Spinal cord injury

Spinal cord injury

Chapter 59 SPINAL CORD INJURY Thomas N. Bryce, MD 1. Which of the following terms are currently favored to describe impairment or loss of motor an...

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59

SPINAL CORD INJURY Thomas N. Bryce, MD

1. Which of the following terms are currently favored to describe impairment or loss of motor and/or sensory function due to damage of neural elements within the spinal canal: (1) tetraplegia, (2) paraplegia, (3) quadriplegia, (4) quadriparesis, and/or (5) paraparesis? Tetraplegia refers to the impairments resulting from damage to neural elements within the cervical spinal canal, whereas paraplegia refers to the impairments resulting from damage to neural elements within the thoracic, lumbar, or sacral spinal canal. As tetra, para, and plegia are of Greek origin and quadri is of Latin origin, to maintain uniformity in word root origins, tetraplegia is preferred over quadriplegia. Because the American Spinal Injury Association (ASIA) Impairment Scale (AIS) (see Question 7) more precisely defines incomplete tetraplegia and paraplegia than the terms quadriparesis and paraparesis, their use is discouraged. 2. What is the difference between a skeletal level and a neurologic level of injury in assessing a person with a traumatic spinal cord injury (SCI)? The skeletal level of injury is defined as the level in the spine where the greatest vertebral damage is found on radiographic examination. The neurologic level of injury is defined as the most caudal segment of the spinal cord with normal sensory and motor function bilaterally. 3. How are the sensory and motor components assessed in the determination of a neurologic level of spinal cord injury? Sensory and motor functions are assessed according to the International Standards for Neurological Classification of Spinal Cord Injury: • Sensory component: Light touch and pinprick sensation are tested for each dermatome and graded on a three-point scale: 0 5 Absent 1 5 Impaired (partial or altered appreciation, including hyperesthesia) 2 5 Normal The sensory level is the most caudal dermatome where both light touch and pinprick are normal and where all rostral dermatomes are also normal. • Motor component: A key muscle is tested from each myotome in a rostral-caudal sequence by manual muscle test and graded on a six-point scale: 0 5 Total paralysis, no palpable or visible contraction 1 5 Palpable or visible contraction 2 5 Active movement, full range of motion (ROM) with gravity eliminated 3 5 Active movement, full ROM against gravity only 4 5 Active movement, full ROM against resistance 5 5 Normal The motor level is the most caudal muscle having grade 3 or better strength where all muscles above are graded 5. If the level of injury is at a site for which there is no key muscle (e.g. C2–C4, T2–L1, S2–S4/5), the motor level is defined by the sensory level. 4. Identify the key muscles that are tested in determining the motor level. C5 5 Elbow flexors (biceps, brachialis) T1 5 Small finger abductors (abductor digiti minimi) C6 5 Wrist extensors (extensor carpi radialis longus L2 5 Hip flexors (iliopsoas) and brevis) L3 5 Knee extensors (quadriceps) C7 5 Elbow extensors (triceps) L4 5 Ankle dorsiflexors (tibialis anterior) C8 5 Finger flexors (flexor digitorum profundus) to L5 5 Long toe extensors (extensor hallucis longus) the middle finger S1 5 Ankle plantar flexors (gastrocnemius, soleus)

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5. Identify the key point for each sensory sensory level. C2 5 Occipital protuberance C3 5 Supraclavicular fossa C4 5 Top of acromioclavicular joint C5 5 Lateral side of antecubital fossa C6 5 Thumb C7 5 Middle finger C8 5 Little finger T1 5 Medial (ulnar) side of antecubital fossa T2 5 Apex of the axilla T3 5 Third intercostal space (IS) T4 5 Fourth IS (nipple line) T5 5 Fifth IS (midway between T4 and T6) T6 5 Sixth IS (level of xiphisternum) T7 5 Seventh IS (midway between T6 and T8)

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dermatome that is tested in determining the T8 5 Eighth IS (midway between T6 and T10) T9 5 Ninth IS (midway between T8 and T10) T10 5 Tenth IS (umbilicus) T11 5 Eleventh IS (midway between T10 and T12) T12 5 Inguinal ligament at mid-point L1 5 Half the distance between T12 and L2 L2 5 Mid-anterior thigh L3 5 Medial femoral condyle L4 5 Medial malleolus L5 5 Dorsum of the foot at the third metatarsal phalangeal joint S1 5 Lateral heel S2 5 Popliteal fossa in the midline S3 5 Ischial tuberosity S4–S5 5 Perianal area (taken as one level)

6. What is the difference between a complete and an incomplete SCI? • Complete spinal cord injury is defined by the total absence of sensory and motor function below the anatomic level of injury in the absence of spinal shock. Recovery from spinal shock typically occurs within 48 hours following an acute spine injury • Incomplete spinal cord injury is present when residual spinal cord and/or nerve root function exists below the anatomic level of injury. Incomplete neurologic injuries are broadly classified by pattern of neurologic deficit into one of several syndromes, which is helpful in determining prognosis 7. How is the severity of a spinal cord injury classified? The AIS, a component of the International Standards for Neurological Classification of Spinal Cord Injury, is a 5-point scale (A, B, C, D, E) used to specify the severity of injury. It includes definitions of complete and incomplete injuries. • A 5 Complete: No sensory or motor function is preserved in the sacral segments S4–S5 • B 5 Incomplete: Sensory but not motor function is preserved below the neurologic level and includes the sacral segments S4–S5 • C 5 Incomplete: Motor function is preserved below the neurologic level, and more than half of key muscles below the neurologic level have a muscle grade less than 3 • D 5 Incomplete: Motor function is preserved below the neurologic level, and at least half of key muscles below the neurologic level have a muscle grade 3 or greater • E 5 Normal: Sensory and motor function are normal 8. Identify and describe six different patterns of incomplete neurologic injury which may be present following a traumatic spinal injury. • Cruciate paralysis: damage to the anterior spinal cord at the C2 level (level of corticospinal tract decussation) with greater loss of motor function in upper extremities compared with the lower extremities, variable sensory loss, and variable cranial nerve deficits. • Central cord syndrome: damage to the central spinal cord below the C2 level with greater loss of motor function in upper extremities (especially in the hands) compared with the lower extremities with variable sensory loss, at least partial sacral sparing, and variable bowel and bladder involvement • Anterior cord syndrome: damage to the anterior spinal cord with relative preservation of proprioception and variable loss of pain sensation, temperature sensation, and motor function. • Brown-Séquard syndrome: damage to the lateral half of the spinal cord with relative ipsilateral proprioception and motor function loss and contralateral pain and temperature sensation loss. • Conus medullaris syndrome: damage to the sacral segments of the spinal cord located in the conus medullaris, which typically results in an areflexic bowel and bladder, lower extremity sensory loss, and incomplete paraplegia. • Cauda equina syndrome: damage to lumbosacral nerve roots within the neural canal results in variable lower extremity motor and sensory function, bowel and bladder dysfunction, and saddle anesthesia. 9. What is the rationale for administering medications, such as methylprednisolone, following an acute spinal cord injury? The pathophysiology of acute spinal cord injury involves both primary and secondary injury mechanisms. • Primary injury to the spinal cord results from mechanical forces applied to the spinal column at the time of injury and is not correctable. • Secondary injury to uninvolved neurologic tissue in the vicinity of the primary injury may occur due to a variety of mechanisms and potentially can be modified via pharmacotherapy. Methylprednisolone has been advocated based on its antioxidant and cell membrane stabilizing properties. A loading dose of 30 mg/kg is followed by 5.4 mg/kg for 23 hours if administered within 3 hours of injury or for 48 hours if administered between 3 and 8 hours after injury. Use of methylprednisolone remains controversial due to complications,

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such as infection, gastrointestinal bleeding, pulmonary and endocrine problems, and an adverse effect on healing of spinal fusions. Research regarding alternative pharmacologic agents is currently under way. 10. Identify six complications of SCI that may manifest within the first 2 days after injury. Hypotension, bradycardia, hypothermia, hypoventilation, gastrointestinal bleeding, and ileus. 11. What causes hypotension, bradycardia, and hypothermia? Acute cervical or upper thoracic spinal cord injuries are associated with a functional total sympathectomy with resultant loss of vasoconstrictor tone in the trunk and extremities and loss of beta-adrenergic cardiostimulation, leading to a clinical picture of hypotension with paradoxical bradycardia. The loss of sympathetic tone also leads to an inability to regulate body temperature. After it is clearly established that no visceral or extremity injury is causing occult hemorrhage and blood loss, hypotension is best treated with sympathomimetic agents. 12. What causes hypoventilation? The innervation to the diaphragm, the major muscle responsible for inspiration, is C3 to C5 (“3, 4, 5 keeps you alive”). The innervation to the internal intercostals and the abdominal muscles, the major muscles responsible for forced expiration (e.g. cough), are local thoracic and abdominal segmental nerves. Thus, a cervical or thoracic spinal cord injury can affect inspiration, cough, or both, depending on the level of injury. Patients with a C1–C2 complete SCI have no volitional diaphragmatic function and require mechanical ventilation or placement of a diaphragm/phrenic pacer. Patients with a C3–C4 complete SCI have severe diaphragmatic weakness and commonly require mechanical ventilation, at least temporarily. Patients with C5 to T1 complete SCI are usually able to maintain independent breathing but remain at high risk for pulmonary complications due to loss of innervation to the intercostal and abdominal muscles. Pneumonia is the most common cause of early death for persons with tetraplegia and is often related to aspiration of stomach or oropharyngeal contents, commonly occurring at or shortly after the initial injury. Atelectasis may result from hypoexpansion of the chest due to either pain or muscle weakness or to inadequate cough predisposing to inadequate clearing of secretions. Respiratory failure may develop immediately after SCI or over several days. Close monitoring of respiratory function is warranted in persons with cervical SCI during the first week after injury. See Table 59-1.

Table 59-1.  Respiratory Function and Spinal Injury INJURY LEVEL

RESPIRATORY SYSTEM CHANGES

MECHANICAL VENTILATION

Occiput–C2

(2) Diaphragm, (2) intercostals

Always needed

C3–C4

(1/2) Diaphragm, (2) intercostals

Often needed acutely

C5–T1

(1) Diaphragm, (2) intercostals

Only needed if there are associated pulmonary complications

T2–T12

(1) Diaphragm, (1/2) intercostals

Usually not needed

13. What causes gastrointestinal bleeding? Risk is increased with any physical or psychologic trauma and is exacerbated by the standard high-dose steroid protocols used after SCI. 14. What causes ileus? Adynamic (paralytic) ileus occurs after acute SCI in 8% of cases. After its resolution, usually within 2 to 3 days, a bowel routine of stool softeners, stimulant laxatives, and bowel evacuants is initiated to facilitate regularly timed evacuations of the bowel. 15. When should anticoagulant prophylaxis against venous thromboembolus (VTE) be started after SCI? VTE is found in one half to three quarters of persons with traumatic SCI who are not receiving anticoagulant prophylaxis. The highest risk is within the first week after SCI. Therefore, anticoagulant prophylaxis should be started as soon as hemostasis has been achieved, unless there is a contraindication. Randomized controlled studies have shown a low risk of major bleeding when either low-molecular-weight heparin (LMWH) or unfractionated heparin prophylaxis is started within 72 hours of injury. LMWH has been shown to be more effective than unfractionated heparin in preventing pulmonary embolus. Mechanical compression devices have been shown to decrease the risk of VTE when used in conjunction with anticoagulant prophylaxis. 16. When should an inferior vena cava (IVC) filter be placed? An IVC filter should only be placed in those in whom active bleeding is anticipated to last more than 72 hours or in those in whom adequate anticoagulant prophylaxis cannot be started. If an IVC filter is used, a temporary one should be chosen, and it should be removed within 8 to 12 weeks if no VTE develops. Historically, one third of those who receive permanent IVC filters ultimately develop VTE.



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17. How can incontinence of stool be prevented after SCI? A neurogenic bowel after SCI affects mainly the colon and rectum distal to the splenic flexure and can be classified as an upper motor neuron (UMN) type if sacral reflexes are present (e.g. bulbocavernosus or anocutaneous) or lower motor neuron (LMN) type if these reflexes are absent. Institution of a bowel routine or daily timed evacuation of the colon can prevent incontinence by allowing predictable evacuations in nearly everyone with SCI. During a UMN-type bowel routine, digital stimulation of the rectum triggers reflex evacuation of stool. This can be further facilitated by inserting an irritant suppository or mini-enema into the rectum and performing this routinely after a meal to take advantage of the gastrocolic reflex. During a LMN-type bowel routine, digital evacuation of the rectum empties the rectum of stool. Stool-bulking agents or fiber are useful in maintaining an optimal consistency of stool, because water absorption is usually impaired within an areflexic colon. Oral irritant or osmotic laxatives given 8 to 12 hours before the routine may be necessary to help propel the stool through the colon to the distal portion where it can be evacuated. 18. How should a neurogenic bladder be initially managed after an SCI? An indwelling transurethral catheter (or suprapubic tube if indicated) should be placed as soon as feasible and should remain in place until the patient’s fluid status has stabilized. 19. Identify five interventions that can help prevent the development of pressure ulcers after acute SCI. 1. The length of time spent on a spine board should be minimized, and pressure relief should be provided every 30 minutes if the time on the board exceeds 2 hours. 2. Patients in spinal traction should be immobilized on rotating kinetic beds. 3. Patients must be turned from side to side (30°–45° from supine) every 2 hours around the clock while in bed to prevent prolonged pressure over bony prominences. 4. Bowel and bladder incontinence should be managed with timed bowel evacuations and catheter drainage of the bladder. 5. Shear pressure on the skin can be avoided by lifting rather than dragging immobile patients. 20. Identify six reasons for transferring a person with tetraplegia to a specialized SCI center. • Overall survival rates increase • Complication rates (e.g. incidence of new pressure ulcers) decrease • Length of hospital stay decreases • Functional gains during rehabilitation are greater • Home discharge is more likely • Rehospitalization rates are lower 21. What is the prognosis for neurologic recovery of a patient with a complete tetraplegia? Only 2% to 3% of persons who have an initial Asia Impairment Scale (AIS) score of A convert to AIS D by 1 year. However, 30% to 80% of persons with motor complete tetraplegia recover a single motor level (gaining functional motor strength at that level) within 1 year of injury. A muscle with grade 1 or 2 strength at 1 month has a 90% chance of reaching grade 3 by 1 year, whereas a muscle with grade 0 strength has only a 25% chance to reach grade 3 or better by 1 year. The chance of functional recovery of a muscle two levels below the motor level of injury, when the first muscle below the motor level is grade 0, is exceedingly rare. 22. What is the prognosis for neurologic recovery of someone who has an incomplete tetraplegia? Among sensory incomplete patients, the type of sensation preserved below the level of injury is prognostically important. Persons with preservation of perianal pinprick sensation have a greater than 70% chance of regaining ambulatory ability, whereas persons who have spared light touch sensation only in the same region are unlikely to regain ambulatory ability. Among persons with motor incomplete SCI, age and initial motor strength seem to be major determinants of ambulation. In one study of 105 persons with incomplete motor tetraplegia, in which age 50 was arbitrarily chosen as a cutoff, 91% of all persons younger than 50 years, either AIS C or D, ambulated at 1 year; all persons older than 50 years and AIS D ambulated; while only 40% of persons older than 50 years and AIS C ambulated. 23. What is the prognosis for neurologic recovery for someone who has paraplegia? Among persons with complete paraplegia, 75% retain the same neurologic level of injury (NLI) at 1 year that they had at 1-month postinjury, 20% gain a single level, and 5% gain two neurologic levels. Persons with T1 to T8 complete paraplegia do not recover lower limb voluntary movement. Fifteen percent of persons with T9 to T11 complete paraplegia recover some lower limb function, while 55% of persons with T12 or below complete paraplegia recover some lower limb function. Persons with incomplete paraplegia have the best prognosis for ambulation among all the groups of persons with traumatic SCI. Eighty percent of individuals with incomplete paraplegia regain functional hip flexion and knee extension within 1 year of injury, making both indoor and community-based ambulation possible.

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24. What typical lower extremity motor function is required for community ambulation? Typically, community ambulation requires bilateral grade 3 hip flexor strength and at least one knee with grade 3 knee extensor strength. 25. Compare the expected patterns of muscular weakness and the expected functional outcomes for eating, bed/wheelchair transfers, and wheelchair propulsion for persons with C1 to C3, C4, and C5 neurologic levels. See Table 59-2.

Table 59-2.  Functional Outcomes for C1 to C5 Spinal Cord Injuries C1–C3

C4

C5

Patterns of Muscular Weakness

Total paralysis of trunk, upper extremities, lower extremities, dependent on ventilator

Paralysis of trunk, upper extremities, lower extremities; inability to cough, endurance and respiratory reserve low secondary to paralysis of intercostals

Absence of elbow extension, pronation, all wrist and hand movement, total paralysis of trunk and lower extremities

Eating

Total assist

Total assist

Total assist for setup, then independent eating with equipment

Bed/Wheelchair Transfers

Total assist

Total assist

Total assist

Wheelchair Propulsion

Manual: total assist Power: independent with equipment

Manual: total assist Power: independent with equipment (sip and puff control or head array)

Manual: independent to some assist indoors on noncarpet, level surface; some to total assist outdoors Power: independent

26. Compare the expected patterns of muscular weakness and the expected functional outcomes for wheelchair propulsion and ambulation for persons with C6, C7–C8, T1 to T9, and T10 to L1 neurologic levels. See Table 59-3.

Table 59-3.  Functional Outcomes for C6 to L1 Spinal Cord Injuries C6

C7–C8

T1–T9

T10–L1

Patterns of Muscular Weakness

Absence of wrist flexion, elbow extension, hand movement; total paralysis of trunk and lower extremities

Paralysis of trunk and lower extremities; limited grasp release and dexterity secondary to partial intrinsic muscles of hand

Lower trunk paralysis; total paralysis of lower extremities

Paralysis of lower extremities

Wheelchair Propulsion

Manual: independent indoors; some to total assist outdoors Power: independent with standard arm drive on all surfaces

Manual: independent all indoor surfaces and level outdoor terrain; some assist with uneven terrain

Independent

Independent

Ambulation

Standing: total assist Ambulation: not indicated

Standing: independent to some assist in standing frame Ambulation: not indicated

Standing: independent in standing frame Ambulation: typically not functional

Standing: independent with equipment Ambulation: functional, some assist to independent with knee, ankle, foot orthosis and forearm crutches or walker



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27. What is spasticity and what peripheral factors can cause an exacerbation of spasticity? Spasticity is a motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex as one component of the upper motor neuron syndrome. Peripheral factors that may exacerbate spasticity include heterotopic ossification, urolithiasis, urinary tract infections, stool impaction, pressure ulcers, fracture/dislocations, and ingrown toenails. 28. Name six pathologic changes associated with late neurologic deterioration after SCI. 1. Posttraumatic cysts 2. Delayed spinal deformity 3. Residual cord compression 4. Tethering 5. Fibrosis 6. Subarachnoid cysts 29. A tetraplegic patient develops an L2–L3 destructive spinal lesion 10 years after a C5–C6 fracture-dislocation. Workup reveals no evidence of a spinal tumor or infection. What is the most likely cause of this lesion? Neuropathic spinal arthropathy (Charcot spine). Destructive spinal lesions can develop in spinal cord–injured patients due to repetitive loads placed on the denervated spine in the course of daily activities. The most common clinical presentation is a spinal deformity. Patients may present with audible clicking or crepitus due to spinal instability, loss of sitting balance, cauda equina syndrome, nerve root compression, or obstructive uropathy. Surgical treatment is challenging and associated with a high complication rate. 30. What are the three most common causes of death after SCI? 1. Diseases of the respiratory system 2. Other heart disease 3. Infective and parasitic diseases

Key Points 1. Perform baseline and serial neurologic assessments using the International Standards for Neurological Classification of Spinal Cord Injury to detect neurologic changes, as well as to define the severity of injury. 2. Patients with spinal cord injury should be initially managed in an intensive care unit setting due to the high risk of respiratory complications and hypotension. 3. Early surgical stabilization allows earlier mobilization, enables more intensive rehabilitation, and results in a shorter hospital stay. 4. Persons with preserved perianal pinprick sensation, with or without motor function, have a good prognosis for functional motor recovery and ambulation.

Websites Clinical practice guidelines, developed by the Consortium for Spinal Cord Medicine, are available for download at www.pva.org Bladder Management for Adults with Spinal Cord Injury Preservation of Upper Limb Function Following Spinal Cord Injury Respiratory Management Following Spinal Cord Injury Depression Following Spinal Cord Injury Neurogenic Bowel Management in Adults with Spinal Cord Injury Outcomes Following Traumatic Spinal Cord Injury Acute Management of Autonomic Dysreflexia Pressure Ulcer Prevention and Treatment Following Spinal Cord Injury Prevention of Thromboembolism in Spinal Cord Injury

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Bibliography 1. Bryce TN, Ragnarsson KT, Stein AS. Spinal cord injury. In: Braddom RL, editor. Physical Medicine and Rehabilitation. 3rd ed. Philadelphia: Saunders; 2007. p. 1285–1349. 2. Capagnolo DI, Heary RF. Acute medical and surgical management of spinal cord injury. In Kirshblum S, Capagnolo DI, DeLisa JA, editors. Spinal Cord Medicine. Philadelphia: Lippincott, Williams and Wilkins; 2002. p. 96–107. 3. Consortium for Spinal Cord Medicine. Early acute management in adults with spinal cord injury: A clinical practice guideline for healthcare professionals. J Spinal Cord Med 2008:31(4):403–79. 4. Consortium for Spinal Cord Medicine. Neurogenic bowel management in adults with spinal cord injury. J Spinal Cord Med 1998;21(3):248–93. 5. Consortium for Spinal Cord Medicine. Outcomes following traumatic spinal cord injury: Clinical pratice guidelines for health-care professionals. J Spinal Cord Med 2000;23(4):289–316. 6. Marino RJ, Barros T, Biering-Sorensen, et al. International standards for neurological classification of spinal cord injury. J Spinal Cord Med 2003;26(Suppl 1):S50–6. 7. National Spinal Cord Injury Statistical Center, University of Alabama at Birmingham, 2006 annual statistical report, July 2006, University of Alabama, Birmingham. https://www.nscisc.uab.edu/public_content/pdf/NSCIC%20Annual%2006.pdf . 8. Piepmeier J. Late sequelae of spinal cord injury. In: Narayan R, Wilberger J, Povlishock J, editors. Neurotrauma. New York: McGraw-Hill; 1996. p. 1237–44. 9. Reference manual for the International Standards for Neurological Classification of Spinal Cord Injury. Chicago: American Spinal Injury Association; 2003. p. 21–45. 10. Yarkony G, Formal C, Cawley M. Spinal cord injury rehabilitation: Assessment and management during acute care. Arch Phys Med Rehabil 1997;78:S48–S52.