Postictal (Todd's) Paralysis: Evaluation and Management
In a patient with new weakness after a seizure, the primary goal is to rapidly distinguish Todd's paralysis from acute stroke, which requires emergent neuroimaging (CT or MRI with angiography/perfusion sequences) and careful clinical assessment, while avoiding thrombolytic therapy until stroke is definitively excluded. 1
Clinical Recognition and Differential Diagnosis
Key Clinical Features of Todd's Paralysis
Todd's paralysis occurs after 6-13% of seizures and presents with transient focal neurological deficits that can persist from 30 minutes to 36 hours (mean 15 hours). 2, 3
Clinical presentation is highly variable and may include: 3
- Motor weakness in any combination of face, arm, or leg (ranging from mild weakness to complete plegia)
- Variable muscle tone (spastic, flaccid, or normal)
- Variable reflexes (increased, decreased, or normal)
- Aphasia (particularly in patients with underlying structural lesions)
- Gaze palsy
- Sensory loss (uncommon, occurring in only rare cases)
Critical Distinguishing Features from Stroke
The fundamental challenge: Both Todd's paralysis and acute stroke with seizure at onset present identically on clinical examination and may show similar imaging findings. 1, 2, 4
High-risk indicators suggesting underlying structural pathology: 5
- Old stroke is an independent risk factor for Todd's paralysis (positive likelihood ratio of 11.2 for remote seizure etiologies)
- Older age
- Convulsive status epilepticus
- Longer duration of convulsion
- Remote structural brain lesions (present in 19.7% of cases with Todd's paralysis)
Diagnostic Evaluation Algorithm
Immediate Assessment (Within Minutes)
Obtain focused history for: 1
- Witnessed seizure activity (critical for diagnosis)
- Prior seizure history
- Known structural brain lesions or prior stroke
- Medication compliance in known epilepsy patients
- Recent head trauma
- Fever or signs of CNS infection
Point-of-care testing: 1
- Fingerstick glucose (mandatory in all patients—hypoglycemia occurs in 1-2% of first-time seizures even with normal mental status)
- Vital signs including oxygen saturation
Laboratory Workup
For patients who have returned to baseline neurologic status: 1
- Laboratory testing has very low yield when history and physical examination are normal
- Glucose and sodium abnormalities are most common but usually predicted by clinical findings
- Consider: serum sodium, complete metabolic panel, antiepileptic drug levels (if applicable), toxicology screen based on clinical suspicion
For patients with persistent deficits (suspected Todd's paralysis): 1
- Complete metabolic panel
- Serum sodium, calcium, magnesium
- Antiepileptic drug levels if on therapy
Neuroimaging Strategy
Emergent neuroimaging is mandatory when: 1, 6
- Postictal focal deficit that does not quickly resolve
- Patient has not returned to baseline within several hours after seizure
- First-time seizure
- Known or suspected malignancy
- Anticoagulation use
- Head trauma
- Fever with concern for CNS infection
Imaging modality selection: 1, 2, 4
- MRI with diffusion-weighted imaging (DWI) and perfusion sequences is preferred to differentiate Todd's paralysis from acute stroke
- CT angiography or MR angiography can confirm vascular occlusion in acute stroke
- Important caveat: Todd's paralysis may show cytotoxic edema on diffusion MRI that mimics acute stroke, but this resolves on follow-up imaging 4
EEG Monitoring
Consider emergent EEG when: 1, 6
- Persistent altered consciousness despite apparent seizure termination
- Concern for non-convulsive status epilepticus
- Patient received long-acting paralytics
- Patient in drug-induced coma
Management Approach
Acute Management of Active Seizures
If seizure activity is ongoing (not self-limiting within 5 minutes): 6, 7
- First-line: IV lorazepam 4 mg at 2 mg/min (65% efficacy)
- Second-line (if seizures persist):
- Valproate 20-30 mg/kg IV (88% efficacy, 0% hypotension risk)
- Levetiracetam 30 mg/kg IV (68-73% efficacy, minimal cardiovascular effects)
- Fosphenytoin 20 mg PE/kg IV (84% efficacy, 12% hypotension risk)
Management of Todd's Paralysis Specifically
Once Todd's paralysis is confirmed (stroke excluded): 1
- Supportive care and observation
- No specific treatment for the paralysis itself—it resolves spontaneously
- Address underlying seizure etiology
- Do NOT administer thrombolytics (critical to avoid if stroke has been excluded)
Disposition decisions: 1
- Patients with first unprovoked seizure who have returned to clinical baseline need not be admitted
- Consider admission for:
- Persistent neurologic deficits
- Concern for underlying acute process
- Status epilepticus
- Inability to ensure outpatient follow-up
Long-term Antiepileptic Management
For provoked seizures (including those with Todd's paralysis due to metabolic causes): 8
- Identify and treat the underlying cause rather than initiating long-term antiseizure medications
- Correct metabolic abnormalities (hyponatremia, hypocalcemia, hypoglycemia)
- Address medication non-compliance if applicable
For unprovoked seizures: 1
- Single unprovoked seizure: waiting until second seizure before initiating antiepileptic medication is appropriate
- Remote symptomatic seizures (history of stroke, trauma, tumor): treatment after first seizure is appropriate due to higher recurrence risk
Critical Pitfalls to Avoid
Do not administer thrombolytics based on clinical presentation alone when seizure at onset is suspected—advanced imaging (MRI with DWI/PWI or CT angiography/perfusion CT) is required to confirm ischemic stroke. 1
Do not assume all post-seizure weakness is Todd's paralysis—the diagnosis of Todd's paralysis is one of exclusion and requires ruling out acute stroke, particularly in patients with: 5
- Old stroke (19.7% of Todd's paralysis cases have remote structural etiologies)
- Advanced age
- Prolonged or status epilepticus presentation
Do not delay neuroimaging to obtain laboratory results in patients with persistent focal deficits. 6
Do not attribute persistent altered mental status solely to post-ictal state—obtain urgent EEG if patient does not awaken within expected timeframe, as non-convulsive status epilepticus occurs in up to 8% of comatose patients. 1, 6