Swayback refers to abnormal bent-back postures in humans and in quadrupeds, especially horses.

Swayback posture in humans is characterised by the posterior displacement of the rib cage in comparison to the pelvis. It looks like the person has a hyperextension of the natural lordosis, however this is not necessarily the case. Most sway-back exhibits a posteriorly tilted pelvis; the lumbar region is usually flat (too flexed) and not hyperlordotic (too extended).

Although hyperlordosis gives an impression of a stronger back, incongruently it can lead to moderate to severe lower back pain. The most problematic symptom is that of herniated disc where the dancer has put so much strain on their back that the discs between the vertebrae have been damaged or have ruptured. Technical problems with dancing such as difficulty in the positions of attitude and arabesque can be a sign of weak iliopsoas. Tightness of the iliopsoas results in a dancer having difficulty lifting their leg into high positions. Abdominal muscles being weak and the rectus femoris of the quadriceps being tight are signs that improper muscles are being worked while dancing which leads to lumbar hyperlordosis. The most obvious signs of lumbar hyperlordosis is lower back pain in dancing and pedestrian activities as well as having the appearance of a swayed back.

Lumbar hyperlordosis is a condition that occurs when the lumbar region (lower back) experiences stress or extra weight and is arched to point of muscle pain or spasms. Lumbar hyperlordosis is a common postural position where the natural curve of the lumbar region of the back is slightly or dramatically accentuated. Commonly known as swayback, it is common in dancers. Imbalances in muscle strength and length are also a cause, such as weak hamstrings, or tight hip flexors (psoas). A major feature of lumbar hyperlordosis is a forward pelvic tilt, resulting in the pelvis resting on top of the thighs.

Other health conditions and disorders can cause hyperlordosis. Achondroplasia (a disorder where bones grow abnormally which can result in short stature as in dwarfism), Spondylolisthesis (a condition in which vertebrae slip forward) and osteoporosis (the most common bone disease in which bone density is lost resulting in bone weakness and increased likelihood of fracture) are some of the most common causes of hyperlordosis. Other causes include obesity, hyperkyphosis (spine curvature disorder in which the thoracic curvature is abnormally rounded), discitits (an inflammation of the intervertebral disc space caused by infection) and benign juvenile lordosis. Other factors may also include those with rare diseases, as is the case with Ehlers Danlos Syndrome (EDS), where hyper-extensive and usually unstable joints (e.g. joints that are problematically much more flexible, frequently to the point of partial or full dislocation) are quite common throughout the body. With such hyper-extensibility, it is also quite common (if not the norm) to find the muscles surrounding the joints to be a major source of compensation when such instability exists.

Excessive lordotic curvature – lumbar hyperlordosis, is also called hollow back, and saddle back (after a similar condition that affects some horses); swayback usually refers to a nearly opposite postural misalignment that can initially look quite similar. Common causes of lumbar hyperlordosis include tight low back muscles, excessive visceral fat, and pregnancy. Rickets, a vitamin D deficiency in children, can cause lumbar lordosis.

The vertebral column, also known as the backbone or spine, is part of the axial skeleton. The vertebral column is the defining characteristic of a vertebrate, in which the notochord (a flexible rod of uniform composition) found in all chordates has been replaced by a segmented series of bones—vertebrae separated by intervertebral discs. The vertebral column houses the spinal canal, a cavity that encloses and protects the spinal cord.

There are about 50,000 species of animals that have a vertebral column. The human vertebral column is one of the most-studied examples.

Excessive or abnormal spinal curvature is classed as a spinal disease or dorsopathy and includes the following abnormal curvatures:

- Kyphosis is an exaggerated kyphotic (concave) curvature in the thoracic region, also called hyperkyphosis. This produces the so-called "humpback" or "dowager's hump", a condition commonly resulting from osteoporosis.

- Lordosis as an exaggerated lordotic (convex) curvature of the lumbar region, is known as lumbar hyperlordosis and also as "swayback". Temporary lordosis is common during pregnancy.

- Scoliosis, lateral curvature, is the most common abnormal curvature, occurring in 0.5% of the population. It is more common among females and may result from unequal growth of the two sides of one or more vertebrae, so that they do not fuse properly. It can also be caused by pulmonary atelectasis (partial or complete deflation of one or more lobes of the lungs) as observed in asthma or pneumothorax.

- Kyphoscoliosis, a combination of kyphosis and scoliosis.

Another common symptom of copper deficiency is peripheral neuropathy, which is numbness or tingling that can start in the extremities and can sometimes progress radially inward towards the torso. In an Advances in Clinical Neuroscience & Rehabilitation (ACNR) published case report, a 69-year-old patient had progressively worsened neurological symptoms. These symptoms included diminished upper limb reflexes with abnormal lower limb reflexes, sensation to light touch and pin prick was diminished above the waist, vibration sensation was lost in the sternum, and markedly reduced proprioception or sensation about the self’s orientation. Many people suffering from the neurological effects of copper deficiency complain about very similar or identical symptoms as the patient. This numbness and tingling poses danger for the elderly because it increases their risk of falling and injuring themselves. Peripheral neuropathy can become very disabling leaving some patients dependent on wheel chairs or walking canes for mobility if there is lack of correct diagnosis. Rarely can copper deficiency cause major disabling symptoms. The deficiency will have to be present for an extensive amount of time until such disabling conditions manifest.

Copper deficiency myelopathy in humans was discovered and first described by Schleper and Stuerenburg in 2001. They described a patient with a history of gastrectomy and partial colonic resection who presented with severe tetraparesis and painful paraesthesias and who was found on imaging to have dorsomedial cervical cord T2 hyperintensity. Upon further analysis, it was found that the patient had decreased levels of serum coeruloplasmin, serum copper, and CSF copper. The patient was treated with parenteral copper and the patient`s paraesthesias did resolve. Since this discovery, there has been heightened and increasing awareness of copper-deficiency myelopathy and its treatment, and this disorder has been reviewed by Kumar.

Sufferers typically present difficulty walking (gait difficulty) caused by sensory ataxia (irregular muscle coordination) due to dorsal column dysfunction or degeneration of the spinal cord (myelopathy). Patients with ataxic gait have problems balancing and display an unstable wide walk. They often feel tremors in their torso, causing side way jerks and lunges.

In brain MRI, there is often an increased T2 signalling at the posterior columns of the spinal cord in patients with myelopathy caused by copper deficiency. T2 signalling is often an indicator of some kind of neurodegeneration. There are some changes in the spinal cord MRI involving the thoracic cord, the cervical cord or sometimes both. Copper deficiency myelopathy is often compared to subacute combined degeneration (SCD). Subacute combined degeneration is also a degeneration of the spinal cord, but instead vitamin B12 deficiency is the cause of the spinal degeneration. SCD also has the same high T2 signalling intensities in the posterior column as copper deficient patient in MRI imaging.