 hyperintensity with restriction of diffusion, presence of hypointensity in GRE sequences and evidence of axonal damage in the corticospinal tracts in the cerebral peduncle in diffusion tensor imaging and MR tractography. The pathological basis of such changes may be variable or a combination of several pathological processes, which may all be related to the impact/compression of the contralateral crus with the tentorial margin. These include contusion, compression, demyelination, and perhaps most importantly microvascular damage including microbleeds. The role of uncal herniation is debatable. It appears that as a result of massive lateral shift in the supratentorial compartment, there is a transient forceful impact of the opposite cerebral peduncle against the rigid tentorial border to induce one or more of the abovementioned phenomena to explain the imaging findings. The limitation of these studies is that most of them have been done in the post-operative periods and surgical manipulations can surely alter anatomical relationships between intracranial structures. The exact sequence of events happening intracranially in the face of rapidly expanding supratentorial mass lesions is largely unknown. Even with rapid progress in neuroimaging, documentation of such changes during life are difficult, principally for logistic reasons. Consequently, the very truth of the much taught about phenomenon of uncal herniation and the resultant Kernohan-Woltman notch phenomenon and the false localizing sign of unilateral motor weakness and contralateral pupillary dilation have been questioned. Animal experimentation and autopsy studies have not contributed much in our understanding of the actual process happening intracranially in such an emergent situation. The midbrain undoubtedly is the key structure bearing the brunt of the effect of brain shift which is more lateral than downward in cases with unilateral expanding lesions. Structural changes in the cerebral peduncles have now been visualized with modern neuroimaging. These alterations may result from the interplay of one or more factors which include compression, contusion, demyelination, and perhaps most importantly microvascular ischemia and hemorrhage resulting from a forceful yet transient impact of the cerebral peduncle with the tough tentorial margin. The last mentioned hypothesis would be in conformity with Kernohan and Woltman's concept of elastic deformation of the midbrain. In the present article an attempt is made to provide a historical account of the changing concepts in relation to brain herniation as systematically and chronologically as possible, and then, critically review recent neuroimaging observations with a view to hypothesize on the sequence of events during transtentorial brain herniation.