Кеңіршек жүйке синдромы және омыртқа арқасы зақымдануы

Nerve damage at the end of the spinal cord
CES is generally treated surgically via laminectomy. It was first described in 1934.

After the conus medullaris (near lumbar vertebral levels 1 (L1) and 2 (L2), occasionally lower), the spinal canal contains a bundle of nerve fibers (the cauda equina or "horse tail") that branches off the lower end of the spinal cord and contains the nerve roots from L1–L5 and S1–S5. The nerve roots from L4–S4 join in the sacral plexus which affects the sciatic nerve, which travels caudally (toward the feet). Compression, trauma or other damage to this region of the spinal canal can result in cauda equina syndrome. The symptoms may also appear as a temporary side effect of a sacral extra dural injection.

Direct trauma can also cause cauda equina syndrome. Most common causes include as a complication of lumbar punctures, burst fractures resulting in posterior migration of fragments of the vertebral body, severe disc herniations, spinal anaesthesia involving trauma from catheters and high local anaesthetic concentrations around the cauda equina, penetrating trauma such as knife wounds or ballistic trauma. Cauda equina syndrome may also be caused by blunt trauma suffered in an event such as a car accident or fall.

CES can be caused by lumbar spinal stenosis, which is when the diameter of the spinal canal narrows. This could be the result of a degenerative process of the spine (such as osteoarthritis) or a developmental defect which is present at birth. In the most severe cases of spondylolisthesis cauda equina syndrome can result.

Diagnosis is first suspected clinically based on history and physical exam and usually confirmed by an MRI scan or CT scan, depending on availability. Changes in sensation can start as pins and needles leading to numbness. Changes in bladder function may be changes to stream or inability to fully empty the bladder. If a person progresses to full retention intervention is less likely to be successful.

The management of true cauda equina syndrome frequently involves surgical decompression. When cauda equina syndrome is caused by a herniated disk early surgical decompression is recommended. Sudden onset cauda equina syndrome is regarded as a medical/surgical emergency. Surgical decompression by means of laminectomy or other approaches may be undertaken within 6, 24 or 48 hours of symptoms developing if a compressive lesion (e. g., ruptured disc, epidural abscess, tumor or hematoma) is demonstrated. Early treatment may significantly improve the chance that long term neurological damage will be avoided. Cauda equina syndrome can occur during pregnancy due to lumbar disc herniation. The risk of cauda equina syndrome during pregnancy increases with age of the mother. Surgery can still be performed and pregnancy does not adversely affect treatment. Treatment for those with cauda equina can and should be carried out at any time during pregnancy. Lifestyle issues may need to be addressed post treatment. Issues could include the person's need for physiotherapy and occupational therapy due to lower limb dysfunction. Obesity might also need to be tackled. Once surgery is performed, resting is required until the bladder and bowel dysfunction can be assessed. Urinary catheterization may help with bladder control. Gravity and exercise can help control bowel movement (Hodges, 2004). Pelvic floor exercises assist in controlling bowel movements (Pelvic Floor Exercises, 2010). These exercises can be done standing, lying, or on all fours with the knees slightly separated. Full recovery of bowel and bladder control can take as long as two years.

The prognosis for complete recovery is dependent upon many factors. The most important of these is the severity and duration of compression upon the damaged nerve(s). Generally, the longer the time before intervention to remove the compression causing nerve damage, the greater the damage caused to the nerve(s). Damage can be so severe that nerve regrowth is impossible, and the nerve damage will be permanent. In cases where the nerve has been damaged but is still capable of regrowth, recovery time is widely variable. Surgical intervention with decompression of the cauda equina can assist recovery. Delayed or severe nerve damage can mean up to several years' recovery time because nerve growth is exceptionally slow. Review of the literature indicates that around 50–70% of patients have urinary retention (CES R) on presentation with 30–50% having an incomplete syndrome (CES I). The latter group, especially if the history is less than a few days, usually requires emergency MRI to confirm the diagnosis followed by prompt decompression. CES I with its more favourable prognosis may become CES R at a later stage.

Various etiologies of CES include fractures, abscesses, hematomas, and any compression of the relevant nerve roots. Injuries to the thoracolumbar spine will not necessarily result in a clinical diagnosis of CES, but in all such cases it is necessary to consider. Few epidemiological studies of CES have been done in the United States, owing to difficulties such as amassing sufficient cases as well as defining the affected population, therefore this is an area deserving of additional scrutiny. Traumatic spinal cord injuries occur in approximately 40 people per million annually in the United States, resulting from traumas due to motor vehicle accidents, sporting injuries, falls, and other factors. An estimated 10 to 25% of vertebral fractures will result in injury to the spinal cord. The most frequent injuries of the thoracolumbar region are to the conus medullaris and the cauda equina, particularly between T12 and L2. It is not a typical diagnosis, developing in only 4 to 7 out of every 10,000 to 100,000 patients, and is more likely to occur proximally.

Degenerative lumbosacral stenosis (DLSS), also known as cauda equina syndrome, is a pathologic degeneration in the lumbosacral disk in dogs. DLSS affects the articulation, nerve progression, and tissue and joint connections of the disk. This degeneration causes compressions in soft tissues and nerve root locations in the caudal area of the medulla, causing neuropathic pain in the lumbar vertebrae.