The condition is named after Robert Bentley Todd (1809-1860), an Irish-born London physiologist who first described the phenomenon in 1849. It may occur in as many as 13% cases of seizures. 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.
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. 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. There have been case reports of longer durations of paresis, ranging to as long as days.
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, and rare genetic causes of hemiplegia and seizures.
Todd's paresis is more common after any clonic seizure activity, and particularly if generalized tonic-clonic seizures occur.
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.