Life-threatening bradycardia after bilateral paramedian thalamic and midbrain infarction

Abstract

Dear Sirs,Bilateral symmetric thalamic infarcts are uncommon pre-sentations of ischemic stroke that mostly occur in the ter-ritories of the paramedian thalamic arteries [1]. Thesearteries arise either separately from the posterior cerebralarteries (PCAs) or exceptionally from a single commontrunk the artery of Percheron [2]. In this article, a case ofbithalamic paramedian and midbrain stroke presenting withdrowsiness, ophtalmoplegia, and life-threatening brady-cardia is presented. Despite it is known that different stroketopographic patterns can produce slowing of heart rate andasystolia, this is the first report of acute bradycardia inconcomitance to bilateral midbrain infarction [3–5].A 51-year-old man with a 3-year history of idiopathicarterial hypertension (on zofenopril) was admitted to ouremergency room after being found unresponsive in bed. Onadmission he showed fluctuating level of consciousness,dysarthria, anisocoria, and vertical gaze palsy (NIHSS 7,GCS 9). During examination, the patient suddenly devel-oped severe sinus bradycardia (pulse rate \30 beats perminute (bpm), for 3 minutes) that improved only afteratropine administration. Arterial blood pressure (BP),blood exams, toxicological screening, and brain CT scanwere all normal. Within 1 h, another self-limiting episodeof drowsiness and concomitant bradycardia ensued. Dif-fusion-weighted (DW) sequences on brain MRI demon-strated symmetric bilateral thalamic, hypothalamic, andmidbrain acute infarctions, thus, advocating the occlusionof a putative artery of Percheron (Fig. 1a). Top-of-the-basilar syndrome was ruled out documenting patency ofthe basilar artery and both PCAs by MRI angiography.Extensive cardiological workup showed no signs ofhypertensive cardiomyopathy both on ECG and echocar-diography, but revealed a patent foramen ovale (PFO) withsevere right-to-left atrial shunt. Anticoagulant therapy was,therefore, started and PFO closure suggested. In the fol-lowing days, episodes of bradycardia (nadir of 38 bpm,without major alterations of BP) tended to recur duringdrowsiness and night sleep. Particularly, diurnal fluctua-tions of vigilance paralleled recurrent sleep spindle patternson electroencephalography (Fig. 1b). Sinus bradycardiaoccurred less often and heart rate gradually increased in thefollowing weeks. At the 3-month follow-up, despite fullresolution of gaze palsy and arrhythmia, the patient stillpresented recurring episodes of hypersomnolence andimportant disability due to long-lasting apathy.Infarcts at the mesencephalic–diencephalic junctionresult in complex clinical syndromes contingent on thedeep brain structures involved. Supranuclear vertical gazepalsy and associated abnormal ocular reflexes are related tolesions of the rostral interstitial and Edinger–Westphalnuclei [6]. Fluctuating level of consciousness, coma, andhypersomnolence are attributed to the involvement ofintralaminar nuclei and reticular mesencephalic formation[7]. Notably, while presenting symptoms usually reverseover time, cognitive dysfunctions caused by limbic loopinterruption lead to long-term disability [8]. In our patient