A patient on antiepileptic drugs presents with frequent lip‑smacking—is this a drug‑induced movement disorder or an ictal automatisms, and how should it be evaluated and managed?

Lip-Smacking in Patients on Antiepileptic Drugs: Ictal Automatism vs. Drug-Induced Movement Disorder

Lip-smacking in a patient on antiepileptic drugs is most likely an ictal automatism representing a complex partial seizure (focal seizure with impaired awareness) rather than a drug-induced movement disorder, and requires immediate EEG evaluation to confirm seizure activity and guide antiepileptic drug optimization. 1

Clinical Distinction: Key Differentiating Features

Features Strongly Suggesting Ictal Automatism (Seizure)

Clear automatisms such as chewing or lip-smacking are characteristic of partial seizures, particularly those of temporal lobe origin. 1 The European Heart Journal guidelines specifically identify these as seizure-likely findings when observed during loss of consciousness 1.

Critical distinguishing features include:

• Stereotyped, repetitive pattern - Lip-smacking occurs in a rhythmic, repetitive pattern that interrupts speech 2, 3
• Associated features - Presence of epigastric aura, altered consciousness (though consciousness can occasionally be preserved), postictal confusion, or tongue biting 1, 3
• Temporal relationship - Automatisms coincide with or immediately follow the onset of altered consciousness 1
• Duration - Episodes are typically brief (seconds to 2-3 minutes) 4
• Insulo-opercular involvement - Ictal activity involving the insulo-opercular cortex consistently correlates with oroalimentary automatisms in temporal lobe seizures 4

Features Suggesting Drug-Induced Movement Disorder

Drug-induced orofacial dyskinesia presents differently:

• Arrhythmic, non-stereotyped movements - Involuntary spasms causing irregular movements of tongue, lips, and jaw without the repetitive pattern seen in seizures 2
• Continuous or intermittent throughout the day - Not episodic like seizures 1, 5
• Associated with dopamine-blocking agents - Tardive dyskinesia is primarily associated with antipsychotics (neuroleptics), not traditional antiepileptic drugs 1, 2
• Gradual onset - Develops over weeks to months of medication exposure, not acutely 1

Critical Evaluation Algorithm

Step 1: Obtain Detailed Seizure Semiology

• Witness description is essential - Ask specifically about the timing of lip-smacking relative to consciousness changes 1
• Look for temporal lobe seizure features: epigastric aura, olfactory hallucinations, déjà vu, postictal confusion, or amnesia for the event 1, 6
• Document frequency and duration - Seizures are episodic; movement disorders are more continuous 1, 4

Step 2: Emergency EEG with Video Monitoring

Video-EEG is the definitive diagnostic test to distinguish ictal automatisms from movement disorders. 6, 3

• Ictal automatisms will show focal epileptiform discharges originating from temporal regions (particularly mesial temporal or insulo-opercular cortex) during the lip-smacking episodes 6, 3, 4
• Drug-induced movement disorders show normal interictal EEG during the movements 1
• Capture multiple episodes on video-EEG to correlate clinical phenomena with electrical activity 6, 3

Step 3: Review Current Antiepileptic Drug Regimen

Most traditional antiepileptic drugs do not cause orofacial dyskinesia; this is primarily an antipsychotic side effect. 7

However, consider:

• Phenytoin can worsen or induce movement disorders and should be avoided if movement disorder is suspected 7
• Lamotrigine, vigabatrin, tiagabine have been reported to worsen movement disorders 7
• Carbamazepine and valproate have variable effects on movement disorders 7
• Levetiracetam, gabapentin, pregabalin are less likely to cause movement disorders 7

Step 4: Assess for Inadequate Seizure Control

If EEG confirms seizure activity, the lip-smacking represents breakthrough seizures requiring antiepileptic drug optimization, not drug discontinuation. 8

• Check antiepileptic drug levels to ensure therapeutic range 8
• Evaluate medication adherence 8
• Consider drug interactions or recent medication changes 8
• Assess for new structural lesions with MRI if seizure pattern has changed 6, 3

Management Based on Diagnosis

If Confirmed Ictal Automatism (Most Likely Scenario)

Optimize antiepileptic therapy rather than discontinuing medications:

• Increase current antiepileptic drug dose if subtherapeutic levels or inadequate seizure control 8
• Add or switch to medications effective for temporal lobe epilepsy: carbamazepine, lamotrigine, levetiracetam, or lacosamide 8
• Consider surgical evaluation if medically refractory temporal lobe epilepsy is confirmed 3, 4
• Avoid benzodiazepines for chronic management as they may affect arousal more than other agents 8

If Confirmed Drug-Induced Movement Disorder (Rare with Antiepileptics)

Immediate discontinuation of the offending agent is the primary treatment, but this is rarely applicable to traditional antiepileptic drugs. 5

• If patient is on antipsychotics (not antiepileptics), discontinue immediately 5
• If on phenytoin, lamotrigine, or vigabatrin and movement disorder confirmed, switch to alternative antiepileptic drug 7
• Do NOT use anticholinergics - they are ineffective for tardive dyskinesia and may worsen symptoms 5
• Consider VMAT2 inhibitors (valbenazine or deutetrabenazine) for persistent, disabling tardive dyskinesia 5

Common Pitfalls to Avoid

• Do not assume lip-smacking is a drug side effect without EEG confirmation - this is almost always an ictal phenomenon in patients with epilepsy 1, 4
• Do not discontinue antiepileptic drugs based on clinical suspicion alone - this could precipitate status epilepticus if the movements are actually breakthrough seizures 6
• Do not confuse brief postictal movements in syncope with seizure automatisms - syncope-related movements are brief (<15 seconds) and occur AFTER loss of consciousness, while seizure automatisms coincide with or precede the fall 1
• Do not attribute orofacial movements to tardive dyskinesia in patients only on antiepileptic drugs - tardive dyskinesia is primarily caused by dopamine-blocking antipsychotics, not antiepileptics 1, 2, 7

Prognosis and Follow-Up

• Early identification and treatment of breakthrough seizures prevents progression to status epilepticus and reduces injury risk 6
• Temporal lobe seizures with oroalimentary automatisms may be amenable to surgical treatment if medically refractory 3, 4
• True drug-induced tardive dyskinesia has up to 50% chance of resolution if the offending agent is discontinued early 5