Todd Paresis

Etiology

The cause of Todd paresis is a seizure immediately preceding the clinical manifestation of Todd paresis. The clinical manifestation occurring during the period following the seizure and lasting until the brain recovers all its functions is known as the postictal syndrome. Some seizures may not have it, or it cannot be recognized, like absence seizures, myoclonic seizures, and, in short, focal seizures.[1] Todd paresis will always correspond to the ictal topography, and the symptoms presented will localize the area in the brain where the seizure occurred.[1] This is important in those patients where the seizure was unseen, as the majority of the seizures last less than five minutes. 

The current and most accepted understanding of the condition is theorized to be the exhaustion of the primary motor cortex (or any other area of the brain) after neuronal hyperexcitation in a seizure state or due to hypoperfusion to the affected area of the brain through vasoconstriction mechanisms, thus limiting the function of that area through relative oxygen starvation.

Epidemiology

Approximately 13% of all seizures show signs of Todd paresis in one presentation or another.[5][6] It does not have a gender tendency and can occur at any specific age and in any race.

Approximately 90% of the patients with postictal paralysis displayed visible clonic motor movement during the seizure activity, while only 10% of them had no ictal motor activity.[5] Unilateral clonic activity is the most common predictor of postictal paralysis in 56% of patients.

Pathophysiology

The pathophysiology is most commonly theorized to result from one of three mechanisms.[1] The first theory is that the area in question is depolarized so vigorously during the seizure that it enters a prolonged refractory period. This theory attributed to the refractory period can be contradicted by status epilepticus, where there is a prolonged unlimited depolarization. The second theory is that there is a prolonged local inhibition by surrounding structures as a protective measure employed by the brain to prevent further seizure activity.[7][8][9][10] The third theory explains this phenomenon by hypoperfusion to the affected area of the brain through vasoconstriction, thus limiting the function of that area through relative oxygen starvation.[11][12][13]

A study using rodent models found that during the postictal period, hypoperfusion occurs in the areas that had epileptogenic discharges. Significant decreases in pO2 (pO2 < 10 mmHg) were found in localized regions of the brain leading to memory and behavioral impairments.[14] An association between L-type calcium channels and cyclooxygenase-2 (COX-2) activity as potential causative mechanisms behind the hypoperfusion was found. COX-2 catalyzes the production of vasoactive products that will act on the L-type calcium channels in the vessel wall to allow the influx of calcium causing vasoconstriction. Rats pretreated before the seizure with nifedipine, an L-type calcium channel inhibitor, showed no weakness in grip strength when compared to an untreated group. Rats treated with acetaminophen or ibuprofen, a COX antagonist, prevented amnesic postictal episodes. Despite this new information on the potential mechanisms behind this condition, all the data must be interpreted with caution when using basic science results.[15]

In humans, similar focal tissue hypoperfusion was found by measuring the cerebral blood using arterial spin labeling magnetic resonance imaging (MRI) with flow reductions of at least 10 mL/100 g/min.[14] The hypoperfused areas corresponded to the areas involved in the seizure, indicating that it is a local phenomenon. Brief and mild seizures can produce prolonged hypoperfusion events. There is no significant effect on postictal severe hypoxia by acutely administering antiepileptic drugs.[14]

Severe hypoperfusion/hypoxia, which occurs in specific brain areas after a focal seizure or a generalized seizure, is responsible for the negative sequelae following the seizure.[16] Several events like central inflammation, glial activation, altered blood-brain barrier permeability, and neuronal loss will follow the ischemic event, causing cognitive and behavioral changes.[16][17][18][19][20]

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 confusion, amnesia, alteration of consciousness, aphasia, agitation, psychosis, gaze palsy, neglect, numbness, and visual field deficits depending on the particular anatomic epileptic focus.[1][2][5][21] Careful physical examination of the patient can help to localize the seizure focus.

It is essential to understand that pure focal seizures may cause this condition, but it may also be observed in focal-onset seizures that are generalized. The key difference is that a focal-onset seizure begins with twitching in one limb (or other effects depending on the initial focus), then affects one complete half of the body, and later appears as a more generalized seizure pattern (Jacksonian march). A pure focal seizure persists in the affected area of the body and does not become generalized.[2] Aphasia can be a manifestation of left temporal lobe epilepsy.[22] Amnesia and confusion are more common after generalized seizures but can be a sequela from repetitive partial seizures.[23]

This postictal syndrome may last anywhere from minutes to days, with the vast majority of patients seeing spontaneous and complete resolution within 36 hours.[1][2] The median time for complete resolution of symptoms is 15 hours.[2]

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

Evaluation

Symptoms can sometimes be alarming to the clinician, such as agitation, psychosis, and alteration of consciousness. Recognition of the diagnosis of Todd paresis in a patient will avoid unnecessary tests and treatments.

No laboratory studies help with the diagnosis of postictal paralysis. 

Computed tomographic (CT) perfusion scan anomalies are often found but are not consistent and thus nondiagnostic. It can show a hypoperfusion state at the site of the epileptic focus.[12][24][25]

CT angiography is unremarkable in postictal paralysis. This study can be used to differentiate between this condition and acute cerebrovascular accident (stroke) in which a major arterial branch can be seen occluded.[12][26]

Brain magnetic resonance imaging (MRI) will show findings consistent with a seizure, such as a transiently increased T2 signal at the site of the epileptic focus. This is due to increased edema at the site, which is bright on T2 imaging. It is best appreciated on fluid-attenuated inversion recovery (FLAIR) images.[1][4][12][27] These findings do not correspond to Todd paresis as the seizure causes them.

Electroencephalography (EEG) will show a focal or generalized slowing.[1] Rarely, there is a suppression of the activity. When the brain is recovering, background activity is restored with a decreased amplitude of signals. Even after EEG is restored, behavioral dysfunction can persist for several days.[16] This study can help to differentiate Todd paresis from a non-convulsive status epilepticus.

Treatment / Management

Treatment of this condition is primarily supportive as it resolves without any intervention. The evaluating clinician must recognize the diagnosis to prevent unnecessary procedures. Orotracheal intubation is only required in those patients who can not protect their airway. Patients do not require acute infusion of antiepileptic medication to treat Todd paresis; however, the usual prescribed medication should be continued. In those patients who had low therapeutic levels, loading, and optimization should be done to prevent recurrent episodes of seizures.

Differential Diagnosis

• Non-convulsive status epilepticus: Usually occurs after a prolonged seizure and may have minor ictal motor manifestations but does not show improvement. EEG will show ictal activity.[1] 
• Cerebrovascular accident (stroke): This may be distinguished by CT angiography, brain MRI, magnetic resonance angiography, or head CT scan. Care must be taken with the interpretation of a perfusion CT scan, as there could be hypoperfusion following a focal or generalized epileptic seizure similar to a stroke.
• Hemiplegic migraine: This is a rare genetic mutation or familial migraine variant in which the patient presents with severe, typically unilateral headache, weakness, ataxia, or paralysis.[28]
• 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.[29]
• Hypoglycemia: It is a well-known mimic of stroke syndromes.
• Psychogenic non-epileptic seizure: Presentation varies in intensity and does not follow an anatomic progression. Patients will present in an unresponsive state, will show a fast recovery, and can have episodes of postictal paresis.[1][30] Patients characteristically showed a triad, including asking what happened, blinking their eyes, and looking disoriented in place.[31]

Prognosis

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

Complications

No complications are expected as the paresis is self-limiting. On occasions, some patients are exposed to unnecessary procedures if the diagnosis is not identified.