Scientists are investigating various avenues for treatment of spinal cord injury. Therapeutic research is focused on two main areas: neuroprotection and neuroregeneration. The former seeks to prevent the harm that occurs from secondary injury in the minutes to weeks following the insult, and the latter aims to reconnect the broken circuits in the spinal cord to allow function to return. Neuroprotective drugs target secondary injury effects including inflammation, damage by free radicals, excitotoxicity (neuronal damage by excessive glutamate signaling), and apoptosis (cell suicide). Several potentially neuroprotective agents that target pathways like these are under investigation in human clinical trials.

Stem cell transplantation is an important avenue for SCI research: the goal is to replace lost spinal cord cells, allow reconnection in broken neural circuits by regrowing axons, and to create an environment in the tissues that is favorable to growth. A key avenue of SCI research is research on stem cells, which can differentiate into other types of cells—including those lost after SCI. Types of cells being researched for use in SCI include embryonic stem cells, neural stem cells, mesenchymal stem cells, olfactory ensheathing cells, Schwann cells, activated macrophages, and induced pluripotent stem cells. Hundreds of stem cell studies have been done in humans, with promising but inconclusive results. An ongoing Phase 2 trial in 2016 presented data showing that after 90 days, 2 out of 4 subjects had already improved two motor levels and had thus already achieved its endpoint of 2/5 patients improving two levels within 6–12 months. Six-month data is expected in January 2017.

Another type of approach is tissue engineering, using biomaterials to help scaffold and rebuild damaged tissues. Biomaterials being investigated include natural substances such as collagen or agarose and synthetic ones like polymers and nitrocellulose. They fall into two categories: hydrogels and nanofibers. These materials can also be used as a vehicle for delivering gene therapy to tissues.

One avenue being explored to allow paralyzed people to walk and to aid in rehabilitation of those with some walking ability is the use of wearable powered robotic exoskeletons. The devices, which have motorized joints, are put on over the legs and supply a source of power to move and walk. Several such devices are already available for sale, but investigation is still underway as to how they can be made more useful.

Vehicle-related SCI is prevented with measures including societal and individual efforts to reduce driving under the influence of drugs or alcohol, distracted driving, and drowsy driving. Other efforts include increasing road safety (such as marking hazards and adding lighting) and vehicle safety, both to prevent accidents (such as routine maintenance and antilock brakes) and to mitigate the damage of crashes (such as head restraints, air bags, seat belts, and child safety seats). Falls can be prevented by making changes to the environment, such as nonslip materials and grab bars in bathtubs and showers, railings for stairs, child and safety gates for windows. Gun-related injuries can be prevented with conflict resolution training, gun safety education campaigns, and changes to the technology of guns (such as trigger locks) to improve their safety. Sports injuries can be prevented with changes to sports rules and equipment to increase safety, and education campaigns to reduce risky practices such as diving into water of unknown depth or head-first tackling in association football.

Neurogenic shock is a distributive type of shock resulting in low blood pressure, occasionally with a slowed heart rate, that is attributed to the disruption of the autonomic pathways within the spinal cord. It can occur after damage to the central nervous system such as spinal cord injury. Low blood pressure occurs due to decreased systemic vascular resistance resulting in pooling of blood within the extremities lacking sympathetic tone. The slowed heart rate results from unopposed vagal activity and has been found to be exacerbated by hypoxia and endobronchial suction.

Neurogenic shock can be a potentially devastating complication, leading to organ dysfunction and death if not promptly recognized and treated. It is not to be confused with spinal shock, which is not circulatory in nature.

Spinal shock was first defined by Whytt in 1750 as a loss of accompanied by motor paralysis with initial loss but gradual recovery of reflexes, following a spinal cord injury (SCI) – most often a complete transection. Reflexes in the spinal cord below the level of injury are depressed (hyporeflexia) or absent (areflexia), while those above the level of the injury remain unaffected. The 'shock' in spinal shock does not refer to circulatory collapse, and should not be confused with neurogenic shock, which is life-threatening

There is no known treatment to reverse nerve damage due to myelomalacia. In some cases, surgery may slow or stop further damage. As motor function degenerates, muscle spasticity and atrophy may occur. Steroids may be prescribed to reduce swelling of the spinal cord, pain, and spasticity.

Research is underway to consider the potential of stem cells for treatment of neurodegenerative diseases. There are, however, no approved stem cell therapies for myelomalacia.

Anterior spinal artery syndrome (also known as "anterior spinal cord syndrome", or "Beck's syndrome") is a medical condition where the anterior spinal artery, the primary blood supply to the anterior portion of the spinal cord, is interrupted, causing ischemia or infarction of the spinal cord in the anterior two-thirds of the spinal cord and medulla oblongata. It is characterized by loss of motor function below the level of injury, loss of sensations carried by the anterior columns of the spinal cord (pain and temperature), and preservation of sensations carried by the posterior columns (fine touch, vibration and proprioception). Anterior spinal artery syndrome is the most common form of spinal cord infarction.

Because it causes a loss of sympathetic tone, which plays a major role in other forms of shock, neurogenic shock causes a unique and atypical presentation.

Typically, in other forms of shock, the sympathetic nervous system triggers various compensatory mechanisms by releasing epinephrine and norepinephrine, its major chemical mediators. These neurotransmitters trigger an increased heart rate, faster breathing, and sweating. They also trigger vasoconstriction, to shunt blood away from the extremities and to the vital organs.

In neurogenic shock, the body loses its ability to activate the sympathetic nervous system and cannot trigger these compensatory mechanisms. Only parasympathetic tone remains. Consequently, neurogenic shock's unique presentation includes:

- Instantaneous hypotension due to sudden, massive vasodilation

- Warm, flushed skin due to vasodilation and inability to vasoconstrict

- Priapism, also due to vasodilation

- The patient will be unable to get tachycardic, and may become bradycardic

- If the injury is below the 5th cervical vertebra, the patient will exhibit diaphragmatic breathing due to loss of nervous control of the intercostal muscles (which are required for thoracic breathing).

- If the injury is above the 3rd cervical vertebra, the patient will go into respiratory arrest immediately following the injury, due to loss of nervous control of the diaphragm.

Treatment is directed at the pathology causing the paralysis. If it is because of trauma such as a gunshot or knife wound, there may be other life-threatening conditions such as bleeding or major organ damage which should be dealt with on an emergent basis. If the syndrome is caused by a spinal fracture, this should be identified and treated appropriately. Although steroids may be used to decrease cord swelling and inflammation, the usual therapy for spinal cord injury is expectant.

Brown-Séquard syndrome is rare as the trauma would have to be something that damaged the nerve fibres on just one half of the spinal cord.

The treatment and prognosis of myelopathy depends on the underlying cause: myelopathy caused by infection requires medical treatment with pathogen specific antibiotics. Similarly, specific treatments exist for multiple sclerosis, which may also present with myelopathy. As outlined above, the most common form of myelopathy is secondary to degeneration of the cervical spine. Newer findings have challenged the existing controversy with respect to surgery for cervical spondylotic myelopathy by demonstrating that patients benefit from surgery.

The application of MRI plays a significant role in the early diagnosis and treatment of SCIWORA in children and adults. Recently, systematic reviews on SCIWORA described the clinical and radiological patterns and correlations with neurological outcome.C.K. Boese und P. Lechler: "Spinal cord injury without radiologic abnormalities in adults: a systematic review." In: "Journal of Trauma and Acute Care Surgery." 78, 2015, S. 320-330 .Boese CK, Oppermann J, Siewe J, Eysel P, Scheyerer MJ, Lechler P.: "Spinal cord injury without radiologic abnormality in children: a systematic review and meta-analysis." In: "Journal of Trauma and Acute Care Surgery." 75, 2013. Boese and Lechler proposed a MRI-based classification for SCIWORA which correlated with the neurological outcome:

Due to extensive physical contact and activity, many athletes become victim to myelomalacia. Any accidents or injuries attained during athletic competition to the spinal cord may result in myelomalacia. Accounts of awkward landing on the ground or being hit intensively have attested to spinal cord injury.

Treatment is determined based on the primary cause of anterior cord syndrome. When the diagnosis of anterior cord syndrome is determined, the prognosis is unfortunate. The mortality rate is approximately 20%, with 50% of individuals living with anterior cord syndrome having very little or no changes in symptoms.

Myelopathy describes any neurologic deficit related to the spinal cord. When due to trauma, it is known as (acute) spinal cord injury. When inflammatory, it is known as myelitis. Disease that is vascular in nature is known as vascular myelopathy. The most common form of myelopathy in human, "cervical spondylotic myelopathy (CSM)", is caused by arthritic changes (spondylosis) of the cervical spine, which result in narrowing of the spinal canal (spinal stenosis) ultimately causing compression of the spinal cord. In Asian populations, spinal cord compression often occurs due to a different, inflammatory process affecting the posterior longitudinal ligament.

Vascular myelopathy (vascular disease of the spinal cord) refers to an abnormality of the spinal cord in regard to its blood supply. The blood supply is complicated and supplied by two major vessel groups: the posterior spinal arteries and the anterior spinal arteries—of which the Artery of Adamkiewicz is the largest. Both the posterior and anterior spinal arteries run the entire length of the spinal cord and receive anastomotic (conjoined) vessels in many places. The anterior spinal artery has a less efficient supply of blood and is therefore more susceptible to vascular disease. Whilst atherosclerosis of spinal arteries is rare, necrosis (death of tissue) in the anterior artery can be caused by disease in vessels originating from the segmental arteries such as atheroma (arterial wall swelling) or aortic dissection (a tear in the aorta).

Spinal cord injury without radiographic abnormality (SCIWORA) is a spinal cord injury (SCI) with no evidence of injury to the spinal column present on radiographs. Spinal column injury is trauma that causes fracture of the bone or instability of the ligaments in the spine; this can coexist with or result in injury to the spinal cord itself but each injury can occur without the other. Abnormalities might show up on magnetic resonance imaging (MRI), but the term was coined before MRI was in common use.

According to medical professionals with the Cleveland Clinic, once an athlete suffers from an episode of cervical spinal cord, team physician or athletic trainer first stabilize the head and neck followed by a thorough neurologic inspection. If the injury is deemed severe, injured parties should be taken to a hospital for evaluation. Athletes that suffer from severe episodes of neurapraxia are urged to consult orthopaedic or spinal medical specialists. In mild cases of neurapraxia, the athlete is able to remove themselves from the field of play. However, the athlete is still advised to seek medical consultation.

Because neurological deficits are generally irreversible, early surgery is recommended when symptoms begin to worsen. In children, early surgery is recommended to prevent further neurological deterioration, including but not limited to chronic urinary incontinence.

In adults, surgery to detether (free) the spinal cord can reduce the size and further development of cysts in the cord and may restore some function or alleviate other symptoms. Although detethering is the common surgical approach to TCS, another surgical option for adults is a spine-shortening vertebral osteotomy. A vertebral osteotomy aims to indirectly relieve the excess tension on the spinal cord by removing a portion of the spine, shortening it. This procedure offers a unique benefit in that the spinal cord remains fixated to the spine, preventing retethering and spinal cord injury as possible surgical complications. However, its complexity and limited “track record” presently keeps vertebral osteotomies reserved as an option for patients who have failed in preventing retethering after detethering procedure(s).

Other treatment is symptomatic and supportive. Medications such as NSAIDs, opiates, synthetic opiates, COX-2 inhibitors, and off-label applications of tricyclic antidepressants combined with anti-seizure compounds have yet to prove they are of value in treatment of this affliction's pain manifestations. There is anecdotal evidence that TENS units may benefit some patients.

Treatment may be needed in adults who, while previously asymptomatic, begin to experience pain, lower back degeneration, scoliosis, neck and upper back problems and bladder control issues. Surgery on adults with minimal symptoms is somewhat controversial. For example, a website from the Columbia University Department of Neurosurgery says, "For the child that has reached adult height with minimal if any symptoms, some neurosurgeons would advocate careful observation only." However, surgery for those who have worsening symptoms is less controversial. If the only abnormality is a thickened, shortened filum, then a limited lumbosacral laminectomy with division of the filum may be sufficient to relieve the symptoms.

This syndrome was first noticed in the late 19th century. While information has been available for years, little widespread blind research has been done. More research has been called for, and doctors have conducted many studies with good results. There is a low morbidity rate, and no complications have been documented other than those typical of any type of back surgery. The association of this condition with others has been noticed, and needs further research to understand such relationships. TCS is causally linked to Chiari malformation and any affirmative diagnosis of TCS must be followed by screening for Chiari's several degrees. TCS may also be related to Ehlers-Danlos syndrome, or Klippel-Feil syndrome, which should also be screened for upon a positive TCS diagnosis. Spinal compression and the resulting relief is a known issue with this disorder. Like with the early-onset form, this disease form is linked to the Arnold-Chiari malformation, in which the brain is pulled or lowers into the top of the spine.

In cases of neurapraxia, the function of the nerves are temporarily impaired. However, the prognosis for recovery from neurapraxia is efficient and quick. Recovery begins within two to three weeks after the injury occurs, and it is complete within six to eight weeks. There are instances when function is not completely restored until four months after the instance of injury. The recovery period of neurapraxia is not an entirely ordered process, but the recovery is always complete and fast.

Ditunno et al. proposed a four-phase model for spinal shock in 2004 as follows:

Phase 1 is characterized by a complete loss—or weakening—of all reflexes below the SCI. This phase lasts for a day. The neurons involved in various reflex arcs normally receive a basal level of excitatory stimulation from the brain. After an SCI, these cells lose this input, and the neurons involved become hyperpolarized and therefore less responsive to stimuli.

Phase 2 occurs over the next two days, and is characterized by the return of some, but not all, reflexes below the SCI. The first reflexes to reappear are polysynaptic in nature, such as the bulbocavernosus reflex. Monosynaptic reflexes, such as the deep tendon reflexes, are not restored until Phase 3. Restoration of reflexes is not rostral to caudal as previously (and commonly) believed, but instead proceeds from polysynaptic to monosynaptic. The reason reflexes return is the hypersensitivity of reflex muscles following denervation – more receptors for neurotransmitters are expressed and are therefore easier to stimulate.

Phases 3 and 4 are characterized by hyperreflexia, or abnormally strong reflexes usually produced with minimal stimulation. Interneurons and lower motor neurons below the SCI begin sprouting, attempting to re-establish synapses. The first synapses to form are from shorter axons, usually from interneurons – this categorizes Phase 3. Phase 4 on the other hand, is soma-mediated, and will take longer for the soma to transport various growth factors, including proteins, to the end of the axon.

The evidence for the use of medical interventions for lumbar spinal stenosis is poor. Injectable but not nasal calcitonin may be useful for short term pain relief. Epidural blocks may also transiently decrease pain, but there is no evidence of long-term effect. Adding steroids to these injections does not improve the result; the use of epidural steroid injections (ESIs) is controversial and evidence of their efficacy is contradictory.

Non-steroidal anti-inflammatory drugs (NSAIDs), muscle relaxants and opioid analgesics are often used to treat low back pain, but evidence of their efficacy is lacking.

The best evidence exists for the treatment of septic shock in adults and as the pathophysiology appears similar in children and other types of shock treatment this has been extrapolated to these areas. Management may include securing the airway via intubation if necessary to decrease the work of breathing and for guarding against respiratory arrest. Oxygen supplementation, intravenous fluids, passive leg raising (not Trendelenburg position) should be started and blood transfusions added if blood loss is severe. It is important to keep the person warm as well as adequately manage pain and anxiety as these can increase oxygen consumption.

Treatment options are either surgical or non-surgical. Overall evidence is inconclusive whether non-surgical or surgical treatment is the better for lumbar spinal stenosis.

The effectiveness of non surgical treatments is unclear as they have not been well studied.

- Education about the course of the condition and how to relieve symptoms

- Medicines to relieve pain and inflammation, such as acetaminophen, nonsteroidal anti-inflammatory drugs (NSAIDs)

- Exercise, to maintain or achieve overall good health, aerobic exercise, such as riding a stationary bicycle, which allows for a forward lean, walking, or swimming can relieve symptoms

- Weight loss, to relieve symptoms and slow progression of the stenosis

- Physical therapy to support self-care. Also may give instructs on stretching and strength exercises that may lead to a decrease in pain and other symptoms.

- Lumbar epidural steroid or anesthetic injections have low quality evidence to support their use.

Surgery appears to lead to better outcomes if there are ongoing symptoms after three to six months of conservative treatment. Laminectomy is the most effective of the surgical treatments. In those who worsen despite conservative treatments surgery leads to improvement in 60–70% of cases. Another procedure using an interspinous distraction device known as X-STOP was less effective and more expensive when more than one spinal level is repaired. Both surgical procedures are more expensive than medical management.