Differential diagnosis in bilateral thalamic infarct: clinical and radiological aspects

Abstract

Keywords Top of the basilar syndrome Artery ofpercheron Stroke Bithalamic infarctionA 77-year-old hypertensive man, presented with suddenleft hemiparesis and dysarthria, rapidly progressing to lossof consciousness. He was admitted, with a Glasgow ComaScale (GCS) score of 6/15 and left hemiplegia. A cranialCT showed no acute changes. Brain T2-weighted MagneticResonance Imaging (MRI) showed bilateral signal changesin the medial thalamus and the rostral portion of the mid-brain (Fig. 1).Electrocardiography (ECG), transthoracic echocardi-ography, Holter ECG and a study of the cervical Mag-netic Resonance Angiography (MRA) showed nosignificant abnormalities. A cerebral MRA showed severestenosis at the P1 segment of the right posterior cerebralartery, at the likely emergence of the Artery of Perche-ron (AOP). The basilar and vertebral arteries were patent(Fig. 2). During hospitalization, the patient improvedprogressively. Upon discharge, the patient had mild lefthemiparesis (4/5), dysmetria and dysdiadochokinesia, andinternuclear ophthalmoplegia associated with memoryimpairment.The bilateral thalamic infarct may be found in threeclinical conditions:1. Top of the basilar syndrome: circulatory disturbance atthe top of the basilar artery that involves five arterialbranches: the superior cerebellar arteries, the posteriorcerebral arteries and basilar artery itself between theirjunctions [1].2. Occlusion of the AOP: a single branch of the P1segment of one of the PCA, which also contributes torostral irrigation of the brainstem, in roughly half of allcases [2, 3].3. Deep cerebral venous thrombosis [2–4]: in our case,we can state that it is not this situation. There are nosigns of venous thrombosis from the cerebral MRA;there are no clinical symptoms of thrombosis (head-ache, vomiting, papilloedema and seizure) and thepatient improved without needing anticoagulation (theideal treatment for this pathological condition) [2–4].Conversely, the possibility of the top of the basilarsyndrome or AOP occlusion requires discussion.Regarding the clinical characteristics, both present mentalconfusion, vertical gaze paralysis and memory impairment[2, 3, 5]. Signs and symptoms characteristic of the top ofthe basilar syndrome are: visual field defects, agitatedbehaviour and amnesia, due to involvement of theoccipital and temporal lobes [2]. Some common signs andsymptoms of occlusion of the AOP: oculomotor distur-bances, ataxia, and hemiparesia can also be seen in thetop of the basilar syndrome in the presence of mesence-phalic involvement [1, 5]. Ataxia also can occur in top ofthe basilar syndrome when the superior cerebellar arteryis affected [1, 2]. Just the clinical symptoms, therefore,are insufficient for determining the aetiology in the casedescribed.