P18 Non epileptic seizures and Todd's paresis: case series and literature review

Abstract

Objective Todd9s paresis is a transient focal weakness of a hand, arm or leg which follows a partial seizure activity within that limb. This was first described by Robert Bentley Todd in 1849. The weakness can range from severity from mild to complete paralysis and usually occurs on just one side of the body. The paralysis can last from minutes to hours. There have been case reports of longer duration of paresis, ranging to as long as days. It may occur in up to 13% of seizure cases. Todd9s paresis may affect speech, eye gaze or vision. It most commonly occurs after generalised tonic clonic seizures. There is literature on Todd9s paresis and its association with epilepsy since it was first described in 1849. There is dearth of literature on its association with non-epileptic seizures. Its presentation in patients with NEAD whether represents a true epileptic event or it represents a pseudo paralysis was something we were interested in. The interest was primarily driven by the three patients we had of non-epileptic attack disorder who presented with focal weakness. Method We did an electronic literature search using PubMed, Medline and Trip database. The key words used were—epilepsy, Todd9s paresis, non-epileptic attack disorder, post ictal paresis, pseudo Todd9s paresis and pseudoneurological symptoms. The case series is as follows: Case 1 : A 48-year-old gentleman with history of non-epileptic attack disorder (NEAD) was admitted to hospital following another episode of NEAD. He reported having an attack of cluster of absent seizures following which he complained of being paralysed down one side. He complained of loss of function of left arm and leg. He was admitted to hospital where he had a full neurological screen done. Objectively, there was no evidence of any focal deficits. He reported being unable to feel anything on left side but was able to respond appropriately to lateralised tactile stimulation with eyes closed. Gate was antalgic with a reduced support phase on left. He had video telemetry done with no evidence of seizures and CT exam was unremarkable. Patient was discharged with the diagnosis of NEAD. Case 2 : 37-year-old, female with history of non-epileptic attack disorder was admitted to hospital following an episode of non-epileptic seizure. Patient reported right sided paresis; difficulty lifting her right arm and leg. The weakness lasted 2–3 h, settled on its own. No evidence of any focal deficits on neurological examination. EEG was unremarkable. MRI showed slight asymmetry of left pre central gyrus. No convincing signal abnormality and the appearances were constitutional. Case 3 : A 33-year-old lady with history of non-epileptic attack disorder was seen in the outpatient clinics. She had an NEAD attack which was generalised and following that she complained of left sided facial weakness. No dysphasia or problems with vision reported. The weakness lasted for only few minutes and subsided on its own. She had further episodes of seizures but never had a weakness afterwards. On assessment there was no evidence of any change in the nature or degree of her seizure pattern. Results Our three patients above had diagnosis of NEAD and they all complained of motor weakness or Todd9s paresis which is more characteristic of Epilepsy. This raised doubts in our minds that whether these patients actually had a seizure and that resulted in Todd9s paresis. The first two patients had investigations re done to establish that but no cause was found. The third patient was seen well after the episode of facial weakness. We did not notice any change in her seizure episodes from the past so further investigations were not carried out. We wanted to establish if there is any association between Todd9s paresis and NEAD .We tried to find the answer by doing a literature search but unfortunately it did not help much as we could find only one case report and nothing else useful. Conclusion There will always be ethical dilemma that whether patients with NEAD should be re investigated or not if they complained of neurological symptoms. We believe that each case should be dealt on its merit and the patients to be managed accordingly. It is not uncommon for patients with NEAD to have epilepsy and as a result Todd9s paresis. The literature search was not very useful in finding the right answer.