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Paralysis / Spinal Cord Introduction


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Anatomically, the spine, or vertebral column, is comprised of vertebral bodies separated by intervertebral discs and supported by many ligaments. The vertebral column is divided into cervical, thoracic, lumbar, sacral and coccygeal regions. There are seven cervical, twelve thoracic, five lumbar, five fused sacral and four fused coccygeal vertebrae. Structurally, a typical vertebra is comprised of an anterior portion called the vertebral body and a posterior portion called the neural arch. The neural arch consists of a pair of anterolateral pedicles, a pair of posterolateral laminae, four articular processes, two transverse processes and one spinous process. The bony portion of the spine provides structural integrity to the entire vertebral column.

The spinal cord is encased in supporting structures that protect its fragile, gelatinous nature. These supporting structures include bone and ligaments. Although there are eight ligaments that help to maintain spinal stability, the most important supporting structures are the anterior longitudinal ligament, the posterior longitudinal ligament and the intervertebral discs. When there are insignificant or no bony fractures in a spinal injury, the stability of the vertebral column lies with the integrity of the ligaments.

The bony vertebral column and the supporting ligaments determine the amount of motion that is possible in the spine. In the cervical spine, there is greater range of lateral flexion and rotation than in any other portion of the spinal column. Maximum bending in flexion and extension occurs between C4 and C6. The thoracic region is less flexible but more stable than the cervical region because of the limitations provided by the rib cage. The lower thoracic and lumbar spine has the capability to resist an imposed load (stiffness) secondary to the design of the facet joints in these areas.

SPINAL CORD INJURIES

Traumatic spinal cord injuries are associated with skeletal and ligamentous as well as intraspinal pathology. The most common cervical level for spinal cord injury is C5, followed by C6 and then C4. T12 is the most common thoracic level for spinal cord injury.

Traumatic spinal cord injuries are most commonly secondary to motor vehicle accidents and gunshot wounds, followed by falls, bicycle accidents, and pedestrian verses auto accidents. Fractures, dislocations, bleeding and swelling can precipitate trauma to the cord. A common misnomer is that the cord is "transected" when injured; however, the spinal cord is rarely physically transected. It may be stated that the cord is "physiologically transected" as it loses it's supply of oxygen and glucose as a result of traumatized blood vessels that supply that level of the cord, inducing inflammation and irreversible damage to the central neurons.

Depending on the type of skeletal and intraspinal pathology sustained in a spinal cord injury, an associated neurologic picture will result. This neurologic picture is based on the organization that is present in the spinal cord where motor, sensory and autonomic nerve tracts run systematically from the periphery to the brain. In the majority of traumatic spinal cord injuries, there is skeletal as well as ligamentous damage associated with spinal instability, which necessitates surgical intervention such as fusion. However, there are cases such as gun shot wounds, where mere shock waves can induce enough trauma to the cord to produce swelling and hemorrhage, leaving the vertebral column intact but resulting in a complete lesion.

SCI CLASSIFICATION

The classification for spinal cord injury is based upon the initial neurologic examination. The term "tetraplegia" has replaced "quadriplegia," and refers to injury to the cervical region of the spinal cord. The term "paraplegia" refers to injury to the spinal cord in the thoracic, lumbar, and sacral segments.

The spinal cord "level of injury" is named for the last preserved or normal level of motor and sensory function. Therefore, with a C5 quadriplegia, the motor and sensory nerves are intact down to the C5 level; C6 and below are affected. Spinal cord injuries can either be complete or incomplete in nature. Complete injuries are defined as having no detectable motor or sensory findings below the level of injury and abnormal autonomic function. Incomplete injuries have some preserved motor, sensory or autonomic function below the level of injury.

The American Spinal Injury Association has defined the ASIA IMPAIRMENT SCALE for spinal cord injury. This taxonomy supersedes the previously well used Frankel Classification system.

  1. = Complete: No motor or sensory function is preserved in the sacral segments S4-S5.
  2. = Incomplete: Sensory but not motor function is preserved below the neurologic level and extends through the sacral segmentsS4-S5.
  3. = Incomplete: Motor function is preserved below the neurologic level and the majority of key muscles below the neurological level have a muscle grade of less than 3.
  4. = Incomplete: Motor function is preserved below the neurologic level and the majority of key muscles below the neurological level have a muscle grade greater than or equal to 3.
  5. = Normal: Motor and sensory function is normal.

The ASIA Classification is divided into complete and incomplete injuries and utilizes the nomenclature A, B, C, and D. A patient with ASIA A has more neurologic deficits than a person with ASIA D. Keep in mind that the more neurologic function preserved, the more potential a patient has regarding activities of daily living and mobility. Therefore, a patient with a C6 ASIA Classification of D has potential for a more functional lifestyle than one with a C6 ASIA Classification of A. In spinal cord injury rehabilitation, long and short-term goals are established based upon the patient's neurologic level and degree of preserved function below the level of injury.

Key Muscles for Determining the Level of Lesion are as follows:

C5 Elbow flexors (biceps flexes forearm)
C6 Wrist Extensors (cock-up wrist)
C7 Elbow Extensors (triceps straightens elbow)
C8 Finger flexors (flex fingers to grip)
T1 Small finger abductors (spreads fingers)
L2 Hip Flexors (flexes hip)
L3 Knee Extensors (quadriceps straightens knee)
L4 Ankle dorsiflexors (bends ankle up and lifts foot)
L5 Long toes extensors (lifts big toe)
S1 Ankle plantarflexors (calf muscles push foot down)

The following Clinical Syndromes of Spinal Cord Injury are recognized:

Central Cord Syndrome
A lesion, occurring almost exclusively in the cervical region, that produces sacral sparing and greater weakness in the upper limbs than in the lower limbs.

Brown-Sequard Syndrome
A lesion that produces rather greater ipsilateral (same-sided) proprioceptive and motor loss and contralateral (other side) loss of sensitivity to pin and temperature.

Anterior Cord Syndrome
A lesion that produces variable loss of motor function and of sensitivity to pin and temperature, while preserving proprioception.

Conus Medullaris Syndrome
Injury of the sacral cord (conus) and lumbar nerve roots within the neural canal that usually results in areflexic (reflex loss) bladder, bowel and lower limbs. Sacral segments may occasionally show preserved reflexes (bulbocavernosus and micturition reflexes).

Cauda Equina Syndrome
Injury to the lumbosacral nerve roots within the neural canal resulting in areflexic bladder, bowel and lower limbs.

ACUTE MANAGEMENT

The emergency medical care system is the patient's point of entry into the medical care system. The goal during this period is for the SCI patient is to immobilize the spine to prevent further damage to the spinal cord prior to reaching the emergency room. Maintenance of an adequate airway, cardiopulmonary resuscitation, and fluid management are required to ensure survival and limit secondary damage.

The acute management of traumatic spinal cord injury is unique and requires specialized medical training. Among the issues addressed are spinal stabilization, pulmonary rehabilitation, gastrointestinal and urinary function, hemodynamics and thermodynamics. Although this discussion will focus on these medical issues, it should be remembered that SCI is associated with psychosocial adjustment, and oftentimes substance abuse withdrawal and head injury.

In acute spinal cord injury, it is considered standard of care to implement high doses of intravenous (IV) steroids (methylprednisolone), which has been scientifically shown to decrease the swelling in the spinal cord after a traumatic insult. The protocol is administered within the first eight hours of the injury and is completed within 24 hours. There has been no documented medical benefit supporting the administration of methylprednisolone after the initial eight-hour period. In spinal cord injury research and development, there are nerve regenerating medications as well as surgeries that are being investigated throughout the country. Most notable is the Gm-1 Ganglioside (Sygen). The intended purpose of this medication is to improve the patient's neurologic function when administered within 72 hours of injury. The results of the multi-center investigation are slated to be available February 1998.

As stated above, spinal cord injury is most often associated with skeletal instability. This can occur at the cervical, thoracic or lumbar level. Patients are optimally managed in a rotokinetic bed, but may be "log-rolled" by trained staff every two hours. The rotokinetic bed acts as a body cast to stabilize the spine until surgical fusion. Cervical injuries, in addition, usually require weighted traction via a halo ring or tongs. After cervical fusion, depending on the type of surgical stabilization, continued external immobilization via a halo vest or a cervical orthotic (Philadelphia collar) is required for a period of time defined by the surgeon. Although spinal stabilization is necessary to correct fractures and dislocations, it must be remembered that it rarely improves the neurologic function of the patient. In the majority of cases, therefore, the neurologic level that the patient has at the time of injury is the level of function that the patient has to work with during rehabilitation and live with for a lifetime.

In the acute trauma setting, patients with spinal cord injury are routinely hypotensive. This is manifest by low blood pressure that is most often corrected by intravenous fluids. However, this type of hypotension is a result of neurogenic shock or "spinal shock," which is secondary to autonomic nervous system dysfunction. Until the patient is determined to be spinal cord injured, high volumes of IV fluids are introduced which puts the patient at a hemodynamic disadvantage, and places the respiratory status at risk for pulmonary edema. Once the patient is known to be spinal cord injured above the level of T9, IV fluids are gingerly administered and the pulmonary status must be monitored very closely. Blood gases are ordered. The patient typically receives oxygen via nasal canula and begins respiratory therapy exercises. There is a low threshold for intubation especially in patients with cervical injury and a history of smoking or asthma. In the acute spinal cord setting, the two most common causes of death are infection and respiratory complications. The patient's pulmonary status is aggressively monitored and treated.

In addition to neurogenic shock, other organ systems also slow down. An ileus develops (bowel functions slows or ceases) in the gastrointestinal system, and the risk for associated stress gastritis is present. The patient is treated with bowel rest and IV administration of an H2 blocker. Occasionally, with severe gastritis, blood transfusions are necessary. The bladder is also affected by these autonomic changes, becoming hypotonic and non-contractile. Treatment is with indwelling (Foley) catheterization.

Finally, during spinal shock, patients have difficulty maintaining a stable core body temperature. They tend to take on the room temperature; if it is hot, they are hot, and conversely if it is cold, they will be cold. Patients commonly arrive at the acute care setting with hypothermia or hyperthermia, and must be managed by someone skilled in the rehabilitation of acute spinal cord injury.

Preventing pressure sores is an ongoing challenge during the acute care phase. In the supine position, the back of the head, the sacrum and heels are at particularly risk. Special mattresses are available as well as seating cushions. While in bed, a regular turning schedule is emphasized. Non-blanching erythema (redness) is considered a grade I ulcer and a precursor to skin ulceration.

Joint contractures should be prevented by frequent range of motion and orthotics may be needed as well. The individual in bed with a spinal cord injury is at significant risk for a deep venous thrombosis and prophylaxis (up to twelve weeks) should be started early with a short-acting anti-coagulant (such as low molecular weight heparin) which can be supplemented with support stocking and intermittent compression boots.

SCI REHABILITATION

In a comprehensive rehabilitation facility, interdisciplinary intervention begins as soon as the patient is medically stable enough to tolerate therapy. This may be as soon as the day following injury. In fact, the sooner therapies begin, the better chance there is of preventing SCI complications such as the formation of joint contractures. The Rehabilitation Team should be meeting two to three times per week to facilitate progress in the patient's short and long-term goals, modifying them appropriately as the medical status dictates. An example of this is an associated head injury where the cognitive signs may not become apparent until therapies ensue, necessitating drastic changes in anticipated long-term goals.

During rehabilitation, the patient learns the fundamentals of spinal cord injury with the ultimate goal of being as independent as the neurologic level and ASIA Classification allow. Discharge planning, mobility, self care, cognition, bowel and bladder, durable medical equipment, education, vocational retraining, adjustment to disability and family training are among the areas addressed during aninpatient stay.

LEVEL OF INJURY MOBILITY ADL’S
C1, C2, C3, C4 power wheelchair (chin drive or sip-n-puff) dependent transfers dependent for all careadapted computer use
C5 power wheelchair (arm
drive) assisted sliding board transfers
self-feed after set up, light
hygienewrites with equipment
C6 manual and/or power chairsliding board transfers above plus: 25% dressing modified weight shifts
C7 manual chair transfers w/o sliding board above plus: 50% dressing depression weight shifts
C8 same as above (has finger function) independent with all ADL’s
T1-T6 same as above independent with all ADL’s
T7 - T11 same as above with better
trunk control
independent with all ADL’s
T12 and below same as above may potentially ambulate independent with all ADL’s

It is apparent that the more function a patient has, the more independent he or she may be. The neurologic level generally dictates the potential functional capability of the injured person for rehabilitation. Breathing with or without assistance is no exception. A C1, C2, or C3 complete (ASIA A) tetraplegic will be ventilator dependent. C1 and C2 tetraplegics have the potential for the surgical implantation of phrenic nerve pacemakers so that they may breathe without a ventilator attached to the tracheotomy. Otherwise healthy patients with a C4 injury or below can be weaned completely from the ventilator. A C3 complete tetraplegic like Christopher Reeves may breathe for short periods off the ventilator and talk using a special "talking" trach. Functional expectations similarly apply to mobility and self care. The following table represents general capabilities of an ASIA A tetraplegic with the stated level of injury. Some patients may do more and some less depending on many factors including age, motivation, premorbid health, home environment, and associated diagnoses such as head injury or depression.

Independence and privacy are significant issues in the self-care activity of bowel and bladder management. Learning how to manage these functions of elimination is a complex and sensitive task. Oftentimes a family member, such as a spouse or mother, must perform the care because the patient does not have enough function to master it independently. The neurogenic bladder is optimally managed with intermittent catheterization via the clean technique approximately every 4-5 hours. This requires a clean (but not necessarily sterile) urinary catheter and lubricant. Although debated, another preferred method of management of the male bladder is a sphincterotomy and condom catheter. The choice between the two is usually physician-specific. The next best way to care for the bladder is with a suprapubic catheter, followed by an indwelling urethral catheter. It is important to note that any indwelling catheter increases the risk of urinary tract infection, and it is still unclear as to whether prophylactic antibiotics are beneficial. In a neurogenic bowel, the gastrointestinal tract functions normally until the fecal matter reaches the descending colon, where peristalsis essentially stops. For evacuation to occur, a scheduled bowel program is performed. It consists of oral and rectal medications plus digital stimulation. Again, someone often must perform this personal activity other than the patient, as it requires adequate hand (finger) function.

With spinal cord injury being so complex, many complications are possible in the short and long term. In the acute medical setting, after the resolution of spinal shock, autonomic dysreflexia (or hyperreflexia) may occur and is considered a medical emergency. Most physicians do not know what this problem is or how to treat it; therefore, patients and families should not leave the hospital without thoroughly understanding how to recognize the symptoms of dysreflexia and what to do about it. In patients with lesions above T9, the dysfunctional autonomic nervous system can induce dangerously high blood pressures when a noxious stimulus affects the body below the level of injury. This stimulus is most frequently a distended bladder, but may be a urinary tract infection, full bowel, new decubitus ulcer, ingrown toenail, or even sunburn. The symptoms of autonomic dysreflexia are severe headache, flushing of the face, sweating above the level of injury, post nasal drip, anxiety...signs that the sympathetic nervous system has been hyper-activated. Blood pressures of 200/100 may develop in patients whose pressures are normally 90/60 now that they have a spinal injury. The consequences of untreated, ongoing dysreflexia may be devastating leading to stroke, coma, seizure or death. The treatment of this SCI-related phenomenon focuses on safely lowering the blood pressure and removing the initial noxious stimulus. Patients should carry cards or medals that will identify the syndrome and outline appropriate medical intervention.

Another complication of SCI is the development of decubitus ulcers that may occur at any time in the person's life. The more severe (large and deep) the sore is, the more at risk for a complication such as superimposed infection. The consequences of a severe decubitus may be as radical as amputation or death, and the costs incurred are potentially staggering. Although treatment may require bed rest, dressing changes, or flap surgery, prevention is the best way to deal with pressure sores which is why frequent pressure relief via weight shifts is imperative.

Less devastating but equally important complications of spinal cord injury are spasticity, contractures, and heterotopic ossification. Spasticity is considered a normal part of SCI as it is a manifestation of an injury to the central nervous system. The management pyramid stretches from range of motion and medications to baclofen pumps and the surgical release of tendons. Joint contractures may develop as a result of severe spasticity and are not only disfiguring but can diminish the amount of function (and therefore independence) a person has. Heterotopic ossification is the development of bone across a joint, leading to less range and therefore less function. It may cause a once adequate wheelchair to become non-useful, as the person cannot sit properly or activate the arm drive. It most commonly occurs in the hips and knees, but can also be seen in the shoulders and elbows. There is no known reason as to why heterotopic ossification develops in one patient and not another, and treatment with oral medications such as NSAIDs or etidronate are controversial and often not effective. Research is ongoing for successful early intervention. In the meantime, aggressive range of motion is useful in its early stages of development.

Rehabilitation is a lifelong process for the person with a spinal cord injury. Formal training may continue from the inpatient setting to outpatient and home as appropriate. It takes months of learning and practice for a patient to physically manage paralysis; yet it often takes much longer to emotionally accept his or her life as a disabled person. The transition from inpatient to outpatient or home and from home to community-based services should therefore be well coordinated via case management to ensure the most successful outcome possible.

HOPE FOR THE FUTURE

Generally, the earlier recovery begins and the more rapid its progress, the better the prognosis. In scientific studies, most recovery occurs during the first six months, and may continue up to two years post injury. Patients with incomplete spinal cord injury lesions have a better chance of recovery than those with complete lesions.

Research and development for "fixing severed spinal cords" has been ongoing for decades. Allocation of funds for this disorder, however, is scarce when compared to more common maladies such as coronary artery disease. Since the unfortunate accident of Christopher Reeves that rendered him a ventilator-dependent tetraplegic, SCI has entered into the limelight and more money has been donated from the private sector. It is therefore hoped that within the next few decades a breakthrough for SCI may be established. It is the dream of many individuals that complete paralysis of acute SCI may be prevented and chronically injured persons may regain motor function.

In the meantime, because of medical advances in early and appropriate intervention in acute SCI, patients are living longer and experiencing more related complications as a result. The medical cost may be considerable as the SCI patient may live many years post injury. Experience shows that the more comprehensive the initial education and training are, the better the patient and family are in understanding the manifestations of spinal injury and in preventing complications through the years.

A person with SCI, especially with a diagnosis of ASIA A tetraplegia, should be regularly followed by a team of physicians including a primary care practitioner annually, a specialist in SCI rehabilitation (such as a physiatrist) at least every other year and for special circumstances and a urologist per medical discretion. Referrals to medical and ancillary specialists should not be delayed. One example of potential cost savings is to have a therapist rather than a vendor evaluate a patient for a new wheelchair. With more patients "recovering" from SCI as well as living longer, money should be thoughtfully spent as penny-wise in the short run may prove to be pound-foolish in the long run. The goal is to provide first-rate, cost-effective medical care to this disabled population.

SUMMARY

Rehabilitation of the spinal cord injured patient is complex. It is a continuum of treatment provided by specialty-trained professionals who assist the patient in learning to deal with his or her new disability. Intervention should begin as early as the day of injury and continue throughout the patient's lifetime. Despite being permanently disabled, patients have the potential to be as independent as they can, provided they are given appropriate tools and training. Comprehensive spinal cord injury rehabilitation can create accomplishment and independence from catastrophe and disability, offering hope and optimism to patients with spinal cord injury.

* Steven D. Feinberg, M.D. and co-author
Maureen Miner, M.D.
CWCE Magazine
August 1997

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