Angular deformity of the spine
Introduction
Introduction Spinal deformity : The human spine develops faster during the embryonic period and all structures are completed within a few weeks. After the spine is formed, it has its shape and stability. The entire development process is divided into four phases. The first phase, called the spinal cord, is formed on the fifteenth day of the embryo, and the remaining part of the embryo survives, called the nucleus pulposus; the second phase is called the membranous phase, starting from the 21st day to the end of three months; the third phase is the cartilage Period, from 5 to 6 weeks to before birth; the fourth period is the skeletal period, from two months to the completion of a part of birth. When the embryo develops to the 14th to 21st day, the lamellar cell layer separates the amniotic cavity and the yolk sac. From then on, it is divided into ectoderm, mesoderm and endoderm. The ectoderm forms a neural plate, which is submerged into a sulcus, which in turn develops into a neural tube. The spinal cord originates from the mesenchymal cells and is located in the deep layer of the neural tube. A pair of body segments are formed around the notch along the midline. The mesoderm gradually evolves into a "bone joint" along the neural tube, forming a "bone joint", developing along the neural tube and the notochord, and finally forming a vertebral body.
Cause
Cause
First, structural scoliosis
1. Idiopathic scoliosis: The cause of the disease is unknown, and it is generally considered to be related to a variety of factors. In addition to genetic abnormalities, it is considered to be related to postnatal posture and movement. Some small babies always lie in a single direction without turning over, causing the undeveloped soft skull and pelvis to be deformed by gravitation, and the compression of the thorax affects the spine, which may be the cause of idiopathic scoliosis.
A. Infant type (0-3 years old).
B. Juvenile type (2-10 years old).
C. Adolescent (greater than 10 years old).
2. Neuromuscular scoliosis
A. Neurological diseases:
(1) Upper motor neuron lesions: cerebral palsy, spinal cerebellar degenerative disease, syringomyelia, spinal cord tumor, spinal cord trauma.
(2) Lower motor neuron lesions: polio, other viral myelitis, spinal cord trauma, spinal muscular atrophy, paralytic spinal meningocele.
(3) Painless (Riley-Day Syndrome).
(4) Others.
B. Muscle disease:
(1) Muscular multiple joint contracture
(2) Progressive muscular dystrophy
3. Congenital scoliosis congenital spinal deformity is associated with abnormal development of the embryo during the first 8 weeks of pregnancy.
A vertebral body formation:
(1) Wedge-shaped vertebral body.
(2) Half vertebral body.
B vertebral segmentation is poor:
(1) Unilateral bone bridge (unsegmented bar).
(2) bilateral bone bridge.
(3) Mixed type.
4. Neurofibromatosis
5. Mesenchymal disease: Ma Fan syndrome. Ehrlers-Danlos syndrome, etc.
6. Rheumatoid disease
7. Traumatic scoliosis
A fracture.
B After laminectomy, after thoracoplasty.
C After radiation therapy.
8. Soft tissue contracture around the spine
A empyema.
B after burns.
9. Osteochondral malnutrition
A. Bone deformity dwarf.
B. Mucopolysaccharidosis.
C. Spinal epiphysis dysplasia.
D. Multiple epiphyseal dysplasia.
10. Acute and chronic infection of the bone
11. Metabolic disease
A. Rickets.
B. Osteogenesis is incomplete.
C. homocystinuria.
D. Other.
12. Lumbosacral joint related diseases
A. Spine slippage.
B. Congenital dysplasia of the lumbosacral spine.
13. Tumor
A. Spinal tumors (osteoid osteoma, histiocytosis X).
B. Spinal cord tumors.
Second, non-structural scoliosis
Posture
2. Caries
3. Disc herniation or tumor-induced nerve root stimulation
4. Inflammation (appendicitis)
5. Secondary in the lower limbs unequal length
6. Contracture around the hip joint
Third, kyphosis
1 posture
2 spinal osteochondrosis
3 congenital
A vertebral body formation is poor.
B vertebral body segmentation is poor.
C mixed type.
4. Neuromuscular kyphosis
5. Meningocele
A developmental type (paralysis).
B Congenital type.
6 traumatic kyphosis
A No bone or ligament damage damaged by the spinal cord.
B has bone or ligament damage that is damaged by the spinal cord.
7 postoperative kyphosis
A after laminectomy.
B after vertebral resection.
8 radiotherapy kyphosis
9 metabolic kyphosis
A Osteoporosis.
B rickets.
C Osteogenesis is incomplete.
D Other.
10 bone dysplasia
A Osteophytes are dysplastic.
B mucopolysaccharidosis.
C neurofibromatosis.
11 Collagen disease: ankylosing spondylitis.
12 neoplastic kyphosis
13 inflammatory kyphosis
Fourth, lordosis
1. Posture.
2. Congenital.
3. Neuromuscular.
4. After laminectomy.
5. Hip flexion contracture.
Examine
an examination
Related inspection
Spinal MRI examination of erythrocyte sedimentation rate (ESR)
The diagnosis of this disease is not difficult to make according to children's nutritional history and x-ray examination. The forehead is prominent, the chest is easy to see beaded, but the limbs and fingers are short and thick, the lumbar vertebrae are obviously lordosis, the blood calcium and phosphorus are normal, the dry energy end is wide, but the contour is still Finishing.
First, scoliosis
1. Ask about the family history, the time, extent and development of scoliosis, and whether there are any history of trauma, infection, tumor and metabolic diseases.
2. Measure the height, check the degree of scoliosis, and pay attention to the development of the whole body, especially the chest shape and cardiopulmonary function, whether there is a knife-like deformity.
3. X-ray examination to determine the presence or absence of hemivertebra deformity, except for acquired lesions, and to measure the angle of scoliosis according to the Cobb method. At the same time, the degree of spine development should be estimated. If necessary, you should rotate the position film.
4. Perform a myelography or MRI if necessary.
5. Cardiac function tests should be performed in patients with severe deformities.
Second, kyphosis
1. Ask if there is a family history, whether there is any history of trauma, infection, tumor and metabolic disease, whether there is stiffness in the lower back, dyspnea and hip pain after morning, and the time, extent and development of kyphosis.
2. Check the degree of kyphosis, limited spinal activity, and cardiopulmonary function. Bilateral hip joints have no tenderness and limited mobility.
3. Laboratory tests mainly include: erythrocyte sedimentation rate, anti-streptolysin O, rheumatoid factor, serum HLA-B27 examination.
4. X-ray examination should include the spine and pelvis to observe the deformity angle and whether it involves the hip joint.
Diagnosis
Differential diagnosis
(1) Kashin-Beck disease
Also known as "Kashin-Beck disease", the cause is still unclear, mostly in the eastern part of Siberia in the former Soviet Union and adjacent areas in the northeast of China, and distributed in a strip shape from northeast to southwest in China. The age of onset of this disease is mostly from pre-school to pre-puberty, and adults can also develop disease, but it is rare. Kaschin-Beck disease mainly invades the bones and joint system, usually chronic, with few systemic symptoms. The whole body joints are generally affected, and the limbs are more common. The damage is bilateral but not necessarily symmetrical. Among them, the interphalangeal joint is more common and early, followed by the elbow, ankle, knee, wrist, marrow and shoulder. The damage of the spine is rare. Can be heavier. The onset is more insidious. At first, there is often only pain, numbness, ant movement, or joint activity is not flexible. After the morning, the joints are stiff. The first thing to pay attention to is the interphalangeal joint or the ankle joint. Sometimes the patient has no symptoms and the joints are found to be thick or frizzy. Individual patients have only symptoms such as fatigue and fatigue, but lack local symptoms. In the examination, the joints are thickened, and there are frictional sounds during flexion and extension. The early joint movements are not necessarily limited, and the X-ray examination can also be seen without abnormalities. As the disease progresses, the joints gradually thicken and dysfunction occurs. In the later stage, the limbs and fingers were significantly shortened, the joints were thick, the pain was limited, the muscles were atrophied, and there were severe short-finger deformities and short stature. X-ray films with interphalangeal joints, tendons and knee joints are more typical, showing that the joint surface is uneven, and the subchondral bone is dense. There is currently no specific method for the diagnosis of Kashin-Beck disease, and the diagnosis is generally based on a comprehensive analysis of medical history, physical examination and X-ray examination. The area where the patient lives is helpful for diagnosis.
(two) rheumatoid arthritis
The disease is a systemic disease characterized by joint inflammation and unclear etiology. The disease is most common in women aged 25-45. Prodromal symptoms are weakness, fatigue, and loss of appetite. Then there is a joint lesion characterized by multiple, symmetric joint involvement, slow and recurrent episodes, joint swelling and pain with progressive aggravation. In general, early manifestations of the disease include joint exudation, tenderness and limited mobility, and finally deformities, including incomplete dislocation of the joints, and joint contractures. Laboratory tests can have mild anemia, increased white blood cell counts, and increased erythrocyte sedimentation rate. About 75% of patients are positive for rheumatoid factor. The joint fluid is turbid, the formation of partial protein blocks is poor, the cell count is increased, and polymorphonuclear granulocytes are increased. X-ray examination showed soft tissue swelling and osteoporosis in the early stage, and the joint space was narrowed, erosion and deformity in the later stage.
(3) Congenital polyarticular contracture
The disease is a congenital malformation, involving the joints of the extremities. It is characterized by limited active and passive activities of the joint, fixed in the straight or flexed position, and the joint has only a few degrees of painless passive activity. The skin is not normally wrinkled and tightened; the skin of the joint has a small pit flexion deformity on the flex side with a span formed by skin and subcutaneous tissue. Often there are deformities such as clubfoot, dislocation of the silver joint, dislocation of the bones, scoliosis, etc., and may be accompanied by congenital heart disease and kidney deformity.
(4) Vitamin D deficiency
Mainly due to the lack of vitamin D, the absorption of calcium and phosphorus in the intestine is reduced, and the product of blood calcium and phosphorus is decreased, causing the temporary calcification zone to thicken and bone. It can increase the rib beading and hand silver seen in the clinic. The ankles are marked by X and the growth of the bones is stagnant. The main skeletal system of the disease changes as follows;
l, the head skull softens, more common in 3-6 months of babies, fingers gently press the occipital bone or the center of the parietal bone, like the feeling of pressing table tennis. Square skull, more common in patients 8-9 months or more, severe cases can be saddle-shaped, cruciform cranial. The front bunker is closed. Delayed teething.
2, chest ribs beading, rib groove, chicken chest or funnel chest, the above deformity is more common in children around 1 year old.
3, limbs wrist deformity, more common in patients over 6 months, the distal end of the forearm calf long bone can and even see the thick bone marrow, forming a blunt ring-shaped bulge, called rickets hand or foot silver. An "O" shaped leg or an "X" shaped leg may appear after the patient walks.
4, other pediatrics can cause posterior or lateral curvature of the spine after sitting, and the anterior and posterior diameter of the severe pelvis becomes shorter to form a flat pelvis.
The diagnosis of this disease is not difficult to make based on the child's nutritional history and X-ray examination.
(5) Cartilage malnutrition
The head is large, the forehead is prominent, the long bone marrow bulges, the chest is easy to see beading, the abdomen is similar to the rickets, but the limbs and fingers are short and thick, the five fingers are flush, the lumbar vertebrae are lordosis, and the hips are kyphosis. Blood calcium and phosphorus are normal. The X-ray shows that the long bone is short and thick and curved, and the dry energy end is widened and has a flared shape, but the contour is still smooth, and sometimes some of the bone marrow is buried in the dry energy end.
A physical examination can be diagnosed.
