Tag Archives: neurological level

Chronic Spinal Pain

Partial Spinal Cord Injury And Syndromes

Neurological symptoms don’t always follow a classic pattern or demonstrate a clear neurological level. For this reason, spinal cord injuries are sometimes misdiagnosed and become attributed to hysterical or conversion paralysis. Neurological symptoms indicating spinal cord injury and spinal cord syndromes should never be dismissed until spinal cord injury has been proven to not exist by means of thorough examinations and appropriate clinical investigations.

When a spinal cord injury has been confirmed through comprehensive primary and secondary hospital examinations a clinical diagnosis of spinal cord injury can be made. The diagnosis comprises of a level, completeness, and is often attributed to a type of syndrome, before a prognosis of expected long term outcomes is delivered. Given any spinal cord injury syndrome where lesions display as complete from the outset, recovery is far less likely than for incomplete lesions.

Spinal Pain

Spinal Pain

Most spinal cord injury syndromes are considered a rare disease by the United States National Institute of Health as the incidence rates for each number less than 200,000 people in the American population. In total approximately 250,000 Americans are living with some form of SCI.

At an incidence rate of 10,000/year many are classed under a syndrome. And while we do offer detailed statistics throughout this website it is important to remember spinal cord injury is about people’s lives not numbers or expectation. A full life is lived when you make the most of what you have got, not what you have lost. Where there is life there is hope and where there is a wheel there is a way.

Anterior Cord Syndrome

Damage to the anterior (front) of the spinal cord is usually caused by a compression fracture, or by a flexion-rotation force on the spine producing an anterior dislocation. There is often anterior spinal artery compression so that the corticospinal (between spinal cord and brain cortex) and spinothalamic (between spinal cord and thalamus) tracts are damaged by a combination of direct trauma and inadequate blood flow. This results in loss of power as well as reduced pain and temperature sensation below the lesion.

Brown Sequard Syndrome

The signs of Brown-Sequard syndrome are hemisection (cutting) of the spinal cord resulting from stab injuries but also common in lateral mass fractures of the vertebrae. Power is reduced or absent but pain and temperature sensation are relatively normal on the side of the injury because the spinothalamic tract crosses over to the opposite side of the cord. The uninjured side therefore has good power but reduced or absent sensation to pin prick and temperature.

Central Cord Syndrome

The most common spinal cord syndrome, an incomplete spinal cord injury is also known as, “inverse paraplegia” because the hands and arms are paralyzed while the legs and lower extremities work correctly. Typically seen in older patients with cervical spondylosis central cord syndrome is a hyperextension injury often from relatively minor trauma to the cervical regions of the spinal cord. The more centrally situated cervical tracts supplying the arms suffer the brunt of the injury resulting in a flaccid (lower motor neurone) weakness of the arms and relatively strong but spastic (upper motor neurone) leg function. Sacral sensation and bladder and bowel function are often partial. The ability to walk is regained in most cases with some residual disability.

Conus Medullaris Syndrome

Resulting from injury to the tip of the spinal cord, located at vertebra L1 the effect of injury to the sacral cord (conus medullaris) and lumbar nerve roots is usually loss of bladder, bowel and lower limb reflexes. Lesions high in the conus may occasionally represent upper motor neurone defects and function may then be preserved in the sacral reflexes, for example the bulbospongiosus and micturition reflexes.

Posterior Cord Syndrome

This syndrome is most commonly seen in hyperextension injuries with fractures of the posterior (rear) elements of the vertebrae. Contusion of the posterior columns may cause the patient to have good power, pain and temperature sensations, but poor perception of movement and spatial orientation, making walking very difficult.

Tethered Spinal Cord Syndrome

Tethered spinal cord syndrome (also known as occult spinal dysraphism) is a condition arising from an abnormally stretched spinal cord. The sensory and motor symptoms of lower back pain and leg weakness can usually be relieved by surgery that may involve the cutting of spinal cord nerve roots. Tethered spinal cord damage affecting bowel or bladder function however is typically non-treatable and permanent.


Spinal cord injuries resulting in paraplegia and quadriplegia (tetraplegia) are permanent debilitating conditions of paralysis involving much more than loss of limb function and sensation. Thorough primary and secondary hospital examinations are essential in forming an accurate early diagnosis and long term prognosis of spinal cord injury classification and outcomes.

Given the same neurological examination and findings, neurologists and physiatrists may not assign the same spinal cord injury level. For example, a patient with fractured C5 vertebrae who has normal C4 sensation and absent C5, a physiatrist may call a C4 level injury whereas a neurologist or neurosurgeon may call it C5. Most orthopedic surgeons will refer to the bony level of injury C5 as the level of injury.

Outside of clinical environments it matters little if C4 or C5. Both require use of a wheelchair for life. Many of the rights and opportunities afforded to able-bodied people are not afforded to wheelchair users with spinal cord injury.


Kind Regards
Graham Streets

Spinal Reflex Hammer

Testing Reflexes Redefining Spinal Shock

Vital information on the nervous system is gathered by testing reflexes after spinal cord injury. The path reflex neurons follow (the reflex arc) do not rely on intact nerve paths to the brain. They synapse (jump a small gap between nerve ends) in the spinal cord returning along motor nerves to quickly trigger muscles. Impulses travel along these refex arc nerves at 127 mph.

Stimulus to a reflex tendon creates an impulse that travels along sensory nerve axons (long middle section of nerve) to the spinal cord where it returns along motor nerves to trigger a muscle response, without the delay of routing signals via the brain, although (in a healthy spinal cord) the brain will receive motor (muscle) sensory feedback when the reflex arc fires.

spinal cord reflex arc

Basic Reflex Arc

There are two types of reflex arc — autonomic (affecting inner organs) and somatic (affecting muscles), — an accurate assessment of reflex arc function determines the location and severity of spinal cord injury, resulting amount of paralysis, and formulates expected long term outcomes. Testing reflexes also gives strong indications whether a spinal cord injury is incomplete or complete.

After severe spinal cord injury paralysis and limited to no sensation below the level of injury is typical, but it is rare to present no reflexes – spinal shock. Almost one third of patients examined within 1-3 hours of injury do present some reflexes. Describing spinal shock as the period following injury during which all spinal reflexes are absent is being phased out.

The evolution of reflexes over several days following spinal cord injury are now considered more relevant to prognosis than the use of the term spinal shock and the presence or absence of reflexes on the actual day of injury.

Reflexes and Corresponding Spinal Cord Nerve Supply Level

spinal cord injury reflex testing hammer with retractable pin prick

Reflex testing hammer with pin prick

  • Biceps jerk C5, C6
  • Supinator jerk C6
  • Extensor digitorum reflex C7
  • Triceps jerk C7, C8
  • Abdominal reflex T8-T12
  • Knee jerk L2-L4
  • Ankle jerk L5, S1, S2
  • Bulbospongiosus reflex S2-S4
  • Anal reflex S5
  • Plantar reflex L5-S2


Delayed Plantar Response Reflex

Delayed Plantar Response (DPR) is a reflex present in all patients with complete spinal cord injury. DPR is demonstrated by pressing a blunt instrument firmly from the heel along the lateral (outer) sole of the foot and continuing slowly across the metatarsal heads (where foot bones connect to toes). Following this stimulus the toes flex and relax in delayed sequence. Caution should be taken to not misinterpret the flexion component as a normal plantar response.

Deep Tendon Reflex

Deep tendon (stretch) reflexes provide information on the integrity of the central and peripheral nervous system. Generally, decreased reflexes indicate a peripheral problem and lively or exaggerated reflexes a central one. Deep tendon reflexes are usually absent in complete spinal cord injuries as both peripheral and central nervous systems have been compromised, and conversely are present in the majority of patients with incomplete spinal cord injuries.

Anal and Bulbospongiosus Reflex

Understanding the usefulness of sacral reflex arcs in determining the location and severity of spinal cord injury requires definition of the term bulbospongiosus. Imagine a diamond between your legs (no girls, not that kind of diamond lol), the perineum, a diamond shaped erogenous zone that includes the anus and penis or vagina.

Bulbospongiosus muscles are superficial (surface) muscles of the perineum. In males that includes the base of the penis to halfway up the penis shaft. Its function is to empty the urethra and contributes to erection, ejaculation, and the feelings of orgasm. In females, residing either side of the vagina, bulbospongiosus muscles are responsible for clenching the vagina closed and contribute to clitoral erection and the feelings of orgasm. Both anal and bulbospongiosus reflexes rely on intact sacral reflex arcs.

Anal reflex is an externally visible contraction of the anal sphincter triggered by pin prick. The bulbospongiosus reflex is a similar contraction of the anal sphincter in response to firmly squeezing the penis head or clitoris.

Testing anal and bulbospongiosus reflex arcs aid in distinguishing between upper motor neuron lesions in which the reflex may not return for several days, and lower motor neuron lesions in which the reflex remains abaited unless neurological recovery occurs.

  • Upper motor neuron lesion; injury of upper motor neurons are common because of the large amount of cortex occupied by the motor areas, and because motor pathways extend all the way from the cerebral cortex to the lower end of the spinal cord.
  • Lower motor neuron lesion; injury of lower motor neurons are less common as they are typically secondary injuries. Lower motor neurons relay the movement instructions provided by upper motor neurons, from spinal cord to the relevant muscles. When the lower motor neurons are damaged the result is muscle weakness, twitching and atrophy.


As a part of primary and secondary initial hospital assessments the testing of reflexes delivers conclusive information relevant in determining the level and completeness of a spinal cord injury. The term spinal shock is being phased out. The evolution of reflexes over several days to weeks following spinal cord injury are considered significant factors in determining long term outcomes.


chest sensation

Incomplete vs Complete Spinal Cord Injury

A key component of initial hospital examinations and treatment is the diagnosis of a spinal cord injury as incomplete or complete. Incomplete means some sensory (feeling) or motor (muscle) function exists below the neurological level of injury, including the lowest sacral segment (S4-S5). Complete means no sensory or motor function exists below the neurological level of injury, including the lowest sacral segment (S4-S5).

  • Incomplete means some
  • Complete means none

Diagnosis of a spinal cord injury as incomplete verses complete is made by locating the neurological level of injury and determining which myotomes and dermatomes remain intact. We covered this in the previous article and move on here to explore some real life examples and the long term outcomes of incomplete verses complete spinal cord injury.

It may not seem a big difference but the outcomes certainly are. To understand the broader implications of incomplete verses complete spinal cord injury we first need to consider the following real life examples. Incomplete and complete translate into being able to achieve a sustainable erection or not, having sensation in forearms or not, having wrist extension or not, to name but three examples.

While at first, the difference between some and none may seem subtle, after further consideration the full impact upon relationships, employment, health and independence become more obvious.

Real Life Examples of Incomplete vs Complete

Taking our first real life example, the inability to achieve a sustainable erection and satisfy your partner sexually is self demoralizing and can place a huge strain on an existing relationship or marriage. Impotency drastically reduces the number of potential partners interested in forming new sexual and intimate life-long relationships and greatly suppresses ones sexual self awareness, sexual development and sexual expression. Testosterone levels, impotency and virility have long been proven to have widespread influence upon the male psyche.

sexual imperfection

Sexual expression and sustainable erection following spinal cord injury

Hence, the inability to achieve a sustainable erection following spinal cord injury vastly reduces the opportunities available to men in finding a life partner, getting married, and fathering children. These undeniably huge life events are keenly sought by most men, and as such, they are possibly the greatest example of difference between an incomplete and complete spinal cord injury.

As a C4 incomplete quadriplegic I have no sensation from the nipples down or elbows out, though I feel compelled to state, I can achieve sustainable erections. I can only imagine the dent, the blow to ego and self becoming impotent a man. That said, there are many ways to sexually please a person and we advocate these throughout our website.

In our second real life example, having no forearm sensation makes it virtually impossible to determine by leaning on an object if it’s hot or cold, acidic, dirty, sharp, sticky, wet etc. Often clothing that cuts off circulation to hands goes unnoticed. Void of forearm sensation it’s impossible to estimate the weight of an object by holding it. Likewise, it’s impossible to sense when a limb is under so much pressure it’s about to break. Absolutely any area of skin or body part void of sensation is vulnerable to many forms of harm.

chest sensation

Chest sensation

As an incomplete quadriplegic I have limited forearm sensation, areas of my body void of sensation seem to have a way of eventually getting the message through. Technically I am paralyzed and void of sensation from the chest down but as I’m incomplete my legs and feet spasm frequently. I experience warm or buzzing sensations in my lower limbs in response to pain. Typically those with complete spinal cord injury do not spasm or “feel” any sensation whatsoever below the neurological level of injury.

While eating dinner one night a complete quadriplegic friend of mine realized his roast pumpkin was missing, totally unaware it had fallen onto his bare foot causing third degree burns. Had that been my foot, I most likely would have noticed a dull sensation after five minutes and/or noticed increased spasm in that leg. Being incomplete is not always good however. I once calculated my feet spasm approx 8640 times per day.

Our third real life example of wrist extension means moving the back of the hand toward the back of the forearm (upward). Wrist flexion is moving the palm of the hand toward the front of the forearm (downward). When no wrist function exists and a diagnosis of incomplete is given there is small chance of regaining some wrist extension. Usually this would occur within 3 to 12 months of injury. When no wrist function exists and a diagnosis of complete is given, change is extremely rare.

disability friendly vehicle hand controls

Disability friendly vehicle hand controls

In many countries to legally operate a vehicle on a public road requires wrist extension. When “some” wrist extension exists, bending the wrist upward automatically closes the hand and fingers, fashioning a grip sufficient enough to operate the standard hands controls of a disability friendly vehicle. The ability to drive (or not) has universal impact on employment opportunities, independence, freedom of travel, maintaining friendships, living in rural and remote areas, participation in the community, outings and social integration in general.

I have no wrist extension and cannot legally drive a car (not because my injury is incomplete). My spinal cord was damaged above the neurological section responsible for wrist extensors – C6. Having held A and C class, omnibus, motorcycle, forklift, cherry picker, scissor lift, and speedboat licenses, being active and adventurous driving is something I miss terribly.

“Losing my legs was hard to deal with but losing my hands is a real bitch.” –Graham Streets

Outomes of Incomplete vs Complete Spinal Cord Injury

professor wise young

Professor Wise Young

Professor Wise Young, Ph.D., M.D. who co-chaired the committee defining the currently accepted ASIA (American Spinal Injury Association) classification suggests many doctors today frequently become confused when determining spinal cord injury levels, the definition of complete and incomplete, and the classification of spinal cord injury.

“In the end, the whole issue of complete versus incomplete injury may be a moot issue. The absence of motor and sensory function below the injury site does not necessarily mean that there are no axons that cross the injury site. Many clinicians equate a complete spinal cord injury with the lack of axons crossing the injury site. However, much animal and clinical data suggest that an animal or person with no function below the injury site can recover some function when the spinal cord is reperfused (in the case of an arteriovenous malformation causing ischemia to the cord), decompressed (in the case of a spinal cord that is chronically compressed), or treated with a drug such as 4-aminopyridine. The labeling of a person as being complete or incomplete, in my opinion, should not be used to deny a person hope or therapy.” —Professor Wise Young, Ph.D., M.D.

I agree, my GP admitted he knew about spinal cord injury in general but would assist in finding a local spinal injuries specialist with concise knowledge and experience if I wish. I see specialists annually so kept my GP who has been brilliant in learning with me the intricacies of quadriplegia and spinal cord injury.

Incomplete or complete many of the challenges in life after spinal cord injury are being met through advances in medicine, assistive devices and education. Research and studies highlight the need of improved therapies and treatments for spinal cord injury. Technology such as computers and disability schemes are broadening employment opportunities after spinal cord injury. Laws for wheelchair friendly buildings and environments are increasingly becoming legislated. And greater sexual awareness and rights for wheelchair users are being established globally.


Spinal cord injury is a life changing event. Stem cell research and advances in medicine are narrowing the differences between incomplete verses complete spinal cord injury. Still, the differences are significant and should be considered on an individual and whole basis. A diagnosis of complete is not absolute, some will regain function. A complete spinal cord injury does not mean an incomplete life. Emphasis is best placed on life after diagnosis rather than the diagnosis itself.

People with complete spinal cord injury may not be able to achieve a sustainable erection but many enjoy healthy active sexual relationships. Many are getting married and fathering children. Many are furthering their education and gaining meaningful employment. Incomplete verses complete spinal cord injury does not affect a person’s ability to love, respect, achieve and live a full satisfying life.


SCI Info Pages; http://www.sci-info-pages.com/levels.html

Dermatomes are areas of the skin

Neurological Examination and Assessment

During spinal cord injury primary and secondary examinations neurological examinations are carried out to assess the severity and location of damage to the spinal cord. These examinations aim to provide information on the neurological level of spinal cord injury, extent of injury to the spinal cord, and the resulting degree of impairment. Performed upon initial hospitalization and repeated periodically during rehabilitation, the collated results assist in determining how much support may be required upon discharge from hospital. For initial assessment purposes a typical neurological examination where spinal cord injury is suspected will include the following tests;

  • Cranial nerve function: There are 12 cranial nerves which are nerves that originate in the head, coming off the brain and brain stem. The examination of these nerves and their functions is complex but includes areas such as smell, vision and eye movements, facial sensation, reflexes and movement, hearing, taste, tongue and palate movements and even movements of the head, neck and shoulders.
  • Power of muscle groups according to the Medical Research Council scale: This part of the examination tests the motor function, or movement, of the major muscle groups, most notably in the shoulders, arms, hips and legs. The muscles are tested for mass, muscle tone, and strength.
  • Reflexes including abdominal, anal, and bulbospongiosus: Various reflexes are tested throughout the body. While these can indicate problems with sensation and/or motor function, they can also reveal other aspects of nervous system dysfunction as well.
  • Sensation to pin prick, fine touch and joint position sense: The sensory exam part of the neurological exam evaluates the sensation of the patient. This includes not just normal touch but also pain and temperature and sensation of limb position and movement.

Detailed neurological examinations may include CAT, IVP and MRI scans, a cerebral angiogram, electroencephalogram, electromyogram, and nerve conduction study.

Myotomes and Dermatomes

Dermatomes are regions of the skin

Dermatomes – last region of skin with healthy sensation indicates neurological level of injury

Each myotome (muscle) and dermatome (region of skin) of the body is supplied by a particular level or section of the spinal cord and by its corresponding spinal nerve. There are eight cervical nerves, twelve thoracic nerves, five lumbar nerves and five sacral nerves. Each of these nerves relays sensation (including pain) from a particular muscle or region of skin to the brain. By examining the dermatomes and myotomes this way, a motor score, level and completeness of a spinal cord injury can be determined.

According to the American Spinal Injury Association (ASIA) standard neurological classification guide the last dermatome or region of skin with healthy intact sensation displaying normal spinal cord function is considered the neurological level of injury. This does not necessarily correspond with the vertebral (spinal column bone or disc) level of injury. Therefore both neurological and vertebral diagnoses are recorded. Additionally while the following muscles grades are not included in determining the ASIA motor score and level they should still be assessed and noted.

  • Diaphragm – C3,4,5
  • Shoulder abductors – C5
  • Supinators/pronators – C6
  • Wrist flexors – C7
  • Finger extensors – C7
  • Intrinsic hand muscles – T1
  • Hip adductors – L2,3
  • Knee flexors – L4,5 S1
  • Toe flexors – S1, S2

Neurological Level of Spinal Cord Injury

A significant proportion, 55% of cases admitted to spinal units involve the cervical segments C1-C7. This type of impairment is referred to as tetraplegia (or quadriplegia). Injury at the thoracic, lumbar or sacral levels, are referred to as paraplegia. In Australia over the past eight years cervical spine injuries have accounted for between 50% and 59% of all SCI. The most common cervical spine injuries involved C4-C5. This group accounted for 61% of cervical SCI cases and 32% of all 241 documented neurological injuries reported in 2007-08.

Neurological levels of spinal cord injury

Neurological levels recorded for 241 spinal cord injury patients

The next most common neurologic level of spinal cord injury is the thoraco-lumbar junction with 11% of cases reporting neurological impairment at T12-L1. Injuries to the thoracic spine accounted for 32% of all injuries reported. The number of thoracic spinal injuries ranged between 64 in 2003-04 to a high of 93 in 2004-05 in Australia. Reports from 2000 to 2010 show an annual average of 31% of all SCI occurred at the thoracic levels T1-T12. Lumbar and sacral injuries make up the remaining cases.

Neurological Category of Spinal Cord Injury

The overall severity of spinal cord injury is measured by a combination of the neurological level of injury (tetraplegia or paraplegia) and extent of injury (complete or incomplete). These are divided into five neurological categories;

  • Complete Tetraplegia
  • Incomplete Tetraplegia
  • Complete Paraplegia
  • Incomplete Paraplegia
  • Complete Recovery

Approximately 65% of all spinal cord injury cases are diagnosed as incomplete injuries. In 2007-08 a study group of 241 Australian patients with permanent spinal cord injury were diagnosed under the following categories;

  • Incomplete Tetraplegia 38%
  • Incomplete Paraplegia 27%
  • Complete Paraplegia 20%
  • Complete Tetraplegia 15%

This distribution of neurological injury is relatively consistent from year to year. Similar results have been found in Europe although a slightly different model appears in the United States where reports show greater proportions of complete SCI cases, mostly attributed to a higher proportion of penetrating gunshot injuries.

Spinal Cord Injury Explained

Injury to the spinal cord can be caused by acute (sudden) or chronic (developing) trauma as well as medical conditions. Frequent causes of chronic compression injuries are herniated disks and primary or secondary tumors. Compromised blood perfusion, the delivery of nutritive arterial blood to capillary bed, as in anterior spinal cord syndrome can also be severely detrimental to spinal cord function. However the most damaging Spinal Cord Injury is one of acute trauma resulting in permanent paralysis.


Traumatic spinal cord injury have been classified into five categories by the American Spinal Injury Association and the International Spinal Cord Injury Classification System:


    Spinal cord injury where no motor or sensory function remains in the sacral segments S4-S5.


    Spinal cord injury sensory but not motor function remains below the neurological level and includes the sacral segments S4-S5. Typically a transient phase and if the person recovers any motor function below the neurological level, they’are considered motor incomplete and classified C or D.


    Spinal cord injury where motor function remains 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.


    Spinal cord injury where motor function exists 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 – NORMAL

    Where motor and sensory scores are normal. It is possible to have spinal cord injury and neurological deficits with completely normal motor and sensory scores.


The annual incidence rate of spinal cord injury varies from country to country, ranging from 15 to 71 per million (/m). In 2008 the incidence of spinal cord injury in the United Kingdom around 13 /m, Australia 14 /m, Canadi 35 /m, China 65 /m and the United States 35 /m per year. This suggests around 40 per million or 52,000 spinal injuries occur every year globally.   

Of the 12,000 new cases of paraplegia and quadriplegia that occur in the United States each year 4,000 patients die before reaching hospital. Causes of acute spinal cord injury include motor vehicle accidents, work-related accidents, recreational accidents, falls and violence (shootings and stab wounds).   

Paralysis occurs our times as often in males as females where about 60% of victims are under 30 years of age and 5% under 13 years of age (the pediatric age group). Falls from a height greater than their own is the largest cause of spinal trauma amongst the pediatric age group. A long-term outcome study of patients aged 25 to 34 who had suffered acute traumatic SCI before the pediatric age showed an employment rate of 54% while the employment rate in the general population for the same age group was 84%.   

Limitation or complete loss of the capability to achieve economic independence following SCI combined with additional medical costs causes severe economic hardship for many living with paralysis and their immediate family. Further limitations to living a full social life are architectural barriers, buildings only accessible by stairs and a lack of ramps on sidewalks for example.   

Increased awareness through education has played a key role in resolving these barriers and those created by negative or overprotective attitudes of healthy, non-injured people toward persons with spinal cord injury. When persons with spinal cord injury cannot fully participate society suffers. Not only are ethical standards, artistic and financial contributions to society lost, huge expenses for specialised lifelong care are incurred.   

80% of SCI occur in people under the age of 30. The average life-time cost of thoracic paraplegia is $1.25 million and high level cervical quadriplegia such as those on ventilators $25 million USD. In 1990 the cost for acute and long term care of surviving spinal cord injury victims was estimated at $4 billion in the United States alone.   


Road traffic accidents 45%   

  • Motorcycle 20%
  • Car, van, coach, truck 16%
  • Bicycle 6%
  • Pedestrian 2%
  • Aircraft, helicopter 1%

Domestic and industrial accidents 34%   

  • Domestic: falls from stairs, trees, ladders, roofs etc. 22%
  • Industrial: work falls from scaffolding, ladders, crush etc. 12%

Sporting injuries 15%   

  • General:?gymnastics, motocross, skiing, etc, 7%
  • Diving into shallow water 4%
  • Horse riding 3%
  • Rugby 1%

Self harm and criminal assault 6%   

  • Self harm 5%
  • Criminal assault 1%


Ancient Egyptian Edwin Smith Papyrus
Ancient Egyptian Edwin Smith Papyrus

The first known description of acute spinal cord trauma and resulting neurological deficits was in the Edwin Smith papyrus which is believed to be more than 3,500 years old. In this ancient Egyptian document Smith accurately described the clinical symptoms and traumatic effects of quadriplegia (tetraplegia) “an ailment not to be treated.” An indication of the feelings helplessness medical practitioners suffered at the time, a doctor’s value measured by the extent of cure achieved.  

No strategies ensuring longterm survival for patients with spinal cord injury existed. A view which prevailed well into the early 1900’s. In the First World War the mortality rate for those with a spinal cord injury was 95%, mainly attributed to urinary sepsis and complications from pressure sores. Less than 1% survived for more than twenty years.  

During World War II the number of casualties from spinal cord injuries both military and civilian increased dramatically in Europe. Specialized hospital units known as “peripheral nerve centers” developed between the wars in Germany and the United States demonstrating the advantages of concentrating special needs patients under specialized care. Great importance was placed on the unique opportunities offered by these specialized units. Gaining new insight in the natural course of the disease and further development of new therapeutic strategies.  

Building on those experiences, specialized spinal cord injury units started opening throughout England in the 1940s. Mortality rates from a spinal cord injury were recorded at 35% in the 1960s. Today nearly every capital city operates an acute care spinal unit.  

Sir Ludwig Guttmann
Sir Ludwig Guttmann

Dr. Ludwig Guttmann and his colleagues at the Spinal Cord Unit of Stoke Mandeville Hospital developed new treatment approaches including frequent repositioning of paralyzed patients to avoid developing bedsores, a potential source of sepsis and intermittent sterile catheterization to prevent urinary sepsis. The success in patient survival was dramatic enough to require development of completely new strategies for social reintegration of patients with spinal cord injury. Adapted workplaces and wheelchair accessible housing championed in the 1940s and 1950s by the English Red Cross has today become an integral component in the framework of social politics in most industrialized countries. Respiratory complications are now the leading cause of death in patients admitted with SCI. Secondary are heart disease, septicemia (blood poisoning), pulmonary emboli (blood clot in lungs), suicide, and unintentional injuries.  


Paralympic Games Wheelchair Athletes
Paralympic Games Wheelchair Athletes

Dr. Guttmann and his colleagues viewed physical rehabilitation as the basis of social reintegration both physically and psychologically. Supporting the idea of athletic competition in disciplines adequate and adapted to the physical capacity of their patients. Starting with two teams a competition in 1948 paralleling the Olympic Games in England, the idea of competitive sports for the paralyzed developed rapidly.  

In 1960 the first Paralympic Games were held in Rome. The Paralympic games were held in the same year as the Olympic Games for the able-bodied using the same facilities, a tradition that has been followed ever since. The idea of competitive sports was extended to include people with a multitude of physical handicaps other than spinal cord injury emerging as the Paralympics we know today.  


In many countries initiatives have risen at communal and national levels with the intent to decrease the incidence of spinal cord trauma and offer support and advice to both those with spinal cord injuries and their families. Many generously offer financial support for scientific and clinical research.  

The prevention oriented “Think First” initiative, Canadian-based CORD and Wheels in Motion, the Christopher Reeve Paralysis Foundation, the U.K. Spinal Cord Trust, and the Paralyzed Veterans of America all maintain informative web sites with valuable information on the subject of spinal cord injury.  

Although the overall incidence of SCI has not noticeably decreased the severity of injuries has deceased overall. Fewer now suffer complete injuries and survival rates have increased. This is mostly attributed to improvements in prehospital care including widespread instruction of first aid principles as well as the introduction of spinal cord immobilization and administration of advanced medicines during rescue and transport. Increased public awareness of risk factors leading to head trauma and spinal cord injury, the introduction of mandatory use of safety belts and installation of air bags in modern vehicles has also served to decrease trauma severity.  


Stem Cells Neuron Chain
Stem Cells Neuron Chain

Until recently research suggested once spinal cord trauma had occurred nothing could be done to alter the natural course of developing pathology, that damage to the central nervous system was permanent and repair impossible. At the beginning of the twenty-first century this belief came to change in the minds of scientists, clinicians, patients and their families. Research laboratories around the world adopted two new approaches:  

1. Prevention of secondary injury and repair of manifest damage. The term secondary injury describes the observation that central nervous system structures that survived the primary mechanical trauma die at a later point in time due to deterioration of the milieu (nerve ending sheath) at the site of injury.  

2. The amount and severity of secondary injury damage can be significantly larger than that of the primary injury. Researchers focused on identification of substances and therapeutic methods that help minimize secondary injury effects. In the field of cell biology, isolation and manipulation of specific cell types is being undertaken in effort to induce certain cell types, including stem cells and olfactory ensheathing cells to help repair damaged central nervous system structures.  

Clinical research continues to improve outcomes for those with a spinal cord injury, such as stimulators for bladder control, orthopedic correctional procedures and physical mobilization. Integration of biomedical research like pattern generators, mechanics and kinetics of movement with the latest developments in computer science and engineering has given rise to neuronal networks. Neuroprostheses are being developed which enable paraplegics to move about and walk.  


  • Gary L. Albrecht. 2006. Encyclopedia of Disability. University of Illinois, Chicago.
  • Go, B. K., Michel J. DeVivo, and Scott J. Richards. 1995.  The Epidemiology of Spinal Cord Injury. Clinical Outcomes from the Model Systems, edited by Samuel L. Stover, Joel DeLisa, and Gale G. Whiteneck. Gaithersburg, MD: Aspen.
  • Sekhon, Lali H. S. and Michael G. Fehlings. 2001.  Epidemiology, Demographics, and Pathophysiology of Acute Spinal Cord Injury.
  • Stripling, Thomas E. 1990.  The Cost of Economic Consequences of Traumatic Spinal Cord Injury.  Paraplegia News.
  • Vogel, Lawrence C., L. J. Klaas, John P. Lubicky, and C. J. Anderson. 1998. Long-term outcomes and life satisfaction of adults who had pediatric spinal cord injuries. Archives of Physical Medicine & Rehabilitation.


Autonomic Dysreflexia – Hyperreflexia

When a strong sensory impulse is sent via the spinal cord to the brain it envokes a massive sympathetic reflex and hypertension. Blood pressure rises often resulting in chronic headaches, blurred vision, blotchy skin and sweating. Also known as hyperreflexia, autonomic dysreflexia is a potentially life threatening condition usually affecting individuals with spinal cord injury from a lesion at or above the T6 neurological level. Common amongst quadriplegics early recognition of symptoms and treament can avoid the associated dangers of elevated blood pressure, brain hemorrhage, burst blood vessels, stroke and fitting. If you suffer from autonomic dysreflexia it’s important to educate family, carers and medical professionals about the syndrome and its management.

Epidemiology Of Autonomic Dysreflexia

Dysreflexic Headache

Dysreflexia causes chronic headaches

Below the level of spinal cord injury intact peripheral sensory nerves transmit impulses that ascend in the spinothalamic and posterior columns to stimulate sympathetic neurons located in the intermediolateral gray matter of the spinal cord. A sympathetic production of various neurotransmitters (norepinephrine, dopamine-b-hydroxylase, dopamine) from cerebral vasomotor centres increases but typically are unable to pass below the level of spinal cord injury. Vasoconstriction (narrowing) in arterial vasculature below the SCI and vasodilation (widening) of pain sensitive intracranial vessels above the SCI occurs creating severe headaches.

Vasomotor brainstem reflexes attempt to lower blood pressure by increasing parasympathetic stimulation to the heart through the vagus nerve to cause compensatory bradycardia. This reflex action cannot compensate for severe vasoconstriction, explained by the Poiseuille formula where pressure in a tube is affected to the fourth power by change in radius (vasoconstriction) and only linearly by change in flow rate (bradycardia). Parasympathetic nerves may also prevail above the level of injury which may be characterized by profuse sweating. Vasodilation may also display as blotchy skin, blurred vision and so on. Once the inciting stimulus is removed, reflex hypertension (hyperreflexia) resolves.

Autonomic Dysreflexia In Plain English

When a person with a spinal cord injury (lesion) at or above T6 such as a quadriplegic or tetraplegic breaks their leg the pain messages sent to the brain which usually have you on the ground screaming get mixed up and lost. I often explain it as cutting through a telephone cable with 100,000 wires in it, twist one side 90 degrees and press them back together. Not much chance your call will get through and if it does it will probably be a wrong number.

Finding the source of dysreflexia

Finding the source of dysreflexia

Two years ago I broke my Tibia (shinbone) clean in half and fractured Fibula (thinner one behind it). Broken leg pain messages reached my damaged spinal cord area near C4 and couldn’t go any further. I only knew it was broken because it went off like a firecracker, snap! The message “this hurts” from my leg got transposed at the damaged section C4 of my spinal cord into let’s raise his blood pressure. I developed a mild headache and later a little sweating — autonomic dysreflexia.

An average blood pressure for people with a T6 spinal injury is commonly 90-100/60 when lying and lower when sitting. A BP of 130/90 is considered slightly high and if untreated it can rapidly rise to extreme dangerous levels like 220/140. I myself with C4 quadriplegia once hit 220/160 due to a blocked catheter. I displayed all the classic symptoms. Luckily once layed on a bed the blockage released filling a 2 litre drainage bag in a matter of minutes. I gained instant relief. You would think a badly broken leg would have been worse, but not in my case. Not everyone with a T6 or higher level of spinal cord injury experiences autonomic dysreflexia and the severity will vary per person but in all cases where it does occur it warrants immediate attention.

Common Autonomic Dysreflexia Symptoms

  • Blotchy red, rash like, flushing skin
  • Blurred vision
  • Headache
  • High blood pressure

Possible Autonomic Dysreflexia Symptoms

  • A sudden significant rise in systolic and diastolic blood pressures (usually associated with bradycardia). The normal systolic blood pressure for SCI above T6 is 90-100mm Hg
  • Difficulty breathing
  • Dizzyness
  • Goose bumps above or below the level of the spinal cord injury
  • Nasal congestion
  • Profuse sweating above the level of lesion especially in the face neck and shoulders may be noted but rarely occurs below the level of spinal cord injury because of sympathetic cholinergic activity
  • Spots may appear in the persons visual fields

Occassionaly no symptoms are observed besides elevated blood pressure. Dysreflexic episodes can be triggered by many things though painful, strong irritating stimulus below the level of the spinal cord injury are most frequently the cause of an autonomic dysreflexic reaction.

Causes Of Autonomic Dysreflexia

  • Appendicitis or other abdominal pathology trauma
  • Bladder distension
  • Blisters
  • Blocked catheter
  • Bowel distension
  • Bowel impaction
  • Broken bones fractures or other trauma
  • Burns or sunburn
  • Constrictive clothing shoes or appliances
  • Contact with hard or sharp objects
  • Cystoscopy
  • Deep vein thrombosis (blood clot in vien or artery)
  • Detrusor-sphincter dyssynergia
  • Ejaculation
  • Epididymitis or scrotal compression
  • Gall, bladder or kidney stones
  • Gastric ulcers or gastritis
  • Gastrocolic irritation
  • Hemorrhoids
  • Heterotopic bone
  • Ingrown toenail
  • Insect bites
  • Invasive testing
  • Menstruation
  • Pain
  • Pregnancy, especially labor and delivery
  • Pressure sores or ulcers
  • Pulmonary embolism (blood clot in lungs)
  • Sexual intercourse
  • Sudden temperature changes
  • Surgical or diagnostic procedures
  • Testicular compression
  • Urinary tract infection
  • Urodynamics
  • Vaginitis

It is easier to assist a dysreflexic person when two carers are present, one can monitor blood pressure while the other provides treatment, but this may not always be possible. The person with a spinal cord injury is usually aware of dysreflexia and will often be able to suggest possible causes. In any case it is important that the symptoms are relieved quickly and their BP lowered. Treat all episodes of autonomic dysreflexia as a medical emergency but stay calm and avoid leaving the person alone.

Initial Treatments For Autonomic Dysreflexia

  • Ask if they have just taken a drug to control autonomic dysreflexia
  • Ask the individual and carer if they suspect a cause
  • Elevate the head and lower legs if possible (this will help lower BP until a cause is identified)
  • Loosen any constrictive clothing
  • Check bladder drainage equipment for kinks or other causes of obstruction to flow such as catheter blockage, leg bag problems or an overfull leg bag
  • Monitor BP every 2-5 minutes
  • Avoid pressing?on the bladder

Further Treatments Of Autonomic Dysreflexia

If the person has an Indwelling Catheter or Supra Pubic Catheter:

  • Empty urinary drainage devivce and determine whether or not the bladder is empty, ask if volume is reasonable considering fluid intake and output earlier that day
  • If the catheter is blocked, irrigate GENTLY with no more than 30 mls of sterile water. Drain the bladder slowly, 500 ml initially and 250 ml each 15 minutes afterwards to avoid a sudden drop in blood pressure
  • If this is unsuccessful recatheterize using a generous amount of lubricant containing a local anaesthetic e.g. 2% lignocaine (Xylocaine) jelly
  • Where constipation is suspected check the rectum for faecal loading
  • If the rectum is full check the blood pressure before attempting manual evacuation
  • Gently insert a generous amount of lignocaine jelly into the rectum and gently remove the faecal mass – note: if symptoms are aggravated stop immediately and seek an alternate method of evacuation such as supositories or laxettes

If elevated blood pressure does not start to fall within one or two (1-2) minutes of the above proceedures and the cause cannot be determined treatment with a short-acting anti-hypertensive medication should be commenced concurrently with the search for and treatment of the cause. The blood pressure threshold at which medication should be given may vary a little depending on the individual and type of intervention being undertaken. In general if a systolic blood pressure greater than 170mm prevails consider use of a blood pressure lowering medication.

Glyceryl Trinitrate 

NB: DO NOT use glyceryl trinitrate if sildenafil (Viagra), or vardenafil (Levitra) has been taken in the previous 24 hours or tadalafil (Cialis) in the previous 4 days. Give one spray of glyceryl trinitrate (Nitrolingual Pumpspray) under the tongue. During administration the canister should be held upright and the spray should not be inhaled.

OR: Place a glyceryl trinitrate tablet (Anginine) under the tongue.

OR: Apply 5mg, transdermal patch to chest and upper arms according to manufacturer’s instructions. Remove patch once BP settles or if the BP drops too low.

A hypotensive response (lower blood pressure) should begin within 2 to 3 minutes and last up to 30 minutes. A second spray/tablet may be given in 5 -10 minutes if the reduction in the blood pressure is inadequate or if the blood pressure rises again. If glyceryl trinitrate is not available or unsuitable (e.g. within 24 hours of sildenafil use) give one 10 mg nifedipine tablet (not a slow-release tablet) crushed, mixed with water and swallowed. Avoid sildenafil (Viagra), vardenafil (Levitra) and tadalafil (Cialis) for at least 48 hours after a severe episode of autonomic dysreflexia.

Botox Trials On Autonomic Dysreflexia

A Taiwanese study recently indicated that for patients with Spinal Cord Injury who have detrusor sphincter dyssynergia, using a combination of fluoroscopy and electromyography to localize the external urethral sphincter with a Foley catheter employed to visualize vesicourethral anatomy, makes transperineal injection of botulinum toxin (botox) type A into the external urethral sphincter safe accurate and easy to perform. Such injections have been shown to reduce the occurrence and severity of autonomic dysreflexia as well as vesicoureteral reflux, hydronephrosis, and urinary tract infection.

Kind Regards
Graham Streets
MSC Founder


  • Autonomic Dysreflexia in Spinal Cord Injury : Treatment & Medication by Denise I Campagnolo. Barrow Neurology Clinics. St Joseph’s Hospital and Medical Center. Investigator for Barrow Neurology Clinics.
  • Director NARCOMS Project for Consortium of MS Centers.