ABSTRACT
STUDY DESIGN: A case is reported in which a flexion-induced compression of the upper cervical spinal cord caused symptoms of brainstem compromise in the absence of radiographic evidence of osseous instability. OBJECTIVES: A 41-year-old woman developed postoperative cervical instability with flexion-induced neurologic symptoms referable to the brainstem. The instability was caused by direct compression at the third cervical vertebral body, which in turn was caused by differential movements between the neuraxis and skeletal elements in the upper cervical spine. SUMMARY OF BACKGROUND DATA: Pathologic processes at the craniocervical junction may cause brainstem compromise with neurologic symptoms. The mechanism of brainstem involvement is usually either vertebrobasilar insufficiency or direct mechanical compression. In cases where the brainstem is compressed by skeletal elements, the compressing osseous structures usually are the walls of the foramen magnum or the odontoid process, or, less frequently, the atlas or axis vertebrae. Symptoms of brainstem dysfunction caused by dynamic compression at the level of the third cervical vertebra in the absence of hindbrain herniation are unusual and, to the best of the authors' knowledge, have not been described previously. METHODS: The patient underwent initial examination, evaluation, and periodic follow-up examination with magnetic resonance imaging from the time of her first visit until 26 months after the surgical treatment. The patient experienced postsurgical instability with dynamic compression by the C3 vertebral body, which caused brainstem compromise. Surgical treatment consisted of decompressive C3 corpectomy and fusion of C2 to C6, supplemented by anterior fixation. RESULTS: After undergoing surgical decompression of C3, reconstruction, and anterior internal fixation of C2 to C6, the patient had dramatic neurologic improvement. Diplopia, paresthesia, and nystagmus disappeared immediately after surgery. Swallowing difficulties, hoarseness, and vertigo improved gradually. At follow-up examination 26 months after surgery, the patient was asymptomatic. Magnetic resonance imaging showed good position of the construct, with no evidence of compression of the spinal cord or brainstem. CONCLUSIONS: Instability of the cervical spine may result in symptoms of brainstem dysfunction, even in the absence of hindbrain herniation. This instability is explained by the differential movement between the bony structures and neuraxis in the upper cervical region. Diagnosis and adequate management of this instability alleviates the neurologic symptoms and prevents possible hazardous complications.
