Yoshihiko Kato

Biomechanical study of cervical flexion myelopathy using a three-dimensional finite element method

OBJECT The goal of this study was to perform a biomechanical study of cervical flexion myelopathy (CFM) using a finite element method. METHODS A 3D finite element model of the spinal cord was established consisting of gray matter, white matter, and pia mater. After the application of semi-static compression, the model underwent anterior flexion to simulate CFM. The flexion angles used were 5 degrees and 10 degrees , and stress distributions inside the spinal cord were then evaluated. RESULTS Stresses on the spinal cord were very low under semi-static compression but increased after 5 degrees of flexion was applied. Stresses were concentrated in the gray matter, especially the anterior and posterior horns. The stresses became much higher after application of 10 degrees of flexion and were observed in the gray matter, posterior funiculus, and a portion of the lateral funiculus. CONCLUSIONS The 5 degrees model was considered to represent the mild type of CFM. This type corresponds to the cases described in the original report by Hirayama and colleagues. The main symptom of this type of CFM is muscle atrophy and weakness caused by the lesion of the anterior horn. The 10 degrees model was considered to represent a severe type of CFM and was associated with lesions in the posterior fand lateral funiculi. This type of CFM corresponds to the more recently reported clinical cases with combined long tract signs and sensory disturbance.

Investigation of motor dominant C5 paralysis after laminoplasty from the results of evoked spinal cord responses.

Background Postoperative motor dominant C5 paralysis was known as one of several complications after laminoplasty. Several theories have been proposed for postoperative segmental paralysis after laminoplasty, but its etiology remains unclear. Objective To investigate the possible mechanism for postoperative motor dominant C5 paralysis from intraoperative electrophysiological studies using evoked spinal cord potentials (ESCPs). Methods A total of 66 patients who had undergone laminoplasty due to compressive cervical myelopathy were studied retrospectively. In all patients, the symptomatic intervertebral levels of cervical myelopathy were identified by several types of the ESCPs. Motor dominant C5 paralysis was determined as at least 1 level down compared with pre-operative shoulder abduction according to the manual muscle testing. Results Five patients (7.6%) showed postoperative motor dominant C5 paralysis. C5 paralysis occurred from 1 to 3 days after surgery and compromised unilaterally in all 5 patients. The causes of cervical myelopathy were cervical spondylosis in 3 patients and ossification of the posterior longitudinal ligament in 2 patients. One patient with severe impairment (2 in manual muscle-testing [MMT] scale) did not show clinical recovery. The other 4 patients recovered to 4 or 5 on the MMT score from 3 to 6 months after the onset. Based on the findings of ESCPs, the C4-5 level was affected by cervical myelopathy in all 5 patients with postoperative motor dominant C5 paralysis (C4-5 level in 3 patients, both C4-5 and C5-6 levels in 2 patients). A high signal intensity area on T2-weighted magnetic resonance imaging (MRI) was observed in all patients who showed apparent motor dominant C5 paralysis in this study. Conclusions Cervical myelopathy at the C4-5 level is a potential risk for motor dominant C5 paralysis. Although it is merely a speculation, when C5 radiculopathy occurs after laminoplasty, C5 paralysis becomes clinically apparent because the deltoid muscle gets predominantly innervated by C5 root due to intramedullary spinal cord damage on the C6 segment in C4-5 myelopathy before surgery. It may represent the high signal intensity area on T2-weighted MRI at the C4-5 level.

A study of stiffness protocol as exemplified by testing of a burst fracture model in sagittal plane.

Study Design. An in vitro biomechanical study of lumbar spine segments. Objective. To study the characteristics of the stiffness test protocol. Summary of Background Data. In an in vitro study using a flexibility protocol, forces are applied and motions are measured; no center of rotation needs to be specified. In a study using a stiffness protocol, the forces are measured and the motions are applied. This does require the center of rotation to be specified. Many biomechanical studies of the spine are available, but there is lack of clarity concerning which of these two test protocols is appropriate to achieve a certain study goal. Methods. Five-vertebrae lumbar spine specimens with burst fractures in the middle vertebrae (L1) were used. Specially designed apparatus applied flexion and extension rotations around five centers of rotations located on anteroposterior line through the middle of L1. Maximum moment of 4 Nm was applied. Results. The authors found load-displacement curves, ranges of motion, and neutral zones obtained at the five centers of rotations to be markedly different. The center of rotation located at the posterior longitudinal ligament produced large range of motion and neutral zones in comparison to the centers of rotation located at the anterior longitudinal ligament and the spinous process tip (P < 0.01). Conclusions. The stiffness protocol requires that a center of rotation be specified. Shown here is the significant variability in the load-displacement curves, depending on the choice of the location of the center of rotation. Certain center of rotation locations may block the natural motions of the spine and may result in tissue damage.

Biomechanical study of the effect of degree of static compression of the spinal cord in ossification of the posterior longitudinal ligament.

OBJECT The authors evaluated the biomechanical effect of 3 different degrees of static compression in a model of the spinal cord in order to investigate the effect of cord compression in patients with ossification of the posterior longitudinal ligament (OPLL). METHODS A 3D finite element spinal cord model consisting of gray matter, white matter, and pia mater was established. As a simulation of OPLL-induced compression, a rigid plate compressed the anterior surface of the cord. The degrees of compression were 10, 20, and 40% of the anteroposterior (AP) diameter of the cord. The cord was supported from behind by the rigid body along its the posterior border, simulating the lamina. Stress distributions inside of the cord were evaluated. RESULTS The stresses on the cord were very low under 10% compression. At 20% compression, the stresses on the cord increased very slightly. At 40% compression, the stresses on the cord became much higher than with 20% compression, and high stress distributions were observed in gray matter and the lateral and posterior funiculus. The stresses on the compressed layers were much higher than those on the uncompressed layer. CONCLUSIONS The stress distributions at 10 and 20% compression of the AP diameter of the spinal cord were very low. The stress distribution at 40% compression was much higher. The authors conclude that a critical point may exist between 20 and 40% compression of the AP diameter of the cord such that when the degree of the compression exceeds this point, the stress distribution becomes much higher, and that this may contribute to myelopathy.

Etiology of cervical myelopathy induced by ossification of the posterior longitudinal ligament: determining the responsible level of OPLL myelopathy by correlating static compression and dynamic factors.

Study Design Retrospective study. Objective To determine the responsible level of cervical myelopathy induced by ossification of the posterior longitudinal ligament (OPLL). This was achieved by correlating the intervertebral range of motion (ROM) as the dynamic factor with the space available for spinal cord (SAC) as the static compression factor. Summary of Background Data The association between spinal canal stenosis and the occurrence of the myelopathy has previously been reported for OPLL patients, but not the detailed relationship between SAC, ROM, and myelopathy. Methods We investigated OPLL type, SAC, and ROM in relation to the responsible level of cervical OPLL myelopathy in 27 cases. SAC and ROM were measured at each vertebral and intervertebral levels. The responsible level was diagnosed using spinal cord-evoked potentials and classified as group A, whereas the nonresponsible level was classified as group B. Results Spinal cord-evoked potentials revealed 21 cases with a single responsible level and 6 cases with 2 responsible levels. The mean ROM of group A (8.9 degrees) was significantly higher (P<0.01) than that of group B (5.7 degrees). The mean SAC of group A (8.2 mm) was significantly lower (P<0.01) than that of group B (12.4 mm). Using discriminate analysis, significant differences for both SAC and ROM were observed between groups A and B [Boxs M test: χ2=3.31 <χ23 (0.05)]. The discriminate formula for the borderline of symptomatic spinal compression can be described as: Z=−0.21ROM+0.47SAC−2.76. Conclusions Cervical OPLL myelopathy is induced by static factors, dynamic factors, or a combination of both. The discriminate formula for symptomatic cervical OPLL myelopathy contains both ROM and SAC.

Use of the finite element method to study the mechanism of spinal cord injury without radiological abnormality in the cervical spine.

Study Design. Three-dimensional C3–C5 and C3–C4 finite element (FE) models were used to analyze biomechanical responses under compression and extension moments. Objective. To validate our models against other published FE models and experimental studies and improve our understanding of the mechanism of spinal cord injury without radiologic abnormality (SCIWORA) in cervical spine. Summary of Background Data. The underlying mechanism for SCIWORA remains unclear. We hypothesized that the incidence of SCIWORA was associated with facet joint morphology and bony pincers mechanism. Methods. FE models were constructed using data from computed tomography scans of the cervical spine of a healthy young man. The C3–C5 FE models consisted of bony vertebra, articulating facets, and intervertebral disc. Facet surfaces were oriented at 30°, 45°, and 60° from the transverse plane. These models were constrained in all degrees of freedom at the C5 inferior vertebral body and a uniform axial displacement of 1 mm was applied to the superior nodes of C3. Three model versions changed to C3–C4 models with ligaments. The C4 inferior-most bony nodes were constrained, whereas the top of the C3 superior-most bony nodes were left unconstrained. These models were subjected to an axial compression load of 73.6 N with extension moments (1.8 Nm) applied to the upper bony section C3 vertebra. The predicted responses were compared with published results. Results. The response under axial compression was validated and corresponded closely with published results. Under sagittal moment, the C3–C4 FE model with 60° facet was the most flexible in extension (4.22°). Total translation was highest for the model with 60° facet. Conclusion. The load displacement response of C3–C5 FE models was in agreement with published data. We confirmed that the C3–C4 FE model with 60° facet was the most susceptible to SCIWORA and that the bony pincers mechanism was dependent on facet joint inclination.

Warfarin-induced impairment of cortical bone material quality and compensatory adaptation of cortical bone structure to mechanical stimuli.

Long-term warfarin use has been reported to increase fracture risk of rib and vertebra but not hip in elderly patients, but the mechanisms remain unknown. We hypothesized that warfarin would impair bone material quality but could not weaken bone strength under conditions with higher mechanical stimuli. To test this hypothesis, rats were randomized to vehicle or warfarin group at 4 weeks of age and subsequently weight matched into a sedentary or jumping exercise group at 12 weeks of age. At 6 months of age, osteocalcin content, bone mineral density (BMD), mineral size, material properties, morphological parameters, and biomechanical properties of cortical bones were evaluated. In order to seek evidence for a common mechanism of action, effects of nucleation rate of mineral crystals on their rigidity were also investigated using computer simulation. In humeral cortical bones, warfarin did not change BMD, but markedly decreased osteocalcin content, diminished mineral size, and impaired material hardness. Consistent with these results, our computer-simulation model showed that osteocalcin-induced delay of mineral crystal nucleation decreased mineral formation rate, increased mean and distribution of mineral sizes, and strengthened mineral rigidity. In tibial cortical bones, warfarin decreased material ultimate stress; however, under jumping exercise, warfarin increased cross-sectional total and bone areas of these tibiae and completely maintained their biomechanical properties including work to failure. Collectively, our findings suggest that long-term warfarin therapy weakens rib and vertebra by impairing cortical bone material quality due to a marked decrease in osteocalcin content but could not reduce hip strength through compensatory adaptation of cortical bone structure to higher mechanical stimuli.

Distal-type cervical spondylotic amyotrophy: assessment of pathophysiology from radiological findings on magnetic resonance imaging and epidurally recorded spinal cord responses.

Study Design. Six cases with distal-type cervical spondylotic amyotrophy are reported. Objective. To investigate the pathophysiology of distal-type cervical spondylotic amyotrophy from magnetic resonance imaging and intraoperative evoked spinal cord responses. Summary of Background Data. Cervical spondylotic amyotrophy had a characteristic clinical symptom of severe muscular atrophy with no or insignificant sensory deficit. Selective ventral root lesions or intrinsic spinal cord lesions have been proposed as the pathophysiology of cervical spondylotic amyotrophy, but they have not been well understood. Method. Six patients with distal-type cervical spondylotic amyotrophy were described, and their magnetic resonance imaging and evoked spinal cord potentials after median nerve, motor cortex, and spinal cord stimulation were investigated. Results. Sagittal T2-weighted magnetic resonance imaging showed high signal intensity change within the spinal cord at C4–C5, C5–C6, and C6–C7. All patients underwent laminoplasty. The attenuation of postsynaptic potentials with preserved presynaptic potentials at C4–C5, C5–C6, and C6–C7 was characteristic in the evoked spinal cord potentials after median nerve stimulation. The amplitude of the evoked spinal cord potentials after median nerve stimulation was preserved at C2–C3. This means that lateral posterior column in the spinal cord had less or no involvement in distal-type cervical spondylotic amyotrophy. Concomitant hyperactivity of the patellar tendon reflex was correlated with the abnormality in the evoked spinal cord potentials after transcranial electric stimulation. Conclusions. The results suggest a longitudinal gray matter lesion as one pathophysiologic feature, and that less damage to the lateral posterior column is the reason for the preservation of sensory function in the patients with distal-type cervical spondylotic amyotrophy described in this study.

Biomechanical study of the spinal cord in thoracic ossification of the posterior longitudinal ligament.

Abstract Background Ossification of the posterior longitudinal ligament (OPLL) in the thoracic spine produces myelopathy. This is often progressive and is not affected by conservative treatment. Therefore, decompressive surgery is usually chosen. Objective To conduct a stress analysis of the thoracic OPLL. Methods The three-dimensional finite element spinal cord model was established. We used local ossification angle (LOA) for the degree of compression of spinal cord. LOA was the medial angle at the intersection between a line from the superior posterior margin at the cranial vertebral body of maximum OPLL to the top of OPLL with beak type, and a line from the lower posterior margin at the caudal vertebral body of the maximum OPLL to the top of OPLL with beak type. LOA 20°, LOA 25°, and LOA 30° compression was applied to the spinal cord in a preoperative model, the posterior decompressive model, and a model for the development of kyphosis. Results In a preoperative model, at more than LOA 20° compression, high stress distributions in the spinal cord were observed. In a posterior decompressive model, the stresses were lower than in the preoperative model. In the model for development of kyphosis, high-stress distributions were observed in the spinal cord at more than LOA 20° compression. Conclusions Posterior decompression was an effective operative method. However, when the preoperative LOA is more than 20°, it is very likely that symptoms will worsen. If operation is performed at greater than LOA 20°, then correction of kyphosis by fixation of instruments or by forward decompression should be considered.

Flexion Model Simulating Spinal Cord Injury Without Radiographic Abnormality in Patients With Ossification of the Longitudinal Ligament: The Influence of Flexion Speed on the Cervical Spine

Abstract Background/Objective: It is suspected that the speed of the motion of the spinal cord under static compression may be the cause of spinal cord injury (SCI). However, little is known about the relationship between the speed of the motion of the spinal cord and its stress distributions. The objective was to carry out a biomechanical study of SCI in patients with ossification of the longitudinal ligament without radiologic evidence of injury. Methods: A 3-dimensional finite element spinal cord model was established. After the application of static compression, the model underwent anterior flexion to simulate SCI in ossification of the longitudinal ligament patients without radiologic abnormality. Flexion of the spine was assumed to occur at 1 motor segment. Flexion angle was 5°, and flexion speeds were 0.5°/s, 5°/s, and 50°/s. Stress distributions inside of the spinal cord were evaluated. Results: Stresses on the spinal cord increased slightly after the application of 5° of flexion at a speed of 0.5°/s. Stresses became much higher at a speed of 5°/s and increased further at 50°s. Conclusions: The stress distribution of the spinal cord under static compression increased with faster flexion speed of the spinal cord. High-speed motion of the spinal cord under static compression may be one of the causes of SCI in the absence of radiologic abnormality.