Spinal stenosis
In 1910, Sumita first described lumbar spinal stenosis in patients with chondrodysplasia, followed by Donath and Vogl, and in 1953, Schlesinger and Taverus gave a more comprehensive description. Verbiest and Epstenin in 1962 successively proposed neurological complications due to lumbar spinal stenosis with compression of the cauda equina. 1964 Brish and 1966 Jaffe et al. described intermittent rupture associated with spinal stenosis. Zhang Yafeng, Department of Spinal Orthopedics, Wuxi Hospital of Traditional Chinese Medicine
[Etiology
Developmental spinal stenosis, also known as primary spinal stenosis: this spinal stenosis is caused by congenital developmental abnormalities. Therefore, the anterior and posterior diameters and the left and right diameters of the spinal canal are consistently narrowed. The capacity of the spinal canal is small, and any of the causes can further narrow the spinal canal, causing irritation or compression of the spinal cord, cauda equina, or nerve roots. If the transverse canal transection is trilobar shaped it can often narrow the lateral saphenous fossa. Degenerative spinal stenosis, also known as secondary spinal stenosis, is mainly caused by degenerative lesions of the spine. Due to degenerative disease of the spine, the intervertebral disc atrophy and absorption, narrowing of the intervertebral space, and loosening of the annular ligament, pseudo-slip or hyperplasia of the spine may occur. More due to spinal laxity, the vertebral plate and the ligamentum flavum can be thickened by abnormal stimulation (e.g., the thickness of the vertebral plate exceeds 5 mm and the thickness of the ligamentum flavum exceeds 4 mm, which is abnormal), and the epidural fat becomes variable and fibrotic, so that the dura is compressed, causing a series of cauda equina and nerve compression or irritation symptoms. Spinal slip stenosis, if the patient has spinal collapse disorder or lumbar isthmus discontinuity, can often occur. When there is spinal slippage, the spinal canal can be further narrowed due to anterior and posterior displacement of the upper and lower spinal canal. Due to spinal slippage, degeneration can be promoted and fibrocartilage proliferation in the isthmus can add to the narrowing of the spinal canal, compressing nerve roots in the cauda equina or lateral saphenous fossa and causing spinal stenosis. Medical spinal stenosis, due to the stimulation of various surgical treatments, especially after the implementation of spinal fusion implants, can often cause hypertrophy of the interspinous ligament and ligamentum flavum or thickening of all the vertebral plates in the implant, resulting in narrowing of the spinal canal and compression of the cauda equina or nerve roots, causing spinal stenosis. Traumatic spinal stenosis, when the spine is traumatized, especially when the trauma is severe enough to cause a spinal fracture or dislocation, often causes spinal stenosis, compressing or stimulating the cauda equina or nerve roots, causing spinal stenosis. Spinal stenosis caused by other bone diseases, such as deformity and fluorosis, can be caused by thickening of the vertebral body, vertebral plate, and soft tissues, which reduces the content of the spinal canal and compresses or stimulates the nerve roots, causing spinal stenosis. Clinical manifestations】The disease is most common in lumbar spine 4-5 and lumbar 5-sacral 1. The main symptom is lumbar and leg pain, often occurring on one or both sides of the radicular radicular neuralgia. In severe cases, it can cause weakness of both lower limbs, sphincter relaxation, diplegia or light paralysis. Another major symptom of spinal stenosis is intermittent rupture. In most patients, when standing or walking, the symptoms of lumbar and leg pain are aggravated, and when walking a shorter distance, they feel pain and numbness in the lower limbs, and the more they walk, the heavier they become. When squatting or sitting slightly, the symptoms of low back pain and streaking are relieved. The main cause of intermittent claudication may be related to irritation or compression of the cauda equina or nerve roots. 1803 Portal was the first to notice that the narrowing of the anterior and posterior diameters of the spinal canal could compress the nerves in the spinal canal. 1858 Charcot believed that insufficient blood supply to the skeletal muscles due to vascular lesions in the lower extremities could also cause intermittent claudication, so intermittent claudication was divided into two major categories: neurological intermittent claudication and vascular intermittent claudication. In 1949, Boyd pointed out that vascular intermittent claudication occurs only after walking with spasmodic pain in the thigh or calf muscles, and the clinical symptoms can be relieved after rest. In contrast, intermittent claudication caused by compression of lumbosacral nerve roots due to spinal stenosis is also called neurogenic intermittent claudication. It can be caused by the change of position of the lower extremity radiating neuralgia, especially whenever the lumbar spine is hyperextended, the symptoms of lumbar and leg pain are aggravated. This is because when the lumbar spine is hyperextended, the anterior part of the lumbar spinal space widens and the posterior part narrows, often causing the lumbar intervertebral disc and the fibrous ring to protrude into the spinal canal, which further narrows the spinal canal and stimulates or compresses the nerve roots. It also causes nerve root or cauda equina irritation due to shortening and thickening of the lumbar hyperextension nerve roots, which are easily compressed. At the same time of dorsal extension, the ligamentum flavum of the lumbar spine also relaxes and forms a thickened crease, making the intervertebral foramen smaller and also compressing or stimulating the cauda equina and nerve roots, causing irritation of the cauda equina and nerve roots. When the lumbar spine is bent forward, the above clinical symptoms can be reduced by the elongation of the tissue behind the spinal canal, the reduction of the content of the spinal canal and the retraction of the prolapsed intervertebral disc, etc. They can also be reduced by squatting slightly, sitting slightly or resting in bed. Therefore, those who suffer from lumbar spinal stenosis tend to have more and heavier conscious symptoms and fewer positive signs. This is because the clinical signs may have resolved or disappeared by the time the patient is examined in bed. The common clinical signs, in addition to symptom reduction during lumbar forward flexion and aggravation of lumbar leg pain during lumbar dorsiflexion, are often positive or negative for straight leg raising, often the same on both sides, and abnormal or diminished sensation in the lower extremities. Weakness in both legs, abnormal knee Achilles tendon reflex and sphincter weakness, and dysfunctional bowel movements. Measurement of the spinal canal: From 1975 to 1977, Verbiest’s spinal stenosis was based on the central sagittal diameter of the spinal canal (m-s diameter) and the spinal canal flaw. 1. Absolute type, that is, the central sagittal diameter of the spinal canal is less than or equal to 10 mm, is absolute spinal stenosis (m-s ≤ 10 mm). 2. ～3. mixed type, in which the central sagittal diameter (m-s diameter) is less than 11.5 mm, is definitely pathological. If the ratio of the central sagittal diameter of the cephalic or caudal side of the lumbar spinal canal is greater than 1, it is an abnormal phenomenon (the ratio of m-s diameter is less than when the cephalic and caudal sides are normal). Transverse diameter: i.e., the maximum distance of the vertebral arch, the average value is 23 mm. the lower limit of its normal value is 13 mm (15 mm for X-ray pictures). [Auxiliary examination] The orthogonal X-ray often shows mild lumbar scoliosis, the inter-articular distance between the synapses becomes smaller, and there are degenerative changes. Lateral radiographs often show a small central sagittal diameter of the spinal canal, and less than 15 mm indicates the possibility of stenosis. If necessary, lumbar puncture, Quaker test, cerebrospinal fluid testing, and myelography can be performed. Myelography is a reliable method for diagnosing this condition. Orthopantomographs can clearly show the size of the dural cavity. If there is a striated or whisker-like shadow, it indicates compression of the cauda equina nerve root or total obstruction, and if the shadow column is segmentally narrowed or interrupted, it indicates multiple or total obstruction. CT and MRI examination: the size ratio of the sphincter and bony vertebrae both change, the sphincter and nerve roots are compressed, the epidural fat disappears or decreases, the articular process hypertrophy makes the lateral saphenous fossa and spinal canal narrow, the trilobar spinal canal, and the interarch ligament and posterior longitudinal ligament are hypertrophied. Diagnosis】It is not difficult to diagnose based on detailed history, clinical symptoms and signs, radiographs and myelography, but it needs to be differentiated from lumbar disc herniation and thrombo-occlusive vasculitis, etc. Treatment measures] For atypical cases, non-surgical treatment should be used first, such as bed rest, traction, massage, physiotherapy and medication. At the same time, cold and overexertion should be avoided to promote the recovery of symptoms of nerve irritation. In typical cases where non-surgical treatment is ineffective, surgical treatment should be considered. Surgery is based on total laminectomy and complete decompression. By complete decompression, it is meant that the lamina should not only be high and wide enough when it is removed, but also the hyperplastic bone in the posterior part of the vertebral body (anterior part of the spinal canal) and the lateral saphenous fossa should be released so that all compression of the cauda equina and nerve roots can be completely removed.