| | Paraplegia After Aortic Aneurysm Repair Versus Traumatic Spinal Cord Injury: Functional Outcome, Complications, and Therapy Intensity of Inpatient RehabilitationAbstract Yokoyama O, Sakuma F, Itoh R, Sashika H. Paraplegia after aortic aneurysm repair versus traumatic spinal cord injury: functional outcome, complications, and therapy intensity of inpatient rehabilitation. ObjectiveTo compare outcomes, complications, and therapy intensity of inpatient rehabilitation in patients with paraplegia caused by spinal cord injury associated with aortic aneurysm repair (SCI-AA) versus patients with traumatic spinal cord injury (SCI). DesignCase-controlled study. SettingSCI unit in a rehabilitation center. ParticipantsSeventeen patients with SCI-AA and 17 patients with traumatic SCI. InterventionStandard rehabilitation therapy for SCI. Main Outcome MeasuresLength of stay (LOS) in acute and rehabilitation hospitals; FIM instrument scores; FIM change; FIM efficiency; complications; therapy intensity; and ambulatory state and return to community at discharge. ResultsNo significant differences were noted in acute and rehabilitation LOS and admission FIM scores. Discharge FIM scores, FIM change, and FIM efficiencies were significantly lower in the SCI-AA group, which had many complications related to AA and SCI. Intensity of rehabilitation sports therapy in the SCI-AA group was significantly lower than that of the traumatic SCI group, but total therapy intensity did not differ significantly. Both had similar rates of return to ambulatory state and discharge to the community. ConclusionsSCI-AA patients had many complications that interfered with rehabilitation therapy, and could not achieve functional gains comparable to those with traumatic SCI. However, both groups achieved comparable success with return to ambulatory state and discharge to the community.
AFTER THE SURGICAL REPAIR of an aortic aneurysm (AA), spinal cord injury (SCI) with paraplegia is among the most devastating and unpredictable complications. Spinal cord ischemia is caused by aortic cross-clamping and interruption of blood flow to the spinal cord via critical intercostal arteries. The causation of SCI during AA repair is thought to depend on various factors, including clamping time, reperfusion injury, and hemodynamics.1 As for the arterial blood supply of the spinal cord, the mid-thoracic area is poorly vascularized with 1 (or, occasionally, no) anterior medullary artery that originates from the intercostal artery. In the thoracic area, the distance between medullary arteries is the greatest, and the watershed effect is most striking.2 Various methods have been devised to protect against spinal cord ischemia during surgery for AA, such as cerebrospinal fluid drainage,3 hypothermia,4, 5 monitoring of somatosensory and motor-evoked potentials,6 intercostal artery reattachment,7 distal aortic perfusion,8 and direct spinal cord cooling.9 The incidence of SCI as a complication of AA repair is 3.0% to 18.0%.1, 3, 10, 11, 12, 13
A paucity of information exists on rehabilitation for SCI caused by AA. Some authors reported outcomes in patients with particular subtypes of nontraumatic SCI,14, 15, 16 and spinal infarction caused by AA was included as part of the vascular etiology of nontraumatic SCI.17
These reports did not discuss the number of therapy sessions, therapy intensity (total number of therapy sessions divided by the length of stay [LOS]), or complications during inpatient rehabilitation. Some studies18, 19, 20 reported that more intense rehabilitation (therapy dosages) may contribute to greater functional gains. However, Heinemann et al21 reported that a relationship between therapy intensity and outcomes had not been demonstrated for patients receiving rehabilitation for SCI. They showed that interrupted rehabilitation due to complications and comorbidities was associated with decreased achievement of motor gains.
The purpose of this study was to investigate the outcome of inpatient rehabilitation, complications during rehabilitation hospitalization, preexisting medical comorbidities, and therapy intensity in patients with paraplegia after AA repair (SCI-AA) versus patients with traumatic SCI. A comparison between SCI-AA and traumatic SCI controlling for age, level of injury, and American Spinal Injury Association (ASIA) classification22 was used to enhance generalizations.
Patients with nontraumatic SCI, compared with those with traumatic SCI, presented with associated medical complications, such as cardiopulmonary disease, or diabetes, which could lead to decreased functional outcomes.23 AA was strongly associated with cardiovascular disease. After AA repair, serious organ dysfunction commonly occurs and limits functional recovery.10 We hypothesized that patients with SCI-AA compared with those with traumatic SCI would have the following: (1) lower FIM instrument scores at discharge and lower FIM efficiency, (2) lower return to ambulatory state and return to the community at discharge, (3) more complications and preexisting medical comorbidities, and (4) lower therapy intensity.
Methods  Participants Our hospital was a rehabilitation center with 280 beds, including 80 beds in a spinal cord rehabilitation ward. Our hospital had 29 physical therapists, 18 occupational therapists, and 7 rehabilitation sports instructors. We collected retrospective data on consecutive patients with SCI-AA or traumatic SCI who were admitted to the spinal cord rehabilitation ward between 2000 and 2004. We established the following inclusion criteria for patients in this study: (1) complete data available for age, injury level, completeness of injury, LOS in an acute care hospital and LOS in the rehabilitation center, FIM scores, ambulatory state, rehabilitation exercise time, discharge placement, complications during rehabilitation hospitalization, and preexisting medical comorbidities; and (2) admittance from the acute care hospital more than 3 weeks after injury. This was the reason that all the patients with SCI-AA admitted to our hospital after acute medical management, and more than 3 weeks later after injury. The established exclusion criteria were as follows: (1) patients with cognitive disturbances that inhibited them from participating in the rehabilitation program; (2) patients who had severe upper-limb dysfunction that prevented them from participating in the rehabilitation program due to peripheral nerve palsy, severe hemiplegia, or severe restriction of range of motion with fracture; and (3) patients who were transferred to an acute medical hospital for the treatment of medical complications. There were 20 patients with SCI-AA admitted during the 5-year period. One patient was excluded because he was transferred to an acute medical hospital for the treatment of a medical complication. Three patients had cerebral infarction, but they were not excluded because they had very mild hemiparesis (Brunnstrom stage V or VI of the upper extremity and hand) that did not prevent them from participating in the rehabilitation program. There were 352 patients in the traumatic SCI group. Twenty-eight were excluded because of cognitive disturbances. Three patients were excluded due to upper-limb dysfunction (plexus injury, n=2; fracture, n=1). The remaining 19 patients in the SCI-AA group and 321 patients in the traumatic SCI group were enrolled in this study. Matching Procedure For outcomes evaluation, we used a block-design matching procedure to control for the covariant effects of injury characteristics and age at injury on the etiology effect. Three matching variables were selected: (1) level of neurologic injury, (2) ASIA impairment classification, and (3) age at time of injury. The level of injury in all patients in the SCI-AA group was in the thoracic regions. Thus, we classified the level of injury into 2 groups: the upper thoracic region (T2-6) group and the lower thoracic region (T7-12) group. ASIA impairment classification comprised 4 grades (A through D) (table 1). Age category at time of injury comprised 2 groups: a “younger” group (<50y) and an “older” group (≥50y). The choice of age 50 years as a break point was made on the basis of previous reports.24, 25, 26 Each patient was identified by an injury type and age group classification and categorized based on etiology characteristic. Patients were selected by age (within 10y), further controlling for the covariant effects of age at injury on the etiology effect, from each etiology group to create matched dyads on the basis of the injury type and age group classification. When multiple SCI-AA and traumatic SCI patients were identified within the same injury type and age group classification, the patients were randomly matched until no more aortic aneurysmal and traumatic dyads could be created. Seventeen patients with SCI-AA were successfully matched with 17 counterparts with traumatic SCI (table 2). | | |  | Grade | Classification |  |
 | A | Complete: No motor or sensory function is preserved in the sacral segments S4–S5. |  |
 | B | Incomplete: Sensory but not motor function is preserved below the neurological level and extends through the sacral segments S4–S5. |  |
 | C | Incomplete: Motor function is preserved below the neurological level, and more than half of key muscles below the neurological level have a muscle grade less than 3. |  |
 | D | Incomplete: Motor function is preserved below the neurological level, and at least half of key muscles below the neurological level have a muscle grade of 3 or more. |  |
 | E | Normal: Motor and sensory function are normal. |  | | | |
| | |  | Patients | SCI-AA | Traumatic SCI |  |
|---|
 | (n=17) | (n=17) |  |
|---|
 | (Age [y]/LOI/ASIA grade) | (Age [y]/LOI/ASIA grade) |  |
 | 1 | 46/T12/A | 45/T9/A |  |
 | 2 | 52/T8/A | 53/T11/A |  |
 | 3 | 59/T7/A | 57/T11/A |  |
 | 4 | 64/T9/A | 58/T9/A |  |
 | 5 | 64/T7/A | 63/T10/A |  |
 | 6 | 65/T5/A | 67/T5/A |  |
 | 7 | 68/T11/A | 65/T12/A |  |
 | 8 | 70/T7/A | 70/T12/A |  |
 | 9 | 32/T10/B | 35/T12/B |  |
 | 10 | 46/T12/B | 46/T12/B |  |
 | 11 | 56/T9/C | 51/T12/C |  |
 | 12 | 61/T10/C | 53/T12/C |  |
 | 13 | 68/T7/C | 65/T12/C |  |
 | 14 | 56/T9/D | 55/T9/D |  |
 | 15 | 60/T12/D | 56/T12/D |  |
 | 16 | 63/T9/D | 62/T9/D |  |
 | 17 | 67/T12/D | 71/T12/D |  | | | |
Therapy Intensity The standard rehabilitation program for patients with paraplegia was composed of 40 minutes of physical therapy (PT), 40 minutes of occupational therapy (OT), and 40 minutes of rehabilitation sports therapy per day, 5 days a week. We counted every 40 minutes of exercise in the gymnasium as 1 therapy session. Bedside exercises were not included, because aggressive exercises could not be done in those circumstances. We counted the number of patients receiving each therapy, the total number of therapy sessions during the rehabilitation hospitalization, and the therapy intensity. Outcome Measures Outcomes variables were as follows: LOS in the acute and rehabilitation hospitals; FIM score27; FIM change (discharge FIM minus admission FIM); FIM efficiency (FIM change divided by LOS); ambulatory state at discharge; discharge to the community; total therapy sessions and therapy intensity; complications during rehabilitation hospitalization; and preexisting medical comorbidities. Ambulatory state was classified into 2 groups: ambulatory and nonambulatory. The ambulatory subjects were defined as those who could walk within homes with or without orthoses or devices. Complications during rehabilitation hospitalization and preexisting medical comorbidities were collected from medical records. Data Analysis We conducted data analyses to compare the relationship between patients with SCI-AA and their counterparts with traumatic SCI. Independent 2-tailed t tests were performed between the 2 groups for parametric data. Chi-square analyses were also performed to determine group differences for nonparametric data. The level of statistical significance was set at P less than .05.
Results  Participants The etiology of the SCI-AA group (n=17) was dissecting aneurysm in 13 (76.4%) patients, descending thoracic AA in 1 (5.9%) patient, thoracoabdominal AA in 2 (11.8%) patients, and infrarenal abdominal AA in 1 (5.9%) patient. DeBakey classification of dissecting aneurysms was the following: type I, 4 patients; type II, 1 patient; type IIIa, no patients; and type IIIb, 8 patients. The identifiable etiology for the dissection was Marfan syndrome (1 patient). Thirteen (76.4%) patients underwent surgical therapy and 4 (23.6%) patients were treated medically. Surgical therapy was elective in 6 patients for rapid expansion, and urgent or emergency in 7 patients for symptoms such as chest pain, back pain, or abdominal pain. Of these 13 patients who underwent surgical therapy, 3 patients had preoperative paraplegia and 10 patients became paraplegic after surgery. In all 4 patients who were treated medically, paraplegia was observed on admission into the acute hospital. The etiology of the traumatic SCI group (n=17) was fall in 13 (76.4%) patients and motor vehicle collision in 4 (23.6%) patients. The mean age of subjects in the SCI-AA group and the traumatic SCI group was similar (58.6y vs 57.2y, respectively). The level of injury of each of the 2 groups was from T5 to T12. As for the ASIA classification of the 2 groups, 8 patients were grade A, 2 patients were grade B, 3 patients were grade C, and 4 patients were grade D. FIM Comparison There were no significant differences between the 2 groups in the admission FIM total, motor, and cognitive scores. Significant differences were noted between the SCI-AA and SCI groups, respectively, in the discharge FIM total scores (95.6 vs 107.2, P<.05), FIM motor scores (62.7 vs 72.8, P<.05), FIM total change (23.5 vs 33.2, P<.05), FIM motor change (23.4 vs 32.8, P<.05), and FIM efficiency (.182 vs .308, P<.01). There were no significant differences between the 2 groups in the discharge FIM cognitive score and FIM cognitive change (table 4). | | |  | FIM Measures | SCI-AA | Traumatic SCI | P |  |
|---|
 | (n=17) | (n=17) |  |
 | Admission FIM | 72.1±16.1 | 74.1±14.0 | .72 |  |
 | Discharge FIM | 95.6±16.2 | 107.2±11.1 | .02 |  |
 | FIM change | 23.5±10.6 | 33.2±13.5 | .03 |  |
 | FIM efficiency | 0.182±0.095 | 0.308±0.128 | <.01 |  |
 | Admission FIM motor | 39.4±15.7 | 40.1±13.6 | .89 |  |
 | Discharge FIM motor | 62.8±15.0 | 72.8±10.4 | .03 |  |
 | FIM motor change | 23.4±10.6 | 32.8±13.3 | .03 |  |
 | Admission FIM cognitive | 32.8±3.77 | 34.0±2.00 | .25 |  |
 | Discharge FIM cognitive | 32.9±3.55 | 34.4±1.28 | .11 |  |
 | FIM cognitive change | 0.12±0.47 | 0.41±1.70 | .51 |  | | | |
Ambulatory State and Discharge to the Community There were no significant differences between the 2 groups in the rate of return to an ambulatory state (17.6% for SCI-AA vs 35.3% for SCI) and return to community (82.4% for SCI-AA vs 100% for SCI) at discharge (see table 3). Complications and Preexisting Medical Comorbidities There were no significant differences between the 2 groups in the occurrences of complications related to SCI, such as pressure ulcers, urinary tract infections, bladder stones, heterotopic ossification, ileus, and pain during rehabilitation hospitalization. Complications related to AA or atherosclerotic disease, such as cerebral infarction in 1 patient and cardiac disease in 2 patients and occlusion of peripheral artery in 1 patient during rehabilitation hospitalization, were noted in patients in the SCI-AA group. One patient with SCI-AA had recurrent pneumonia and required tracheostomy during the rehabilitation hospitalization (table 5). | | |  | Complications and Comorbidities | SCI-AA | Traumatic SCI | P |  |
|---|
 | (n=17) | (n=17) |  |
 | Complications during rehabilitation hospitalization | | | |  |
 | Pressure ulcers | 8 | 4 | .151 |  |
 | Urinary tract infections | 6 | 5 | .714 |  |
 | Bladder stones | 2 | 1 | .545 |  |
 | Heterotopic ossification | 2 | 0 | .141 |  |
 | Pain | 2 | 1 | .545 |  |
 | Ileus | 1 | 0 | .31 |  |
 | Cardiac disease | 2 | 0 | .141 |  |
 |  Angina pectoris | 2 | 0 | .141 |  |
 | Cerebral infarction | 1 | 0 | .31 |  |
 | Occlusion of peripheral artery | 1 | 0 | .31 |  |
 | Pneumonia | 1 | 0 | .31 |  |
 | Tracheostomy insertion | 1 | 0 | .31 |  |
 | Preexisting medical comorbidities | | | |  |
 | Hypertension | 16 | 4 | <.01 |  |
 | Cardiac disease | 7 | 1 | .01 |  |
 |  Angina pectoris | 3 | 1 | .29 |  |
 |  Myocardial infarction | 1 | 0 | .31 |  |
 |  Chronic heart failure | 1 | 0 | .31 |  |
 |  Sick sinus syndrome | 1 | 0 | .31 |  |
 |  Atrial fibrillation | 1 | 0 | .31 |  |
 | Renal insufficiency | 1 | 0 | .31 |  |
 | Cerebral infarction | 2 | 0 | .141 |  |
 | Hyperlipemia | 3 | 0 | .07 |  |
 | Patency of the false lumen | 1 | 0 | .31 |  |
 | Hyperuricemia | 2 | 0 | .141 |  |
 | Diabetes mellitus | 0 | 2 | .141 |  |
 |  Insulin-dependent diabetes mellitus | 0 | 1 | .31 |  |
 |  Non-insulin−dependent diabetes mellitus | 0 | 1 | .31 |  | | | |
Significant differences were noted in the preexisting medical comorbidities between the 2 groups, such as the prevalence of hypertension and cardiac complications (angina pectoris, prior myocardial infarction, chronic heart failure, arrhythmias). There were no significant differences between these groups in the preexisting medical comorbidities, such as hyperlipemia, hyperuricemia, or diabetes mellitus. In the SCI-AA group, 1 patient had a patent false lumen that was thought to contribute to a risk of rupture or dissection.28 Another patient in the SCI-AA group had renal insufficiency, which was defined as a serum creatinine level of 2.0mg/dL or more. A serum creatinine of this patient was simply elevated, and he was not on hemodialysis. Two patients in the SCI-AA group had a preexisting cerebral infarction (see table 5). Therapy Comparison There were no significant differences between the SCI-AA and SCI groups in the number of patients receiving PT (17 vs 17, respectively) and OT (14 vs 10, respectively). Significant differences were noted between these groups in the number of patients receiving rehabilitation sports therapy (0 vs 7, respectively; P<.01). The amount and the intensity of PT and OT were similar between the SCI-AA and SCI groups (PT amount, 75.5 vs 69.8 sessions, respectively; PT intensity, .58 vs .65, respectively; OT amount, 41.8 vs 32.3 sessions, respectively; OT intensity, .31 vs .26, respectively). Significant differences were noted between the SCI-AA and SCI groups in the amount and intensity of rehabilitation sports therapy (amount, 0.0 vs 12.4 sessions, respectively, P<.05; intensity, 0.00 vs 0.11, respectively, P<.05). The amount of total therapy sessions during the rehabilitation hospitalization was similar between the SCI-AA and SCI groups (117.3 vs 114.6 sessions, respectively), and no significant differences were noted in therapy intensity (0.889 vs 1.024, respectively) (table 6).
Discussion  LOS in acute hospitals for the SCI-AA group was comparable to that of the traumatic SCI group. The traumatic SCI patients may have had medical issues from the trauma itself, such as vertebral instability, hemodynamic stabilization, multiple fractures, abdominal injuries, and concomitant brain injury. Similarly, the SCI-AA patients may have had medical issues such as treating hypertension to prevent rupture, hemodynamic stabilization, pneumonia, cardiac disease, and prolonged delirium. These medical issues caused in each group may have affected the LOS in the acute hospital.15, 29 In addition, the admission FIM scores for the SCI-AA and traumatic SCI groups were similar in this study. This was probably due to controlling for age, level of injury, and completeness. These factors, such as age, level of injury, and completeness, might affect the functional outcome; therefore they had to be controlled for matching process in this study. McKinley et al showed similar FIM efficiency of rehabilitation outcome between neoplastic SCI and traumatic SCI patients15 and between nontraumatic SCI patients and traumatic SCI patients.29 New17 described that the occurrence of many complications was less common in nontraumatic SCI patients than in traumatic SCI patients. Significantly lower discharge FIM total scores, FIM motor scores, FIM change, FIM motor change, and FIM efficiency in the SCI-AA group were noted as compared with the traumatic SCI group in this study. This was probably affected by complications and preexisting medical comorbidities. The occurrence of those complications related to SCI with the SCI-AA group was comparable to that of the traumatic SCI group. The SCI-AA group had more complications during hospitalization and preexisting medical comorbidities related to AA such as hypertension and cardiac disease, cerebral infarction, patent false lumen, recurrent pneumonia, and peripheral artery occlusion. These complications and preexisting medical comorbidities could interfere with the rehabilitation process. According to the therapy comparison, no patients in the SCI-AA group were receiving rehabilitation sports therapy. The reason for this was to prevent the risk of rupture or enlarging of the AA due to markedly increasing blood pressure by aggressive exercise of rehabilitation sports therapy. The total number of sessions in the PT SCI-AA group was comparable to that of the traumatic SCI group. But the PT intensity in the SCI-AA group was less than that in the traumatic SCI group. Furthermore, the amount of total therapy sessions in the SCI-AA group was almost the same as that in the traumatic group, and the intensity of total therapy in the SCI-AA group was less than that of the traumatic SCI group. However, these differences were not significant. Thus, patients in the SCI-AA group had complications during the rehabilitation hospitalization, and these complications prevented successive rehabilitation therapy, diminished therapy intensity, and may have led to decreased functional outcomes as compared with the traumatic SCI group. During and after training of the patients in the SCI-AA group, vital signs were monitored, the diastolic blood pressure was not allowed to increase more than 20mmHg above the diastolic blood pressure at rest, and the heart rate was not allowed to reach more than 50% of the predicted maximum heart rate. Our patients had no complaints of chest or back pain during training, but 1 patient, who was excluded from this study, was noted to have an enlarged dissecting aneurysm and complicated disseminated intravascular coagulation syndrome. This patient was transferred to an acute medical hospital to treat these complications and could not continue an intensive rehabilitation program due to the complications. As well as complications and preexisting medical comorbidities related to AA and recurrent pneumonia, these limitations for exercise to prevent rupture or enlargement of the AA could lead to decreased therapy intensity and to lower functional outcomes as compared with the traumatic SCI group. The rate of ambulation at discharge in the SCI-AA group was half of that in the traumatic SCI group, but significant differences were not noted. The rate of return to community life was similar between the 2 groups. In both the SCI-AA group and the traumatic SCI group, more than 80% of patients were able to return to their own home. Study Limitations This study had several limitations. The number of subjects was relatively small, which increased the chance of error. Furthermore, because the results reflect the practice and referral pattern of only 1 rehabilitation center, the generalization of the findings is limited. Patients with SCI-AA not admitted to the spinal cord rehabilitation ward included the following: those who died at the acute hospital, those with very mild ischemia who recovered quickly at the acute hospital and did not need inpatient rehabilitation therapy, and those who had a poor prognosis for rehabilitation and were transferred to another hospital, nursing home, or palliative care unit. The matching process in this study was broad in age, level of injury, and ASIA impairment classification. Other factors or preexisting medical comorbidities will affect both outcome and potential recovery after AA repair. But preexisting medical comorbidities were different between the SCI-AA and traumatic SCI groups. The implication of the results of the present study is that prospective studies of patients with SCI-AA are needed. Future studies should include a larger sample size, should be done by multicenter research, including acute hospitals, documentation of complications and preexisting medical comorbidities, rehabilitation therapy from the acute hospital, and long-term follow-up outcome.
Conclusions  Patients with SCI-AA had numerous medical complications and preexisting medical comorbidities related to AA and SCI. These complications and comorbidities prevented rehabilitation therapy and diminished therapy intensity. Consequently, patients with SCI-AA have lower discharge FIM scores and FIM efficiency compared with those of traumatic SCI counterparts. However, they achieved comparable rates of return to an ambulatory state and return to community life at discharge.
References  1.
1
Tabayashi K
.
Spinal cord protection during thoracoabdominal aneurysm repair
.
Surg Today
. 2005;35:1–6
.
MEDLINE |
CrossRef
2.
2
Sliwa JA
, Maclean IC
.
Ischemic myelopathy
(a review of spinal vasculature and related clinical syndromes)
.
Arch Phys Med Rehabil
. 1992;73:365–372
.
MEDLINE |
CrossRef
3.
3
Coselli JS
, Le Maire SA
, Koksoy C
, Schmitting ZC
, Curling PE
.
Cerebrospinal fluid drainage reduces paraplegia following thoracoabdominal aortic aneurysm repair
(results of a prospective randomized trial)
.
J Vasc Surg
. 2002;35:631–639
.
Abstract | Full Text |
Full-Text PDF (89 KB)
|
CrossRef
4.
4
Tabayashi K
, Niibori K
, Konno H
, Mohri H
.
Protection from postischemic spinal cord injury by perfusion cooling of the epidural space
.
Ann Thorac Surg
. 1993;56:494–498
.
MEDLINE 5.
5
Marsala M
, Vanicky I
, Galik J
, Radonak J
, Kundrat I
, Marsala J
.
Panmyelic epidural cooling protects against ischemic spinal cord damage
.
J Surg Res
. 1993;55:21–31
.
MEDLINE |
CrossRef
6.
6
Laschinger JC
, Owen J
, Rosenbloom M
, Cox JL
, Kouchoukos NT
.
Direct noninvasive monitoring of spinal cord motor function during thoracic aortic occlusion
(use of motor evoked potentials)
.
J Vasc Surg
. 1988;7:161–171
.
Abstract | Full Text |
Full-Text PDF (1097 KB)
|
CrossRef
7.
7
Griepp RB
, Ergin MA
, Galla JD
, et al.
Looking for the artery of Adamkiewicz
(a quest to minimize paraplegia after operations for aneurysms of the descending thoracic and thoracoabdominal aorta)
.
J Thorac Cardiovasc Surg
. 1996;112:1202–1213
.
Abstract | Full Text |
Full-Text PDF (1563 KB)
|
CrossRef
8.
8
Safi HJ
, Miller CC
, Huynh TT
, et al.
Distal aortic perfusion and cerebrospinal fluid drainage for thoracoabdominal and descending thoracic aortic repair
(ten years of organ protection)
.
Ann Surg
. 2003;238:372–380
.
MEDLINE 9.
9
Cambria RP
, Davison JK
, Zannetti S
, et al.
Clinical experience with epidural cooling for spinal cord protection during thoracic and thoracoabdominal aneurysm repair
.
J Vasc Surg
. 1997;25:234–241
.
Abstract | Full Text 10.
10
Rectenwald JE
, Huber TS
, Martin TD
, et al.
Functional outcome after thoracoabdominal aortic aneurysm repair
.
J Vasc Surg
. 2002;35:640–647
.
Abstract | Full Text |
Full-Text PDF (103 KB)
|
CrossRef
11.
11
Estrera AL
, Miller CC
, Huynh TT
, Porat E
, Safi HJ
.
Neurologic outcome after thoracic and thoracoabdominal aortic aneurysm repair
.
Ann Thorac Surg
. 2001;120:224–229
.
12.
12
Murray MJ
, Bower TC
, Oliver WC
, Werner E
, Gloviczki P
.
Effects of cerebrospinal fluid drainage in patients undergoing thoracic and thoracoabdominal aortic surgery
.
J Cardiothorac Vasc Anesth
. 1993;7:266–272
.
MEDLINE |
CrossRef
13.
13
Grabitz K
, Sandmann W
, Stuhmeier K
, et al.
The risk of ischemic spinal cord injury in patients undergoing graft replacement for thoracoabdominal aortic aneurysms
.
J Vasc Surg
. 1996;23:230–240
.
Abstract | Full Text |
Full-Text PDF (2077 KB)
|
CrossRef
14.
14
McKinley WO
, Conti-Wyneken AR
, Vokac CW
, Cifu DW
.
Rehabilitative functional outcome of patients with neoplastic spinal cord compression
.
Arch Phys Med Rehabil
. 1996;77:892–895
.
Abstract |
Full-Text PDF (434 KB)
|
CrossRef
15.
15
McKinley WO
, Huang ME
, Brunsvold KT
.
Neoplastic versus traumatic spinal cord injury
(an outcome comparison after inpatient rehabilitation)
.
Arch Phys Med Rehabil
. 1999;80:1253–1257
.
Abstract |
Full-Text PDF (698 KB)
|
CrossRef
16.
16
McKinley WO
, Tellis AA
, Cifu DX
, et al.
Rehabilitation outcome of individuals with nontraumatic myelopathy resulting from spinal stenosis
.
J Spinal Cord Med
. 1998;21:131–136
.
MEDLINE 17.
17
New PE
.
Functional outcomes and disability after nontraumatic spinal cord injury rehabilitation
(results from a retrospective study)
.
Arch Phys Med Rehabil
. 2005;86:250–261
.
Abstract | Full Text |
Full-Text PDF (160 KB)
|
CrossRef
18.
18
Kwakkel G
, Wagenaar RC
, Twisk JW
, Lankhorst GJ
, Koetsier JC
.
Intensity of leg and arm training after primary middle-cerebral artery stroke
(a randomized trial)
.
Lancet
. 1999;354:191–196
.
CrossRef
19.
19
Jette DU
, Warren RL
, Wirtalla C
.
The relation between therapy intensity and outcomes of rehabilitation in skilled nursing facilities
.
Arch Phys Med Rehabil
. 2005;86:373–379
.
Abstract | Full Text |
Full-Text PDF (118 KB)
|
CrossRef
20.
20
Sonoda S
, Saitoh E
, Nagai S
, Kawakita M
, Kanada Y
.
Full-time integrated treatment program, a new system for stroke rehabilitation in Japan
(comparison with conventional rehabilitation)
.
Am J Phys Med Rehabil
. 2004;83:88–93
.
MEDLINE |
CrossRef
21.
21
Heinemann AW
, Hamilton B
, Linacre JM
, Wright BD
, Granger CV
.
Functional status and therapeutic intensity during inpatient rehabilitation
.
Am J Phys Med Rehabil
. 1995;74:315–326
.
MEDLINE |
CrossRef
22.
22
Ditunno JF
, Young W
, Donovan WH
, Creasey G
.
The international standards booklet for neurological and functional classification of spinal cord injury. American Spinal Injury Association
.
Paraplegia
. 1994;32:70–80
.
MEDLINE 23.
23
Kirshblum SC
, Groah SL
, McKinley WO
, Gittler MS
, Stiens SA
.
Spinal cord injury medicine. 1. Etiology, classification, and acute medical management
.
Arch Phys Med Rehabil
. 2002;83(Suppl 1):S50–S57
.
Abstract |
CrossRef
24.
24
Scivoletto G
, Morganti B
, Ditunno P
, Ditunno JF
, Molinari M
.
Effects on age on spinal cord lesion patients’ rehabilitation
.
Spinal Cord
. 2003;41:457–464
.
MEDLINE |
CrossRef
25.
25
Penrod LE
, Hedge SK
, Ditunno JF
.
Age effects on prognosis for functional recovery in acute traumatic central cord syndrome
.
Arch Phys Med Rehabil
. 1990;71:963–968
.
MEDLINE 26.
26
Roth EJ
, Lovell L
, Heinemann AW
, Lee MY
, Yarkony GM
.
The older adult with a spinal cord injury
.
Paraplegia
. 1992;30:520–526
.
MEDLINE 27.
27
Hamilton B
, Granger C
, Sherwin F
, Zielezny M
, Tashman JA
.
Uniform national data system for medical rehabilitation
.
In:
Fuhrer MJ
editors.
Rehabilitation outcome
(analysis and measurement)
. Baltimore: PH Brooks; 1987;p. 137–147
.
28.
28
Dinsmore RE
, Willerson JT
, Buckley MJ
.
Dissecting aneurysm of the aorta
(aortographic features affecting prognosis)
.
Radiology
. 1972;105:567–570
.
MEDLINE 29.
29
McKinley WO
, Seel RT
, Gadi RK
, Tewksbury MA
.
Nontraumatic vs. traumatic spinal cord injury
(a rehabilitation outcome comparison)
.
Am J Phys Med Rehabil
. 2001;80:693–699
.
MEDLINE |
CrossRef
a Department of Rehabilitation Medicine, Kanagawa Rehabilitation Hospital, Japan b Department of Rehabilitation Medicine, Yokohama City University School of Medicine, Yokohama, Japan Reprint requests to Osamu Yokoyama, MD, Kanagawa Rehabilitation Hospital, 516 Nanasawa, Atsugi-city, Kanagawa Prefecture, 243-0121, Japan
No commercial party having a direct financial interest in the results of the research supporting this article has or will confer a benefit upon the author(s) or upon any organization with which the author(s) is/are associated. PII: S0003-9993(06)00469-2 doi:10.1016/j.apmr.2006.05.017 © 2006 American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation. Published by Elsevier Inc. All rights reserved. | |
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