Spinal cord injuries at the cervical (neck) level result in full or partial tetraplegia (also called quadriplegia). Depending on the specific location and severity of trauma, limited function may be retained.

Additional signs and symptoms of cervical injuries include low heart rate, low blood pressure, problems regulating body temperature, and breathing dysfunction. 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.

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.

Pain, especially headache, is a common complication following a TBI. Being unconscious and lying still for long periods can cause blood clots to form (deep venous thrombosis), which can cause pulmonary embolism. Other serious complications for patients who are unconscious, in a coma, or in a vegetative state include pressure sores, pneumonia or other infections, and progressive multiple organ failure.

The risk of post-traumatic seizures increases with severity of trauma (image at right) and is particularly elevated with certain types of brain trauma such as cerebral contusions or hematomas. As many as 50% of people with penetrating head injuries will develop seizures. People with early seizures, those occurring within a week of injury, have an increased risk of post-traumatic epilepsy (recurrent seizures occurring more than a week after the initial trauma) though seizures can appear a decade or more after the initial injury and the common seizure type may also change over time. Generally, medical professionals use anticonvulsant medications to treat seizures in TBI patients within the first week of injury only and after that only if the seizures persist.

Neurostorms may occur after a severe TBI. The lower the Glasgow Coma Score (GCS), the higher the chance of Neurostorming. Neurostorms occur when the patient's Autonomic Nervous System (ANS), Central Nervous System (CNS), Sympathetic Nervous System (SNS), and ParaSympathetic Nervous System (PSNS) become severely compromised https://www.brainline.org/story/neurostorm-century-part-1-3-medical-terminology . This in turn can create the following potential life-threatening symptoms: increased IntraCranial Pressure (ICP), tachycardia, tremors, seizures, fevers, increased blood pressure, increased Cerebral Spinal Fluid (CSF), and diaphoresis https://www.brainline.org/story/neurostorm-century-part-1-3-medical-terminology. A variety of medication may be used to help decrease or control Neurostorm episodes https://www.brainline.org/story/neurostorm-century-part-3-3-new-way-life.

Parkinson's disease and other motor problems as a result of TBI are rare but can occur. Parkinson's disease, a chronic and progressive disorder, may develop years after TBI as a result of damage to the basal ganglia. Other movement disorders that may develop after TBI include tremor, ataxia (uncoordinated muscle movements), and myoclonus (shock-like contractions of muscles).

Skull fractures can tear the meninges, the membranes that cover the brain, leading to leaks of cerebrospinal fluid (CSF). A tear between the dura and the arachnoid membranes, called a CSF fistula, can cause CSF to leak out of the subarachnoid space into the subdural space; this is called a subdural hygroma. CSF can also leak from the nose and the ear. These tears can also allow bacteria into the cavity, potentially causing infections such as meningitis. Pneumocephalus occurs when air enters the intracranial cavity and becomes trapped in the subarachnoid space. Infections within the intracranial cavity are a dangerous complication of TBI. They may occur outside of the dura mater, below the dura, below the arachnoid (meningitis), or within the brain itself (abscess). Most of these injuries develop within a few weeks of the initial trauma and result from skull fractures or penetrating injuries. Standard treatment involves antibiotics and sometimes surgery to remove the infected tissue.

Injuries to the base of the skull can damage nerves that emerge directly from the brain (cranial nerves). Cranial nerve damage may result in:

- Paralysis of facial muscles

- Damage to the nerves responsible for eye movements, which can cause double vision

- Damage to the nerves that provide sense of smell

- Loss of vision

- Loss of facial sensation

- Swallowing problems

Hydrocephalus, post-traumatic ventricular enlargement, occurs when CSF accumulates in the brain, resulting in dilation of the cerebral ventricles and an increase in ICP. This condition can develop during the acute stage of TBI or may not appear until later. Generally it occurs within the first year of the injury and is characterized by worsening neurological outcome, impaired consciousness, behavioral changes, ataxia (lack of coordination or balance), incontinence, or signs of elevated ICP.

Any damage to the head or brain usually results in some damage to the vascular system, which provides blood to the cells of the brain. The body can repair small blood vessels, but damage to larger ones can result in serious complications. Damage to one of the major arteries leading to the brain can cause a stroke, either through bleeding from the artery or through the formation of a blood clot at the site of injury, blocking blood flow to the brain. Blood clots also can develop in other parts of the head. Other types of vascular complications include vasospasm, in which blood vessels constrict and restrict blood flow, and the formation of aneurysms, in which the side of a blood vessel weakens and balloons out.

Fluid and hormonal imbalances can also complicate treatment. Hormonal problems can result from dysfunction of the pituitary, the thyroid, and other glands throughout the body. Two common hormonal complications of TBI are syndrome of inappropriate secretion of antidiuretic hormone and hypothyroidism.

Another common problem is spasticity. In this situation, certain muscles of the body are tight or hypertonic because they cannot fully relax.

Traumatic brain injury (TBI, physical trauma to the brain) can cause a variety of complications, health effects that are not TBI themselves but that result from it. The risk of complications increases with the severity of the trauma; however even mild traumatic brain injury can result in disabilities that interfere with social interactions, employment, and everyday living. TBI can cause a variety of problems including physical, cognitive, emotional, and behavioral complications.

Symptoms that may occur after a concussion – a minor form of traumatic brain injury – are referred to as post-concussion syndrome.

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,

Any type of traumatic brain injury (TBI) or injury done to the spinal cord can result in a wide spectrum of disabilities in a person. Depending on the section of the brain or spinal cord that suffers the trauma, the outcome may be anticipated.

Depending on the cause of the disease, such clinical conditions manifest different speed in progression of symptoms in a matter of hours to days. Most myelitis manifests fast progression in muscle weakness or paralysis starting with the legs and then arms with varying degrees of severity. Sometimes the dysfunction of arms or legs cause instability of posture and difficulty in walking or any movement. Also symptoms generally include paresthesia which is a sensation of tickling, tingling, burning, pricking, or numbness of a person's skin with no apparent long-term physical effect. Adult patients often report pain in the back, extremities, or abdomen. Patients also present increased urinary urgency, bowel or bladder dysfunctions such as bladder incontinence, difficulty or inability to void, and incomplete evacuation of bowel or constipation. Others also report fever, respiratory problems and intractable vomiting.

The spinal cord transmits sensory reception from the peripheral nervous system. It also conducts motor information to the body's skeletal muscles, cardiac muscles, smooth muscles, and glands. There are 31 pairs of spinal nerves along the spinal cord, all of which consist of both sensory and motor neurons. The spinal cord is protected by vertebrae and connects the peripheral nervous system to the brain, and it acts as a "minor" coordinating center.

Myelitis lesions usually occur in a narrow region but can be spread and affect many areas.

- Poliomyelitis: disease caused by viral infection in the gray matter with symptoms of muscle paralysis or weakness

- Leukomyelitis: lesions in the white matter

- Transverse Myelitis: caused by axonal demyelination encompassing both sides of the spinal cord

- Meningococcal Myelitis (or meningomyelitis): lesions occurring in the region of meninges and the spinal cord

Geriatric trauma refers to a traumatic injury that occurs to an elderly person. The three prevailing causes of traumatic death in the elderly are falls (which account for 40% of traumatic death in this age group), traffic collisions and burns.

A progressive decline in central nervous system function leads to a loss of proprioception, balance and overall motor coordination, as well as a reduction in eye–hand coordination, reaction time and an unsteady gait. These degenerative changes are often accompanied by osteoarthritis (degenerative joint disease), which leads to a reduction in the range of motion of the head, neck and extremities. Furthermore, elderly people frequently take multiple medications for control of various diseases and conditions. The side effects of some of these medications may either predispose to injury, or may cause a minor trauma to result in a much more severe condition. For example, a person taking warfarin (Coumadin) and/or clopidogrel (Plavix) may experience a life-threatening intracranial hemorrhage after sustaining a relatively minor closed head injury, as a result of the defect in the hemostatic mechanism caused by such medications. The combined effects of these changes greatly predisposes elderly people to traumatic injury. Both the incidence of falls and the severity of associated complications increase with advancing age.

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.

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.

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.

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.

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.

Nervous system disease refers to a small class of medical conditions affecting the nervous system.

The Nervous System Diseases can be divided into two categories:

- Central nervous system disease in the CNS

- Peripheral neuropathy in the PNS

The "DSM-IV" specifies that ASD must be accompanied by the presence of dissociative symptoms, which largely differentiates it from PTSD.

Dissociative symptoms include a sense of numbing or detachment from emotional reactions, a sense of physical detachment, such as seeing oneself from another perspective, decreased awareness of one’s surroundings, the perception that one’s environment is unreal or dreamlike, and the inability to recall critical aspects of the traumatic event (dissociative amnesia).

In addition to the characteristic dissociative symptoms, ASD shares many of the symptoms with PTSD, including:

- the experience or witnessing of a threatening event that resulted in intense fear or horror

- the re-experiencing of the event by means of flashbacks, recurrent thoughts or dreams, and distress when reminded of the event

- the avoidance of stimuli that serve as reminders of the event, such as feelings, thoughts, places, individuals, and activities

- anxiety, including restlessness, difficulty sleeping and concentrating, and hypervigilance

- a significant disruption in normal social or work functioning

Acute stress reaction (also called acute stress disorder, psychological shock, mental shock, or simply shock) is a psychological condition arising in response to a terrifying or traumatic event, or witnessing a traumatic event that induces a strong emotional response within the individual. It should not be confused with the unrelated circulatory condition of shock/hypoperfusion. Acute stress reaction (ASR) may develop into delayed stress reaction (better known as PTSD) if stress is not correctly managed. ASR is characterized by re-living and avoiding reminders of an aversive event, as well as generalized hypervigilance after initial exposure to a traumatic event. ASD is differentiated from PTSD as a disorder that precedes it, and if symptoms last for more than one month, it will develop into PTSD. It can thus be thought of as the acute phase of PTSD.

Clinical features of CRPS have been found to be inflammation resulting from the release of certain pro-inflammatory chemical signals from the nerves, sensitized nerve receptors that send pain signals to the brain, dysfunction of the local blood vessels' ability to constrict and dilate appropriately, and maladaptive neuroplasticity.

The signs and symptoms of CRPS usually initially manifest near the site of a (typically minor) injury. The most common symptoms are pain sensations, including burning, stabbing, grinding, and throbbing. Moving or touching the limb is often intolerable. The patient may also experience muscle spasms; local swelling; extreme sensitivity to things such as wind and water, touch and vibrations; abnormally increased sweating; changes in skin temperature (usually hot but sometimes cold) and color (bright red or a reddish violet); softening and thinning of bones; joint tenderness or stiffness; changes in nail and hair growth and/or restricted or painful movement. Drop attacks (falls), almost fainting, and fainting spells are infrequently reported, as are visual problems. The symptoms of CRPS vary in severity and duration. Since CRPS is a systemic problem, potentially any organ can be affected.

The pain of CRPS is continuous although varies in severity. It is widely recognized that it can be heightened by emotional or physical stress.

Previously it was considered that CRPS had three stages; it is now believed that people affected by CRPS do not progress through these stages sequentially. These stages may not be time-constrained and could possibly be event-related, such as ground-level falls or re-injuries of previously damaged areas. Thus, rather than a progression of CRPS from bad to worse, it is now thought, instead, that such individuals are likely to have one of the three following types of disease progression:

1. "Stage" one is characterized by severe, burning pain at the site of the injury, muscle spasms, joint stiffness, restricted mobility, rapid hair and nail growth, and vasospasm. The vasospasm is that which causes the changes in the color and temperature of the skin. Some may experience hyperhydrosis (increased sweating). In mild cases this stage lasts a few weeks, in which it can subside spontaneously or respond rapidly to treatment (physical therapy, pain specialist).

2. "Stage" two is characterized by more intense pain. Swelling spreads, hair growth diminishes, nails become cracked, brittle, grooved and spotty, osteoporosis becomes severe and diffuse, joints thicken, and muscles atrophy.

3. "Stage" three is characterized by irreversible changes in the skin and bones, while the pain becomes unyielding and may involve the entire limb. There is marked muscle atrophy, severely limited mobility of the affected area, and flexor tendon contractions (contractions of the muscles and tendons that flex the joints). Occasionally the limb is displaced from its normal position, and marked bone softening and thinning is more dispersed.

The symptoms of cerebritis may range from mild to severe.

The severity of the symptoms varies based on the degree of swelling and on how elevated is the intracranial pressure. Mild symptoms include headaches, depression, anxiety and in some cases, memory loss. In some cases inflammation of brain can be seen if the brain or the nervous system is attacked as a result of problems with the immune system. The serious problems caused because of inflammation include headaches, seizures, vision problems, dizziness, behavior changes and even stroke.

Severe lupus cerebritis symptoms include psychosis, dementia, peripheral neuropathy, cerebellar ataxia (failure of muscular coordination, usually on one side of the body), and chorea (jerky, involuntary movements). Stroke incidence is 3-20% in systemic lupus patients, and is highest in the first five years of the disease. Peripheral neuropathy (carpal tunnel syndrome, for example) occurs in more than 20% of systemic lupus patients and cranial nerve palsies occur in 10-15%.

The signs and symptoms of autonomic neuropathy include the following:

- Urinary bladder conditions: bladder incontinence or urinary retention

- Gastrointestinal tract: dysphagia, abdominal pain, nausea, vomiting, malabsorption, fecal incontinence, gastroparesis, diarrhoea, constipation

- Cardiovascular system: disturbances of heart rate (tachycardia, bradycardia), orthostatic hypotension, inadequate increase of heart rate on exertion

- Respiratory system: impairments in the signals associated with regulation of breathing and gas exchange (central sleep apnea, hypopnea, bradypnea).

- Nervous system: pupillary defect, exaggerated hippus, dizziness or lightheadedness.

- Other areas: hypoglycemia unawareness, genital impotence, sweat disturbances, sicca (dryness).

Syringomyelia is a generic term referring to a disorder in which a cyst or cavity forms within the spinal cord. This cyst, called a syrinx, can expand and elongate over time, destroying the spinal cord. The damage may result in loss of pain, paralysis, weakness, and stiffness in the back, shoulders, and extremities. Syringomyelia may also cause a loss of the ability to feel extremes of hot or cold, especially in the hands. It may also lead to a cape-like bilateral loss of pain and temperature sensation along the upper chest and arms. Each patient experiences a different combination of symptoms. These symptoms typically vary depending on the extent and, often more critically, to the location of the syrinx within the spinal cord.

Syringomyelia has a prevalence estimated at 8.4 cases per 100,000 people, with symptoms usually beginning in young adulthood. Signs of the disorder tend to develop slowly, although sudden onset may occur with coughing, straining, or myelopathy.

Peripheral neuropathy may be classified according to the number and distribution of nerves affected (mononeuropathy, mononeuritis multiplex, or polyneuropathy), the type of nerve fiber predominantly affected (motor, sensory, autonomic), or the process affecting the nerves; e.g., inflammation (neuritis), compression (compression neuropathy), chemotherapy (chemotherapy-induced peripheral neuropathy).