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Case Reports
. 2018 Oct 30:13:14-17.
doi: 10.1016/j.ensci.2018.10.001. eCollection 2018 Dec.

Recurrent thrombolysis of a stuttering lacunar infarction captured on serial MRIs

Affiliations
Case Reports

Recurrent thrombolysis of a stuttering lacunar infarction captured on serial MRIs

Imama Naqvi et al. eNeurologicalSci. .

Abstract

Lacunar strokes account for about a fourth of all ischemic strokes. Pontine infarcts often present with stuttering symptoms, referred to as pontine warning syndrome (PWS). Patients presenting with fluctuating symptoms can appear to have rapidly improving symptoms and thus often go untreated despite the risk of recurrent deficits. MRI carries a higher sensitivity in detecting posterior circulation strokes compared to computed topagraphy, but does not always indicate irreversible injury. Here we present the first description of a stuttering lacune, captured radiographically on serial magnetic resonance imaging (MRI), that was initially averted with the administration of intravenous (IV) tissue plasminogen activator (tPA), only to return a month later and progress on imaging despite re-administration of tPA. During the first admission, our patient had spontaneous resolution of symptoms with complete reversal on restricted diffusion soon after IV tPA administration. On the second admission, the stuttering symptoms returned as did the same pontine lesion. Although his stuttering lesions lasted for several days, and the pontine lesion did ultimately progress to partial infarction on MRI, he was discharged home without neurologic deficits. Our case suggests that tPA may be of benefit in patients with lacunar pontine strokes even if symptoms rapidly improve or resolve.

Keywords: Ischemic stroke; Ischemic tolerance; Lacunar infarct; MRI; Rapidly improving stroke symptoms; Small vessel disease; Thrombolysis.

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Figures

Fig. 1
Fig. 1
This visual timeline depicts the patient's clinical course with corresponding representative MR diffusion sequences.
Fig. 2
Fig. 2
The right pontine infarct and perfusion lesion (A) resolved 24 h after thrombolysis (B), and re-occurred 30 days later (C). The diffusion lesion resolved approximately 1 h after thrombolysis was given, but the perfusion deficit persisted (D). By the time of discharge, the patient was still clinically asymptomatic despite having a persistent perfusion deficit for 4 days and a diffusion lesion evident on the FLAIR.

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