What is Todd Paralysis?
Todd paralysis is a transient neurological deficit—most commonly limb weakness or hemiplegia—that occurs immediately following an epileptic seizure and resolves completely within hours to days without permanent consequences. 1, 2
Clinical Definition and Characteristics
Todd paralysis (also called Todd's paresis or postictal paralysis) presents as temporary focal neurological deficits after seizure activity. The condition was named after Robert Bentley Todd, who first described this phenomenon. 2
Key clinical features include:
- Onset: Occurs immediately following a seizure, most commonly after partial (focal) seizures or generalized tonic-clonic seizures 2, 3
- Duration: Typically lasts minutes to hours, but can persist up to 36-48 hours (rarely up to 70 hours in variant presentations) 2, 4, 3
- Frequency: Occurs after approximately 6-13% of all seizures 3
- Resolution: Complete recovery without permanent neurological sequelae 1, 2
Clinical Presentations
The most common manifestation is unilateral limb weakness or hemiplegia, but Todd paralysis can present with various focal neurological deficits: 2, 4
- Hemiparesis or hemiplegia (most common) 1, 2
- Paresthesias 5
- Aphasia 5
- Hemianopsia 5
- Altered consciousness 5
- Ideomotor limb apraxia (rare variant) 4
- Severe hemineglect syndrome (rare variant) 4
Risk Factors and Associated Conditions
Certain patient populations have significantly higher risk of developing Todd paralysis: 1, 2
- Old stroke history: The most important independent risk factor—Todd paralysis occurred in 19.7% of seizures with remote stroke etiology, with a positive likelihood ratio of 11.2 1
- Advanced age: Older patients are at increased risk 1, 2
- Pre-existing structural brain lesions: Any cortical structural damage increases risk 1, 2
- Convulsive status epilepticus: Associated with higher incidence 1
- Longer seizure duration: Prolonged convulsions increase likelihood 1
Pathophysiology
The underlying mechanism involves cerebral perfusion abnormalities following seizure activity. 2 The exact pathophysiology remains incompletely understood, but current evidence suggests post-seizure metabolic exhaustion and vascular changes in the affected cortical regions contribute to the temporary dysfunction. 2, 3
Critical Diagnostic Challenge: Distinguishing from Acute Stroke
Todd paralysis is a well-recognized stroke mimic that poses significant diagnostic challenges in emergency settings, particularly because both conditions present with acute focal neurological deficits. 1, 2, 5, 3
Key differentiating features:
- Temporal relationship: Todd paralysis occurs immediately after witnessed or suspected seizure activity 2, 3
- History of epilepsy or prior stroke: Strongly suggests Todd paralysis over new stroke 1, 2
- Complete resolution: Symptoms resolve completely within hours to days 2, 3
- MRI findings: May show transient cytotoxic edema with diffusion restriction that resolves on follow-up imaging, unlike stroke where restriction persists 5
Common pitfall: Patients presenting with acute stroke may have a seizure at symptom onset, making differentiation extremely difficult clinically. 3 In these cases, advanced imaging including cerebral CT and MRI with angiography is recommended to avoid misdiagnosis. 3
Diagnostic Approach
When Todd paralysis is suspected, the following evaluation is recommended: 3
- Document the temporal relationship between seizure and neurological deficit 2, 3
- Obtain detailed history of prior seizures, epilepsy, or stroke 1, 2
- Perform cerebral CT and MRI with angiography to exclude acute stroke 3
- Consider that diffusion restriction on MRI may be present but reversible in Todd paralysis 5
- Monitor for complete resolution of deficits, which confirms the diagnosis retrospectively 2, 3
Clinical Significance
The diagnosis of Todd paralysis strongly suggests underlying structural brain pathology, particularly old stroke. 1 This consideration is critical for:
- Reducing misdiagnosis of acute stroke in emergency settings 1
- Guiding appropriate antiepileptic treatment rather than thrombolytic therapy 1
- Identifying patients who need further evaluation for structural brain lesions 1
- Avoiding unnecessary stroke interventions in patients with postictal deficits 5, 3