Supranuclear infarction mimicking Bell’s palsy: a case report of splenial infarction

Abstract

Background

The classic distinguishing feature between peripheral and central facial palsy is the preservation of forehead wrinkles; however, in rare instances, supranuclear lesions can present as peripheral-type facial palsy involving both the upper and lower face, and cases caused by splenial infarction are particularly uncommon among them.

Case presentation

We report a 61-year-old woman who presented with isolated left-sided peripheral-type facial palsy. No predominance of lower facial involvement or dissociation between emotional and volitional facial movements was observed. Magnetic resonance imaging (MRI) on the day after symptom onset revealed an acute infarction in the right splenium of the corpus callosum, with no evidence of brainstem or peripheral responsible lesions. Bilateral facial nerve conduction studies and needle electromyography showed no abnormalities. The splenial lesion was considered the most likely cause of her facial palsy. Following treatment with antiplatelet agents, lipid-lowering therapy, and neurotrophic support, her facial palsy began to improve on day 3 of hospitalization and had markedly improved by discharge on day 6. At six-month follow-up, she had recovered well without recurrence.

Conclusions

This case further expands the spectrum of supranuclear lesions that can present as peripheral-type facial palsy and provides preliminary evidence that splenial infarction may be associated with isolated peripheral-type facial palsy. However, further accumulation of cases is needed to validate this association.

Supplementary Information

The online version contains supplementary material available at 10.1186/s12883-026-05167-y.

Introduction

Acute unilateral facial weakness involving both the upper and lower face is a common presentation in emergency and neurology practice, with idiopathic Bell‘s palsy being the most frequent cause [1]. According to traditional teaching, the key to distinguishing central from peripheral facial palsy lies in examining upper facial function, including forehead wrinkling, eyebrow elevation, and eye closure. Because the subnucleus of the facial motor nucleus that supplies the upper face receives bilateral cortical input, a unilateral supranuclear lesion typically results in contralateral lower facial weakness while sparing the forehead [2]. Conversely, when both the upper and lower face are affected, the lesion is generally considered to involve the facial nucleus or its peripheral fibers.

This conventional framework, however, has been increasingly challenged. A small number of case reports have described supranuclear lesions—such as precentral gyrus infarction or hemorrhage and lenticulostriate artery infarction—that can affect both the contralateral upper and lower face, mimicking peripheral facial palsy [3–7]. Cattaneo et al. [8] further found that upper facial movement is only relatively spared in middle cerebral artery (MCA) territory infarction, and may be accompanied by lip opening weakness; in contrast, eyelid closure weakness was associated with anterior cerebral artery (ACA) territory infarction. These observations suggest that bilateral innervation of the upper facial muscles is not absolute and that considerable interindividual variation in corticobulbar projections may exist [9]. Despite these reports, the literature on this phenomenon remains sparse. Here, we describe a patient with an acute splenial infarction confirmed by brain MRI, who presented with isolated peripheral-type facial palsy as the sole clinical manifestation. This case aims to expand the spectrum of supranuclear lesions that can cause peripheral-type facial palsy and to raise clinicians’ awareness of this diagnostic pitfall.

Case presentation

A 61-year-old woman was found by her family at approximately 9:00 AM on the day of symptom onset to have left-sided facial palsy, presenting as right-sided mouth deviation and left eyelid closure weakness. Because the symptoms persisted, she presented to our emergency department at 7:00 PM that evening. An emergency head computed tomography scan showed no acute hemorrhage or space-occupying lesions. There was no preceding infection, and the patient reported no periauricular vesicles, postauricular pain, hyperacusis, dysgeusia, excessive tearing, headache, dizziness, blurred vision, diplopia, limb weakness, numbness, dysarthria, or dysphagia. There was also no evidence of agraphia, alien hand syndrome, alexia, prosopagnosia, or epileptic seizures. She had no history of chronic diseases, family history of genetic disorders, smoking, or alcohol use. There was no prior history of right facial nerve palsy, and she had not noticed any facial asymmetry previously.

On admission, her blood pressure was 132/70 mmHg and heart rate was 75 beats per minute. She was alert and oriented, with fluent speech and normal memory. Pupils were equal and round (3 mm in diameter) with prompt light reflexes. No eye position abnormality was observed; extraocular movements were full in all directions without nystagmus. Facial sensation was intact. On the left side, forehead wrinkles were markedly diminished, eyelid closure was weak, and eyebrow wrinkling and frowning were impossible. The left nasolabial fold was shallow, and she showed right-sided mouth deviation when showing her teeth, accompanied by cheek puffing with air leakage, food retention in the cheek, and water leakage while drinking. No clear predominance of lower facial involvement or dissociation between emotional and volitional facial movements was observed. Tongue protrusion was midline. Palatal elevation was symmetric, and the gag reflex was present. Muscle strength was grade 5/5 in all four limbs with normal tone. Coordination testing (finger-to-nose, heel-to-shin, and rapid alternating movements) was normal. Sensation to light touch and pinprick was intact. Deep tendon reflexes were symmetric, and no Babinski sign or meningeal signs were elicited.

Laboratory studies revealed mildly elevated homocysteine (17.40 µmol/L), triglycerides (2.10 mmol/L), and low-density lipoprotein (2.7 mmol/L), as well as occult blood (++) on urinalysis, the latter being considered clinically insignificant in the setting of acute facial palsy. Complete blood count, coagulation profile, liver and kidney function tests, electrolytes, infectious disease screening, and stool examination were all within normal limits. Additional laboratory results are provided in Supplementary Table 1. The initial differential diagnosis included cerebral infarction and peripheral facial palsy, and she was started on methylprednisolone (40 mg once daily), vitamin B1 (100 mg three times daily), mecobalamin (0.5 mg three times daily), aspirin (100 mg once daily), atorvastatin (20 mg once daily), and rehabilitation therapy.

On the second hospital day, brain magnetic resonance imaging (MRI) revealed a focal hyperintensity on diffusion-weighted imaging (DWI) in the right splenium of the corpus callosum, with corresponding hypointensity on the apparent diffusion coefficient (ADC) map, consistent with acute infarction. The lesion appeared hyperintense on T2-weighted imaging, with well-defined borders and no mass effect (Fig. 1A-C). Magnetic resonance angiography (MRA) showed mild focal narrowing of the intracranial segment of the left vertebral artery, while the remaining major intracranial vessels had a normal course and smooth walls without significant stenosis or occlusion. No infarction or abnormal signal was detected in the pontine facial nucleus (Fig. 1D-F), facial nerve fascicles, or geniculate ganglion region. On the third hospital day, bilateral facial nerve conduction studies were symmetric and normal, and needle electromyography showed no abnormalities. Echocardiography revealed grade I left ventricular diastolic dysfunction and mild tricuspid regurgitation. Carotid artery ultrasonography showed no significant plaque or stenosis. Electrocardiography was normal. Abdominal ultrasonography revealed fatty liver, with no abnormalities of the gallbladder, pancreas, spleen, kidneys, ureters, or bladder.

Fig. 1.

Brain magnetic resonance imaging (MRI) findings. Diffusion-weighted imaging (DWI) (A) and apparent diffusion coefficient (ADC) (B) show a focal hyperintense lesion in the right splenium of the corpus callosum (arrows), with corresponding hypointensity on ADC, consistent with acute infarction. T2-weighted imaging (C) shows the lesion as hyperintense with well-defined borders and no mass effect (arrow). Diffusion-weighted images at the level of the pons and adjacent regions (D-F) reveal no abnormal signal in the facial nucleus or fascicles

Given the temporal coincidence of facial palsy with the acute infarct, the exclusion of brainstem or peripheral responsible lesions by MRI, and normal findings on both facial nerve conduction studies and needle electromyography, the right acute splenial infarction was considered the most likely cause of her facial palsy. The stroke mechanism was consistent with small artery occlusion. Accordingly, the treatment regimen was adjusted: methylprednisolone was discontinued, and she was started on dual antiplatelet therapy with aspirin (100 mg/day) and clopidogrel (75 mg/day), combined with atorvastatin (20 mg/day) and ezetimibe (10 mg/day) for lipid-lowering and plaque stabilization, along with neurotrophic support and rehabilitation. On hospital day 3, her facial palsy began to improve. By the time of discharge on day 6, her left forehead wrinkles had largely recovered, eyelid closure was stronger, and only mild residual mouth deviation remained. A telephone follow-up at six months after discharge revealed good recovery without recurrence of facial palsy.

Discussion

Previous case reports have described supranuclear lesions presenting as peripheral-type facial palsy, with responsible lesions located in the precentral gyrus (ischemic or hemorrhagic) [3, 4], subcortical frontal lobe [6], lenticulostriate artery territory [5], and bilateral corona radiata [7] (see Table 1 for a summary of previous and the present case). This case suggests that splenial infarction can also lead to a similar presentation.

Table 1.

Supranuclear infarction presenting as peripheral-type facial palsy: summary of reported cases

Author, year	Age/Sex	Lesion location	Facial palsy features	Other neurological symptoms	Facial nerve electromyography
Hebant et al., 2018 [3]	78/F	Left precentral gyrus	Right peripheral-type facial palsy	None	-
Hebant et al., 2020 [4]	35/F	Left precentral gyrus cavernoma hemorrhage	Right peripheral-type facial palsy; predominance of lower face; dissociation present (symmetrical smiling)	None	-
Kubota-Hanya et al., 2024 [5]	82/F	Left lenticulostriate artery	Right pseudoptosis (upper facial weakness)	Right hemiparesis	Bilateral symmetrical nerve conduction
Onder et al., 2017 [6]	69/F	Right frontal lobe cortex and subcortex	Left peripheral-type facial palsy	Left hemiparesis	-
Zheng-Hua et al., 2025 [7]	56/M	Bilateral corona radiata (left lacunar, right acute)	Right peripheral-type facial palsy	Left lower limb weakness	needle EMG unremarkable
Present case	61/F	Right splenium of corpus callosum	Left peripheral-type facial palsy; no predominance of lower face; no emotional-volitional dissociat	None	Bilateral facial nerve conduction and needle EMG were normal

At present, the precise functions of the splenium of the corpus callosum remain incompletely understood; nevertheless, lesions in this region can disrupt interhemispheric information transfer, giving rise to a variety of clinical manifestations. These include disturbances of consciousness, ataxia, epilepsy, hemiparesis, as well as interhemispheric disconnection phenomena such as aphasia, agraphia, and sensory abnormalities, with considerable interindividual variability [10]. Notably, disruption of interhemispheric motor integration can lead to craniofacial dysfunction. Korn et al. [11] and Chung et al. [12] respectively reported contralateral eyelid closure difficulty and dysarthria resulting from infarction of the anterior part and the body of the corpus callosum. Previous reports have confirmed that callosal damage can lead to contralateral facial palsy, which may occur even when the primary motor cortex remains intact. Yin et al. [13] reported a patient with left anterior cerebral artery territory infarction involving the genu, body, and splenium of the corpus callosum, who presented with right central facial palsy; Trivilegio et al. [14] documented a case of right central facial palsy following infarction of the body and splenium of the corpus callosum. Both cases involved the body and splenium of the corpus callosum, suggesting an association between facial palsy and involvement of these regions. Furthermore, Tahara et al. [15] reported a pair of monozygotic twin children with mild encephalitis/encephalopathy, in whom MRI showed hyperintense lesions in the splenium of the corpus callosum and bilateral deep cerebral white matter; one of the twins exhibited transient facial palsy. Takemaru et al. [16] described a female patient with X-linked Charcot-Marie-Tooth disease (CMTX1) whose MRI revealed hyperintense signals in the cerebral white matter, the splenium of the corpus callosum, and the posterior limb of the internal capsule, and who presented clinically with bilateral central facial palsy. Ward et al. [17] reported a patient with post-partum cytotoxic lesions of the corpus callosum (CLOCCs) who presented with bilateral facial palsy; unfortunately, the original imaging data were not provided. Although these cases had different etiologies (ischemic, inflammatory, genetic, and post-partum), splenial involvement was a common feature, suggesting that splenial damage may be a key factor in the development of facial palsy.

The precise mechanism by which a splenial lesion leads to facial palsy remains unclear. The classic corticobulbar tract does not pass through the corpus callosum, making it difficult to explain this phenomenon solely by direct damage to this pathway. One plausible mechanism is that motor control of the left face is highly dependent on coordinated commands transmitted from the right hemisphere via the corpus callosum. Tractography studies have confirmed that the splenium acts as a structural hub connecting the bilateral facial motor cortices [18]. Furthermore, transcranial magnetic stimulation combined with electroencephalography has provided direct evidence of transcallosal connections between the two facial motor cortices [19, 20]. Infarction of the splenium of the corpus callosum can lead to disconnection in the coordination and transmission of interhemispheric motor commands, thereby resulting in contralateral facial palsy. An additional hypothesis is that, in the presence of pre-existing structural compromise—such as congenital anatomical variation in the corticobulbar tract or subclinical white matter lesions—an acute splenial infarction may further disrupt the original compensatory mechanisms. This can lead to decompensation of an already fragile interhemispheric coordination, thereby “amplifying” or “unmasking” a latent neurological deficit and ultimately manifesting as contralateral complete facial palsy. This hypothesis helps to explain why the same lesion location can present with markedly heterogeneous clinical manifestations across different patients: interindividual differences in pre-existing anatomical and functional reserve determine the degree of decompensation and the resulting symptom profile following acute injury [21].

Notably, our patient did not exhibit dissociation between emotional and volitional facial movements. This dissociation has been supported by previous literature [22, 23] : volitional movements are primarily regulated by the primary motor cortex, whereas emotional expressions depend on the cingulate cortex and its limbic connections. The lesion in our patient was located in the right splenium of the corpus callosum, adjacent to the posterior part of the cingulate cortex. We speculate that the infarct may have simultaneously involved both types of fibers, or that individual anatomical variation may account for this finding.

This case also highlights a diagnostic pitfall that warrants attention. Acute-onset “peripheral-type” facial palsy is not synonymous with Bell’s palsy. A surveillance study of nearly 44,000 patients diagnosed with Bell’s palsy found that 0.8% received an alternative diagnosis within 90 days of follow-up, with stroke accounting for a substantial proportion [24]. The “isolated” presentation of our patient—absence of any limb, speech, or ataxic symptoms—represents precisely this pitfall, making it highly likely to be misdiagnosed as Bell’s palsy, thereby delaying etiological treatment. Central causes of facial palsy may present with subtle clinical differences from typical peripheral facial palsy. As previously noted, the presence of predominant lower facial involvement or dissociation between emotional and volitional facial movements should raise suspicion of a central etiology [4].

Limitations

This study has several limitations. First, the anatomical mechanism by which right splenial infarction leads to left-sided facial palsy remains unclear, as the classic corticobulbar tract does not directly traverse the corpus callosum. We have proposed an “interhemispheric disconnection” hypothesis as a possible explanation; however, this hypothesis requires further validation through functional neuroimaging studies. Moreover, as this is a single case report, accumulation of additional similar cases is needed to support this association. In addition, this was a retrospective report, and no facial photographs documenting the patient‘s facial palsy were obtained at the time of presentation. Second, coronal DWI and thin-section brainstem imaging were not performed in this case, which may have resulted in missing small lesions. Furthermore, the lack of follow-up MRI makes it impossible to completely exclude the possibility of delayed appearance of lesions in the brainstem or other regions. Third, due to the absence of serial electromyography data, the possibility that the facial palsy represented an independent peripheral lesion (i.e., coincidentally coexisting with the cerebral infarction) cannot be completely ruled out.

Conclusion

This case further expands the spectrum of supranuclear lesions that can present as peripheral-type facial palsy and provides preliminary evidence that splenial infarction may be associated with isolated peripheral-type facial palsy. However, further accumulation of cases is needed to validate this association. Clinicians should be aware that acute-onset “peripheral” facial palsy may be caused by cerebral infarction, even in the absence of limb, speech, or ataxic symptoms. Facial weakness of central origin may show subtle clinical differences from classic peripheral facial palsy, and careful semiological analysis—such as identifying predominance of lower facial involvement or dissociation between emotional and volitional facial movements—remains key to avoiding misdiagnosis.

Abbreviations

ACA

Anterior Cerebral Artery

ADC

Apparent diffusion coefficient

CLOCCs

Cytotoxic lesions of the corpus callosum

CMTX1

X-linked Charcot-Marie-Tooth disease type 1

DWI

Diffusion-weighted imaging

MCA

Middle Cerebral Artery

MRA

Magnetic resonance angiography

MRI

Magnetic resonance imaging

EMG

Electromyography

T2WI

T2-weighted imaging

Authors’ contributions

Y.Y., L.L., and Z.Z. conceived and designed the study. Y.Y., L.L., and Z.Z. acquired, analyzed, and interpreted the patient data. Y.Y., L.L., and Z.Z. drafted the original manuscript. Y.Y., L.L., and Z.Z. critically reviewed and revised the manuscript for important intellectual content. Z.Z. supervised the study and is the corresponding author. All authors reviewed and approved the final version of the manuscript and agreed to be accountable for all aspects of the work.

Funding

No funding was received for this study.

Data availability

The datasets used and/or analysed during the current study are available from the corresponding author on reasonable request.

Declarations

Ethics approval and consent to participate

Ethical approval was not required for this case report in accordance with the local legislation and institutional requirements. Written informed consent was obtained from the patient for participation in this case report.

Consent for publication

Written informed consent was obtained from the patient for the publication of this case report and any accompanying images.

Competing interests

The authors declare no competing interests.