Reply to Letter to Editor regarding the article, "Stroke mimic: Perfusion magnetic resonance imaging of a patient with ictal paralysis".

Thank you for your interest in our case report on magnetic resonance perfusion imaging of a stroke mimic and the insightful comments on controversies regarding the subject matter published as a letter to the editor. We presented an uncommon case of clinically diagnosed window period stroke investigated by diffusion–perfusion magnetic resonance imaging (MRI) and diagnosed as ictal paralysis on MRI; likely due to focal inhibitory seizures. Our case report emphasizes the importance of perfusion MRI in establishing the diagnosis of stroke mimic; thereby avoiding expensive and unnecessary intravenous thrombolytic treatment.[1]

We agree that absence of early electroencephalogram (EEG) at the time of ictus is a significant shortcoming in substantiating our diagnosis. We agree that seizures presenting with ictal paralysis constitute considerably rare entities. However, in our opinion, the presence of localized hyperperfusion recorded by MRI and coinciding with a clinical neurological deficit is important evidence for ictal paralysis. Negative diffusion imaging definitively ruled out acute ischemic stroke in our case. By contrast, postictal or Todds paralysis is marked by hypoperfusion on computed tomography or MRI. The absence of a history of seizures and a normal EEG recorded 2 days later should not preclude the diagnosis of stroke mimic due to negative motor seizures. We agree that hemiplegic migraine is a differential diagnosis in the list of stroke mimics that would also include hysteria, hypoxic hemiplegia, and hypoglycemia.[2] The patient described in this case had no previous history of migraine. Furthermore, the MRI perfusion abnormality in hemiplegic migraine is more often localized decreased perfusion.[3]

It is persuasive that hemiplegia should be attributed to the frontal lobe; parietal hyperperfusion demonstrated in our case possibly may be due to the spread of seizure activity from the primary focus. Indeed, recent reports highlight the role of pre-supplementary motor area and inferior frontal gyrus as “negative motor areas” in the pathophysiology of negative motor seizures.[4] Furthermore, primary sensorimotor mechanisms play an important role in generating phasic inhibitory motor responses, such as cortical negative myoclonus or silent periods in humans.[56]

In conclusion, we highlight the expanding body of evidence[67] on the advantage of MRI in bettering safety and efficacy of reperfusion therapies in acute ischemic strokes and particularly to avoid unwarranted thrombolysis in stroke mimics. Once again, we appreciate the comments and suggestions of the author of the letter to the editor regarding the subject matter of our case report.

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