OBJECT: The authors describe 4 cases of delayed dural laceration by hydroxyapatite (HA) spacer causing tetra-paresis following double-door laminoplasty. There are few reports of iatrogenic spinal cord lesions developing after double-door laminoplasty, although some complications such as postoperative C-5 paralysis or axial symptoms have been reported. The purpose of this report is to draw attention to the possibility of delayed dural laceration and its triggering mechanism. METHODS: One hundred thirty patients treated for cervical myelopathy were followed up for an average of 2 years and 9 months after laminoplasty. RESULTS: Four patients experienced aggravation of cervical myelopathy. Anterior dislodgement of HA spacers was shown on plain lateral radiographs. Follow-up T2-weighted magnetic resonance imaging demonstrated that the dislodged HA spacers were surrounded by cerebrospinal fluid at the time of aggravation. The dislodged HA spacers were removed and the dural membrane defects were repaired by patching with the fascia of the gluteus maximus muscle. The preoperative symptoms improved after the second operation in all patients. CONCLUSIONS: It is hypothesized that the loosening of the HA spacer in split spinous processes could occur with the movement of the cervical spine and/or the breakage of the suture before bone bonding. Anterior dislodgement of the HA spacer toward the spinal canal would cause dural laceration by direct friction between the dural membrane and the dislodged HA spacer, resulting in clinical aggravation. Despite the well-documented advantages of using HA spacers for double-door laminoplasty, possible laceration due to a dislodged HA spacer should be considered as a late complication.
OBJECT: The authors describe 4 cases of delayed dural laceration by hydroxyapatite (HA) spacer causing tetra-paresis following double-door laminoplasty. There are few reports of iatrogenic spinal cord lesions developing after double-door laminoplasty, although some complications such as postoperative C-5 paralysis or axial symptoms have been reported. The purpose of this report is to draw attention to the possibility of delayed dural laceration and its triggering mechanism. METHODS: One hundred thirty patients treated for cervical myelopathy were followed up for an average of 2 years and 9 months after laminoplasty. RESULTS: Four patients experienced aggravation of cervical myelopathy. Anterior dislodgement of HA spacers was shown on plain lateral radiographs. Follow-up T2-weighted magnetic resonance imaging demonstrated that the dislodged HA spacers were surrounded by cerebrospinal fluid at the time of aggravation. The dislodged HA spacers were removed and the dural membrane defects were repaired by patching with the fascia of the gluteus maximus muscle. The preoperative symptoms improved after the second operation in all patients. CONCLUSIONS: It is hypothesized that the loosening of the HA spacer in split spinous processes could occur with the movement of the cervical spine and/or the breakage of the suture before bone bonding. Anterior dislodgement of the HA spacer toward the spinal canal would cause dural laceration by direct friction between the dural membrane and the dislodged HA spacer, resulting in clinical aggravation. Despite the well-documented advantages of using HA spacers for double-door laminoplasty, possible laceration due to a dislodged HA spacer should be considered as a late complication.