Kernohan–Woltman notch phenomenon in patient with subdural hematoma and ipsilateral hemiparesis in Bukavu

Key Clinical Message Kernohan–Woltman phenomenon is a rare and paradoxical neurological situation in which a transtentorial lesion leads to compression of the contralateral cerebral peduncle responsible for compression of the descending corticospinal fibers with clinical consequence of a motor deficit ipsilateral to the primary lesion. This phenomenon should attract the attention of clinicians in order to avoid unfortunate incidents such as wrong‐side craniotomy in neurosurgical practice. In this work, we report a similar situation. Abstract The Kernohan–Woltman notch phenomenon is a rare and paradoxical neurological situation in which transtentorial damage is observed leading to compression of the contralateral cerebral peduncle responsible for compression of descending corticospinal fibers with the clinical consequence of a motor deficit ipsilateral to the primary lesion. This phenomenon has been found in several situations including tumors and cerebral hematomas after craniocerebral trauma. In this work, we have reported the case of a 52‐year‐old man with hemiparesis ipsilateral to a large chronic subdural hematoma.


| INTRODUCTION
The Kernohan-Woltman notch phenomenon is a neurological situation in which the patient presents with hemiparesis ipsilateral to a primary lesion in the setting of transtentorial involvement, where the contralateral cerebral peduncle is compressed against the free edge of the tentorium, responsible for compression of fibers of the descending corticospinal tract. 1,2 This phenomenon is a false sign of localization that can lead to confusion of topographic diagnosis in neurosurgical practice. It was first described by Kernohan and Woltman in 1929, through postmortem studies of 297 patients following cases of false localization observed at the time. 3 The causes of this phenomenon are multiple and among them, we have slowly evolving supratentorial extraparenchymal mass lesions; such as neoplasms or chronic subdural hematomas. 4 We report the case of a 52-year-old man who presented a few days after being beaten, a decreased level of consciousness, right mydriasis, and motor deficit of the right hemisphere caused by a large chronic right hemispheric subdural hematoma, which was immediately evacuated with a good clinical course.

| CASE REPORT
We report the case of a 52-year-old man who, 1 month before his admission to our hospital, received a blow to the head in the right parietal region, then fell, the mechanism of which was not specified by those accompanying him, and presented with a brief initial loss of consciousness. One week after the fall, he began to present with holocranial headaches. Due to a lack of means to seek medical attention, he attended a prayer room with no change in symptomatology. Six hours before his admission, he presented with an abrupt alteration in consciousness, which motivated his relatives to bring him to our hospital for better management. On admission, he had a Glasgow score of 12 (O3V4M5), anisocoric pupils with reflex mydriasis to right light. He also had right central facial paralysis and right hemiparesis. A brain scan was performed which showed a large right hemispheric subdural hematoma with subfalcoral involvement ( Figure 1) and a Kernohan-Woltman phenomenon ( Figure 2). He was taken to the operating room for evacuation of the hematoma; two drill holes were made, which allowed evacuation under pressure of 300 mL of digested blood. A subdural drain ending in the right occipitotemporal was left. On awakening, the patient had a maximum Glasgow, the right central facial palsy and right hemiparesis had disappeared, and the pupils were of good reflection diameter.
On the second day, the drain was removed after bringing back a total of 150 cc of serohematic fluid, and on the fifth day, he was discharged without any neurological deficit.

| DISCUSSION
The corticospinal pathways originate from the motor cortex in the frontal lobes and descend through the internal capsules and then through the midbrain and annular protrusions, before the majority of these motor fibers (80%) undergo decussation in the medulla oblongata. 7 This decussation of these motor fibers will explain the fact that the left cerebral motor cortex controls the movements of the right side of the human body and vice versa. It is therefore logical that a lesion of a cerebral hemisphere with compression of the motor fibers passing through it should manifest itself by a contralateral motor deficit. However, this clinic is paradoxical in a rare situation.

The
Kernohan-Woltman notch phenomenon ( Figure 3) is a deceptively localized neurological sign that manifests as a motor deficit ipsilateral to the primary lesion and occurs in the setting of a transtentorial hernia, where the contralateral cerebral peduncle is compressed against the free edge of the tentorium, resulting in compression of fibers of the descending corticospinal tract. 2 This paradoxical neurologic sign or false localization was first described in 1929 by Kernohan and colleagues during autopsy examination of a patient with a brain tumor whose brain was nicked by the peduncle of a contralateral hernia. 8 This phenomenon has been associated with brain tumors and supratentorial hematomas. 3,9 Compression of the contralateral peduncle is thought to disrupt fibers of the corticospinal tract above the decussation, resulting in hemiparesis ipsilateral to the primary lesion. 3 Our patient presented with a right hemiparesis ipsilateral to a large chronic subdural hematoma responsible for the Kernohan-Woltman phenomenon visible on brain CT.
Other clinical signs, apart from hemiplegia or hemiparesis, may be observed, including ipsilateral mydriasis, divergent gaze, or ptosis secondary to the primary lesion with oculomotor nerve involvement, and ipsilateral paralysis of the superior motor nerve of the face due to involvement of corticobulbar fibers of the cerebral peduncle. 3,10 And other authors mention altered consciousness as a clinical sign often found. 11 Our patient presented on admission with altered consciousness; right mydriasis and right central facial palsy ipsilateral to his large chronic subdural hematoma.
A good neurological examination combined with medical imaging plays an important role in the diagnosis. Brain magnetic resonance imaging may show T2 hyperintensity of the contralateral cerebral peduncle. 3 A brain scan may be performed. Several authors have suggested that some individuals are susceptible to developing this syndrome due to anatomical factors. 12,13 Adher and Milhorat autopsied and analyzed the tentorium morphology of 100 individuals, and found that they differed in the diameter of the tentorium notch, which ranged from 24.5 to 39.0 mm. 14 Based on these data, it is possible to speculate that individuals with a smaller diameter of this structure tend to herniate and may generate contralateral compression of the cerebral peduncle more readily than those with a larger diameter.
It is very crucial to recognize this syndrome because of the risk of error in the neurosurgical procedure by operating on the wrong side with respect to the location of the lesion. Wolf RFE and colleagues 15 reported an unfortunate incident in which a patient who had a subdural hematoma after being hit by a golf ball, the patient had a motor deficit on the left side and the brain scan showed an ipsilateral subdural hematoma. The surgeons thought that the CT indexes were misplaced, so they performed a craniotomy on the side opposite to the motor deficit (the healthy side), which did not reveal a hematoma; a follow-up brain CT scan was performed postoperatively and showed that the hematoma was contralateral to the surgical site. 15

| CONCLUSION
The Kernohan-Wotman phenomenon is a rare, paradoxical situation but not to be ignored in clinical neurosurgical practice. Several factors can lead to this phenomenon among which we have cerebral hematoma after cranioencephalic trauma. A good neurological examination and magnetic resonance imaging or CT scan are necessary for diagnosis. This phenomenon should attract the attention of clinicians in order to avoid unfortunate incidents such as craniotomy on the wrong side in neurosurgical practice.

CONFLICT OF INTEREST STATEMENT
The authors have no conflict of interest to declare.

FUNDING INFORMATION
None.

DATA AVAILABILITY STATEMENT
All the materials used in this study are available on request.

ETHICS STATEMENT
This case report received ethical clearance from the Ethical committee of the catholic University of Bukavu.

PATIENT CONSENT STATEMENT
Written informed consent was signed by the patient prior to the publication of this paper.