Beyond uncal herniation: An updated diagnostic reappraisal of ipsilateral hemiparesis and the Kernohan-Woltman notch phenomenon.

PURPOSE

This works comprehensively analyses a modern cohort of patients with ipsilateral hemiparesis (IH) and discusses the pathophysiological theories elaborated to explain this paradoxical neurological sign according to the findings from contemporary neuroimaging and neurophysiological techniques.

METHODS

A descriptive analysis of the epidemiological, clinical, neuroradiological, neurophysiological, and outcome data in a series of 102 case reports of IH published on since the introduction of CT/MRI diagnostic methods (years 1977-2021) was performed.

RESULTS

IH mostly developed acutely (75.8%) after traumatic brain injury (50%), as a consequence of the encephalic distortions exerted by an intracranial haemorrhage eventually causing contralateral peduncle compression. Sixty-one patients developed a structural lesion involving the contralateral cerebral peduncle (SLCP) demonstrated by modern imaging tools. This SLCP showed certain variability in its morphology and topography, but it seems pathologically consistent with the lesion originally described in 1929 by Kernohan & Woltman. The study of motor evoked potentials was seldom employed for the diagnosis of IH. Most patients underwent surgical decompression, and a 69.1% experienced some improvement of the motor deficit.

CONCLUSIONS

Modern diagnostic methods support that most cases in the present series developed IH following the KWNP model. The SLCP is presumably the consequence of either compression or contusion of the cerebral peduncle against the tentorial border, although focal arterial ischemia may also play a contributing role. Some improvement of the motor deficit should be expected even in the presence of a SLCP, provided the axons of the CST were not completely severed.