BACKGROUND: Neurologic deficits in patients with Klippel-Feil syndrome usually are attributed to direct compression of neuronal structures or hypoperfusion secondary to compression of the vertebral arteries by bony abnormalities. OBJECTIVE: To describe a 38-year-old woman with known Klippel-Feil syndrome who developed lateropulsion. RESULTS: The results of magnetic resonance imaging were consistent with rubrothalamic stroke. The cerebral angiogram confirmed vertebral artery dissection at the level of her previously observed bony abnormality. CONCLUSIONS: Hypermobility adjacent to fused vertebrae subjects the vertebral artery to increased shear forces. Thus, Klippel-Feil syndrome may be a predisposing factor for vertebral artery dissection. Moreover, to our knowledge, this case represents the second known case of rubral lateropulsion.
BACKGROUND:Neurologic deficits in patients with Klippel-Feil syndrome usually are attributed to direct compression of neuronal structures or hypoperfusion secondary to compression of the vertebral arteries by bony abnormalities. OBJECTIVE: To describe a 38-year-old woman with known Klippel-Feil syndrome who developed lateropulsion. RESULTS: The results of magnetic resonance imaging were consistent with rubrothalamic stroke. The cerebral angiogram confirmed vertebral artery dissection at the level of her previously observed bony abnormality. CONCLUSIONS: Hypermobility adjacent to fused vertebrae subjects the vertebral artery to increased shear forces. Thus, Klippel-Feil syndrome may be a predisposing factor for vertebral artery dissection. Moreover, to our knowledge, this case represents the second known case of rubral lateropulsion.