Thoracolumbar spinal deformity in achondroplasia

2003 ◽  
Vol 14 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Sanjay N. Misra ◽  
Howard W. Morgan

The authors review the management of thoracolumbar kyphotic deformity in cases of achondroplasia. The presence of angular thoracolumbar kyphosis in achondroplasia is well recognized. In children this is initially a nonfixed deformity that persists, however, in more than 10% of individuals and becomes a fixed thoracolumbar kyphotic deformity. Additionally, with the coexistent spinal canal stenosis, neurological damage can occur and manifest as spinal cord or cauda equina compression. The nature of this condition, the natural history, and management options are discussed. Anatomical and biomechanical factors relevant to the condition are specifically highlighted. Avoidance of pitfalls in the management of these patients is discussed for both pediatric and adult patients.

2009 ◽  
Vol 10 (2) ◽  
pp. 122-128 ◽  
Author(s):  
Macondo Mochizuki ◽  
Atsuomi Aiba ◽  
Mitsuhiro Hashimoto ◽  
Takayuki Fujiyoshi ◽  
Masashi Yamazaki

Object The authors assessed the clinical course in patients with a narrowed cervical spinal canal caused by ossification of the posterior longitudinal ligament (OPLL), but who have no or only mild myelopathy. Additionally, the authors analyzed the factors contributing to the development and aggravation of myelopathy in patients with OPLLinduced spinal canal stenosis. Methods Between 1997 and 2004, the authors selected treatments for patients with cervical OPLL in whom the residual space available for the spinal cord was ≤ 12 mm. Treatment decisions were based on the severity of myelopathy at presentation. Twenty-one patients with no or mild myelopathy (defined as a Japanese Orthopaedic Association [JOA] scale score ≥ 14 points) received conservative treatment, with a mean follow-up period of 4.5 years. In 20 patients with moderate or severe myelopathy (JOA scale score < 14 points), the authors performed surgery via an anterior approach. The clinical course in these patients was assessed with the JOA scale and the OPLL types were classified. The authors evaluated the range of motion between C-1 and C-7, the developmental segmental sagittal diameter, the percentage of spinal canal diameter occupied by the OPLL (% ratio), and the residual space available for the spinal cord on cervical radiographs; T2-weighted MR images were examined for high signal changes (HSCs). Results In the conservative treatment group, 8 patients showed improvement, 12 remained unchanged, and 1 patient's condition became slightly worse during the observation period. Fifteen patients in this group had mixedtype, 3 had continuous-type, 2 had localized-type, and 1 had a segmental-type OPLL. In the surgically treated group, there were 12 patients with segmental-type, 10 patients with mixed-type, and 1 with localized-type OPLL. The mean range of motion at C1–7 was 36.4° in the conservatively treated group and 46.5° in the surgical group (p < 0.05). No significant difference was seen between the groups in terms of developmental segmental sagittal diameter, % ratio, or residual space available for the cord. No HSCs were noted in the conservative group, while 17 patients in the surgical group had HSCs (p < 0.05). Conclusions In the present study, the authors demonstrate that the mobility of the cervical spine and the type of OPLL are important factors contributing to the development and aggravation of myelopathy in patients with OPLLinduced spinal canal stenosis. The authors advocate conservative treatment in most patients with OPLLs who have no or only mild myelopathy, even in the presence of spinal canal narrowing.


2020 ◽  
pp. 77-77
Author(s):  
Vuk Aleksic ◽  
Rosanda Ilic ◽  
Mihailo Milicevic ◽  
Filip Milisavljevic ◽  
Milos Jokovic

Introduction. The spine is involved in less than 1% of all tuberculosis (TB) cases, and it is a very dangerous type of skeletal TB as it can be associated with neurologic deficit and even paraplegia due to compression of adjacent neural structures and significant spinal deformity. The spine TB is one of the most common causes for an angular kyphotic deformity of spine. Patients with 60 or more degree kyphosis at dorsolumbar spine are at great risk to develop late onset neurological deficit and paraplegia due to chronic compression and stretching of the spinal cord over bonny ridges. In small portion of cases other conditions may lead to neurological deficit in patients with long standing angular kyphosis which also alters the treatment strategy that otherwise involves prolonged and mutilant surgery. Case outline. We present a case of a 61-year-old male patient with concomitant 90-degree dorsolumbar spine kyphosis due to spinal TB and ligamentum flavum hypertrophy, which led to spinal canal stenosis with myelopathy and consequent paraplegia. The patient undergoes dorsal decompression with removal of the hypertrophic yellow ligament after which he recovered to the level of walking. Conclusion. Many authors propose guidelines for treatment of spinal TB taking into account the stage of the disease, the age of the patient, the angle of kyphosis, and other factors. We find that the best approach for each patient is personalized medical approach.


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Baasanjav Uranbileg ◽  
Nobuko Ito ◽  
Makoto Kurano ◽  
Daisuke Saigusa ◽  
Ritsumi Saito ◽  
...  

Abstract Cauda equina compression (CEC) is a major cause of neurogenic claudication and progresses to neuropathic pain (NP). A lipid mediator, lysophosphatidic acid (LPA), is known to induce NP via the LPA1 receptor. To know a possible mechanism of LPA production in neurogenic claudication, we determined the levels of LPA, lysophosphatidylcholine (LPC) and LPA-producing enzyme autotaxin (ATX), in the cerebrospinal fluid (CSF) and spinal cord (SC) using a CEC as a possible model of neurogenic claudication. Using silicon blocks within the lumbar epidural space, we developed a CEC model in rats with motor dysfunction. LPC and LPA levels in the CSF were significantly increased from day 1. Importantly, specific LPA species (16:0, 18:2, 20:4) were upregulated, which have been shown to produce by ATX detected in the CSF, without changes on its level. In SC, the LPC and LPA levels did not change, but mass spectrometry imaging analysis revealed that LPC was present in a region where the silicon blocks were inserted. These results propose a model for LPA production in SC and CSF upon neurogenic claudication that LPC produced locally by tissue damages is converted to LPA by ATX, which then leak out into the CSF.


1972 ◽  
Vol 37 (1) ◽  
pp. 83-88 ◽  
Author(s):  
Hiroshi Yamada ◽  
Masaki Ohya ◽  
Tsuguo Okada ◽  
Zenji Shiozawa

✓ Five patients with intermittent claudication due to compression of the cauda equina in the presence of lumbar spinal canal stenosis or midline intervertebral disc protrusion are described. The characteristic myelographic evidence was complete obstruction during extension of the spine and release of the block with flexion. The cause of this syndrome is considered to be intermittent bulging of the ligamentum flavum into a narrow spinal canal so as to compress the cauda equina during extension of the back.


1976 ◽  
Vol 44 (5) ◽  
pp. 613-616 ◽  
Author(s):  
Glen S. Merry ◽  
D. Barry Appleton

✓ A case is reported of spinal aneurysm in a child with a family history of hereditary hemorrhagic telangiectasia causing spinal cord and cauda equina compression. The operative approach is discussed.


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