Posterior Spinal Column Research Articles

The use of interbody cage devices for spinal deformity: a biomechanical perspective.

Spinal instrumentation has revolutionized the treatment of spinal deformities and offers a plethora of techniques and designs to surgically treat deformity conditions. The authors address the biomechanical properties afforded by various posterior and anterior spinal instrumentation mechanisms, with and without intervertebral reconstruction, and the principles associated with optimal reconstruction techniques. The integration of multiple strategies can improve anterior and posterior construct stiffness in the treatment of spinal deformities. Structural interbody support probably is the best method to minimize longitudinal rod and screw-bone interface strain. Moreover, anterior load-bearing structural grafts and interbody devices have been shown to increase construct stiffness, decrease the incidence posterior implant failure, permit the use of smaller diameter longitudinal rods, and may enhance the rate of successful spinal arthrodesis. From a biomechanical standpoint, treatment of medium to high-grade spondylolisthesis with stand-alone interbody or transvertebral cages, in the absence of supplemental posterior fixation, is contraindicated. Collectively, the included studies reinforce the principles of load sharing between the anterior and posterior spinal columns and affirm the biomechanical dominance of anterior column support in circumferential spinal arthrodesis.

Neurotoxicity of 1-bromopropane in rats

Neurotoxicity of 1-bromopropane (1-BP) used as an alternative solvent of fluorocarbons was experimentally studied. Eight rats in the experimental group were exposed to 1-BP at 1500 ppm for six hours a day, five days a week for four weeks in an exposure chamber. Another eight rats in the control group were exposed to room air in a similar exposure chamber as those in the experimental group. During the latter half of the fourth week of exposure, all the rats in the experimental group showed a loss of body weight and ataxic gait compared with control rats. At the end of the fourth week, the rats in both groups were perfused through the ascending aorta and fixed. The cerebellum, medulla oblongata, spinal cord and peripheral nerve were processed for histopathological studies. No statistically significant difference in the frequency of axonal degeneration in both peroneal and sural nerves was found between the experimental and control groups. In the cerebellum, the frequency of degeneration of Purkinje cells in both the vermis and hemisphere was higher in the experimental group than in the control group (P < 0.05). There was no significant difference in the frequency of myelin ovoids in the fifth thoracic and in the third cervical posterior columns of the spinal cord between control and experimental groups. There was also no significant difference in the frequency of axonal swelling in the nucleus gracilis of the medulla oblongata between control and experimental groups. Ataxic gait was considered to be induced by degeneration of Purkinje cells in the cerebellum due to 1-BP exposure. However, degenerative findings of nerve fibers in the peripheral nerve, spinal posterior column and nucleus gracilis of the medulla oblongata due to 1-BP exposure were not evident. At the end of the fourth week of exposure, rats in the experimental group showed loss of body weight and markedly decreased motor activities, and it was considered that they would die if we continued the exposure into the fifth week. Therefore, we feel that our experimental schedule should be reconsidered before undertaking any further studies on the peripheral nerve toxicity of 1-BP.

Maturation of the Posterolateral Spinal Fusion and Its Effect on Load-Sharing of Spinal Instrumentation

We investigated the temporal relationship among the biomechanical, radiographic, and histological properties of a posterolateral spinal fusion mass to elucidate the changes in load-sharing of the spinal instrumentation and that of the fusion mass throughout the healing process. Destabilization of the posterior spinal column and transpedicular screw fixation at the segments between the third and fourth and the fifth and sixth lumbar vertebrae was performed in twenty-four sheep. A posterolateral spinal arthrodesis with use of autologous corticocancellous bone graft was done randomly at one of the two segments; the other segment (without bone graft) served as the instrumented control. Six animals each were killed at four, eight, twelve, and sixteen weeks postoperatively. Biomechanical testing showed that the posterolateral fusion mass had increased mechanical stiffness after the fourth week. The strain on the hardware, measured with use of rods instrumented with strain-gauges, decreased significantly (p < 0.01) beginning at eight weeks. Radiographically, three independent observations of each of the six animals at each time-period showed that, although all of the fusion masses were considered solid unions at sixteen weeks, bridging of trabecular bone was noted during only ten of eighteen observations at twelve weeks, three of eighteen observations at eight weeks, and none of eighteen observations at four weeks. Computerized tomography and histomorphometric analyses demonstrated that mineralization in the fusion mass increased in a linear fashion even after eight weeks. Histologically, the fusion mass consisted predominantly of woven bone at eight weeks; thereafter, it was gradually trabeculated. We found a great discrepancy between biomechanical stability and histological maturation of the posterolateral fusion mass. The biomechanical properties of a stable spinal fusion preceded the radiographic appearance of a solid fusion by at least eight weeks, suggesting that immature woven bone provided substantial stiffness to the fusion mass. The spinal instrumentation was subjected predominantly to bending stress rather than to axial stress, and the load-sharing of the spinal instrumentation decreased concurrently with the development of the spinal fusion.

Spinal tract degeneration confined to the bilateral posterior columns in malnutrition: Report of an autopsy case

An autopsy case of malnutrition with spinal tract degeneration confined to the bilateral posterior columns is reported. The patient had schizophrenia in adolescence, and suffered from aplastic anemia in late middle age. Subsequently, he took little food due to delusions for 18 months until his death. He had malnutrition resulting in severe hypoproteinemia. He developed gait disturbance, loss of deep tendon reflexes and paresthesia of limbs. Neuropathological examination disclosed tract degeneration confined to the bilateral spinal posterior columns, in addition to the findings of aplastic anemia and hypoxic encephalopathy in the cerebrum. The myelin and axons were severely affected throughout the spinal cord; status spongiosus with many fatty-laden macrophages was seen in these lesions. Neurons in the posterior column nuclei were intact, while the dorsal roots and their ganglia were moderately affected. The unusual distribution and extension of the degeneration of the bilateral posterior columns in the poor nutritional state is discussed.

Morphological changes in brain and spinal cord tissues following low intensity laser irradiation

The influence of laser emission on opened infact brain and spinal cord was studied in two series of 92 animals. Semiconductor laser (L = 830 nm) was used in series I, and He-Ne laser (L=630) in series II. Output power of each laser was 4 mVt. Exposure time was 3.5, 15 and 30 minutes in each series of experiment. Cerebral tissue was examined during acute period in 24 hours, 5 and 15 days after the radiation by means of conventional hystological viewing technique. The most pronounced morphological changes in the brain and the spinal cord were revealed in 24 hours after radiation by semiconductor laser with the exposure time being 30 minutes. The most were damages take place in subcortical layer of the brain and in pyramidal cells of posterior horns of the spinal cord. These changes may be classified as pyknosis and Kariorrhexis of glial cells. The manifestation of edema to the extent of kribrosis changes in the white matter catches the eye. The cerebral cortex suffers the least. At 5 days examination the changes in pyramidal cells of the spinal cord and glial cells of the brain appear less severe. The edema of cerebral tissue is still noticeable. At 15 days examination the structure of nerve cells is changed not significantly. The edema of the white matter is less pronounced. The examination of cerebral specimens in acute period and in 24 hours after He-Ne laser radiation reveals significantly less morphological changes as compared with previous series. Minimal damages of the cortex and the white matter of the brain and posterior horn neurons of the spinal cord manifest themselves in irragular granulation of cortex neurons with minimal tigrolysis in isolated cells. The edema of the white matter of the brain and the dorsal columns of the spinal cord is uncomparably less manifestated. At 5 days cortex cells of the brain and pyramidal cells of posterior columns of the spinal cord appear infact. Signs of pericellular edema are practically absent. At 15 days the hystological picture is normalized. Thus, the experimental comparison studies of two types of lasers have revealed the principal difference of their influence in the structure of nerve cells. Subcortical layer of brain glial tissue and pyramidal cells of the posterior spinal columns are the most damagable by the semiconductor laser emission. Yet these changes regress rapidly and at 15 days only the signs of regressing edema of the cerebral matters, and very light dystrophic changes in neurons in regressive phase are preserved. The most infact structure of cellular and extracellular elements of white and grey matter is preserved in case of the exposure to He-Ne laser. The changes are practically not detectable at 5 days of the experiment and at 15 days the cerebral tissue appears intact.

Neurotoxicity of methyl bromide--neuropathologic evaluation--preliminary study

Methyl bromide exposure produces disorders of the central and peripheral nervous system. In the literature, there are many neuropathologic studies on the nervous system, especially on the central nervous system, of experimental animals intoxicated with methyl bromide presented. However, in our opinion, a variety of lesions of the nervous system described in the human methyl bromide intoxication have not been well reproduced in the experimental animals. In this study, male Wistar rats were subjected to a 6-hour exposure a day to methyl bromide at a concentration of 500 or 290 ppm 3 days a week for 3 to 8 weeks. The systematic neuropathologic studies of their central and peripheral nervous systems were carried out to reproduce the nervous system lesions in the human methyl bromide intoxication hitherto not produced in the experimental animals. Among the rats exposed to methyl bromide at a concentration of 500 ppm for 10 to 18 days, the axonal degeneration of myelinated fibers at the cervical level of the fasciculus gracilis, which probably corresponds to the degeneration of the spinal posterior column in humans, and the necrosis of the caudate-putamen and atrophy of neurons and pallor of the neuropile in caudate-putamen, thalamus and cingulate cortex, which probably correspond to the degenerative findings of the cerebrum in humans, were found. The rats exposed to methyl bromide at a concentration of 290 ppm for 8 weeks (24 days) did not show any noticeable abnormalities histologically.(ABSTRACT TRUNCATED AT 250 WORDS)

An Autopsy Case of Atypical Motor Neuron Disease with Bunina Bodies in the Lower Motor and Subthalamic Neurons

We report a 37-year-old male without any family history of neurological disease who suffered progressive muscular atrophy and sensory impairment of 4 years' duration. Autopsy revealed neuronal loss in the anterior horns of the spinal cord and in the hypoglossal and facial nuclei of the brain stem. The corticospinal tracts of the spinal cord showed only mild degeneration. In addition, there were obvious degenerative lesions manifested by loss of neurons, myelin and axons in the spinal posterior columns, Clarke's column, spinocerebellar tracts and dorsal root ganglia as well as in the subthalamic nucleus, globus pallidus, substantia nigra and cerebellar dentate nucleus. Furthermore, we frequently encountered Bunina bodies not only in the lower motor neurons but also in the subthalamic neurons. We consider this case to be an atypical example of motor neuron disease with features of multisystem degeneration. The fact that Bunina bodies were observed in both lower motor and subthalamic neurons in this case suggests a common etiology of neuronal degeneration in these two different systems.

Serial somatosensory evoked potentials in a patient with familial hypobetalipoproteinemia, and vitamin E deficiency.

Serial somatosensory evoked potentials (SEPs) to median and posterior tibial nerve stimulation in a case with familial heterozygous hypobetalipoproteinemia and vitamin E deficiency were investigated over a period of 4 years. In serial SEPs to posterior tibial nerve stimulation, interpeak latencies between N20 and P2 were delayed even in the early clinical stage, although the peak latency of N20 was normal. N20 latency was delayed when the patient noted paresthesia of the lower extremities. Interpeak latencies between N20 and P2 were progressively prolonged, and finally both peaks disappeared. Progressive dysfunctions of spinal posterior columns and peripheral somatosensory pathways were discovered by serial SEP studies.

A biomechanical evaluation of cervical spinal stabilization methods in a bovine model. Static and cyclical loading.

A bovine model was developed for biomechanical evaluation of surgical procedures stabilizing traumatic cervical injuries disrupting the anterior and posterior spinal column. Cervical spinal segments and C4-5 functional spinal units were tested statically, and C4-5 functional spinal units were tested cyclically in evaluation of 1) the intact cervical spine, 2) Rogers' wiring method, 3) Bohlman's triple-wire technique, 4) sublaminar wiring, 5) anterior cervical plate instrumentation, and 6) posterior hook plate stabilization. Anterior cervical plate instrumentation proved inadequate, and was the least rigid, with axial and flexural loading (P less than 0.05). There was no significant difference between each of the three posterior wiring methods, and all generally restored stability to equal that of the uninjured intact cervical spine. Posterior hook plating with an interspinous bone graft serving as an extension block was the most effective method in reducing flexural stress across the injured C4-5 segment (P less than 0.05). Cyclical in vitro testing was the most sensitive method in highlighting mechanical differences between instrumentation systems, particularly with "on-line" continuous measurement of anterior and posterior strains. Anterior cervical plate stabilization does not appear to confer enough stability in cervical facet injuries to obviate the need for posterior cervical stabilization procedures. The recently developed posterior hook plate technique offers biomechanical advantages that should be weighed against the greater technical precision needed for insertion and the increased potential for neurologic and vascular complications.

Transverse Myelitis Associated with &lt;i&gt;Mycoplasma pneumoniae &lt;/i&gt;Infections

43-year-old man developed transverse myelitis following an infection with Mycoplasma pneumoniae. Among the uncommon neurological complications following infection with this organism, transverse myelitis has been reported rarely but may be more frequent than previously thought. Posterior spinal column involvement might result in a permanent neurological deficit despite the usually good prognosis.

Experimental myelo-optic neuropathy induced by clioquinol.

To elucidate the neurotoxicity of clioquinol, 20 mongrels, 8 beagles, 27 cats and a Japanese monkey were given clioquinol orally for a long period. 12 mongrels, 7 beagles and 6 cats manifested neurologic signs clinically which began with side-swaying of the hips and ataxic gait followed by muscle weakness and increased tendon-jerks in the hindlegs. The longer the period of administration, the more severe the signs became. Visual acuity was also impaired in long surviving animals. Autopsy of these severely affected animals revealed marked degenerative changes in the distal portions of nerve fibres in the posterior spinal column and optic tract predominantly. The changes involved axons first, then demyelination and later these foci were replaced by fat granules and glial cells. Spinal root ganglia and peripheral nerves were also affected. Postmortem examination of the animals with none or minimal clinical manifestations showed, nevertheless, mild pathological changes in the same portions as above mentioned. The myelo-optic neuropathy seen in these animals is well in accord with the changes observed in “subacute myelo-optic neuropathy” (SMON) in humans. There are, however, differences in strains as well as species of animals for the neurotoxicity of clioquinol.