What is the management approach for patients with facial Upper Motor Neuron (UMN) or Lower Motor Neuron (LMN) lesions?

Facial Upper Motor Neuron (UMN) vs Lower Motor Neuron (LMN) Lesions

Clinical Distinction: The Critical First Step

The key to distinguishing UMN from LMN facial lesions is forehead involvement: LMN lesions affect the entire hemiface including forehead, while UMN lesions spare the forehead due to bilateral cortical innervation of the upper facial muscles. 1

Examination Findings

LMN Pattern (Peripheral Facial Palsy):

• Complete hemifacial weakness including inability to wrinkle forehead, close eye, or smile on affected side 2
• Loss of nasolabial fold and drooping of mouth corner 2
• All facial muscles on one side are affected equally 1

UMN Pattern (Central Facial Palsy):

• Forehead movement preserved (can wrinkle forehead and close eyes) 1
• Lower face weakness only (difficulty smiling, showing teeth) 1
• Often accompanied by contralateral limb weakness suggesting stroke 1, 3

Critical Pitfall: Central Causes Can Present as LMN Pattern

A dorsal pontine lesion affecting the facial colliculus can produce an LMN facial palsy pattern despite being a central lesion. 3 This occurs because the lesion affects the facial nerve fascicles before they exit the brainstem. Associated findings include:

• Ipsilateral conjugate gaze palsy (abducens nerve involvement) 3
• Cerebellar signs (ataxia, nystagmus) 3
• Other cranial nerve palsies 3

Any LMN facial palsy with additional neurological signs warrants immediate brain imaging to exclude stroke or space-occupying lesions, even in young patients without vascular risk factors. 3

Diagnostic Approach

When to Image

For isolated LMN facial palsy (Bell's palsy), imaging is not routinely indicated unless: 2, 4

• Symptoms are atypical or recurrent 4
• No improvement after 2-4 months 4
• Other neurological signs are present 2, 3
• Progressive or complete paralysis from onset 5

For UMN facial palsy with limb weakness, immediate stroke protocol imaging (CT or MRI) is mandatory. 1

Imaging Protocol When Indicated

MRI is the preferred modality for evaluating facial nerve pathology: 2, 4

• Pre- and post-contrast sequences with sensitivity 73-100% for detecting lesions 4
• High-resolution thin-cut sequences through entire facial nerve course 4
• Coverage must include brainstem, cerebellopontine angle, temporal bone segments, and parotid gland 4
• 3D heavily T2-weighted sequences for vascular compression evaluation 4

High-resolution temporal bone CT provides complementary information for: 4

• Osseous integrity of facial nerve canal 4
• Trauma or suspected fractures 4
• Facial nerve canal dehiscence 1

Electrodiagnostic Testing

For Bell's palsy with incomplete paralysis, electrodiagnostic testing should not be performed. 2

For complete facial paralysis, electroneurography (ENoG) and electromyography (EMG) may be offered to guide surgical decisions: 2, 1

• ENoG showing >90% amplitude reduction suggests severe denervation 1
• Absent volitional activity on EMG indicates complete denervation 1
• Testing should be performed 3-14 days after symptom onset 1

Management Based on Lesion Type

LMN Lesions (Bell's Palsy)

Medical Management:

• Oral corticosteroids (prednisone 1-1.5 mg/kg daily) within 72 hours of symptom onset is the standard of care, achieving 94% recovery rates. 2, 1
• Antiviral monotherapy alone should not be prescribed 2
• Antiviral therapy may be added to steroids as an option 2

Eye Protection:

• Implement eye protection immediately for patients with impaired eye closure to prevent exposure keratitis or corneal abrasion. 2
• This includes artificial tears, lubricating ointment, and eye taping 2

Surgical Decompression:

• Consider middle fossa decompression only for highly selected patients with complete paralysis, >90% ENoG amplitude reduction, absent EMG activity, and surgery within 3-14 days of onset. 1
• Achieves House-Brackmann grade I/II in 91% versus 42% with steroids alone in selected patients 1
• Target is the labyrinthine segment at the meatal foramen 1
• Most Bell's palsy patients (70-94%) recover without surgery—surgical intervention is reserved for the small subset with severe electrodiagnostic findings. 1

Follow-up:

• Reassess or refer patients with: (1) new/worsening neurological findings at any point, (2) ocular symptoms developing at any point, or (3) incomplete recovery at 3 months. 2

UMN Lesions (Stroke/Central Causes)

Immediate stroke protocol management is required: 1

• Central facial pattern (forehead spared) plus limb weakness equals stroke until proven otherwise. 1
• Activate stroke team for thrombolysis/thrombectomy evaluation 1
• Admit for comprehensive stroke workup and secondary prevention 1

Tumor-Related Facial Nerve Pathology

Surgical principles for tumor management: 1

• Preserve facial nerve when preoperative function is intact AND dissection plane exists between tumor and nerve 1
• Resect involved nerve branches when preoperative facial movement is impaired OR nerve is encased/grossly involved by malignancy 1

For perineural tumor spread (most commonly trigeminal and facial nerves): 2

• MRI is preferred for detecting perineural spread with thin-section protocol 2
• CT visualizes neural foramina expansion 2
• FDG-PET/CT may be useful for localization and treatment response monitoring 2

Traumatic Facial Nerve Injury

Use electrodiagnostic testing to guide treatment decisions, with surgical decompression considered for severe denervation. 1

Special Considerations

Cranial Nerve Examination in Surgical Contexts

For patients undergoing head and neck surgery or radiotherapy, perform thorough cranial nerve examination and laryngoscopy before and after intervention. 2

• Evaluate cranial nerves VII-XII systematically 2
• Assess symmetric facial movement, hearing, swallowing, palate rise, shoulder elevation, and tongue mobility 2
• New cranial neuropathies occur in 30-33% even with observation alone 2

Distinguishing from Other Motor Neuron Disorders

In amyotrophic lateral sclerosis (ALS), facial nerve involvement is rare but UMN signs may be subtle. 6, 7 Motor cortex thickness on MRI is more sensitive than clinical examination for detecting UMN degeneration and can identify changes before signs become clinically evident. 7