A 53-year-old right-handed white man presented to the emergency room of our institution with a 2-day history of double vision, dysarthria, and difficulty with swallowing and walking. His symptoms were sudden in onset with gradual worsening. He could not walk owing to fear of falling and was unable to eat or drink because of choking. His double vision was worse with horizontal gaze to the left side. He noticed clumsiness and incoordination in both upper and lower extremities. A review of systems was unremarkable for headache, nausea, vomiting, fever, facial pain, new-onset weakness or numbness, neck pain or stiffness, or weight and appetite loss. The patient’s past medical history was significant for hypertension, type 2 diabetes mellitus, hyperlipidemia, obstructive sleep apnea, and right medullary infarction 2 years prior to presentation. He had residual left-sided weakness and ambulated with a cane at baseline. He denied smoking, drinking alcohol, and use of recreational drugs. His home medications included amlodipine, atenolol, clopidogrel, gabapentin, insulin, losartan, metformin, spironolactone, and ibuprofen. At presentation, the patient’s systolic blood pressure was elevated in the range of 200–220 mmHg. His physical examination was significant for disconjugate eye movements with multidirectional nystagmus, right-sided medial rectus palsy on left-sided horizontal gaze suggestive of right-sided internuclear ophthalmoplegia (INO), no afferent pupillary defect, and a normal pupillary reflex and fundus examination. His facial sensations were normal to fine touch and painful stimuli. There was no facial muscle weakness. He had continuous, involuntary, and rhythmic contractions of the soft palate without an audible clicking sound. The results of the patient’s motor examination were significant for spasticity, mild weakness, and brisk deep tendon reflexes in the left upper and lower extremities. His sensations were diminished to vibration up to the ankles bilaterally with unremarkable fine touch and pain sensation. He had abnormal finger-to-nose and heel-to-shin test results in the upper and lower extremities bilaterally. He was unable to stand with his eyes open. No tremors were noticed in his head or upper and lower extremities. His National Institutes of Health Stroke Scale score was 6 (2 points each for dysarthria, ataxia, and left-sided upper and lower extremity drift). The differential diagnoses considered were possible multifocal infarction in the posterior circulation; demyelinating diseases such as acute demyelinating encephalomyelitis, multiple sclerosis, and neuromyelitis optica; and neuroinfectious diseases such as Whipple’s disease and neurosarcoidosis. Acute stroke was considered high in the differential diagnosis, given his multiple uncontrolled vascular risk factors, prior history of stroke, and the acuity of symptom onset. The patient’s blood workup revealed leukocytosis of 18,900 cells/mm3 (reference range 3600–11,200 cells/mm3), which decreased to 14,800 cells/mm3 the next day. He had mild elevation of blood urea nitrogen at 27 mg/dl (reference range 9–25 mg/dl) and creatinine at 1.34 mg/dl (reference range 0.7–1.3 mg/dl) at admission, which were normalized the following day with intravenous hydration. We thought that the patient’s leukocytosis and slightly elevated renal parameters were due to dehydration. The result of his urine toxicology screen was unremarkable. A clopidogrel resistance panel showed a subtherapeutic response with adenosine diphosphate inhibition of 31% (reference range 50–100%). He had a glycated hemoglobin A1c of 7.6 g %, low-density lipoprotein level of 178 mg/dl, and triglyceride level of 359 mg/dl. A computed tomographic (CT) scan of the patient’s head showed mild burden of small vessel disease without hemorrhage or early signs of ischemic stroke. CT angiography of his head and neck showed chronic occlusion of the V4 segment of the right vertebral artery with distal reconstitution by collateral branches 5 mm before the origin of the basilar artery with a sessile aneurysm measuring 7 mm × 7 mm at the basilar tip. On day 2 of the patient’s admission, magnetic resonance imaging of the brain showed a small area of restricted diffusion in the right caudal midbrain suggestive of acute lacunar infarct with additional findings of chronic infarction in the right caudal medulla and T2 hyperintensity with hypertrophy of the right inferior olivary nucleus. His electrocardiogram showed sinus rhythm with no arrhythmias on continuous telemetric monitoring during hospitalization. A transthoracic echocardiogram showed normal ejection fraction, moderate concentric left ventricular hypertrophy along with diastolic dysfunction, and no right-to-left shunting. The etiology of stroke was possibly secondary to vessel-to-vessel thromboembolism resulting from severe intracranial atherosclerotic disease of the right vertebral artery. He was started on dual antiplatelet therapy with aspirin and clopidogrel. We also optimized his modifiable vascular risk factors by adjusting his antihypertensive and statin medications for secondary prevention of ischemic stroke. He was discharged to an inpatient rehabilitation center on day 3. The patient was lost to follow-up.