Karimi Morvarid, Razavi Mehrdad, Fattal Deema
Department of Neurology, University of Iowa Hospitals and Clinics, Iowa City, USA.
Arch Neurol. 2004 Apr;61(4):583-5. doi: 10.1001/archneur.61.4.583.
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.
To describe a 38-year-old woman with known Klippel-Feil syndrome who developed lateropulsion.
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.
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.
Klippel-Feil综合征患者的神经功能缺损通常归因于神经元结构的直接受压或继发于骨异常对椎动脉压迫的灌注不足。
描述一名已知患有Klippel-Feil综合征且出现向外侧推挤症状的38岁女性。
磁共振成像结果与红核丘脑中风相符。脑血管造影证实了在其先前观察到的骨异常水平处存在椎动脉夹层。
融合椎体相邻部位的活动度过高会使椎动脉受到更大的剪切力。因此，Klippel-Feil综合征可能是椎动脉夹层的一个易感因素。此外，据我们所知，该病例是已知的第二例红核性向外侧推挤病例。
