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)