Although the most obvious symptom is impairment to the limbs, functioning is also impaired in the torso. This can mean a loss or impairment in controlling bowel and bladder, sexual function, digestion, breathing and other autonomic functions. Furthermore, sensation is usually impaired in affected areas. This can manifest as numbness, reduced sensation or burning neuropathic pain.

Secondarily, because of their depressed functioning and immobility, people with tetraplegia are often more vulnerable to pressure sores, osteoporosis and fractures, frozen joints, spasticity, respiratory complications and infections, autonomic dysreflexia, deep vein thrombosis, and cardiovascular disease.

Severity depends on both the level at which the spinal cord is injured and the extent of the injury.

An individual with an injury at C1 (the highest cervical vertebra, at the base of the skull) will probably lose function from the neck down and be ventilator-dependent. An individual with a C7 injury may lose function from the chest down but still retain use of the arms and much of the hands.

The extent of the injury is also important. A complete severing of the spinal cord will result in complete loss of function from that vertebra down. A partial severing or even bruising of the spinal cord results in varying degrees of mixed function and paralysis. A common misconception with tetraplegia is that the victim cannot move legs, arms or any of the major function; this is often not the case. Some individuals with tetraplegia can walk and use their hands, as though they did not have a spinal cord injury, while others may use wheelchairs and they can still have function of their arms and mild finger movement; again, that varies on the spinal cord damage.

It is common to have movement in limbs, such as the ability to move the arms but not the hands or to be able to use the fingers but not to the same extent, as before the injury. Furthermore, the deficit in the limbs may not be the same on both sides of the body; either left or right side may be more affected, depending on the location of the lesion on the spinal cord.

Spinal cord injuries are classified as complete and incomplete by the American Spinal Injury Association (ASIA) classification. The ASIA scale grades patients based on their functional impairment as a result of the injury, grading a patient from A to D (see table 1 for criteria). This has considerable consequences for surgical planning and therapy.

Table 1: ASIA impairment scale

Paraplegia is an impairment in motor or sensory function of the lower extremities. The word comes from Ionic Greek παραπληγίη "half-striking". It is usually caused by spinal cord injury or a congenital condition that affects the neural (brain) elements of the spinal canal. The area of the spinal canal that is affected in paraplegia is either the thoracic, lumbar, or sacral regions. Common victims of this impairment are veterans or members of the armed forces. If four limbs are affected by paralysis, tetraplegia or quadriplegia is the correct term. If only one limb is affected, the correct term is monoplegia.

Spastic paraplegia is a form of paraplegia defined by spasticity of the affected muscles, rather than flaccid paralysis.

The American Spinal Injury Association classifies spinal cord injury severity. ASIA A being the complete loss of sensory function and motor skills below the injury. ASIA B is having some sensory function below the injury, but no motor function. ASIA C some motor function below level of injury, but half the muscles cannot move against gravity. ASIA D, more than half of the muscles below the level of injury can move against gravity. ASIA E which is the restoration of all neurologic function.

Symptoms depend on the type of HSP inherited. The main feature of the disease is progressive spasticity in the lower limbs due to pyramidal tract dysfunction. This also results in brisk reflexes, extensor plantar reflexes, muscle weakness, and variable bladder disturbances. Furthermore, among the core symptoms of HSP are also included abnormal gait and difficulty in walking, decreased vibratory sense at the ankles, and paresthesia.

Initial symptoms are typically difficulty with balance, stubbing the toe or stumbling. Symptoms of HSP may begin at any age, from infancy to older than 60 years. If symptoms begin during the teenage years or later, then spastic gait disturbance usually progresses over many years. Canes, walkers, and wheelchairs may eventually be required, although some people never require assistance devices.

More specifically, patients with the autosomal dominant pure form of HSP reveal normal facial and extraocular movement. Although jaw jerk may be brisk in older subjects, there is no speech disturbance or difficulty of swallowing. Upper extremity muscle tone and strength are normal. In the lower extremities, muscle tone is increased at the hamstrings, quadriceps and ankles. Weakness is most notable at the iliopsoas, tibialis anterior, and to a lesser extent, hamstring muscles.

In the complex form of the disorder, additional symptoms are present. These include: peripheral neuropathy, amyotrophy, ataxia, mental retardation, ichthyosis, epilepsy, optic neuropathy, dementia, deafness, or problems with speech, swallowing or breathing.

Anita Harding classified the HSP in a pure and complicated form. Pure HSP presents with spasticity in the lower limbs, associated with neurogenic bladder disturbance as well as lack of vibration sensitivity (pallhypesthesia). On the other hand, HSP is classified as complex when lower limb spasticity is combined with any additional neurological symptom.

This classification is subjective and patients with complex HSPs are sometimes diagnosed as having cerebellar ataxia with spasticity, mental retardation (with spasticity), or leukodystrophy. Some of the genes listed below have been described in other diseases than HSP before. Therefore, some key genes overlap with other disease groups.

In the past, HSP has been classified as early onset beginning in early childhood or later onset in adulthood. The age of onsets has two points of maximum at age 2 and around age 40. New findings propose that an earlier onset leads to a longer disease duration without loss of ambulation or the need for the use of a wheelchair. This was also described earlier, that later onset forms evolve more rapidly.

Facial diplegia refers to people with paralysis of both sides of their face. Bilateral occurs when the onset of the second side occurs within one month of the onset of the first side. Facial diplegia occurs in 50% of patients with Guillain–Barré syndrome. Facioscapulohumeral muscular dystrophy (FSHD) is the second most common adult-onset muscular dystrophy with facial weakness being a distinct feature of FSHD in over 90% of cases.

Facial paralysis is usually caused by traumatic, infectious, neurological, metabolic, toxic, vascular, and idiopathic conditions. While over 50% of the cases of unilateral facial paralysis are caused by idiopathic conditions, less than 20% of bilateral cases are idiopathic. The most common infectious cause of facial diplegia is Lyme disease.

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.

Posterior cord syndrome, 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. This rare syndrome causes the loss of proprioception and sense of vibration below the level of injury while motor function and sensation of pain, temperature, and touch remain intact. Usually posterior cord injuries result from insults like disease or vitamin deficiency rather than trauma. Tabes dorsalis, due to injury to the posterior part of the spinal cord caused by syphilis, results in loss of touch and proprioceptive sensation.

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.

Individuals with paraplegia can range in their level of disability, requiring treatments to vary from case to case. From a rehabilitation standpoint, the most important factor is to gain as much functionality and independence back as possible. Physiotherapists spend many hours within a rehabilitation setting working on strength, range of motion/stretching and transfer skills. Wheelchair mobility is also an important skill to learn. Most paraplegics will be dependent on a wheelchair as a mode of transportation. Thus it is extremely important to teach them the basic skills to gain their independence. Activities of daily living (ADLs) can be quite challenging at first for those with a spinal cord injury (SCI). With the aid of physiotherapists and occupational therapists, individuals with an SCI can learn new skills and adapt previous ones to maximize independence, often living independently within the community.

Primary lateral sclerosis (PLS) usually presents with gradual-onset, progressive, lower-extremity stiffness and pain due to muscle spasticity. Onset is often asymmetrical. Although the muscles do not appear to atrophy as in ALS (at least initially), the disabling aspect of PLS is muscle spasticity and cramping, and intense pain when those muscles are stretched, resulting in joint immobility. A normal walking stride may become a tiny step shuffle with related instability and falling.

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.

Onset of PLS usually occurs spontaneously after age 50 and progresses gradually over a number of years, or even decades. The disorder usually begins in the legs, but it may start in the tongue or the hands. Symptoms may include difficulty with balance, weakness and stiffness in the legs, and clumsiness. Other common symptoms are spasticity (involuntary muscle contraction due to the stretching of muscle, which depends on the velocity of the stretch) in the hands, feet, or legs, foot dragging, and speech and swallowing problems due to involvement of the facial muscles. Breathing may also become compromised in the later stages of the disease, causing those patients who develop ventilatory failure to require noninvasive ventilatory support. Hyperreflexia is another key feature of PLS as seen in patients presenting with the Babinski's sign. Some people present with emotional lability and bladder urgency, and occasionally people with PLS experience mild cognitive changes detectable on neuropsychological testing, particularly on measures of executive function.

PLS is not considered hereditary when onset is in adulthood; however, juvenile primary lateral sclerosis (JPLS) has been linked to a mutation in the ALS2 gene which encodes the cell-signalling protein alsin.

The issue of whether PLS exists as a different entity from ALS is not clear, as some patients initially diagnosed as having PLS ultimately develop lower motor neuron signs.

There are no specific tests for the diagnosis of PLS. Therefore, the diagnosis occurs as the result of eliminating other possible causes of the symptoms and by an extended observation period.

Foot drop is characterized by steppage gait. While walking, people suffering the condition drag their toes along the ground or bend their knees to lift their foot higher than usual to avoid the dragging. This serves to raise the foot high enough to prevent the toe from dragging and prevents the slapping. To accommodate the toe drop, the patient may use a characteristic tiptoe walk on the opposite leg, raising the thigh excessively, as if walking upstairs, while letting the toe drop. Other gaits such as a wide outward leg swing (to avoid lifting the thigh excessively or to turn corners in the opposite direction of the affected limb) may also indicate foot drop.

Patients with painful disorders of sensation (dysesthesia) of the soles of the feet may have a similar gait but do not have foot drop. Because of the extreme pain evoked by even the slightest pressure on the feet, the patient walks as if walking barefoot on hot sand.

Severe back pain, saddle anesthesia, incontinence and sexual dysfunction are considered "red flags", i.e. features which require urgent investigation.

Examination for pain sensation, by pinprick, shows leg (lumbar nerves) analgesia with perineal (sacral nerves) escape. The maintenance of perineal sensation with absence of pain sensation over the lumbar nerve roots is typical for an extra-medullary and intra-thecal (outside the cord and within the dural sheath) process. Inability to walk, with this unusual sensory examination completes a triad of signs and usually represents spinal tuberculosis. The triad is paraplegia with lumbar loss of pain sensation and presence of perineal altered sensation.

Diagnosis is usually confirmed by an MRI scan or CT scan, depending on availability. Early surgery in acute onset of severe cases has been reported to be important.

The causes of foot drop, as for all causes of neurological lesions, should be approached using a localization-focused approach before etiologies are considered. Most of the time, foot drop is the result of neurological disorder; only rarely is the muscle diseased or nonfunctional. The source for the neurological impairment can be central (spinal cord or brain) or peripheral (nerves located connecting from the spinal cord to an end-site muscle or sensory receptor). Foot drop is rarely the result of a pathology involving the muscles or bones that make up the lower leg. The anterior tibialis is the muscle that picks up the foot. Although the anterior tibialis plays a major role in dorsiflexion, it is assisted by the fibularis tertius, extensor digitorum longus and the extensor halluces longus. If the drop foot is caused by neurological disorder all of these muscles could be affected because they are all innervated by the deep fibular (peroneal) nerve, which branches from the sciatic nerve. The sciatic nerve exits the lumbar plexus with its root arising from the fifth lumbar nerve space. Occasionally, spasticity in the muscles opposite the anterior tibialis, the gastrocnemius and soleus, exists in the presence of foot drop, making the pathology much more complex than foot drop. Isolated foot drop is usually a flaccid condition. There are gradations of weakness that can be seen with foot drop, as follows: 0=complete paralysis, 1=flicker of contraction, 2=contraction with gravity eliminated alone, 3=contraction against gravity alone, 4=contraction against gravity and some resistance, and 5=contraction against powerful resistance (normal power). Foot drop is different from foot slap, which is the audible slapping of the foot to the floor with each step that occurs when the foot first hits the floor on each step, although they often are concurrent.

Treated systematically, possible lesion sites causing foot drop include (going from peripheral to central):

1. Neuromuscular disease;

2. Peroneal nerve (common, i.e., frequent) —chemical, mechanical, disease;

3. Sciatic nerve—direct trauma, iatrogenic;

4. Lumbosacral plexus;

5. L5 nerve root (common, especially in association with pain in back radiating down leg);

6. Cauda equina syndrome, which is cause by impingement of the nerve roots within the spinal canal distal to the end of the spinal cord;

7. Spinal cord (rarely causes isolated foot drop) —poliomyelitis, tumor;

8. Brain (uncommon, but often overlooked) —stroke, TIA, tumor;

9. Genetic (as in Charcot-Marie-Tooth Disease and hereditary neuropathy with liability to pressure palsies);

10. Nonorganic causes.

If the L5 nerve root is involved, the most common cause is a herniated disc. Other causes of foot drop are diabetes (due to generalized peripheral neuropathy), trauma, motor neuron disease (MND), adverse reaction to a drug or alcohol, and multiple sclerosis.

Motor neuron diseases affect either upper motor neurons (UMN) or lower motor neurons (LMN), or both:

In the United States, the term is often used to denote ALS, the most common disorder in the group. In the United Kingdom, the term is also spelled "motor neurone disease" (MND) and is sometimes used for the entire group; but mostly it refers to ALS.

While MND refers to a specific subset of similar diseases, there are numerous other diseases of motor neurons that are referred to collectively as "motor neuron disorders", for instance disease belonging to spinal muscular atrophies. However, they are not classified as "motor neuron diseases" by the tenth International Statistical Classification of Diseases and Related Health Problems (ICD-10), which is the definition followed in this article.

The first symptoms of Guillain–Barré syndrome are numbness, tingling, and pain, alone or in combination. This is followed by weakness of the legs and arms that affects both sides equally and worsens over time. The weakness can take half a day to over two weeks to reach maximum severity, and then becomes steady. In one in five people, the weakness continues to progress for as long as four weeks. The muscles of the neck may also be affected, and about half experience involvement of the cranial nerves which supply the head and face; this may lead to weakness of the muscles of the face, swallowing difficulties and sometimes weakness of the eye muscles. In 8%, the weakness affects only the legs (paraplegia or paraparesis). Involvement of the muscles that control the bladder and anus is unusual. In total, about a third of people with Guillain–Barré syndrome continue to be able to walk. Once the weakness has stopped progressing, it persists at a stable level ("plateau phase") before improvement occurs. The plateau phase can take between two days and six months, but the most common duration is a week. Pain-related symptoms affect more than half, and include back pain, painful tingling, muscle pain and pain in the head and neck relating to irritation of the lining of the brain.

Many people with Guillain–Barré syndrome have experienced the signs and symptoms of an infection in the 3–6 weeks prior to the onset of the neurological symptoms. This may consist of upper respiratory tract infection (rhinitis, sore throat) or diarrhea.

In children, particularly those younger than six years old, the diagnosis can be difficult and the condition is often initially mistaken (sometimes for up to two weeks) for other causes of pains and difficulty walking, such as viral infections, or bone and joint problems.

On neurological examination, characteristic features are the reduced power and reduced or absent tendon reflexes (hypo- or areflexia, respectively). However, a small proportion has normal reflexes in affected limbs before developing areflexia, and some may have exaggerated reflexes. In the "Miller Fisher variant" subtype of Guillain–Barré syndrome (see below), a triad of weakness of the eye muscles, abnormalities in coordination, as well as absent reflexes can be found. The level of consciousness is normally unaffected in Guillain–Barré syndrome, but the Bickerstaff brainstem encephalitis subtype may feature drowsiness, sleepiness, or coma.

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

Transient ischemic attacks (TIAs) rarely affect the spinal cord and usually affect the brain; however, cases have been documented in these areas. Spinal ateriovenous malformations are the main cause and are represented later in this article. However, TIAs can result from emboli in calcific aortic disease and aortic coarctation.

A quarter of all people with Guillain–Barré syndrome develop weakness of the breathing muscles leading to respiratory failure, the inability to breathe adequately to maintain healthy levels of oxygen and/or carbon dioxide in the blood. This life-threatening scenario is complicated by other medical problems such as pneumonia, severe infections, blood clots in the lungs and bleeding in the digestive tract in 60% of those who require artificial ventilation.

Phantom pain is pain felt in a part of the body that has been amputated, or from which the brain no longer receives signals. It is a type of neuropathic pain.

The prevalence of phantom pain in upper limb amputees is nearly 82%, and in lower limb amputees is 54%. One study found that eight days after amputation, 72% of patients had phantom limb pain, and six months later, 67% reported it. Some amputees experience continuous pain that varies in intensity or quality; others experience several bouts of pain per day, or it may reoccur less often. It is often described as shooting, crushing, burning or cramping. If the pain is continuous for a long period, parts of the intact body may become sensitized, so that touching them evokes pain in the phantom limb. Phantom limb pain may accompany urination or defecation.

Local anesthetic injections into the nerves or sensitive areas of the stump may relieve pain for days, weeks, or sometimes permanently, despite the drug wearing off in a matter of hours; and small injections of saline into the soft tissue between vertebrae produces local pain that radiates into the phantom limb for ten minutes or so and may be followed by hours, weeks or even longer of partial or total relief from phantom pain. Vigorous vibration or electrical stimulation of the stump, or current from electrodes surgically implanted onto the spinal cord, all produce relief in some patients.

Mirror box therapy produces the illusion of movement and touch in a phantom limb which in turn may cause a reduction in pain.

Paraplegia, the loss of sensation and voluntary motor control after serious spinal cord damage, may be accompanied by girdle pain at the level of the spinal cord damage, visceral pain evoked by a filling bladder or bowel, or, in five to ten per cent of paraplegics, phantom body pain in areas of complete sensory loss. This phantom body pain is initially described as burning or tingling, but may evolve into severe crushing or pinching pain, or the sensation of fire running down the legs or of a knife twisting in the flesh. Onset may be immediate or may not occur until years after the disabling injury. Surgical treatment rarely provides lasting relief.