Reply to the Comments on “Comments on Published Articles: Reversal of Abulia with Atomoxetine in Unilateral Basal Ganglia Infarct: A Case Report”

Dear Commentators,

We appreciate your interest in our case report “Reversal of Abulia with Atomoxetine in Unilateral Basal Ganglia Infarct: A Case Report.” ¹ We read the comments and have the following response.

We are grateful to the correspondents for reminding us about the etiopathophysiological classification of stroke. Given the journal requirements and word limitations, it was not possible to give a detailed account of the exclusion of possible etiologies of stroke. When not specifically mentioned and the medical history is declared to be unremarkable in the report, it stands to reason that the investigations were non-contributory. We aimed to report a novel clinical phenomenon as a presenting feature of ischemic stroke. We did not believe that the description of the pathomechanism of stroke was significantly relevant. However, we would like to bring to your kind attention that this patient had a lacunar infarct (TOAST classification: 3) without any large intracranial or extracranial vessel or cardiac abnormalities. Her hypertension was uncontrolled, consequent to irregular compliance with medications; however, it did not result in any hypertensive crises. Moreover, a thorough evaluation of the possible etiologies of stroke was carried out as is the standard protocol followed in our center, including testing for SARS-CoV-2 infection; the patient did not have any evidence of carotid artery disease, connective tissue disorders, small vessel disease, hematological disease, malignancy, diabetes, dyslipidemia, cardiac disease, smoking or cardiac arrhythmias or SARS-CoV-2 infection. She took her booster dose of SARS-CoV-2 vaccination (COVISHIELD) 18 months prior to stroke onset, lessening the possibility of it being the etiology of stroke.

The report documented clear improvement at two months, after which atomoxetine was tapered and stopped over the next two weeks with full recovery. There were no residual symptoms at 6 and 12-month follow-ups, not necessitating any additional antidepressants or other medications. As has been succinctly demonstrated, spontaneous recovery was not considered since the symptoms recurred when a trial of discontinuation of atomoxetine was tried at one month of initiation.

Abulia in stroke is a rare phenomenon described in this case report. From our understanding of clinical neurology, the constellation of any abrupt onset of neurological deficit with uncontrolled hypertension requires the exclusion of stroke. Moreover, ancillary investigations, including brain imaging without any other contributory neurological or systemic symptoms, suggested stroke as the most likely etiology. The MRI brain, as demonstrated in the report, confirmed the presence of an acute stroke while ruling out other possibilities. We want to highlight the pathogenesis that we described. The ventral globus pallidus and nucleus accumbens receive dopaminergic fibers from the ventral tegmental area comprising the motivation and reward circuit disruption, which is associated with abulia, similar to other cases of abulia reported earlier although in association with bilateral globus pallidus damage, unlike our case which had unilateral involvement. ²

As far as the exclusion of non-convulsive status epilepticus (NCSE) is concerned, a normal EEG (done before the patient presented to us) and clinical improvement without antiseizure medications and anesthetics is considered sufficient enough by the authors to exclude NCSE as the etiology of abulia reasonably.

We apologize if we could not list all the negative investigations and clinical differentials in the manuscript in the original report that we considered were beyond the scope of our submission and were not relevant to this case. We are grateful for this chance to expand on our submission.