Surgical treatment of spinal disorder in patients with Parkinson’s disease is often problematic because of its high risk of instrument-related complications and revision surgery [1–3]. Babat et al. reported that revision surgery was required in 12 of 14 of their cases of spine surgery complicated by Parkinson’s disease and concluded that the increased risk is caused by persistent kyphosis or instability at the operated or adjacent vertebral levels . Several reports have also described that patients with Parkinson’s disease frequently have poor bone quality, suggesting increased risk of fractures [11, 12]. Despite the higher risk of spinal fracture, there are only a few reports describing the details of surgical results of spinal fracture repair in patients with Parkinson’s disease. In one of the 14 cases reported by Babat et al., a case of L1 osteoporotic burst fracture treated by T11-L2 segmental instrumented fusion was described. Unfortunately, this case required revision surgery because of hook and screw pullout . Nakashima et al. reported three cases of osteoporotic vertebral fracture complicated by Parkinson’s disease, all of which showed significant deterioration of sagittal alignment due to postoperative compression fracture or sinking of the fusion cage, suggesting the difficulty of maintaining sagittal alignment even with posteroanterior surgery .
As previously stated, patients with ankylosed spine are prone to spinal fracture, and delay in diagnosis often occurs because of the difficulty of initial diagnosis. Westerveld et al. reported that, of 28 patients with thoracolumbar fracture in patients with ankylosed spine, 27 were the result of hyperextension injury . Our patient had no history of trauma, and showed minimum displacement of fractured site at the first presentation. Ankylosed spine had not been diagnosed before the injury, because kyphosis and spinal rigidity had been thought to be symptoms due to Parkinson’s disease. In such conditions, early diagnosis of spinal fracture in ankylosed spine seemed to be relatively difficult. As reviewed by Heyde et al., beause of pathological tension and shearing force with lacking flexibility due to kyphosis and spinal rigidity, spinal fracture may occur even after minor trauma in ankylosed spine . Secondery osteoporosis and loss of muscle strength also cause the fragility of the spine . Therefore, in severely ankylosed spine, spinal fracture may occur without history of trauma [14, 15]. It has been suggested that neurological deficit is due not only to the initial injury, but also to secondary neurological deterioration [9, 16]. Because delayed diagnosis of spinal fractures in ankylosed spine often leads to secondary neurological deterioration, clinicians must be cautious not to misdiagnose at first examination even patients have no history of trauma.
Regrettably, the clinical outcome for patients fracturing their ankylosed spine is worse compared to the general spine trauma population, particularly when treated conservatively . Three-column fractures are common in the ankylosed spine and surgical treatment is required in such cases [7–9]. Although Caron et al. reported that 14% of surgically treated patients required revision surgery, no patients required revision surgery when treated by multilevel posterior segmental fixation with at least three bilateral points of fixation above and below the injury . From these observations, long-segment spinal fusion is generally recommended to treat thoracolumbar fracture in the severely ankylosed spine.
Because our patient had a severely ankylosed spine, fusion surgery was performed at levels 3-below and 3-above the fracture level. The patient also had Parkinson’s disease, suggestive of a poor surgical outcome. However, we experienced excellent surgical results with no complications at the two-year follow-up. Because the surgically treated segments had been completely ankylosed before the fracture, it is possible that the excellent results in our case arose from the fact that fusion surgery did not change the number of fused segments. Consequently, the postoperative risk of adjacent segment disease did not increase after fusion surgery in our patient. In addition, the surgically treated levels were completely ankylosed, thus, no stress force existed between adjacent vertebral bodies, except at the fracture site. This fact indicates a decreased risk of pedicle screw breakage or pullout, even though the patient had Parkinson’s disease. A total of six pedicle screws were inserted into the ankylosed vertebral bodies, on cranial and caudal segments respectively, providing more rigidity of pedicle screw fixation. While an ankylosed spine is usually unfavorable for treating patients with spinal fracture, it seems possible that ankylosis around the fracture site may prove advantageous for patients with Parkinson’s disease.
Although our patient had Parkinson’s disease and an ankylosed spine, both of which increase the risk of poor surgical outcomes after spinal surgery, the results for this patient were excellent, suggesting that spinal fracture in an ankylosed spinal segment is a less adverse condition for patients with Parkinson’s disease when treated with long-segment spinal fusion.
To date, there was no previous report describing thoracic spine fracture in a patient with severely ankylosed spine complicated by Parkinson’s disease. However, our experience led us to think that a combination of Parkinson’s disease with severely ankylosed spine does not necessarily suggest unsatisfactory outcomes after surgical treatment of spinal fracture.