Other studies have focused on the association between initial motor strength in a muscle and expected magnitude of recovery. Several studies in complete tetraplegia have found that more than 90% of muscles with Grade 1 of 5 or Grade 2 of 5 strength from 1 week to 1 month after injury will eventually recover to Grade ≥3 of 5 strength. 17,62 In contrast, muscles with Grade 0 of 5 strength 1 month after injury and located one neurologic level below the most caudal level having motor function regained Grade ≥3 of 5 strength in only 27% of cases at 1 year. 62 Muscles two levels below the most caudal level with motor function regained Grade ≥3 of 5 strength in only 1% of cases. Late conversion, i.e., >1 month postinjury, from complete to incomplete injury had little bearing on the ultimate motor recovery.
In another study on complete paraplegia using a 1-month baseline examination, Waters et al reported that in 73% (108 of 148) of patients, the neurologic level of injury did not change at 1 year. 61 Only two patients recovered >2 levels. None of the patients with an initial neurologic level above T9 regained any lower extremity motor function. In muscles with an initial Grade of 1 of 5 or 2 of 5, approximately 70% recovered to Grade 3 of 5 or greater at 1 year. In contrast, 3–7% of initially Grade 0 of 5 muscles progressed to Grade 3 of 5 at 1 year. In cases with initially “present” lower abdominal muscles, 26% of hip flexors recovered to Grade ≥3 of 5. Four percent (6 of 148) of the patients converted “late” to incomplete injuries. Three of six late converters regained bowel/bladder continence, and two of six ambulated with a reciprocal gait.
The majority of neurorecovery in complete patients occurs during the first 6 to 9 months. 17,61,62 Afterwards, the rate of improvement rapidly drops off with a plateau being reached 12 to 18 months postinjury with little additional improvement (Figure 3). 17,19,21,61,62
Incomplete injuries of the cervical spinal cord recover to a greater extent than complete injuries. A recent multicenter study compared the recovery of upper extremity strength in complete and incomplete tetraplegics. 21 Greater than 90% of incomplete injuries gained at least one additional motor level in the upper extremities compared with 70% to 85% of complete injuries. There is an excellent chance (92%) of recovery to ≥3–5 motor strength for initially 0–5 muscles if pinprick is spared at the same dermatome. 50
In the majority of incomplete tetraplegics and paraplegics, there was an approximately 12- to 14-point increase in lower extremity motor scores during the first year and minimal improvement during the second year using the 50-point scale. The exception was incomplete tetraplegics without sharp–dull discrimination who failed to demonstrate any lower extremity motor recovery. In tetraplegics upper extremity motor scores improved 11 points by 1 year with little additional improvement by 2 years.
In incomplete paraplegia 85% of muscles that were Grade 1–5 or 2–5 at 1 month recovered to ≥3–5 by 1 year. In comparison, of 212 muscles that were Grade 0–5 at 1 month, 55% (117 of 212) recovered some volitional control, but only 26% (55 of 212) recovered “motor useful” (≥3–5) function. The study on incomplete tetraplegia found similar magnitudes of neurorecovery. 64 In both incomplete paraplegia and tetraplegia, the majority of improvement occurred within the first 6 to 9 months and a plateau was reached by 12 months (Figure 3). 63–64
The anterior spinal syndrome predominantly affects the spinothalamic tracts and corticospinal tracts while sparing the posterior columns. Motor recovery is thought to be significantly less in these patients in comparison with other incomplete patients. 12,26 Central cord syndrome is characterized by disproportionately more motor impairment of the upper than the lower extremities. Prior studies have reported that 57% to 86% of patients with this syndrome will independently ambulate. 2,46 Penrod et al 47 assessed the impact of age in central cord syndrome and noted that 97% (29 of 30) of patients younger than 50 years ambulated compared with 41% (7 of 17) of patients older than 50 years. Foo 27 found that in central cord syndrome due to cervical spondylosis, only 31% of patients ambulated, with the mean age of study subjects being 65 years. The Brown-Sequard syndrome produces relatively greater ipsilateral proprioceptive and motor loss and contralateral loss of sensitivity to pin and temperature. The prognosis is also favorable with this syndrome, and almost all patients will ambulate successfully. 2,47,57 It has been theorized that axons in the contralateral cord may facilitate recovery. 41 Motor return also tends to occur in a proximal-to-distal pattern with extension returning before flexion. 41
It has been clearly established that patients with complete spinal cord injuries rarely walk. 44 In one study on complete paraplegics, 5% (7 of 148) of complete injuries at 1 month were eventually able to reciprocally ambulate using conventional orthoses and crutches. 61 Two of these patients were late converters to incomplete status. In a similar study on 61 complete tetraplegics, 90% had no return of volitional lower extremity function and no patients were reported to ambulate. 62
In comparison with incomplete paraplegics, incomplete tetraplegics are less likely to ambulate. Waters et al found that only 46% of incomplete tetraplegics (vs. 76% of incomplete paraplegics) were community ambulators 1 year postinjury 64; they attributed this to the fact that upper extremity strength is often severely compromised in the tetraplegic and therefore insufficient to enable crutch-assisted ambulation. Burns et al also focused on the recovery of ambulation in motor incomplete tetraplegic patients. 7 Ninety-one percent (30 of 33) of ASIA C patients younger than 50 years of age ambulated compared with 42% (13 of 31) of ASIA C patients age 50 or older. All (41 of 41) ASIA D patients ambulated regardless of age. Foo 27 focused on SCI related to cervical spondylosis. Thirty-one percent (10 of 32) of the incomplete patients became independent ambulators; however, the average age of study patients was 65 years. 27 Both the studies by Burns et al 7 and Foo 27 emphasize the impact of age on ultimate prognosis.
A unique subcategory of incomplete injuries is the individuals with preserved sensation but no motor function (“motor complete”). Maynard et al 44 found that 44% (8 of 18) of initially motor complete (preserved sensation but no motor function) patients ambulated. Crozier et al 12 later demonstrated that the preservation of pinprick significantly impacts the prognosis for ambulation in motor complete patients. Using a 72-hour baseline examination, 89% of patients with pinprick ambulated compared with 11% with preserved light touch but no pinprick. This is thought to be explained by the proximity of the spinothalamic tracts, which mediate pinprick, to the lateral corticospinal tracts.
The first attempt to relate functional capacity to level of injury was based on clinical observation and published in 1955 by Long and Lawton. 42 Their astute observations 42 have stood the test of time and have served as a guide for estimating functional capacity based on the neurologic examination and level for close to 50 years (Table 3). Recent textbooks have used a similar outline with minor revisions. 28,55 Other investigators have also examined the impact of injury level on function. 66,73 The Consortium for Spinal Cord Medicine recently published an excellent set of clinical practice guidelines on expected outcomes after traumatic SCI. 11 For this discussion, level of injury refers to motor level. It has been previously shown that motor level correlates with self-care function and is superior to the single neurologic level. 43 Motor level and neurologic level were previously defined above. It is also assumed for the sake of discussion that patients are complete and sharply demarcated at their described motor level.
C1–C4 patients are dependent for activities of daily living (ADLs), bed mobility, and transfers. They can often use a motorized wheelchair with specialized control mechanisms such as sip-and-puff. C1–C3 patients are also usually permanently dependent on mechanical ventilation. 40,69 C5 patients have active elbow flexion and can perform some simple ADLs with setup and special hand devices. This group of patients is otherwise dependent on an attendant for ADLs and transfers. They are unable to roll over or come to a sitting position in bed without additional adaptive devices. They can use a motorized wheelchair with hand controls, but they are unable to propel themselves in a manual wheelchair.
C6 patients have full innervation of the rotator cuff musculature and added shoulder stability. More importantly, active wrist extension is possible using the extensor carpi radialis. Active wrist extension is accompanied by passive finger flexion and opposition of the second digit with the thumb. This passive grip is referred to as a tenodesis grip and can be developed with appropriate occupational therapy to grasp and manipulate objects. Tenodesis grip can be strengthened using a wrist-driven flexor-hinge orthosis. Nevertheless, most of these patients still require assistance for ADLs, bed mobility, and transfers. Wheelchair propulsion is also possible for short distances on smooth, level surfaces. Hand rim projections (knobs) can facilitate this.
C7 patients gain functional strength in the triceps. The ability to forcefully extend the elbow allows the patient to lift their body weight. These patients can roll over, sit up in bed, and move about in the sitting position. Motivated patients can also transfer independently. Some assistance may still be required for toileting and dressing activities, particularly for the lower extremities. Eating can be done independently except for cutting. Independent wheelchair propulsion is possible for long distances on smooth surfaces.
C8 and T1 patients gain increasingly greater intrinsic hand function. This results in improved grasp strength and dexterity. This patient should be independent with bed mobility and transfers. Individuals with levels of C8 and below should also be independent with ADLs. Patients with injuries below T1 are at a minimum independent at wheelchair level. Prospects for meaningful ambulation depend on the variables discussed above. Sitting balance progressively improves with lower thoracic levels.
In the near future, it can be expected that there will be an increasing number of pharmacologic interventions directed at improving the long-term outcome from spinal cord injury. 39 For the purposes of objectively evaluating new treatment interventions, more precise outcome measures will be needed. Currently, the Functional Independence Measure defines community ambulation as the ability to ambulate 150 ft but does not distinguish between devices so that a person ambulating with a walker and two long leg braces is rated the same as another person ambulating with one cane and no braces. Although the Functional Independence Measure may have value for describing extent of independence or conversely the amount of assistance required, it will have limited value in clinical trials requiring a more precise measure of walking ability. New outcome measures for walking, such as the Walking Index for Spinal Cord Injury and subscales of the Spinal Cord Injury Independence Measure, may provide more accurate measures of improvement in walking. 9,22
Within the past 15 years, studies have been published on agents directed at minimizing secondary injury from SCI, facilitating neurorecovery, and enhancing function of compromised axons. Methylprednisolone in the acute setting has been accepted as the standard of care in the United States and is thought to improve long-term recovery. 3,4 There has also been preliminary evidence suggesting that GM-1 ganglioside might improve neurorecovery. 30,59 It is thought to work by augmenting axonal sprouting. Results of a multicenter study to confirm its efficacy are pending publication. 31 4-Aminopyridine is being evaluated as a potential intervention for chronic spinal cord injury. 32,48,49,53,54 It is a voltage-gated, fast potassium channel blocker that is believed to improve axonal conduction by facilitating the propagation of action potentials in demyelinated nerve fibers. The interaction of these agents with specific therapy programs and their role in optimizing functional independence remain to be elucidated. In addition, regeneration research continues in animals, and trials of cell transplantation are underway in humans. 70
Another exciting, new intervention that directly involves physical retraining is body weight support gait training. The explanation for how this might work is based on the theoretical existence of a secondary central pattern generator in the lumbar spinal cord. Based on animal and human work, it has been postulated that training this pattern generator with body weight support might facilitate the recovery of walking. 14,15,24,39,67,68 Currently, a National Institutes of Health funded multicenter study is being conducted to evaluate its potential efficacy in humans. In the future, methods that use the concept of activity-dependent neuroplasticity will most likely play an increasing role in the rehabilitation of SCI patients.
The role of electrical stimulation in gait training also needs to be elucidated. 39 Functional neuromuscular stimulation (FNS) is defined as the use of electrical stimulation to activate paralyzed or paretic muscles in precise sequence and intensity to assist in the performance of ADLs. 10 Devices that provide FNS are called neuroprostheses.
A processor controls the delivery of electrical stimulation to targeted muscles. Open loop systems do not receive input from the environment and therefore do not correct for differences between actual and intended movements. In closed loop systems the processor receives some form of input from the environment and adjusts output accordingly. The majority of the current clinical devices are open loop.
Another important variable is the mechanism of delivery for electrical current. Current can be applied externally or internally through implantation. With implantation there is the risk of infection, but selectivity and efficiency of activation are improved. Also, current requirements are significantly reduced. One implantable device approved by the Food and Drug Administration is the Freehand System (NeuroControl Corporation in Cleveland, OH).
Clinically, hand neuroprosthesis devices are being predominantly used in C5 and C6 patients to provide grasp using either a lateral pinch or palmar prehension. The applicability in C4 and above patients is currently limited secondarily to an inability to move their arms in space. In C7 and below patients, grasp can usually be augmented by alternative procedures such as tendon transfers.
Functional neuromuscular stimulation is also being used for standing and walking in SCI. One such device that uses surface stimulation and that has been approved by the Food and Drug Administration is the Parastep System (Sigmedics, Inc., Northfield, IL). It uses a walker in conjunction with FNS and requires some upper extremity function. Constant stimulation of the antigravity muscles can lead to fatigue and limits distance walked. Currently, gait with FNS remains inefficient with significantly higher energy consumption in comparison with normal gait. Researchers are also developing implantable devices. 10
The role of electric stimulation in managing bowel and bladder dysfunction as well as the collection of semen for artificial insemination are described in an accompanying article in this issue of Spine. 6 Research also continues on other applications of electrical stimulation such as the treatment of pressure ulcers and pain. 1,8,29,37,58,72
In summary, advances in pharmacologic treatment, training, and FNS, along with the potential for future regeneration strategies, have led to increased optimism and excitement regarding the prospects for future successful rehabilitation interventions.
Over the past two decades, landmark studies have been published on the natural history of neurorecovery after SCI. As clinicians, we can now predict long-term outcome for most SCIs with a reasonable degree of confidence. This will become increasingly important as third-party payers continue their efforts to efficiently ration medical services. Furthermore, current research gives rise to the hope that in the near future clinicians will be actively intervening in an attempt to alter and augment natural recovery. As this comes to fruition, functional outcomes and quality of life for SCI patients should improve.
1. Akers TK, Gabreilson AL. The effect of high voltage galvanic stimulation on the rate of healing of decubitus ulcers. Biomed Sci Instrum 1984; 20: 99–100.
2. Bosch A, Stauffer ES, Nickel VL. Incomplete traumatic quadriplegia: a ten year review. JAMA 1971; 216: 473–8.
3. Bracken MB, Shephard MJ, Collins WF, et al. A randomized trial of methylprednisolone or naloxone in the treatment of acute spinal cord injury
. N Engl J Med 1990; 322: 1405–11.
4. Bracken MB, Shephard MJ, Holford TR, et al. Administration of methylprednisolone for 24–48 hrs or tirilazad mesylate for 48 hrs in the treatment of acute spinal cord injury
. JAMA 1997; 277: 1597–604.
5. Brown PJ, Marino RJ, Herbison GJ, et al. The 72-hour examination as a predictor of recovery
in motor complete quadriplegia. Arch Phys Med Rehabil 1991; 72: 546–8.
6. Burns AS, Rivas DA, Ditunno JF. The management of neurogenic bladder and sexual dysfunction following spinal cord injury
. Spine 200;26:S129–36.
7. Burns SP, Golding DG, Rolle WA, et al. Recovery
of ambulation in motor-incomplete tetraplegia. Arch Phys Med Rehabil 1997; 78: 1169–72.
8. Carley PJ, Wainapel SF. Electrotherapy for acceleration of wound healing: low intensity direct current. Arch Phys Med Rehabil 1985; 66: 443–6.
9. Catz A, Itzkovich M, Agranov E, et al. SCIM—spinal cord independence measure: a new disability scale for patients with spinal cord lesions. Spinal Cord 1998; 36: 734–5.
10. Chae J, Kilgore K, Triolo R, et al. Functional Neuromuscular Stimulation in Spinal Cord Injury
. Phys Med Rehabil Clin North Am 2000; 11: 209–26.
11. Consortium for Spinal Cord Medicine. Outcomes
Following Traumatic Spinal Cord Injury
: Clinical Practice Guidelines for Health-Care Professionals. Paralyzed Veterans of America (PVA), 1999.
12. Crozier KS, Graziani V, Ditunno JF Jr, et al. Spinal cord injury
for ambulation based on sensory examination in patients who are initially motor complete. Arch Phys Med Rehabil 1991; 72: 119–21.
13. Crozier KS, Cheng LL, Graziani V, et al. Spinal cord injury
for ambulation based on quadriceps recovery
. Paraplegia 1992; 30: 762–7.
14. de Leon RD, Hodgson JA, Roy RR, et al. Locomotor capacity attributable to step training versus spontaneous recovery
after spinalization in adult cats. J Neurophysiol 1998; 79: 1329–40.
15. Dietz V, Wirz M, Curt A, et al. Locomotor pattern in paraplegic patients: training effects and recovery
of spinal cord function. Spinal Cord 1998; 36: 380–90.
16. Ditunno JF Jr, Sipski ML, Posuniak EA, et al. Wrist extensor recovery
in traumatic quadriplegia. Arch Phys Med Rehabil 1987; 68 (5 Part 1):287–90.
17. Ditunno JF, Stover SL, Freed MM, et al. Motor recovery
of the upper extremities in traumatic quadriplegia: a multicenter study. Arch Phys Med Rehabil 1992; 73: 431–6.
18. Ditunno JF. Rehabilitation assessment and management in the acute spinal cord injury
(SCI) patient. In: Narayan RK, Wilberger JE, Povlishock JT, eds. Neurotrauma. New York: McGraw-Hill, 1996: 1259–66.
19. Ditunno JF Jr, Cohen ME, Hauck W. Early prediction of upper extremity motor recovery
in tetraplegia: results of a 10 year multicenter study. J Spinal Cord Med 1998; 21: 162.
20. Ditunno JF Jr. The John Stanley Coulter Lecture. Predicting recovery
after spinal cord injury
: a rehabilitation imperative. Arch Phys Med Rehabil 1999; 80: 361–4.
21. Ditunno JF Jr, Cohen ME, Hauck WW, et al. Recovery
of upper-extremity strength in complete and incomplete tetraplegia: a multicenter study. Arch Phys Med Rehabil 2000; 81: 389–93.
22. Ditunno JF Jr, Ditunno PL, Graziani V, et al. Walking index for spinal cord injury
(WISCI): an international multicenter validity and reliability study. Spinal Cord 2000; 38: 234–43.
23. Eastwood EA, Hagglund KJ, Ragnarsson KT, et al. Medical rehabilitation length of stay and outcomes
for persons with traumatic spinal cord injury
: 1990–1997. Arch Phys Med Rehabil 1999; 80: 1457–63.
24. Edgerton VR, de Leon RD, Tillakaratne N, et al. Use-dependent plasticity in spinal stepping and standing. Adv Neurol 1997; 72: 233–47.
25. Fiedler IG, Laud PW, Maiman DJ, et al. Economics of managed care in spinal cord injury
. Arch Phys Med Rehabil 1999; 80: 1441–9.
26. Foo D, Subrahmanyan TS, Rossier AS. Post-traumatic acute anterior spinal cord syndrome. Paraplegia 1981; 19: 201–5.
27. Foo D. Spinal cord injury
in forty-four patients with cervical spondylosis. Paraplegia 1986; 24: 301–6.
28. Freed MM. Traumatic and congenital lesions of the spinal cord. In: Kottke FJ, Leo-Summers L, eds. Krusen’s Handbook of Physical Medicine and Rehabilitation. Philadelphia: Saunders, 1990: 717–48.
29. Gardner SE, Frantz RA, Schmidt FL. Effect of electrical stimulation on chronic wound healing: a meta-analysis. Wound Repair Regen 1999; 7: 495–503.
30. Geisler FH, Dorsey FC, Coleman WP. Recovery
of motor function after spinal-cord injury: a randomized, placebo-controlled trial with GM-1 ganglioside. N Engl J Med 1991; 324: 1829–38.
31. Geisler FH, Dorsey FC, Coleman WP. Past and current clinical studies with GM-1 ganglioside in acute spinal cord injury
. Ann Emerg Med 1993; 22: 1041–7.
32. Hansebout RR, Blight AR, Fawcett S, et al. 4-Aminopyridine in chronic spinal cord injury
: a controlled, double-blind, crossover study in eight patients. J Neurotrauma 1993; 10: 1–18.
33. Hussey RW, Stauffer ES. Spinal cord injury
: requirements for ambulation. Arch Phys Med Rehabil 1973; 54: 544–7.
34. International Standards for Neurological Classification of Spinal Cord Injury
. Chicago: American Spinal Injury Association, 2000.
35. Kirshblum SC, O’Connor KC. Predicting neurological recovery
in traumatic spinal cord injury
. Arch Phys Med Rehabil 1998; 79: 1456–66.
36. Kirshblum SC, O’Connor KC. Levels of spinal cord injury
and predictors of neurologic recovery
. Phys Med Rehabil Clin North Am 2000; 11: 1–27.
37. Kloth LC, Feedar JA. Acceleration of wound healing with high voltage, monophasic, pulsed current. Phys Ther 1988; 68: 503–8.
38. Ko HY, Ditunno JF, Graziani V, et al. The pattern of reflex recovery
during spinal shock. Spinal Cord 1999; 37: 402–9.
39. Ladouceur M, Pepin A, Norman KE, et al. Recovery
of walking after spinal cord injury
. Adv Neurol 1997; 72: 249–55.
40. Lanig IS, Lammertse DP. The respiratory system in spinal cord injury
. Phys Med Rehabil Clin North Am 1992; 3: 725–40.
41. Little JW, Halar E. Temporal course of motor recovery
after Brown-Sequard spinal cord injury
. Paraplegia 1985; 23: 39–46.
42. Long C, Lawton EB. Functional significance of spinal cord lesion level. Arch Phys Med Rehabil 1955; 36: 249–55.
43. Marino RJ, Rider-Foster D, Maissel G, et al. Superiority of motor level over single neurological level in categorizing tetraplegia. Paraplegia 1995; 33: 510–3.
44. Maynard FM, Reynolds GG, Fountain S, et al. Neurological prognosis
after traumatic quadriplegia: three year experience of California Regional Spinal Cord Injury
Care System. J Neurosurg 1979; 50: 611–6.
45. Maynard FM Jr, Bracken MB, Creasey G, et al. International standards for neurological and functional classification of spinal cord injury
patients (revised). Spinal Cord 1997; 35: 266–74.
46. Merriam WF, Taylor TKF, Ruff SJ, et al. A reappraisal of acute traumatic central cord syndrome. J Bone Joint Surg Br 1986; 68: 708–13.
47. Penrod LE, Hegde SK, Ditunno JF. Age effect on prognosis
for functional recovery
in acute, traumatic central cord syndrome. Arch Phys Med Rehabil 1990; 71: 963–8.
48. Potter PJ, Hayes KC, Segal JL, et al. Randomized double-blind crossover trial of fampridine-SR (sustained release 4-aminopyridine) in patients with incomplete spinal cord injury
. J Neurotrauma 1998; 15: 837–49.
49. Potter PJ, Hayes KC, Hsieh JT, et al. Sustained improvements in neurological function in spinal cord injured patients treated with oral 4-aminopyridine: three cases. Spinal Cord 1998; 36: 147–55.
50. Poynton AR, O’Farrel DA, Shannon F, et al. Sparing of sensation to pinprick predicts recovery
of a motor segment after injury to the spinal cord. J Bone Joint Surg Br 1997; 79: 952–4.
51. Rogers JC, Figone JJ. Traumatic quadriplegia: follow-up study of self-care skills. Arch Phys Med Rehabil 1980; 61: 316–21.
52. Runge M. Follow-up study of self-care activities in traumatic spinal cord injury
quadriplegics and quadriparetics. Am J Occup Ther 1966; 20: 241–9.
53. Segal JL, Brunnemann SR. 4-Aminopyridine alters gait characteristics and enhances locomotion in spinal cord injured humans. J Spinal Cord Med 1998; 21: 200–4.
54. Segal JL, Pathak MS, Hernandez JP, et al. Safety and efficacy of 4-aminopyridine in humans with spinal cord injury
: a long-term, controlled trial. Pharmacotherapy 1999; 19: 713–23.
55. Staas WE Jr, Formal CS, Gershkoff AM, et al. Rehabilitation of the spinal cord-injured patient. In: DeLisa JA, ed. Rehabilitation Medicine: Principles and Practice. Philadelphia: Lippincott, 1988: 635–59.
56. Stauffer ES. Rehabilitation of posttraumatic cervical spinal cord quadriplegia and pentaplegia. In: Cervical Spine Research Society, eds. The Cervical Spine. Philadelphia: Lippincott, 1983.
57. Taylor RG, Gleave JRW. Incomplete spinal cord injuries: Brown-Sequard phenomena. J Bone Joint Surg Br 1957; 39: 438–50.
58. ten Vaarwerk IA, Staal MJ. Spinal cord stimulation in chronic pain syndromes. Spinal Cord 1998; 36: 671–82.
59. Walker JB, Harris M. GM-1 ganglioside administration combined with physical therapy restores ambulation in humans with chronic spinal cord injury
. Neurosci Lett 1993; 161: 174–8.
60. Waters RL, Adkins RH, Yakura JS. Definition of complete spinal cord injury
. Paraplegia 1991; 29: 573–81.
61. Waters RL, Yakura JS, Adkins RH, et al. Recovery
following complete paraplegia. Arch Phys Med Rehabil 1992; 73: 784–9.
62. Waters RL, Adkins RH, Yakura JS, et al. Motor and sensory recovery
following complete tetraplegia. Arch Phys Med Rehabil 1993; 74: 242–7.
63. Waters RL, Adkins RH, Yakura JS, et al. Motor and sensory recovery
following incomplete paraplegia. Arch Phys Med Rehabil 1994; 75: 67–72.
64. Waters RL, Adkins RH, Yakura JS, et al. Motor and sensory recovery
following incomplete tetraplegia. Arch Phys Med Rehabil 1994; 75: 306–11.
65. Waters RL. Donald Munro lecture: functional and neurologic recovery
following acute SCI. J Spinal Cord Med 1998; 21: 195–9.
66. Welch RD, Lobley SJ, O’Sullivan SB, et al. Functional independence in quadriplegia: critical levels. Arch Phys Med Rehabil 1986; 67: 235–40.
67. Wernig A, Muller S, Nanassy A, et al. Laufband therapy based on rules of spinal locomotion is effective in spinal cord injured persons. Eur J Neurosci 1995; 7: 823–9.
68. Wickelgren I. Teaching the spinal cord to walk. Science 1998; 279: 319–21.
69. Wicks AB, Mentor RR. Long term outlook in quadriplegic patients with initial ventilation dependency. Chest 1986; 90: 406–10.
70. Wirth ED III, Fessler RG, Reier PJ, et al. Feasibility and safety of neural tissue transplantation in patients with syringomyelia. Soc Neurosci Abstr 1998; 24: 70.
71. Yarkony GM, Roth EJ, Heinemann AW, et al. Functional skills after spinal cord injury
rehabilitation: three-year longitudinal follow-up. Arch Phys Med Rehabil 1988; 69: 111–4.
72. Yarkony GM, Roth EJ, Cybulski GR, et al. Neuromuscular stimulation in spinal cord injury
: II. Prevention of secondary complications. Arch Phys Med Rehabil 1992; 73: 195–200.
73. Zafonte RD, Demangone DA, Herbison GJ, et al. Daily self-care in quadriplegic subjects. Neurol Rehabil 1991; 1: 17–24.