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.

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.

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. A person with a lowered level of consciousness may show a response to a painful stimulus above a certain point but not below it.

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.

The specific parts of the body affected by loss of function are determined by the level of injury.

Central cord syndrome (CCS) is the most common form of cervical spinal cord injury. It is characterized by loss of motion and sensation in arms and hands. It usually results from trauma which causes damage to the neck, leading to major injury to the central grey matter of the spinal cord. The syndrome is more common in people over the age of 50 because osteoarthritis in the neck region causes weakening of the vertebrae. CCS most frequently occurs among older persons with cervical spondylosis, however, it also may occur in younger individuals.

CCS is the most common incomplete spinal cord injury syndrome. It accounts for approximately 9% of traumatic SCIs. After an incomplete injury, the brain still has the capacity to send and receive some signals below the site of injury. Sending and receiving of signals to and from parts of the body is reduced, not entirely blocked. CCS gives a greater motor loss in the upper limbs than in the lower limbs, with variable sensory loss.

It was first described by Schneider in 1954. It is generally associated with favorable prognosis for some degree of neurological and functional recovery. However, factors such as age, preexisting conditions, and extent of injury will affect the recovery process.

Symptoms vary depending on whether the spinal cord, brain stem, nerves or their blood supply is affected by the pressure.

Symptoms become apparent when the neck is bent. They include:

- Posterior head pain

- Neck weakness

- Periods of confusion

- Dysarthria (difficulty swallowing or talking due to loss of muscle control)

- Dizziness

- Loss of sensation

- Cranial nerve disturbance

- Loss of the ability to know how joints are positioned

- Lhermitte's sign ('electric shock sensation' down spine and/or to the extremities when the neck is flexed forward)

- Weakness of the arms and legs

- Orthostatic hypotension

- Patients will go into a pool and notice that below their belly button the water is not as cold as it is above.

Complications from this can include hydrocephalus, pseudotumor cerebri or syringomyelia because it blocks the flow of fluid around the brain and spinal cord.

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.

The onset of myelomalacia may be so subtle that it is overlooked. Depending on the extent of the spinal cord injury, the symptoms may vary. In some cases, the symptom may be as common as hypertension. Though every case is different, several cases reported loss of motor functions in the extremities, areflexia or sudden jerks of the limbs, loss of pain perception, or even paralysis; all of which are possible indicators of a damaged and softened spinal cord. In the most severe cases, paralysis of the respiratory system manifests in death.

Symptoms usually occur very quickly and are often experienced within one hour of the initial damage. MRI can detect the magnitude and location of the damage 10–15 hours after the initiation of symptoms. Diffusion-weighted imaging may be used as it is able to identify the damage within a few minutes of symptomatic onset.

Clinical features include paraparesis or quadriparesis (depending on the level of the injury) and impaired pain and temperature sensation. Complete motor paralysis below the level of the lesion due to interruption of the corticospinal tract, and loss of pain and temperature sensation at and below the level of the lesion. Proprioception and vibratory sensation is preserved, as it is in the dorsal side of the spinal cord.

Clinical signs and symptoms depend on which spinal cord level (cervical, thoracic or lumbar) is affected and the extent (anterior, posterior or lateral) of the pathology, and may include:

- upper motor neuron signs—weakness, spasticity, clumsiness, altered tonus, hyperreflexia and pathological reflexes, including Hoffmann's sign and inverted Plantar reflex (positive Babinski sign);

- lower motor neuron signs—weakness, clumsiness in the muscle group innervated at the level of spinal cord compromise, muscle atrophy, hyporeflexia, muscle hypotonicity or flaccidity, fasciculations;

- sensory deficits;

- bowel/bladder symptoms and sexual dysfunction.

Symptoms suggestive of cord compression are back pain, a dermatome of increased sensation, paralysis of limbs below the level of compression, decreased sensation below the level of compression, urinary and fecal incontinence and/or urinary retention. Lhermitte's sign (intermittent shooting electrical sensation) and hyperreflexia may be present.

Basilar invagination is invagination (infolding) of the base of the skull that occurs when the top of the C2 vertebra migrates upward. It can cause narrowing of the foramen magnum (the opening in the skull where the spinal cord passes through to the brain). It also may press on the lower brainstem.

This is similar to Chiari malformation. That, however, is usually present at birth.

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.

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.

There are disturbances in sensory nerves and motor nerves and dysfunction of the autonomic nervous system at the level of the lesion or below. Therefore, the signs and symptoms depend on the area of spine involved:

- Cervical: If the upper cervical cord is involved, all four limbs may be involved and there is risk of respiratory paralysis (cervical nerve segments C3, 4, 5 innervate the abdominal diaphragm). Lesions of the lower cervical (C5–T1) region will cause a combination of upper and lower motor neuron signs in the upper limbs, and exclusively upper motor neuron signs in the lower limbs. Cervical lesions account for about 20% of cases.

- Thoracic: A lesion of the thoracic spinal cord (T1–12) will produce upper motor neuron signs in the lower limbs, presenting as a spastic diplegia. This is the most common location of the lesion,

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

Myelomalacia is a pathological term referring to the softening of the spinal cord. Hemorrhagic infarction (bleeding) of the spinal cord can occur as a sequela to acute injury, such as that caused by intervertebral disc extrusion (being forced or pressed out).

The disorder causes flaccid paraplegia (impairment of motor function in lower extremities), total areflexia (below normal or absence of reflexes) of the pelvic limbs and anus, loss of deep pain perception caudal (toward the coccyx, or tail) to the site of spinal cord injury, muscular atrophy (wasting away of muscle tissue), depressed mental state, and respiratory difficulty due to intercostal (muscles that run between the ribs) and diaphragmatic paralysis. Gradual cranial migration of the neurological deficits (problems relating to the nervous system), is known as ascending syndrome and is said to be a typical feature of diffuse myelomalacia. Although clinical signs of myelomalacia are observed within the onset (start) of paraplegia, sometimes they may become evident only in the post-operative period, or even days after the onset of paraplegia. Death from myelomalacia may occur as a result of respiratory paralysis when the ascending lesion (abnormal damaged tissue) reaches the motor nuclei of the phrenic nerves (nerves between the C3-C5 region of the spine) in the cervical (neck) region.

In children, symptoms may include:

- Lesions, hairy patches, dimples, or fatty tumours on the lower back

- Foot and spinal deformities

- Weakness in the legs (loss of muscle strength and tone)

- Change in or abnormal gait including awkwardness while running or wearing the tips or side of one shoe

- Low back pain

- Scoliosis (abnormal curvature of the spine to the left or right)

- Urinary irregularities (incontinence or retention)

Tethered spinal cord syndrome may go undiagnosed until adulthood, when sensory, motor, bowel, and bladder control issues emerge. This delayed presentation of symptoms relates to the degree of strain on the spinal cord over time.

Tethering may also develop after spinal cord injury. Scar tissue can block the flow of fluids around the spinal cord. Fluid pressure may cause cysts to form in the spinal cord, a condition called syringomyelia. This can lead to additional loss of movement or feeling, or the onset of pain or autonomic nervous system symptoms.

In adults, onset of symptoms typically include:

- Severe pain (in the lower back and radiating into the legs, groin, and perineum)

- Bilateral muscle weakness and numbness

- Loss of feeling and movement in lower extremities

- Urinary irregularities (incontinence or retention)

- Bowel control issues

Neurological symptoms can include a mixed picture of upper and lower motor neuron findings, such as amyotrophy, hyperreflexia, and pathologic plantar response, occurring in the same limb. Profound sensory changes, such as loss of pain, temperature, and proprioceptive sensations, are common. Last, progressive symptoms of a neuropathic bladder are noted on over 70% of adult patients, versus only 20% to 30% of children. These symptoms include urinary frequency and urgency, feeling of incomplete voiding, poor voluntary control, and urge and stress incontinence. Chronic recurrent infections are common and occasionally lead to nephrolithiasis (kidney stones), renal failure, or renal transplantation. Female patients also give a history of ineffective labor and postpartum rectal prolapse, presumably due to an atonic pelvic floor.

Brown-Séquard syndrome may be caused by a spinal cord tumour, trauma [such as a gunshot wound or puncture wound to the cervical (neck) or thoracic spine (back)], ischemia (obstruction of a blood vessel), or infectious or inflammatory diseases such as tuberculosis, or multiple sclerosis. In its pure form, it is rarely seen. The most common cause is penetrating trauma such as a gunshot wound or stab wound to the spinal cord. Decompression sickness may also be a cause of Brown-Séquard syndrome.

The presentation can be progressive and incomplete. It can advance from a typical Brown-Séquard syndrome to complete paralysis. It is not always permanent and progression or resolution depends on the severity of the original spinal cord injury and the underlying pathology that caused it in the first place.

Syringomyelia causes a wide variety of neuropathic symptoms due to damage of the spinal cord and the nerves inside. Patients may experience severe chronic pain, abnormal sensations and loss of sensation particularly in the hands. Some patients experience paralysis or paresis temporarily or permanently. A syrinx may also cause disruptions in the parasympathetic and sympathetic nervous systems, leading to abnormal body temperature or sweating, bowel control issues, or other problems. If the syrinx is higher up in the spinal cord or affecting the brainstem as in syringobulbia, vocal cord paralysis, ipsilateral tongue wasting, trigeminal nerve sensory loss, and other signs may occur. Rarely, bladder stones can occur in the onset of weakness in the lower extremities.

Classically, syringomyelia spares the dorsal column/medial lemniscus of the spinal cord, leaving pressure, vibration, touch and proprioception intact in the upper extremities. Neuropathic arthropathy, also known as a Charcot joint, can occur, particularly in the shoulders, in patients with syringomyelia. The loss of sensory fibers to the joint is theorized to lead to damage of the joint over time.

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

Understanding the meaning of signs and symptoms for the clinical syndrome of lumbar stenosis requires an understanding of what the syndrome is, and the prevalence of the condition. A recent review on lumbar stenosis in the Journal of the American Medical Association's "Rational Clinical Examination Series" emphasized that the syndrome can be considered when lower extremity pain occurs in combination with back pain. This syndrome occurs in 12% of older community dwelling men and up to 21% of those in retirement communities.

The leg symptoms in lumbar spinal stenosis (LSS) are similar to those found with vascular claudication, giving rise to the term pseudoclaudication. These symptoms include pain, weakness, and tingling of the legs, which may radiate down the leg to the feet. Additional symptoms in the legs may be fatigue, heaviness, weakness, a sensation of tingling, pricking, or numbness and leg cramps, as well as bladder symptoms. Symptoms are most commonly bilateral and symmetrical, but they may be unilateral; leg pain is usually more troubling than back pain.

Pseudoclaudication, now referred to as neurogenic claudication, typically worsen with standing or walking and improve with sitting. The occurrence is often related to posture and lumbar extension. Lying on the side is often more comfortable than lying flat, since it permits greater lumbar flexion. Vascular claudication can resemble spinal stenosis, and some individuals experience unilateral or bilateral symptoms radiating down the legs rather than true claudication.

The first symptoms of stenosis include bouts of low back pain. After a few months or years, this may progress to claudication. The pain may be radicular, following the classic neurologic pathways. This occurs as the spinal nerves or spinal cord become increasingly trapped in a smaller space within the canal. It can be difficult to determine whether pain in the elderly is caused by lack of blood supply or stenosis; testing can usually differentiate between them but patients can have both vascular disease in the legs and spinal stenosis.

Among people with lower extremity pain in combination with back pain, lumbar stenosis as the cause is two times more likely in those older than 70 years of age while those younger than 60 years it is 0.40 as likely. The character of the pain is also useful. When the discomfort does not occur while seated, the likelihood of LSS increases considerably around 7.4 times. Other features increasing the likelihood of lumbar stenosis are improvement in symptoms on bending forward 6.4 times, pain that occurs in both buttocks or legs 6.3 times, and the presence of neurogenic claudication 3.7 times. Alternately, the absence of neurogenic claudication makes lumbar stenosis much less likely as the explanation for the pain.

Diagnosis is by X-rays but preferably magnetic resonance imaging (MRI) of the whole spine. The most common causes of cord compression are tumors, but abscesses and granulomas (e.g. in tuberculosis) are equally capable of producing the syndrome. Tumors that commonly cause cord compression are lung cancer (non-small cell type), breast cancer, prostate cancer, renal cell carcinoma, thyroid cancer, lymphoma and multiple myeloma.

Posterior spinal artery syndrome is much rarer than its anterior counterpart as the white matter structures that are present are much less vulnerable to ischemia since they have a better blood supply. When posterior spinal artery syndrome does occur, dorsal columns are damaged and ischemia may spread into the posterior horns. Clinically the syndrome presents as a loss of tendon reflexes and loss of joint position sense

Magnetic resonance imaging (MRI) is the imaging of choice in spinal cord lesions.

Brown-Séquard syndrome is an incomplete spinal cord lesion characterized by findings on clinical examination which reflect hemisection of the spinal cord (cutting the spinal cord in half on one or the other side). It is diagnosed by finding motor (muscle) paralysis on the same (ipsilateral) side as the lesion and deficits in pain and temperature sensation on the opposite (contralateral) side. This is called ipsilateral hemiplegia and contralateral pain and temperature sensation deficits. The loss of sensation on the opposite side of the lesion is because the nerve fibers of the spinothalamic tract (which carry information about pain and temperature) crossover once they meet the spinal cord from the peripheries.

Transverse myelitis is a neurological condition in which the spinal cord is inflamed. The inflammation damages nerve fibers, and causes them to lose their myelin coating leading to decreased electrical conductivity in the central nervous system. "Transverse" implies that the inflammation extends across the entire width of the spinal cord. Partial transverse myelitis and partial myelitis are terms used to define inflammation of the spinal cord that affects part of the width of the spinal cord.

Lumbar spinal stenosis (LSS) is a medical condition in which the spinal canal narrows and compresses the nerves at the level of the lumbar vertebrae. This is usually due to the common occurrence of spinal degeneration that occurs with aging. It can also sometimes be caused by spinal disc herniation, osteoporosis, a tumor, or trauma. In the cervical (neck) and lumbar (low back) region it can be a congenital condition to varying degrees.

It is also a common symptom for those who suffer from various skeletal dysplasias such as with pseudoachondroplasia and achondroplasia at an early age.

Spinal stenosis may affect the cervical or thoracic region in which case it is known as cervical spinal stenosis or thoracic spinal stenosis. In some cases, it may be present in all three places in the same patient. Lumbar spinal stenosis can cause low back pain, abnormal sensations, and the absence of sensation (numbness) in the legs, thighs, feet or buttocks, or loss of bladder and bowel control.