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At least 595 records · Page 33Linked to original sources
PubMed1992

[Remodeling of the spinal canal after comminuted fracture of the spine. Apropos of a case].

A burst fracture of T 12, without neurological impairment, was treated by plaster cast. Prior to treatment, there was a significant narrowing of the spinal canal, due to posterior displacement of a bone fragment. This was not modified by treatment, as the narrowing was unchanged on the second CT scan, done eight days later. At 17 months, there was no more narrowing on the CT scan, as a consequence of vertebral body remodeling. The patient had no pain and performed several sport activities.

Adult↗
PubMedDate not supplied

Narrowing of thoraco-lumbar spinal canal in achondroplasia.

The incidence of neurological deficits in achondroplastic subject is by no means negligible. We considered the clinico-radiological and therapeutic data of 35 achondroplasic patients (5 personal cases and 30 published in the available literature) harbouring myelo-radicular deficits related to narrowing of thoraco-lumbar canal. There was no significant sex prevalence. The clinical symptoms appear most frequently in the III or IV decades of life. Actually morphological anomalies of the spinal canal are already present at birth in achondroplasic dwarfs, and signs of cervical cord involvement are not uncommon in achondroplasic children. The delayed occurrence of clinical symptoms related to narrow toracho-lumbar canal may be explained by the pathogenetic role of acquired cofactors as prolapse of intervertebral disks and for degenerative spondyloartrosis. The clinical history is usually of insidious onset. Most frequent symptoms are motor weakness of the lower limbs (82.8%) and low-back pain (77.1%). Sensory and/or sphincter disturbances appeared to be less frequent (about 40% of the examined subjects). Plain X-rays, myelography, CT, CT-myelography and MRI are the diagnostic examination of choice. Surgical treatment consists of anterior decompression with fusion, when thoraco-lumbar kyphosis is prevalent, and/or posterior decompression, when the symptoms are mainly caused by canal stenosis. From the prognostic point of view, two groups of patients are recognized, in relationship to the presence of marked dorsal kyphosis. Those with kyphosis showed almost invariably poor functional results. In the remaining ones the results were satisfactory, provided that the clinical history lasted less than 3 years and the symptomatology was not already too advanced.

Achondroplasia↗
PubMed1997

Spinal canal compromise in Proteus syndrome: case report and review of the literature.

A 24-year-old Vietnamese man with Proteus syndrome presented to the emergency department with progressive paraplegia and underwent urgent operative decompression of an angiolipomatous mass compressing the spinal cord. The associated spinal deformity and difficulty in imaging the mass, together with the paucity of discussion regarding the spinal cord sequelae of this rare syndrome in the literature, made this an extremely challenging case. Spinal cord compromise in patients with Proteus syndrome can result from either infiltration of the spinal canal by an angiolipomatous mass or canal narrowing as a result of vertebral hypertrophy. Regardless of the cause, the prognosis for neural recovery remains poor.

Adult↗
PubMed1991

A study and analysis of spinal canal diseases in the Black Lion Hospital by myelography.

Sixty seven lumbar and thoracic myelographic examinations were performed during the period February 1987 to September 1988. Fourteen patients (21%) had normal myelography while 53 (79%) patients had pathological findings. Spinal canal tumours accounted for the majority of complete CSF blocks (76.7%) Seventy-five per cent of the intradural tumours showed no abnormality on plain films of the vertebral column, whereas 75% of the extradural tumours had pathological findings. Dorsal (central) disc herniation was more frequent (70%) than lateral herniation with almost equal distribution at L5-S1 and L4-L5 disc spaces. Central disc herniation was more common at L4-L5 (71%). The measurement of the interpedicular distance on plain radiograph was not found to be diagnostic in our single case of spinal stenosis.

Adolescent↗
PubMed2007

Glial phosphorylated p38 MAP kinase mediates pain in a rat model of lumbar disc herniation and induces motor dysfunction in a rat model of lumbar spinal canal stenosis.

STUDY DESIGN: Immunohistochemical and behavioral study using rat models of lumbar disc herniation and cauda equina syndrome. OBJECTIVE: To investigate the expression of activated p38 mitogen-activated protein kinases (p38 MAP kinase; p38) in the spinal cord and to determine the effect of intrathecal administration of a specific p38 inhibitor on pain in a lumbar disc herniation model and on motor function and hypoalgesia in a spinal canal stenosis (SCS) model. SUMMARY OF BACKGROUND DATA: In pathologic lumbar disc herniation-induced neuropathic pain and compression of cauda equina-induced motor dysfunction and hypoalgesia caused by SCS, glia are activated and produce certain cytokines, including tumor necrosis factor-alpha (TNF-alpha) and interleukins, which play a crucial role in the pathogenesis of nerve degeneration. p38 is phosphorylated by these cytokines, suggesting that it may play an important role in pain transmission and nerve degeneration. Here we have examined the role of p38 in rat models of lumbar disc herniation and SCS. METHODS: Six-week-old male Sprague-Dawley rats were used. For the disc herniation model, autologous nucleus pulposus was applied to L5 nerve roots, which were then crushed. For the SCS model, a piece of silicon was placed under the lamina of the fourth lumbar vertebra. We assessed mechanical allodynia, hypoalgesia, and motor function using von Frey hairs, treadmill tests, and immunohistochemical localization of phosphorylated p38 (P-p38) in the cauda equina, dorsal root ganglion (DRG), and spinal cord, which were also double-stained with NeuN (neuronal marker), GFAP (astrocyte/Schwann cell marker), or isolectin B4 (IB4; microglia marker). We also examined the effects of intrathecal administration of a specific p38 inhibitor, FR167653, on nucleus pulposus-induced pain, hypoalgesia, and motor dysfunction following SCS. RESULTS: We demonstrated that activated P-p38-immunoreactive cells in the spinal cord and cauda equina were not observed before nerve injury but appeared in the cauda equina, DRG, and spinal dorsal horn in the disc herniation and SCS models. Double-labeling revealed that most P-p38-immunoreactive cells were isolectin B4-labeled microglia and GFAP-immunoreactive Schwann cells. Intrathecal administration of the p38 inhibitor FR167653 decreased mechanical allodynia in the disc herniation model and improved hypoalgesia and intermittent motor dysfunction in the SCS model. CONCLUSIONS: Our findings suggest that activated p38 may play an important role in the involvement of microglia in the pathophysiology of pain following lumbar disc herniation and mechanical hypoalgesia, and motor nerve dysfunction of cauda equina following SCS.

Animals↗