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Todd's paresis
ICD-10 G83.8
ICD-9 344.89
MeSH D010243

Todd's paresis or Todd's paralysis (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 generalised tonic-clonic seizures ("grand mal"), and may last for hours or occasionally days after the initial seizure. 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 fibres are involved.

Todd's paresis, as defined as any motor deficit after seizure, occurs in 13% of all seizures.[3] This was evaluated in a study of 513 patients with epilepsy with video-electroencephalography. The same study also showed that the mean duration of postictal paresis was 173 seconds, with ranges of 11 seconds to 22 minutes.[3] There have been case reports of longer durations of paresis, ranging to as long as days.[4]

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,[5] and rare genetic causes of hemiplegia and seizures.[6]

Todd's paresis is more common after any clonic seizure activity, and particularly if generalized tonic-clonic seizures occur.[3]


The cause of Todd's paresis is unknown but there are two hypotheses to its cause. The first is the depletion theory, where the motor cortex is exhausted leading to prolonged neuronal hyperpolarization. The second is that there is transient inactivation of motor fibres caused by activation of NMDA receptors. Neither has been extensively evaluated.


Treatment of Todd's paralysis is symptomatic and supportive because the paralysis disappears quickly.


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.[7]

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.[8]


  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. PMID 8158178.  
  3. ^ a b c d 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. PMID 15210875.  
  4. ^ Kimura M, Sejima H, Ozasa H, Yamaguchi S (1998). "Technetium-99m-HMPAO SPECT in patients with hemiconvulsions followed by Todd's paralysis.". Pediatr Radiol 28 (2): 92–4. doi:10.1007/s002470050300. PMID 9472051.  
  5. ^ 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.  
  6. ^ 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. PMID 1361034.  
  7. ^ 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.  
  8. ^ Nelson K,Ellenberg J; Prognosis in Children With Febrile Seizures Paediatrics; 61, 5: 720-727


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