Neurologic dysfunction or iatrogenic neurologic deficits after lumbar spine surgery are arguably the most severe complications of spinal surgery. They may result in neurological symptoms, such as radiculopathy, lower extremity weaknesses, postoperative neuropathic pains or even short-term, permanent damage to the nervous system. Delamarter et al  demonstrated in a study on dogs that when compressions to the spinal cord last for six hours, there is no neurological recovery and progressive spinal cord necrosis. Other studies indicate that if patients with an acute spinal cord compression have had surgical decompressions within eight hours, their nerurological functions will make good or partial recovery [5, 6]. A timely diagnosis and urgent management of neurologic complications are very important when helping patients recover from neurological deficits after lumbar spine surgeries. CT scans and MRIs are mainstream examinations that help in the diagnosis of neurological deficits.
Neurological deficits after lumber spine surgeries are rare complications and their occurrence rate varies widely in different studies. There are also patient variables, including age, general level of health, and previous surgical procedures/lumber fusions. Kamerlink et al  found that hyperkyphotic patients undergoing anteroposterior deformity corrections were at a relatively higher risk of postoperative neurological deficits. This is due to a disruption of blood flow to the thoracic spinal cord through segmented arterial feeders from the aorta. Carreon et al demonstrated in a retrospective study that the occurrence rate of perioperative neurological deficits was 2% (2/98) after posterior lumbar decompression and arthrodesis in older adults (≥ 65 years of age). Daubs et al found in another retrospective study that the rate of neurologic deficits in patients ≥ 60 years of age who underwent major spinal deformity surgeries and required a minimum level-5 arthrodesis procedure was 8.7% (4/46). Another study by Bydon et al into 500 lumber discectomies found a 2.61% rate of postoperative weakness. A recent meta-analysis study by Ghobrial et al  showed that 37 out of 2,052 (1.9%) patients had a neurologic injury after posterior decompressions and fusions. Disparities between these studies are as to be expected, due to statistical and operative factors, variations on the definitions of postoperative neurological deficits, inclusion and exclusion criteria, surgical complexities and the number of levels instrumented. In this study, we found that the incidence rate of lower extremity weaknesses was 0.74%(30/4078)after posterior lumber spine fusion surgeries. The exclusion criterion for the present study was where there were cases of symptoms easing after neurological deficits, due to traditional methods of treatment. We should be aware, of course, that there is a greater rate of morbidity where there are neurological deficit complications.
Our study demonstrated that the malposition or loosening of fixations was one of the most common causes of weakness after spinal fusion surgery. Ghobrial et al  showed that in a study of 37 patients suffering neurological injury after spinal fusion surgery, a malposition of screws resulted in 11 injuries and 9 patients were affected by the placement of instrumentation [11–14]. Lee at al  reported in his study that CT scans detected a rate of screw malposition as 3.9%. Numerous studies show that the use of image-guided technologies to identify pedicle screw placements could significantly decrease the pedicle breach rate during a procedure [16, 17]. Neuromonitoring and SSEPs enable the earlier detection of potential injuries and significantly limit neurological deficits .
Our study found that epidural hematomas were one of the most common causes of weaknesses. In addition, the weaknesses caused by epidural hematomas occurred within the shortest average time after surgery: 1.4 days. There should be a considerable diagnosis for acute epidural hematomas if neurological deficits are found shortly after surgery. Kou et al found that patients requiring multilevel lumbar procedures, especially those with preoperative coagulopathy, were at a significantly higher risk of developing a postoperative epidural hematoma. In our study, one patient underwent L3-S1 fusion procedures and suffered a preoperative congenital deficiency of coagulation factor XIII. Lower extremity motor weaknesses occurred the day after surgery and an acute epidural hematoma was found on an MRI.
Other minor causes of lower extremity weaknesses after spinal fusion surgery were insufficient decompressions during surgery, and nerve root edemas. In our study, we found three patients with unilateral lower extremity symptoms prior to surgery. Decompression procedures were performed, but patients complained of motor weaknesses on the other side of the lower extremity. They had had no symptoms before the fusion surgery. The reason for this is still unknown. A possible reason is that there has been a relative shift of the vertebrae due to internal instrumentation during surgery. This may have resulted in the stimulation and/or compression of nerve roots. In addition, tractions of never roots during surgery and a congestive reaction after surgery can lead to an edema of nerve roots, thus results in radiculopathy, neuropathic pain and motor weakness. Several studies demonstrated that steroid administration could modify the edema and the inflammatory response of nerve roots in patients, without increased incidence of postoperative infection or suture failures [18, 19]. In our surgical center, an intravenous infusion of methylprednisolone was routine after lumber decompressions and fusion surgeries. We found that only five patients needed secondary surgery because of a post-operative nerve root edema.
There are several limitations in this study. First, the study was retrospective. Secondly, patients were collected from a single institute and the number of patients was relatively small because of the low number of neurological complications after spinal surgery. To resolve these limitations, a prospective multi-institutional study is suggested.