Artery of Percheron Ischaemic Stroke: A Classic Presentation of a Rare Case

The artery of Percheron (AoP) is a rare anatomic variant, where the paramedian thalami and the rostral midbrain are supplied by an artery emerging from the P1 segment of the posterior cerebral artery. Ischaemic infarction of the artery of Percheron occurs rarely, accounting for 0.1 to 2% of all ischaemic strokes. AoP occlusion can lead to an infarction of the paramedian thalami and mesencephalon, resulting in a triad of clinical features; namely, altered mental status, vertical gaze palsy and memory impairment. A larger mesencephalon infarction can also feature oculomotor disturbances. We describe here the case of an 88-year-old patient, presenting with this triad of features.

Bilateral facial colliculus syndrome caused by pontine tegmentum infarction: a case report

Background Bilateral facial colliculus syndrome is a rare clinical presentation in patient with pontine infarction. We herein described a case of bilateral facial paralysis and complete horizontal gaze palsy possibly caused by paradoxical embolization from patent foramen ovale related stroke. Case presentation A 55-year-old male presented with sudden onset of complete peripheral facial palsy and horizontal gaze palsy after Valsava maneuver. MRI revealed symmetric involvement of bilateral pontine tegmentum in accordance with the location of facial colliculus. CSF analysis and follow-up MRI showed no evidence of central demyelinating disease. Subsequent echocardiography revealed patent foramen ovale and closure surgery was performed. Conclusions Facial colliculus syndrome with symmetric dorsal pontine tegmentum involvement may a rare manifestation in posterior circulation stroke.

Compound Heterozygous ROBO3 Mutation in Two Siblings Presenting with Horizontal Gaze Palsy without Scoliosis: Case-Based Review

Horizontal gaze palsy with progressive scoliosis (HGPPS) is a rare, autosomal recessively inherited disorder characterized by a congenital absence of conjugated horizontal eye movements with progressive scoliosis developing in childhood and adolescence. HGPPS is caused by mutations of the ROBO3 gene that disrupts the midline crossing of the descending corticospinal and ascending lemniscal sensory tracts in the medulla. We present two siblings, 5-year-old and 2-year-old boys with HGPPS, from non-consanguineous parents. The older brother was brought for the evaluation of moderate psychomotor retardation. He had bilateral horizontal gaze palsy with preserved vertical gaze and convergence. Scoliosis was absent. Cranial MRI showed brainstem abnormalities, and diffusion tensor imaging showed absent decussation of cortico-spinal tracts in the medulla. Clinical diagnosis of HGPPS was confirmed by sequencing of ROBO3 gene, IVS4–1G > A (c.767–1G > A) and c.328_329delinsCCC (p.Asp110Profs*57) compound heterozygous variations were found, and segregated in parents. The younger boy was first reported at 16 months of age and had the same clinical and neuroradiological findings, unlike mild psychomotor retardation. ROBO3 gene analysis showed the same variants in his brother. Our cases show the importance of evaluating eye movements in children with neurodevelopmental abnormalities and looking for brainstem abnormalities in children with bilateral horizontal gaze palsy.

Wall-eyed bilateral internuclear ophthalmoplegia in posterior circulation stroke-a case report

Internuclear ophthalmoplegia is characterised by restricted ocular motility in lateral gaze in which the affected eye shows impairment of adduction and it results from damage to medial longitudinal fasciculus (MLF). Wall-eyed bilateral internuclear ophthalmoplegia (WEBINO) is an extremely rare neurological manifestation which has typical signs including primary gaze exotropia, vertical gaze palsy, ptosis, abducting nystagmus. The common and serious etiological factor is cerebrovascular accident involving the vessels supplying MLF and many cases have life threatening associated neurological impairment. In this case report we have discussed about a gentleman who presented with bilateral ptosis, primary gaze exotropia and headache. Patient found to have vertical gaze palsy and abducting nystagmus on examination. Computed tomography (CT) imaging shows infarct in pontine region and CT angiography revealed basilar artery occlusion supplying region of pons with involvement of posterior cerebral artery. Patient treated with antiplatelet and diplopia managed. Patient showed improvement on subsequent follow-up visits.

Upward gaze palsy and convergence insufficiency as a rare presentation of primary intraventricular haemorrhage

A primary intraventricular haemorrhage (PIVH) usually presents with non-localised neurological symptoms since the haematoma is limited to the ventricles. However, it is sometimes associated with focal neurological signs, whose pathophysiologies are not confirmed. Here, we report on a case of PIVH who showed rare manifestations in the acute stage: upward gaze palsy and convergence insufficiency. The CT and MRI showed intraventricular haematoma without evidence of parenchymal haemorrhage, local mass effect around midbrain or hydrocephalus. There had been bilateral papilloedema, and it resolved along with improvement of the ophthalmic symptoms, suggesting a possible causal relation to increased intracranial pressure. The ophthalmic abnormalities suggested injury of the rostral part of the midbrain, especially the region around the dorsal midbrain tectum. It should be known that PIVH is one of the causes of acutely developing upward gaze palsy and convergence insufficiency.

Isolated abducens nucleus syndrome due to pontine tegmentum infarction

Introduction: Abnormalities of horizontal gaze could be caused by damage of the abducens nucleus due to ischemic lesion. We report a patient with isolated horizontal gaze palsy as a result of a small ischemic lesion of the pontine tegmentum. Observation: A 61-year-old man, with medical history of diabetes mellitus, dyslipidemia and high blood pressure, was hospitalized after 12 hours of transient dizziness and diplopia. On examination, he had conjugate eye deviation to the right side with horizontal gaze paralysis toward controlateral side. Vertical eye movements, convergence and pupillary reflex were preserved with no peripheral facial palsy. Brain MRI revealed a small lesion in the left pontine tegmentum. Patient received aspirin with atorvastatin and the gaze palsy has been disappeared three weeks later. Discussion: Conjugate lateral eye movement paralysis is commonly attributed to lesions of the caudal pons involving the abducens nucleus. horizontal gaze palsy is often associated to an ipsilateral peripheral facial palsy. In our case, the left lateral gaze palsy was isolated. The pontine lesion should be strictly confined the abducens nucleus which is extremely rare. the outcome of eye movement deviation in brainstem lesions is favorable within few weeks. Conclusion: Our case provides evidence that small pontine lesions can damage the abducens nerve nucleus without causing ipsilateral peripheral facial palsy.