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Frontal lobe ischemic stroke presenting with peripheral type facial palsy: A crucial diagnostic challenge in emergency practice

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Halil Önder at Ankara Etlik City Hospital
Halil Önder
  • Ankara Etlik City Hospital
Levent Albayrak at Bozok University
Levent Albayrak
Halil Polat
Halil Polat
Halil Polat
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Here, we illustrate a 69-year old female admitting with weakness on left side of the face who firstly considered peripheral facial palsy in the forefront. However, detailed neurological examination and cranial MRI findings finally yielded the proper diagnosis of right hemisphere ischemic stroke. Via this remarkable presentation, we point out the clinical challenges in evaluation processes of patients with facial palsy in emergency practice and emphasize the importance of detailed examination for the proper diagnosis as well as initiation of appropriate treatment agents without delay.
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Case Report
Frontal lobe ischemic stroke presenting with peripheral type facial
palsy: A crucial diagnostic challenge in emergency practice
Halil Onder
a
,
*
, Levent Albayrak
b
, Halil Polat
c
a
Yozgat State Hospital, Department of Neurology, Yozgat, Turkey
b
Yozgat State Hospital, Department of Emergency Medicine, Yozgat, Turkey
c
Yozgat State Hospital, Department of Otorhinolaryngology, Yozgat, Turkey
article info
Article history:
Received 20 February 2017
Received in revised form
18 April 2017
Accepted 21 April 2017
Available online xxx
Keywords:
Facial paralysis
Stroke
Emergency department
Facial innervation
Pathophysiology
abstract
Here, we illustrate a 69-year old female admitting with weakness on left side of the face who firstly
considered peripheral facial palsy in the forefront. However, detailed neurological examination and
cranial MRI findings finally yielded the proper diagnosis of right hemisphere ischemic stroke. Via this
remarkable presentation, we point out the clinical challenges in evaluation processes of patients with
facial palsy in emergency practice and emphasize the importance of detailed examination for the proper
diagnosis as well as initiation of appropriate treatment agents without delay.
Copyright ©2017 The Emergency Medicine Association of Turkey. Production and hosting by Elsevier B.V.
on behalf of the Owner. This is an open access article under the CC BY-NC-ND license (http://
creativecommons.org/licenses/by-nc-nd/4.0/).
1. Introduction
Peripheral facial nerve paralysis is an acute facial nerve affection
which is encountered frequently in emergency medicine practice.
Typically, the diagnosis can be made based on the weakness of all
muscles innervated by the facial nerve branches. The discrimina-
tion between peripheral and central facial nerve palsies can be
made according to whether the upper facial muscles are spared or
not [1]. However, in contrast with common knowledge, upper facial
weakness has also been reported to exist in patients with central
facial palsy associated with unilateral stroke syndromes [2,3].From
a distinct point of view, via the remarkable clinical follow-up of our
patient, we point out challenges associated with clinical evaluation
of patients presenting with facial palsy in emergency departments.
We emphasize the importance of a detailed examination for the
proper diagnosis as well as the initiation of appropriate treatment
agents without delay.
2. Case report
A-69-year old female patient with a medical history of diabetes
mellitus and hypertension presented with a left facial weakness,
which had started abruptly 4 hours prior to his admission to ED. A
neurological examination revealed that both upper and lower parts
of the face were involved in a grade 3 facial nerve palsy based on
the HBS grading system (Fig. 1). Hence, a preliminary diagnosis of
peripheral facial nerve palsy was made and an otorhinolaryngology
consultation was requested. However, a reassessment of the patient
revealed a left-sided hemiparesis (MRC grade 4) which had not
been expressed by the patient's relatives. Taken together, a central
nervous system disorder was considered at the forefront and a
neurology consultation was requested. Based on a provisional
diagnosis of stroke, a cranial MRI was performed which showed a
right frontal lobe infarction corresponding to the territory of the
superior division of the right middle cerebral artery (Fig. 2). Anti-
platelet and anticoagulant therapies were started and the patient
was admitted to the neurology ward. Further investigations,
including computed tomography angiography of the brain and the
neck, echocardiogram, electrocardiogram did not demonstrate any
other abnormality. However, paroxysmal atrial fibrillation attacks
Abbreviations: HBS, HouseeBrackmann score; INR, International normalized
ratio; MRC, Medical Research Council.
*Corresponding author. Yozgat State Hospital, Department of Neurology, Yozgat,
66700, Turkey.
E-mail address: halilnder@yahoo.com (H. Onder).
Peer review under responsibility of The Emergency Medicine Association of
Turkey.
Contents lists available at ScienceDirect
Turkish Journal of Emergency Medicine
journal homepage: http://www.elsevier.com/locate/TJEM
http://dx.doi.org/10.1016/j.tjem.2017.04.001
2452-2473/Copyright ©2017 The Emergency Medicine Association of Turkey. Production and hosting by Elsevier B.V. on behalf of the Owner. This is an open access article
under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
Turkish Journal of Emergency Medicine xxx (2017) 1e3
Please cite this article in press as: Onder H, et al., Frontal lobe ischemic stroke presenting with peripheral type facial palsy: A crucial diagnostic
challenge in emergency practice, Turkish Journal of Emergency Medicine (2017), http://dx.doi.org/10.1016/j.tjem.2017.04.001
were observed during HOLTER monitoring which led to the initia-
tion of warfarin therapy. After the INR values within the target
range were achieved, the patient was discharged with residual left
sided peripheral-type facial paralysis and a moderate left
hemiparesis.
3. Discussion
Here, we present an interesting patient diagnosed with central
facial paralysis associated with unilateral cortical ischemic infarc-
tion whose diagnosis constituted a distractive experience in the
emergency department. Findings of upper and lower facial weak-
ness firstly suggested a diagnosis of peripheral facial palsy, however
a detailed examination of the patient revealed a left sided hemi-
paresis, in addition to the facial weakness. Finally, cranial MRI
findings enabled a proper diagnosis of right frontal lobe ischemic
stroke in the MCA territory.
Facial paralysis is classically categorized as ‘upper motor neuron’
or ‘lower motor neuron’types [4]. Upper motor neuron paralysis
refers to ‘central’paralysis, whereas lower motor neuron paralysis
is known as ‘peripheral’facial paralysis. Peripheral facial palsy can
be defined as acute peripheral facial nerve affection, and can be
classified as idiopathic or secondary to a number of conditions
including infections, metabolic diseases, tumors, surgery, etc. Of
note, rare cases of strokes associated with peripheral type facial
paralysis have been reported in the literature [5e7]. However, in
these reports, patients were diagnosed with brain stem infarcts and
the responsible mechanisms were explained in the setting of lower
motor neuron damage (facial nucleus). On the other hand, it is also
a recognized fact that the weakness of upper facial muscles which is
Fig. 1. Grade 3 upper and lower face paralysis according to HB grading system (A, B, C).
Fig. 2. Diffusion weighted cranial MRI findings showing a right frontal lobe infarction corresponding to the superior division of the right middle cerebral artery (arrows).
H. Onder et al. / Turkish Journal of Emergency Medicine xxx (2017) 1e32
Please cite this article in press as: Onder H, et al., Frontal lobe ischemic stroke presenting with peripheral type facial palsy: A crucial diagnostic
challenge in emergency practice, Turkish Journal of Emergency Medicine (2017), http://dx.doi.org/10.1016/j.tjem.2017.04.001
typically attributed to peripheral facial paralysis can be seen in
association with central facial paralysis [2,3]. In a study, it was re-
ported to appear up to 6.6% of the patients with unilateral stroke
and central facial paralysis [2]. Of note, right hemisphere involve-
ment was suggested as a risk factor for upper facial weakness
which was also the case in our patient [2]. Nonetheless, underlying
pathophysiology and pathways of this atypical manifestation (pe-
ripheral-type facial paralysis) associated with upper motor neuron
injury still remain to be clarified. Moreover, these discussions seem
to be relatively underestimated in the literature. The basic knowl-
edge states that upper facial muscles receive bilateral cortical
innervation, but lower facial muscles are innervated by the
contralateral cortex. However, currently, it is suggested that there
may be some controversies regarding the mechanisms of facial
innervation [8]. For example, studies conducted in adult rhesus
monkeys using neuronal labelling techniques revealed that both
upper and lower facial nucleus received bilateral cortical innerva-
tion which was in contrast to the classical knowledge, and
remarkably, the upper facial nucleus received less cortical inner-
vation than the lower facial nucleus [9,10]. These conclusions have
also been confirmed by post mortem anatomical studies in humans
[11].
In the literature, this atypical manifestation of upper facial
weakness has been stated in a limited number of reports and
basically, clinical presentations, patient characteristics, prognosis
and neuroimaging findings were the major points focused on in
these studies [1,3]. However, from a distinct point of view, our
report may add substantial data pointing out clinical challenges in
the differential diagnosis of facial paralysis associated with cortical
stroke which mimics peripheral type, particularly in emergency
departments. We emphasize the importance of a detailed evalua-
tion to make a proper diagnosis and initiate appropriate treatments
without delay. We believe that the presence of comorbidities (hy-
pertension, diabetes mellitus, coronary disease etc.) or an abrupt
clinical onset should lead the clinicians to be more careful while a
complete neurological examination should be performed in all
patients presenting with facial palsy, even in typical peripheral
subtypes. In addition, we think that documentation of these
atypical presentations in future reports of larger case series may
further clarify the unknown mechanisms underlying innervation
pathways of facial nerve, while these study results may add crucial
data to the evaluation processes as well as treatment approaches in
these atypical cases.
Conflict of interest
None.
Acknowledgements
None.
References
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H. Onder et al. / Turkish Journal of Emergency Medicine xxx (2017) 1e33
Please cite this article in press as: Onder H, et al., Frontal lobe ischemic stroke presenting with peripheral type facial palsy: A crucial diagnostic
challenge in emergency practice, Turkish Journal of Emergency Medicine (2017), http://dx.doi.org/10.1016/j.tjem.2017.04.001
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Background: Upper facial dysfunction is not generally considered a feature of central facial paralysis after unilateral hemispheric stroke; however, weakness of eye closure (WEC) has been observed in some cases. We aimed to investigate the frequency and characteristics of WEC in unilateral stroke and its association with stroke prognosis. Methods: Patients with unilateral stroke and central facial paralysis were prospectively recruited within 7 days of onset. Facial paralysis was evaluated via the fourth item in the National Institute of Health Stroke Scale (NIHSS-4) and the Japan Facial Score (JFS) on admission, and at days 7, 14, 21, and 30 after stroke. Eye closure strength was measured daily using an ergometer for 30 days after stroke. Primary outcome was assessed using the modified Rankin Scale (mRS) at 90 and 180 days. Univariate and multivariate analyses were performed to investigate risk factors of WEC. Results: WEC was identified in 16 of 242 patients (6.6%). Baseline characteristics, stroke risk factors, and lesion volume were not significantly different between patients with and patients without WEC. Patients with WEC featured higher NIHSS-4 scores and lower JFS between admission and at 21 days after stroke. Severe central facial paralysis (odds ratio [OR] = 8.1, 95% confidence interval [CI] = 2.3-28.6, P = .001) and right hemispheric stroke (OR = 13.7, 95% CI = 3.7-51.2, P < .001) were potential predictors of WEC. At 180 days after stroke, patients with WEC demonstrated a lower rate of functional independence (mRS = 0-2: 37.5% versus 72.1%, P < .001). Conclusions: WEC, which predicts a worse functional outcome at 180 days after unilateral stroke, demonstrates an association with severe central facial paralysis and right hemispheric stroke.
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Historically, paralysis of facial muscles has been divided into "upper motor neuron injury" and "lower motor neuron injury". Patients who experience a stroke in the cortex or internal capsule have UMN injury and cannot purse their lips or smile on command. They are, however, able to wrinkle their forehead, raise their eyebrows, and completely close their eyes. Patients with LMN injury, in addition to the aforementioned impairments cannot raise their eyebrows. The classical explanations for these clinical findings are that the upper facial muscles receive bilateral innervation from the cerebral cortex and the lower facial muscles receive only unilateral innervation from the contralateral cerebral cortex. However, a review of the basic science literature indicates that commonly accepted explanations and the pattern of cortical projections are not consistent with anatomical studies. Studies in monkeys demonstrate that both the upper facial nucleus and the lower facial nucleus receive bilateral cortical projections. As well, there is no direct anatomical evidence in human beings that the facial nucleus (upper or lower) receives any innervation from the cortex.
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Peripheral Type Facial Palsy in a Patient with Dorsolateral Medullary Infarction with Infranuclear Involvement of the Caudal Pons
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The corticobulbar tract fibers descend near the corticospinal tract, mostly to the upper medulla, where they decussate and ascend in the dorsolateral medulla to connect with the contralateral facial nucleus. Therefore, central type facial palsy can be present in patients with ipsilateral dorsolateral upper medullar lesion. We describe a 71-year-old man with lateral medullary infarction who showed ipsilateral peripheral type facial palsy. Brain diffusion-weighted image showed hyperintensities on the left dorsolateral portion of upper medulla and adjacent inferomedial tegmentum of the lower pons. Transfemoral cerebral angiography depicted prominence of ipsilateral posterior inferior cerebellar artery with focal stenosis. Left posterior inferior cerebellar artery might supply the inferolateral tegmentum of the lower pons, which is usually supplied from anterior inferior cerebellar artery. The peripheral type facial palsy in our patient may have resulted from facial infranuclear involvement of the caudal pons extended from dorsolateral upper medullary lesion in ascending pathway of corticobulbar tract fibers.
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Organization of the facial nucleus and corticofacial projection in the monkey: A reconsideration of the upper motor neuron facial palsy
Article
  • Jul 1987
The somatotopic organization of the facial nucleus and the distribution of the corticofacial projection in the monkey were studied by the use of retrograde and anterograde transport of horseradish peroxidase. Facial motor neurons innervating lower facial muscles were primarily found in the lateral part of the nucleus, those supplying upper facial muscles in the dorsal part of the nucleus, and those innervating the platysma and posterior auricular muscles in the medial part of the nucleus. Descending corticofacial fibers innervated the lower facial motor nuclear region bilaterally, although with contralateral predominance. The upper facial motor nuclear regions received scant direct cortical innervation on either side of the brain. Our results indicate that upper facial movement, like that at the shoulder, is relatively preserved in upper motor neuron palsy because these motor neurons receive little direct cortical input. By contrast, the lower facial muscles, like those of the hand, are more severely affected because their motor neurons normally depend upon significant cortical innervation.
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Seventh nerve palsies may be the only clinical sign of small pontine infarctions in diabetic and hypertensive patients
Article
  • Dec 2002
Small brainstem infarctions are increasingly recognized as a cause of isolated ocular motor and vestibular nerve palsies in diabetic and/or hypertensive patients. This raises the question whether there are also isolated 7(th) nerve palsies due to pontine infarctions in patients with such risk factors for the development of cerebrovascular diseases. Over an 11-year-period, we retrospectively identified 10 diabetic and/or hypertensive patients with isolated 7(th) nerve palsies and electrophysiological abnormalities indicating pontine dysfunction. All patients had examinations of masseter and blink reflexes, brainstem auditory evoked potentials, direct current electro-oculography including bithermal caloric testing, and T1- and T2-weighted MRI (slice thickness: 4-7 mm). Electrophysiological abnormalities on the side of the 7(th) nerve palsy included delayed masseter reflex latencies (4 patients), slowed abduction saccades (4 patients), vestibular paresis (2 patients), and abnormal following eye movements (2 patients). Electrophysiological abnormalities were always improved or normalized at re-examination, which was always associated with clinical improvement. MRI revealed an ipsilateral pontine infarction in 2 patients. Another 2 had bilateral hyperintense intrapontine lesions, and one an ipsilateral cerebellar infarction. Simultaneous improvement or recovery of abnormal clinical and electrophysiological findings strongly indicated that both were caused by the same actual pontine lesions. A 7(th) nerve palsy may be the only clinical sign of a pontine infarction in diabetic and/or hypertensive patients. Such mechanism may be underestimated if based on MRI only.
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