Scoliosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Rohan A. Bhimani, M.B.B.S., D.N.B., M.Ch.[2]

Scoliosis is defined as a deviation of the normal vertical line of the spine, consisting of a lateral curvature with rotation of the vertebrae within the curve.^[1] Typically, for scoliosis to be considered, there should be at least 10° of spinal angulation on the posterior-anterior radiograph associated with vertebral rotation (1). The causes of scoliosis vary and are classified broadly as congenital, neuromuscular, syndrome-related, idiopathic and spinal curvature due to secondary reasons. Congenital scoliosis is due to a vertebral abnormality causing the mechanical deviation of the normal spinal alignment. Scoliosis can be due to neurological conditions (eg, cerebral palsy or paralysis), muscular abnormalities (eg, Duchenne muscular dystrophy) or other syndromes (eg, Marfan’s syndrome and neurofibromatosis). Occasionally, significant lateral deviation of the spine can occur with little or no rotation of the spine and without bony abnormalities. In these cases, the scoliosis can be the result of pain, spinal cord abnormalities, tumors (both intraspinal and extraspinal) and infection.The natural history relates to the etiology and age at presentation, and usually dictates the treatment. However, it is the patient’s history, physical examination and radiographs that are critical in the initial evaluation of scoliosis and in determining which patients need additional evaluation and consideration.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Rohan A. Bhimani, M.B.B.S., D.N.B., M.Ch.[2]

In 490 BC, Hippocrates described scoliosis for the first time. In 1890, Lewis Sayre popularized plaster of Paris casts that he applied to patients while they were standing in a vertical suspension device and attempted to correct both lateral and rotational deformities and held them with a cast. In 1931, Hibbs along with Risser and Ferguson suggested of the turnbuckle cast for preoperative correction and creation of a window in the back of the cast through which to operate, while maintaining correction. In 1948, John Cobb described a method of measuring scoliosis curve magnitude radiologically and is still widely used today. In the same year, Walter Blount, together with Albert Schmidt, popularized their Milwaukee brace. In 1955, Paul Harrington developed Harrington distraction instrumentation which was a clear milestone in scoliosis surgery providing for the first time, a reliable means of obtaining and maintaining maximal deformity correction. In 1970s, Hall and Miller developed the Boston brace which has remained a popular choice in the nonoperative treatment of scoliosis. In the same period, Luque further developed the segmental spinal instrumentation system using sublaminar wires at each vertebral level connected to Harrington rods or L-shaped Luque rods. Cotrel and Dubousset introduced their segmental instrumentation method of fixation to provide three-dimensional correction of the scoliotic deformity in late 1980s.

• The word scoliosis is derived from the greek word meaning ‘crooked’.^[1][2][3]
• In 490 BC, Hippocrates described scoliosis for the first time. ^[4]
• In 131-201 BC, Galen coined the terms scoliosis, kyphosis, and lordosis to describe spinal deformity.
• In 1510-1590, Ambrose Pare first described congenital scoliosis and appreciated spinal cord compression as a possible cause of paraplegia.
• In 1741, Nicholas Andre coined the word “orthopedia” meaning “straight child”. He emphasized that scoliosis was the result of muscle imbalance, a consequence of poor sitting posture.^[5]

• In 490 BC, Hippocrates described distraction devices for treatment of scoliosis.^[4]
• In 131-201 BC, Galen advised various chest binders and jackets in an effort to control spinal curves.
• In 1510-1590, Ambrose Pare advocated the use of iron corsets fabricated by armorers, in addition to axial traction. He also recommended new breast plates to be made every 3 months for growing individuals.
• In 1741, Nicholas Andre Proper recommended construction and use of tables and chairs for students in preventing scoliosis. For the treatment of scoliosis, he endorsed periods of recumbence, as well as braces or corsets.
• In 1768, Francois LeVacher described the “Jurymast” brace, which allowed for axial distraction while the patient was upright. This was accomplished by a tight fitting cap suspended from a posterior bar arising from the back of the brace.
• In 1780, Jean-Andre Venel founded the first orthopedic hospital specializing in the treatment of skeletal deformities. In addition, to an orthopedic traction bed, Venel developed a brace which applied horizontal forces attempting to derotate the spine, as well as the extension forces.^[6][7]
• In 1839, Jules Guerin used percutaneous myotomies of the vertebral musculature in conjunction with bracing to correct the deformity.

• In 1889, Volkman attempted to resect rib deformities, the first known scoliosis surgery on bony structures.
• In 1890, Lewis Sayre popularized plaster of Paris casts that he applied to patients while they were standing in a vertical suspension device and attempted to correct both lateral and rotational deformities and held them with a cast.
• In 1902, Lange used steel rods and wire anchored to the spinous processes bilaterally in the treatment of tuberculosis kyphosis.^[8]
• In 1911, Albee described his technique of spinal fusion for Pott’s disease of the spine using tibial autograft.
• In 1924, Hibbs reported his results on 59 cases of scoliosis that were treated with fusion. Hibbs’ method utilized preoperative traction jackets and/or head-pelvic traction to obtain correction and used cast immobilization for 6 to 12 months post-operatively to maintain correction.
• In 1931, Hibbs along with Risser and Ferguson suggested of the turnbuckle cast for preoperative correction and creation of a window in the back of the cast through which to operate, while maintaining correction.^[9]
• In 1941, Research Committee of the American Orthopedic Association reviewed treatment for scoliosis and found overall end results discouraging with 69% rated as fair or poor, while only 31% as good or excellent.
• In 1948, John Cobb described a method of measuring scoliosis curve magnitude radiologically and is still widely used today.
• In 1948, Walter Blount, together with Albert Schmidt, popularized their Milwaukee brace.
• In 1955, Paul Harrington developed Harrington distraction instrumentation which was a clear milestone in scoliosis surgery providing for the first time, a reliable means of obtaining and maintaining maximal deformity correction.^[10]
• In 1958, Joseph Risser described the Risser’s Sign, documenting the coincidental development of vertebral endplate growth and the excursion of ossification of the iliac apophysis. This remains a useful tool in the management of scoliosis.
• In 1958, John Moe endorsed surgical technique that emphasized on facet fusion, thorough decortication, and addition of autologous bone.
• In 1959, Nickel and Perry developed halo distraction apparatus to provide firm control of the neck and cervical spine.
• In 1965, A. R. Hodgson reported relative success with transthoracic approach with anterior wedge resection, hemivertebrae excision, and interbody fusion.
• In 1968, Dwyer further advanced anterior spinal surgery by developing instrumentation system utilizing specialized screws that crossed the vertebral body. The heads of

the screws had a large hole to accept the flexible cable. Segmental compression at each level proved to be effective especially in treating scoliosis of neuromuscular origin.

• In 1975, Hall and Miller developed the Boston brace which has remained a popular choice in the nonoperative treatment of scoliosis.
• In 1978, Luque further developed the segmental spinal instrumentation system using sublaminar wires at each vertebral level connected to Harrington rods or L-shaped Luque rods.^[11]
• In 1982, Drummond developed instrumentation utilizing wires passed through a hole made at the base of each spinous process.
• In 1984, Cotrel and Dubousset introduced their segmental instrumentation method of fixation to provide three-dimensional correction of the scoliotic deformity, in some cases improving sagittal alignment.^[12]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Rohan A. Bhimani, M.B.B.S., D.N.B., M.Ch.[2]

Scoliosis can be classified into congenital scoliosis (due to failure of vertebral formation or segmentation of affected vertebrae), idiopathic scoliosis(when the cause is not known) or neuromuscular scoliosis (due to loss of muscle strength or voluntary muscle control).

• Congenital scoliosis is subdivided based on radiological finding, combined structural component involved and 3-D CT.^[1][2]

• Idiopathic scoliosis may be further classified into three types based on age of onset and anatomical level involved.^[3][4]

• Infantile idipathic scoliosis (birth to 3 years)
• Juvenile idiopathic scoliosis (4 to 9 years)
• Adolescent idiopathic scoliosis (10 to 20 years)

King and Moe defined five curve types:

• Type 1: an S shape deformity, in which both curves are structural and cross the CSVL, with the lumbar curve being larger than the thoracic one
• Type 2: an S shape deformity, in which both curves are structural and cross the CSVL, with the thoracic curve being larger or equal to the lumbar one
• Type 3: major thoracic curve in which only the thoracic curve is structural and crosses the CSVL
• Type 4: long C shape thoracic curve in which the fifth lumbar vertebra is centered over the sacrum and the fourth lumbar vertebra is tilted into the thoracic curve
• Type 5: double thoracic curve

• Neuromuscular scoliosis can be further subdivided based on the classification of scoliosis research society.^[5]
  • Primary neuropathies
  • Upper motor neuron neuropathies
    • Cerebral palsy
    • Spinocerebellar degeneration
      • Friedreich ataxia
      • Roussy-Levy disease
      • Spinocerebellar ataxia
    • Syringomyelia
    • Spinal cord tumor
    • Spinal cord trauma
  • Lower motor neuron neuropathies
    • Poliomyelitis
    • Other viral myelitides
    • Traumatic
    • Charcot-Marie-Tooth disease
    • Spinal muscular atrophy
      • Werdnig-Hoffmann disease (SMA type 1)
      • Kugelberg-Welander disease (SMA type 2)
    • Dysautonomia
      • Riley-Day syndrome
    • Combined upper and lower pathologies
      • Amyotrophic lateral sclerosis
      • Myelomeningocele
      • Tether cord
  • Primary myopathies
    • Muscular dystrophy
      • Duchenne muscular dystrophy
      • Limb-girdle dystrophy
      • Facioscapulohumeral dystrophy
    • Arthrogryposis
    • Congenital hypotonia
    • Myotonia dystrophica

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Rohan A. Bhimani, M.B.B.S., D.N.B., M.Ch.[2]

The exact pathogenesis of scoliosis is not fully understood. It is thought that scoliosis is the result of nutritional, endocrine, or genetic factors.The observation that curve development and progression correlate with the period of rapid adolescent growth appears to support a biomechanical contribution. However, multiple theories exist that attempt to explain the process by which the development takes place, and while each makes sense from a biomechanical standpoint. Malfunctioning melatonin and calmodulin signal pathway have been proposed for development of idiopathic scoliosis. In addition, theories suggesting a relative anterior spinal overgrowth (RASO) or an uncoupled neuro-osseus growth as a cause of idiopathic scoliosis. Skeletal immaturity is the major risk factor for the curve progression. It has been noted that girls with adolescent IS are taller and have a higher growth velocity during puberty in comparison to healthy individuals. A lower bone mineral density, leptin, cartilage oligomeric matrix protein and a high levels of growth hormone have seen to be influencing development of the disease. The effect of genetics on idiopathic scoliosis is well established. From the genetic standpoint, scoliosis is not easily explained by existing inheritance models. It has been recently seen the disease to be associated with loci on OS1, OS2, OS3, OS4, OS5, CHD7 and PAX1 gene.

• Idiopathic scoliosis(IS) is the most common form of spinal deformity seen in healthy children and adoloscent during growth.
• The pathophysiology of scoliosis in not clearly understood.
• Many hypothesis have been postulated.

Role of Melatonin and Calmodulin

• Animal studies have shown that pinealectomies lead to development of scoliosis due to lack of melatonin.^[1][2][3]
• Dysfunctional melatonin signal pathway involving MT2 receptors affecting osteoblast have been recommended.^[4][5]
• Calmodulin, a calcium-binding receptor protein, controls contraction in platelets and muscles, and interacts with melatonin. Increased levels of calmodulin in platelets and a disproportionate distribution of calmodulin in paraspinal muscles have been suggested in IS patients.^[6][7][8]

Biomechanical Derangement

• In literature, it has been shown that bone growth in the period of skeletal immaturity is retarded by mechanical compression on the growth plate and accelerated by growth plate tension.^[9]
• Because of the physiologic curvature in the normal thoracic spine, compressive force is delivered on the ventrally located part of the vertebral column, whereas distractive force is delivered on the dorsally located part.
• This process leads to abnormal spinal curvature which is thought to be initiated by the rotation of vertebral bodies in the axial plane, which causes discrepant axial loading between the ventrally and dorsally located portions of the involved vertebrae.
• Over time, the discrepancy manifests as a change in the directionality of spinal curvature; that is, the ventrally located part of the vertebral column becomes the concave side and the dorsally located part becomes the convex side of a lateral curve.
• On MRI scans of IS patients, it seen that the length of the spinal cord is shorter in relation to the vertebral column and there is an increased prevalence of cerebellar tonsillar ectopia as well as an uncoordinated growth of the vertebral bodies in relation to the dorsal elements.^[10][11][12]
• This has led to theories proposing a relative anterior spinal overgrowth (RASO) or an uncoupled neuro-osseus growth as a cause of IS.^[13]
• The risk of curve progression in IS is related to skeletal immaturity.
• It has also been shown that girls with adolescent IS are taller and have a higher growth velocity during puberty in comparison to healthy individuals.^[14][15][16]

Role of Bone Mineral Density, Growth and Sex Hormones

• Bone mineral density, growth, and sex hormones have been studied in the pathogenesis of IS.
• Adolescent girls with IS have lower bone mineral density and a higher bone turnover rate.^[17][18]
• In addition, a decreased level of cartilage oligomeric matrix protein (COMP) in serum is seen in IS patients.^[19]
• A raised levels of growth hormone (GH) and insulin-like growth factor 1 (IGF-1) have been associated with IS.^[20][21]

Role of Leptin

• A lower circulating levels of leptin, the “satiety” hormone have been suggested in pathogenesis of IS.^[22][23][24]
• Leptin is primarily secreted by adipocytes, and leptin receptor can be detected in chondrocytes and osteoblasts.
• Leptin regulates the osteogenic differentiation of bone marrow stem cells and the function of chondrocytes by directly binding to leptin receptors.
• Leptin functions to promotes chondrocyte proliferation and differentiation; regulates chondrocyte function by enhancing the production of collagen, matrix metalloproteinase (MMP), and bone morphogenetic protein (BMP) and remodels the cytoskeleton.

• The recognition of genetic influences in IS is well-documented.^[25][26]
• The general consensus is that, while families with dominant inheritance may exist, IS is generally a complex genetic disease that is not easily explained by existing inheritance models.^[27]
• A higher concordance seen in monozygotic (MZ) compared to dizygotic (DZ) twins.^[28]
• Polymorphisms in the collagen genes COL1A1, COL1A2, the fibrillin 1 gene FBN1, and the elastin gene ELN have been tested in family collections, but the results did not reveal evidence of linkage.^[29][30]
• Studies have shown five IS loci, OS1 (chr19p13.3), OS2 (chr 17p11), OS3 (chr 8q12.1-12.2), OS4 (chr 9q31-q34) and OS5 (chr 17q25-qter).^[31]
• Common single-nucleotide polymorphisms (SNPs) for gene within OS3, CHD7 have been associated with IS.^{[32][33][34][35]}
• Recently, a new IS susceptibility locus in an ~100-kb region of chromosome 20p11.22 downstream of PAX1 has been identified by Texas Scottish Rite Hospital for Children.^[36]

Scoliosis is sometimes associated with other conditions such as

• Cerebral palsy
• Spinal muscular atrophy
• Familial dysautonomia
• CHARGE syndrome
• Friedreich’s ataxia
• Spina bifida
• Marfan’s syndrome
• Neurofibromatosis
• Connective tissue disorder
• Craniospinal axis disorders (e.g., syringomyelia, Arnold-Chiari malformation).
• Roussy-levy disease
• Charcot-marie-tooth disease
• Duchenne muscular dystrophy
• Limb girdle dystrophy
• Arthrogyposis

However, the majority of people with adolescent scoliosis have no pain or other abnormalities.

There are no gross pathology findings associated with scoliosis.

• On microscopic histopathological analysis,cells of convex side of deformation are chondroblasts. Cells isolated from the growth plates of the concave side of the deformation showed numerous features of neuro- and glioblasts. These cells form synapses, contain neurofilaments, and expressed neural and glial proteins.^[37]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Rohan A. Bhimani, M.B.B.S., D.N.B., M.Ch.[2]

The most common cause of scoliosis is idiopathic. Less common causes of scoliosis include congenital and neuromuscular.

There are three general causes of scoliosis:

• Congenital (present at birth) scoliosis is due to failure of vertebral formation or segmentation of affected vertebrae in utero.^[1][2]
• Neuromuscular scoliosis is caused by problems such as poor muscle control or muscle weakness, or paralysis due to diseases such as cerebral palsy, muscular dystrophy, spina bifida, and polio.^[3]
• Idiopathic scoliosis is scoliosis of unknown cause. Idiopathic scoliosis in adolescents is the most common type.^[4]

• There are no life-threatening causes of scoliosis, however complications resulting from untreated scoliosis is common.

Common causes of scoliosis include:^[4]

• Idiopathic

Less Common causes of scoliosis can be divided into:^[3][4]

Nonstructural scoliosis

• Appendicitis
• Local inflammation
• Leg length discrepancy
• Muscle spasms

Structural scoliosis

• Amyoplasia congenita
• Arthrogryposis
• Bechterew’s Disease
• Benign tumors
• Brucella infection of the spine
• Cerebral Palsy
• Chondrodysplasia
• Dislocation
• Dwarfism
• Ehlers-Danlos syndrome
• Fredrick’s Ataxia
• Hemivertebra
• Homocystinuria
• Irradiation
• Malignant tumors
• Marfan’s Syndrome
• Morquio’s Disease
• Muscular Dystrophy
• Osteogenesis imperfecta
• Osteomalacia
• Osteoporosis
• Polyomyelitis
• Postoperative
• Rheumatic disease of the spine
• Rheumatoid Arthritis
• Rickets
• Salmonella infection of the spine
• Scheuermann’s disease
• Spinal cord trauma
• Spinal muscular atrophy
• Still’s Disease
• Syringomyelia
• Tuberculosis of the spine
• Unilateral bar
• VonRecklinghausen’s Disease

• Scoliosis may be caused by a mutations in the Mendelian gene, including:
  • CHD7 gene
  • PAX1 gene

List the causes of the disease in alphabetical order:

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Rohan A. Bhimani, M.B.B.S., D.N.B., M.Ch.[2]

Scoliosis must be differentiated from syringomyelia, spina bifida, arnold-chiari malformation and leg length discrepancy.

• Scoliosis must be differentiated from other diseases that causes spinal deformity, neurologic abnormalities and gait abnormalities, such as syringomyelia, spina bifida, arnold-chiari malformation and leg length discrepancy.^[1][2]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Rohan A. Bhimani, M.B.B.S., D.N.B., M.Ch.[2]

Scoliosis is the most common spinal deformity. The prevalence of scoliosis is approximately 470-5200 per 100,000 individuals worldwide. Patients of all age groups may develop scoliosis. Curves convex to the right are more common than those to the left, and single or ‘C’ curves are slightly more common than double or ‘S’ curve patterns. Scoliosis usually affects individuals of African-American race more than any other race. The female to male ratio is approximately 1.5-3 to 1 for idiopathic scoliosis, whereas its equal gender predilection for congenital scoliosis.

Scoliosis is the most common spinal deformity. Highest incidence of scoliosis is in adoloscent women. Epidemiology and demographics of scoliosis is as follows:^[1]

• The prevalence of scoliosis is approximately 470-5200 per 100,000 individuals worldwide.^[1]

• Patients of all age groups may develop scoliosis.
• Congenital scoliosis develops at the age of 0–3 years and have a prevalence of 1000 per 100,000 individuals.^[1]
• Adolescent scoliosis develops at the age of 11–18 years and accounts for approximately 90 % of cases of idiopathic scoliosis in children.
• Scoliosis has a prevalence of more than 8000 per 100,000 in adults over the age of 25 and rises up 68000 per 100,000 individuals in the age of over 60 years, caused by degenerative changes in the aging spine.

• Scoliosis usually affects individuals of African-American race.^[2]

The severity of curve according to race is as follows:^[3]

• Females are more commonly affected by idiopathic scoliosis than males. The female to male ratio is approximately 1.5-3 to 1.^{[1][4][5][6][7]}
• Congenital scoliosis affects males and females equally.

• The majority of scoliosis cases are reported in Germany.^[1]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Rohan A. Bhimani, M.B.B.S., D.N.B., M.Ch.[2]

Common risk factors in the development of scoliosis include Age (growth spurt), female gender and family history.

Common risk factors in the development of scoliosis include:^[1]

Age

• Signs and symptoms typically begin during the growth spurt that occurs just prior to puberty.

Gender

• Although both boys and girls develop mild scoliosis at about the same rate, girls have a much higher risk of the curve worsening and requiring treatment.
• Scoliosis in infants and young children are less common, and commonly affect boys and girls equally.

Family history

• Scoliosis can run in families, but most children with scoliosis don’t have a family history of the disease.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Rohan A. Bhimani, M.B.B.S., D.N.B., M.Ch.[2]

According to the US Preventive Services Task Force, American Academy of Orthopaedic Surgeons and Scoliosis Research Society, screening for scoliosis by visual inspection of the spine as well as Adam’s forward bend test looking for curvature is recommended in childhood, after age 10 years in schools.

• According to the US Preventive Services Task Force(UPSTF), American Academy of Orthopaedic Surgeons(AAOS), Pediatric Orthopaedic Society of North America (POSNA) and Scoliosis Research Society(SRS), screening for by visual inspection of the spine, shoulder and hips as well as Adam’s forward bend test with scoliometer looking for curvature is recommended in childhood, after age 10 years in schools.^{[1][2][3][4][5][6]}

• The females should be screened twice, at 10 and 12 years and boys once, at age 13 or 14 years.^[1][2]

• This is a simple screening test that can detect potential problems.
• Ask kids to bend at the waist as if they were touching their toes.
• Get eyes level with the child’s back to look for one side being higher than the other or any asymmetry of the back.

• Ask the child to slowly bend forward until the shoulders are level with the hips.
• View the child from the back with eyes at the same level as the back.
• Adjust the bending position height so the deformity of the spine is most pronounced.
• Gently lay the scoliometer across the deformity at right angles to the body, with the marking centered over the curve.
• Observe the scoliometer reading.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Rohan A. Bhimani, M.B.B.S., D.N.B., M.Ch.[2]

The literature on the natural history of untreated scoliosis is fairly limited. With curve progression, it can have effects on socioeconomic and marital status, increased disability due to back pain and late complications like pulmonary hypertension and cor pulmonale. The prognosis of scoliosis depends on the likelihood of curve progression. The general dictum of progression are that larger curves carry a higher risk of progression than smaller curves, and that thoracic and double primary curves carry a higher risk of progression than single lumbar or thoracolumbar curves. Moreover, patients who have not yet reached skeletal maturity have a higher likelihood of progression.

• The literature on the natural history of untreated Adolescent Idiopathic Scoliosis is fairly limited.^[1][2]
• Past studies revealed a grim prognosis,1-3 mostly as a result of socioeconomic effects on work and marital status, the development of cor pulmonale, and increased disability secondary to back pain.
• The major threat, though, is how the pulmonary function is affected over time.^[3][4][5][1]
• Pulmonary function is considered to be at its peak around the age of 20 years or just after, and a slow deterioration begins thereafter as part of the ageing process.^[5][1]
• If left untreated, an increase of the curve size further adds to the reduction of the pulmonary function.
• Thus,radiographs have to be performed at regular follow-up while observing for curve progression.

• Emotional problems or lowered self-esteem may occur as a result of the condition or its treatment (specifically, wearing a brace)
• Pseudoarthrosis (very rare in idiopathic scoliosis)^[5]
• Low back arthritis and pain as an adult^[5]
• Respiratory problems from severe curve with significant decline in pulmonary function leading to pulmonary hypertension and cor pulmonale^[5]
• Spinal cord or nerve damage from surgery or severe, uncorrected curve
• Spine infection after surgery
• Intracranial hemorrhage following surgery^[6]

• The outcome depends on the cause, location, and severity of the curve. The greater the curve, the greater the chance the curve will get worse after growth has stopped.
• The greater the initial curve of the spine, the greater the chance the scoliosis will get worse after growth is complete. Severe scoliosis (curves in the spine greater than 80 degrees) with early onset can cause cardio-pulmonary problems such as loss of vital capacity, pulmonary hypertension, and cor pulmonale, especially with thoracic curves.^[5]
• The mortality rate increased 2.2 times in all patients with idiopathic scoliosis and 3.2 times for patients above 45 years of age.^[5]
• Mild cases treated with bracing alone do very well. People with these kinds of conditions do not tend to have long-term problems, except an increased rate of low back pain when they get older.This leads to poor quality of life.
• People with surgically corrected idiopathic scoliosis can do very well and can lead active, healthy lives.
• Patients with neuromuscular scoliosis have another serious disorder (like cerebral palsy or muscular dystrophy) so their goals are much different. Often the goal of surgery is simply to allow a child to be able to sit upright in a wheelchair.
• In addition, the patients are usually self-conscious or depressed about their body shape.
• Babies with congenital scoliosis have a wide variety of underlying birth defects. Management of this disease is difficult and often requires many surgeries.
• The prognosis of scoliosis depends on the likelihood of progression. The general rules of progression are that larger curves carry a higher risk of progression than smaller curves, and that thoracic and double primary curves carry a higher risk of progression than single lumbar or thoracolumbar curves. In addition, patients who have not yet reached skeletal maturity have a higher likelihood of progression.

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