Discussion:
Cerebral infarcts affecting both paramedian thalami are unusual and may raise suspicion of occlusion of a single arterial trunk known as the artery of Percheron (4,5) . This is the third anatomical arterial variant (Type IIb) which vascularises the thalami and/or the midbrain (3) (see table 1). These structures are responsible for the regulation of the sleep-wake cycle. Therefore, thalamic infarcts ca cause paresthesias or numbness, speech and cognition disturbance, memory impairment, and stupor (6). Our patient presented a motor deficit associated with consciousness discturbance like stupor. This anatomical variant occurs in 33% of the population (7) and infarcts of this artery account for 4-18% of all thalamic infarcts and 0.1-2% of all strokes (8). Macedo et al. who had one of the most representative series found a frequency of 0.17%(9). The classic clinical presentation of an infarction of Percheron’s artery is a triad of altered consciousness, paralysis of verticality of gaze and memory disorders (2) . The association of these signs with Weber’s syndrome in our patient constitutes one of the main particularities of our clinical case. Indeed, Weber’s syndrome is part of the midbrain syndrome and is characterised by a contralateral hemiplegia associated with an attack on the homolateral common oculomotor nerve. Its incidence is unknown and it rarely occurs in isolation (10,11). Mesencephalic and Percheron’s artery infarction with Weber’s syndrome is a rare and difficult clinical finding (12). In our patient, the common oculomotor nerve damage was not accompanied by pupillary damage. The most plausible hypothesis would be an absence of damage to the nuclei of the superior mesencephalon, responsible for pupillary innervation. Thus, a careful clinical examination allows the diagnosis to be suspected. Brain CT allowed to exclude the infarction involving occipital lobe (or lobes), that could suggest basilar artery occlusion, but it did revealed symmetrical ischemic lesions in both thalami and anteromedial midbrain, which were consistent with clinical presentation (13)(6). Carotid and basilar Doppler ultrasound was irrelevant. CT angiography was performed (arterial and venous phases), which revealed no signs of arterial or venous thrombosis. Although it also did not show evidence for artery of Percheron (AOP) occlusion. It is not unusual as artery of Percheron is rarely visible on angio-MRI or angio-CT or conventional angiography. In our patient the CT angiogram showed an vertebral occlusion. Our patient did not benefit from intravenous thrombolysis because it was not available in our region. Finally, the treatment of Percheron’s artery infarction must be oriented according to the underlying pathological process. It can range from antiaggregation treatment to anticoagulation depending on the aetiology (14). The long-term evolution had not been done in our patient who was lost to follow-up. We could not determine if she presented persistent vigilance disorders or dementia as reported by Macedo et al. In his series of 8 patients, he found hypersomnia in 3 patients. (9)