Journal of Clinical Neuroscience 16 (2009) 1628–1631

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Journal of Clinical Neuroscience
journal homepage: www.elsevier.com/locate/jocn

Case Reports

Kernohan-Woltman notch phenomenon caused by an acute subdural hematoma
Rodrigo Carrasco a,*, José M. Pascual a, Marta Navas a, Pedro Martínez-Flórez a,
Rafael Manzanares-Soler b, Rafael G. Sola a
a
b

Department of Neurosurgery, La Princesa University Hospital, C/- Diego de León 62, 28006 Madrid, Spain
Department of Neuroradiology, La Princesa University Hospital, Madrid, Spain

a r t i c l e

i n f o

Article history:
Received 25 November 2008
Accepted 3 February 2009

Keywords:
Cerebral peduncle
Kernohan’s notch
False localizing signs
Ipsilateral hemiparesis
Subdural hematoma
Tentorial incisura
Uncal herniation

a b s t r a c t
Uncal herniation through the tentorial notch is occasionally associated with false localizing ipsilateral
hemiparesis, known as the Kernohan-Woltman notch phenomenon (KWNP). We report an 81-year-old
female who presented with a decreased level of consciousness, a right mydriasis and an ipsilateral motor
deficit caused by a large right hemispheric subdural hematoma that was immediately evacuated. The
patient recovered well, although her right hemiplegia persisted. A follow-up MRI showed a residual
lesion in the left cerebral peduncle, corresponding to KWNP. The presence of such a structural lesion suggests a poor prognosis for recovery from the initial motor deficit.
Ó 2009 Elsevier Ltd. All rights reserved.

1. Introduction
The Kernohan-Woltman notch phenomenon (KWNP) defines
the paradoxical neurological deficits associated with a compressive
injury of the cerebral peduncle against the edge of the tentorium
due to the expansion of a contralateral supratentorial lesion. It is
characterized by a hemiparesis ipsilateral to the mydriasis observed in patients with altered levels of consciousness.1 The presence of false localizing neurological signs can preclude a correct
topographical diagnosis of the associated pathological lesions
within the central nervous system, leading to surgical treatment
of the wrong site.2 However, modern neuroradiological methods
facilitate the recognition of the structural lesions of the nervous
system as well as the pathophysiological mechanisms underlying
this paradoxical phenomenon.3,4 We report a patient with KWNP
caused by an acute subdural hemorrhage, providing CT scan and
MRI evidence of the structural midbrain lesion located within the
contralateral cerebral peduncle.
2. Case report
An 81-year-old female received a medical consultation after
suffering an accidental minor head injury. She had been treated
with anticoagulants because of a chronic atrial fibrillation. While
in the emergency room, the patient suffered a sudden deterioration
of her level of consciousness to the point of coma (Glasgow Coma
Scale of 7/15), and showed a right mydriasis and a complete right
motor deficit on the neurological examination. A CT scan demon* Corresponding author. Tel.: +34 91 520 23 88.
E-mail address: rocamo@gmail.com (R. Carrasco)

strated a large right hemispheric acute subdural hemorrhage
(Fig. 1). The clot was immediately evacuated through a right frontoparietotemporal craniotomy. Postoperatively, the patient had no
complications. She gradually regained normal consciousness and
a normal pupillary function. Nevertheless, the paradoxical right
hemiplegia persisted. Postoperative CT and MRI scans were obtained after 4 weeks, and demonstrated a structural lesion within
the left cerebral peduncle, probably caused by compression against
the free tentorial edge (Figs. 2, 3). The motor deficit was moderately improved after 3 months.
3. Discussion
The tentorial incisura is located between the tentorial edges and
communicates the supratentorial and infratentorial spaces. This
area can be divided into three spaces: anterior, middle (lateral
to), and posterior to the brainstem. The middle incisural space is
close to the midbrain and the upper pons at the level of the pontomesencephalic sulcus. Mesial temporal lobe structures such as
the uncus, the parahippocampal gyrus and the hippocampal formation, are also intimately related to the incisura. The principal
vascular structures coursing along the middle incisural space are
the posterior cerebral artery and the superior cerebellar artery
which pass around the brainstem, parallel to the free tentorial
edge. The incisura has also a close relationship with the first 6 cranial nerves.5
Symptoms associated with tentorial herniation may result from
displacement, compression and stretching of the brainstem and
cranial nerves, and/or hemorrhage and infarction caused by compression and tearing of arteries and veins coursing along the tentorial incisura. A downward shift of mesial temporal lobe structures

Case Reports / Journal of Clinical Neuroscience 16 (2009) 1628–1631

1629

Fig. 1. Axial brain CT scans showing (A) an extensive right hemispheric acute subdural hematoma, causing a 2 cm midline shift and (B) a right uncal herniation with
deformation of both cerebral peduncles and obliteration of the perimesencephalic cisterns.

Fig. 2. (A) Axial brain CT scan showing brain re-expansion after surgical evacuation of the subdural hematoma. A well-defined rounded hypointense signal is evident within
the anterolateral left midbrain. T2-weighted MRI showing a hyperintense signal in both (B) axial and (C) coronal slices (white arrow).

Fig. 3. Maximum notch width measurements on (A) postoperative coronal T2-weighted MRI and (B) axial T2-weighted gradient-echo MRI sections. The distance measured
between the free tentorial edges was less than the mean value (29.6 mm) and near the first quartile value (27.0 mm) of Adler and Milhorat’s morphometric tentorial notch
analysis based on 100 human autopsies.14 A slight discrepancy of less than 1.0 mm was measured between the axial and coronal slices. In the gradient-echo MRI a linear
hypointense signal can be observed at the lowest border of the peduncular lesion, indicating a paramagnetic effect probably due to iron deposition.

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Case Reports / Journal of Clinical Neuroscience 16 (2009) 1628–1631

is typical of tentorial herniation, resulting in kinking and grooving
of the uncus and parahippocampal girus. Compression of the ipsilateral cerebral peduncle causes contralateral pyramidal signs and,
if the lateral displacement of the brainstem is severe, the contralateral cerebral peduncle may be forced against the free edge, thus
producing a groove on the peduncle called a Kernohan’s notch,
with ipsilateral pyramidal signs.5,6 Hemorrhage into the brainstem
as a result of tearing of arteries and veins without cerebral herniation may occur if the incisura hugs the brainstem so tightly that it
prevents cerebral herniation while allowing axial displacement of
the brainstem.5
The notion of ‘‘false localizing signs” refers to neurological
signs that reflect a dysfunction that is remote from the expected
anatomical site of pathology.2 Collier first reported the frequency
of these phenomena to be as high as 12.4% in his own series, with
most occurring in patients with raised intracranial pressure due
to supratentorial masses.7–9 However, prior to the availability of
CT technology, a wide range of variation in the percentage of patients demonstrating false localizing signs was reported, ranging
from 7 to 50% of patients.10,11 In particular, the finding of mydriasis and ipsilateral hemiparesis in patients harbouring a supratentorial expanding mass led clinicians to a topographical
misdiagnosis and, in many cases, to surgical treatment of the
wrong side.12 Kernohan and Woltman first described the correlation between this paradoxical ipsilateral motor deficit and the
groove deformation and/or tissue destruction observed in the
contralateral cerebral peduncle.1
Pathological mechanisms by which KWNP is produced,
whether by a brisk displacement of diencephalic structures or
by the pressure exerted on the brainstem by the herniated uncus,
still remain unclear.13 Several factors, mainly the growing rate of
the supratentorial mass, the degree of lateral displacement of the
brainstem and the individual width of the tentorial incisura, may
contribute to the development of KWNP, but there is still little
evidence to support these hypotheses.3,14,15 The morphometric
analysis of the tentorial notch variations performed by Adler
and Milhorat in 100 autopsies has classified the maximum notch
width in narrow (24.5–27.0 mm), typical (27.1–31.9 mm) and
wide (32.0–39.0 mm) categories.14 Among the different measurements considered for the tentorial notch in this study, we believe
the maximum notch width may represent a fundamental anatomical factor predisposing patients who suffer from uncal herniation
to KWNP. In our patient, the maximum notch width was determined by postoperative MRI, yielding a value close to the first
quartile (27.0 mm) and far from the maximum width (39.0 mm)
found on necropsy specimens (Fig. 3).14 Although no definite conclusions can be drawn as to the effects of this parameter based on
this observation, our finding suggests that individual anatomical
variations of the tentorial incisura can influence the development
of KWNP.
Neuroradiological evidence of KWNP obtained with CT and MRI
technologies is scarce.16–18 KWNP has been mostly observed in
adult patients with traumatic intracranial hematomas, but it has
also been reported in both elderly and young patients.15,19,3 For patients with a severe traumatic brain injury, it is essential to distinguish KWNP from other possible causes of ipsilateral motor
weakness such as contralateral cortical damage, arterial infarction,
primary brainstem lesion and spinal cord injury.17,3
Morphological changes associated with KWNP may correspond to either: (i) a reversible indentation of the cerebral
peduncle caused by midbrain compression against the free tentorial edge; or (ii) irreversible tissue destruction of the adjacent
corticospinal tract.1,20 MRI studies performed in awake patients
with gradually expanding lesions usually show an indentation
deformity in the contralateral cerebral peduncle as the unique
morphological change associated with KWNP.19,3 This early mor-

phological deformation, similar to that observed in necropsy
studies by Kernohan and Woltman, could theoretically be associated with a better functional motor outcome given the potential
reversibility of such elastic deformation.1,3 However, most MRI
studies investigating KWNP have been performed after the evacuation of intracranial hematomas in patients with critical head
injuries.4,3 In these patients, the initial brainstem deformities
have usually reverted. Nevertheless, a residual rounded lesion
in the cerebral peduncle, that is typically hypodense on a CT
scan, hypointense or isointense on T1-weighted MRI, and hyperintense on T2-weighted MRI and fluid-attenuated inversion
recovery-MRI, can be observed.16,17 This lesion represents a
degeneration of myelinized fibres within the corticospinal tract,
caused by a sustained midbrain compression against the free
tentorial edge, and may predict a poor functional outcome.3,20
In our patient, a gradient-echo MRI axial slice at the level of
the pontomesencephalic union showed a hypointense linear signal located at the inferior limit of the lesion involving the corticospinal tract (Fig. 3B). To our knowledge, this is the first
gradient-echo MRI performed in a patient with KWNP and is
indicative of a paramagnetic effect caused by iron, probably related to hemosiderin deposition.21 This signal may correspond
to a small peripheral rim of blood extravasation as first reported
by Kernohan and Woltman, who described the presence of previous or recent petechial hemorrhages at the peripheral borders
of the mechanical corticospinal lesion associated with the deepest brainstem grooves.1
This signal must be differentiated from other brainstem hemorrhagic lesions, namely Duret hemorrhages, which can develop secondarily to a descending tentorial herniation of any cause. Duret
hemorrhages usually arise in the midline of the lower mesencephalon and upper pons and are thought to be caused by the stretching
and spasm of perforating brainstem arteries, and are associated
with a high mortality.22 Other types of traumatic brainstem hemorrhages, such as primary shearing petechiae caused by rotational
forces applied to the brainstem, are usually found in the posterolateral quadrants and not within the peduncles.23 Spontaneous
hypertensive hemorrhages are also usually located in the dorsal region at the caudal pons.23

4. Conclusion
Mechanical lesions of the brainstem associated with KWNP are
caused by a sustained notching of the nervous tissue against the
tentorial edge and present a specific pathological change that must
be differentiated from other brainstem lesions caused by tentorial
herniation. KWNP was initially related to the final stages of supratentorial tumors but here is reported in patients harbouring supratentorial traumatic hemorrhages. CT and MRI scans can show the
focal brainstem lesion that explains the presence of the false localizing hemiplegia.
References
1. Kernohan J, Woltman H. Incisura of the crus due to contralateral brain tumor.
Arch Neurol 1929;21:274–87.
2. Larner AJ. False localising signs. J Neurol Neurosurg Psychiatry 2003;74:415–8.
3. Moon KS, Lee JK, Joo SP, et al. Kernohan’s notch phenomenon in chronic
subdural hematoma: MRI findings. J Clin Neurosci 2007;14:989–92.
4. Osborn AG. Diagnosis of descending transtentorial herniation by cranial
computed tomography. Radiology 1977;123:93–6.
5. Rothon Jr AL. Tentorial incisura. Neurosurgery 2000;47(Suppl. 3):131–53.
6. Sunderland S. The tentorial notch and complications produced by herniations of
the brain through that aperture. Br J Surg 1958;45:422–38.
7. Collier J. The false localizing signs of intracranial tumors. Brain 1904;27:
490–508.
8. Meyer A. Herniation of the brain. Arch Neurol Psychiatry 1920;4:387–400.
9. Pearce JMS. Kernohan’s notch. Eur Neurol 2006;55:230–2.

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10. Cabieses F, Jeri R. Transtentorial lobe herniation. Acta Neurol Lat Am
1955;1:67–79.
11. McKissock W, Richardson A, Bloom WH. Subdural hematoma. A review of 389
cases. Lancet 1960;1:1365–9.
12. Wolf RF, ter Weeme CA, Krikke AP. Kernohan’s notch and misdiagnosis. Lancet
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13. Maramattom BV, Wijdicks EFM. Uncal herniation. Arch Neurol 2005;62:1932–5.
14. Adler DE, Milhorat TH. The tentorial notch: anatomical variation,
morphometric analysis, and classification in 100 human autopsy cases. J
Neurosurg 2002;96:1103–12.
15. Namura S, Kang Y, Matsuda I, et al. Magnetic resonance imaging of sequelae of
temporal lobe herniation secondary to traumatic acute subdural hematoma:
Kernohan’s notch and posterior cerebral artery territory infarctions
contralateral to the supratentorial lesion. Neurol Med Chir (Tokyo)
1997;37:32–5.
16. Cohen AR, Wilson J. Magnetic resonance imaging of Kernohan’s notch.
Neurosurgery 1990;27:205–7.
17. Giménez-Pando J, Cabezudo-Artero JM, Fernández-Portales I, et al. Lesión
mesencefálica contralateral por hernia cerebral. Imagen en resonancia

magnética de la Hendidura de Kernohan (Kernohan’s Notch). Neurocirugía
(Astur) 2004;15:384–7.
18. Iwama T, Kuroda T, Sugimoto S, et al. MRI demonstration of Kernohan’s notch:
case report. Neuroradiology 1992;34:225–6.
19. Itoyama Y, Fujioka S, Ushio Y. Kernohan’s notch in chronic subdural hematoma:
findings on magnetic resonance imaging. J Neurosurg 1995;82:645–6.
20. Yoo W-K, Kim D-S, Kwon YH, et al. Kernohan’s notch phenomenon
demonstrated by diffusion tensor imaging and transcranial magnetic
stimulation. J Neurol Neurosurg Psychiatry 2008;79:1295–7.
21. Kim J, Kim DI, Lee SK, et al. Imaging of the inflammatory response in
reperfusion injury after transient cerebral ischemia in rats: Correlation of
superparamagnetic iron oxide-enhanced magnetic resonance imaging with
histopathology. Acta Radiol 2008;49:580–8.
22. Fujimoto Y, Aguiar PH, Freitas ABR, et al. Recovery from Duret hemorrhage: A
rare complication after craniotomy. Case report. Neurol Med Chir (Tokyo)
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23. Parizel PM, Makkat S, Jorens PG, et al. Brainstem hemorrhage in descending
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doi:10.1016/j.jocn.2009.02.015

Very late thrombosis in a patient with a drug-eluting stent for intracranial
atherosclerotic stenosis
Qinghai Huang, Bo Hong, Yi Xu, Jianmin Liu *
Department of Neurosurgery, Changhai Hospital, 168 Changhai Road, Shanghai 200433, China

a r t i c l e

i n f o

Article history:
Received 19 November 2008
Accepted 19 January 2009

Keywords:
Angioplasty
Atherosclerosis
Intracranial stenting
Ischemic stroke
Stenosis

a b s t r a c t
Late stent thrombosis is an infrequent, but severe, complication after implantation of a drug-eluting
stent. We report one such patient, a 69-year-old man with intracranial vertebral artery stenosis. He experienced very late stent thrombosis after discontinuation of clopidogrel therapy, about 16 months after the
insertion of a Taxus StentÒ (Boston Scientific Corporation, Natick, MA, USA). The patient recovered well,
with good clinical outcome, after the re-initiation of dual antiplatelet and anticoagulation therapy. No
abnormality within the stent was identified on a repeat angiogram taken 4 weeks after treatment reinitiation.
Ó 2009 Elsevier Ltd. All rights reserved.

1. Introduction

2. Case report

Intracranial atherosclerotic disease is a common cause of stroke,
particularly in the Asian population.1 Preliminary observational
studies have suggested that combined angioplasty and stenting
may reduce the risk of stroke in patients who have symptomatic
intracranial stenosis.2,3 In-stent restenosis is also known to be a
key factor influencing the effect of intracranial stenting. Based on
the successful use of the technique in cardiology, some investigators have used drug-eluting stents (DESs) for the treatment of
intracranial atherosclerotic stenosis.4,5 Stent thrombosis is an
infrequent, but severe, complication that can occur after implantation of a DES. We present a patient with a very late thrombosis
after discontinuation of clopidogrel therapy, about 16 months after
the insertion of a paclitaxel-eluting coronary stent (Taxus StentÒ,
Boston Scientific Corporation, Natick, MA, USA).

A 69-year-old man with a history of systemic hypertension and
diabetes mellitus presented to our facility with recurrent dizziness
and diplopia. MRI performed at the time of admission showed
infarction of the right cerebellar hemisphere. Cerebral angiography
demonstrated a 60% stenosis of the right vertebral artery (VA)
(Fig. 1A) and total occlusion of the left VA. The posterior communicating arteries were not shown on digital subtraction angiography
(DSA). We decided to perform percutaneous transluminal angioplasty and stenting (PTAS) to prevent further progression of stroke.
Aspirin and clopidogrel were administered for 7 days before the
procedure.
The PTAS procedure was performed under general anesthesia. A
6 French guiding catheter (Envoy, Endovascular Corporation, Miami, FL, USA) was positioned in the right distal VA. The stenotic segment was crossed with a Transend microwire (Boston Snientific
Corporation). A Taxus stent (4.5 mm in diameter, 16 mm in length)
was gently advanced over the microwire. However, the delivery of

* Corresponding author. Tel./fax: +86 21 8187 3446.
E-mail address: ocin2007@163.com (J. Liu)