Ann Rehabil Med.  2013 Dec;37(6):879-885. 10.5535/arm.2013.37.6.879.

Diffusion Tensor Tractography in Two Cases of Kernohan-Woltman Notch Phenomenon

• Jang SG
• Pyun SB

• KMID: 2266568
• DOI: http://doi.org/10.5535/arm.2013.37.6.879

Abstract

Kernohan-Woltman notch phenomenon (KWP) is an ipsilateral motor weakness due to compression of the contralateral cerebral peduncle. We report two cases of KWP following traumatic brain injury. In case 1, ipsilateral hemiplegia was noted after right subdural hemorrhage. Although magnetic resonance imaging showed no abnormal signal changes on cerebral peduncle, diffusion tensor tractography (DTT) revealed interruption of corticospinal tract (CST) at lower level of the midbrain level. In case 2, there was abnormal signal change of the right cerebral peduncle contralateral to the primary lesion and we could not reconstruct right CST. Case 1 showed unsatisfactory motor recovery even after 15 months, and follow-up DTT showed no change. In case 2, follow-up DTT was not performed, but her ipsilateral hemiparesis had almost disappeared during the 15 months. DTT would be useful in detecting ipsilateral hemiparesis due to KWP and the clinical course may differ according to the lesion characteristics.

Keyword

Traumatic brain injury; Hemiplegia; Diffusion tractography; Pyramidal tract

MeSH Terms

Brain Injuries
Diffusion Tensor Imaging
Diffusion*
Follow-Up Studies
Hematoma, Subdural
Hemiplegia
Magnetic Resonance Imaging
Mesencephalon
Paresis
Pyramidal Tracts
Tegmentum Mesencephali

Figure

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  Fig. 1 (A) Brain computed tomography at the onset of injury in case 1. The images show massive subdural hemorrhage on the right frontotemporal lobe with uncal herniation to the left causing compression of the cerebral peduncle against the tentorial egde (arrows). (B) The T1- and (C) T2-weighted axial magnetic resonance (MR) images 5 days after injury. (D) T1-weighted coronal MR images 5 days after injury. The uncal herniation improved after surgery but the images showed mild shifting of cerebral peduncle to the left tentorial edge (arrow heads). There were no abnormal signal changes on MR images.

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  Fig. 2 (A) Diffusion tensor image with tractography for the corticospinal tract and (B) axial image of the fractional anisotropy (FA) color map 4 weeks after the onset of injury. (C) Follow-up tractography and (D) axial image of FA color map 9 months after the onset of injury (left hemisphere, blue; right hemisphere, green). Disruptions of corticospinal tract around the left pons were noted in initial and follow-up images (arrows). FA color map showed disrupted blue fibers in the left anterior pons compared with the right side (open arrows).

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  Fig. 3 (A) Brain computed tomography at the onset of injury in case 2. The images show a large amount of left frontotemporal subdural hemorrhage, frontal intracranial hemorrhage, and contralateral shift of midline and transtentorial herniation (arrows). (B) The T1- and (C) T2-weighted axial magnetic resoance images 10 days after injury. Low intensity signal change in the right crus cerebri on T1-weighted image, and high signal intensity change on T2-weighted image (arrow heads).

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  Fig. 4 (A) Diffusion tensor image with tractography (DTT) for the corticospinal tract (CST) 8 weeks after the onset of injury in case 2 (left hemisphere, blue). Although tentorial herniation caused brain stem damage in Kernohan-Woltman notch phenomenon, right CST tract was also not visualized from cerebral cortex to posterior limb of internal capsule (PLIC) after reconstruction, which was not the case in DTT image of case 1. (B) CST was reconstructed after using different region of interest (ROI) method. One ROI was placed on the CST portion of the anterior mid pons and the other was placed on the CST portion of PLIC (left hemisphere, blue; right hemisphere, green). Disruption of CST around midbrain level was noted (arrow).

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