Development Of Spinal Deformity Research Articles

Dietary fatty acids and inflammation in the vertebral column of Atlantic salmon, Salmo salar L., smolts: a possible link to spinal deformities

Vegetable oils (Vo) are an alternative to fish oil (Fo) in aquaculture feeds. This study aimed to evaluate the effect of dietary soybean oil (Vo diet), rich in linoleic acid, and of dietary fish oil (Fo diet) on the development of spinal deformities under bacterial lipopolysaccharide (LPS)-induced chronic inflammation conditions in Atlantic salmon, Salmo salar L. Fish [25 g body weight (BW)] were fed the experimental diets for 99 days. On day 47 of feeding (40 g BW), fish were subjected to four experimental regimes: (i) intramuscular injections with LPS, (ii) sham-injected phosphate-buffered saline (PBS), (iii) intraperitoneally injected commercial oil adjuvant vaccine, or (iv) no treatment. The fish continued under a common feeding regime in sea water for 165 more days. Body weight was temporarily higher in the Vo group than in the Fo group prior to immunization and was also affected by the type of immunization. At the end of the trial, no differences were seen between the dietary groups. The overall prevalence of spinal deformities was approximately 14% at the end of the experiment. The Vo diet affected vertebral shape but did not induce spinal deformities. In groups injected with LPS and PBS, spinal deformities ranged between 21% and 38%, diet independent. Deformed vertebrae were located at or in proximity to the injection point. Assessment of inflammatory markers revealed high levels of plasma prostaglandin E₂ (PGE₂) in the Vo-fed and LPS-injected groups, suggesting an inflammatory response to LPS. Cyclooxigenase 2 (COX-2) mRNA expression in bone was higher in fish fed Fo compared to Vo-fed fish. Gene expression of immunoglobulin M (IgM) was up-regulated in bone of all LPS-injected groups irrespective of dietary oil. In conclusion, the study suggests that Vo is not a risk factor for the development of inflammation-related spinal deformities. At the same time, we found evidence that localized injection-related processes could trigger the development of vertebral body malformations.

Spinal Deformity in Patients With DiGeorge Syndrome

Retrospective review of a case series. To present the clinical characteristics and treatment of spinal deformity in DiGeorge syndrome. There are no data on the development of spinal deformity in this condition. A high rate of wound infection could be expected after spinal surgery due to congenital thymic hypoplasia. The medical records and spinal radiographs of 4 consecutive patients were reviewed. All patients were followed for a minimum of 2.5 years after spinal surgery. The mean age at diagnosis of spinal deformity was 9.9 years. The type of deformity was not uniform but the curves progressed in all patients requiring a spinal arthrodesis at a mean age of 16.1 years. Two patients developed a thoracolumbar scoliosis and underwent an anterior spinal arthrodesis with instrumentation, which produced a good outcome. The remaining 2 patients developed a double thoracic and lumbar scoliosis with increased thoracic kyphosis. Brace treatment was unsuccessful to control the deformity in one of these patients. Both patients underwent a posterior spinal arthrodesis with segmental instrumentation, which achieved satisfactory correction of the scoliosis with no loss of correction or detected pseudarthrosis at follow-up. However, both patients developed junctional kyphosis above the proximal end of the instrumentation. This was asymptomatic and nonprogressive; therefore, cephalad extension of the fusion was not required. Irradiated blood products were administered in all patients to prevent graft-versus-host disease. The postoperative course was uncomplicated and none of the patients developed wound healing problems or infections. The development of spinal deformity in patients with DiGeorge syndrome may be associated to the presence of marked ligamentous laxity and congenital cardiac disease. There is significant variability on the pattern of spinal deformity, which in our series was progressive in all patients and required surgical correction with no perioperative complications.

Morphometric Analysis of Neurocentral Synchondrosis Using Magnetic Resonance Imaging in the Normal Skeletally Immature Spine

Morphometric analysis of the neurocentral synchondrosis (NCS) using magnetic resonance imaging in the normal infantile and juvenile patients. To assess the developmental stages of the neurocentral synchondrosis (NCS) by determining the age at which closure of the NCS occurs at specific levels of the spine and to evaluate whether symmetric growth of the NCS occurs during the different developmental stages in normal immature spine. The function and developmental stage of the NCS are controversial because of a lack of agreement on the exact age of closure. To date, most authors believe that the NCS is actively open at a very early age, but the reported age of closure of the NCS varies from age 3 to 16 years. This various closure age of the NCS has resulted in some confusion about the role of the NCS in the normal spinal growth or the development of spinal deformity. A total of 34 normal pediatric patients who had axial magnetic resonance images from first thoracic vertebra to fifth lumbar vertebra were assigned into following 3 groups: infantile group (n = 11), 0 to 3 years of age; juvenile-young group (n = 16), 4 to 7 years of age; and juvenile-old group (n = 7), 8 to 10 years of age. T2-weighted axial magnetic resonance images were used to analyze the NCS developmental stages using a custom 6-point scale (0: actively open with 0% closure; 5: 100% NCS closure). For the stage 0 closure NCS, the width and thickness of the NCS were measured. The NCS was actively open without closure for all less than 4-year-old patients at all levels. The NCS had approximate 75% closure in the lumbar region at 4 years of age while the thoracic NCS remained nearly open. After 5 years of age, the middle-lower thoracic NCS began to close with closure rate less than 25%. At the 10 years of age, the NCS in the lumbar region had near 100% closure, whereas the thoracic NCS demonstrated approximate 50% closure. For the NCS without closure, the average width and thickness were 7.6 x 1.3 mm on the left and 7.9 x 1.3 mm on the right, which was not significantly different. For the NCS with closure, the left and right NCS closure rates were not significantly different. The NCS developmental stage is age- and vertebral level-dependent. The NCS closes from the lumbar and proximal thoracic spine to the middle-distal thoracic spine and times from very early juvenile to the adolescent. The NCS symmetry bilaterally occurred not only during the active open, but also the long closure period. The NCS symmetric open and/or closure may be important to maintain the normal spine alignment.

Spinal Deformity in Patients With Sotos Syndrome (Cerebral Gigantism)

Retrospective review of a case series. To present the clinical characteristics and progression of spinal deformity in patients with Sotos syndrome. There is limited information on the development of spinal deformity and the need for treatment in this condition. The medical records and spinal radiographs of 5 consecutive patients were reviewed. All patients were followed to skeletal maturity (mean follow-up: 6.6 y). The mean age at diagnosis of spinal deformity was 11.9 years (range: 5.8 to 14.5) with 4 patients presenting in adolescence. The type of deformity was not uniform. Two patients presented in adolescence with relatively small and nonprogressive thoracolumbar and lumbar scoliosis, which required observation but no treatment until the end of spinal growth. Three patients underwent spinal deformity correction at a mean age of 11.7 years (range: 6 to 15.4). The first patient developed a double structural thoracic and lumbar scoliosis and underwent a posterior spinal arthrodesis extending from T3 to L4. Five years later, she developed marked degenerative changes at the L4/L5 level causing symptomatic bilateral lateral recess stenosis and affecting the L5 nerve roots. She underwent spinal decompression at L4/L5 and L5/S1 levels followed by extension of the fusion to the sacrum. The second patient developed a severe thoracic kyphosis and underwent a posterior spinal arthrodesis. The remaining patient presented at the age of 5.9 years with a severe thoracic kyphoscoliosis and underwent a 2-stage antero-posterior spinal arthrodesis. The development of spinal deformity is a common finding in children with Sotos syndrome and in our series it occurred in adolescence in 4 out of 5 patients. There is significant variability on the pattern of spine deformity, ranging from a scoliosis through kyphoscoliosis to a pure kyphosis, and also the age at presentation and need for treatment.

STRUCTURAL AND FUNCTIONAL PECULIARITIES OF SPINE DEFORMITY DEVELOPMENTIN NEUROFIBROMATOSIS NF-1

Objective. To study pathogenetic mechanisms of the development of spinal deformity in neurofibromatosis. Material and Methods. Structural components of the spine were presented as specimens obtained after surgical correction of spinal deformity performed in 10 children with III–IV grade scoliosis associated with neurofibromatosis. Tissues were investigated by conventional histochemical and ultrastructural methods. The levels of aggrecan and lumnican gene expression were studied using PCR method. Results. Etiologic factor of the development of spinal deformity in neurofibromatosis is a mutation of the NF-1 gene in cells of ganglious lamella. Migration of cells carrying mutant gene into one of the sclerotome zones results in oncogene activation and intensive proliferation of chondro-, osteo-, and fibroblasts in the growth plate, intervertebral disc, and vertebral body. Since the mutation involves the earliest stages of embriogenesis, the formation of definitive structural components in pathologically altered zones is disturbed. Conclusion. Progressive development of the spinal deformity after surgical intervention is accounted both for proliferation of chondro- and fibroblasts in the vertebral body and intervertebral disc and for disturbance of the lumnican gene expression.

Retrospective Study on the Development of Spinal Deformities Following Sternotomy for Congenital Heart Disease

Retrospective Study on the Development of Spinal Deformities Following Sternotomy for Congenital Heart Disease

Neurofibromatous sensory neuropathy of the thigh in a 7-year-old boy

Neuropathy is considered to be an unusual complication of neurofibromatosis 1 (NF1). Neurofibromatous neuropathy is extremely rare in the setting of paediatric age group, pure sensory mononeuropathy and NF1. The following is a description of a 7-year-old boy who presented with complains of discomfort and parasthesia on the anterior aspect of his left thigh which is an unusual mode of presentation and site of involvement. Clinical examination and imaging revealed an isolated sensory neuropathy of the left anterior femoral cutaneous nerve of the thigh secondary to plexiform neurofibromatosis involving the L1-L4 nerve roots and the anterior femoral cutaneous nerve of thigh. The main abnormality in this patient was segmental hypertrophy of the left lower limb and dilatation of left lumbar neural foramens. Subtotal excision of the neurofibromas of the anterior femoral cutaneous nerve was performed and the patient was asymptomatic at the end of 27 months (2.25 years) of followup. Although the result of treatment in this case was good, long-term followup is necessary in view of greater risk of malignant transformation and development of spinal deformity and overall long-term poor prognosis in this particular patient subgroup of NF1.

Retrospective Study on the Development of Spinal Deformities Following Sternotomy for Congenital Heart Disease

Retrospective review with a minimum of 3 years of follow-up. We hypothesize that following median sternotomy there may be an increase incidence of both sagittal and coronal spinal deformity. We also think that heart size and a cyanotic cardiac condition are also risk factors for development of spinal deformity. The purpose of this study was to determine the incidence and characteristics of spinal deformity in patients following sternotomy for congenital heart disease. Patients with congenital heart disease are at an increased risk to develop scoliosis. A total of 108 patients underwent a median sternotomy for the treatment of congenital heart disease and met inclusion criteria. The medical record was reviewed to gather demographic data and medical and surgical history. Serial chest and spine radiographs were reviewed. Scoliosis developed in 28% of the patients (10 males, 20 females). The mean follow-up was 13 years (range, 3-26 years). The mean coronal Cobb angle was 25 degrees (range, 11 degrees-88 degrees). Of these, 7 patients presented with curves of > or = 30 degrees. The mean age at diagnosis of scoliosis was 14 years (range, 2-33 years). A kyphotic deformity developed in 22% (24 patients). In patients with scoliosis, the mean sagittal kyphosis was 34 degrees (range, 2 degrees-73 degrees). Patients with a cyanotic cardiac condition had a trend toward severe scoliosis. There was no correlation between the development of scoliosis or kyphosis and the age at time of procedures, number of surgeries, gender, or heart size. The risk of developing scoliosis in children with congenital heart disease is more than 10 times that of idiopathic scoliosis. Spinal deformities, including scoliosis and/or kyphosis, were found in 34% of the patients. The sagittal alignment in scoliosis patients tends toward kyphosis.

Spinal Deformity Secondary to Impaired Neurologic Control

Spinal deformity occurs in children who have problems with motor control involving the trunk muscles. This lack of control allows the growing spine to collapse. Most commonly, this collapse is due to spasticity in children with the quadriplegic pattern of cerebral palsy. The most typical collapse pattern is scoliosis, although kyphosis or lordosis may also develop. Children who have severe hypotonia may also have development of spinal deformities, often with substantial kyphosis. Individuals with severe extensor posturing may have development of total spinal lordosis. A severe lack of motor control, expressed as a movement disorder such as athetosis or dystonia, is associated with a lower incidence of scoliosis than spasticity is. The incidence of scoliosis in institutionalized individuals, most of whom have a spastic quadriplegic pattern, has been reported to be 64%, with a strong inverse relationship to ambulatory ability1. This means that individuals who are dependent sitters with no head control may have a rate of scoliosis as high as 90%. We are not aware of published data on the incidence of spinal deformity with other movement disorders. Friedreich ataxia is a condition in which the primary neurologic manifestation is also a lack of motor control and in which the development of spinal deformities, primarily scoliosis, is common. Progressive scoliosis requiring surgical stabilization develops in approximately 50% of these individuals2. Individuals with motor-control problems tend to have development of spinal deformity in late childhood. Initially, the child often has very flexible postural curves and tends to lean toward one side. Typically, as the child enters early adolescent growth, the spine develops a structural torsional deformity with increasing stiffness. This structural curve may become so stiff that physical correction, even when the child is in a lying position, is impossible. The stiffness typically increases as the …

Growth Considerations of the Immature Spine

It is a well-known fact that the human spine grows during the infantile, juvenile, and adolescent periods of life. Less known and less obvious are the specifics of vertebral column growth, including the total amount of growth per year and the amount of growth that occurs at each vertebral segment and in each of the various planes (axial, coronal, sagittal, and transverse). We do know that the growth rate of the spine varies according to age. In utero, the spine grows at an extremely accelerated rate; from birth to two years of age, it develops at an increased rate; from two to ten years of age, it proceeds to grow at a steady rate; and finally, during the prepubescent growth phase, it grows at an increased rate once again. There is a relationship between growth of the spine and the development of spinal deformity. Progression of scoliotic spinal deformity occurs during periods of peak growth velocity1,2. The first spinal growth peak occurs after the postnatal period until two years of age, and the second peak occurs during the prepubescent period as a result of a strong hormonal influence2. Estimates of average total vertebral column growth and vertebral column growth by region have been proposed by Dimeglio and Ferran3. Anderson et al.4 described the remaining vertebral column growth based on sitting heights. These methods delineate differences in growth between boys and girls and among different skeletal ages. According to Dimeglio and Ferran3, the longitudinal growth of the thoracic and lumbar vertebrae is 0.8 and 1.1 mm per year, respectively. According to Roaf5 and Taylor6, the intervertebral thoracic discs grow between 0.2 and 0.6 mm per year and the intervertebral lumbar discs grow between 0.3 and 0.8 mm …

The transformation of spinal curvature into spinal deformity: pathological processes and implications for treatment

BackgroundThis review summarizes what is known about the pathological processes (e.g. structural and functional changes), by which spinal curvatures develop and evolve into spinal deformities.MethodsComprehensive review of articles (English language only) published on 'scoliosis,' whose content yielded data on the pathological changes associated with spinal curvatures. Medline, Science Citation Index and other searches yielded > 10,000 titles each of which was surveyed for content related to 'pathology' and related terms such as 'etiology,' 'inheritance,' 'pathomechanism,' 'signs and symptoms.' Additional resources included all books published on 'scoliosis' and available through the Arizona Health Sciences Library, Interlibrary Loan, or through direct contact with the authors or publishers.ResultsA lateral curvature of the spine–'scoliosis'–can develop in association with postural imbalance due to genetic defects and injury as well as pain and scarring from trauma or surgery. Irrespective of the factor that triggers its appearance, a sustained postural imbalance can result, over time, in establishment of a state of continuous asymmetric loading relative to the spinal axis. Recent studies support the longstanding hypothesis that spinal deformity results directly from such postural imbalance, irrespective of the primary trigger, because the dynamics of growth within vertebrae are altered by continuous asymmetric mechanical loading. These data suggest that, as long as growth potential remains, evolution of a spinal curvature into a spinal deformity can be prevented by reversing the state of continuous asymmetric loading.ConclusionSpinal curvatures can routinely be diagnosed in early stages, before pathological deformity of the vertebral elements is induced in response to asymmetric loading. Current clinical approaches involve 'watching and waiting' while mild reversible spinal curvatures develop into spinal deformities with potential to cause symptoms throughout life. Research to define patient-specific mechanics of spinal loading may allow quantification of a critical threshold at which curvature establishment and progression become inevitable, and thereby yield strategies to prevent development of spinal deformity.Even within the normal spine there is considerable flexibility with the possibility of producing many types of curves that can be altered during the course of normal movements. To create these curves during normal movement simply requires an imbalance of forces along the spine and, extending this concept a little further, a scoliotic curve is produced simply by a small but sustained imbalance of forces along the spine. In fact I would argue that no matter what you believe to be the cause of AIS, ultimately the problem can be reduced to the production of an imbalance of forces along the spine [1].

Analysis of Zinc and Magnesium Levels in Pinealectomized Chicks: Roles on Development of Spinal Deformity?

Melatonin is the main product of the pineal gland, and trace metals play a critical role in growth and development. The purpose of this study was to assess the serum zinc (Zn) and magnesium (Mg) levels in pinealectomized chicks and their possible interactions with the development of spinal deformity. Chicks were divided into two equal groups: unoperated controls (group M) and pinealectomized chicks (group N). Pinealectomies were performed at the age of 3 d. After 8 wk, serum Zn and Mg levels of 10 animals from each group were measured by spectrophotometric assay. The results of analyses were compared using the Mann-Whitney U-test. The correlation between serum Zn and Mg levels were assessed by Spearman's correlation. In this study, it was obvious that the serum Zn levels in group N were significantly lower than those in group M (2.8 +/- 0.10 vs 4.2 +/- 0.14 ppm; p < 0.0005). In contrast, Mg levels in group N was high compared with the values in group M, although there was no significant difference (17.8 +/- 0.69 vs 15.7 +/- 0.85 ppm; p > 0.05). In pinealectomized animals, serum Zn levels declined significantly while serum Mg levels increased, albeit insignificantly. Thus, there was a moderately positive but not statistically significant correlation between Mg and Zn levels in unoperated controls (r = 0. 273, p > 0.05), whereas there was a negative but not statistically significant correlation between Zn and Mg levels in pinealectomized chicks (r = -0.115, p > 0.05). In addition, the serum Mg to serum Zn ratio was significantly higher in group N than in the group M control (6. 39 +/- 0.32 vs 3.75 +/- 0.22, respectively; p < 0.001). From the results of the current study, it is clear that surgical pinealectomy in newly hatched Hybro Broiler chicks has a significant effect on serum Zn level. However, the serum Mg did not change significantly. Because serum Mg is not a good indicator of Mg status in chicks, it is speculated that other tissues, such as muscle or spine, might productively be explored as a more sensitive Mg biomarker for this model. The present study provides experimental evidence that serum trace metal levels might be affected in pinealectomized animals because of the lack of its main neurohormone melatonin.

Chronic changes in cerebrospinal fluid pathways produced by subarachnoid kaolin injection and experimental spinal cord trauma in the rabbit: their relationship with the development of spinal deformity

Post-traumatic cystic changes in cerebrospinal fluid (CSF) pathways such as ventriculomegaly and/or hydrosyringomyelia are not uncommon, but their characteristics have not yet been fully clarified. This study was designed to investigate the alterations affecting the CSF pathways in rabbits at a late stage, and to clarify the relationship between these changes and the development of spinal deformity. In this study, a total of 60 New Zealand white rabbits were used and they were segregated into four different groups of 15 animals each: sham-operation group, kaolin group, and kaolin plus mild trauma group and kaolin plus severe trauma group. The animals were subjected to radiological investigation using direct X-ray study and magnetic resonance imaging (MRI) after 4 months. The thoracic spinal cords of the animals were dissected after intracardiac perfusion-fixation with 10% formalin for light microscopy and 2.5% glutaraldehyde for transmission electron microscopic study. Following the sectioning and staining procedures, the histological characteristics of the spinal cords were evaluated with light microscopy and transmission electron microscopy. A spinal deformity developed in 90% in rabbits in both kaolin injection group and spinal trauma groups. MRI revealed generalized dilatation of the ventricular system and the central canal of the spinal cord after the kaolin injection with/without trauma in this study. Gross morphologic examination showed some enlargement of entire CSF pathways in these groups. All animals with central canal dilatation had mild or severe scoliotic and kyphotic deformities. In a light microscopic study, a denuded ependymal line and multicyst formations in periependymal areas were found in both kaolin injection and spinal trauma groups. Ultrastructurally, an apical flattening of the ependyma, microcysts in the ependymal cells, axonal degeneration, demyelination, and loss of ependymal cells adjacent mild spongy were found in the spinal cords of animals in these groups. To the best of our knowledge, this is the first study to investigate the chronic effects of spinal cord injury (SCI) on the CSF pathways and their relationship with the development of spinal deformity in an experimental model of kaolin injection and trauma, using MRI as well as light and transmission electron microscopy. In the light of this study, the severity of spinal cord injury on the development of some degenerative findings in the spinal cord was clear, but further clinical and experimental studies using dynamic imaging techniques will be valuable.

Spinal deformities after selective dorsal rhizotomy for spastic cerebral palsy

Spinal deformities are significant problems in children with spastic cerebral palsy. The treatment of their spasticity by selective dorsal rhizotomy (SDR) may worsen or improve these problems. The purpose of this study was to determine the incidence of and change in degree of thoracolumbar scoliosis, thoracic kyphosis, and lumbar lordosis in children who have undergone SDR. A retrospective review was conducted of children younger than 18 years of age, who had undergone SDR at British Columbia's Children's Hospital from 1987 to 2001 and in whom preoperative and postoperative spine radiographs have been obtained. Angles for thoracolumbar scoliosis, thoracic kyphosis, and lumbar lordosis were measured. The study group comprised 105 patients. The mean age at surgery was 5.2 years (range 2.7-14.6 years), with a mean time to most recent follow-up radiographs of 4.3 years (1-13.6 years). Sixty-two children had spastic diplegia (59%), 34 spastic quadriplegia (32%), and nine quadriplegia and intellectual delay (9%). A total of 104 children underwent laminoplasty with replacement of the laminae, usually from L-1 to S-1 and 54.8% of children had scoliosis at last follow up, with 25% having worsening of 10 degrees or more. The incidence of abnormal kyphosis at the last follow-up visit was 38.6%, with 31.8% having worsening of 15 degrees or more. The incidence of hyperlordosis at last follow up was 21.3%, with 36% having worsening of 15 degrees or more. The factors in this series impacting development of spinal deformities have been analyzed and are discussed. The relatively high incidence of spinal deformity in children who have undergone SDR via multi-level lumbosacral laminoplasties should raise some concern.

Langerhans cell histiocytosis of the spine in children. Long-term follow-up.

Langerhans cell histiocytosis causes destructive lesions in a child's spine. Few large, long-term studies have evaluated the clinical and radiographic presentation, natural history, outcomes of modern treatment approaches, and maintenance of normal spinal growth and stability after the diagnosis of this disease in children. Twenty-six children with biopsy-proven Langerhans cell histiocytosis involving the spine were treated at our institution between 1970 and 2003. They had a total of forty-four involved vertebrae (twenty cervical, fourteen thoracic, and ten lumbar). Vertebral body collapse was measured on radiographs and classified as grade I (0% to 50% collapse) or grade II (51% to 100% collapse) and subclassified as A (symmetric collapse) or B (asymmetric collapse). Lesions of the posterior elements of the spine were classified as grade III. Twenty-three children were followed for two years or more (mean, 9.4 years), and the analyses of treatment and long-term outcomes were performed in that group of patients. There was a predominance of lesions in the cervical spine (p </= 0.02). Sixteen (62%) of the twenty-six children were found to have multifocal skeletal disease. Cervical and lumbar lesions were more commonly associated with multilevel spinal disease. The extent of the initial collapse seen radiographically was grade IA for twenty vertebrae, IB for three, IIA for ten, IIB for nine, and III for two. Grade-I lesions were more likely to be associated with symmetric collapse than were grade-II lesions. Spinal deformity developed in four children, and two later required spinal fusion. No relationship was observed between the grade of the initial collapse and the subsequent development of spinal deformity. Despite heterogeneous treatment, all patients were alive and well with resolution of all presenting signs and symptoms and no evidence of active disease at the time of the most recent follow-up. We found a particularly high prevalence of lesions in the cervical spine and a high prevalence of multiple skeletal lesions. In contrast to the classic finding of vertebra plana, we found that more severe lesions often led to asymmetric collapse; yet, asymmetric collapse was not found to be associated with the development of subsequent spinal deformity. The natural history of these lesions in the spine in the absence of systemic disease or spinal deformity is such that aggressive surgical management is usually not indicated; only follow-up is necessary to monitor recovery and spinal balance.

The effects of pineal gland transplantation on the production of spinal deformity and serum melatonin level following pinealectomy in the chicken.

Pinealectomy frequently produces spinal deformity in some animal models, but the precise biological mechanism of this phenomenon remains obscure. The current study investigated the effects of an autograft pineal body on the development of spinal deformity and serum melatonin (MLT) concentration after pinealectomy in the chicken. Thirty-six chickens (2 days of age) were divided into three equal groups. While the removal of the pineal gland was performed in groups B and C, a pineal body autograft was surgically implanted into the body wall musculature only in the pineal transplantation group (group C). Chickens in which no surgical intervention was performed served as intact controls (group A). Posteroanterior radiographs of the spines of the chickens were taken at the age of 8 weeks. These were used to determine Cobb angles and to measure the rib-vertebra angles (RVA) on the concave and convex sides of the curves, from which data the difference between the convex and concave RVA (the RVAD) was calculated. At the end of the study, serum MLT levels were determined using the enzyme-linked immunosorbent assay method, and histopathological examination of specimens from all the groups was performed. The results were compared using one-way analysis of variance followed by Duncan's test for pairwise comparisons or by the Kruskal-Wallis test followed by the Mann-Whitney U tests for comparisons between two groups. In this study, the serum MLT levels in groups B and C were significantly lower than those in group A ( P<0.05). However, scoliosis developed in only 7 of 12 (58%) in group B and 6 of 12 (50%) in group C. The average Cobb angle and RVAD in groups B and C were significantly larger than those found in group A ( P=0.000 and P=0.001, respectively). Interestingly, there were no significant differences in either serum MLT levels or development of scoliosis between groups B and C. From the results of the current study, it is evident that the intramuscular pineal gland transplantation following pinealectomy in young Hybro Broiler chickens has no significant effect on the development of spinal deformity and serum MLT level. In the light of this result, the role of MLT in the development of spinal deformity in chickens after pinealectomy remains controversial, and further investigations are warranted.

Cervical laminoplasty: a critical review.

The technique of cervical laminoplasty was developed to decompress the spinal canal in patients with multi-level anterior compression caused by ossification of the posterior longitudinal ligament or cervical spondylosis. There is a paucity of data confirming its superiority to laminectomy with regard to neurological outcome, preserving spinal stability, preventing postlaminectomy kyphosis, and the development of the "postlaminectomy membrane." The authors conducted a metaanalysis of the English-language laminoplasty literature, assessing neurological outcome, change in range of motion (ROM), development of spinal deformity, and complications. Seventy-one series were reviewed, comprising more than 2000 patients. All studies were retrospective, uncontrolled, nonrandomized case series. Forty-one series provided postoperative recovery rate data in which the Japanese Orthopaedic Association Scale was used for assessing myelopathy. The mean recovery rate was 55% (range 20-80%). The authors of 23 papers provided data on the percentage of patients improving (mean approximately 80%). There was no difference in neurological outcome based on the different laminoplasty techniques or when laminoplasty was compared with laminectomy. There was postlaminoplasty worsening of cervical alignment in approximately 35% and with development of postoperative kyphosis in approximately 10% of patients who underwent long-term follow-up review. Cervical ROM decreased substantially after laminoplasty (mean decrease 50%, range 17-80%). The authors of studies with long-term follow up found that there was progressive loss of cervical ROM, and final ROM similar to that seen in patients who had undergone laminectomy and fusion. In their review of the laminectomy literature the authors could not confirm the occurrence of postlaminectomy membrane causing clinically significant deterioration of neurological function. Postoperative complications differed substantially among series. In only seven articles did the writers quantify the rates of postoperative axial neck pain, noting an incidence between 6 and 60%. In approximately 8% of patients, C-5 nerve root dysfunction developed based on the 12 articles in which this complication was reported. The literature has yet to support the purported benefits of laminoplasty. Neurological outcome and change in spinal alignment are similar after laminectomy and laminoplasty. Patients treated with laminoplasty develop progressive limitation of cervical ROM similar to that seen after laminectomy and fusion.

Does genotype predict development of the spinal deformity in patients with diastrophic dysplasia?

This study analyzed whether genotype can be used to predict development of spinal deformity in patients with diastrophic dysplasia (DD). Severity and natural history of scoliosis vary among patients, but the magnitude of the curves is similar among siblings. Plain radiographs were taken of 69 patients aged 16 years or older. The degree of scoliosis was measured according to Cobb's method. Blood samples were collected from patients clinically diagnosed as having DD and the genotype was determined. Fifty-six patients were found to be homozygous for the Finnish founder DTD mutation, DTDST(Fin). Of these 56, 51 (91%) had scoliosis, with an average curve of 43 degrees (range 12 degrees-188 degrees ). The DTDST(Fin)/R279 W genotype was found in nine patients, and of these, eight (89%) had scoliosis, with an average curve of 34 degrees (range 11 degrees-70 degrees ). The DTDST(Fin)/nondetermined genotype was found in four patients. Three (75%) of them had scoliosis, with an average curve of 126 degrees (range 77 degrees-188 degrees ). Statistical analysis found no difference in the prevalence or magnitude of curves between subgroups. The development and severity of the scoliosis cannot, therefore, be predicted from the genotype. It seems possible that scoliosis development is affected by several genes as well as by external factors.

Biomechanical study of the development of scoliosis, using a thoracolumbar spine model

A thoracolumbar spine model was made using synthetic resin vertebrae and silicon discs. The model was fixed to a metal frame and spinal deformation caused by loading was determined relative to three-dimensional coordinates set in the frame. A three-dimensional evaluation of the development of spinal deformity was performed by applying rotational, lordotic, and lateral flexional forces in various orders to the model. The most severe scoliosis occurred when loading was done in the order of rotational force, lordotic force, and lateral flexional force.

Development of spinal deformities in Atlantic salmon and Arctic charr fed diets supplemented with oxytetracycline

Some individuals within populations of Atlantic salmon Salmo salar and Arctic charr Salvelinus alpinus fed diets supplemented with oxytetracycline (OTC) developed spinal deformations. Possible differences in feed intake and growth of spinally deformed fish relative to fish without any deformities were investigated. Amongst Atlantic salmon, 17% of the fish fed OTC-supplemented feed developed spinal fractures, whereas none of the fish receiving the basic feed did so. Despite deformation of the spinal column, the injured fish continued to feed and grow, but at lower rates than unaffected individuals. In contrast to Atlantic salmon, Arctic charr showed no signs of spinal fractures at any time during the 65-day experiment.