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Clinically Complete Recovery after Bilateral Paramedian Thalamic Infarction

Dear Editor, A 61-year-old woman presented to the emergency department with a reduced level of consciousness. On arrival, her Glasgow Coma scale (GCS) was 6/15 (eye: 1, verbal: 1, motor: 4). On physical examination, the patient grimaced to painful stimuli and plantar reflexes were positive bilaterally. The pupils were unequal and mydriatic, both unresponsive to light. Her blood pressure was 180/120 mmHg and blood glucose level, body temperature, heart rate, and respiratory rate were within normal limits. The National Institutes of Health Stroke Scale (NIHSS) score was 25. Cardiovascular and respiratory examinations were normal. There were no signs of hemorrhage in brain computed tomography (CT). Diffusion-weighted magnetic resonance imaging (MRI) showed bilateral paramedian thalamic infarction (Figure 1A, 1B). The patient was intubated and admitted to the intensive care unit. She was started on 300 mg/day acetylsalicylic acid for ischemic stroke. Additionally, amantadine 200 mg/day was started to increase wakefulness. Due to the high NIHSS score, the lack of information regarding the exact time when the event started, and the high risk of hemorrhage, thrombolytic therapy was not considered. The patient was extubated after 48 hours. On the second physical examination, the right pupil was mydriatic and unresponsive and there was vertical gaze palsy and skew deviation in the same eye. Muscle strength of the four extremities was 5/5, bilateral plantar reflex was positive, and GCS was 13 (E3, V4, M6). After five days from hospitalization, the GCS was 15 and a neurologic examination was normal. A crain CT scan and carotid-vertebral angiogram excluded any major intracranial artery occlusion (Figure 2). A 24-h Holter monitor showed paroxysmal atrial fibrillation; therefore, warfarin therapy was started. Bilateral thalamic infarction is rare, representing 0.6% of all ischemic strokes, with paramedian thalamic infarction being the most common subtype (75%) (1). The etiology of vertebrobasilar ischemia remains controversial. Recent studies have demonstrated that cardiac embolism is responsible for about one-fifth of the cases of brain embolism that manifest with the signs and symptoms of vertebrobasilar insufficiency (2). In our patient, the a Holter monitor showed paroxysmal atrial fibrillation that could cause