Missed Warnings: The Silent Danger of Cerebellar Stroke

Introduction

Cerebellar infarcts account for roughly 2% of ischemic strokes yet carry a mortality rate near 23%. Their subtle presentation often delays diagnosis, raising the risk of life-threatening complications. Occlusion of the posterior inferior cerebellar artery (PICA) is the most common cause, typically presenting with dizziness, vertigo, and imbalance. This case illustrates the diagnostic challenge of cerebellar infarction presenting with deceptively mild initial symptoms.

Case Presentation

A 67-year-old male with hypertension and hyperlipidemia presented after a fall triggered by lightheadedness upon standing, with associated headache, nausea, blurry vision, and mild dyspnea. Given stroke concern, he received loading doses of aspirin and clopidogrel. Initial blood pressure was 161/66 mmHg, and ECG showed normal sinus rhythm with occasional PVCs.

Non-contrast head CT showed no acute abnormality, and neurology found no focal deficits, nystagmus, or ataxia. NIHSS was 0, precluding thrombolytics. Despite reassuring findings, MRI was ordered to evaluate for TIA.

Approximately 29 hours after admission, he developed worsening nausea, vomiting, headache, left facial droop, and slurred speech. Repeat CT revealed evolving left cerebellar (PICA territory) infarction with cytotoxic edema, fourth ventricle mass effect, and early hydrocephalus. Neurosurgery recommended posterior fossa decompression; however, per the family's wishes and the patient's DNR status, comfort care was pursued. He died approximately 48 hours after admission.

Discussion

This case highlights the difficulty of diagnosing cerebellar infarction when patients present with nonspecific symptoms — dizziness, headache — without focal deficits. Initial non-contrast CT missed early ischemic changes, and a NIHSS of 0 masked the severity of underlying pathology.

Cerebellar strokes are frequently misdiagnosed because they mimic benign vestibular disorders. Symptoms like headache, nausea, vomiting, ataxia, and dizziness warrant a high index of suspicion, especially in patients with vascular risk factors. Given the limited sensitivity of non-contrast CT for posterior fossa infarcts, repeat imaging and close clinical reassessment are essential when symptoms evolve.

Ultimately, this case reinforces the need for vigilance with persistent dizziness, since missed cerebellar infarction can progress to brainstem compression and herniation. Meticulous history-taking, serial neurologic exams, and timely imaging remain key to early recognition and improved outcomes.