Upper cervical structural disease can alter vertebral artery biomechanics, although a mechanical contribution cannot be established by anatomical proximity alone. We describe an older woman with seronegative inflammatory arthritis and chronic atlantoaxial abnormality who developed abrupt vertigo, nausea, and inability to walk despite a National Institutes of Health Stroke Scale (NIHSS) score of 0. Computed tomography angiography (CTA) demonstrated left V3 vertebral artery dissection with pseudoaneurysmal dilation at the craniovertebral junction. Magnetic resonance imaging (MRI) showed a dominant acute left posterior inferior cerebellar artery (PICA)-territory infarction. Cervical imaging demonstrated atlantoaxial deformity, pannus-like peri-odontoid tissue, and a C1 arch abnormality adjacent to the affected V3 segment. Echocardiography and inpatient telemetry did not identify an embolic source. Anatomical colocalization of the C1-C2 abnormality and V3 lesion, together with the ipsilateral PICA infarction, suggests a possible mechanical contribution to the dissection, with subsequent artery-to-artery thromboembolism to the cerebellum. Dynamic compression was not demonstrated; spontaneous dissection, intracranial atherosclerosis, and occult embolism remain alternative or additional mechanisms. The patient received dual antiplatelet therapy followed by aspirin, statin therapy, and rehabilitation. This case emphasizes the limitations of the NIHSS in posterior circulation stroke and the importance of evaluating the craniovertebral junction when a V3 lesion occurs near upper cervical structural disease.
Rheumatoid arthritis-related diseases of the cervical spine, especially atlantoaxial subluxation with pannus, may cause a mechanical force on the V3 portion of the vertebral arteries and predispose to vertebral artery injury and posterior circulatory stroke. The report gives an account of an elderly woman with long-term seronegative inflammatory arthritis and chronic cervical degeneration presenting with sudden severe vertigo and nausea later identified to have a left anterior inferior cerebellar artery infarct. A CT angiography vascular imaging revealed left V3 vertebral artery dissection with pseudoaneurysm and no anterior circulation, and an MRI showed acute PICA territory cerebellar infarct with other small anterior circulation lesions. The cervical spine images showed chronic rheumatoid atlantoaxial changes and C1 arch malformation in keeping with the convergence of structural RA pathology and systemic vascular risk to develop mechanical vertebral artery dissection. She was medically managed on short-course dual antiplatelet therapy and then aspirin, high-intensity statin therapy, and multidisciplinary rehabilitation, and a neurosurgical examination considered her cervical disease inoperable. This case underscores the importance of early posterior circulation vascular imaging even in low-NIHSS presentations of isolated vertigo to avoid missed diagnoses. It highlights the need for diagnostic vigilance in RA patients with new posterior circulation symptoms, as prompt recognition of uncommon causes like mechanical VAD can guide timely management and improve outcomes.