Rehabilitation in the case of total right leg paresis caused by disc herniation--case report.

Disorders of normal relations within the intervertebral joints are among the most important secondary consequences of intervertebral disc injury. Not only the joint mechanics are impaired, but since the disintegration of nucleus pulposus causes backward movement of the axis of movement, there are also secondary degenerative changes inflicted which, in turn, accelerate wear of the facet joints. In normal conditions, body weight and additional compensation forces are transferred to the nucleus pulposus which, thanks to principles of hydrodynamics, distributes them evenly on the entire surface of the vertebra body and fibrous ring of intervertebral disk. Upon disintegration of the nucleus this action ceases to function, which results in changes in the vertebral bone structure caused by nonuniform loads. Additionally, the facet joints are subject to excessive compressions. Narrowing of the vertebral separation impairs and disrupts the function of facet joints. This eventually leads to the occurrence of degenerative changes in them. These changes also affect negatively the posterior ligaments of the spine, the over-stretching of which leads to their thickening and hypertrophy. The symptoms of lumbar intervertebral disc lesion relate primarily to low-back pain and sciatic nerve pain in one or both lower limbs. The wear of an intervertebral disc takes place during the first phase, followed by chronic degeneration, and later by posterior displacement of the nucleus pulposus with varying degrees of its degeneration. The role of immune factors in low-back pain is cited by Dziak. He states that during the process of degeneration of an intervertebral disc some of the breakdown products stimulate the immunological response of the body. This reaction is accompanied by swelling that causes the pain. Additional confirmation of the reaction of immunological factors is provided by observation of inflammation, granulation and fibrosis of intervertebral discs removed during surgery [1, 2, 3, 4, 5]. The majority of cases of lumbar intervertebral disc liasons are accompanied by lower limbs symptoms, such as pain, hypoesthesia, weakness, muscle atrophy, and range of motion deviations. With the exception of deep pain, all of these symptoms are associated with irritation of nerve roots or cauda equina by a liaison of nucleus pulposus and annulus. Compression of the sciatic nerve in the buttock region causes hypoesthesia and paresis, but it does not inflict pain. In the normal health condition, nerves of the cauda equina occupy about 21% of the dural sac. The remaining space of the subarachnoid cavity is filled with cerebrospinal fluid protecting the nerve roots before they leave the spinal canal through the intervertebral foramina. The nerve roots occupy from 1/6 – 1/3 of the inside diameter of the intervertebral foramina. The seizure of these channels by subdural structures results first in fibrosis and atrophy of epidural fat, the layer of which in normal health conditions acts as a protective layer, both in the spinal cord canal and in the nerve root canals. If compression increases, then the circulation of cerebrospinal fluid is disturbed; thus, collapse or even adhesion of vascular cells may occur. If the constriction continues, a direct nerve compression takes place and causes degeneration of nerve fibres. At first, nerve compression increases its electric irritability, therefore stimulating spontaneous discharges, and after about 10 minutes causes total blockage of transmission. Motor neurons are the most sensitive to the lack of conductivity. Sensory neurons first lose the sense of the spatial position of a body part with respect to the whole body, which is necessary for proper functioning of the system controlling body mechanics. They arise unconsciously in proprioceptive receptors in muscles, tendons, joints and vestibular system of the inner ear. Subsequently there is a loss of the sense of touch, pain and temperature. It has to be remembered that damaged nerves are more susceptible to hypoxia. Partial ability of nerve transmission returns at the moment when the pressure is relieved, but regaining its full conductivity might take up to a year [6, 7, 8, 9, 10, 11].