Stroke mimic: Hemiplegia in a case of acute aortic dissection

A 68-year-old man was emergently transported to the hospital due to a sudden onset of motor paralysis and sensory impairment in the left upper and lower limbs. He arrived 90 minutes after symptom onset. He reported no headache, chest pain, or back pain. His vital signs on admission were as follows: body temperature, 36.0°C; blood pressure, 130/102 mmHg; heart rate, 98 beats per minute (regular); respiratory rate, 20 breaths per minute; and peripheral saturation in oxygen, 95% on room air. His consciousness was clear, with no conjugate gaze deviation or dysarthria. On physical examination, he had muscle weakness (Medical Research Council grade 4) and decreased superficial sensation in the left upper and lower limbs. The National Institutes of Health Stroke Scale score was 3. Carotid ultrasound revealed good-color Doppler signals in both carotid arteries, with no evidence of arterial dissection. There were no apparent stroke findings on head computed tomography (CT) and magnetic resonance imaging. Laboratory tests revealed a markedly elevated D-dimer level (33.0 μg/mL). Additionally, supine chest radiography showed mild mediastinal widening (9 cm in the upper mediastinum). The pulses in the left radial and dorsalis pedis arteries were not palpable. Contrast-enhanced CT demonstrated extensive aortic dissection extending from the ascending aorta to the level of the common iliac arteries, with pericardial effusion. Blood flow beyond the left subclavian artery and left common iliac artery was completely occluded (Figure 1), but the dissection did not extend into the carotid or intracranial arteries. The patient was diagnosed with Stanford type A acute aortic dissection (AAD). He was transferred to a higher-level medical facility but developed cardiac arrest because of cardiac tamponade during transport. Despite resuscitative efforts and intensive care, he did not survive. In Stanford type A AAD, aortic dissection frequently extends beyond the carotid arteries, leading to cerebral infarction and subsequent unilateral upper and lower limb neurological deficits.1 However, cases in which unilateral upper and lower limb paralysis and sensory impairment mimic stroke because of simultaneous dissection-related arterial occlusion are exceedingly rare. There have been reports of AAD causing unilateral lower limb paresthesia and pain2, 3 and of acute limb ischemia presenting as unilateral upper and lower limb paresthesia.4 These findings underscore the importance of differentiating ischemia from neurological disorders in cases of acute unilateral symptoms. In our case, the absence of pain made differentiation from stroke even more challenging. When urgent evaluation is required to administer intravenous thrombolysis (t-PA) for acute ischemic stroke, carotid ultrasound is often useful in ruling out AAD.5 However, as demonstrated in this case, carotid ultrasound alone may not be sufficient in certain scenarios. In general, when cerebral infarction is identified, the possibility of AAD as an underlying cause should always be considered. Furthermore, as highlighted by this case, even when hemiparesis occurs in the absence of cerebral infarction, AAD should still be considered as a potential cause. Fundamental physical examinations, including the assessment of peripheral arterial pulses and routine coagulation testing in emergency settings, are essential for early and accurate diagnosis. Masahiro Biyajima: Conceptualization; methodology; validation; resources; writing – original draft; writing – review and editing; formal analysis; visualization; project administration; data curation; investigation. Juri Sato: Methodology; writing – review and editing. Jun Tsuyuzaki: Writing – review and editing; supervision. Ryuichi Kai: Methodology; writing – review and editing; supervision; validation. The authors have nothing to report. The authors have stated explicitly that there are no conflicts of interest in connection with this article. Ethics approval statement: Ethical approval was not required for this case report. Written informed consent for publication was obtained from the patient's wife. Participant consent statement: Written informed consent for publication of this case report and the accompanying images was obtained from the patient's wife. Clinical trial registration: None. All relevant data have been included in the report.