Cauda equina injury

Introduction The cauda equina is also called the peripheral nerve. The cauda equina syndrome refers to the cauda equina due to external factors such as paralysis, disorder or insufficiency. It can not regulate the regulation of movement, sensation, pain, perception, temperature, etc., such as neurological ischemia. Excessive time or concurrent edema and paralysis can lead to paraplegia. Fracture and dislocation below the second lumbar vertebra can cause cauda equina injury. A complete break of the horse's tail is rare, which may result in the disappearance of sensory motion and the weakness of the bladder below the damage plane. If the cauda equina is completely broken, or sutured after fracture, the function can be completely or largely restored by nerve regeneration.

Cause

Fracture and dislocation of the second lumbar vertebra.

The damage is more common in the clinic. Most of them are caused by a variety of congenital or acquired causes. The lumbar spinal canal is absolutely or relatively narrow, and the cauda equina is compressed to produce a series of neurological dysfunction. Verbiest's first clinical report in 1949 and named it Caudaequinasyndrome CES.

After peripheral nerve injury, recovery is slow and often incomplete recovery, which is common. The cauda equina is a peripheral nerve that also recovers slowly after injury.

However, the cauda equina nerve recovers more slowly than other peripheral nerves. The reason may be: the spinal nerve root and the dorsal root ganglion, and the blood is obtained from the artery supplying the spinal nerve from the lateral side into the intervertebral foramen and the central blood vessel supplying the spinal cord. There is no local or segmental supply of arteries in the spinal nerve roots in the cauda equina.

Developmental lumbar spinal stenosis:

In 1910, Sumita first reported lumbar spinal stenosis in patients with achondroplasia. Subsequently, British doctors reported nerve compression syndrome caused by hypertrophy of the lamina or ligamentum flavum and nerve root compression caused by lateral recess stenosis. In 1977, Verbiest first reported the experience of surgical treatment of developmental lumbar spinal stenosis with the diagnosis of "lumbar spinal stenosis". In the following years, American scholar Ehmi Wimsteim reported a special clinical manifestation of partial developmental lumbar spinal stenosis, CES. It is now clear that lumbar spinal stenosis is the primary pathological basis of CES.

Ankylosing spondylitis:

Ankylosing spondylitis is a common disease that is rarely associated with neurological complications in the early and middle stages. It has been reported that the late cauda equina structure of this disease can be combined with cauda equina syndrome, and more than 60 such reports have been accumulated in the world. The mechanism of CES caused by ankylosing spondylitis was discussed separately. It is believed that ankylosing spondylitis can be associated with arachnoiditis, which in turn forms a diverticuloid cyst and expands, leading to enlargement of the spinal canal, posterior vertebral body, vertebral arch and laminar bone compression, arachnoid cyst formation, spinal conus or / The cauda equina is compressed and the clinical manifestation is CES, which is a long process. Coscia et al. used CT and MRI techniques to study these patients and reached the same conclusion.

Lumbar degenerative dislocation or lumbar fracture:

Lumbar degeneration and spondylolisthesis often cause spinal stenosis. At this time, the lower edge of the lamina and the ligamentum flavum attached to the laminae are thickened, the epiphyseal hyperplasia, and the fibrous tissue surrounding the dura mater and lateral crypt can compress the cauda equina and Nerve root. Marhouitz et al. reported that manual massage caused the vertebral body to slip and cause compression of the cauda equina to cause CES. Vertebral or accessory fractures, fracture blocks or broken intervertebral discs occupy the space inside the spinal canal and directly compress the cauda equina. The fracture block can also penetrate into the dura mater to cause direct damage of the cauda equina, hemorrhage, scarring, vertebral compression fracture, which constitutes the soft tissue of the spinal canal to the spinal canal fold, the spinal canal is extremely narrow, can produce serious or irreversible Symptoms of cauda equina injury.

Soft tissue compression factor

The literature reports that CES is 5.4% to 10.6% in lumbar disc herniation, accounting for 9.3% of surgical treatment of lumbar disc herniation and lumbar spinal stenosis. Because lumbar disc herniation and lumbar spinal stenosis are common diseases, CES is more common. It has also been reported that the incidence of lumbar disc herniation with CES is about 7%. At the same time, the segment of the disc herniation, the location and extent of each segment, and the prognosis of the operation are described in detail. It is considered that there are acute and chronic disc herniations. . In the acute protrusion, the protrusion not only oppresses the cauda equina nerve, but also has a momentary impact force on the cauda equina when it is free from the spinal canal, which makes the cauda equina nerve ischemia and edema aggravate, affecting the normal cerebrospinal fluid circulation. Professor Hou Shuxun of the 304 Hospital reported that 75% of the nerve root nutrition in the root sleeve segment comes from the cerebrospinal fluid, and 25% comes from the blood supply. Therefore, most of the nutrients are lost when the cerebrospinal fluid is blocked. After the cauda equina edema subsided, the surrounding adhesions formed. Even if the laminectomy was performed, the protrusions were removed and decompressed. The cerebrospinal fluid circulation could not be established for a period of time, and the secondary injury of the cauda equina continued to increase. Therefore, the acute injury is worse after the injury. Chronic onset is often accompanied by symptoms of lumbar spinal stenosis, incomplete damage to the cauda equina, repeated symptoms, and good decompression.

Tandon analyzed and classified CES caused by disc factors. According to the rapid onset of the disease, it is divided into: type I, acute onset, sudden onset of horsetail injury; type II, acute onset, horsetail injury occurs on days or weeks after waist and leg pain; type III, chronic onset, long history, more With the symptoms of lumbar spinal stenosis, the horsetail injury is incomplete and the symptoms are repeated. Kstuik divides it into two types: type A, acute horsetail injury occurs within 1 week; type B, progressive horsetail damage occurs within months and weeks. According to the degree of injury, it is divided into: (a) complete injury, complete loss of sphincter function, numbness in the saddle area, muscle spasm in the calf; (b) incomplete acute injury, the above sensory movement is only partially lost.

Firearm damage

Firearm injuries are caused by direct or indirect violence, and are more common during wartime. Recent literature has also reported that John conducted in-depth research on patients with CES caused by firearm injuries. It is believed that bullets or bullet fragments are injected into the spinal canal or paravertebral. The trajectory undergoes a series of inflammatory reactions over a period of time, fibrous tissue hyperplasia, followed by scar formation, and scar tissue involving the cauda equina. On the other hand, bullets are generally made of metal. When they enter the human body, they produce a series of chemical reactions. The resulting chemicals stimulate the cauda equina to cause inflammatory changes. It has been reported that 1 case of the bullet stays in the L45 intervertebral space. A few years later, arachnoiditis occurs in the corresponding segment, and the arachnoid and cauda equina are extensively adhered. Some people also observed in the observed cases that no obvious CES was observed for a period of time when the bullet was injected. When the symptoms appeared, the body found a large cyst in the same segment of the spinal canal as the bullet. Emphasis is placed on the damage of bone and soft tissue leading to damage and re-repair of nerve tissue. The scar tissue surrounding the cauda equina nerve produces compression and chemical stimulation. The cauda equina is the main cause of CES.

Bleeding

Schmidt et al. studied progressive CES caused by fistula aneurysms. According to the information provided by the symptoms and signs, the lesion is located in the lumbosacral region. MRI examination showed dural sac compression and intraspinal space occupying. The angiography revealed that the space was active hemorrhage, and the hematoma oppressed the cauda equina to cause CES.

Spinal anesthesia

There have been more reports of CES caused by spinal anesthesia. Drasner et al. studied CES caused by epidural anesthesia, and concluded that there are three reasons: (1) epidural anesthesia needles directly into the subarachnoid space directly damage the cauda equina nerve to make the cauda equina edema and adhesion; (2) needle injury Epidural choroid plexus forms an epidural hematoma, oppressing the cauda equina nerve; (3) toxic effects of anesthetics. Such reports are often found in non-fresh chemical substances.

Some people have used intervertebral disc injection of intervertebral disc lytic enzyme to treat CES caused by disc herniation. Samuel et al. analyzed 3 patients, 1 of whom used this method to cause incomplete paralysis of the lower extremities. The other 2 cases produced severe CES. The reason may be that the lytic enzyme dissolves the intervertebral disc incompletely, forming intervertebral disc fragments, which enter the spinal canal and cause compression of the cauda equina. It may also cause arachnoid edema adhesion caused by arachnoiditis caused by lytic enzyme intrusion or invasion into the subarachnoid space, and the degree of this pathological change is directly proportional to the severity of the symptoms.

surgery

More common in lumbar discectomy and spinal canal enlargement, Kardaun et al. analyzed the causes of CES after lumbar disc surgery: (1) surgical action is rough or in order to seek protrusions, nerve strippers are too hard to squeeze Membrane sac and cauda equina directly damage the cauda equina and nerve roots; (2) Unreasonable laminectomy and decompression, leading to instability or slippage of the lumbar spine; (3) scar formation directly compresses the cauda equina after surgery.

an examination

Related inspection

Spinal MRI examination, CT examination, neurological examination

Lumbar X-ray examination

Lumbar X-ray can be used to macroscopically observe lumbar degeneration or external injury, which is the basis for the diagnosis of lumbar disease, and can not be ignored. X-ray films of lumbar degenerative spondylolisthesis, lumbar intervertebral disc degeneration, intervertebral space narrowing, transitional vertebrae, fractures, bone tumors, etc. have important diagnostic significance, combined with clinical diagnosis of cauda equina nerve damage.

Myelography

The nerve root and the dural sac are developed, and the degree of filling thereof reflects its own lesion or damage from another angle. But angiography itself is a kind of trauma.

CT and MRI

CT and MRI and various contrast agents, whether water-soluble or water-insoluble as chemical factors, may damage the arachnoid or cauda equina more or less, and sometimes may cause headache, dizziness, fever, iodine allergy, and increased primary symptoms. Adverse reactions such as convulsions, severe refractory adhesive arachnoiditis, contrast agents should be carefully selected, and Ommupaque is currently used. Most patients with cauda equina syndrome have a clear cause of the disease and should be selected according to the specific circumstances.

Differential diagnosis

Lumbar spondylolisthesis refers to a condition in which part or all of the lumbar vertebrae are dislocated. It is generally called the vertebral body in the clinic, and the upper vertebral body is generally slipped forward.

Degenerative lumbar spondylolisthesis is caused by prolonged sustained lumbar instability, which causes degenerative changes in the corresponding facet joints, and the level of joint abrupt changes, combined with degeneration of the intervertebral disc, making the connection between the vertebrae loose and unstable, and gradually occurs. Lumbar spondylolisthesis. This disease is also called pseudo-slip due to the integrity of the isthmus.

The lumbar spondylolisthesis is caused by the isthmus cracking. The cause of the isthmic cracking is still unclear. It may be related to the narrow and weak isthmus of the lumbar spine. On this basis, the isthmus is prone to fatigue fracture and fracture, and then the fracture does not heal. The isthmus was cracked. The isthmus cracking may not be combined with lumbar spondylolisthesis, but the degree of lumbar spondylolisthesis formed after isthmus cracking can be very heavy.

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