What causes facial twitch and how is it treated?

Facial Twitching: Causes and Treatment

Facial twitching requires immediate assessment to distinguish between benign eyelid twitching, Bell's palsy, hemifacial spasm, paroxysmal kinesigenic dyskinesia, or seizure activity, as each has distinct treatment pathways and prognoses.

Initial Diagnostic Approach

You must perform a focused history and physical examination to exclude identifiable causes of facial movement disorders before assuming a benign etiology. 1

Key Historical Features to Elicit:

• Onset timing: Symptoms developing over less than 72 hours suggest Bell's palsy, while gradual progression beyond 72 hours indicates tumor or infection 2, 3
• Distribution pattern: Unilateral involvement of both upper and lower face (including forehead) indicates Bell's palsy, while isolated lower face weakness with forehead sparing suggests stroke 3
• Trigger identification: Sudden voluntary movements triggering facial twitching suggest paroxysmal kinesigenic dyskinesia 1
• Presence of aura: Approximately 78-82% of paroxysmal kinesigenic dyskinesia patients experience numbness, tingling, or muscle weakness before attacks 1
• Associated neurological symptoms: Limb weakness, sensory changes, diplopia, or dysphagia exclude Bell's palsy and require consideration of stroke, Guillain-Barré syndrome, or brainstem pathology 2, 3

Critical Physical Examination Findings:

• Forehead involvement: Inability to raise eyebrow or wrinkle forehead on affected side confirms peripheral facial nerve involvement (Bell's palsy) rather than central causes 3
• Eye closure: Incomplete eye closure indicates Bell's palsy; complete inability suggests more severe pathology 3
• Bilateral involvement: Extremely rare in Bell's palsy; consider Guillain-Barré syndrome or sarcoidosis 3
• Isolated branch paralysis: Suggests alternative diagnosis to Bell's palsy 3

Specific Causes and Their Characteristics

Bell's Palsy (Acute Facial Nerve Paralysis)

Bell's palsy presents with rapid unilateral facial weakness affecting both upper and lower face, developing over less than 72 hours. 1

• Patients experience ipsilateral ear/face pain, hyperacusis, and taste disturbance on anterior two-thirds of tongue 3
• No other neurological deficits should be present 3
• Recovery rate is 70% without treatment, 94% with steroids 1

Hemifacial Spasm

Hemifacial spasm manifests as involuntary unilateral contractions of facial muscles, typically starting in the eyelid and progressing to involve the entire side of face. 4, 5

• Caused by neurovascular compression of facial nerve at root exit zone 5
• Bilateral hemifacial spasm is rare, with asymmetric and asynchronous facial contractions 4
• When bilateral, second side involvement occurs average 8.4 years after initial side 4
• Imaging may reveal tortuous vertebrobasilar arteries 4

Paroxysmal Kinesigenic Dyskinesia

Paroxysmal kinesigenic dyskinesia presents with brief episodes (less than 1 minute in 98% of cases) of facial twitching triggered by sudden voluntary movements. 1

• Face involvement occurs in approximately 70% of patients, manifesting as facial twitching, rigidity, or dysarthria 1
• Attack frequency ranges from several times yearly to over 100 times daily 1
• Peaks during puberty, decreases after age 20, may remit after age 30 1
• PRRT2 gene is the major causative gene 1

Chronic Eyelid Twitching

Chronic eyelid twitching (persisting more than 2 weeks) represents a minor form of facial nerve neuropathy, more common in women (3:1 ratio) and cold weather. 6

• 50% demonstrate delayed or absent R2 response in blink reflex 6
• 45.8% have prolonged facial nerve latency indicating conduction defect 6
• Despite being considered benign, electrophysiological studies confirm underlying facial nerve pathology 6

Hemifacial Seizures

Hemifacial seizures present with stereotyped facial contractions but lack the upward eyebrow elevation typical of hemifacial spasm and show no "lateral spread" on EMG. 7

• Associated with brainstem lesions such as ganglioglioma 7
• MRI reveals absence of clear vascular compression of facial nerve 7
• Often refractory to antiepileptic drugs 7

Diagnostic Testing

When NOT to Order Tests:

Do not obtain routine laboratory testing in patients with new-onset Bell's palsy. 1

Do not routinely perform diagnostic imaging for patients with new-onset Bell's palsy. 1

Do not perform electrodiagnostic testing in Bell's palsy patients with incomplete facial paralysis. 1

When Testing IS Indicated:

• Electrodiagnostic testing: Offer to Bell's palsy patients with complete facial paralysis to identify subset with greater than 90% amplitude reduction who have poor prognosis 1
• Imaging: Indicated when atypical features suggest tumor, stroke, or structural pathology 2
• EMG: Useful to distinguish hemifacial spasm (shows "lateral spread") from hemifacial seizures (no lateral spread) 7

Treatment Approaches

Bell's Palsy Treatment:

Prescribe oral corticosteroids within 72 hours of symptom onset for Bell's palsy patients 16 years and older. 1, 3

• Steroids achieve 83% recovery at 3 months versus 63.6% with placebo 3
• Do not prescribe oral antiviral therapy alone 1
• May offer oral antiviral therapy in addition to steroids within 72 hours 1

Implement mandatory eye protection for impaired eye closure: 1, 3

• Lubricating drops and ointments
• Moisture chambers
• Eye patching
• Sunglasses

Hemifacial Spasm Treatment:

Botulinum toxin injection is the treatment of choice for hemifacial spasm. 4, 5

• Successfully treats bilateral hemifacial spasm 4
• Dose of 4 Units per injection site, maximum 20 Units total for facial treatment 8
• Retreatment no more frequently than every 3 months 8

Gabapentin (900-1,600 mg daily) provides rapid improvement with minimal side effects as alternative to botulinum toxin. 5

Paroxysmal Kinesigenic Dyskinesia Treatment:

• Carbamazepine is first-line treatment (specific dosing not provided in guidelines) 1
• Patients may learn to abort attacks by slowing movements when experiencing aura 1

Critical Follow-Up Requirements

Reassess or refer to facial nerve specialist for Bell's palsy patients with: 1

• New or worsening neurological findings at any point
• Ocular symptoms developing at any point
• Incomplete facial recovery 3 months after initial symptom onset

Common Pitfalls to Avoid

• Do not diagnose Bell's palsy if forehead is spared - this indicates stroke requiring immediate activation of stroke protocol 3
• Do not diagnose Bell's palsy if any other neurological deficits are present - requires consideration of alternative diagnoses 2, 3
• Do not assume bilateral facial weakness is Bell's palsy - consider Guillain-Barré syndrome or sarcoidosis 3
• Do not confuse hemifacial spasm with hemifacial seizures - misdiagnosis leads to inappropriate surgical decompression 7
• Do not inject botulinum toxin closer than 1 cm above central eyebrow to avoid eyelid ptosis 8