Autonomic Dysreflexia

Autonomic Dysreflexia, also known as Hyperreflexia, is a potentially life threatening condition which can be considered a medical emergency requiring immediate attention. It occurs where the blood pressure in a person with a spinal cord injury (SCI) above T5-6 becomes excessively high due to the over activity of the Autonomic Nervous System.

The most common symptoms of autonomic dysreflexia are sweating, pounding headache, tingling sensation on the face and neck, blotchy skin around the neck and goose bumps.

Not all the symptoms always appear at once, and their severity may vary. In untreated and extreme cases of autonomic dysreflexia, it can lead to a stroke and death.

Mechanism of Autonomic Dysreflexia

Autonomic Dysreflexia is usually caused when a painful stimulus occurs below the level of spinal cord injury. The stimulus is then mediated through the Central Nervous System (CNS) and the Peripheral Nervous System (PNS).

The CNS is made up of the spinal cord and brain, which control voluntary acts and end organs via their respective nerves. The PNS is made up from 12 pairs of cranial nerves, spinal nerves and peripheral nerves. The PNS also is divided into the somatic nervous system and the autonomic nervous system. The autonomic nervous system is responsible for the signs and symptoms of autonomic

 

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dysreflexia. The autonomic nervous system normally maintains body homeostasis via its two branches, the parasympathetic autonomic nervous system (PANS) and the sympathetic autonomic nervous system (SANS). These branches have complementary roles through a negative-feedback system; that is, when one branch is stimulated, the other branch is suppressed.

The SANS is associated with the flight-or-fight response, causing dilation of the pupils, increased heart rate, vasoconstriction, decreased peristalsis and tone of the gut, release of epinephrine and norepinephrine, as well as other effects. The effects of PANS stimulation are the opposite of the SANS; for the most part, these are constriction of the pupil, decreased heart rate, as well as increased peristalsis and tone of the gut.

The PANS and SANS exit at different sites in the CNS. The PANS exits via the midbrain, pons, medulla (cranial nerves [CN] III, VII, IX, and X), and the sacral level of the spinal cord. The SANS exits via the thoracic and lumbar segments of the spinal cord. There is a major sympathetic output (called the splanchnic outflow) between T5 and L2.

In someone with a high-level spinal cord injury, intact lower motor neurons sense the painful stimuli below the level of injury and transmit the message up the spinal cord (see diagram). At the level of the spinal cord injury, the pain signal is interrupted and prevented from being transmitted to the cerebral cortex. The site of the spinal cord injury also interrupts the two branches of the autonomic nervous system and disconnects the feedback loop, causing the two branches to function independently.

The ascending information reaches the major splanchnic sympathetic outflow (T5-T6) and stimulates a sympathetic response. The sympathetic response causes vasoconstriction, resulting in hypertension, pounding headache, visual changes, anxiety, pallor, and goose bumps below the level of injury. This hypertension stimulates the baroreceptors in the carotid sinuses and aortic arch. The PANS is unable to counteract these effects through the injured spinal cord, however. Instead, the PANS attempts to maintain homeostasis by slowing down the heart rate. The brainstem stimulates the heart, through the vagus nerve, causing bradycardia and vasodilation above the level of injury. The PANS impulses are unable to descend past the lesion, and therefore no changes occur below the level of injury.

Causes of Autonomic Dysreflexia

There can be many stimuli that cause autonomic dysreflexia. Anything that would have been painful, uncomfortable, or physically irritating before the injury may cause autonomic dysreflexia after the injury.

The most common cause seems to be overfilling of the bladder. This could be due to a blockage in the urinary drainage device, bladder infection (cystitis), inadequate bladder emptying, bladder spasms, or possibly stones in the bladder.

The second most common cause is a bowel that is full of stool or gas. Any stimulus to the rectum, such as digital stimulation, can trigger a reaction, leading to autonomic dysreflexia.

In 85% of cases autonomic dysreflexia is related to either bladder distention or bowel impaction (Teasell et al. 2000; Mathias & Frankel 2002).

Other causes include skin irritations, wounds, pressure sores, burns, broken bones, pregnancy, ingrown toenails, appendicitis, and other medical complications.

In general, noxious stimuli (irritants, things which would ordinarily cause pain) to areas of body below the level of spinal injury. Things to consider include:

Bladder (most common)Overstretch or irritation of bladder wall Urinary tract infectionUrinary retentionBlocked catheterOverfilled collection bagBladder stonesNoncompliance with intermittent catheterisation program

BowelOver distention or irritation Constipation / impactionDistention during bowel program (digital stimulation)Haemorrhoids or anal fissuresInfection or irritation (eg. appendicitis)

Skin-related DisordersAny direct irritant below the level of injury (eg. - prolonged pressure by object in shoe or wheelchair, cut, bruise, abrasion)Pressure sores (decubitus ulcer)Ingrown toenailsBurns (eg. - sunburn, burns from using hot water)Tight or restrictive clothing or pressure to skin from sitting on wrinkled clothing

Sexual ActivityOver stimulation during sexual activity [stimuli to the pelvic region which would ordinarily be painful if sensation were present]Menstrual crampsLabour and delivery

OtherHeterotopic ossification ("Myositis ossificans", "Heterotopic bone")Acute abdominal conditions (gastric ulcer, colitis, peritonitis)Skeletal fractures

Functional Electrical Stimulation (FES)

There have been reports of autonomic dysreflexia resulting in headaches in individuals undertaking functional electrical stimulation. Caution should be exercised in the use of functional electrical stimulation by people with a spinal cord injury with lesion levels above the major splanchnic outflow (T6).

If an autonomic headache is experienced whilst undertaking functional electrical stimulation, the program should be halted, which in most cases will result in the cessation of autonomic dysreflexia. If a muscle tear or fracture has occurred, then the headaches may continue after stimulation has ceased. Generally, individuals with osteoporosis, severe spasticity, contractures and pressure sores may experience autonomic dysreflexia symptoms whilst using functional electrical stimulation. In some cases autonomic dysreflexia is causes by the electrical current passing through, and activating the muscles.

If any of the above sources of pain are found, they must be addressed in order for Autonomic Dysreflexia to be relieved.

Function of the Urinary System

The body's urinary system processes and removes a type of waste product from the bloodstream called urea. Urea is a compound produced when foods containing protein, such as meat, poultry, and certain vegetables, are broken down in the body, and is removed from the blood with water to form urine in the kidneys.

After the urine has been filtered from the blood in the kidneys, it travels down two narrow tubes called ureters to be stored in the bladder. The ureters are about 16 to 25 cm long. Tiny muscles in the ureter walls constantly contract and relax to push urine downward from the kidneys. Every 10 to 15 seconds, small amounts of urine are deposited in the bladder from the ureters, ready for urination.

The bladder is a hollow muscular, and distensible (or elastic) organ shaped like

a balloon. The bladder is positioned in your pelvis and is held in place by ligaments

attached to other organs and the pelvic bones. The bladder stores urine until you are ready to go to the bathroom to empty it in a process called urination through the urethra. The urethra is a tube which connects the urinary bladder to the outside of the body, and has an excretory function in both sexes. The bladder swells into a round shape when it is full and gets smaller when empty.

Circular muscles around the urethra called sphincters act as a valve and help keep urine from leaking from the bladder. The sphincter muscles close tightly like a rubber band around the opening of the bladder into the urethra, the tube that allows urine to pass outside the body.

At a certain point during the bladder filling from the ureters, the internal pressure within the bladder becomes powerful enough to activate stretch receptors in the bladder wall. When these stretch receptors signal a message to the nervous system, small contractile waves occur in the detrusor muscle, and the internal urethral sphincter automatically relaxes and becomes funnel shaped. The external sphincter must now be consciously tightened, and the urge to urinate becomes very apparent. To urinate, a person must relax the external sphincter and contract the detrusor muscle to empty the bladder.

When you feel it is time to urinate, your brain sends signals to the bladder muscles to tighten more, forcing urine out of the bladder. In a joint action, the brain also signals the sphincter muscles in the urethra to relax. As the sphincter muscles relax, urine exits the bladder through the urethra. When all the signals occur in the correct order, normal urination occurs.

Function of the Bowel System

When we eat or drink, the food and fluids that are swallowed enter the stomach, where enzymes begin to break down the contents for digestion. The stomach can expand to hold between 2-4 litres of food. It is a temporary food storage area, and in the process of digestion, the food goes into the stomach first before entering the small bowel (small intestine).

The bowel is the lower part of the digestive tract, and its' role is to digest the food and fluids that we eat and drink, absorb the nutrients, and then to process and expel the waste products that the body cannot use.

The bowel is made up of two sections, the small bowel (small intestine) and the large bowel (large intestine).

The small bowel receives food from the stomach, which has been broken down by acids and enzymes secreted by the stomach lining. The small bowel then removes nutrients from the broken down food, and passes the nutrients into the bloodstream to be processed by the liver.

From the small bowel, the waste food is then passed into the large bowel, where fluid is absorbed for use by the body. As the waste moves around the large bowel, it gradually forms into stools.

The waste products (stools or faeces), are then stored in the left hand side of the large bowel until they are emptied from the body at a convenient time, by means of a bowel movement. A bowel movement happens when the rectum, which is the last section of the bowel is full.

As the rectum fills with stool it expands, and this triggers stretch receptors in the wall of the bowel to send messages to other parts of the body. One message triggers muscles to move the stool down through the bowel. Another message lets you know it is time to go to the bathroom, by sending a message to your brain via the spinal cord, and controls the muscle at the opening of the rectum (anus). This muscle called the anal sphincter, and allows you to control when the waste (stool) leaves the body. This is often called a bowel movement or BM.

The digestive process starts at the mouth and is completed at the anus.

Spasticity Following a Spinal Cord Injury

Following a spinal cord injury the nerve cells below the level of injury become disconnected from the brain at the level of injury. This is due to scar tissue which forms in the structure of the damaged area of the spinal cord, blocking messages from below the level of injury reaching the brain. Spasticity does not occur immediately following a spinal cord injury. When an injury occurs to the

spinal cord the body goes into spinal shock, which may last several weeks. During this time changes take place to the nerve cells which control muscle activity.

Once spinal shock wears off, the natural reflex which is present in everyone reappears. Spasticity is an exaggeration of the normal reflexes that occur when the body is stimulated in certain ways. In an abled bodied person, a stimulus to the skin is sensed, and a sensory signal is sent to the reflex arch where it travels to the brain via the spinal cord, the brain then assesses the stimulant, and if the stimulant is thought not to be dangerous, an inhibitory signal is sent down the spinal cord, and cancels the reflex from moving the muscle.

In a person with a spinal cord injury this inhibitory signal is blocked by the structural damage in the cord, and the natural reflex is allowed to continue resulting in a contraction of the muscle.

Triggering of Spasticity

Muscle spasms can occur in a person with a spinal cord injury any time the body is stimulated below the level of injury. This is usually noticeable when a muscle is stretched, or there is a painful stimulant below the level of injury. Because of the injury to the spinal cord, these sensations can trigger the reflex resulting in the muscle to contract or spasm.

Almost anything can trigger spasticity. Some things, however, can make spasticity more of a problem. A bladder infection or kidney infection will often cause spasticity to increase a great deal. A skin breakdown will also increase spasms. In a person who does not perform regular range of motion exercises, muscles and joints become less flexible and almost any minor stimulation can cause severe spasticity.

Some spasticity may always be present. The best way to manage or reduce excessive spasms is to perform a daily range of motion exercise program. Avoiding situations such as bladder infections, skin breakdowns, or injuries to the feet and legs may also help to control spasticity. There are four primary medications used to treat spasticity, baclofen, diazepam (Valium), dantrolene (Dantrium) and tizanidine (zanaflex). All have some side effects and do not completely eliminate spasticity.

Benefits of Spasticity

There are some benefits to spasticity. It can serve as a warning mechanism to identify pain or problems in areas where there is no sensation. Many people know when a urinary tract infection is coming on by the increase in muscle spasms. Spasticity is also an advantage to help maintain muscle size and bone strength. It does not replace walking, but it does help to some degree in preventing osteoporosis. Spasticity helps maintain circulation in the legs and can be used to improve certain functional activities such as performing transfers or walking with braces. For these reasons, treatment is usually started only when spasticity interferes with sleep or limits an individual's functional capacity.

Surgical Intervention of Spasticity

A surgical procedure called a radiofrequency rhizotomy is sometimes indicated in the treatment of severe spasticity. Another treatment of severe Spasticity is the implantation of a Baclofen Pump. The pump delivers a programmable amount of baclofen directly to the fluid surrounding the spinal cord. The drug inhibits the reflex signal in the reflex arch of the cord and therefore inhibiting muscle spasm. Because the drug is delivered directly to the spinal cord, a very small amount can be used in comparison to a large amount which may have to be taken orally. Once a baclofen pump is implanted, oral anti spasmodic drugs are usually stopped.

Spinal Shock Overview

Spinal shock following a spinal cord injury is a specific term that relates to the loss of all neurological activity below the level of injury. This loss of neurological activity include loss of motor, sensory, reflex and autonomic function. Spinal shock is a short term temporary physiologic disorganisation of spinal cord function that can start between 30-60 minutes following a spinal cord injury. Spinal shock can last up to six weeks post injury.

Mechanism for Spinal Shock

The mechanism for spinal shock involves the sudden loss of conduction in the spinal cord as a result of the migration of potassium ions from the intracellular to extracellular spaces. This is associated with a

transient loss of somatic and automatic reflex activity below the level of spinal cord segment damage. The spinal cord reflex arcs that are immediately above the injury may also be severely disrupted.

Early Stages of Spinal Shock

Spinal shock following a spinal cord injury results in flaccid paralysis, areflexia and anaesthesia below the level of injury. The return of the reflexes indicates the end of spinal shock. Assessment of the end of spinal shock is based on the return of reflexes, with the bulbocavernosus reflex typically being the first to return. However, some clinicians may classify the end of spinal shock as the return of deep tendon reflexes or the return of reflexive detrusor function, which may be months after injury.

Return of Reflexes Following Spinal Shock

Return of reflexes between 1-12 months post injury are characterised by hyper-reflexia, or abnormally strong reflexes usually produced with minimal stimulation. Inter neurons and lower motor neurons below the SCI begin sprouting, attempting to re-establish synapses. The first synapses to form are from shorter axons, usually from inter neurons - later changes are soma-mediated, and will take longer for the soma to transport various growth factors, including proteins, to the end of the axon.

Autonomic Effects of Spinal Shock

In spinal cord injuries in the thoracic spinal segments of T6 and above, autonomic dysreflexia may occur, from the loss of autonomic innervation from the brain. Sacral parasympathetics (S2-S4) are lost, as are many sympathetic levels, depending on the level of the spinal cord injury. Cervical lesions cause total loss of sympathetic innervation and lead to vasovagal hypotension and bradyarrythmias – which resolve in 3–6 weeks. Autonomic dysreflexia is permanent, and occurs with the return of reflexes. Autonomic dysreflexia is characterised by unchecked sympathetic stimulation below the SCI (from a loss of cranial regulation), leading to often extreme hypertension, loss of bladder/bowel control, sweating, headaches, and other sympathetic effects.

Historical Documentation of Spinal Shock

Spinal shock was first defined by Whytt in 1750 as a loss of sensation accompanied by motor paralysis with initial loss but gradual recovery of reflexes, following a spinal cord injury – most often a complete transection.

Spinal Cord Injury Pressure Sores

Pressure sores must be taken seriously, if left unchecked, a pressure sore can lead to amputation or in the worst case death. Even when well cared for, a pressure sore can still become infected such as was the case with Christopher Reeve in October 2004. Christopher had the best care and was looked after by dedicated staff at Northern Westchester Hospital, but still his sore became severely infected, resulting in a serious

systemic infection. This in turn led to a heart attack and coma from which he did not recover. Check yourself for red marks and sores daily, it should be a routine which is as second nature as brushing your teeth.

Causes of Pressure Sores

A pressure sore, also known as a bed sore, is an injury to the skin and the tissue under it. A pressure sore develops when the blood supplying the tissue with oxygen and nutrients is cut off, and the tissue no longer receiving oxygen and nutrients dies. The oxygen and nutrients are essential to maintain healthy tissue. Sitting in the same position for a prolonged period of time can start the process of tissue breakdown.

People who smoke are also at an increased risk of developing a pressure sore due to reduced blood flow to the skin. Those who are overweight or diabetic are also at increased risk.

Prevention of Pressure Sores

If you have been paralyzed, you may not feel a pressure sore developing, therefore it is essential to change your position on regular intervals to allow the circulation of blood throughout pressured areas. Normally in an able bodied person, if you are uncomfortable in your seating position, messages from nerves in the skin will be sent via your spinal cord to the brain to indicate discomfort. However in a person with a spinal cord injury, these messages are blocked at the level of injury, and the disabled person may not even be aware at the level of potential damage the skin is in.

Types of Pressure Sore

Pressure sores are also be referred to as pressure ulcers or decubitus ulcers. The damage from a pressure sore will range from slight discoloration of the skin (stage 1) to open sores that go all the way to the bone (severe). The affected area may feel warmer than the surrounding tissue. In light-skinned people, the discoloration may appear as dark purple or red. In darker-skinned people, the discoloration will appear darker than the surrounding tissue.

Stage One Pressure Sore

How to recognise: Skin is not broken but is red or discolored. The redness or change in color does not fade within 30 minutes after pressure is removed. The hardness or firmness (with an edge you can feel) is called induration and is one of the most common signs of a

stage I pressure ulcer.

NEVER massage over a pressure ulcer like this. It will increase the damage and can cause it to progress to an open (stage II or deeper) pressure ulcer.

Stage Two Pressure SoreHow to recognise: The epidermis or topmost layer of the skin is broken, creating a shallow open sore. Drainage may or may not be present.

Stage Three Pressure Sore How to recognise: The break in the skin extends through the dermis (second skin layer) into the subcutaneous and fat tissue. The wound is deeper than in Stage Two.

Stage Four Pressure Sore How to recognise: The breakdown extends into the muscle and can extend as far down as the bone. Usually lots of dead tissue and drainage are present.

If the skin is at stage 1, the red area can be healed by keeping the pressure off the affected area. If the sore does not heal in a few days or recurs, consult your health care provider.

If the skin is thought to be at stages 2 - 3, you should consult your health care provider for further treatment.

Diagnosis of Incomplete Spinal Cord Injuries

In order to

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diagnose someone for an incomplete spinal cord injury, a thorough neurological examination must be performed upon admission to the hospital, and re-evaluated on an on-going basis months after spinal shock and inflammation of the spinal cord has subsided.

Incomplete spinal cord injuries can present themselves in a multitude of ways. It only takes several nerve fibres within the spinal cord to be preserved to carry messages to or from the brain, for an individual to be classified as an incomplete spinal cord injury resulting in incomplete paraplegia or incomplete tetraplegia.

If after an initial neurological examination of an individual with a spinal cord injury, the diagnosis is determined to be incomplete with preservation of motor or sensory function, the chances of recovery are greatly increased. Incomplete spinal cord injuries can present themselves in three general ways:

The damage to the spinal cord can be so mild that the muscle weakness or sensory impairment can be hardly noticeable.

The damage to the spinal cord can be so severe that the muscle or sensory weakness or loss can resemble that of a complete injury.

The symptom of the incomplete spinal cord injury can be somewhere between the two above examples.

Incomplete Spinal Cord Injury Classification

Incomplete spinal cord injuries are classified using the American Spinal Association (ASIA) Impairment scale. The examination to determine the ASIA classification is based on touch and pinprick sensations, tested at key dermatome levels. Motor (muscle) function is also tested at 10 key points on each side of the body. The resultant evaluation is categorised into five different classifications of spinal cord injury.

A indicates a "complete" spinal cord injury where no motor or sensory function is preserved in the sacral segments S4-S5.

B indicates an "incomplete" spinal cord injury where sensory but not motor function is preserved below the neurological level and includes the sacral segments S4-S5. This is typically a transient phase and if the person recovers any motor function below the neurological level, that person essentially becomes a motor incomplete, i.e. ASIA C or D.

C indicates an "incomplete" spinal cord injury where motor function is preserved below the neurological level and more than half of key muscles below the neurological level have a muscle grade of less than 3, which indicates active movement with full range of motion against gravity.

D indicates an "incomplete" spinal cord injury where motor function is preserved below the neurological level and at least half of the key muscles below the neurological level have a muscle grade of 3 or more.

E indicates "normal" where motor and sensory scores are normal. Note that it is possible to have spinal cord injury and neurological deficits with completely normal motor and sensory scores.

Incomplete Spinal Cord Injury Statistics Upon Discharge From Hospital

At the time of discharge neurologically incomplete tetraplegia ranked first for level of injury at time of discharge (30.9%), followed by neurologically complete paraplegia (25.1%),neurologically complete tetraplegia (19.8%), and neurologically incomplete paraplegia (18.6%). Source: 2011 NSCISC Annual Statistical Report.

The degree of incompleteness is unique from person to person, and may or may not be an indicator to full recovery from a spinal cord injury.

Types of Incomplete Spinal Cord Injury

The symptoms of incomplete spinal cord lesions depend upon the area of the spinal cord (front, back, side, etc) damaged. The part of the cord affected depends on the direction and power of the forces involved during the initial injury.

Causes of Paraplegia

Paraplegia due to a spinal cord injury results in an impairment in motor or sensory function of the lower half of a person's body. The condition occurs due to damage to the cellular structure of the spinal cord within the spinal canal. The area of the spinal cord which is affected in paraplegia is either the thoracic, lumbar, or sacral regions of the spinal column. If the arms are also affected by paralysis, quadriplegia/tetraplegia is the correct terminology.

Symptoms of Paraplegia

Injury to the spinal cord at the thoracic level and below result in paraplegia, with the arms and hands not affected. People with injuries to the spinal cord segments T-1 to T-8 usually retain control of the arms and hands but have poor trunk control and balance due

Note: The cervical spinal nerves exit the vertebrae above the cervical vertebrae, except for C7, where the C8 spinal nerve exits below the C7

vertebrae.

All spinal nerves then exit below the thoracic, lumbar and sacral

vertebrae.

to the lack of abdominal muscle control. Lower thoracic injuries (T-9 to T-12) retain good truck control and good abdominal muscle control. The sitting balance of people with lower spinal cord injuries is usually very good. Lumbar and Sacral injuries result in decreased control of the hip flexors and legs.

Spinal Nerves and Levels

Each part of the body is supplied by a particular level or segment of the spinal cord and its corresponding spinal nerve. Function below the level of spinal cord injury will be either lost or impaired

This is approximately the same for every person:

Function of the spinal nerves in the cervical section of the spinal cord are usually unaffected by paraplegia and remain fully functional in a paraplegic individual.

C3,4 and 5 Supply the diaphragm (mostly C4) (the large muscle between the chest and the belly that we use to breath).

C5 also supplies the shoulder muscles (deltoid) and the muscle that we use to bend our elbow (bicep).

C6 Bends the wrist back (extension), and externally rotates the arm (supinates).

C7 Straightens the elbow and wrist (triceps and wrist extensors); pronates wrist.

C8 Bends the fingers (flexion).

Function of the spinal nerves below the cervical sections of the spinal cord are usually impaired due to damage in either the thoracic, lumbar or sacral areas, resulting in paraplegia.

T1 Spreads the fingers and supplies small muscles of the hand.

T1 –T12 supplies the chest wall (intercostal muscles) and abdominal muscles.

T10 - L2 Psychogenic erections (thought controlled).

L2 Bends the hip.

L1, L2, L3, L4 Thigh flexion.

L2, L3, L4 Extension of leg at the knee (quadriceps femoris)

L2, L3, L4 Thigh adduction.

L4, L5, S1 Thigh abduction.

L4, L5, S1 Dorsiflexion of foot (tibialis anterior).

L4, L5, S1 Extension of toes.

L4, L5, S1, S2 Flexion of leg at the knee (hamstrings).

L5, S1, S2 Extension of leg at the hip (gluteus maximus).

L5, S1, S2 Plantar flexion of foot.

L5, S1, S2 Flexion of toes.

S2, S3, S4 Control a man's ability to have a reflex erection.

S2, S3, S4 Ejaculation is generated by the bulbospongiosus muscle under the control of a spinal reflex via the pudendal nerve.

S3,4 and 5 supply the bladder, bowel and sex organs and the anal and other pelvic muscles.

Secondary Medical Complications

As a result of the decreased loss of feeling or function in the lower extremities, paraplegics can be susceptible to a number of secondary medical complications. These include pressure sores (decubitus), thrombosis, low blood pressure, autonomic dysreflexia and pneumonia. Dysfunction of the bowel and bladder will usually also occur. Sexual functioning is frequently impaired or lost with SCI. Men may have their fertility affected, while a women's fertility is generally not affected. Physiotherapy and various assistive technology, such as a standing frame, as well as vigilant self observation and care may aid in helping to prevent future and mitigate existing complications.

As paraplegia is most often the result of a traumatic injury to the spinal cord tissue and the resulting inflammation, other nerve related complications can and do occur. Cases of chronic nerve pain in the areas surrounding the point of injury are not uncommon. There is speculation that the "phantom pains" experienced by individuals suffering from paralysis could be a direct result of these collateral nerve injuries misinterpreted by the brain.

ASIA impairment scale

Spinal cord injuries are classified 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

A Complete no motor or sensory function is preserved in the sacral segments S4–

S5.

BIncomplete

sensory but not motor function is preserved below the neurological level and includes the sacral segments S4–S5.

CIncomplete

Incomplete: motor function is preserved below the neurological level, and more than half of key muscles below the neurological level have a muscle grade less than 3.

DIncomplete

Incomplete: motor function is preserved below the neurological level, and at least half of key muscles below the neurological level have a muscle grade of 3 or more.

E Normal

Causes of Quadriplegia

Quadriplegia is caused by damage to the cervical spinal cord segments at levels C1-C8. Damage to the spinal cord is usually secondary to an injury to the spinal vertebrae in the cervical section of the spinal column. The injury to the structure of the spinal cord is known as a lesion and may result in the loss of partial or total function in all four limbs, meaning the arms and the legs.

Typical causes of quadriplegia from damage to the spinal cord are trauma (such as car crash, fall or sports injury), disease (such as transverse myelitis or polio) or congenital disorders, such as muscular dystrophy. It is possible to injure the spinal cord without fracturing the spine, such as when a ruptured disc or bony spur on the vertebra protrudes into the spinal column.

The condition quadriplegia is also termed tetraplegia. Both terms mean "paralysis of four limbs"; tetraplegia is more commonly used in Europe than in the United States. In 1991, when the American Spinal Cord Injury Classification system was revised, it was recommended that the term tetraplegia be used to improve consistency ("tetra", like "plegia", has a Greek root, whereas "quadra" has a Latin root).

Symptoms of Quadriplegia

Upon visual inspection of a quadriplegic patient, the first symptom of quadriplegia is impairment to the arms and legs. Function is also impaired in the torso. The loss of

Note: The cervical spinal nerves exit the vertebrae above the cervical vertebrae, except for C7, where the C8 spinal nerve exits below the C7

vertebrae.

All spinal nerves then exit below the thoracic, lumbar and sacral

vertebrae.

function in the torso usually results in a loss or impairment in controlling the 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 sore burning neuropathic pain.

Quadriplegia is defined in different ways depending on the level of injury to the spinal cord. C1–C4 usually affects arm sensation and movement more so than a C5–C7 injury; however, all quadriplegics have or have had some kind of finger dysfunction.

A person with damage to the spinal cord at the cervical spinal cord segment C1 (the highest cervical vertebra, at the base of the skull) will probably lose function from the neck down and require permanent assistance with breathing in the form of a machine called a ventilator. A person with a C8 spinal cord injury may lose function from the chest down, but still retain use of the arms and much of the hands.

The degree of the injury to the cellular structures of the spinal cord is very important. A complete severing of the spinal cord will result in complete loss of function from that spinal segment down. A partial severing or even bruising or swelling of the spinal cord results in varying degrees of mixed function and paralysis. A common misconception with quadriplegia is that the victim cannot move legs, arms or control any of the major bodily functions; this is often not the case. Some quadriplegic individuals can walk and use their hands as though they did not have a spinal cord injury, while others may use wheelchairs although they may still have function in their arms and mild finger movement, this is dependent on the degree of damage done to the spinal cord.

Spinal Nerves and Levels

The body is supplied by a particular level or segment of the spinal cord and its corresponding spinal nerve. Function below the level of spinal cord injury will be either lost or impaired

This is approximately the same for every person:

Quadriplegia will result in complete loss or impaired function below the following cervical levels of injury.

C3,4 and 5 Supply the diaphragm (mostly C4) (the large muscle between the chest and the belly that we use to breath).

C5 also supplies the shoulder muscles (deltoid) and the muscle that we use to bend our elbow (bicep).

C6 Bends the wrist back (extension), and externally rotates the arm (supinates).

C7 Straightens the elbow and wrist (triceps and wrist extensors); pronates wrist.

C8 Bends the fingers (flexion).

Injury below the spinal segments supplying the following spinal nerves will result in paraplegia. All the functions below will be lost or impaired in a quadriplegic injury.

T1 Spreads the fingers and supplies small muscles of the hand.

T1 –T12 supplies the chest wall (intercostal muscles) and abdominal muscles.

T10 - L2 Psychogenic erections (thought controlled).

L2 Bends the hip.

L1, L2, L3, L4 Thigh flexion.

L2, L3, L4 Extension of leg at the knee (quadriceps femoris)

L2, L3, L4 Thigh adduction.

L4, L5, S1 Thigh abduction.

L4, L5, S1 Dorsiflexion of foot (tibialis anterior).

L4, L5, S1 Extension of toes.

L4, L5, S1, S2 Flexion of leg at the knee (hamstrings).

L5, S1, S2 Extension of leg at the hip (gluteus maximus).

L5, S1, S2 Plantar flexion of foot.

L5, S1, S2 Flexion of toes.

S2, S3, S4 Control a man's ability to have a reflex erection.

S2, S3, S4 Ejaculation is generated by the bulbospongiosus muscle under the control of a spinal reflex via the pudendal nerve.

S3,4 and 5 supply the bladder, bowel and sex organs and the anal and other pelvic muscles.

Secondary Complications of Quadriplegia

Secondarily, because of a quadriplegic's depressed functioning and immobility, they are often more susceptible to pressure sores, spasticity, osteoporosis and fractures, frozen

joints, pneumonia, respiratory complications and infections, kidney stones, autonomic dysreflexia, deep vein thrombosis, and cardiovascular disease.

ASIA impairment scale

Spinal cord injuries are classified 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

A Completeno motor or sensory function is preserved in the sacral segments S4–S5.

BIncomplete

sensory but not motor function is preserved below the neurological level and includes the sacral segments S4–S5.

CIncomplete

Incomplete: motor function is preserved below the neurological level, and more than half of key muscles below the neurological level have a muscle grade less than 3.

DIncomplete

Incomplete: motor function is preserved below the neurological level, and at least half of key muscles below the neurological level have a muscle grade of 3 or more.

E Normal