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Spinal cord injury
Spinal cord injury
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Spinal cord injury
MRI of a fractured and dislocated cervical vertebra (C4) in the neck that is compressing the spinal cord
SpecialtyNeurosurgery
TypesComplete, incomplete[1]
Diagnostic methodBased on symptoms, medical imaging[1]
TreatmentSpinal motion restriction, intravenous fluids, vasopressors[1]
Frequencyc. 12,000 annually in the United States[2]

A spinal cord injury (SCI) is damage to the spinal cord that causes temporary or permanent changes in its function. It is a destructive neurological and pathological state that causes major motor, sensory and autonomic dysfunctions.[3]

Symptoms of spinal cord injury may include loss of muscle function, sensation, or autonomic function in the parts of the body served by the spinal cord below the level of the injury. Injury can occur at any level of the spinal cord and can be complete, with a total loss of sensation and muscle function at lower sacral segments, or incomplete, meaning some nervous signals are able to travel past the injured area of the cord up to the Sacral S4-5 spinal cord segments. Depending on the location and severity of damage, the symptoms vary, from numbness to paralysis, including bowel or bladder incontinence. Long term outcomes also range widely, from full recovery to permanent tetraplegia (also called quadriplegia) or paraplegia. Complications can include muscle atrophy, loss of voluntary motor control, spasticity, pressure sores, infections, and breathing problems.

In the majority of cases the damage results from physical trauma such as car accidents, gunshot wounds, falls, or sports injuries, but it can also result from nontraumatic causes such as infection, insufficient blood flow, and tumors. Just over half of injuries affect the cervical spine, while 15% occur in each of the thoracic spine, border between the thoracic and lumbar spine, and lumbar spine alone.[1] Diagnosis is typically based on symptoms and medical imaging.[1]

Efforts to prevent SCI include individual measures such as using safety equipment, societal measures such as safety regulations in sports and traffic, and improvements to equipment. Treatment starts with restricting further motion of the spine and maintaining adequate blood pressure.[1] Corticosteroids have not been found to be useful.[1] Other interventions vary depending on the location and extent of the injury, from bed rest to surgery. In many cases, spinal cord injuries require long-term physical and occupational therapy, especially if it interferes with activities of daily living.

In the United States, about 12,000 people annually survive a spinal cord injury.[2] The most commonly affected group are young adult males.[2] SCI has seen great improvements in its care since the middle of the 20th century. Research into potential treatments includes stem cell implantation, hypothermia, engineered materials for tissue support, epidural spinal stimulation, and wearable robotic exoskeletons.[4]

Classification

[edit]
A human spinal column A person with dermatomes mapped out on the skin
The effects of injury depend on the level along the spinal column (left). A dermatome is an area of the skin that sends sensory messages to a specific spinal nerve (right).
diagram of vertebrae and spinal nerves
Spinal nerves exit the spinal cord between each pair of vertebrae.

Spinal cord injury can be traumatic or nontraumatic,[5] and can be classified into three types based on cause: mechanical forces, toxic, and ischemic from lack of blood flow.[6] The damage can also be divided into primary and secondary injury: the cell death that occurs immediately in the original injury, and biochemical cascades that are initiated by the original insult and cause further tissue damage.[7] These secondary injury pathways include the ischemic cascade, inflammation, swelling, cell suicide, and neurotransmitter imbalances.[7] They can take place for minutes or weeks following the injury.[8]

At each level of the spinal column, spinal nerves branch off from either side of the spinal cord and exit between a pair of vertebrae, to innervate a specific part of the body. The area of skin innervated by a specific spinal nerve is called a dermatome, and the group of muscles innervated by a single spinal nerve is called a myotome. The part of the spinal cord that was damaged corresponds to the spinal nerves at that level and below. Injuries can be cervical 1–8 (C1–C8), thoracic 1–12 (T1–T12), lumbar 1–5 (L1–L5),[9] or sacral (S1–S5).[10] A person's level of injury is defined as the lowest level of full sensation and function.[11] Paraplegia occurs when the legs are affected by the spinal cord damage (in thoracic, lumbar, or sacral injuries), and tetraplegia occurs when all four limbs are affected (cervical damage).[12]

SCI is also classified by the degree of impairment. The International Standards for Neurological Classification of Spinal Cord Injury (ISNCSCI), published by the American Spinal Injury Association (ASIA), is widely used to document sensory and motor impairments following SCI.[13] It is based on neurological responses, touch and pinprick sensations tested in each dermatome, and strength of the muscles that control key motions on both sides of the body.[14] Muscle strength is scored on a scale of 0–5 according to the table on the right, and sensation is graded on a scale of 0–2: 0 is no sensation, 1 is altered or decreased sensation, and 2 is full sensation.[15] Each side of the body is graded independently.[15]

Muscle strength[16] ASIA Impairment Scale for classifying spinal cord injury[14][17]
Grade Muscle function Grade Description
0 No muscle contraction A Complete injury. No motor or sensory function is preserved in the sacral segments S4 or S5.
1 Muscle flickers B Sensory incomplete. Sensory but not motor function is preserved below the level of injury, including the sacral segments.
2 Full range of motion, gravity eliminated C Motor incomplete. Motor function is preserved below the level of injury, and more than half of muscles tested below the level of injury have a muscle grade less than 3 (see muscle strength scores, left).
3 Full range of motion, against gravity D Motor incomplete. Motor function is preserved below the level of injury and at least half of the key muscles below the neurological level have a muscle grade of 3 or more.
4 Full range of motion against resistance E Normal. No motor or sensory deficits, but deficits existed in the past.
5 Normal strength

Complete and incomplete injuries

[edit]
Level and completeness of injuries[18]
Complete Incomplete
Tetraplegia 18.3% 34.1%
Paraplegia 23.0% 18.5%

In a "complete" spinal injury, all functions below the injured area are lost, whether or not the spinal cord is severed.[10] An "incomplete" spinal cord injury involves preservation of motor or sensory function below the level of injury in the spinal cord.[19] To be classed as incomplete, there must be some preservation of sensation or motion in the areas innervated by S4 to S5,[20] including voluntary external anal sphincter contraction.[19] The nerves in this area are connected to the very lowest region of the spinal cord, and retaining sensation and function in these parts of the body indicates that the spinal cord is only partially damaged. Incomplete injury by definition includes a phenomenon known as sacral sparing: some degree of sensation is preserved in the sacral dermatomes, even though sensation may be more impaired in other, higher dermatomes below the level of the lesion.[21] Sacral sparing has been attributed to the fact that the sacral spinal pathways are not as likely as the other spinal pathways to become compressed after injury due to the lamination of fibers within the spinal cord.[21]

Spinal cord injury without radiographic abnormality

[edit]

Spinal cord injury without radiographic abnormality exists when spinal cord injury is present but there is no evidence of spinal column injury on radiographs.[22] Spinal column injury is trauma that causes fracture of the bone or instability of the ligaments in the spine; this can coexist with or cause injury to the spinal cord, but each injury can occur without the other.[23] Abnormalities might show up on magnetic resonance imaging (MRI), but the term was coined before MRI was in common use.[24]

Central cord syndrome

[edit]
Incomplete lesions of the spinal cord: Central cord syndrome (top), Anterior cord syndrome (middle), and Brown-Séquard syndrome (bottom)

Central cord syndrome, almost always resulting from damage to the cervical spinal cord, is characterized by weakness in the arms with relative sparing of the legs, and spared sensation in regions served by the sacral segments.[25] There is loss of sensation of pain, temperature, light touch, and pressure below the level of injury.[26] The spinal tracts that serve the arms are more affected due to their central location in the spinal cord, while the corticospinal fibers destined for the legs are spared due to their more external location.[26]

The most common of the incomplete SCI syndromes, central cord syndrome usually results from neck hyperextension in older people with spinal stenosis. In younger people, it most commonly results from neck flexion.[27] The most common causes are falls and vehicle accidents; however other possible causes include spinal stenosis and impingement on the spinal cord by a tumor or intervertebral disc.[28]

Anterior spinal artery syndrome

[edit]

Anterior spinal artery syndrome also known as anterior spinal cord syndrome, due to damage to the front portion of the spinal cord or reduction in the blood supply from the anterior spinal artery, can be caused by fractures or dislocations of vertebrae or herniated disks.[26] Below the level of injury, motor function, pain sensation, and temperature sensation are lost, while sense of touch and proprioception (sense of position in space) remain intact.[29][27] These differences are due to the relative locations of the spinal tracts responsible for each type of function.

Brown-Séquard syndrome

[edit]

Brown-Séquard syndrome occurs when the spinal cord is injured on one side much more than the other.[30] It is rare for the spinal cord to be truly hemisected (severed on one side), but partial lesions due to penetrating wounds (such as gunshot or knife wounds) or fractured vertebrae or tumors are common.[31] On the ipsilateral side of the injury (same side), the body loses motor function, proprioception, and senses of vibration and touch.[30] On the contralateral (opposite side) of the injury, there is a loss of pain and temperature sensations. If the injury is above pyramidal decussation there is contralateral hemiplegia, at the level of decussation there is completed motor loss on both sides and below pyramidal decussation there is ipsilateral hemiplegia.

[28][30]Spinothalamic tracts are in charge for pain and temperature sensation and because these tracts cross to the opposite side and above the spinal cord there is loss on the contralateral side.[32]

Posterior spinal artery syndrome

[edit]

Posterior spinal artery syndrome (PSAS), in which just the dorsal columns of the spinal cord are affected, is usually seen in cases of chronic myelopathy but can also occur with infarction of the posterior spinal artery.[33] This rare syndrome causes the loss of proprioception and sense of vibration below the level of injury[27] while motor function and sensation of pain, temperature, and touch remain intact.[34] Usually posterior cord injuries result from insults like disease or vitamin deficiency rather than trauma.[35] Tabes dorsalis, due to injury to the posterior part of the spinal cord caused by syphilis, results in loss of touch and proprioceptive sensation.[36]

Conus medullaris and cauda equina syndromes

[edit]

Conus medullaris syndrome is an injury to the end of the spinal cord the conus medullaris, located at about the T12–L2 vertebrae in adults.[30] This region contains the S4–S5 spinal segments, responsible for bowel, bladder, and some sexual functions, so these can be disrupted in this type of injury.[30] In addition, sensation and the Achilles reflex can be disrupted.[30] Causes include tumors, physical trauma, and ischemia.[37] Cauda equina syndrome may also be caused by central disc prolapse or slipped disc, infections such as epidural abscess, spinal haemorrhages, secondary to medical procedures and birth abnormalities.[38]

Cauda equina syndrome (CES) results from a lesion below the level at which the spinal cord ends. Descending nerve roots continue as the cauda equina[35] at levels L2–S5 below the conus medullaris before exiting through intervertebral foraminae.[39] Thus it is not a true spinal cord syndrome since it is nerve roots that are damaged and not the cord itself; however, it is common for several of these nerves to be damaged at the same time due to their proximity.[37] CES can occur by itself or alongside conus medullaris syndrome.[39] It can cause low back pain, weakness or paralysis in the lower limbs, loss of sensation, bowel and bladder dysfunction, and loss of reflexes.[39] There may be bilateral sciatica with central disc prolapse and altered gait.[38] Unlike conus medullaris syndrome, symptoms often occur only on one side of the body.[37] The cause is often compression, e.g. by a ruptured intervertebral disk or tumor.[37] Since the nerves damaged in CES are actually peripheral nerves because they have already branched off from the spinal cord, the injury has better prognosis for recovery of function: the peripheral nervous system has a greater capacity for healing than the central nervous system.[39]

Signs and symptoms

[edit]
Actions of the spinal nerves
Level Motor Function
C1C6 Neck flexors
C1T1 Neck extensors
C3, C4, C5 Supply diaphragm (mostly C4)
C5, C6 Move shoulder, raise arm (deltoid); flex elbow (biceps)
C6 externally rotate (supinate) the arm
C6, C7 Extend elbow and wrist (triceps and wrist extensors); pronate wrist
C7, T1 Flex wrist; supply small muscles of the hand
T1T6 Intercostals and trunk above the waist
T7L1 Abdominal muscles
L1L4 Flex thigh
L2, L3, L4 Adduct thigh; Extend leg at the knee (quadriceps femoris)
L4, L5, S1 abduct thigh; Flex leg at the knee (hamstrings); Dorsiflex foot (tibialis anterior); Extend toes
L5, S1, S2 Extend leg at the hip (gluteus maximus); Plantar flex foot and flex toes

Signs (observed by a clinician) and symptoms (experienced by a patient) vary depending on where the spine is injured and the extent of the injury.

Dermatome

[edit]

A section of skin innervated through a specific part of the spine is called a dermatome, and injury to that part of the spine can cause pain, numbness, or a loss of sensation in the related areas. Paraesthesia, a tingling or burning sensation in affected areas of the skin, is another symptom.[40] A person with a lowered level of consciousness may show a response to a painful stimulus above a certain point but not below it.[41]

Muscle function

[edit]

A group of muscles innervated through a specific part of the spine is called a myotome, and injury to that part of the spinal cord can cause problems with movements that involve those muscles. The muscles may contract uncontrollably (spasticity), become weak, or be completely paralysed. Spinal shock, loss of neural activity including reflexes below the level of injury, occurs shortly after the injury and usually goes away within a day.[42] Priapism, an erection of the penis may be a sign of acute spinal cord injury.[43]

The specific parts of the body affected by loss of function are determined by the level of injury. Some signs, such as bowel and bladder dysfunction can occur at any level. Neurogenic bladder involves a compromised ability to empty the bladder and is a common symptom of spinal cord injury. This can lead to high pressures in the bladder that can damage the kidneys.[44]

Spinal cord injury locations

[edit]

Cervical spine

[edit]
Muscle mass is reduced as muscles atrophy with disuse.
Function after complete cervical spinal cord injury[45]
Level Motor Function Respiratory function
C1–C4 Full paralysis of the limbs Cannot breathe without mechanical ventilation
C5 Paralysis of the wrists, hands, and triceps Difficulty coughing; may need help clearing secretions
C6 Paralysis of the wrist flexors, triceps, and hands
C7–C8 Some hand muscle weakness, difficulty grasping and releasing

Spinal cord injuries at the cervical vertebrae (neck) level result in full or partial tetraplegia, also called quadriplegia.[25] Depending on the specific location and severity of trauma, limited function may be retained. Additional symptoms of cervical injuries include low heart rate, low blood pressure, problems regulating body temperature, and breathing dysfunction.[46] If the injury is high enough in the neck to impair the muscles involved in breathing, the person may not be able to breathe without the help of an endotracheal tube and mechanical ventilator.[10]

Lumbosacral

[edit]

The effects of injuries at or above the lumbar or sacral regions of the spinal cord (lower back and pelvis) include decreased control of the legs and hips, genitourinary system, and anus. People injured below level L2 may still have use of their hip flexor and knee extensor muscles.[47] Bowel and bladder function are regulated by the sacral region. It is common to experience sexual dysfunction after injury, as well as dysfunction of the bowel and bladder, including fecal and urinary incontinence.[10]

Expected spinal cord injury complications by level of injury.

Thoracic

[edit]

In addition to the problems found in lower-level injuries, thorax (chest height) spinal lesions can affect the muscles in the trunk. Injuries at the level of T1 to T8 result in inability to control the abdominal muscles. Trunk stability may be affected; even more so in higher level injuries.[48] The lower the level of injury, the less extensive its effects. Injuries from T9 to T12 result in partial loss of trunk and abdominal muscle control. Thoracic spinal injuries result in paraplegia, but function of the hands, arms, and neck are not affected.[49]

Autonomic dysreflexia

[edit]

One condition that occurs typically in lesions above the T6 level is autonomic dysreflexia (AD), in which the blood pressure increases to dangerous levels, high enough to cause potentially deadly stroke.[9][50] It results from an overreaction of the system to a stimulus such as pain below the level of injury, because inhibitory signals from the brain cannot pass the lesion to dampen the excitatory sympathetic nervous system response.[6] Signs and symptoms of AD include anxiety, headache, nausea, ringing in the ears, blurred vision, flushed skin, and nasal congestion.[6] It can occur shortly after the injury or not until years later.[6]

Other autonomic functions may also be disrupted. For example, problems with body temperature regulation mostly occur in injuries at T8 and above.[47]

Neurogenic shock

[edit]

Another serious complication that can result from lesions above T6 is neurogenic shock, which results from an interruption in output from the sympathetic nervous system responsible for maintaining muscle tone in the blood vessels.[6][50] Without the sympathetic input, the vessels relax and dilate.[6][50] Neurogenic shock presents with dangerously low blood pressure, low heart rate, and blood pooling in the limbs—which results in insufficient blood flow to the spinal cord and potentially further damage to it.[51]

Complications

[edit]

Complications of spinal cord injuries include pulmonary edema, respiratory failure, neurogenic shock, and paralysis below the injury site.

Muscle atrophy

[edit]

In the long term, the loss of muscle function can have additional effects from disuse, including muscle atrophy. Immobility also can lead to pressure sores, particularly in bony areas, requiring precautions such as extra cushioning and turning in bed every two hours (in the acute setting) to relieve pressure.[52]

In the long term, people in wheelchairs must shift periodically to relieve pressure.[53] Another complication is pain, including nociceptive pain (indication of potential or actual tissue damage) and neuropathic pain, when nerves affected by damage convey erroneous pain signals in the absence of noxious stimuli.[54] Spasticity, the uncontrollable tensing of muscles below the level of injury, occurs in 65–78% of chronic SCI.[55] It results from lack of input from the brain that quells muscle responses to stretch reflexes.[56] It can be treated with drugs and physical therapy.[56] Spasticity increases the risk of contractures (shortening of muscles, tendons, or ligaments that result from lack of use of a limb); this problem can be prevented by moving the limb through its full range of motion multiple times a day.[57] Another problem lack of mobility can cause is loss of bone density and changes in bone structure.[58][59] Loss of bone density (bone demineralization), thought to be due to lack of input from weakened or paralysed muscles, can increase the risk of fractures.[60] Conversely, a poorly understood phenomenon is the overgrowth of bone tissue in soft tissue areas, called heterotopic ossification.[61] It occurs below the level of injury, possibly as a result of inflammation, and happens to a clinically significant extent in 27% of people.[61]

Cardiovascular and respiratory complications

[edit]

People with spinal cord injury are at especially high risk for respiratory and cardiovascular problems, so hospital staff must be watchful to avoid them.[62] Respiratory problems (especially pneumonia) are the leading cause of death in people with SCI, followed by infections, usually of pressure sores, urinary tract infections, and respiratory infections.[63] Pneumonia can be accompanied by shortness of breath, fever, and anxiety.[25]

Deep venous thrombosis

[edit]

Another potentially deadly threat to respiration is deep venous thrombosis (DVT), in which blood forms a clot in immobile limbs; the clot can break off and form a pulmonary embolism, lodging in the lung and cutting off blood supply to it.[64] DVT is an especially high risk in SCI, particularly within 10 days of injury, occurring in over 13% in the acute care setting.[65] Preventative measures include anticoagulants, pressure hose, and moving the patient's limbs.[65] The usual signs and symptoms of DVT and pulmonary embolism may be masked in SCI cases due to effects such as alterations in pain perception and nervous system functioning.[65]

Urinary tract infection

[edit]

Urinary tract infection (UTI) is another risk that may not display the usual symptoms (pain, urgency, and frequency); it may instead be associated with worsened spasticity.[25] The risk of UTI, likely the most common complication in the long term, is heightened by use of indwelling urinary catheters.[52] Catheterization may be necessary because SCI interferes with the bladder's ability to empty when it gets too full, which could trigger autonomic dysreflexia or damage the bladder permanently.[52] The use of intermittent catheterization to empty the bladder at regular intervals throughout the day has decreased the mortality due to kidney failure from UTI in the first world, but it is still a serious problem in developing countries.[60]

Clinical depression

[edit]

An estimated 24–45% of people with spinal cord injuries have major depressive disorder, and the suicide rate is as much as six times that of the rest of the population.[66] The risk of suicide is worst in the first five years after injury.[67] In young people with SCI, suicide is the leading cause of death.[68] Depression is associated with an increased risk of other complications such as UTI and pressure ulcers that occur more when self-care is neglected.[68]

Causes

[edit]
Falling as a part of recreational activities can cause spinal cord injuries.

Spinal cord injuries are most often caused by physical trauma.[22][69] Forces involved can be hyperflexion (forward movement of the head); hyperextension (backward movement); lateral stress (sideways movement); rotation (twisting of the head); compression (force along the axis of the spine downward from the head or upward from the pelvis); or distraction (pulling apart of the vertebrae).[70] Traumatic SCI can result in contusion, compression, or stretch injury.[5] It is a major risk of many types of vertebral fracture.[71] Pre-existing asymptomatic congenital anomalies can cause major neurological deficits, such as hemiparesis, to result from otherwise minor trauma.[72]

In the U.S., motor vehicle accidents are the most common cause of SCIs; second are falls, then violence such as gunshot wounds, then sports injuries.[73] Another study from Asia, found that the most common cause of the SCI is fall (31.70%) from various sites such as fall from roof-tops (9.75%), electric pole (7.31%), fall from tree (7.31%) etc. Whereas road traffic accidents count for 19.51%, firearm injuries (12.19%), slipped foot (7.31%) and sports injuries (4.87%). As a result of injury, 26.82%[74]In some countries falls are more common, even surpassing vehicle crashes as the leading cause of SCI.[75] The rates of violence-related SCI depend heavily on place and time.[75] Of all sports-related SCIs, shallow water dives are the most common cause; winter sports and water sports have been increasing as causes while association football and trampoline injuries have been declining.[76] Hanging can cause injury to the cervical spine, as may occur in attempted suicide.[77] Military conflicts are another cause, and when they occur they are associated with increased rates of SCI.[78] Another potential cause of SCI is iatrogenic injury, caused by an improperly done medical procedure such as an injection into the spinal column.[79]

SCI can also be of a nontraumatic origin. The percentage varies by locale, influenced by efforts to prevent trauma.[80] Developed countries have higher percentages of SCI due to degenerative conditions and tumors than developing countries.[81] In developed countries, the most common cause of nontraumatic SCI is degenerative diseases, followed by tumors; in many developing countries the leading cause is infection such as HIV and tuberculosis.[82] SCI may occur in intervertebral disc disease, and spinal cord vascular disease.[83] Spontaneous bleeding can occur within or outside of the protective membranes that line the cord, and intervertebral disks can herniate.[12] Damage can result from dysfunction of the blood vessels, as in arteriovenous malformation, or when a blood clot becomes lodged in a blood vessel and cuts off blood supply to the cord.[84] When systemic blood pressure drops, blood flow to the spinal cord may be reduced, potentially causing a loss of sensation and voluntary movement in the areas supplied by the affected level of the spinal cord.[85] Congenital conditions and tumors that compress the cord can also cause SCI, as can vertebral spondylosis and ischemia.[5] Multiple sclerosis is a disease that can damage the spinal cord, as can infectious or inflammatory conditions such as tuberculosis, herpes zoster or herpes simplex, meningitis, myelitis, and syphilis.[12]

Prevention

[edit]

Vehicle-related spinal cord injury is prevented with measures including societal and individual efforts to reduce driving under the influence of drugs or alcohol, distracted driving, and drowsy driving.[86] 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.[86] There are also approaches mitigate the damage of crashes, such as head restraints, air bags, seat belts, and child safety seats.[86] 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.[87] Gun-related injuries can be prevented with conflict resolution training, gun safety education campaigns, and changes to the technology of guns, including trigger locks to improve their safety.[87] 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.[88]

Diagnosis

[edit]
X-rays (left) are more available, but can miss details like herniated disks that MRIs can show (right).[89]

A person's presentation in context of trauma or non-traumatic background determines suspicion for a spinal cord injury. The features are namely paralysis, sensory loss, or both at any level. Other symptoms may include incontinence.[90]

A radiographic evaluation using an X-ray, CT scan, or MRI can determine if there is damage to the spinal column and where it is located.[10] X-rays are commonly available[89] and can detect instability or misalignment of the spinal column, but do not give very detailed images and can miss injuries to the spinal cord or displacement of ligaments or disks that do not have accompanying spinal column damage.[10] Thus when X-ray findings are normal but SCI is still suspected due to pain or SCI symptoms, CT or MRI scans are used.[89] CT gives greater detail than X-rays, but exposes the patient to more radiation,[91] and it still does not give images of the spinal cord or ligaments; MRI shows body structures in the greatest detail.[10] Thus it is the standard for anyone who has neurological deficits found in SCI or is thought to have an unstable spinal column injury.[92]

Neurological evaluations to help determine the degree of impairment are performed initially and repeatedly in the early stages of treatment; this determines the rate of improvement or deterioration and informs treatment and prognosis.[93][94] The ASIA Impairment Scale outlined above is used to determine the level and severity of injury.[10]

Management

[edit]

Pre-hospital treatment

[edit]
Spinal precaution with use of a long spinal board

The first stage in the management of a suspected spinal cord injury is geared toward basic life support and preventing further injury: maintaining airway, breathing, circulation, and restricting further motion of the spine.[24]

Spinal motion restriction

[edit]

In the emergency setting, most people who has been subjected to forces strong enough to cause SCI are treated as though they have instability in the spinal column and have spinal motion restricted to prevent damage to the spinal cord.[95] Injuries or fractures in the head, neck, or pelvis as well as penetrating trauma near the spine and falls from heights are assumed to be associated with an unstable spinal column until it is ruled out in the hospital.[10] High-speed vehicle crashes, sports injuries involving the head or neck, and diving injuries are other mechanisms that indicate a high SCI risk.[96] Since head and spinal trauma frequently coexist, anyone who is unconscious or has a lowered level of consciousness as a result of a head injury is spinal motion restricted.[97]

Devices

[edit]

A rigid cervical collar is applied to the neck, and the head is held with blocks on either side and the person is strapped to a backboard.[95] Extrication devices are used to move people without excessively moving the spine[98] if they are still inside a vehicle or other confined space. The use of a cervical collar has been shown to increase mortality in people with penetrating trauma and is thus not routinely recommended in this group.[99]

Modern trauma care includes a step called clearing the cervical spine, ruling out spinal cord injury if the patient is fully conscious and not under the influence of drugs or alcohol, displays no neurological deficits, has no pain in the middle of the neck and no other painful injuries that could distract from neck pain.[35] If these are all absent, no spinal motion restriction is necessary.[98]

If an unstable spinal column injury is moved, damage may occur to the spinal cord.[100] Between 3 and 25% of SCIs occur not at the time of the initial trauma but later during treatment or transport.[24] While some of this is due to the nature of the injury itself, particularly in the case of multiple or massive trauma, some of it reflects the failure to adequately restrict motion of the spine. SCI can impair the body's ability to keep warm, so warming blankets may be needed.[97]

Early hospital treatment

[edit]

Initial care in the hospital, as in the prehospital setting, aims to ensure adequate airway, breathing, cardiovascular function, and spinal motion restriction.[101] Imaging of the spine to determine the presence of a SCI may need to wait if emergency surgery is needed to stabilize other life-threatening injuries.[102] Acute SCI merits treatment in an intensive care unit, especially injuries to the cervical spinal cord.[101] People with SCI need repeated neurological assessments and treatment by neurosurgeons.[103] People should be removed from the spine board as rapidly as possible to prevent complications from its use.[104]

Blood pressure

[edit]

If the systolic blood pressure falls below 90 mmHg within days of the injury, blood supply to the spinal cord may be reduced, resulting in further damage.[51] Thus it is important to maintain the blood pressure which may be done using intravenous fluids and vasopressors.[105] Vasopressors used include phenylephrine, dopamine, or norepinephrine.[1] Mean arterial blood pressure is measured and kept at 85 to 90 mmHg for seven days after injury.[106]

The CAMPER Trial led by Dr Kwon and subsequent studies by the UCSF TRACK-SCI group (Dhall) have shown that spinal cord perfusion pressure (SCPP) goals are more closely associated with better neurologic recovery than MAP goals. Some institutions have adopted these SCPP goals and lumbar CSF drain placement as a standard of care.[107] The treatment for shock from blood loss is different from that for neurogenic shock, and could harm people with the latter type, so it is necessary to determine why someone is in shock.[105] However it is also possible for both causes to exist at the same time.[1] Another important aspect of care is prevention of insufficient oxygen in the bloodstream, which could deprive the spinal cord of oxygen.[108] People with cervical or high thoracic injuries may experience a dangerously slowed heart rate; treatment to speed it may include atropine.[1]

Steroid treatment

[edit]

The corticosteroid medication methylprednisolone has been studied for use in spinal cord injury patients with the hope of limiting swelling and secondary injury.[109] As there does not appear to be long term benefits and the medication is associated with risks such as gastrointestinal bleeding and infection its use is not recommended as of 2018.[1][109] Its use in traumatic brain injury is also not recommended.[104]

Surgery

[edit]

Surgery may be necessary, e.g. to relieve excess pressure on the cord, to stabilize the spine, or to put vertebrae back in their proper place.[106] In cases involving instability or compression, failing to operate can lead to worsening of the condition.[106] Surgery is also necessary when something is pressing on the cord, such as bone fragments, blood, material from ligaments or intervertebral discs,[110] or a lodged object from a penetrating injury.[89] Although the ideal timing of surgery is still debated, studies have found that earlier surgical intervention (within 12 hours of injury) is associated with better outcomes.[111] This type of surgery is often referred to as "Ultra-Early", coined by Burke et al. at UCSF. Sometimes a patient has too many other injuries to be a surgical candidate this early.[106] Surgery is controversial because it has potential complications (such as infection), so in cases where it is not clearly needed (e.g. the cord is being compressed), doctors must decide whether to perform surgery based on aspects of the patient's condition and their own beliefs about its risks and benefits.[112] Recent large-scale studies have shown that patients who do undergo earlier surgery (within 12–24 hours) experience significantly lower rates of life-threatening complications and spend less time in hospital and critical care.[113][114]

However, in cases where a more conservative approach is chosen, bed rest, cervical collars, motion restriction devices, and optionally traction are used.[115] Surgeons may opt to put traction on the spine to remove pressure from the spinal cord by putting dislocated vertebrae back into alignment, but herniation of intervertebral disks may prevent this technique from relieving pressure.[116] Gardner-Wells tongs are one tool used to exert spinal traction to reduce a fracture or dislocation and to reduce motion to the affected areas.[117]

Rehabilitation

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A drop foot orthosis lifts the forefoot in order to compensate for a weakness in the dorsiflexors. If other muscle groups, such as the plantar flexors, are weak, additional functional elements must be considered. An ankle-foot orthoses (AFO) is not suitable for the care of patients with weakness in other muscle groups.
A patient after incomplete paraplegia (lesion height L3) with a knee-ankle-foot orthosis (KAFO) with an integrated stance phase control knee joint

Spinal cord injury patients often require extended treatment in specialized spinal unit or an intensive care unit.[118] The rehabilitation process typically begins in the acute care setting. Usually, the inpatient phase lasts 8–12 weeks and then the outpatient rehabilitation phase lasts 3–12 months after that, followed by yearly medical and functional evaluation.[9] Physical therapists, occupational therapists, recreational therapists, nurses, social workers, psychologists, and other health care professionals work as a team under the coordination of a physiatrist[10] to decide on goals with the patient and develop a plan of discharge that is appropriate for the person's condition.

In the acute phase physical therapists focus on the patient's respiratory status, prevention of indirect complications (such as pressure ulcers), maintaining range of motion, and keeping available musculature active.[119]

For people whose injuries are high enough to interfere with breathing, there is great emphasis on airway clearance during this stage of recovery.[120] Weakness of respiratory muscles impairs the ability to cough effectively, allowing secretions to accumulate within the lungs.[121] As SCI patients have reduced total lung capacity and tidal volume,[122] physical therapists teach them accessory breathing techniques (e.g. apical breathing, glossopharyngeal breathing) that typically are not taught to healthy individuals. Physical therapy treatment for airway clearance may include manual percussions and vibrations, postural drainage,[120] respiratory muscle training, and assisted cough techniques.[121] Patients are taught to increase their intra-abdominal pressure by leaning forward to induce cough and clear mild secretions.[121] The quad cough technique is done lying on the back with the therapist applying pressure on the abdomen in the rhythm of the cough to maximize expiratory flow and mobilize secretions.[121] Manual abdominal compression is another technique used to increase expiratory flow which later improves coughing.[120] Other techniques used to manage respiratory dysfunction include respiratory muscle pacing, use of a constricting abdominal binder, ventilator-assisted speech, and mechanical ventilation.[121]

The amount of functional recovery and independence achieved in terms of activities of daily living, recreational activities, and employment is affected by the level and severity of injury.[123] The Functional Independence Measure (FIM) is an assessment tool that aims to evaluate the function of patients throughout the rehabilitation process following a spinal cord injury or other serious illness or injury.[124] It can track a patient's progress and degree of independence during rehabilitation.[124] People with SCI may need to use specialized devices and to make modifications to their environment in order to handle activities of daily living and to function independently. Weak joints can be stabilized with devices such as ankle-foot orthoses (AFOs) or knee-ankle-foot orthoses (KAFOs), but walking may still require a lot of effort.[125] Increasing activity will increase chances of recovery.[126]

For treatment of paralysis levels in the lower thoracic spine or lower, starting therapy with an orthosis is promising from the intermediate phase (2–26 weeks after the incident).[127][128][129] In patients with complete paraplegia (ASIA A), this applies to lesion heights between T12 and S5. In patients with incomplete paraplegia (ASIA B-D), orthoses are even suitable for lesion heights above T12. In both cases, however, a detailed muscle function test must be carried out to precisely plan the construction with an orthosis.[130]

Prognosis

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Holly Koester, who incurred a spinal injury as a result of a motor vehicle collision, is now a wheelchair racer.

Spinal cord injuries generally result in at least some incurable impairment even with the best possible treatment. The best predictor of prognosis is the level and completeness of injury, as measured by the ASIA impairment scale.[131] The neurological score at the initial evaluation done 72 hours after injury is the best predictor of how much function will return.[132] Most people with ASIA scores of A (complete injuries) do not have functional motor recovery, but improvement can occur.[131][133] Most patients with incomplete injuries recover at least some function.[133] Chances of recovering the ability to walk improve with each AIS grade found at the initial examination; e.g. an ASIA D score confers a better chance of walking than a score of C.[132] The symptoms of incomplete injuries can vary and it is difficult to make an accurate prediction of the outcome. A person with a mild, incomplete injury at the T5 vertebra will have a much better chance of using his or her legs than a person with a severe, complete injury at exactly the same place. Of the incomplete SCI syndromes, Brown-Séquard and central cord syndromes have the best prognosis for recovery and anterior cord syndrome has the worst.[29]

People with nontraumatic causes of SCI have been found to be less likely to develop complete injuries and some complications such as pressure sores and deep vein thrombosis, and to have shorter hospital stays.[12] Their scores on functional tests were better than those of people with traumatic SCI upon hospital admission, but when they were tested upon discharge, those with traumatic SCI had improved such that both groups' results were the same.[12] In addition to the completeness and level of the injury, age and concurrent health problems affect the extent to which a person with SCI will be able to live independently and to walk.[9] However, in general people with injuries to L3 or below will likely be able to walk functionally, T10 and below to walk around the house with bracing, and C7 and below to live independently.[9] New therapies are beginning to provide hope for better outcomes in patients with SCI, but most are in the experimental/translational stage.[4]

One important predictor of motor recovery in an area is presence of sensation there, particularly pain perception.[39] Most motor recovery occurs in the first year post-injury, but modest improvements can continue for years; sensory recovery is more limited.[134] Recovery is typically quickest during the first six months.[135] Spinal shock, in which reflexes are suppressed, occurs immediately after the injury and resolves largely within three months but continues resolving gradually for another 15.[136]

Sexual dysfunction after spinal injury is common. Problems that can occur include erectile dysfunction, loss of ability to ejaculate, insufficient lubrication of the vagina, and reduced sensation and impaired ability to orgasm.[55] Despite this, many people learn ways to adapt their sexual practices so they can lead satisfying sex lives.[137]

Although life expectancy has improved with better care options, it is still not as good as the uninjured population. The higher the level of injury, and the more complete the injury, the greater the reduction in life expectancy.[84] Mortality is very elevated within a year of injury.[84]

Epidemiology

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Breakdown of age at time of injury in the US from 1995–1999.[138]
  1. 0–15 (3.00%)
  2. 16–30 (42.1%)
  3. 31–45 (28.1%)
  4. 46–60 (15.1%)
  5. 61–75 (8.50%)
  6. 76+ (3.20%)

Worldwide, the number of new cases since 1995 of SCI ranges from 10.4 to 83 people per million per year.[106] This wide range of numbers is probably partly due to differences among regions in whether and how injuries are reported.[106] In North America, about 39 people per every million incur SCI traumatically each year, and in Western Europe, the incidence is 16 per million.[139][140] In the United States, the incidence of spinal cord injury has been estimated to be about 40 cases per 1 million people per year or around 12,000 cases per year.[141] In China, the incidence is approximately 60,000 per year.[142]

The estimated number of people living with SCI in the world ranges from 236 to 4187 per million.[106] Estimates vary widely due to differences in how data are collected and what techniques are used to extrapolate the figures.[143] Little information is available from Asia, and even less from Africa and South America.[106] In Western Europe the estimated prevalence is 300 per million people and in North America it is 853 per million.[140] It is estimated at 440 per million in Iran, 526 per million in Iceland, and 681 per million in Australia.[143] In the United States there are between 225,000 and 296,000 individuals living with spinal cord injuries,[144] and different studies have estimated prevalences from 525 to 906 per million.[143]

SCI is present in about 2% of all cases of blunt force trauma.[100] Anyone who has undergone force sufficient to cause a thoracic spinal injury is at high risk for other injuries also.[102] In 44% of SCI cases, other serious injuries are sustained at the same time; 14% of SCI patients also have head trauma or facial trauma.[22] Other commonly associated injuries include chest trauma, abdominal trauma, pelvic fractures, and long bone fractures.[94]

Males account for four out of five traumatic spinal cord injuries.[25] Most of these injuries occur in men under 30 years of age.[10] The average age at the time of injury has slowly increased from about 29 years in the 1970s to 41.[25] In Pakistan, spinal cord injury is more common in males (92.68%) as compared to females in the 20–30 years of age group with a median age of 40 years, although people from 12–70 years of age suffered from spinal cord injury[74] Rates of injury are at their lowest in children, at their highest in the late teens to early twenties, then get progressively lower in older age groups; however rates may rise in the elderly.[145] In Sweden between 50 and 70% of all cases of SCI occur in people under 30, and 25% occur in those over 50.[75] While SCI rates are highest among people age 15–20,[146] fewer than 3% of SCIs occur in people under 15.[147] Neonatal SCI occurs in one in 60,000 births, e.g. from breech births or injuries by forceps.[148] The difference in rates between the sexes diminishes in injuries at age 3 and younger; the same number of girls are injured as boys, or possibly more.[149] Another cause of pediatric injury is child abuse such as shaken baby syndrome.[148] For children, the most common cause of SCI (56%) is vehicle crashes.[150] High numbers of adolescent injuries are attributable in a large part to traffic accidents and sports injuries.[151] For people over 65, falls are the most common cause of traumatic SCI.[5] The elderly and people with severe arthritis are at high risk for SCI because of defects in the spinal column.[152] In nontraumatic SCI, the gender difference is smaller, the average age of occurrence is greater, and incomplete lesions are more common.[132]

History

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The ancient Egyptian Edwin Smith Papyrus, who provided the earliest known description of spinal cord injury[153]

Spinal cord injury has been known to be devastating for millennia; the ancient Egyptian Edwin Smith Papyrus from 2500 BC, the first known description of the injury, says it is "not to be treated".[153] Hindu texts dating back to 1800 BC also mention SCI and describe traction techniques to straighten the spine.[153] The Greek physician Hippocrates, born in the fifth century BC, described SCI in his Hippocratic Corpus and invented traction devices to straighten dislocated vertebrae.[154] But it was not until Aulus Cornelius Celsus, born 30 BC, noted that a cervical injury resulted in rapid death that the spinal cord itself was implicated in the condition.[153] In the second century AD the Greek physician Galen experimented on monkeys and reported that a horizontal cut through the spinal cord caused them to lose all sensation and motion below the level of the cut.[155] The seventh-century Greek physician Paul of Aegina described surgical techniques for treatment of broken vertebrae by removing bone fragments, as well as surgery to relieve pressure on the spine.[153] Little medical progress was made during the Middle Ages in Europe; it was not until the Renaissance that the spine and nerves were accurately depicted in human anatomy drawings by Leonardo da Vinci and Andreas Vesalius.[155]

In 1762, Andre Louis, a surgeon, removed a bullet from the lumbar spine of a patient, who regained motion in the legs.[155] In 1829, Gilpin Smith, a surgeon, performed a successful laminectomy that improved the patient's sensation.[156] However, the idea that SCI was untreatable remained predominant until the early 20th century.[157] In 1934, the mortality rate in the first two years after injury was over 80%, mostly due to infections of the urinary tract and pressure sores,[158] the latter of which were believed to be intrinsic to SCI rather than a result of continuous bedrest.[159] It was not until the second half of the century that breakthroughs in imaging, surgery, medical care, and rehabilitation medicine contributed to a substantial improvement in SCI care.[157] The relative incidence of incomplete compared to complete injuries has improved since the mid-20th century, due mainly to the emphasis on faster and better initial care and stabilization of spinal cord injury patients.[160] The creation of emergency medical services to professionally transport people to the hospital is given partial credit for an improvement in outcomes since the 1970s.[161] Improvements in care have been accompanied by increased life expectancy of people with SCI; survival times have improved by about 2000% since 1940.[162] In 2015/2016 23% of people in nine spinal injury centres in England had their discharge delayed because of disputes about who should pay for the equipment they needed.[163]

Research directions

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Human bone marrow derived mesenchymal stem cells seen under phase contrast microscope at 63-times magnification)

Scientists are investigating various avenues for treatment of spinal cord injury. Therapeutic research is focused on two main areas: neuroprotection and neuroregeneration.[78] 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.[78] Neuroprotective drugs target secondary injury effects including inflammation, damage by free radicals, excitotoxicity (neuronal damage by excessive glutamate signaling), and apoptosis (cell suicide).[78] Several potentially neuroprotective agents that target pathways like these are under investigation in human clinical trials.[78]

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.[78] A key avenue of SCI research is research on stem cells, which can differentiate into other types of cells—including those lost after SCI.[78] 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.[164] Hundreds of stem cell studies have been done in humans, with promising but inconclusive results.[151] An ongoing Phase 2 trial in 2016 presented data[165] 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 was expected in January 2017.[166]

Another type of approach is tissue engineering, using biomaterials to help scaffold and rebuild damaged tissues.[78] Biomaterials being investigated include natural substances such as collagen or agarose and synthetic ones like polymers and nitrocellulose.[78] They fall into two categories: hydrogels and nanofibers.[78] These materials can also be used as a vehicle for delivering gene therapy to tissues.[78]

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.[167] The devices, which have motorized joints, are put on over the legs and supply a source of power to move and walk.[167] Several such devices are already available for sale, but investigation is still underway as to how they can be made more useful.[167]

Preliminary studies of epidural spinal cord stimulators for motor complete injuries have demonstrated some improvement,[168] and in some cases to enable walking to some degree bypassing the injury.[169][170]

In 2014, Darek Fidyka underwent pioneering spinal surgery that used nerve grafts, from his ankle, to bridge the gap in his severed spinal cord and olfactory ensheathing cells (OECs) to stimulate the spinal cord cells. The surgery was performed in Poland in collaboration with Prof. Geoff Raisman, chair of neural regeneration at University College London's Institute of Neurology, and his research team. The OECs were taken from the patient's olfactory bulbs in his brain and then grown in the lab, these cells were then injected above and below the impaired spinal tissue.[171][38]

There have been a number of advances in technological spinal cord injury treatment, including the use of implants that provided a "digital bridge" between the brain and the spinal cord. In a study published in May 2023 in the journal Nature, researchers in Switzerland described such implants which allowed a 40-year old man, paralyzed from the hips down for 12 years, to stand, walk and ascend a steep ramp with only the assistance of a walker. More than a year after the implant was inserted, he has retained these abilities and was walking with crutches even when the implant was switched off.[172]

In March 2025, researchers reported that a paralyzed man stood for the first time after being injected of neural stem cells to treat his spinal cord injury. The first-of-its-kind study, which is not yet peer reviewed, is encouraging scientists to consider if reprogrammed stem cells can be used in the future to treat people who are fully paralyzed. Reprogrammed cells are adult cells that are reverted to an embryonic-like state, from which they can be coaxed to develop into other cell types.[173]

See also

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References

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Bibliography

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Revisions and contributorsEdit on WikipediaRead on Wikipedia
from Grokipedia
A spinal cord injury (SCI) is damage to the —the bundle of and nerve fibers that transmits signals between the and the rest of the body—or to the at the end of the , such as the , resulting in permanent changes to strength, sensation, and other body functions below the level of injury. These injuries disrupt motor, sensory, and autonomic pathways, often leading to partial or complete loss of function depending on the severity and location. Globally, over 15 million people live with SCI, with the condition contributing to more than 4.5 million years lived with in 2021, and it disproportionately affects males while reducing due to secondary complications. SCIs are classified as traumatic or non-traumatic. Traumatic injuries, which account for the majority of cases and are largely preventable, stem from external forces such as accidents (the leading cause, responsible for about 38% of new cases annually in the United States since 2015), falls (especially among those over 65), (about 14%), and sports or recreational activities (around 8%). Non-traumatic causes include medical conditions like , cancer, infections, disk herniation, or degenerative diseases that gradually damage the without direct trauma. Risk factors encompass male gender (80% of cases), age groups 16–30 (over 50% of injuries) or over 65, alcohol or substance use (involved in about 25% of cases), and lack of safety measures like seatbelts or protective gear. Symptoms of SCI vary by the injury's location and completeness but typically include immediate loss of sensation or movement below the injury site, with complete injuries severing all nerve communication (resulting in total ) and incomplete injuries preserving some function. Common manifestations encompass numbness, , , breathing difficulties (especially in cervical injuries), loss of or bowel control, circulatory issues like blood clots, pressure sores, muscle spasms or , , and psychological effects such as depression. Injuries higher in the spinal cord (cervical or thoracic levels) affect more body areas, potentially impacting respiratory and function, while or sacral injuries primarily involve the legs and pelvic organs. Treatment begins as a medical emergency to prevent further damage, involving immobilization of the spine, medications to reduce swelling, surgery for decompression or stabilization, and management of vital functions like breathing and circulation. Long-term care emphasizes rehabilitation through physical, occupational, and speech therapy; assistive devices such as wheelchairs; and strategies to address complications like autonomic dysreflexia or osteoporosis. Prevention focuses on road safety, fall-proofing environments, violence reduction, and early intervention for underlying conditions, potentially averting many traumatic cases worldwide. As of February 2026, there is no established cure for spinal cord injury, but significant breakthroughs in regenerative therapies are progressing rapidly and offer growing potential for meaningful recovery. Key developments include the "dancing molecules" supramolecular peptide therapy, which received FDA Orphan Drug Designation in 2025 and demonstrated regenerative effects including reduced scarring and neurite outgrowth in lab-grown human spinal cord organoids in February 2026; grants awarded in January 2026 by the Christopher & Dana Reeve Foundation and Spinal Research to advance preclinical studies on biologics, gene therapies, and stem cell approaches while challenging the view that paralysis is permanent; and a world-first Phase 1 clinical trial initiated in August 2025 using patient-derived olfactory ensheathing cells to create a nerve bridge implant for chronic SCI. Ongoing research targets neuroprotection, cell-based therapies, and neuroplasticity to improve recovery outcomes.

Classification and Types

Complete and incomplete injuries

Spinal cord injuries are classified as complete or incomplete based on the extent of neurological function preserved below the level of injury. A complete injury is defined as the total loss of sensory and motor function in all segments below the neurological level, including the absence of sacral sparing in the S4-S5 segments, which indicates no preserved sensation in the perianal area or voluntary anal contraction. In contrast, an incomplete injury involves partial preservation of sensory or motor function below the injury level, allowing some signal transmission through the despite the damage. The clinical implications of these classifications are profound, as complete injuries typically result in permanent paralysis, such as from cervical-level damage or from thoracic or lumbar injuries, with minimal potential for spontaneous recovery. Incomplete injuries, however, offer variable recovery potential, where patients may regain some mobility or sensation, with studies showing that 20% to 75% of individuals achieve ambulatory capacity within one year depending on the injury severity. This distinction is assessed using tools like the ASIA Impairment Scale, which grades the degree of completeness. For example, a complete cervical spinal cord injury often leads to full , affecting all four limbs and trunk, whereas an incomplete cervical injury might spare partial arm or hand function, enabling limited upper body use.

ASIA Impairment Scale

The American Spinal Injury Association () Impairment Scale (AIS), also known as the International Standards for Neurological Classification of Spinal Cord Injury (ISNCSCI), is a standardized tool used to classify the severity of spinal cord injuries based on sensory and motor function. It provides a five-grade system that differentiates complete from incomplete injuries and guides clinical management. The scale consists of the following grades:
GradeDescription
A (Complete)No sensory or motor function is preserved in the sacral segments S4-S5.
B (Sensory Incomplete)Sensory but not motor function is preserved below the neurological level, including the sacral segments S4-S5 (via light touch, pinprick, or deep anal pressure), and extends no motor function more than three levels below the motor level on either side.
C (Motor Incomplete)Motor function is preserved at the most caudal sacral segments (voluntary anal contraction) or sensory incomplete status is met, but more than half of the key muscle functions below the single neurological level of injury have a muscle grade less than 3.
D (Motor Incomplete)Motor incomplete status as defined above, with at least half (half or more) of the key muscle functions below the single neurological level of injury having a muscle grade greater than or equal to 3.
E (Normal)If sensation and motor function as tested with the ISNCSCI are graded as normal in all segments and the patient had prior deficits, then the AIS grade is E; individuals without an initial SCI do not receive an AIS grade.
Assessment involves sensory testing of light touch and pinprick across 28 dermatomes bilaterally (from C2 to S4-S5), scored from 0 (absent) to 2 (normal); motor testing of 10 key muscles representing myotomes (five upper and five lower extremity pairs, from C5 to S1), graded from 0 (no contraction) to 5 (normal strength); and evaluation of sacral sparing through voluntary anal contraction, deep anal pressure, and S4-S5 sensation to determine completeness. The neurological level of injury is identified as the most caudal segment with intact sensory and motor function, while the AIS grade reflects overall impairment severity. Originally introduced in 1982 by the American Spinal Injury Association, the scale was revised multiple times, with the 2019 update incorporating refinements such as zone of partial preservation adjustments for better applicability in incomplete . In 2025, an expedited version (E-ISNCSCI V2) was released to streamline assessments while preserving accuracy. Its primary utility lies in standardizing initial diagnosis, monitoring neurological recovery over time, and facilitating consistent comparisons in and prognostic evaluations. For instance, a grade C thoracic may preserve weak voluntary movement in the legs (motor score <3 in most below-level muscles) but typically precludes independent walking without assistive devices.

Specific injury syndromes

Specific injury syndromes in spinal cord injury encompass distinct clinical patterns arising from localized damage, each producing characteristic combinations of motor, sensory, and autonomic impairments that reflect the underlying neuroanatomy. These syndromes are often incomplete, allowing for potential functional recovery, and are differentiated by the specific tracts or regions affected, such as central gray matter, anterior cord, or hemicord structures. Understanding these patterns aids in precise diagnosis and targeted management. Central cord syndrome represents the most common form of incomplete , accounting for a significant portion of cervical injuries, with an estimated 3,000 cases annually in the United States (2009-2012 data). It is characterized by disproportionately greater motor weakness in the upper extremities than in the lower extremities, along with variable sensory deficits below the level of injury and sacral sparing. This syndrome typically results from hyperextension trauma in the cervical spine, particularly in older adults with preexisting conditions like cervical spondylosis or , where anterior compression from bony spurs or disc material and posterior buckling of the ligamentum flavum pinch the central cord. Clinically, patients exhibit upper motor neuron signs such as spasticity, more pronounced hand and arm paresis, bladder dysfunction with initial retention, and a "cape-like" distribution of sensory loss; proprioception and vibration sense are often relatively preserved due to sparing of the dorsal columns. Anterior spinal artery syndrome arises from occlusion or hypoperfusion of the anterior spinal artery, leading to infarction of the anterior two-thirds of the spinal cord and representing the most frequent type of spinal cord infarction. It manifests as acute bilateral flaccid paralysis or paraplegia below the lesion level, accompanied by loss of pain and temperature sensation in a dissociated pattern, while deep pressure, proprioception, and vibration sense remain intact via the posterior columns supplied by the posterior spinal arteries. Common etiologies include aortic surgery, atherosclerotic disease, aortic dissection, or trauma disrupting the artery of Adamkiewicz, which supplies the lower thoracic cord in about 75% of individuals originating between T9 and T12. Autonomic features such as neurogenic bladder, bowel dysfunction, and hypotension may occur, with symptoms often preceded by severe back pain at the affected level. Brown-Séquard syndrome results from hemisection or unilateral damage to the spinal cord, producing an asymmetric pattern of deficits that highlights the crossed pathways of spinal tracts. It features ipsilateral loss of motor function (corticospinal tract involvement), proprioception, and vibration sense (dorsal columns), combined with contralateral loss of pain and temperature sensation (spinothalamic tract, which decussates 1-2 levels above the lesion). This syndrome accounts for 1-4% of traumatic spinal cord injuries and is most often caused by penetrating trauma such as stab wounds or fractures, though nontraumatic factors like tumors, ischemia, or multiple sclerosis can also precipitate it, predominantly in the cervical or thoracic regions. Sensory level is typically identifiable, with the motor and proprioceptive deficits aligning to the lesion side and pain/temperature loss emerging 1-3 segments below. Posterior spinal artery syndrome is a rare form of spinal cord infarction due to occlusion of the posterior spinal arteries, affecting the dorsal columns and resulting in selective sensory impairments without significant motor involvement. Patients experience bilateral loss of proprioception, vibration, and light touch sensation below the lesion, often with preserved strength and pain/temperature perception, though total anesthesia at the exact level may occur. It is infrequently reported, typically stemming from embolism, atherosclerosis, or vascular spasm, and underscores the vulnerability of posterior circulation in conditions like aortic disease. Conus medullaris syndrome occurs from injury to the terminal portion of the spinal cord at T12-L2, blending upper and lower motor neuron features due to involvement of sacral segments and lumbar nerve roots. It presents with symmetric bilateral perineal sensory loss (saddle anesthesia), early bladder and bowel dysfunction including areflexic bladder and flaccid anal sphincter, and mixed weakness in the lower extremities with hyperreflexia above and hyporeflexia at the conus level. Common causes include fractures, tumors, or disc herniations compressing the conus, distinguishing it from higher cord lesions by its predominant autonomic and sacral involvement. Cauda equina syndrome involves compression or injury to the lumbosacral nerve roots below the conus medullaris (L1-L5), functioning as a peripheral nerve disorder rather than true spinal cord injury, leading to lower motor neuron deficits. Symptoms include asymmetric or unilateral lower extremity weakness, flaccid paralysis, areflexia, saddle anesthesia, and prominent bladder/bowel/sexual dysfunction such as urinary retention and fecal incontinence, often with severe radicular pain. It is frequently triggered by massive disc herniation, trauma, or spinal stenosis, requiring urgent decompression to prevent permanent deficits. Spinal cord injury without radiographic abnormality (SCIWORA) describes clinical myelopathy with objective neurological deficits but no visible fractures, dislocations, or instability on plain radiographs or computed tomography, comprising 6-19% of pediatric spinal injuries. It predominantly affects children under 8 years due to their elastic ligaments and relatively large head-to-body ratio, allowing cord stretch or contusion from hyperextension/hyperflexion without bony damage, though adults may experience it with preexisting stenosis. Diagnosis relies on magnetic resonance imaging to reveal cord edema, hemorrhage, or transection, emphasizing the need for advanced imaging in trauma with neurological signs despite normal initial studies.

Pathophysiology

Primary injury mechanisms

The primary injury in spinal cord injury (SCI) refers to the initial mechanical insult that directly damages neural tissue at the moment of trauma, resulting in immediate and often irreversible structural disruption. This phase encompasses the direct transfer of kinetic energy to the spinal cord, leading to physical deformation or severance of axons, blood vessels, and supporting structures. Unlike subsequent biochemical cascades, the primary injury is characterized by instantaneous events that halt neural conduction across the injury site. Traumatic primary injuries typically arise from external forces applied to the spine, manifesting as compression, contusion, laceration, or transection. Compression occurs when the spinal cord is squeezed by displaced vertebral bone fragments, herniated discs, or ligaments, often during hyperflexion or hyperextension injuries common in falls or sports. Contusion involves bruising of the cord from blunt impact, such as in vehicular crashes where high-velocity energy transfer causes rapid tissue deformation without penetration. Laceration and transection result from sharp or penetrating forces, including rotation-induced facet dislocations or gunshot wounds, which tear neural pathways and may fully sever the cord. These mechanisms are influenced by biomechanical factors like force magnitude and direction; for instance, axial loading in motor vehicle accidents delivers concentrated energy, exacerbating contusion severity through vertebral collapse. Immediate effects of primary injury include axonal disruption, where stretching or shearing interrupts nerve fiber integrity, leading to loss of sensory and motor conduction below the lesion level. Hemorrhage ensues from vascular rupture at the injury epicenter, forming hematomas that further compress tissue, while ischemia develops due to vessel occlusion or spasm, depriving neurons of oxygen and nutrients. These changes collectively cause spinal shock—a transient flaccid paralysis and areflexia—stemming from disrupted descending pathways. In non-traumatic cases, primary injury can occur gradually through sustained compression by tumors or abscesses, which deform the cord over time and initiate similar structural damage without acute force.

Secondary injury processes

Secondary injury processes in spinal cord injury refer to the cascade of biochemical, cellular, and vascular events that occur after the initial mechanical trauma, exacerbating tissue damage and impairing recovery. These processes begin within minutes to hours post-injury and peak between 24 and 72 hours, providing a potentially modifiable window for intervention. Unlike the irreversible primary injury, secondary mechanisms involve progressive deterioration driven by interconnected pathological pathways. A primary mechanism is excitotoxicity, triggered by excessive release of glutamate from damaged neurons, leading to overactivation of receptors such as NMDA and . This causes massive calcium influx into cells, activating destructive enzymes like proteases, lipases, and endonucleases, which damage neurons and oligodendrocytes. Excitotoxicity peaks within 20-30 minutes but contributes to ongoing cell death over hours. Oxidative stress follows, characterized by the production of reactive oxygen species (ROS) and free radicals from disrupted mitochondria and activated inflammatory cells. These species induce lipid peroxidation of cell membranes, protein oxidation, and DNA damage, further compromising neuronal integrity. Markers such as malondialdehyde, a byproduct of lipid peroxidation, remain elevated from 1 hour to 1 week post-injury. Inflammation plays a central role, initiating a cytokine storm involving pro-inflammatory mediators like TNF-α, IL-1β, and IL-6, released by microglia and astrocytes. This recruits neutrophils, which infiltrate the injury site within hours and peak at 24 hours, releasing additional ROS and proteases that amplify tissue destruction. Subsequent macrophage and lymphocyte involvement sustains the inflammatory response for days to weeks. Apoptosis, or programmed cell death, affects both neurons and oligodendrocytes, contributing to demyelination and axonal loss. Activated by signals from excitotoxicity, oxidative stress, and inflammation, apoptotic pathways peak around 7 days post-injury, leading to the progressive expansion of the lesion cavity. Edema formation, resulting from increased vascular permeability and ionic imbalances, raises intramedullary pressure and compresses microvasculature, inducing secondary ischemia. This hypoxic environment worsens all prior mechanisms, creating a vicious cycle of damage. Vascular changes underpin many secondary processes, including immediate hypoperfusion due to hemorrhage and vasospasm, which reduces oxygen delivery and persists for up to 24 hours. Breakdown of the blood-spinal cord barrier allows influx of serum proteins and immune cells, further promoting edema and inflammation. Therapeutic strategies target these modifiable phases, with antioxidants such as cerium oxide nanoparticles aimed at scavenging ROS to limit oxidative damage, and anti-inflammatories like minocycline or GW2580 designed to suppress cytokine release and neutrophil activity. These approaches seek to halt the cascade and preserve viable tissue.

Signs and Symptoms

Sensory and motor deficits

Spinal cord injury (SCI) primarily disrupts the ascending sensory pathways and descending motor pathways, leading to profound impairments in sensation and voluntary movement below the level of the lesion. Sensory deficits typically manifest as anesthesia (complete loss of sensation) or paresthesia (abnormal sensations such as tingling or numbness) in the dermatomes corresponding to spinal segments caudal to the injury site. Neuropathic pain, characterized by burning, shooting, or electric-like sensations, affects approximately 53% of individuals with SCI and arises from central and peripheral sensitization below the injury level. These deficits affect multiple modalities, including light touch and pressure (mediated by the dorsal column-medial lemniscus pathway), pain and temperature (via the spinothalamic tract), and proprioception (joint position sense, also via dorsal columns). Motor deficits arise from interruption of the corticospinal tract, resulting in weakness or paralysis of muscles innervated by segments below the injury. Initially, following acute SCI, a phase known as spinal shock occurs, characterized by flaccid paralysis, areflexia (loss of reflexes), and temporary hypotension due to disrupted spinal reflexes and autonomic tone; this phase typically lasts from days to weeks, after which hyperreflexia and spasticity may emerge as upper motor neuron signs develop. Above the injury level, motor function remains intact. Below the injury, upper motor neuron signs like spasticity and hyperreflexia may develop in the chronic phase, while the deficits are predominantly lower motor neuron in nature if the injury involves anterior horn cells, leading to flaccid weakness and atrophy. The specific pattern of deficits depends on the injury level. Cervical injuries (C1-C8) often cause tetraplegia, affecting all four limbs, with high cervical lesions (e.g., C1-C4) potentially impairing respiratory muscles innervated by the phrenic nerve (C3-C5), leading to ventilatory dependence. Thoracic injuries (T1-T12) result in paraplegia, sparing the upper limbs but causing trunk instability and loss of intercostal muscle function, which compromises posture and respiration. Lumbar and sacral injuries (L1-S5) primarily involve lower limb weakness or paralysis, with additional impacts on foot muscles and intrinsic functions like bowel and bladder control due to involvement of cauda equina segments. In certain incomplete injury syndromes, such as Brown-Séquard syndrome, deficits are asymmetric, with ipsilateral motor loss and proprioceptive impairment contralateral to pain and temperature deficits.

Autonomic and visceral symptoms

Spinal cord injury (SCI) disrupts the autonomic nervous system, leading to a range of involuntary symptoms that affect cardiovascular regulation, visceral organ function, and respiration. These disruptions arise from the interruption of descending pathways from the brainstem and hypothalamus, resulting in loss of supraspinal control over sympathetic and parasympathetic outflows. Autonomic dysreflexia is a potentially life-threatening syndrome characterized by sudden, severe hypertension, pounding headache, flushing, and sweating above the injury level, triggered by noxious stimuli below the lesion such as bladder distension or bowel impaction. It commonly occurs in individuals with injuries at or above the T6 spinal level, where intact spinal sympathetic reflexes below the injury cause an exaggerated response due to the absence of inhibitory descending modulation. In the acute phase, neurogenic shock manifests as profound hypotension and bradycardia due to the sudden loss of sympathetic vasomotor tone, particularly in cervical and upper thoracic injuries that impair sympathetic outflow from the thoracolumbar region. This condition contrasts with hypovolemic shock by featuring stable or low heart rates, as unopposed vagal parasympathetic activity predominates. Visceral symptoms include neurogenic bladder dysfunction, where detrusor muscle control is lost, resulting in either an atonic (flaccid) bladder with urinary retention or a spastic (hyperreflexic) bladder with involuntary contractions and incontinence, depending on the injury level and completeness. Neurogenic bowel dysfunction similarly impairs colonic motility and sphincter control, leading to chronic constipation, fecal incontinence, or a combination of both, often exacerbated by reduced physical activity and dietary factors. Sexual dysfunction encompasses erectile impotence in males, reduced lubrication and arousal in females, and orgasmic difficulties, stemming from disrupted reflex arcs and psychogenic pathways in the sacral cord. Respiratory involvement varies by injury level; high cervical lesions (above C3) paralyze the diaphragm, necessitating mechanical ventilation, while low cervical injuries (C5-C8) typically spare diaphragmatic function but impair intercostal and abdominal muscles, reducing cough effectiveness and vital capacity. These autonomic and visceral symptoms often coexist with sensory and motor deficits, compounding the overall impact of SCI.

Causes

Traumatic causes

Traumatic causes account for the majority (approximately 60%) of spinal cord injury cases worldwide, primarily resulting from external physical forces that disrupt the spinal column and cord. The leading etiologies globally include falls (particularly among older adults) and motor vehicle crashes, followed by acts of violence and sports or recreational activities, with variations by region (e.g., higher proportions of road traffic crashes and violence in low- and middle-income countries). Common injury mechanisms encompass hyperflexion and hyperextension, as seen in whiplash from motor vehicle accidents, where rapid forward and backward motion strains the cervical spine. Axial loading occurs predominantly in falls, compressing the vertebral column vertically and potentially fracturing bones that impinge on the cord. Penetrating trauma from assaults involves direct disruption by projectiles or blades, severing neural pathways. Key risk factors include high-speed travel without proper restraints, which amplifies forces in crashes, and alcohol impairment, which increases the likelihood of accidents across etiologies. Osteoporosis heightens vulnerability in falls, especially among older adults, by weakening bone resistance to impact. These injuries disproportionately affect young males aged 16-30, who face higher exposure to high-risk activities like driving and contact sports.

Non-traumatic causes

Non-traumatic spinal cord injuries (NTSCI) arise from medical conditions or diseases rather than external physical forces, accounting for approximately 20-50% of all spinal cord injuries in various global populations, with higher proportions in older adults. Unlike traumatic causes, which predominate in younger males from acute events, NTSCI typically presents as incomplete lesions that may progress gradually, often leading to paraplegia and affecting females and individuals over 50 years more frequently. These injuries result from compression, ischemia, inflammation, or direct tissue damage within the spinal cord or surrounding structures. Vascular causes represent a leading etiology of NTSCI, comprising 11-38% of cases depending on the cohort, primarily through ischemia or hemorrhage that disrupts spinal cord blood supply. Spinal cord infarction, often from anterior spinal artery occlusion due to atherosclerosis, embolism, or hypotension, leads to acute onset symptoms like flaccid paralysis below the lesion level; for instance, affects the anterior two-thirds of the cord, sparing dorsal columns. Hemorrhagic events, such as spinal subdural or epidural hematomas, can occur spontaneously or in anticoagulated patients, compressing the cord and causing rapid neurological decline. Infectious causes account for 5-15% of NTSCI, involving direct microbial invasion or inflammatory responses that damage cord tissue. Spinal epidural abscesses, often bacterial (e.g., from ), arise in immunocompromised individuals and present with back pain, fever, and progressive myelopathy if untreated, with an incidence of 0.1-1.2 per 10,000 hospitalizations. Viral infections contribute via transverse myelitis, such as -associated vacuolar myelopathy (affecting 1-5% of advanced cases) or HTLV-1-induced HAM/TSP (2-5% of carriers), leading to demyelination and spastic paraparesis. Less common are remnants of eradicated diseases like , which historically caused asymmetric flaccid paralysis but now occur in fewer than 1,000 global cases annually. Degenerative and neoplastic causes frequently result from chronic structural changes or growths that compress the spinal cord, representing 19-33% of NTSCI cases combined. Degenerative conditions, such as —the most common spinal cord disorder in those over 55—involve osteophytes, ligament hypertrophy, and disc herniation narrowing the canal, with MRI showing cord compression in 86% of symptomatic patients and a 2% overall prevalence. Spinal stenosis exacerbates this in older adults, causing gait instability and hand clumsiness through intermittent ischemia. Neoplastic etiologies include intramedullary tumors like ependymomas (56% benign) or extramedullary metastases (from lung, breast, or prostate cancers in 10% of advanced cases), leading to insidious weakness and sensory loss as the tumor expands. Other causes, including iatrogenic, congenital, and inflammatory processes, encompass the remaining NTSCI spectrum and often manifest progressively in specific populations. Iatrogenic injuries occur post-surgery or radiation, with radiation myelopathy showing early (within 6 months) or delayed (up to 10 years) onset due to vascular endothelial damage. Congenital anomalies like spina bifida (incidence 1 in 2,758 live births) can lead to later myelopathy from tethered cord or syringomyelia complications. Inflammatory conditions, such as multiple sclerosis flares or acute transverse myelitis (incidence 1.3-4.6 per million yearly), cause demyelinating plaques and edema, resulting in 22% of NTSCI cases with relapsing-remitting patterns. Metabolic factors, like vitamin B12 deficiency-induced subacute combined degeneration, add to this category through axonal loss and treatable myelopathy.

Diagnosis

Clinical evaluation

Clinical evaluation of spinal cord injury begins with a detailed history to identify the mechanism of injury and immediate symptoms, such as sudden loss of sensation or movement below the level of injury. The history focuses on the circumstances of the trauma, including high-impact events like motor vehicle accidents or falls, and any preceding symptoms that may indicate the onset of neurological deficits. Red flags prompting urgent evaluation include severe back pain, progressive weakness in the extremities, and changes in bowel or bladder function, which signal potential spinal cord compression or injury. The physical examination determines the neurological level of injury through systematic testing of sensory and motor functions. Sensory assessment involves light touch and pinprick testing across dermatomes to identify the most caudal segment with normal sensation bilaterally. Motor evaluation uses manual muscle testing of key myotomes, prioritizing the supine position for standardization and spinal protection; left and right sides are tested separately, with each muscle scored independently on a 0-5 scale to establish the lowest level with at least grade 3 strength (antigravity). If joint range of motion is less than 50% of normal, the muscle is scored as "NT" (not testable). Confirmation of no compensatory movements—such as spasticity, tendinous action, or gravity assistance—is obtained via palpation or observation, while avoiding elicitation of pain or fatigue and exercising caution with positioning, especially in the acute phase. A digital rectal examination is performed to assess sacral sparing, checking for voluntary anal contraction, deep anal pressure sensation, and perianal sensation, which are critical for distinguishing complete from incomplete injuries. The American Spinal Injury Association (ASIA) protocol integrates these elements into a standardized framework, including sensory and motor scoring to classify the injury's completeness using the ASIA Impairment Scale. The standards were revised in 2019, with a further update in 2025 (E-ISNCSCI Version 2) introducing a streamlined exam while preserving key assessments. This scale grades injuries from A (complete, no sacral sparing) to E (normal), guiding prognosis and further care based on preserved function. The neurological level is defined as the most caudal segment with intact sensory and motor function, provided that there is normal sensory and motor function rostrally.

Imaging and electrophysiological tests

Imaging plays a crucial role in diagnosing (SCI) by visualizing structural damage to the vertebrae, ligaments, and the spinal cord itself. Initial imaging typically begins with plain X-rays to detect fractures, dislocations, or alignment abnormalities in the spinal column, providing a rapid and accessible assessment following trauma. However, X-rays have limitations in visualizing soft tissue or subtle cord injuries. Computed tomography (CT) scans offer superior detail for bony structures and are recommended as the initial imaging modality for evaluating spinal trauma in both adults and children, serving as the reference standard for identifying fractures and assessing spinal stability. CT is particularly valuable in the acute setting due to its speed and ability to detect associated injuries like epidural hematomas. Magnetic resonance imaging (MRI) is considered the gold standard for direct visualization of the spinal cord, revealing intramedullary abnormalities such as edema, hemorrhage, compression, or transection, as well as ligamentous injuries that may not be apparent on X-ray or CT. Electrophysiological tests complement imaging by providing functional assessments of neural pathways. Somatosensory evoked potentials (SSEPs) evaluate the integrity of sensory conduction from peripheral nerves through the spinal cord to the brain, detecting disruptions in dorsal column pathways that may indicate the level and severity of injury. Electromyography (EMG) records electrical activity in skeletal muscles to identify nerve root involvement, denervation, or ongoing reinnervation processes, offering insights into lower motor neuron function. In cases of spinal cord injury without radiographic abnormality (SCIWORA), where X-rays and CT appear normal despite clinical evidence of neurological deficits, MRI is essential to confirm cord pathology, such as contusions or edema, and guide further management. Urgent imaging, ideally within the first few hours post-injury, is critical to delineate the extent of damage and inform acute interventions. Advanced techniques like diffusion tensor imaging (DTI), an MRI-based method, are increasingly used in research to quantify white matter tract integrity by measuring water diffusion anisotropy, providing prognostic insights into axonal damage beyond conventional imaging. These tests, performed after initial clinical evaluation, offer objective data to confirm and characterize SCI.

Prevention

Primary prevention strategies

Primary prevention strategies for spinal cord injury focus on reducing the incidence of trauma through targeted interventions in high-risk scenarios, such as motor vehicle crashes, falls, sports activities, and occupational hazards. These measures emphasize engineering controls, regulatory enforcement, and public education to eliminate or minimize exposure to risks before injuries occur. In traffic safety, seatbelts and airbags have demonstrated substantial effectiveness in mitigating spinal cord injuries from motor vehicle crashes, which account for a significant portion of traumatic cases. Seatbelt use reduces the risk of major injuries by 53% and spinal injuries by 44% among vehicle occupants in crashes. Airbags, when combined with seatbelts, further enhance protection by dissipating crash forces over a larger area, lowering the likelihood of cervical spine damage. Anti-drunk driving laws, including blood alcohol concentration limits and sobriety checkpoints, have proven effective in decreasing alcohol-involved crashes, which contribute to severe spinal trauma due to impaired reaction times and vehicle control. Similarly, strict enforcement of speed limits helps prevent high-impact collisions that exacerbate spinal cord damage, as higher speeds correlate with increased collision severity and injury risk. Fall prevention efforts are particularly vital for older adults, where falls represent a leading cause of spinal cord injuries due to age-related bone fragility and balance issues. Home modifications, such as installing grab bars, improving lighting, and removing tripping hazards like loose rugs, can significantly lower fall risks by addressing environmental factors. Hip protectors, worn under clothing, absorb impact during falls to reduce the risk of hip fractures, a common injury in older adults that underscores the need for comprehensive fall prevention to mitigate overall trauma including potential spinal risks. Educational programs on safe ladder use and balance training further empower individuals to avoid falls during routine activities. Sports regulations play a key role in curbing spinal cord injuries from high-impact or improper techniques. Mandating helmets in contact sports like football and hockey helps protect against head trauma, with primary benefits in reducing brain injuries; evidence for direct prevention of spinal cord injuries is limited, emphasizing the importance of rule changes like tackling techniques. In aquatic settings, "no diving" signs and depth markings at pools prevent shallow-water impacts, a common mechanism for cervical spinal cord injuries during dives. Violence prevention strategies, including community-based programs, firearm safety education, and conflict resolution initiatives, aim to reduce intentional injuries that contribute to spinal cord trauma. These efforts, supported by public health campaigns, have shown promise in lowering rates of violence-related injuries in high-risk populations. Workplace safety standards, enforced by organizations like the (OSHA), target construction and other high-fall-risk industries. OSHA requires fall protection systems—such as guardrails, safety nets, and personal fall arrest equipment—at heights of six feet or more, which has contributed to declining fall-related injury rates, including those involving spinal cord damage. Training on proper equipment use and hazard recognition ensures compliance and proactive risk reduction in these environments.

Secondary prevention measures

Secondary prevention measures for spinal cord injury (SCI) focus on early interventions in at-risk individuals or those with suspected instability to halt progression and avoid further cord damage, distinguishing from primary strategies that emphasize pre-exposure avoidance such as safety equipment use. These measures target high-risk groups exposed to potential injury mechanisms, like trauma survivors or those with degenerative conditions, by stabilizing the spine, screening for underlying pathologies, and promoting modifiable risk factors. In cases of suspected spinal trauma, spinal motion restriction (SMR) is employed prehospital to minimize excessive spine movement that could exacerbate neurologic deficits. SMR typically involves a cervical collar and supportive cot to maintain neutral alignment, replacing rigid backboards due to evidence of complications like pressure ulcers and respiratory compromise from the latter. Guidelines from the American College of Surgeons Committee on Trauma, American College of Emergency Physicians, and National Association of EMS Physicians recommend SMR for blunt trauma patients meeting specific criteria, such as altered mental status or midline tenderness, while contraindicating it in penetrating trauma where it may increase mortality. This approach has been shown not to elevate SCI rates in transitioned protocols. Early screening is crucial for detecting conditions like osteoporosis or tumors that predispose to vertebral fragility and cord compression in high-risk populations. For osteoporosis, dual-energy X-ray absorptiometry (DXA) screening is recommended for women aged 65 and older, or postmenopausal women under 65 with risk factors such as low body weight, smoking, or family history of hip fracture, to identify bone mineral density loss that heightens fracture risk leading to SCI. In individuals with known malignancies, such as breast or prostate cancer, whole-spine MRI within 24 hours of symptoms suggestive of metastatic spinal cord compression (MSCC) is advised to enable timely intervention and prevent irreversible damage. The National Institute for Health and Care Excellence (NICE) guidelines emphasize urgent imaging and multidisciplinary referral for at-risk cancer patients reporting back pain or neurologic changes to avert progression. Smokers, who face elevated vascular compromise risks, should undergo targeted screening as part of risk assessment. Lifestyle modifications play a key role in mitigating vascular and structural risks for SCI. Smoking cessation improves spinal tissue perfusion by reducing atherosclerosis and inflammation, thereby lowering the incidence of degenerative disc disease and associated cord vulnerability, with benefits accruing over time post-quitting. Regular exercise targeting core and back muscles strengthens spinal stability and reduces injury susceptibility; recommended routines include the bridge exercise, where one lies supine and lifts hips to form a straight line from knees to shoulders, holding for three breaths and progressing to 30 repetitions, and the cat stretch, involving alternating arching and sagging of the back on all fours for 3-5 cycles twice daily. These activities enhance flexibility and support without excessive strain, as endorsed by clinical guidelines for back health maintenance. Public health initiatives promote awareness to facilitate early symptom recognition in degenerative spinal conditions, such as cervical myelopathy, where delays in diagnosis—often 2-3 years—lead to worsened outcomes. Campaigns educate on subtle signs like gait instability or hand clumsiness, urging prompt medical evaluation to prevent cord compression; for instance, the AO Spine RECODE-DCM project highlights how increased professional and public knowledge can expedite interventions, improving recovery rates and reducing disability. Such efforts, including annual Spine Health Awareness Month activities, target communities to bridge diagnostic gaps in underrecognized pathologies.

Management

Prehospital and acute care

Prehospital management of suspected prioritizes the assessment and stabilization of airway, breathing, and circulation (ABCs) to ensure vital organ perfusion while minimizing further neurological damage. Emergency medical services personnel apply spinal motion restriction using a rigid cervical collar and manual in-line stabilization during airway interventions, followed by log-roll techniques to secure the patient on a long backboard, vacuum mattress, or scoop stretcher for transport. This immobilization aims to prevent exacerbation of secondary injury mechanisms such as ischemia and cord compression. Rapid transport to a designated trauma center is essential, as outcomes improve with specialized care within the first hour, often termed the "golden hour." In the emergency department, initial acute care focuses on hemodynamic stabilization to counteract hypotension, which is common due to neurogenic shock and can worsen spinal cord perfusion. Intravenous fluid resuscitation with crystalloids is administered to maintain euvolemia, while vasopressors such as norepinephrine may be initiated if systolic blood pressure remains below 90 mmHg despite fluids. Oxygenation is optimized to achieve SpO2 greater than 92%, avoiding hypoxia that could compound ischemic secondary injury. The use of high-dose methylprednisolone remains highly debated; the National Acute Spinal Cord Injury Studies (NASCIS II and III) reported modest neurological benefits when administered within 8 hours of injury, but subsequent analyses highlight significant risks including infection, gastrointestinal bleeding, and mortality without clear long-term gains, leading many guidelines to recommend against routine use. Blood pressure management is critical in the acute phase to optimize spinal cord perfusion pressure and mitigate secondary injury from hypotension. Current guidelines recommend augmenting mean arterial pressure (MAP) to at least 75-80 mmHg, but not exceeding 90-95 mmHg, for the first 3-7 days post-injury using fluids and vasopressors as needed. This target balances perfusion enhancement with risks of over-augmentation, such as cardiac strain. Close monitoring in an intensive care setting includes continuous invasive arterial pressure, pulse oximetry, and end-tidal CO2 to prevent hypoxia (PaO2 <60 mmHg) and hypercapnia (PaCO2 >50 mmHg), which can lead to and further cord ischemia. Intubation and are indicated for respiratory compromise, particularly in cervical injuries above C5, where falls below 15 mL/kg or negative inspiratory force exceeds -20 cm H2O, to secure the airway and support ventilation proactively.

Surgical interventions

Surgical interventions for spinal cord injury (SCI) are primarily indicated in cases of , instability, or progressive neurological deficits, where operative management can alleviate pressure and prevent further deterioration. These indications arise in both traumatic and non-traumatic SCI, with surgery recommended when imaging confirms mechanical compromise contributing to ongoing injury. Recent meta-analyses from 2025 emphasize that performing within 24 hours of injury significantly enhances neurological recovery compared to later intervention, particularly by minimizing secondary ischemic damage. Key procedures include decompression through , which involves removing portions of the vertebral lamina to relieve pressure on the , often combined with and instrumentation such as rods and screws to stabilize the spine and restore alignment. In instances of tumor-related compression, surgical resection of the is performed to directly address the while preserving neural tissue. These approaches follow acute stabilization and are tailored to the injury level and mechanism, with minimally invasive techniques increasingly used to reduce tissue disruption. Debate persists on the optimal timing of , pitting early intervention (within 24 hours) against delayed approaches, with evidence favoring early decompression for better motor score improvements and reduced complications in incomplete injuries. Ultra-early (less than 8 hours) shows promise for incomplete SCI by limiting secondary injury cascades, though logistical challenges and patient stability concerns fuel ongoing controversy. Outcomes of surgical interventions focus on mitigating secondary damage through prompt decompression, which preserves viable neural tissue and improves long-term potential in select cases, yet functional recovery is not universally achieved due to the extent of primary . Complications occur in a minority of patients, with surgical site infections reported in 2-6% of spinal surgeries for SCI, often managed through antibiotics and . Overall, early correlates with shorter hospital stays and lower rates of pulmonary and thromboembolic events, underscoring its role in optimizing prognosis.

Pharmacological and supportive treatments

Pharmacological treatments for acute spinal cord injury (SCI) primarily target to mitigate secondary injury mechanisms, such as and , though no agents have been definitively proven to improve long-term neurological outcomes. High-dose , a , has been controversial due to its potential risks, including gastrointestinal hemorrhage and , outweighing marginal benefits in most cases; current guidelines as of 2025 recommend against its routine use, limiting administration to select scenarios like presentation within 8 hours of injury and after informed discussion of risks. , a sodium-glutamate antagonist that blocks excitotoxic damage by inhibiting glutamate release, shows promise based on Phase III trials; the RISCIS trial demonstrated improved neurological recovery in acute cervical SCI patients treated with riluzole (50 mg twice daily for 14 days) compared to , with meta-analyses confirming and enhanced motor scores at 6 months.00307-X/fulltext) Anticoagulation therapy is essential for preventing venous thromboembolism, a common complication in immobilized SCI patients. Low-molecular-weight heparin (LMWH), such as enoxaparin (30-40 mg subcutaneously daily), is the preferred agent for deep vein thrombosis (DVT) prophylaxis, initiated 24-72 hours post-injury once hemorrhagic risk is deemed low, as supported by clinical practice guidelines that report reduced pulmonary embolism incidence with LMWH over other methods. Prophylaxis typically continues for at least 8-12 weeks or until mobility improves, with mechanical compression devices as adjuncts in high-bleeding-risk cases. Pain management in the acute phase addresses both nociceptive and neuropathic components, with initial reliance on opioids for severe injury-related pain, transitioning to non-opioid agents to minimize dependency risks. , such as (starting at 300 mg daily, titrated to 3600 mg) or , are first-line for , reducing symptoms by 30-50% in SCI patients through modulation; early administration (within 24 hours) may also enhance motor recovery by limiting secondary neuronal damage. For neurogenic bladder overactivity, antispasmodics like (5 mg orally 2-3 times daily) improve bladder compliance and reduce detrusor leak point pressure, preventing upper urinary tract complications in up to 70% of cases. Supportive treatments focus on maintaining physiological stability and preventing secondary complications during the acute phase. Nutritional support emphasizes high-protein enteral feeding (1.25-1.5 g/kg/day) to promote and counteract , with guidelines recommending early initiation to reduce risk by 25% in at-risk patients. prevention involves standardized turning schedules (every 2 hours) and specialized mattresses, as immobility in SCI doubles the incidence of ulcers within the first week; multidisciplinary protocols integrating assessments and moisture management are critical for early intervention.

Rehabilitation and long-term care

Rehabilitation following spinal cord injury (SCI) involves a multidisciplinary approach designed to optimize functional recovery, prevent secondary complications, and enhance overall through structured phases of care. The process is typically divided into acute, subacute, and chronic phases, each building on the previous to support progressive . In the acute phase, bedside therapy begins immediately after stabilization to maintain joint mobility, prevent , and address early respiratory or circulatory needs, often within the intensive care or acute hospital setting. This phase emphasizes passive range-of-motion exercises and basic positioning to mitigate risks like pressure ulcers and contractures. The subacute phase shifts to inpatient rehabilitation facilities, where intensive, coordinated interventions occur over an average of 55 days, though this can vary based on injury severity and individual progress. Key components include for strengthening and mobility training, to develop skills for (ADLs) such as dressing and self-care, and speech-language therapy if cervical injuries affect or communication. Assistive devices, including wheelchairs, orthotic braces, and adaptive utensils, are introduced and customized to promote safe movement and task performance. Psychological support from counselors and psychologists is integrated to address adjustment challenges, depression, and coping strategies. Goals across these early phases focus on preventing further , improving ADLs, and fostering emotional resilience, with multidisciplinary teams—including physicians, nurses, therapists, and social workers—collaborating to tailor programs to the patient's level of injury and needs. For instance, body-weight-supported treadmill training may be used in subacute care to enhance lower extremity function in incomplete injuries. Long-term care transitions into the chronic phase, emphasizing community reintegration and sustained independence beyond the initial 12-18 months post-injury. This includes home modifications such as ramps, widened doorways, and accessible bathrooms to facilitate daily living, often supported by occupational therapists and funding programs. services help individuals identify employment options, acquire new skills, or return to work through job training and accommodations like ergonomic setups. groups provide ongoing emotional and practical guidance, connecting individuals with SCI to others facing similar experiences for shared coping strategies and advocacy. Regular follow-up care addresses evolving needs, such as managing or , to maintain health and prevent rehospitalization.

Complications

Acute complications

Acute complications of spinal cord injury (SCI) encompass a range of life-threatening conditions that emerge within the first days to weeks post-injury, primarily due to disrupted neural control over vital systems. These issues contribute significantly to early morbidity and mortality, with , hemodynamic instability, and thromboembolic events being particularly prevalent in injuries at or above the cervical or high thoracic levels. Autonomic dysfunction often serves as a precursor, manifesting as abnormal temperature regulation or instability that exacerbates these risks. Respiratory complications are among the most critical in acute SCI, especially for cervical injuries, where damage to the (originating from C3-C5) impairs diaphragmatic function. develops in approximately 50% of acute SCI patients, driven by reduced effectiveness, , and aspiration risk, making it a leading cause of early death. dependence is common in high cervical injuries (C1-C4), affecting 21-77% of cases depending on injury severity, with carrying a 20-30% . Overall, respiratory issues account for up to 30% of acute mortality in severe cervical SCI. Cardiovascular instability arises from loss of sympathetic outflow in injuries above T6, leading to and unopposed parasympathetic activity. , characterized by (systolic <90 mmHg) and bradycardia, occurs in about 19% of cervical and high thoracic SCI cases and can persist for weeks if untreated. Arrhythmias, including sinus bradycardia (64-77% incidence) and ventricular ectopic beats (18-27%), further complicate the acute phase, increasing the risk of cardiac arrest. These events underscore the need for vigilant monitoring in the initial post-injury period. Thromboembolic events pose a substantial risk due to immobility, venous stasis, and hypercoagulability following SCI. Deep vein thrombosis (DVT) develops in 47-100% of cases without prophylaxis, with a meta-analysis estimating an overall incidence of 62% in the acute phase. Pulmonary embolism (PE), a potentially fatal sequela, occurs in about 5% of patients within the first year, often within the initial months. These complications highlight the heightened vulnerability in the early recovery window. Gastrointestinal disruptions stem from autonomic imbalance and spinal shock, affecting motility and mucosal integrity. Paralytic ileus, marked by delayed gastric emptying and abdominal distension, is common in the first 4 weeks, occurring in up to 4.7% of patients and potentially leading to complications like perforation if prolonged. Stress ulcers (Cushing's ulcers) form in the gastroduodenal region due to elevated gastrin and splanchnic ischemia, with acute bleeding reported in 4-20% of cases, particularly in injuries above T5. These issues can delay nutrition and increase infection risk.

Chronic complications

Chronic complications of spinal cord injury (SCI) encompass a range of persistent health issues that emerge or endure months to years post-injury, often stemming from immobility, neurogenic changes, and altered physiology, significantly impacting quality of life and requiring ongoing management. These conditions arise due to the disruption of neural control over motor, sensory, and autonomic functions, leading to secondary adaptations that can exacerbate disability if not addressed. Unlike acute complications, which are immediate and often resolve with intervention, chronic issues evolve over time and are frequently preventable through vigilant care. In the musculoskeletal system, osteoporosis is a prominent concern, characterized by rapid bone density loss below the level of injury due to mechanical unloading of paralyzed limbs and hormonal imbalances, resulting in a 5- to 23-fold increased risk of fragility fractures, particularly in the distal femur and proximal tibia. This bone loss begins within weeks of injury and can progress for years, with significant demineralization occurring in the first 12-18 months. Contractures, involving shortening and stiffening of muscles, tendons, and joints, commonly develop from prolonged immobility, spasticity, and lack of passive range-of-motion exercises, leading to reduced mobility, pain, and functional limitations. Pressure ulcers, also known as pressure injuries, affect 10-38% of individuals annually, primarily over bony prominences like the sacrum, ischium, and trochanters due to impaired sensation, moisture, and shear forces from wheelchair use; these can progress to deep tissue damage and systemic infections if untreated. Urological complications are prevalent owing to neurogenic bladder dysfunction, which impairs voluntary control and increases risks of stasis and reflux. Urinary tract infections (UTIs) occur at a mean frequency of 3.6 episodes per year in chronic SCI patients, driven by catheterization practices and bacterial colonization, contributing to frequent hospitalizations and antimicrobial resistance. Chronic kidney disease (CKD) develops in 8-22% of cases, often due to high detrusor pressures exceeding 40 cm H₂O, vesicoureteral reflux, and recurrent infections that cause hydronephrosis and progressive kidney damage; end-stage renal disease affects approximately 4%. Psychological sequelae are common, with clinical depression affecting approximately 30% of individuals one year post-injury, linked to loss of independence, chronic pain, and social isolation, and persisting without significant improvement over time. Anxiety disorders manifest in up to 45% of patients, characterized by excessive worry, panic, or fear related to health uncertainties and lifestyle changes, further compounding emotional distress. Among other chronic issues, spasticity impacts 65-70% of individuals, presenting as velocity-dependent muscle hyperactivity, involuntary spasms, and stiffness that can facilitate or hinder function depending on severity. Autonomic dysreflexia, occurring in up to 90% of patients with injuries at or above T6, presents as episodic hypertension triggered by stimuli below the injury level, requiring prompt recognition and management to prevent stroke or death. Chronic pain, reported by up to 80% of those with , includes neuropathic types from nerve damage and musculoskeletal variants from overuse or immobility, often resistant to standard analgesics and requiring multimodal approaches. Secondary conditions like obesity arise from reduced energy expenditure, altered metabolism, and dietary challenges in the context of immobility, promoting neurogenic obesity that heightens risks for cardiovascular disease and further joint strain.

Prognosis

Factors influencing recovery

The recovery from spinal cord injury (SCI) is influenced by several key factors, including the characteristics of the injury itself, the timing of interventions, patient comorbidities, and emerging biomarkers. These determinants play a critical role in predicting neurological and functional improvements, as assessed by scales such as the American Spinal Injury Association (ASIA) Impairment Scale, which measures changes in sensory and motor function. Injury characteristics significantly affect prognosis. The level of injury impacts recovery potential, with thoracic injuries generally showing the poorest outcomes due to limited collateral vascular supply and smaller cross-sectional area of the cord, leading to less motor recovery compared to cervical or lumbar levels; cervical injuries, while causing more widespread disability due to involvement of upper limbs and respiratory function, often demonstrate better neurological recovery rates than thoracic in complete cases (37.2% marked recovery versus 15.9%). Completeness of the injury is a primary predictor, where incomplete injuries (ASIA grades B-D) yield substantially better results than complete ones (ASIA grade A), with 20-75% of individuals with incomplete SCI regaining some walking capacity within one year. Age at injury also modulates recovery, with younger patients exhibiting greater neurological improvements, such as higher ASIA motor score gains, compared to older individuals, where advanced age is linked to reduced functional outcomes across injury severities. The timing of surgical intervention is another crucial factor. Decompression surgery performed within 24 hours of injury is associated with improved neurological outcomes, including a 70% increased odds of achieving at least one ASIA grade improvement and reduced rates of persistent severe impairment (odds ratio 1.70 for >1 grade improvement). Pre-existing comorbidities and adherence to rehabilitation further shape recovery trajectories. Conditions such as , depression (prevalence 22-28% in SCI patients), or can hinder therapy engagement, leading to lower participation rates and diminished functional gains during inpatient rehabilitation. Similarly, poor adherence to rehabilitation protocols, often exacerbated by these comorbidities, correlates with extended hospital stays and reduced self-management abilities, underscoring the need for integrated psychological support to enhance outcomes. Biomarkers from advanced imaging, particularly diffusion tensor imaging (DTI) with , provide predictive insights into motor recovery. Higher (FA) values at the injury site in the acute phase correlate with better ASIA grades and motor scores, while elevated radial diffusivity indicates poorer prognosis; these metrics allow for early identification of recovery potential by assessing integrity.

Long-term functional outcomes

Long-term functional outcomes following spinal cord injury (SCI) vary significantly based on the injury's completeness and level, with incomplete injuries generally showing better recovery potential than complete ones. Approximately 75% of individuals with American Spinal Injury Association Impairment Scale (AIS) grade C incomplete injuries regain the ability to walk, often with assistive devices, while nearly 100% of those with AIS grade D achieve some form of ambulation within post-injury. In contrast, patients with complete injuries (AIS grade A) rarely regain independent ambulation, with recovery limited to isolated cases involving extensive rehabilitation or adjunct therapies, and most remain non-ambulatory long-term. Overall, about 50% of motor incomplete SCI cases achieve independent walking within , highlighting the prognostic importance of initial neurological status. Survival rates after SCI have improved with modern care, yet life expectancy remains reduced compared to the general population. Among first-year survivors, the 10-year survival rate is approximately 87%, with 20-year rates around 78%. However, individuals with tetraplegia experience a substantial reduction in life expectancy, averaging about 20 years less than age-matched peers without SCI; for example, a 40-year-old with high tetraplegia (C1-C4, AIS A-C) can expect an additional 18.2 years of life, versus 38.8 years for the general population. These outcomes are influenced by factors such as injury level and secondary complications, with tetraplegic patients facing higher mortality risks due to respiratory and cardiovascular issues. Functional independence is achievable for many SCI survivors, though often requiring assistive technologies. Around 70% of individuals live independently or semi-independently in community settings, utilizing mobility aids, adaptive equipment, or home modifications to manage daily activities. Employment rates, however, decline markedly post-injury, dropping to approximately 30-35% within the first decade, with lower rates among those with or complete injuries compared to or incomplete cases. This reduction stems from barriers like physical limitations, workplace , and societal factors, though vocational rehabilitation can mitigate some impacts. As of 2025, advancements in therapies offer promising enhancements to voluntary movement recovery. Epidural or non-invasive , combined with rehabilitation, has enabled volitional leg movements in about 40-50% of chronic complete SCI patients in recent clinical trials, with 5 out of 10 participants demonstrating anti-gravity movements in one study. These interventions activate residual neural circuits, facilitating gains in that were previously unattainable, though long-term efficacy and scalability remain under investigation.

Epidemiology

Incidence and prevalence

Globally, between 250,000 and 500,000 people sustain a spinal cord injury (SCI) each year, with most cases resulting from traumatic events such as falls and road traffic crashes. In 2021, the worldwide incidence reached approximately 0.57 million cases, corresponding to an age-standardized incidence rate (ASIR) of 7.12 per 100,000 population. In the United States, around 18,000 new traumatic SCI cases occur annually, equating to an incidence rate of about 54 cases per million . The global prevalence of SCI is estimated at 15 to 20 million people living with the condition, with 20.6 million individuals affected in 2019 according to Global Burden of Disease (GBD) 2019 data, though GBD 2021 estimates approximately 15.4 million (95% UI: 14.0–17.1 million) as of 2021. That year (2019), SCI also accounted for 6.2 million years lived with (YLDs) worldwide, with GBD 2021 trends indicating stability around 4.5–6 million YLDs in 2021. Projections indicate a rising burden of SCI through 2050, driven by population aging and persistent trauma risks, with global prevalence expected to increase significantly in low- and middle-income countries. In high-income countries, however, incidence trends have shown stabilization or decline over recent decades, attributable to effective measures such as enhanced road safety and fall mitigation programs.

Demographic and regional patterns

Spinal cord injuries (SCI) exhibit distinct demographic patterns, with males accounting for approximately 80% of traumatic cases globally, a disparity largely attributed to higher engagement in high-risk activities such as collisions and occupational hazards. The peak incidence of traumatic SCI occurs in the 20-40 age group, where crashes and predominate, while falls become the leading cause in individuals over 60 years, often resulting from low-height incidents in the elderly population. Non-traumatic SCI, stemming from degenerative diseases, tumors, or infections, is more prevalent among older adults, reflecting the rising burden in aging populations worldwide. Regional variations in SCI incidence highlight stark disparities between high-income and low- to middle-income countries (LMICs), where rates are elevated due to differences in , safety measures, and socioeconomic conditions. , the annual incidence stands at approximately 54 cases per million , primarily from vehicular and recreational traumas. In contrast, LMICs report higher rates, with sub-Saharan African countries showing incidences from 13 to 76 cases per million (e.g., up to 75.6 in ), driven by falls from heights in informal labor and interpersonal . These patterns underscore how environmental and preventive factors influence SCI across geographies. Socioeconomic factors further exacerbate SCI risks and access to care, with higher incidences observed in urban areas plagued by and inadequate safety nets, often affecting low-income communities. Ethnic and racial minorities, including and populations, face disparities in timely access to rehabilitation and surgical interventions, contributing to poorer health outcomes post-injury. Recent analyses from the indicate that in 2021, road injuries alone caused 95,734 incident SCI cases worldwide, with disproportionate impacts in LMICs due to rapid and vulnerabilities.

History

Early historical perspectives

The earliest documented recognition of spinal cord injury (SCI) appears in the , an ancient Egyptian surgical treatise dating to approximately 1600 BCE. This text describes several cases of spinal trauma, including fractures of the cervical and , and explicitly notes that certain injuries involving the —such as those in cases 31 and 33—were untreatable and irreversible, leading to and loss of sensation below the injury site. The papyrus classifies these as "a disease not to be treated," emphasizing the fatal due to complications like inability to control bodily functions. In , (c. 460–377 BCE), often regarded as the father of medicine, provided the first systematic descriptions of following spinal trauma. He detailed how vertebral fractures or dislocations could compress or sever the , resulting in immediate (termed "") and, in complete cases, permanent loss of motor and sensory function below the lesion. observed that such injuries were often hopeless, particularly if accompanied by , and advocated rudimentary interventions like extension and counter-extension using devices such as the Hippocratic board to realign vertebrae, though these were primarily aimed at preventing further damage rather than restoring function. During the medieval period (roughly 500–1500 CE), understanding and treatment of SCI remained limited, with injuries frequently proving fatal due to secondary complications like infections and pressure ulcers. Medical texts, such as those by Paulus of Aegina (625–690 CE), echoed Hippocratic methods but offered little innovation, focusing on conservative management like rest and bandaging. Societally, disabilities from SCI were often interpreted through religious lenses as divine punishment for sin or a test of , influencing care toward palliative or spiritual remedies rather than aggressive intervention; for instance, of (c. 1267 CE) differentiated treatable spinal injuries from those involving the cord, which he deemed incurable and best managed extracorporeally to avoid worsening outcomes. The marked a shift toward experimental , with key insights into function. In 1811, the Bell-Magendie law, independently formulated by and François Magendie, established that anterior spinal roots primarily transmit motor impulses while posterior roots convey sensory information, providing a foundational understanding of neural pathways disrupted in SCI. Building on this, Charles-Édouard Brown-Séquard conducted pivotal experiments in the 1850s, performing hemisections on animal spinal cords to demonstrate ipsilateral motor loss and contralateral sensory deficits, thus elucidating the of tracts and the asymmetrical effects of partial cord injuries. Early treatments emphasized immobilization through splinting or to stabilize fractures, yet mortality remained high—often exceeding 50%—due to unchecked infections from urinary complications and decubitus ulcers, as antisepsis was not yet widespread.

Modern developments and milestones

In the early , the introduction of antibiotics dramatically reduced mortality from infections in spinal cord injury (SCI) patients, transforming SCI from a frequently fatal condition to one with improved survivability. Prior to widespread antibiotic use, complications such as urinary tract infections, cystitis, and often led to and death, with survival rates as low as 50% in the first year post-injury. The in 1928 and its clinical application during the 1940s eliminated many of these infectious risks during both acute and chronic phases of care. World War II marked a pivotal shift toward comprehensive rehabilitation programs for SCI, emphasizing holistic recovery beyond mere survival. In 1944, the in England established the world's first specialized spinal injuries unit under Dr. Ludwig Guttmann, initially treating wounded soldiers with through innovative therapies including sports and psychological support. This approach culminated in the inaugural Stoke Mandeville Games in 1948, a sports event for veterans that evolved into the and underscored the role of in rehabilitation. Mid-20th-century advancements focused on standardized assessment and pharmacological interventions. The American Spinal Injury Association (ASIA) Impairment Scale, first published in 1982, provided a reliable framework for classifying SCI severity based on sensory and motor function, enabling consistent prognosis and treatment planning across clinical settings. In the 1990s, the National Acute Spinal Cord Injury Studies (NASCIS II and III) evaluated high-dose as a neuroprotective agent; NASCIS II (1990) reported modest neurologic improvements when administered within 8 hours of injury, influencing initial guidelines despite later scrutiny. Diagnostic capabilities advanced significantly in the late 20th and early 21st centuries with the adoption of (MRI) in the 1980s, allowing non-invasive visualization of damage, , and hemorrhage to guide surgical decisions and predict outcomes. The controversy surrounding was largely resolved in the , as evidence accumulated showing limited benefits outweighed by risks like and gastrointestinal complications; the 2013 Congress of Neurological Surgeons guidelines explicitly recommended against its routine use in acute SCI. Recent milestones include updated clinical guidelines reflecting evidence-based practices, such as the 2024 AO Spine and Praxis Spinal Cord Institute recommendations (with 2025 editorial updates) emphasizing early surgical decompression within 24 hours and optimized hemodynamic management to enhance recovery. These developments have contributed to substantial improvements in , with first-year post-injury rates rising from approximately 50% in the mid-20th century to over 90% today, driven by advances in infection control, rehabilitation, and .

Research Directions

Regenerative and cellular therapies

Regenerative and cellular therapies represent an emerging frontier in spinal cord injury (SCI) treatment, focusing on biological repair through cell replacement, , and modulation of the injury microenvironment to restore neural connectivity and function. These approaches aim to address the core limitations of by promoting axonal regrowth, reducing secondary damage such as and scarring, and integrating transplanted elements with host tissue. As of February 2026, there is no established cure for spinal cord injury (SCI). However, significant breakthroughs in regenerative therapies are progressing rapidly, offering growing potential for meaningful recovery in preclinical and early clinical stages. Key developments include the "dancing molecules" therapy, a supramolecular injectable therapy developed by Samuel Stupp at Northwestern University that forms nanofibers mimicking the extracellular matrix to promote nerve regeneration and reduce scarring. Preclinical studies demonstrated reversal of paralysis in mouse models, and a February 2026 study showed effectiveness in healing injured lab-grown human spinal cord organoids by stimulating neurite outgrowth and diminishing glial scarring. The therapy received FDA Orphan Drug Designation in July 2025, with human trials targeted for late 2026. In January 2026, the Christopher & Dana Reeve Foundation and Spinal Research awarded $1.5 million in grants to support four preclinical projects advancing biologics, gene therapies, and stem cell approaches for traumatic SCI. These grants aim to bridge the gap to human trials, with foundation leaders noting that function-restoring treatments are becoming available and challenging the long-held view that paralysis is permanent. A world-first Phase 1 clinical trial began in August 2025 using patient-derived olfactory ensheathing cells to create a nerve bridge implant for chronic SCI. Led by Griffith University, the trial primarily assesses safety while also evaluating potential functional improvements in areas such as bladder, bowel, and motor function. Stem cell transplantation is a cornerstone of these therapies, leveraging cells with regenerative potential to repopulate damaged areas and secrete . Neural stem cells (NSCs), often derived from induced pluripotent stem cells (iPSCs), have demonstrated therapeutic potential in human trials. In a pioneering 2025 Japanese phase I trial, iPSC-derived NSCs transplanted into patients with chronic SCI improved motor function in two of four participants, with one paralyzed individual regaining the ability to stand unaided after the procedure. Similarly, a 2024 study reported that NSC transplantation in chronic SCI patients promoted modest neural tissue formation and sensory improvements, suggesting viability for long-term integration. Mesenchymal stem cells (MSCs), typically sourced from or , offer immunomodulatory benefits by attenuating and supporting endogenous repair without direct neuronal differentiation. A 2024 phase I/IIa trial at involving intrathecal MSC administration in ten SCI patients found the therapy safe, with seven participants exhibiting enhanced sensory perception, motor strength, and upper extremity function. Building on this, a 2025 phase II trial combining intrathecal MSCs with rehabilitation in complete SCI cases reported significant reductions in and gains in quality-of-life metrics, attributed to decreased and improved function. Biomaterials enhance these cellular strategies by providing physical bridges across lesions and controlled release of growth factors to guide regrowth. Scaffolds composed of biocompatible polymers like or methacryloyl (GelMA) create three-dimensional matrices that mimic the extracellular environment, fostering and neurite extension. A 2025 review highlighted how such scaffolds, when loaded with , promoted axonal elongation in SCI models compared to controls. , valued for their injectability and tunable stiffness, similarly bridge cavities; for example, a 2024 (BSA)-based co-delivering and basic fibroblast growth factor inhibited formation while stimulating regeneration and motor recovery in animal SCI paradigms. Calcium-neutrophil (CaNeu) hydrogels have also shown early potential in preserving tissue integrity post-injury. Key challenges impede widespread adoption, including immune rejection of transplanted cells, which can trigger graft-versus-host responses requiring , and ethical concerns over sourcing due to destruction. Efficacy translation from preclinical to clinical settings remains inconsistent; models often yield robust outcomes like near-complete locomotor restoration, whereas human trials report more limited gains, such as improvements in American Spinal Injury Association () motor scores, due to factors like injury chronicity and size. As of 2025, combined and trials have advanced, particularly for incomplete injuries where residual pathways exist. Preclinical studies using 3D-printed scaffolds seeded with MSCs or NSCs demonstrated effective bridging and partial function recovery in rat models of partial SCI, outperforming single modalities by synergistically targeting and structural deficits. These approaches, now entering phase I human testing, hold promise for enhancing recovery in patients with incomplete lesions by amplifying endogenous repair mechanisms.

Neuromodulation and neuroprosthetics

techniques, such as epidural and transcutaneous electrical stimulation, target residual neural circuits below the level of injury to facilitate motor recovery in individuals with injury (SCI). These approaches activate dormant spinal networks, enabling volitional control of movement when combined with rehabilitation. A 2022 review highlighted that epidural stimulation (eSCS) and transcutaneous stimulation (tSCS) promote functional restoration, including improved and function, by modulating spinal excitability and enhancing . Epidural stimulation involves implanting electrodes in the to deliver precise electrical pulses to the lumbosacral , activating and motoneurons to bypass disrupted pathways. In a landmark study, three participants with chronic motor-complete SCI achieved independent overground walking with eSCS and locomotor training, demonstrating recovery of voluntary leg movement even in the absence of supraspinal input during stimulation. The 2022 Gill review emphasized that such interventions have enabled standing and stepping in complete injuries, with sustained benefits observed in long-term follow-up for select patients. Transcutaneous stimulation, a noninvasive alternative, applies electrodes externally to deliver similar excitatory signals, showing promise in improving trunk stability and lower limb coordination without surgical risks. The ARC-EX System represents a key advancement in noninvasive , cleared by the FDA in December 2024 for rehabilitation in chronic cervical SCI. This transcutaneous stimulation device targets the cervical spinal cord to enhance hand strength and sensation, with the Up-LIFT trial demonstrating significant improvements in upper extremity function and independence in daily activities when paired with targeted exercises. In the trial, 70% of participants achieved clinically meaningful gains in grasping and pinching, underscoring its role in augmenting rehabilitation outcomes. Neuroprosthetics further extend functional restoration by interfacing with the or musculoskeletal system. Powered exoskeletons like the ReWalk Personal 7.0 provide mechanical support for standing and walking in paraplegic individuals, with FDA clearance since 2014 and evidence from clinical studies showing reduced secondary complications and improved through regular use. Brain-computer interfaces (BCIs) enable thought-controlled movement; for instance, a 2023 brain-spine interface implant allowed a participant with chronic to walk naturally overground by decoding cortical signals and stimulating the lumbar spine in real-time. Neuralink's implant, first used in humans in 2024 for including SCI, facilitates cursor control and device operation via neural activity, with ongoing trials targeting motor restoration. In 2025, the Up-LIFT trial's extended data confirmed that noninvasive stimulation combined with home-based exercise further boosts independence in tasks for SCI patients, with sustained effects up to six months post-treatment. Meanwhile, KP-100IT, a recombinant hepatocyte for acute SCI, received FDA designation in June 2025, advancing its phase III evaluation for in the early injury phase. These developments highlight neuromodulation's evolving integration with to address both acute and chronic SCI challenges.

References

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