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Spinal Cord Trauma and Related Diseases Follow-up

  • Author: Francisco de Assis Aquino Gondim, MD, MSc, PhD, FAAN; Chief Editor: Stephen A Berman, MD, PhD, MBA  more...
 
Updated: Dec 28, 2015
 

Further Outpatient Care

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  • Rehabilitative efforts include physical, occupational, vocational, speech and recreational therapies.
    • In the immediate setting, at least passive range of motion activities to prevent contractures are required if the patient cannot participate actively.
    • Issues that must be addressed in the long term include contractures, postural abnormalities, spasticity, self-care, mobility, psychosocial adaptation, vocational and recreational skills, and adaptive equipment.
    • Spasticity can be addressed with drugs, including intrathecal baclofen, and nonpharmacologic approaches.
    • Special adaptive devices may allow patients with SCI to drive. For further information, the reader is referred to Patient Education.
    • In general, these interventions are more fruitful if family members and other caregivers are included.
  • Rehabilitative efforts also focus on long-term hemodynamic and other medical issues, including autonomic dysreflexia, respiratory care and conditioning, bowel and bladder continence, preventive gastrointestinal and genitourinary care, sexual dysfunction, depression, and skin integrity.
    • Various techniques to restore spinal cord function are under study, including cell transplantation. Despite promising results from animal studies, to date, no strategy has been proven effective in humans.
    • Repetition of task-specific movements can reactivate central pattern generators in the spinal cord and may help with ambulation and endurance. Training is currently under study in a multicenter trial. Techniques include partially supported treadmill walking and electrical stimulation of the extremity muscles to promote gait patterns.
    • Computer controlled transcutaneous activation of leg muscle can help with strength training and cardiovascular conditioning.
    • The Food and Drug Administration (FDA) –approved implantable Brindley-Finetech and Vocare bladder systems activate anterior sacral roots to regulate bladder and large bowel and urethral/anal sphincter contraction.
    • Sexual dysfunction must be systematically approached and treated with mechanical and pharmacologic interventions and psychosocial counseling. Testicular sperm retrieval and intracytoplasmic sperm injection are alternative techniques for failed conservative reproductive treatments in men with SCI seeking to conceive children.
    • Procreation is also an important issue because semen quality and motility is reduced in men because of repeated urinary tract infections. Women may experience life-threatening autonomic hyperreflexia during delivery.
    • Recently, the role of central pattern generators and the possibility of activating standing and stepping circuits after SCI even in chronic injury phase has been addressed.[11]
      • In 1914, Graham Brown demonstrated the existence of central pattern generators for walking in animals. This concept refers to neuronal networks capable of creating rhythmic motor activity in the absence of phasic sensory input.[12]
      • Theoretically, a similar system exists in humans and can be activated by repeated exercise or stimulation of the walking pathways. In cats, the spinal cord "learns" how to generate a continuous walking pattern known as fictive locomotion.[13] Based on these theoretical grounds, exercise programs have been developed, including suspended body weight support system over a treadmill to facilitate walking and bicycles designed for SCI. Reports of return of function several years after high cervical SCI in one patient (Christopher Reeves) have received a lot of attention, and further promising research is underway.[11]
  • After rehabilitation, most of the patients are treated by nonspecialists, but yearly follow-up should address all the topics detailed above and should ideally involve a physiatrist or SCI specialist.
  • Recent guidelines recommend that adults with a SCI should engage in (1) at least 20 minutes of moderate-to-vigorous aerobic activity 2 times per week and (2) strength training exercises 2 times per week, consisting of 3 sets of 8-10 repetitions of each exercise for each major muscle group.[14]
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Further Inpatient Care

The main goal in long-term care is to prevent medical complications, which are the reason for which 30% of patients with spinal cord injury (SCI) require hospital admission every year. For a detailed discussion of medical management, see Sugarman's[15] 1985 article Medical complications of spinal cord injury and the 2002 article by McKinley et al[16] , Comparison of medical complications following nontraumatic and traumatic spinal cord injury. General medical guidelines include the following:

  • Administer empiric antibiotics as indicated, especially if the patient is febrile and epidural abscess is suspected.
  • Always maintain adequate perfusion to prevent further ischemic damage. Mean arterial pressure should ideally be above 70 mm Hg.
  • Intubate the patient if respiratory function is compromised either because of injuries (eg, C3-5, phrenic nerve, neck and/or chest) or because of easy fatigue of respiratory musculature.
  • Prevent nosocomial infections; treat aggressively and early if they occur.
  • Skin care to prevent decubitus ulcers includes vigilance, early treatment, use of air mattresses, frequent rolling and movement, and therapy.
  • Deep vein thrombosis and pulmonary embolism prophylaxis is paramount as well.
  • Bladder and bowel care includes preventing distention, discomfort, impaction, and infection.
    • Foley or intermittent sterile catheterization and/or rectal tube or stool softeners (eg, docusate) or stool bulking agents (eg, psyllium), depending on the extent of voluntary control present, may be needed; furthermore, enemas or suppositories may be needed to prevent or treat impactions.
    • Ascorbic acid (1 g PO qid) may help prevent infections by acidifying the urine; it may also help prevent urinary calculi.
    • Avoiding medications such as anticholinergic agents that can adversely affect bladder emptying is useful. Medications useful in the management of bladder function include bethanechol (used for flaccid paralysis but of questionable efficacy) and oxybutynin (for spastic paralysis). Avoidance of drugs with anticholinergic effect also helps in neurogenic bladder management.
    • Both the bowel and bladder sphincter reflexes can be trained to provide reflex emptying if lesions spare the lower motor neurons involved in micturition.
  • Judicious management of fluids, electrolytes, and nutrition is mandatory.
  • Pain and anxiety control is often required but may be difficult. Narcotics must be used judiciously or be avoided because of bowel and bladder adverse effects. Benzodiazepines, barbiturates, or any drugs causing depression of the CNS should also be used with caution because they can alter respiratory drive and exacerbate respiratory failure in patients with high spinal cord lesions. Such patients already have weak intercostal muscles and may experience further restriction of respiratory movements because of limitation of volitional movements.
  • Gastrointestinal prophylaxis against ulcers is also mandatory. Patients with SCI have a high incidence of stress ulcers, which can also be exacerbated by the concomitant use of steroids in the acute phase. The use of nonsteroidal anti-inflammatory drugs should also be avoided because of the risk of GI bleeding exacerbation.
  • Psychological and emotional support throughout the patient's disease course is necessary and is best provided informally and continuously by the caretakers; however, formal intervention by specialists may be required.
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Inpatient & Outpatient Medications

Medications are administered as required to manage the constellation of medical complications that follow SCI. See Complications.

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Transfer

Referral to a regional trauma center or to a center with expertise on SCI may be advised because of the constellation of complications following SCI. Admission to an intensive care unit may be necessary for close hemodynamic monitoring or if concomitant head or abdominal trauma or multiple fractures are found.

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Deterrence/Prevention

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  • Education programs teaching the general population and paramedics how to handle patients with an unstable neck and to think early about the possibility of SCI after trauma can prevent unnecessary worsening of SCI after injury.
  • In addition, educational programs for adolescents and families demonstrating common causes of SCI and the severity of SCI may help decrease its incidence.
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Complications

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  • In the acute phase, the classic syndrome of complete spinal cord transection at the high cervical level includes a constellation of symptoms called spinal shock. This syndrome consists of the following symptoms:
    • Respiratory insufficiency
    • Quadriplegia with upper and lower extremity areflexia
    • Anesthesia below the affected level
    • Neurogenic shock (ie, hypotension without compensatory tachycardia)
    • Loss of rectal and bladder sphincter tone
    • Urinary and bowel retention leading to abdominal distention, ileus, and delayed gastric emptying
    • Horner syndrome (ie, ipsilateral ptosis, miosis, anhydrosis): This is also present with higher lesions because of interruption of the descending sympathetic pathways originating from the hypothalamus.
  • Lower cervical level injury spares the respiratory muscles. High thoracic lesions lead to paraparesis instead of quadriparesis but autonomic symptoms are still marked. In lower thoracic and lower lesions, hypotension is not present but urinary and bowel retention are.
  • In the subacute phase, spinal shock is replaced by the return of intrinsic activity of spinal neurons. This usually happens in humans within 3 weeks. However, the spinal shock phase may be prolonged by other medical complications, such as infections.
    • Patients have persistent quadriplegia and sensory loss below the level, but spinal reflexes return.
    • Because modulation from supraspinal centers is lost, hyperreflexia with increased tone and extensor plantar responses are noted.
    • At any given level with more extensive involvement of the anterior horn, flaccidity with loss of reflex activity and atrophy are present in a lower motor neuron pattern, which is common in diseases such as poliomyelitis.
  • Autonomic hyperreflexia is also present in the subacute phase. Usually, the initial hypotension after high lesions resolves, although orthostatic hypotension persists.
    • For lesions above the lumbar/sacral centers for bladder control, the initial urinary retention is replaced by the development of an automatic spastic bladder.
    • Lower lesions lead to permanent atonic bladder (lower motor neuron pattern).
    • In humans, constipation persists and may contribute to delayed gastric emptying.
    • Autonomic hyperreflexia in this phase is characterized by massive firing of sympathetic neurons after distention, stimulation, or manipulation of the bladder and bowels.
    • Cutaneous stimulation with painful or cold stimuli can also lead to massive sympathetic firing.
      • This is a life-threatening condition because blood pressure may increase up to 300 mm Hg, leading to intracerebral hemorrhage, confusional states, and death.
      • A response to the massive sympathetic discharge is generated at the brainstem level. However, interruption of descending projections to the spinal cord can prevent the inhibition of the spinal cord sympathetic centers, which continue to fire inappropriately until the stimulus is removed.
      • A vagal inhibitory reflex to the heart is also generated, which leads to bradycardia and worsening symptoms.
  • Long-term, autonomic and somatic hyperreflexia cause severe spasticity and contractures in patients with high SCI. In the early 20th century, the chronic phase was called the third phase. It was characterized by the accumulation of bladder, skin, and bowel disorders, which eventually caused severe wasting and death. Fortunately, modern medical and nursing care have substantially prevented most of the complications.
  • Spasticity is a major complication of SCI, accompanying the other signs of upper motor neuron syndrome (see Spasticity). Its pathophysiology is incompletely understood, but synaptic reorganization within the spinal cord and loss of modulation by descending tracts play an important role.
    • Several strategies are available and should take into account the age, side effects of each treatment, and individual goals. The sedative properties of antispasticity drugs may interfere with learning in children. In addition, the increased lower extremity tone may allow the patient to stand and a decrease in tone may jeopardize mobility.
    • Physiotherapy is the most traditional form of treatment. Oral medications are usually helpful, but sedation is usually a limiting barrier. Benzodiazepines improve passive range of motion, hyperreflexia, painful spasms, and anxiety by affinity to the gamma aminobutyric acid (GABA) type A receptor complex. Baclofen is a GABA agonist, which must be started slowly to prevent sedation. It may be administered orally or through intrathecal infusion, the latter involves lesser adverse effects. Tizanidine is a new alternative. It is an alpha2 agonist and causes less weakness than baclofen and diazepam. Physiotherapy should also take into account the changes in muscle fiber proportion after spinal cord injury. Transformation away from type I fibers starts about 4-7 months after injury, reaching a steady state with predominantly fast glycolytic IIX fibers years after the injury.[17]
    • Injections of botulinum toxin, phenol, alcohol, and lidocaine can also be used in selected patients.
    • Surgical treatments are usually the last option and include selective posterior rhizotomy, lengthening or release of muscles and tendons, and procedures such as osteotomy, used to correct deformities.
  • Sexual dysfunction is common, especially with complete lesions. Many options are available, but 2 recent efficacy and safety trials in men with traumatic SCI revealed that tadalafil[18] (doses of 10 mg and 20 mg) or vardenafil[19] (10-20 mg) were good options for the treatment of erectile dysfunction secondary to traumatic SCI.
  • For a more detailed view of all medical complications in patients with SCI, see Sugarman's 1985 article.[15]
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Prognosis

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  • Spinal trauma and other spinal cord diseases often cause severe physical impairment secondary to motor, sensory, and autonomic impairment.
  • Overall, life expectancy is greatly decreased, although major advances of medical management have markedly prolonged survival.
  • The ability to predict clinical outcome after SCI based on early examination is limited. The most important predictor of improved outcome is retention of sacral sensation (S4-5), especially pinprick, 72 hours to 1 week after injury. In general, most individuals regain one level of motor function, mostly within the first 6 months, although further improvement can be observed years later. Age is also a prognostic factor. In central cord syndrome, 91% of patients younger than 50 years regain ambulation, whereas only 41% of people older than 50 years develop a similar outcome.
  • Transient or chronic reactive mild or severe depression is very common after SCI. In the case of trauma, younger patients often have greater functional improvement from acute spinal injury. The suicide rate among individuals with SCI is nearly 5 times higher than in the general population and is lower for men than for women. In 1998, Hartkopp et al also observed a 2 times higher suicide rate in marginally disabled persons compared to more severely affected individuals.[20]
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Patient Education

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Contributor Information and Disclosures
Author

Francisco de Assis Aquino Gondim, MD, MSc, PhD, FAAN Professor Adjunto of Neurology and Clinical Skills, Department of Internal Medicine, Universidade Federal do Ceará, Brazil

Francisco de Assis Aquino Gondim, MD, MSc, PhD, FAAN is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, International Parkinson and Movement Disorder Society

Disclosure: Received travel grants from for: Aché, Biogen, Genzyme, Ipsen, Novartis.

Coauthor(s)

Florian P Thomas, MD, PhD, Drmed, MA, MS Director, National MS Society Multiple Sclerosis Center; Professor and Director, Clinical Research Unit, Department of Neurology, Adjunct Professor of Physical Therapy, Associate Professor, Institute for Molecular Virology, St Louis University School of Medicine; Editor-in-Chief, Journal of Spinal Cord Medicine

Florian P Thomas, MD, PhD, Drmed, MA, MS is a member of the following medical societies: Academy of Spinal Cord Injury Professionals, American Academy of Neurology, American Neurological Association, Consortium of Multiple Sclerosis Centers, National Multiple Sclerosis Society, Sigma Xi

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Howard S Kirshner, MD Professor of Neurology, Psychiatry and Hearing and Speech Sciences, Vice Chairman, Department of Neurology, Vanderbilt University School of Medicine; Director, Vanderbilt Stroke Center; Program Director, Stroke Service, Vanderbilt Stallworth Rehabilitation Hospital; Consulting Staff, Department of Neurology, Nashville Veterans Affairs Medical Center

Howard S Kirshner, MD is a member of the following medical societies: Alpha Omega Alpha, American Neurological Association, American Society of Neurorehabilitation, American Academy of Neurology, American Heart Association, American Medical Association, National Stroke Association, Phi Beta Kappa, Tennessee Medical Association

Disclosure: Nothing to disclose.

Chief Editor

Stephen A Berman, MD, PhD, MBA Professor of Neurology, University of Central Florida College of Medicine

Stephen A Berman, MD, PhD, MBA is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, Phi Beta Kappa

Disclosure: Nothing to disclose.

Additional Contributors

Stephen A Berman, MD, PhD, MBA Professor of Neurology, University of Central Florida College of Medicine

Stephen A Berman, MD, PhD, MBA is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, Phi Beta Kappa

Disclosure: Nothing to disclose.

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A T1-weighted MRI that depicts a lesion with high signal enhancement inside the cervical spinal cord. This type of signal enhancement is consistent with blood and is most commonly observed secondary to cord trauma.
 
 
 
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