Todd Paresis


Article Author:
James Mastriana
Jeffrey Pay


Article Editor:
Roger Taylor


Editors In Chief:
Rhonda Coffman
Lindsay Iverson
Heather Templin


Managing Editors:
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Frank Smeeks
Kristina Soman-Faulkner
Benjamin Eovaldi
Radia Jamil
Sobhan Daneshfar
Saad Nazir
William Gossman
Pritesh Sheth
Hassam Zulfiqar
Navid Mahabadi
Steve Bhimji
John Shell
Matthew Varacallo
Ahmad Malik
Mark Pellegrini
James Hughes
Beata Beatty
Hajira Basit
Phillip Hynes


Updated:
1/28/2019 11:45:17 PM

Introduction

Todd Paresis is a syndrome associated with weakness or paralysis of part or all of the body after a focal-onset seizure. It most commonly affects one limb or one half of the body but can have a wide range of presentations. 

This condition was originally described by Irish physiologist Robert Bentley Todd in 1849 but has been further defined, researched, and explained by many others over the years. Despite this being a common phenomenon for neurologists, relatively little research has been conducted on the condition.

Etiology

The current and most accepted understanding of the condition is theorized to be exhaustion of the primary motor cortex (or any other area of the brain) after neuronal hyperexcitation in a focal or diffuse seizure state.

Epidemiology

Approximately 13% of all seizures show signs of Todd paresis in one presentation or another.[1] The syndrome does not appear to show a propensity for male, female, or any specific age or race.

A retrospective study on the condition found that postictal paralysis was observed most commonly (78% of patients studied) when patients displayed "obvious" clonic motor movement during the seizure activity. This is compared to only 10% of patients with no ictal motor activity.[1] The same study showed that unilateral clonic activity was the most common predictor of postictal paralysis in 56% of patients. Despite its relatively small sample size of 328, this study has value due to the lack of studies explaining the duration, seizure characteristics, and frequency of Todd paresis; however, it is likely based on the fact that only patients with medically intractable seizures were studied, making the study less likely to accurately apply to the general epileptic community.

Pathophysiology

The pathophysiology is most commonly theorized to be the result of one of three mechanisms. The first theory is that the area in question is depolarized so vigorously during the seizure that it enters a prolonged refractory period, making attempts at excitation require significantly higher voltage for depolarization. The second is that there is prolonged local inhibition by surrounding structures theorized to be a protective measure employed by the brain to prevent further seizure activity. The third explains this phenomenon by theorizing that blood flow to the affected area of the brain is restricted for a time through vasoconstriction thus limiting the function of that area through relative oxygen starvation. None of these theories has been definitively validated or even well studied at the time of this publication. 

With regards to the third theory, a study in 2017 using rodent models found that, during the postictal period,  significant decreases in pO2 (pO2 < 10mmHg) were found in localized areas of the brain leading to "memory and behavioral impairments." They also found an association between L-type calcium channels and cyclooxygenase activity as potential causative mechanisms behind the hypoperfusion. Rodents treated with and without postictal nifedipine treatment were studied. The researches found that untreated animals did indeed have a weakness in grip strength when compared to the nifedipine group. It is also of interest that 8 of 10 human models showed evidence of focal tissue hypoperfusion. Despite all of this exciting information on the potential mechanisms behind this condition, all the data must be interpreted with caution given that this a preliminary study and not well powered.[2]

Histopathology

The histopathologic changes associated with and the origin of this condition is not well understood and only minimally studied at this time.

History and Physical

The classic presentation of this condition is weakness observed in one limb contralateral to the seizure activity after a focal seizure has occurred. This can range from a mild weakness of the limb to complete paralysis; however, this syndrome is not limited to limb weakness and can include gaze palsy, aphasia, and sensory disturbances (e.g., neglect, anesthesia, visual field deficits) depending on the particular anatomic epileptic focus.[1][3][4]

It is important to understand that pure focal seizures may cause this condition, but it may also be observed in focal-onset seizures. The key difference being that a focal-onset seizure begins with twitching in one limb (or other effects depending on the initial focus), then to one complete half of the body, and then appearing as a more generalized seizure pattern (i.e., Jacksonian march). A pure focal seizure remains with the affected area of the body and does not become generalized.[3]

This postictal syndrome may last anywhere from minutes to days, with the vast majority of patients seeing spontaneous and complete resolution within 36 hours. Complete resolution of symptoms is seen within 15 hours on average.[3]

If the seizure was witnessed, it is important to ask the observer if any focal activity was observed prior. While this history can be very helpful, it is often too subtle for the witness to recall. This is especially true in a first seizure episode.

Evaluation

No laboratory studies help in making the diagnosis of postictal paralysis. 

CT perfusion scan anomalies are often noted but are not consistent and thus nondiagnostic. It can show a hyper- or hypoperfusion state at the site of epileptic focus.[5][6][5]

CT angiography is unremarkable in postictal paralysis. This can be used to differentiate between this condition and acute cerebrovascular accident.[7]

MRI will show findings consistent with a seizure such as a transiently increased T2 signal at the site of epileptic focus. This is due to increased edema (i.e., H2O molecules) at the site which is bright on T2 imaging. It is best appreciated on fluid-attenuated inversion recovery (FLAIR).[8]

Treatment / Management

Treatment of this condition is primarily supportive and typically resolves without any intervention. No randomized control trials are available to compare treatment modalities.

Differential Diagnosis

Cerebrovascular accident (embolic, hemorrhagic): This may be distinguished by hypoperfusion on CT angiography and MRI or evidence of intracranial hemorrhage on non-contrasted CT of the brain. 

Hemiplegic migraine: This is a rare genetic mutation or familial migraine variant in which the patient presents with severe, typically, unilateral headache and weakness, ataxia, or paralysis.[9]

Hemiconvulsion: Hemiplegia epilepsy syndrome: This clinical syndrome of infancy or early childhood (generally < 4 years old) is characterized by prolonged hemispheric seizure activity during a febrile disease, resulting in hemispheric atrophy and flaccid hemiplegia followed by focal seizures with an interval of months to years.[10]

Hypoglycemia: Hypoglycemia is a well-known mimic of stroke syndromes.

Prognosis

The prognosis of this condition is very good as the postictal paralytic symptoms are self-limited and require no intervention.

Complications

Typically, no complications are expected as the paresis is self limiting.

Consultations

Neurology is typically consulted to evaluate Todd Paresis.

Enhancing Healthcare Team Outcomes

It is important to communicate findings of Todd Paresis with treating physicians.  Unilateral symptoms should always be addressed and discussed with treating physicians and nursing staff when they occur.  A careful history and physical exam can help exclude other causes of symptoms such as cerebrovascular accidents.  It is important that patients with seizure disorders be educated that this phenomenon can occur to prevent uneccessary over-testing. Patients who have experienced Todd's Paresis in the past should notify members of their care team.


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Todd Paresis - Questions

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In which patients is Todd paresis often seen?



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Which of the following statements about Todd paralysis is correct?



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Which of the following presentations has the highest association with postictal (AKA Todd) paralysis?



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A 62-year-old woman with a history of focal seizures presents to the emergency department after an episode of shaking that began with her left upper extremity and progressed to diffuse tonic-clonic movements of all extremities. She presents confused but protecting her airway with spontaneous movements of all extremities. Her left upper extremity is notable for significantly less spontaneous movement that the other 3. She cannot follow commands for a strength exam. She has no intravenous access at this time. What is the first action?



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A 14-year-old boy presents in a confused state after a "jerking all crazy" episode per his mother. His mother states that her son was playing with a new lego set he'd just gotten and stopped responding to a question she was asking, mid-sentence. She states then his fingers on his right had "started wiggling" and seconds later his entire body was "jerking all crazy." The mother states he has a history of "some brain problem," but she denies anything like this in the past. On physical exam there is a port-wine stain on the right side of his face and that his right upper extremity has been immobile since arrival. What diagnostic test that would be most helpful in confirming the diagnosis regarding his weakness?



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A 61-year-old woman with a history of focal seizures and right parietal cerebrovascular accident with no notable deficits presents to the emergency department after being found down in her apartment for an unknown length of time. She was found by a friendly neighbor who "heard a thud." She has no evidence of head trauma but appears confused. The patient is seen and evaluated the patient. She can follow simple commands, and her neurologic exam reveals 5/5 strength excluding her left upper extremity (LUE) which is 1/5. It is otherwise unremarkable. There is no evidence of swelling, pain or trauma to the extremity. CT brain showed no evidence of intracranial hemorrhage. On rounds the next day her confusion seems to have resolved, but her LUE weakness remains and is unchanged. The MRI brain is complete but is unavailable for review due to what IT calls "technical difficulties." The following day on rounds, approximately 34 hours after being found, the patient has regained 5/5 strength in her LUE. IT has gone on vacation starting yesterday and has not fixed the "technical issue" yet. Which of the following is the most likely cause of the patient's findings?



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Todd Paresis - References

References

Gallmetzer P,Leutmezer F,Serles W,Assem-Hilger E,Spatt J,Baumgartner C, Postictal paresis in focal epilepsies--incidence, duration, and causes: a video-EEG monitoring study. Neurology. 2004 Jun 22     [PubMed]
Lyman KA,Chetkovich D, New Insights Into Postictal Paresis: An Epilepsy-Associated Phenomenon That may not be as Benign as Long Thought. Epilepsy currents. 2017 May-Jun     [PubMed]
Rolak LA,Rutecki P,Ashizawa T,Harati Y, Clinical features of Todd's post-epileptic paralysis. Journal of neurology, neurosurgery, and psychiatry. 1992 Jan     [PubMed]
Fernandes PM,Whiteley WN,Hart SR,Al-Shahi Salman R, Strokes: mimics and chameleons. Practical neurology. 2013 Feb     [PubMed]
Binder DK, A history of Todd and his paralysis. Neurosurgery. 2004 Feb     [PubMed]
Payabvash S,Oswood MC,Truwit CL,McKinney AM, Acute CT perfusion changes in seizure patients presenting to the emergency department with stroke-like symptoms: correlation with clinical and electroencephalography findings. Clinical radiology. 2015 Oct     [PubMed]
Mathews MS,Smith WS,Wintermark M,Dillon WP,Binder DK, Local cortical hypoperfusion imaged with CT perfusion during postictal Todd's paresis. Neuroradiology. 2008 May     [PubMed]
Gelfand JM,Wintermark M,Josephson SA, Cerebral perfusion-CT patterns following seizure. European journal of neurology. 2010 Apr     [PubMed]
Tenney JR,Schapiro MB, Child neurology: hemiconvulsion-hemiplegia-epilepsy syndrome. Neurology. 2012 Jul 3     [PubMed]
Kumar A,Arora R, Headache, Migraine Hemiplegic null. 2018 Jan     [PubMed]

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