Todd's paresis

Todd's paresis
Classification and external resources
Specialty neurology
ICD-10 G83.8
ICD-9-CM 344.89
MeSH D010243

Todd's paresis, Todd's paralysis, or Todd's palsy (or postictal paresis/paralysis, "after seizure") is focal weakness in a part of the body after a seizure. This weakness typically affects appendages and is localized to either the left or right side of the body. It usually subsides completely within 48 hours. Todd's paresis may also affect speech, eye position (gaze), or vision.

The condition is named after Robert Bentley Todd (1809–1860), an Irish-born London physiologist who first described the phenomenon in 1849.[1][2] It may occur in up to 13% of seizure cases.[3] It is most common after a focal motor seizure affecting one limb or one side of the body.[4] The generally postulated cause is the exhaustion of the primary motor cortex, although no conclusive evidence is available to support this.


The classic presentation of Todd's paresis is a transient weakness of a hand, arm, or leg after partial seizure activity within that limb. The weakness may range in severity from mild to complete paralysis.

When seizures affect areas other than the motor cortex, other transient neurological deficits can take place. These include sensory changes if the sensory cortex is involved by the seizure, visual field defects if the occipital lobe is involved, and aphasia if speech, comprehension or conducting fibers are involved.

Postictal paresis (PP), although familiar to neurologists, has not been well-studied. One retrospective observational study evaluated 328 selected patients from ages 16 to 57 years who had prolonged video-electroencephalogram (EEG) monitoring for medically intractable epilepsy and focal seizure onset; those with nonepileptic seizures, status epilepticus, and Lennox-Gastaut syndrome were excluded.[5] The following observations were made:

Of all seizures followed by PP, the following features were noted:

The results of this study are valuable because few other data exist on the frequency, duration, and seizure characteristics associated with PP. However, the study is likely biased by the inclusion only of patients with medically intractable seizures who had undergone video-EEG monitoring, and the results may not extrapolate to a general epilepsy population.

Other post-ictal neurological findings that do not involve activity of the area affected by the seizure have been described. They are thought to be caused by a different mechanism than Todd's paresis, and including paralysis of the contralateral limb,[6] and rare genetic causes of hemiplegia and seizures.[7]


The cause of Todd's paresis is unknown. Current theories propose biological processes in the brain that involve a slow down in either the energy output of neurons or in the motor centers of the brain.


There is no treatment for Todd's paralysis. Individuals must rest as comfortably as possible until the paralysis disappears.


An occurrence of Todd's paralysis indicates that a seizure has occurred. The prognosis for the patient depends upon the effects of the seizure, not the occurrence of the paralysis.


The most significant issue regarding the Todd's paresis is its differentiation from a stroke. The issue is further complicated by the fact that some strokes trigger a focal seizure during the acute phase. A Todd's paresis in this context may overestimate the extent of neurological deficit due to the vascular process itself resulting in erroneous decisions with regards to acute stroke therapy such as thrombolysis. For this reason a seizure during an acute stroke is generally accepted to be a relative contraindication to thrombolytic therapy, especially in the absence of documented cerebrovascular occlusion using vascular imaging techniques.[8]

An infant with Todd's paresis does not necessarily preclude the diagnosis of a febrile convulsion. This view is as a result of a recent study that showed the incidence of Todd's paresis to be in 0.4% of infants that have been diagnosed with a febrile convulsion.[9]


  1. Todd RB (1849). "On the pathology and treatment of convulsive diseases". London Med Gaz. 8: 668.
  2. Pearce JM (March 1994). "Robert Bentley Todd (1809-60) and Todd's paralysis". J. Neurol. Neurosurg. Psychiatr. 57 (3): 315. doi:10.1136/jnnp.57.3.315. PMC 1072820Freely accessible. PMID 8158178.
  3. 1 2 Gallmetzer P, Leutmezer F, Serles W, Assem-Hilger E, Spatt J, Baumgartner C (June 2004). "Postictal paresis in focal epilepsies--incidence, duration, and causes: a video-EEG monitoring study". Neurology. 62 (12): 2160–4. doi:10.1212/wnl.62.12.2160. PMID 15210875.
  4. Uptodate: Evaluation of the first seizure in adults
  5. Gallmetzer P, Leutmezer F, Serles W, Assem-Hilger E, Spatt J, Baumgartner C (June 2004). "Postictal paresis in focal epilepsies--incidence, duration, and causes: a video-EEG monitoring study.". 62 (12): 2160–4. doi:10.1212/wnl.62.12.2160. PMID 15210875.
  6. Oestreich L, Berg M, Bachmann D, Burchfiel J, Erba G (1995). "Ictal contralateral paresis in complex partial seizures". Epilepsia. 36 (7): 671–5. doi:10.1111/j.1528-1157.1995.tb01044.x. PMID 7555983.
  7. Mikati M, Maguire H, Barlow C, Ozelius L, Breakefield X, Klauck S, Korf B, O'Tuama S, Dangond F (1992). "A syndrome of autosomal dominant alternating hemiplegia: clinical presentation mimicking intractable epilepsy; chromosomal studies; and physiologic investigations". Neurology. 42 (12): 2251–7. doi:10.1212/wnl.42.12.2251. PMID 1361034.
  8. Sylaja PN, Dzialowski I, Krol A, Roy J, Federico P, Demchuk AM (2006). "Role of CT angiography in thrombolysis decision-making for patients with presumed seizure at stroke onset". Stroke. 37 (3): 915–7. doi:10.1161/01.STR.0000202678.86234.84. PMID 16456124.
  9. Nelson K,Ellenberg J; Prognosis in Children With Febrile Seizures Paediatrics; 61, 5: 720-727
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