Todd's paresis

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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 (18091860), 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.

Presentation
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.[5]
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]
Todd's paresis is more common after any clonic seizure activity.[3]

Causes

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

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

Prognosis

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.]

Importance
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]

References
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 1072820.
PMID 8158178.
3.

4.
5.

^ 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): 21604. PMID 15210875.
^ Uptodate: Evaluation of the first seizure in adults
^ 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):
924. doi:10.1007/s002470050300. PMID 9472051.

6.

^ Oestreich L, Berg M, Bachmann D, Burchfiel J, Erba G (1995). "Ictal contralateral

paresis in complex partial seizures". Epilepsia 36 (7): 6715. doi:10.1111/j.15281157.1995.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): 22517. 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): 9157. 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