Letter: The History of the Kernohan Notch Revisited

To the Editor:

We read with great interest the article titled “The History of the Kernohan Notch Revisited,” which was recently published in Neurosurgery.¹ In this beautifully written paper, Dammers et al claim the importance of the early contributions of Arnold Groeneveld and Georges Schaltenbrand to understanding the mechanism of paradoxical ipsilateral hemiparesis, in a pioneering article published in 1927,² that is, 2 years before the paramount and well-known study by James W. Kernohan and Henry W. Woltman.³ The authors conclude that the credit should be given to Groeneveld and Schaltenbrand for the first pathophysiological explanation of this false localizing sign, historically attributed to the work of Kernohan and Woltman, from whom the notch phenomenon was named.

Interestingly, the report by Groeneveld and Schaltenbrand was initially conceived to discuss the pathology of labyrinthic and postural reflexes, but the necropsy findings observed in a patient with paradoxical left hemiparesis led them to conclude that this symptom was caused by a lesion of the right peduncle. They assumed that the occurrence of such a lesion was related to the mechanical effect of encephalic distortion, brainstem displacement, and compression of the contralateral peduncle against the free tentorial border and/or the posterior surface of the petrous bone.² Nevertheless, a graphic demonstration of the peduncular lesion is lacking in the original manuscript, which otherwise provides an extraordinarily well-documented clinical and pathological study.²

In 1928, Kernohan and Woltman⁴ published the case of a patient presenting a false localizing sign of hemiparesis in the Proceedings of the Staff Meetings of the Mayo Clinic. In their paper, the authors explain that “the cause of this error—to say that a tumor is on the right side of the brain when it is in reality on the left—was discovered by Dr Kernohan and reported at the neuropathologic conference on May 20, 1927.” The patient was a 47-year-old man who exhibited mental deterioration and experienced headaches, incontinence, and convulsions, which were more prominent on the left side. Upon examination, bilateral papilledema, left hypoacusia, and generalized diminished strength of the extremities with left-sided spasticity and Babinski sign were observed. These findings led to a speculative diagnosis of a tumor involving the right frontal and temporal regions. Nevertheless, an extra-axial expanding mass was found at the left hemisphere during necropsy: “It was noted that the size of this tumor was such that the brain was displaced to the right,” including “the upper portion of the brainstem” (Figure A). Subsequently, the authors reasoned that “the falx cerebri and the tentorium are relatively rigid structures and the displacement of the brain stem brought the most convex portion of the right pes pedunculi against the edge of the tentorium. This edge caused an indentation in the pes which was quite well marked,” and provided the first photographic demonstration in history of a brainstem lesion caused by deformation of the cerebral peduncle against the contralateral free tentorial edge (Figures B-C). Encouraged by this finding, Kernohan and Woltman approached the problem of this paradoxical sign from both a pathological and clinical perspective by studying 276 tumor-affected brain specimens obtained from necropsies. The results of their research were presented in a lecture given in the 54th annual meeting of the American Neurological Association, held in Washington, DC from May 1 to 3, 1928.⁵ This seminal study was published the following year in Archives of Neurology and Psychiatry³ in a well-known paper that predicted important conclusions, such as the differentiation between lesional and nonlesional notch phenomena, each one associating a different prognosis regarding motor recovery, a finding recently verified by modern neuroimaging techniques in living patients.⁶

FIGURE 1.

A, mechanical distortion of the left frontal and temporal lobes exerted by an endothelioma (meningioma). B, right pes pedunculi notching (large arrows) and grooving of the left uncinate girus (small arrow). C, longitudinal section through the peduncle showing the site of compression with myelin destruction (Weigert's myelin sheath stain). Photographs obtained, with permission from Elsevier, from the original manuscript published by Kernohan and Woltman in 1928.⁴

As has happened in other fields of science throughout history, both the German and the North American groups explained in 1927, independently and satisfactorily, the mechanism leading to paradoxical ipsilateral hemiparesis associated with mass-effect lesions involving 1 cerebral hemisphere. As Dammers et al¹ state, both groups failed to define the exact nature of the peduncular lesion and the factors linked to the development of this false localizing sign. Finally, a lesson should be learned: if you are the first to reach the Pole, plant your flag and take a photograph.