INTRODUCTION: Eight and a Half syndrome: a combination of ipsilateral cranial nerve seven palsy plus one and a half syndrome is rare. Exact prevalence of the syndrome has not been reported as of yet. This syndrome is mostly attributed to a vascular etiology such as a pontine tegmental infarction. OBJECTIVE: To present a rare case of a stroke syndrome : eight and a half syndrome (peripheral cranial nerve seven palsy plus a one and an half syndrome) in an adult male. To present the importance of its early clinical recognition in correlation of radiologic imaging, and management. CASE REPORT: This is a case of a sixty-two year old male, who had a one day history of sudden double vision. Cranial nerve examination revealed a frozen right eye; unable to perform any movement on horizontal gaze, and with right sided facial asymmetry. He was hypertensive for more than ten years. Left eye was exotropic, with no adduction. Right eye was frozen on horizontal gaze, and primary gaze was at midline. Right sided peripheral facial palsy was seen on examination. Cranial non-contrast magnetic resonance imaging with time of flight was done revealing an infarct in the right posterior pontine area, and a narrow right vertebral artery due to a probable occlusion. Patient was started on antiplatelet cilostazol 100mg/tab 1 tablet twice daily. Atorvastatin 40mg/tab 1 tablet was given. Anti-hypertensives were started on his fourth hospital day. Smoking cessation, dietary modifications, and compliance to medications were emphasized prior to discharge. DISCUSSION Here we have a stroke syndrome presenting as an ipsilateral lower motor neuron: seventh nerve palsy, and an ipsilateral horizontal gaze palsy with internuclear ophthalmoplegia of the contralateral eye (failure of adduction) termed as CN VII, + 1 ½ syndrome or Eight and a Half Syndrome. This is caused by a lesion involving the paramedian pontine reticular formation (PPRF) which sends signals towards the ipsilateral abducens nerve and contralateral medial longitudinal fasciculus. These structures lie in close proximity to the nucleus and intraaxial fascicles of cranial nerve VII manifesting as facial weakness of the ipsilateral side to the lesion. An occlusion in the tip of the paramedian pontine artery, a branch of the basilar artery, is the most common etiology.