Case Report: Eight-and-a-Half Syndrome from Pontine Infarction in 71-Year-Old Man

A 71-year-old man with vascular risk factors presented with abrupt-onset dizziness, slurred speech, and eye movement abnormalities, ultimately diagnosed with eight-and-a-half syndrome due to an acute pontine infarction. The rare neuro-ophthalmologic condition combines horizontal gaze palsy, internuclear ophthalmoplegia, and ipsilateral facial nerve weakness.

The patient, a right-handed male with a history of hypertension and ischemic heart disease, reported no tobacco or alcohol use and had no prior cerebrovascular events. Neurological examination revealed outward deviation of the right eye in the primary position. On attempted left gaze, there was a complete failure of horizontal eye movement with absent saccades. Rightward gaze demonstrated preserved abduction of the right eye with accompanying gaze-evoked nystagmus. Vertical eye movements and vertical saccades were intact, and the vestibulo-ocular reflex was preserved. A left-sided lower motor neuron facial nerve palsy with Bell’s phenomenon was noted. No ptosis, pupillary abnormality, or involvement of other cranial nerves was observed. Motor, sensory, cerebellar, and meningeal examinations were normal.

Magnetic resonance imaging of the brain showed an acute diffusion-restricted lesion involving the left dorsal pons. The anatomical location of the infarct corresponded to structures governing horizontal gaze and facial nerve function, supporting the diagnosis. A vertebral artery Doppler study revealed mild intimal thickening without significant stenosis, and transthoracic echocardiography demonstrated preserved left ventricular systolic function.

Eight-and-a-half syndrome arises from a single pontine lesion that simultaneously affects multiple functionally related neural pathways. Disruption of the paramedian pontine reticular formation or abducens nucleus produces horizontal gaze palsy, involvement of the medial longitudinal fasciculus results in internuclear ophthalmoplegia, and damage to the facial nerve fascicle at the level of the facial colliculus leads to ipsilateral lower motor neuron facial weakness.

Ischemic injury to the pons, particularly involving perforating branches of the vertebrobasilar circulation, represents a common mechanism underlying this syndrome. Previously reported cases have demonstrated that vascular etiologies typically present with an abrupt onset of symptoms and show close clinicoradiological correlation, whereas demyelinating, infectious, inflammatory, or neoplastic causes often follow a more subacute or progressive course and may be associated with additional neurological findings.

Neuroimaging plays a crucial role in supporting the diagnosis and identifying the underlying etiology. Diffusion-weighted magnetic resonance imaging is particularly valuable in detecting acute pontine infarction, as small strategically located lesions can produce disproportionate clinical deficits due to the dense concentration of neural pathways within the pons.