Todd’s Paralysis disclosing neurocysticercosis
Trevisol-Bittencourt PC 1,2,3, Tomaselli PJ 1, Nahoum RG 1, Collares CF 4, Tournier MB 1, Pioner LM 1, Bittencourt FS 2
1 Federal University of Santa Catarina, Florianópolis/SC, Brazil
Backgrounds: Transient neurological deficits are well-know after epileptic seizures. Robert Bentley Todd (1809–1860), an Irish physician, was the first to describe transient hemiparesis or hemiplegia that may follow some seizures. His remarkable observation was published in 1854 where he noticed it as a neurological state that recovers completely after a few time under the heading “epileptic hemiplegia”. He described a patient who developed hemiplegia after seizure; with complete reversion of the deficit in the subsequent hours after the ictus. Since then many non motor equivalents of Todd’s paralysis (TP) have been described as well. Actually was Hughlings Jackson (1835-1911) who extended the limits of this definition including other transient neurological deficits as TP equivalents; such as cognitive dysfunctions, dysphasia, riots of space construction and visual perception, etc.
Methods: To describe a young woman presenting TP secondary to partial status epilepticus due to neurocysticercosis.
Case report: DA, 26 years old, married, 2 children, peasant, portuguese roots, living in a rural area. She went to a neurological centre due “stroke” that happened less than 24 hours. She presented complete left hemiplegia in the initial assessment. The previous diagnostic of “stroke” was questioned by her age, because she had a normal general clinical examination and due the absence of the classic risk factors for cerebral vascular disease. The clinical history provided other possibility – she was suffering from repetitive tremors in the left arm two years before and as they usually had short duration time she had never complaint of this symptom. In fact she told she was adapted to live with her “strange nervous attacks”.
Discussion: DA is suffering from symptomatic partial epilepsy due to NC and presented a classical picture of TP. We would like to pointed out that TP was the first major symptom of her condition. If you have a look on contemporary neurological literature, this epileptic phenomenon would seems to be rare, however we believe this misconception is a result of poor clinical examination nowadays. TP rarely is proper recognized in people suffering from epilepsy, resulting in repetitive, expensive and sometimes aggressive neurological investigations. The symptoms related to TP usually revert in 24 to 36 hours, although in few patients the recover time can take ten or more days. This condition should be suspected in all patients who develop hemiplegia or another focal neurological deficit, presenting clinical history of epilepsy in the past. Unfortunately partial seizures are underestimates and doctors usually should no pay attention for this common presentation of epilepsy. Very interesting to notice that TP, which had the fast recovery of the neurological deficit, frequently provoke among the health professionals an temptation to diagnose hysteria, and we know well how these peculiar patients labeled as hysterics are treated… overdoses of insults prescribed by doctors and their “collaborators”. As Rolak pointed out most of patients showing TP episodes will have structural cortical injuries. We would like to remain that our patient has one NCC lesion close to the right motor area. Currently the hypothesis most accepted is that transient pos ictal neurological deficits are related with the injuries and its localization, in this case there is a clear involvement of the motor cortex. NCC as etiology for epilepsy must be considered in all patients coming from endemic areas, and DA was living in a region where this trouble is quite common. Finally, NCC lesions are the main etiology of symptomatic epilepsy in Brazil, however its detection by CT would have to be followed by judicious clinical examination to define its clinical and electroencephalographic responsibility, if any.
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