Stroke mimic: Perfusion magnetic resonance imaging of a patient with ictal paralysis

I read with great interest the article by Sanghvi et al. in which they describe an interesting patient admitting with a clinical picture mimicking acute left middle cerebral artery syndrome.[1] After neuroimaging studies, including diffusion-weighted imaging (DWI) and perfusion imaging, ictal paralysis was diagnosed and the patient had recovered totally in following few hours. I agree with the interesting aspect of this patient; however, I would like to comment on the article hoping to provide a better understanding of the issue.

First, in my opinion, making the diagnosis ictal paralysis in this patient may be questioned in many aspects. For instance, not any previous history of seizures was mentioned and electroencephalography (EEG) on day 2 was normal. Furthermore, not an antiepileptic drug (AED) medication was administered avoiding to assess any possible AED response which could support the diagnosis of ictal paralysis. Otherwise, the diagnosis of this patient was based on solely magnetic resonance (MR) perfusion imaging showing hyperperfusion of parietal lobe and normal DWI results. Seizures presenting with ictal paralysis constitute considerably rare entities.[2,3] On the other hand, there is not a consensus for negative motor seizures in MR perfusion imaging to differentiate from stroke as hypoperfusion has also been reported in seizure-related neurological deficits in perfusion imaging studies.[4] Furthermore, hyperperfusion has also been reported in association with other disorders such as hemiplegic migraine attack which can be another leading diagnosis in this patient.[5,6] Otherwise, in a crucial report, the role of EEG, which was normal in the case by Sanghvi et al., has rather been emphasized in discrimination of transient ischemic attack and inhibitory seizures.[7] Taken together, there may be serious questions in the proper diagnosis of this patient. I wonder if the author might give additional data regarding the premorbid medical history of the patient and if migraneous headache accompanied to the clinical manifestations. At this point, I would like to state that follow-up EEG data might add substantial contributions to the understanding of this report.

In addition, the authors indicate that diagnosis of ictal paralysis was made after MR imaging perfusion study, but not any AED medication trial was mentioned. In my opinion, it can be more comprehensible if the authors may explain the reason of not giving AED during the clinical course while ictogenesis was considered in the forefront. Finally, another point to be discussed may be that abnormal perfusion imaging (hyperperfusion) was seen in the left parietal lobe; nonetheless the patient had presented with hemiplegia which rather can be attributed to the frontal lobe in the physiological aspects. Interestingly, recent reports pointed out the role of presupplementary motor area and inferior frontal gyrus as called “negative motor area” in the pathophysiology of negative motor seizures.[8,9] These controversies may constitute important topics for further considerations and should be included in the discussion section.

In conclusion, although some limitations mentioned above need to be clarified, this case represents a crucial report, pointing out stroke mimics in the differential diagnosis of patients presenting with neurological deficits. These alternative diagnoses should be kept in mind among physicians who will avoid unnecessary and potential harmful interventions such as thrombolysis. In addition, I think that perfusion imaging method should be used wider in the future clinical practice which probably may add crucial data regarding the pathophysiology of neurological deficits in other rare conditions of stroke mimics.

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