Spondylosis is a general term for degenerative osteoarthritis of the vertebrae. It may occur at the facet joints, neural foramen, lateral recesses, central canal, or at the vertebral endplates. It results from a change in the normal anatomical weight distribution on the spine. It may result from poor posture, repetitive movements, or any injury to the spine or muscles, which support the spine. The change in weight distribution causes excess bone growth. Degenerative changes occur over many years. Poor posture, muscle weakness, or injury to a spinal muscle results in a change in the normal spinal curvature, which can lead to either increased or decreased kyphosis or lordosis. The constant abnormal pressure on the facet joints and discs results in excess bone growth.

Injured discs frequently result in spondylosis. A disc which loses its elastic properties from disc displacement places significant stress on the facet joints, as well as the vertebral endplates. Excess bone growth occurs at both affected endplates to support the damaged disc. This also occurs at the superior and inferior articulating processes to support the stressed facet joints. The resultant bone is abnormal and forms at the regions of most stress.

Spondylosis will continue to occur, as long as abnormalities exist in the normal anatomic weight distribution of the spine. As the degeneration progresses, excess bone growth may impede vital components of the vertebrae. Resultant arthritis of the facet joints limits range of motion, alters weight distribution, and causes axial pain. As arthritis occurs around the disc at the endplates, neural compromise becomes a concern. The neural foramina may become infiltrated, or the lateral recesses and central may become stenotic.

Spondylolisthesis is the displacement of a vertebral body. Listhesis occurs after a fracture of the pars interacticularis (spondylolysis); most commonly, L5 displaces anteriorly over the sacrum. Another common form is Hangman’s Fracture, a traumatic spondylolisthesis occurring at C2–C3, as the result of severe subluxation from hanging, car crash, or trauma from a sports injury. These events result in fracture of the pedicles and pars interarticularis of the C2 vertebrae and anterior displacement respective to C3. Anterior displacement causes encroachment on the central canal, stretching of the interspinous ligaments, including the ligamentum flavum; thereby resulting in further instability, pain, and radicular symptoms.

Spondylolysis is an injury over the area in the vertebral arch between the superior and inferior articulating processes, the pars interarticularis. The injury most commonly results from strenuous sport or exercise, whereby the spine is hyperextended and rotated repeatedly. This repeated motion can lead to development of a stress fracture in the pars interacticularis, contralateral to the active side. It most commonly occurs in younger, extremely active populations [7]. Participants in certain sports are also more at risk. Repeated vigorous unilateral rotational motion, such as in tennis or football, and repeated hyperextension in gymnastics and cheerleading commonly result in the development of spondylolysis [8]. The injury most commonly occurs in the lower lumbar spine at the L5 vertebrae where the lumbar lordosis transitions to sacral kyphosis, whereby the sacrum is also immovable placing a great deal of stress upon the L5-S1 facet joints [9].

Although many instances of spondylolysis are asymptomatic, which therefore may go untreated unless found through focused examination or imaging, a consequence of the fracture includes weakening of the facet joint, which in turn decreases the spine’s ability to maintain alignment. Untreated or severe cases may progress to spondylolisthesis [10]. When listhesis occurs, further symptoms develop. Facet injury, disc injury, and central canal impingement may occur.

Most instances of spondylolysis are treatable by conservative means, such as activity restriction, bracing, core strengthening, and in the most severe cases, surgery. Most commonly, treatment involves a multi-modal approach , including activity restriction, bracing, and physical therapy regimens focused on strengthening the core. It is vital to avoid any activity which puts undue stress on the spine, such as bending, twisting, heavy lifting, or the activity which caused the injury itself. An anti-lordotic brace worn for short periods each day may relieve symptoms by reducing load on the injured site, placing the spine in slight flexion. The brace is tightly fitted and very rigid, which also limits range of motion. Recovery can be 6–12 weeks depending on severity [10]. Since this injury most commonly occurs in younger highly active individuals, the duration of restriction is vital in the overall rehabilitation process.

Zygapophyseal (facet) arthropathy is any disease of the facet joints. It may be from inflammation, arthritis, or complete joint degeneration. Zygapophyseal arthropathy usually manifests as pain localized over the particular facet joint. It is frequently defined as axial, or non-radiating back pain, which is made worse by extension and rotation. As arthropathy progresses, bone spurs may develop from osteoarthritis, which increase pain, inflammation, and decrease range of motion. The formation of bone spurs is known as facet hypertrophy. These spurs may develop on the anterior portion of the joint and can result in encroachment on the spinal canal, resulting in lateral recess and foraminal spinal stenosis. Absence of identified arthropathy on common imaging techniques, such as radiography and MRI, does not rule out the zygapophyseal joint as a potential pain generator. Pain is usually localized over the affected joints; however, pain across the neck, shoulders, and posterior head is commonly associated with cervical facet arthropathy [11]. Pain referred across the shoulders, posterior ribs, and flanks is common from thoracic facet arthropathy [12]. Lumbar facet arthropathy may present with referral pain across the low back, into the buttock, and posterior legs above the knee [13].

The third occipital nerve is the superficial medial branch of the C3 dorsal ramus. It provides sensory enervation to the posterior neck as well as cutaneous tissue of the sub-occipital region, which is a common region of headaches. This nerve also enervates the C2–C3 zygapophyseal joint. Arthroparthy of this joint from osteoarthritis, or from whiplash injury, may result in irritation of the TON, causing referred pain in the sub-occipital region.

The atlanto-occipital (AO) joint and atlanto-axial (AA) joint are common sources of occipital headaches; however, these syndromes are frequently undiagnosed due to the absence of any non-invasive testing to confirm pain generation. The only diagnostic test is infiltration of a local anesthetic into the joints, in order to assess reduction of pain in the region. These joints are small articular joints, different in structure to the zygapophyseal joints; however, similar pathologies may afflict these joints. AO and AA pain may result from osteoarthritis, inflammation, or injury. Whiplash is a common mechanism for AO and AA pain. Headaches are the most common complaint associated with AO and AA arthropathy. The AO joint is innervated by the C1 ventral rami. The AA joint is innervated by the C2 ventral ramus. Both nerves branch from the trigeminocervical nucleus, which receives afferent input from the upper spine and head. For this reason, referred pain patterns across the upper cervical, suboccipital, mastoid, and even temporal regions may result from AO and AA joint arthropathy [14].

Pathology of the AO and AA joints, as well as the upper cervical facet joints innervated by branches from the trigeminocervical nucleus, may cause cervicogenic headaches. It is hypothesized and repeatedly concluded that the overlap of continued grey matter from the upper spinal dorsal horn and the afferent fibers of the trigeminal nerve in the pars caudalis may be involved [15]. The nociceptive input from the upper cervical nerves causes a misinterpretation at higher brain centers, resulting in pain not only in the watershed of the cervical nerve, but also the trigeminal nerve [16].

The medial aspect of the neural foramen is the lateral recess. The pedicles form the posterior aspect of the neural foramen, the vertebral body, and the anterior aspect of the disc. In the middle of the posterior aspect of the foramen are the facet (zygapophyseal) joints. Stenosis of the lateral recess is caused by bone spur encroachment. Facet arthropathy can lead to bone spur formation. Disc pathologies may also lead to the formation of bone spurs at the endplates. These bone spurs narrow the doorway for the nerve to exit the spinal column, leading to radicular symptoms in the dermatome of the exiting nerve root , or may impinge upon a descending nerve root, leading to radicular symptoms in the corresponding dermatome. Because the facet joints, vertebral bodies, and discs form the entire neural foramen, bone spurs are not limited to formation at the lateral recess. Lateral recess stenosis is usually accompanied by foraminal stenosis, and in some cases, central canal stenosis.

The pedicles form the posterior aspect of the neural foramen, the vertebral body, and the anterior aspect of the disc. In the middle of the posterior aspect of the foramen are the facet (zygapophyseal) joints. Foraminal stenosis is caused by bone spur formation in any or all of these structures, which encroach on the lateral aspect of the neural foramen. It is commonly accompanied by lateral recess stenosis, and likely present if there is central canal stenosis. Foraminal stenosis, like lateral recess stenosis, causes radicular symptoms in the dermatome of the exiting nerve root.

The central canal is formed by the lamina and vertebral bodies, discs, and ligamentum flavum. Damaged or bulging discs may result in the formation of bone spurs on the posterior aspect of the vertebral endplate. These bone spurs may encroach upon the central canal, causing stenosis of the anterior portion. Furthermore, with age, the ligamentum flavum loses elasticity and becomes hypertrophic. This hypertrophy encroaches on the posterior central canal. Radicular symptoms result from canal encroachment. Stenosis may occur in the posterior canal, anterior canal, or along the lateral canal in the vicinity of the medial aspects of the lateral recess. Resultant radicular symptoms may be unilateral or bilateral and may affect the dermatome corresponding to the stenotic canal level.

The dorsal root ganglion (DRG) is located within the foramen of each nerve root. It is the collection of nerve soma from the root dermatome. The DRG receives afferent signal from the distal nerve and transfers these signals to the spinal cord. As a collection of nerve bodies, it is slightly larger in diameter than the rest of the nerve root. Since it lies in the foramen and is slightly larger, the DRG is especially vulnerable to stenosis. Bone spurs from the facet joints, vertebral endplates, or encroachment from the discs may compress or damage the DRG. Dermatomal pain, weakness, and numbness are common symptoms.

Through congenital defect, injury, neuromuscular condition, or degeneration of idiopathic origin, the spine may deform in the sagittal plane or coronal plane. A sagittal deformity is scoliosis, where the spine develops curvature laterally, rather than the normal anterior-posterior S shape. Coronal deformity is either called kyphosis, whereby the normal thoracic kyphosis is increased, or decreased lordosis, whereby the lordosis of the cervical and lumbar spines decreases.

Congenital scoliosis results from abnormal segmentation of the vertebrae during the first trimester in utero. Vertebral bodies may not form completely, may not segment, or may not segment completely, all of which can result in vertebral segments fused bilaterally or unilaterally, or in partial and complete malformations of one or several vertebral bodies. The abnormal structure causes a lateral curvature of varying severity [17]. The progression of congenital scoliosis depends on many factors, which include the type and significance of abnormal segmentation.

Neuromuscular scoliosis is caused by numerous conditions, which affect the brain, spine, and musculature of the spine. Upper or lower motor neuron disorders, which include cerebral palsy, poliomyelitis, and myopathic conditions, which include thoracic myelodysplasia, have exceptionally high instances of neuromuscular scoliosis. Neurological injury from trauma, especially if resulting in paralysis of the spinal musculature, progresses to scoliosis in every instance over 10 years [18]. A condition that affects the muscle tone of the spinal musculature, particularly of the thoracic spine, may hasten the onset of neuromuscular scoliosis. Neuromuscular scoliosis is the most rapidly progressing form of scoliosis and frequently needs surgical correction.

Idiopathic scoliosis accounts for the majority of cases. In these cases, there is no causative injury, congenital condition, or comorbidity. Idiopathic scoliosis is most commonly diagnosed during puberty as adolescent idiopathic scoliosis (AIS).

Minor curvatures typically do not manifest with pain, neuropathy, or organ impingement, thereby such curvatures are usually diagnosed following adolescent school screening, as an incidental finding on a physical exam, or from radiography. Patients with more severe curvature may develop pain and eventual difficulty with breathing. Curvature is measured by a Cobb angle, which is the angle of the intersection of the line of the superior endplate of the cephalad end of the curvature and the line of the inferior endplate of the caudad end of the curvature. Most cases manifest less than a 20-degree Cobb angle and are only observed for progression. As the curvature progresses past 20°–25°, a brace and therapy is warranted. Individuals with higher risk of curve progression are in greater need of therapy and bracing. Therapy and bracing is focused on offloading the curvature, while training the patient to feel comfortable in performing activities of daily living with the curve off loaded and the angle slightly reduced [17]. When the Cobb angle progresses to 40° or greater, surgery may be indicated [19].

Scoliosis may also manifest in adults secondary to comorbidities, which include degenerative disc disease, facet hypertrophy, and spondylosis. Since the lumbar spine is most commonly affected by these disorders, adult degenerative scoliosis manifests most commonly in the lumbar spine [19]. As the discs, ligaments, and zygapophyseal joints lose stability and integrity, the musculature of the back causes a curvature. This curvature increases as the degeneration increases [17]. Other forms of scoliosis are not frequently associated with severe pain. Degenerative scoliosis, accompanying any number of degenerative spine conditions, frequently results in both axial and radicular symptoms, which may or may not be more severe on one side versus the other.

Vertebral compression fractures are frequently the result of bony pathologies causing decreased density, as can occur in post-menopausal women. The cause may be a minor trauma, such as a short fall. Otherwise, fractures may develop over time, with anterior or lateral flexion, due to significant loss in bone density. The vertebral body lacks the strength to support the load of the spine above it, resulting in compression and loss of vertebral height in the anterior column. The compression results in a wedge shape, sloping posterior to anterior, whereby the posterior column is usually unaffected. If the posterior column is affected, neurological symptoms such as radiating pain in the corresponding dermatome may ensue.

Typically, pain is localized to the region surrounding the affected vertebral bodies. Compression fractures are usually managed with conservative measures first. Many patients live with the condition without surgical intervention. Pain usually diminishes over time as the bone heals in the compressed state. Immobilization with rigid LSO or TLSO bracing is used in conjunction with pain medications and physical therapy, which is focused on strengthening and supporting the core musculature. Therapy also includes supplements to address decreased bone density, with the goal of prevention of worsening fracture or development of new fractures.

If pain is not relieved by conservative means, surgical intervention is appropriate before the condition reaches the chronic stage. Minimally invasive surgical procedures, such as vertebroplasty or kyphoplasty, are performed. In the vertebroplasty procedure, a catheter is used to inject cement directly into the affected vertebral body to stabilize the fracture and to relieve pain. There is no restoration of vertebral height with this procedure [20]. With kyphoplasty, a balloon is inserted into the vertebral body and inflated to restore the vertebral body to its natural height. The cavity is then filled with cement to stabilize the fracture and to relieve pain [21]. For further reference, please see dedicated chapter on vertebral augmentation.