Wednesday, June 1, 2011

Cervical Spondylosis - The pathogenesis of cervical spondylosis

Cervical intervertebral disc degeneration is the result. As it wears with age is fragamenteaza loses moisture and suffer collapse.Initial degenerative process begins in the nucleus pulposus.Pathological changes result in incarceration central fiber fiber fiber ring and its external externalization with increased mechanical stress on the cartilage of the vertebral bodies of girls.Subperostial bone formation occurs with the appearance of osteophytes bands that extend along the ventral face of the spinal canal, nerve tissue in some cases prison. They are designed to stabilize the adjacent vertebrae are hipermobile as a result of loss of material from the disk. Hypertrophy process ventrolaterala uncinata incarcereaza portion of the intervertebral foramen. Nerve root irritation as proteoglicanii intervertebral disc are degraded.Posterior longitudinal ligament ossification occurs in advanced disease.
Cervical myelopathyAppears as a result of several physiological factors. They are statico-mechanical, dynamic-mechanical, ischemia and spinal cord injuries associated with stretching. Bone spurs develop as ventral spinal cord space is reduced with the development of myelopathy.
Spinal cord compressionYellow ligament hypertrophy and thickening of the bone marrow lead to collapse deep space. Subluxatiile and degenerative kyphosis are common and may contribute to spinal cord compression in patients with cervical myelopathy. dynamic factors acting through the normal flexion and extension cervical spine that compresses the spinal canal or rigid. Flexion stretches the spinal column and is stretched over the ventral spurs. Yellow ligament in extension and click on the spinal ligaments and pressed between osteophites earlier.Spinal cord ischemia.It plays an important role in cervical myelopathy. histopathological changes observed in people with severe myelopathy involves minimal gray matter white matter lesions characteristic of ischemic brain model. Ischemia is blocked at the microcirculation.

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