Although spinal cord injury (SCI) often causes sexual dysfunction, many people with SCI are able to have satisfying sex lives. Physical limitations acquired from SCI affect sexual function and sexuality in broader areas, which in turn has important effects on quality of life. Damage to the spinal cord impairs its ability to transmit messages between the brain and parts of the body below the level of the lesion. This results in lost or reduced sensation and muscle motion, and affects orgasm, erection, ejaculation, and vaginal lubrication. More indirect causes of sexual dysfunction include pain, weakness, and side effects of medications. Psycho-social causes include depression and altered self-image. Many people with SCI have satisfying sex lives, and many experience sexual arousal and orgasm. People with SCI employ a variety of adaptations to help carry on their sex lives healthily, by focusing on different areas of the body and types of sexual acts. Neural plasticity may account for increases in sensitivity in parts of the body that have not lost sensation, so people often find newly sensitive erotic areas of the skin in erogenous zones or near borders between areas of preserved and lost sensation.

Drugs, devices, surgery, and other interventions exist to help men achieve erection and ejaculation. Although male fertility is reduced, many men with SCI can still father children, particularly with medical interventions. Women's fertility is not usually affected, although precautions must be taken for safe pregnancy and delivery. People with SCI need to take measures during sexual activity to deal with SCI effects such as weakness and movement limitations, and to avoid injuries such as skin damage in areas of reduced sensation. Education and counseling about sexuality is an important part of SCI rehabilitation but is often missing or insufficient. Rehabilitation for children and adolescents aims to promote healthy development of sexuality and includes education for them and their families. Culturally inherited biases and stereotypes negatively affect people with SCI, particularly when held by professional caregivers. Body image and other insecurities affect sexual function, and have profound repercussions on self-esteem and self-concept. SCI causes difficulties in romantic partnerships, due to problems with sexual function and to other stresses introduced by the injury and disability, but many of those with SCI have fulfilling relationships and marriages. Relationships, self-esteem, and reproductive ability are all aspects of sexuality, which encompasses not just sexual practices but a complex array of factors: cultural, social, psychological, and emotional influences.

SCI usually causes sexual dysfunction, due to problems with sensation and the body's arousal responses. The ability to experience sexual pleasure and orgasm are among the top priorities for sexual rehabilitation among injured people.

Much research has been done into erection. By two years post-injury, 80% of men recover at least partial erectile function, though many experience problems with the reliability and duration of their erections if they do not use interventions to enhance them. Studies have found that half or up to 65% of men with SCI have orgasms, although the experience may feel different than it did before the injury. Most men say it feels weaker, and takes longer and more stimulation to achieve.

Common problems women experience post-SCI are pain with intercourse and difficulty achieving orgasm. Around half of women with SCI are able to reach orgasm, usually when their genitals are stimulated. Some women report the sensation of orgasm to be the same as before the injury, and others say the sensation is reduced.

Anejaculation is the pathological inability to ejaculate in males, with ("orgasmic") or without ("anorgasmic") orgasm.

It can depend on one or more of several causes, including:

- Sexual inhibition

- Pharmacological inhibition. They include mostly antidepressant and antipsychotic medication, and the patients experiencing that tend to quit them

- Autonomic nervous system

- Prostatectomy - surgical removal of the prostate.

- Ejaculatory duct obstruction

- Spinal cord injury causes sexual dysfunction including anejaculation. The rate of being able to ejaculate varies with the type of lesion, as detailed in the table at right.

- old age

Anejaculation, especially the "orgasmic" variant, is usually indistinguishable from retrograde ejaculation. However, a negative urinalysis measuring no abnormal presence of spermatozoa in the urine will eliminate a retrograde ejaculation diagnosis.

Thus, if the affected man has the sensations and involuntary muscle-contractions of an orgasm but no or very low-volume semen, ejaculatory duct obstruction is another possible underlying pathology of anejaculation.

Normally, a human being is able to feel pleasure from an orgasm. Upon reaching a climax, chemicals are released in the brain and motor signals are activated that will cause quick cycles of muscle contraction in the corresponding areas of both males and females. Sometimes, these signals can cause other involuntary muscle contractions such as body movements and vocalization. Finally, during orgasm, upward neural signals go to the cerebral cortex and feelings of intense pleasure are experienced. People who have this disorder are aware of reaching an orgasm, as they can feel the physical effects of it, but they experience very limited or no sort of pleasure.

Sexual anhedonia, also known as pleasure dissociative orgasmic disorder, is a condition in which an individual cannot feel pleasure from an orgasm. It is thought to be a variant of hypoactive sexual desire disorder.

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

In the long term, the loss of muscle function can have additional effects from disuse, including atrophy of the muscle. Immobility 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. In the long term, people in wheelchairs must shift periodically to relieve pressure. 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. Spasticity, the uncontrollable tensing of muscles below the level of injury, occurs in 65–78% of chronic SCI. It results from lack of input from the brain that quells muscle responses to stretch reflexes. It can be treated with drugs and physical therapy. 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. Another problem lack of mobility can cause is loss of bone density and changes in bone structure. 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. Conversely, a poorly understood phenomenon is the overgrowth of bone tissue in soft tissue areas, called heterotopic ossification. It occurs below the level of injury, possibly as a result of inflammation, and happens to a clinically significant extent in 27% of people.

People with SCI are at especially high risk for respiratory and cardiovascular problems, so hospital staff must be watchful to avoid them. 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. Pneumonia can be accompanied by shortness of breath, fever, and anxiety.

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. DVT is an especially high risk in SCI, particularly within 10 days of injury, occurring in over 13% in the acute care setting. Preventative measures include anticoagulants, pressure hose, and moving the patient's limbs. 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.

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. The risk of UTI, likely the most common complication in the long term, is heightened by use of indwelling urinary catheters. 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. 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.

An estimated 24–45% of people with SCI suffer disorders of depression, and the suicide rate is as much as six times that of the rest of the population. The risk of suicide is worst in the first five years after injury. In young people with SCI, suicide is the leading cause of death. Depression is associated with an increased risk of other complications such as UTI and pressure ulcers that occur more when self-care is neglected.

In addition to the problems found in lower-level injuries, thoracic (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. 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.

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. 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. Signs and symptoms of AD include anxiety, headache, nausea, ringing in the ears, blurred vision, flushed skin, and nasal congestion. It can occur shortly after the injury or not until years later.

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

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. Without the sympathetic input, the vessels relax and dilate. 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.

A variety of nerve types can be subjected to neurapraxia and therefore symptoms of the injury range in degree and intensity. Common symptoms of neurapraxia are disturbances in sensation, weakness of muscle, vasomotor and sudomotor paralysis in the region of the affected nerve or nerves, and abnormal sensitivity of the nerve at the point of injury. It has been observed that subjective sensory symptoms include numbness, tingling, and burning sensations at the site of the injury. Objective sensory symptoms are generally minimal in regards to touch, pain, heat, and cold. In cases of motor neuron neurapraxia, symptoms consist of flaccid paralysis of the muscles innervated by the injured nerve or nerves.

Symptoms are often transient and only last for a short period of time immediately following the injury. However, in severe cases of neurapraxia, symptoms can persist for weeks or months at a time.

A neurological disorder is any disorder of the nervous system. Structural, biochemical or electrical abnormalities in the brain, spinal cord or other nerves can result in a range of symptoms. Examples of symptoms include paralysis, muscle weakness, poor coordination, loss of sensation, seizures, confusion, pain and altered levels of consciousness. There are many recognized neurological disorders, some relatively common, but many rare. They may be assessed by neurological examination, and studied and treated within the specialities of neurology and clinical neuropsychology.

Interventions for neurological disorders include preventative measures, lifestyle changes, physiotherapy or other therapy, neurorehabilitation, pain management, medication, or operations performed by neurosurgeons. The World Health Organization estimated in 2006 that neurological disorders and their sequelae (direct consequences) affect as many as one billion people worldwide, and identified health inequalities and social stigma/discrimination as major factors contributing to the associated disability and suffering.

Although the brain and spinal cord are surrounded by tough membranes, enclosed in the bones of the skull and spinal vertebrae, and chemically isolated by the blood–brain barrier, they are very susceptible if compromised. Nerves tend to lie deep under the skin but can still become exposed to damage. Individual neurons, and the neural networks and nerves into which they form, are susceptible to electrochemical and structural disruption. Neuroregeneration may occur in the peripheral nervous system and thus overcome or work around injuries to some extent, but it is thought to be rare in the brain and spinal cord.

The specific causes of neurological problems vary, but can include genetic disorders, congenital abnormalities or disorders, infections, lifestyle or environmental health problems including malnutrition, and brain injury, spinal cord injury or nerve injury. The problem may start in another body system that interacts with the nervous system. For example, cerebrovascular disorders involve brain injury due to problems with the blood vessels (cardiovascular system) supplying the brain; autoimmune disorders involve damage caused by the body's own immune system; lysosomal storage diseases such as Niemann-Pick disease can lead to neurological deterioration. The National Institutes of Health recommend considering the evaluation of an underlying celiac disease in people with unexplained neurological symptoms, particularly peripheral neuropathy or ataxia.

In a substantial minority of cases of neurological symptoms, no neural cause can be identified using current testing procedures, and such "idiopathic" conditions can invite different theories about what is occurring.

CCS is characterized by disproportionately greater motor impairment in upper compared to lower extremities, and variable degree of sensory loss below the level of injury in combination with bladder dysfunction and urinary retention. This syndrome differs from that of a complete lesion, which is characterized by total loss of all sensation and movement below the level of the injury.

Neurapraxia is a disorder of the peripheral nervous system in which there is a temporary loss of motor and sensory function due to blockage of nerve conduction, usually lasting an average of six to eight weeks before full recovery. Neurapraxia is derived from the word apraxia, meaning “loss or impairment of the ability to execute complex coordinated movements without muscular or sensory impairment”.

This condition is typically caused by a blunt neural injury due to external blows or shock-like injuries to muscle fibers and skeletal nerve fibers, which leads to repeated or prolonged pressure buildup on the nerve. As a result of this pressure, ischemia occurs, a neural lesion results, and the human body naturally responds with edema extending in all directions from the source of the pressure. This lesion causes a complete or partial action potential conduction block over a segment of a nerve fiber and thus a reduction or loss of function in parts of the neural connection downstream from the lesion, leading to muscle weakness.

Neurapraxia results in temporary damage to the myelin sheath but leaves the nerve intact and is an impermanent condition; thus, Wallerian degeneration does not occur in neurapraxia. In order for the condition to be considered neurapraxia, according to the Seddon classification system of peripheral nerve injury, there must be a complete and relatively rapid recovery of motor and sensory function once nerve conduction has been restored; otherwise, the injury would be classified as axonotmesis or neurotmesis. Thus, neurapraxia is the mildest classification of peripheral nerve injury.

Neurapraxia is very common in professional athletes, especially American football players, and is a condition that can and should be treated by a physician.

In medicine, a stinger, also called a "burner" or "nerve pinch injury", is a neurological injury suffered by athletes, mostly in high-contact sports such as ice hockey, rugby, American football, and wrestling. The spine injury is characterized by a shooting or stinging pain that travels down one arm, followed by numbness and weakness. Many athletes in contact sports have suffered stingers, but they are often unreported to medical professionals.

Anyone who experiences significant trauma to his or her head or neck needs immediate medical evaluation for the possibility of a spinal injury. In fact, it's safest to assume that trauma victims have a spinal injury until proven otherwise because:

- The time between injury and treatment can be critical in determining the extent of complications and the amount of recovery

- A serious spinal injury is not always immediately obvious. If it is not recognized, more severe injury may occur

- Numbness or paralysis may develop immediately or come on gradually as bleeding or swelling occurs in or around the spinal cord

Arachnoid inflammation can lead to many painful and debilitating symptoms which can vary greatly in each case, and not all people experience all symptoms. Chronic pain is common, including neuralgia, while numbness and tingling of the extremities can occur with spinal cord involvement, and bowel, bladder, and sexual functioning can be affected if the lower part of the spinal cord is involved. While arachnoiditis has no consistent pattern of symptoms, it frequently affects the nerves that supply the legs and lower back. Many patients experience difficulty sitting for long (or even short) periods of time due to discomfort or pain, or because of efferent neurological or other motor symptoms, such as difficulties controlling limbs. Difficulty sitting can be problematic for patients who have trouble standing or walking for long periods, as wheelchairs are not always helpful in such cases.

Signs and symptoms may include a limp or paralyzed arm, lack of muscle control in the arm, hand, or wrist, and lack of feeling or sensation in the arm or hand. Although several mechanisms account for brachial plexus injuries, the most common is nerve compression or stretch. Infants, in particular, may suffer brachial plexus injuries during delivery and these present with typical patterns of weakness, depending on which portion of the brachial plexus is involved. The most severe form of injury is nerve root avulsion, which usually accompanies high-velocity impacts that commonly occur during motor-vehicle collisions or bicycle accidents.

Anaphia, also known as tactile anesthesia, is a medical symptom in which there is a total or partial absence of the sense of touch.

Anaphia is a common symptom of spinal cord injury and neuropathy.

A chronic, often debilitating neurological disorder characterized by recurrent moderate to severe headaches, often in association with a number of autonomic nervous system symptoms.

Meningitis is an inflammation of the meninges (membranes) of the brain and spinal cord. It is most often caused by a bacterial or viral infection. Fever, vomiting, and a stiff neck are all symptoms of meningitis.

This condition is distinct and usually episodic, with the people experiencing remarkably high blood pressure (often with systolic readings over 200 mm. Hg), intense headaches, profuse sweating, facial erythema, goosebumps, nasal stuffiness, a "feeling of doom" or apprehension, and blurred vision. An elevation of 40 mm Hg over baseline systolic should be suspicious for dysreflexia.

For the ossificans form of the condition, unenhanced CT may better show the presence and extent of arachnoid ossifications, and is complementary to MRI, as MRI can be less specific and findings can be confused with regions of calcification or hemosiderin.

Based on the location of the nerve damage, brachial plexus injuries can affect part of or the entire arm. For example, musculocutaneous nerve damage weakens elbow flexors, median nerve damage causes proximal forearm pain, and paralysis of the ulnar nerve causes weak grip and finger numbness. In some cases, these injuries can cause total and irreversible paralysis. In less severe cases, these injuries limit use of these limbs and cause pain.

The cardinal signs of brachial plexus injury then, are weakness in the arm, diminished reflexes, and corresponding sensory deficits.

1. Erb's palsy. "The position of the limb, under such conditions, is characteristic: the arm hangs by the side and is rotated medially; the forearm is extended and pronated. The arm cannot be raised from the side; all power of flexion of the elbow is lost, as is also supination of the forearm".

2. In Klumpke's paralysis, a form of paralysis involving the muscles of the forearm and hand, a characteristic sign is the "clawed hand", due to loss of function of the ulnar nerve and the intrinsic muscles of the hand it supplies.

In older patients, CCS most often occurs after acute hyperextension injury in an individual with long-standing cervical spondylosis. A slow, chronic cause in this age group is when the cord gets caught and squeezed between a posterior intervertebral disc herniation against the anterior cord and/or with posterior pressure on the cord from hypertrophy of the ligamentum flavum (Lhermitte's sign may be the experience that causes the patient to seek medical diagnosis). However, CCS is not exclusive to older patients as younger individuals can also sustain an injury leading to CCS. Typically, younger patients are more likely to get CCS as a result of a high-force trauma or a bony instability in the cervical spine. Historically, spinal cord damage was believed to originate from concussion or contusion of the cord with stasis of axoplasmic flow, causing edematous injury rather than destructive hematomyelia. More recently, autopsy studies have demonstrated that CCS may be caused by bleeding into the central part of the cord, portending less favorable prognosis. Studies also have shown from postmortem evaluation that CCS probably is associated with selective axonal disruption in the lateral columns at the level of the injury to the spinal cord with relative preservation of the grey matter.

Autonomic dysreflexia can become chronic and recurrent, often in response to longstanding medical problems like soft tissue ulcers or hemorrhoids. Long term therapy may include alpha blockers or calcium channel blockers.

Complications of severe acute hypertension can include seizures, pulmonary edema, myocardial infarction or cerebral hemorrhage. Additional organs that may be affected include the kidneys and retinas of the eyes.

SCIWORA may present as a complete spinal cord injury (total loss of sensation and function below the lesion) or incomplete spinal cord injury (some sensation and/or function is preserved). It is present in a significant number of children with SCI. Notably, the clinical symptoms can present with a delay of hours to days after the trauma. This phenomenon was primarily seen in children but was reported in adults as well. The duration of symptoms varies widely. A full recovery can be achieved without treatment within minutes to hours and permanent injuries might prevail. Overall, there seems to be a relation between extent of damage to the spinal cord and the clinical prognosis. The prognostic value of intra- and extra-medullary MRI findings is subject of ongoing research in the field of SCIWORA.