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Transient traumatic quadriplegia in a 29-year-old man without predisposing anatomic lesion
1006
CLINICAL NOTES
Transient Traumatic Quadriplegia in a 29-Year-Old Man Without Predisposing Anatomic Lesion Richard S. Kaplan, MD, Kathryn A. Stolp-Smith, AID ABSTRACT. Kaplan RS, Stolp-Smith KA. Transient traumatic quadriplegia in a 29-year-old man without predisposing anatomic lesion. Arch Phys Med Rehabil 1995;76:1006-10. A 29-year-old man presented 45 minutes after sustaining a blow to the right side of his head when his motorcycle slid on gravel and flipped on the side of the road. After walking away from the accident, the patient noted burning pain in his neck. Shortly thereafter, complete quadriplegia with a sensory level at C4 developed. The patient was given a high dose of methylprednisolone and transferred to a tertiary care center. En route, neurological testing demonstrated rapid improvement, and on arrival, all abnormal motor and sensory findings had completely resolved. Radiographic examination and magnetic resonance imaging of the entire spine showed no abnormality. Torg's ratio was > 1 at vertebral level C3 through C6. There was no evidence of developmental stenosis, congenital fusion, cervical instability, or intervertebral disk protrusion.
© 1995 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation RANSIENT TRAUMATIC spinal cord injury was first described by Torg and colleagues ~ and subsequently by MacMillian and Stauffer. 2 Torg 1 defined transient quadriplegia as sensory changes (burning pain, numbness, tingling, or loss of sensation) and motor changes (from weakness to complete paralysis) that resolve completely within 48 hours. MacMillian and Stauffel2 described this entity in thoracic and lumbar spinal injuries. The descriptions of these authors have in common the following features: (1) injury during athletic activity, most commonly during contact sports; (2) a preexisting narrowing of the spinal canal due to developmental stenosis or another structural abnormality; (3) a theorized neurapraxic cause. No cases have been reported of transient traumatic spinal cord injury without an associated fracture, dislocation, or history of a developmental spinal lesion. Because these injuries arereported most frequently in association with athletics, the use of the Torg ratio is common in preparticipation athletic evaluations. Torg j retrospectively reviewed 32 cases of transient quadriplegia in athletes and used neurologically asymptomatic agematched controls to perform radiographic analysis of plain cervical spinal radiographs. On the basis of this analysis, these authors developed a ratio of spinal adequacy, subsequently
T
From the Department of Physical Medicine and Rehabilitation, Mayo Clinic and Mayo Foundation, Rochester, MN. Submitted for publication January 26, 1995. Accepted in revised form May 30, 1995. Presented in part at the 1993 American Spinal Injury Association Meeting, San Diego, CA. No commercial party having a direct or indirect interest in the subject matter of this article has or will confer a benefit upon the authors or upon any organization with which the authors are associated. Reprint requests to Richard S. Kaplan, MD, Uniontown Hospital, Department of Physical Rehabilitation, 500 West Berkeley St, Uniontown, PA 15401. © 1995 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation 0003-9993/95/7611-338453.00/0
Arch Phys Med Rehabil Vol 76, November 1995
termed "Pavlov's ratio" or "Torg's ratio," calculated by comparing the sagittal diameter of the spinal canal (defined as the distance from the midpoint of the posterior aspect of the vertebral body to the nearest point on the spinolaminar line) with the anteroposterior width of the vertebral body (through the midpoint of the body). In 24 of the 32 subjects in their study, Torg's ratio was <.80 in at least one segment from C3 through C6 and all subjects in this subset had radiographically proven spinal stenosis. The other subjects in the study had some other developmental cervical spinal abnormality, ie, developmental stenosis, congenital fusion, cervical instability, or protrusion of an intervertebral disk in association with a decrease in the anteroposterior diameter of the spinal canal. Torg ~concluded that patients with a diminished cervical spinal anteroposterior diameter may experience transient motor and sensory disturbances caused by forced hyperextension or hyperflexion. Although no clear evidence of predisposition toward permanent neurological injury could be found, they recommended that patients with a history of traumatic transient quadriplegia avoid further participation in contact sports and that athletes with a known history of spinal stenosis be counseled about possible risks. Torg and Glasgow 3 later revised this recommendation to a relative rather than absolute contraindication in some cases. The following is a case of transient traumatic quadriplegia that could not have been predicted using Torg's criteria. Although this case was not associated with an athleticrelated injury, the medical history and physical examination findings are compatible with previously reported definitions of transient traumatic quadriplegia. This case is valuable in generating hypotheses about the risk factors for transient traumatic quadriplegia in a population other than male football players. CASE R E P O R T A 29-year-old man who had been riding his motorcycle with a partially secured helmet presented 45 minutes after sustaining a blow to the fight side of his head during an accident in which his motorcycle slid on gravel and flipped on the side of a road. An intoxicated witness reported that the right side of the patient's head hit the ground first; the witness observed the patient walk away from the scene of the accident. After walking away from the scene without any physical complaint, the patient first noted burning pain in his neck, worse with lateral rotation, and then tingling in his fight arm and, finally, in his fight leg. Shortly thereafter, when emergency medical services arrived, the patient was on the side of the road unable to walk. Weakness was noted in all his limbs. A cervical collar and backboard were applied at the scene, and the patient was transferred to an emergency department in a rural hospital. On examination in the emergency department by one of the authors, the patient was noted to meet the April 1990 American Spinal Injury Association's definition for complete bilateral C4 motor and sensory spinal cord injury, with absence of pinprick sensation, light touch, and proprioception below the acromioclavicular joint and trace movement of his deltoid muscles but no other motor function at or below C5. Respirations were spontaneous and unlabored at approximately 18 hreaths/min.
TRANSIENT TRAUMATIC QUADRIPLEGIA, Kaplan
Reflexes were slightly decreased symmetrically in the upper and lower extremities, and no Babinski sign was present. There was no voluntary rectal tone, although a bulbocavernosus reflex was present. The patient was alert and oriented to person, place, and date but apparently unconcerned or unaware of the seriousness of his symptoms. The results of cranial nerve examination were normal. His blood ethanol level was. 17. Body habitus was of medium build. On being questioned later, he denied participation in organized athletic events. The patient was given a high dose of methylprednisolone.4~5 A cross-table lateral radiograph of his cervical spine was obtained and did not show any abnormality. Ten minutes after steroid administration, some return of proprioception was noted in the patient's lower extremities, and 5 minutes later still, trace movements were noted in his distal lower extremities. After another 5 minutes, the patient exhibited good to fair movements of all muscle groups in his lower extremities and trace movement throughout his upper extremities, along with normal findings on sensory examination. The patient was transferred to a tertiary care center. En route, neurological testing demonstrated rapid improvement in his condition, and on arrival, all abnormal motor and sensory findings had completely resolved. Subsequent plain radiographs and magnetic resonance imaging of the spine were interpreted as normal. The Torg ratio was > 1 at C3 through C6, and there was no evidence of developmental stenosis, congenital fusion, cervical instability, or intervertebral disk protrusion (figs 1 and 2). The patient completed 24 hours of treatment with a high dose of steroid and left the hospital against medical advice before more prolonged follow-up could be arranged. When contacted by telephone 1 year later, the patient denied having neurological or other sequelae and refused follow-up head or neck imaging. DISCUSSION We present the first reported case of transient traumatic spinal cord injury without associated spinal abnormalities. This case serves as the basis for discussing the cause of transient quadriplegia, for critically analyzing the study of Torg,~ and for considering the implications of the use of Torg's ratio in counseling various populations of patients. This case is unusual in that it is the first to objectively document quadriplegia due to apparent cervical cord neurapraxia without any apparent predisposing anatomic lesion.6~° Torg ~postulated that a developmental spinal abnormality contributed to the neurapraxic cause of cervical transient quadriplegia. This theory was supported by subsequent case reports. 2 In support of this theory, no case to our knowledge has been reported of transient traumatic spinal cord neurapraxia without an associated traumatic or developmental spinal lesion. This is significant because understanding the cause of such events is essential in allowing us to provide optimum recommendations to patients about the probability of such events occurring in the future. This also has significant implications in formulating recommendations to athletes during preparticipation athletic evaluations as described by Torg. Given this patient's rapid neurological recovery and lack of demonstrable anatomic findings on spinal imaging, we cannot conclude with certainty that his transient neurological lesion was intraspinal in nature. Given the rural hospital emergency department setting, the unavailability of computed tomographic imaging, and the presence of complete quadriplegia, flexion and extension cervical spine films were contraindicated. Because recovery had ensued on arrival at the tertiary care center, this imaging was not pursued. In particular, the initial presentation of paresthesias ipsilateral to the side of the patient' s fall presents
1007
the possibility of a transient head injury with an associated contrecoup injury. Although this pathophysiological mechanism cannot be definitively ruled out by the history and anatomic imaging, the clear segmental distribution of motor and sensory findings on physical examination, the absence of loss of consciousness or mental status changes, and normal findings on cranial nerve examination tend to render head injury unlikely as a cause. Although the patient's level of intoxication could have clouded interpretation of the mental status examination, this was not clearly apparent to the examiner. The patient's ability to accurately denote sensory loss consistent with a dermatomal pattern also supports this impression. It is worthwhile to hypothesize about the possible role of treatment with a high dose of methylprednisolone in our patient's marked neurological recovery. Although it can be hypothesized that steroid administration reduces the magnitude or development of edema caused by traumatic injury, previous work supports a physiological rather than a mechanical mechanism of action of steroids in acute spinal cord injury. 5 In particular, administration of a high dose of steroids is hypothesized to act primarily through inhibition of lipid peroxidation and neurofilament breakdown in the spinal cord, peaking in effect within 8 hours after the initial injury. Thus, the existing literature does not appear to support either a temporal or mechanical role for steroids in promoting recovery from transient traumatic quadriplegia, and we cannot conclude that steroids improved recovery in this case. Although the pathophysiological mechanism of transient spinal cord injury remains to be elucidated, the literature tends to support the role of metabolic or microanatomic factors (or both), which is consistent with the classic definition of neurapraxia. Several investigators have explored the potential role of white matter ischemia in transient spinal cord injury, but Lohse and colleagues, ~j in an experimental animal model, were the first to describe a quantitative analysis of blood flow in transient traumatic paraplegia. Their study demonstrated that transient paraplegia, unlike permanent paraplegia, is not directly associated with white matter ischemia; in fact, their data suggested that transient spinal cord injury might be associated with hyperemia. In their model, blood flow increased while blood pressure decreased; therefore, transient spinal cord injury may (through Poiseuille's law) be associated with decreased vascular resistance and resultant relative ischemia mediated by several vasoactive amines or ions. The radiographic findings in our case are consistent with the concept of a physiological rather than a mechanical cause for at least some cases of transient spinal cord injury. Whether persons have varying predispositions for such an injury is unknown. Therefore, a conservative approach cannot be questioned, given the dramatic implications of any future spinal cord injury. Nonetheless, we cannot agree that the data support Torg's equivocal recommendation against participation in contact sports solely on the basis of a history of transient quadriplegia with spinal stenosis or on the basis of transient quadriplegia without spinal stenosis, as in our case. Such a matter remains an issue of clinical judgment for each case. As Torg's original report ~ noted, none of the subjects in that study with a history of a transient neurological episode subsequently sustained an injury that produced permanent neurological damage. An even more difficult issue to assess is appropriate counseling for amateur athletes or nonathletes about occasional participation in sports if that person is incidentally known to have a decreased Torg ratio but has no history of transient quadriplegia. It is important to realize that the original report of Torg ~ determined " n o r m a l " values for Torg's ratio by comparing
Arch Phys Med Rehabil Vol 76, November 1995
1008
TRANSIENT TRAUMATIC QUADRIPLEGIA, Kaplan
Fig 1. Plain radiographs of (A and B) cervical, (C) thoracic, and (D) lumbar spine showing no evidence of abnormality and with a Torg ratio >1.00 at levels C3 through C6.
32 male athletes 15 to 32 years old (29 were injured playing football and 3 by playing other sports) with age-matched "controls" who were not necessarily athletes. These (presumably skeletally larger) patients may have relatively larger vertebral bodies and an artificially lower ratio of spinal canal to vertebral body. Thus, the applicability of Torg's ratio to others, including female athletes, amateur athletes, participants in contact
Arch Phys Med Rehabil Vol 76, November 1995
sports other than football, and nonathletes, is unclear. Our case of transient traumatic quadriplegia in a nonathlete raises questions about the generalizability of Torg's ratio. The validity of the normal values of Torg ~is further questioned because of the control group, described as 49 male subjects whose ages were similar to those of the patients in our series but without mention of their level of athletic participation. Consequently,
TRANSIENT TRAUMATIC QUADRIPLEGIA, Kaplan
1009
quadriplegia. All the patients in Torg's study reportedly had a cervical radiographic lesion other than a decreased Torg ratio; thus, the clinical validity and usefulness of Torg's ratio are unclear and its routine use theoretically could produce falsenegative diagnoses of spinal stenosis if used without other radiographic data. Torg's study I did not clearly define clinical features required for the diagnosis of transient quadriplegia. In particular, of the 32 cases of transient quadriplegia reported, there were no motor deficits in 7, motor deficits involving the upper extremities alone in 2, sensory deficits limited to both upper extremities in 6, sensory deficits limited to one upper extremity in 1, and sensory deficits limited to one hand in 1. These data suggest that Torg ~ may have classified as a distinct clinical entity what in fact is a spectrum of anatomic and pathophysiological disorders. Three of these patients had symptoms of extremely short duration (ranging from 5 to 60 seconds); thus, the findings probably were not documented by neurological examination. This is similar to a case of Funk and Wells is that Torg cited j° in which a patient noted numbness and paralysis for seconds after hyperextension; yet, the results of subsequent radiographic analysis and neurological examination were normal. Further studies might quantitate spinal stenosis through magnetic resonance imaging analysis of cerebrospinal fluid reserve by using published techniques] 9 Such a technique might help minimize errors resulting from differences in vertebral body size and radiographic magnification.
Fig 2. Spinal magnetic resonance imaging shows normal anatomy, with no evidence of developmental or traumatic abnormality of the cervical spine or cervical cord.
the demographics of the population used to construct normal values for this ratio may result in a high incidence of falsepositives (artificially low ratios ) when applied to a population of football players or to a high incidence of false-negatives (artificially high ratios) when applied to a population of nonfootball players. Although a decreased Torg ratio might be an indication to counsel a football player with a history of transient quadriplegia against subsequent activity, its implications in a routine preparticipation sports examination are less clear and a prospective study of such a ratio in a general population may be worthwhile. Such caution against overinterpretation of a decreased Torg ratio is further supported by the observation that of the 24 subjects Torg j reported who had a Torg ratio <0.8 at at least one measured cervical level, the published data show that less than half (11) met at even one anatomic level the classic definition for cervical stenosis of a spinal sagittal diameter < 14mm. 1°'t2-17 A further criticism of the earlier research of Torg I is that abnormal values of Torg's ratio were calculated on the basis of only 24 of the 32 subjects, because cervical spinal radiographs of the 8 other subjects were not available for review by Torg's colleagues. The study of Torg ~ does not explain whether these 8 subjects excluded from this analysis had a clinical history comparable to the 24 other subjects. Because Torg ~ guardedly counseled against future participation in contact sports for all subjects in their study, it is unclear whether this recommendation was made on the basis of a low Torg ratio, the presence of a congenital or developmental spinal abnormality, or a clinical history compatible with transient
CONCLUSION This unique case of transient traumatic quadriplegia without anatomic spinal abnormality raises significant concerns about the predictive value of a low Torg ratio in the absence of other radiographic findings. We continue to urge caution while interpreting evidence of any developmental spinal abnormality in a professional or amateur athlete. Although a Torg ratio <0.8 may be associated with an increased risk for initial or recurrent transient traumatic quadriplegia in a football player (it has not been shown to be associated with permanent neurological deficit), its applicability to other contact sports, female athletes, or amateur athletes is unclear. Moreover, although the positive predictive value of a low Torg ratio has been explored in relation to transient traumatic quadriplegia, the negative predictive value of a normal Torg ratio has yet to be elucidated. References
1. Torg JS, Pavlov H, Genuario SE, Sennett B, Wisneski RJ, Robie BH, et al. Neurapraxia of the cervical spinal cord with transient quadriplegia. J Bone Joint Surg Am 1986;68:1354-70. 2. MacMillianM, Stauffer ES. Transient neurologic deficitsassociated with thoracic and lumbar spine trauma without fracture of dislocation. Spine 1990;15:466-9. 3. TorgJS, Glasgow SG. Criteria for return to contact activitiesfollowing cervical spine injury. Clin J Sports Med 1991;1:12-26. 4. Bracken MB, Collins WF, Freeman DF, Shepard MJ, Wagner FW, Silten RM, et al. Efficacy of methylprednisolone in acute spinal cord injury. JAMA 1984;251:45-52. 5. Bracken MB, Shepard MJ, Collins WF, Holford TR, Young W, Baskin DS, et al. A randomized,controlled trial of methylprednisolone or naloxone in the treatment of acute spinal-cordinjury: results of Second National Acute Spinal-CordInjury Study. N Engl J Med 1990;322:1405-11. 6. Moiel RH, Raso E, Waltz TA. Central cord syndrome resulting from congenital narrowness of the cervical spinal canal. J Trauma 1970; 10:502-10. 7. Stratford J. Congenital cervical spinal stenosis: a factor in myelopathy. Acta Neurochir (Wien) 1978;41:101-6. 8. Taylor AR. The mechanism of injury to the spinal cord in the neck
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9. 10. 11. 12. 13.
TRANSIENT TRAUMATIC QUADRIPLEGIA, Kaplan
without damage to the vertebral column. J Bone Joint Surg Br 1951;33:543-7. Taylor AR, Blackwood W. Paraplegia in hyperextension cervical injuries with normal radiographic appearances. J Bone Joint Surg Br 1948;30:245-8. Torg JS. Cervical spinal stenosis with cord neurapraxia and transient quadriplegia. Clin Sports Med 1990;9:279-96. Lohse DC, Senter HJ, Kauer JS, Wohns R. Spinal cord blood flow in experimental transient traumatic paraplegia. J Neurosurg 1980; 52: 335-45. Burrows EH. The sagittal diameter of the spinal canal in cervical spondylosis. Clin Radiol 1963; 14:77-86. Countee RW, Vijayanathan T. Congenital stenosis of the cervical spine: diagnosis and management. J Natl Med Assoc 1979;71:25764.
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14. Hinck VC, Gordy PD, Storino HE. Developmental stenosis of the cervical spinal canal: radiological considerations. Neurology 1964; 14:864-8. 15. Hinck VC, Sachdev NS. Developmental stenosis of the cervical spinal canal. Brain 1966;89:27-36. 16. Kessler JT. Congenital narrowing of the cervical spinal canal. J Neurol Neurosurg Psychiatry 1975;38:1218-24. 17. Pallis C, Jones AM, Spillane JD. Cervical spondylosis: incidence and implications. Brain 1954;77:274-89. 18. Funk FJ Jr, Wells RE. Injuries of the cervical spine in football. Clin Orthop 1975; 109:50-8. 19. Schellinger D, LeBihan D, Rajan SS, Cammarata CA, Patronas NJ, Deveikis JP, et al. MR of slow CSF flow in the spine. AJNR Am J Neuroradiol 1992; 13:1393-403.
CLINICAL NOTES
Transient Traumatic Quadriplegia in a 29-Year-Old Man Without Predisposing Anatomic Lesion Richard S. Kaplan, MD, Kathryn A. Stolp-Smith, AID ABSTRACT. Kaplan RS, Stolp-Smith KA. Transient traumatic quadriplegia in a 29-year-old man without predisposing anatomic lesion. Arch Phys Med Rehabil 1995;76:1006-10. A 29-year-old man presented 45 minutes after sustaining a blow to the right side of his head when his motorcycle slid on gravel and flipped on the side of the road. After walking away from the accident, the patient noted burning pain in his neck. Shortly thereafter, complete quadriplegia with a sensory level at C4 developed. The patient was given a high dose of methylprednisolone and transferred to a tertiary care center. En route, neurological testing demonstrated rapid improvement, and on arrival, all abnormal motor and sensory findings had completely resolved. Radiographic examination and magnetic resonance imaging of the entire spine showed no abnormality. Torg's ratio was > 1 at vertebral level C3 through C6. There was no evidence of developmental stenosis, congenital fusion, cervical instability, or intervertebral disk protrusion.
© 1995 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation RANSIENT TRAUMATIC spinal cord injury was first described by Torg and colleagues ~ and subsequently by MacMillian and Stauffer. 2 Torg 1 defined transient quadriplegia as sensory changes (burning pain, numbness, tingling, or loss of sensation) and motor changes (from weakness to complete paralysis) that resolve completely within 48 hours. MacMillian and Stauffel2 described this entity in thoracic and lumbar spinal injuries. The descriptions of these authors have in common the following features: (1) injury during athletic activity, most commonly during contact sports; (2) a preexisting narrowing of the spinal canal due to developmental stenosis or another structural abnormality; (3) a theorized neurapraxic cause. No cases have been reported of transient traumatic spinal cord injury without an associated fracture, dislocation, or history of a developmental spinal lesion. Because these injuries arereported most frequently in association with athletics, the use of the Torg ratio is common in preparticipation athletic evaluations. Torg j retrospectively reviewed 32 cases of transient quadriplegia in athletes and used neurologically asymptomatic agematched controls to perform radiographic analysis of plain cervical spinal radiographs. On the basis of this analysis, these authors developed a ratio of spinal adequacy, subsequently
T
From the Department of Physical Medicine and Rehabilitation, Mayo Clinic and Mayo Foundation, Rochester, MN. Submitted for publication January 26, 1995. Accepted in revised form May 30, 1995. Presented in part at the 1993 American Spinal Injury Association Meeting, San Diego, CA. No commercial party having a direct or indirect interest in the subject matter of this article has or will confer a benefit upon the authors or upon any organization with which the authors are associated. Reprint requests to Richard S. Kaplan, MD, Uniontown Hospital, Department of Physical Rehabilitation, 500 West Berkeley St, Uniontown, PA 15401. © 1995 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation 0003-9993/95/7611-338453.00/0
Arch Phys Med Rehabil Vol 76, November 1995
termed "Pavlov's ratio" or "Torg's ratio," calculated by comparing the sagittal diameter of the spinal canal (defined as the distance from the midpoint of the posterior aspect of the vertebral body to the nearest point on the spinolaminar line) with the anteroposterior width of the vertebral body (through the midpoint of the body). In 24 of the 32 subjects in their study, Torg's ratio was <.80 in at least one segment from C3 through C6 and all subjects in this subset had radiographically proven spinal stenosis. The other subjects in the study had some other developmental cervical spinal abnormality, ie, developmental stenosis, congenital fusion, cervical instability, or protrusion of an intervertebral disk in association with a decrease in the anteroposterior diameter of the spinal canal. Torg ~concluded that patients with a diminished cervical spinal anteroposterior diameter may experience transient motor and sensory disturbances caused by forced hyperextension or hyperflexion. Although no clear evidence of predisposition toward permanent neurological injury could be found, they recommended that patients with a history of traumatic transient quadriplegia avoid further participation in contact sports and that athletes with a known history of spinal stenosis be counseled about possible risks. Torg and Glasgow 3 later revised this recommendation to a relative rather than absolute contraindication in some cases. The following is a case of transient traumatic quadriplegia that could not have been predicted using Torg's criteria. Although this case was not associated with an athleticrelated injury, the medical history and physical examination findings are compatible with previously reported definitions of transient traumatic quadriplegia. This case is valuable in generating hypotheses about the risk factors for transient traumatic quadriplegia in a population other than male football players. CASE R E P O R T A 29-year-old man who had been riding his motorcycle with a partially secured helmet presented 45 minutes after sustaining a blow to the fight side of his head during an accident in which his motorcycle slid on gravel and flipped on the side of a road. An intoxicated witness reported that the right side of the patient's head hit the ground first; the witness observed the patient walk away from the scene of the accident. After walking away from the scene without any physical complaint, the patient first noted burning pain in his neck, worse with lateral rotation, and then tingling in his fight arm and, finally, in his fight leg. Shortly thereafter, when emergency medical services arrived, the patient was on the side of the road unable to walk. Weakness was noted in all his limbs. A cervical collar and backboard were applied at the scene, and the patient was transferred to an emergency department in a rural hospital. On examination in the emergency department by one of the authors, the patient was noted to meet the April 1990 American Spinal Injury Association's definition for complete bilateral C4 motor and sensory spinal cord injury, with absence of pinprick sensation, light touch, and proprioception below the acromioclavicular joint and trace movement of his deltoid muscles but no other motor function at or below C5. Respirations were spontaneous and unlabored at approximately 18 hreaths/min.
TRANSIENT TRAUMATIC QUADRIPLEGIA, Kaplan
Reflexes were slightly decreased symmetrically in the upper and lower extremities, and no Babinski sign was present. There was no voluntary rectal tone, although a bulbocavernosus reflex was present. The patient was alert and oriented to person, place, and date but apparently unconcerned or unaware of the seriousness of his symptoms. The results of cranial nerve examination were normal. His blood ethanol level was. 17. Body habitus was of medium build. On being questioned later, he denied participation in organized athletic events. The patient was given a high dose of methylprednisolone.4~5 A cross-table lateral radiograph of his cervical spine was obtained and did not show any abnormality. Ten minutes after steroid administration, some return of proprioception was noted in the patient's lower extremities, and 5 minutes later still, trace movements were noted in his distal lower extremities. After another 5 minutes, the patient exhibited good to fair movements of all muscle groups in his lower extremities and trace movement throughout his upper extremities, along with normal findings on sensory examination. The patient was transferred to a tertiary care center. En route, neurological testing demonstrated rapid improvement in his condition, and on arrival, all abnormal motor and sensory findings had completely resolved. Subsequent plain radiographs and magnetic resonance imaging of the spine were interpreted as normal. The Torg ratio was > 1 at C3 through C6, and there was no evidence of developmental stenosis, congenital fusion, cervical instability, or intervertebral disk protrusion (figs 1 and 2). The patient completed 24 hours of treatment with a high dose of steroid and left the hospital against medical advice before more prolonged follow-up could be arranged. When contacted by telephone 1 year later, the patient denied having neurological or other sequelae and refused follow-up head or neck imaging. DISCUSSION We present the first reported case of transient traumatic spinal cord injury without associated spinal abnormalities. This case serves as the basis for discussing the cause of transient quadriplegia, for critically analyzing the study of Torg,~ and for considering the implications of the use of Torg's ratio in counseling various populations of patients. This case is unusual in that it is the first to objectively document quadriplegia due to apparent cervical cord neurapraxia without any apparent predisposing anatomic lesion.6~° Torg ~postulated that a developmental spinal abnormality contributed to the neurapraxic cause of cervical transient quadriplegia. This theory was supported by subsequent case reports. 2 In support of this theory, no case to our knowledge has been reported of transient traumatic spinal cord neurapraxia without an associated traumatic or developmental spinal lesion. This is significant because understanding the cause of such events is essential in allowing us to provide optimum recommendations to patients about the probability of such events occurring in the future. This also has significant implications in formulating recommendations to athletes during preparticipation athletic evaluations as described by Torg. Given this patient's rapid neurological recovery and lack of demonstrable anatomic findings on spinal imaging, we cannot conclude with certainty that his transient neurological lesion was intraspinal in nature. Given the rural hospital emergency department setting, the unavailability of computed tomographic imaging, and the presence of complete quadriplegia, flexion and extension cervical spine films were contraindicated. Because recovery had ensued on arrival at the tertiary care center, this imaging was not pursued. In particular, the initial presentation of paresthesias ipsilateral to the side of the patient' s fall presents
1007
the possibility of a transient head injury with an associated contrecoup injury. Although this pathophysiological mechanism cannot be definitively ruled out by the history and anatomic imaging, the clear segmental distribution of motor and sensory findings on physical examination, the absence of loss of consciousness or mental status changes, and normal findings on cranial nerve examination tend to render head injury unlikely as a cause. Although the patient's level of intoxication could have clouded interpretation of the mental status examination, this was not clearly apparent to the examiner. The patient's ability to accurately denote sensory loss consistent with a dermatomal pattern also supports this impression. It is worthwhile to hypothesize about the possible role of treatment with a high dose of methylprednisolone in our patient's marked neurological recovery. Although it can be hypothesized that steroid administration reduces the magnitude or development of edema caused by traumatic injury, previous work supports a physiological rather than a mechanical mechanism of action of steroids in acute spinal cord injury. 5 In particular, administration of a high dose of steroids is hypothesized to act primarily through inhibition of lipid peroxidation and neurofilament breakdown in the spinal cord, peaking in effect within 8 hours after the initial injury. Thus, the existing literature does not appear to support either a temporal or mechanical role for steroids in promoting recovery from transient traumatic quadriplegia, and we cannot conclude that steroids improved recovery in this case. Although the pathophysiological mechanism of transient spinal cord injury remains to be elucidated, the literature tends to support the role of metabolic or microanatomic factors (or both), which is consistent with the classic definition of neurapraxia. Several investigators have explored the potential role of white matter ischemia in transient spinal cord injury, but Lohse and colleagues, ~j in an experimental animal model, were the first to describe a quantitative analysis of blood flow in transient traumatic paraplegia. Their study demonstrated that transient paraplegia, unlike permanent paraplegia, is not directly associated with white matter ischemia; in fact, their data suggested that transient spinal cord injury might be associated with hyperemia. In their model, blood flow increased while blood pressure decreased; therefore, transient spinal cord injury may (through Poiseuille's law) be associated with decreased vascular resistance and resultant relative ischemia mediated by several vasoactive amines or ions. The radiographic findings in our case are consistent with the concept of a physiological rather than a mechanical cause for at least some cases of transient spinal cord injury. Whether persons have varying predispositions for such an injury is unknown. Therefore, a conservative approach cannot be questioned, given the dramatic implications of any future spinal cord injury. Nonetheless, we cannot agree that the data support Torg's equivocal recommendation against participation in contact sports solely on the basis of a history of transient quadriplegia with spinal stenosis or on the basis of transient quadriplegia without spinal stenosis, as in our case. Such a matter remains an issue of clinical judgment for each case. As Torg's original report ~ noted, none of the subjects in that study with a history of a transient neurological episode subsequently sustained an injury that produced permanent neurological damage. An even more difficult issue to assess is appropriate counseling for amateur athletes or nonathletes about occasional participation in sports if that person is incidentally known to have a decreased Torg ratio but has no history of transient quadriplegia. It is important to realize that the original report of Torg ~ determined " n o r m a l " values for Torg's ratio by comparing
Arch Phys Med Rehabil Vol 76, November 1995
1008
TRANSIENT TRAUMATIC QUADRIPLEGIA, Kaplan
Fig 1. Plain radiographs of (A and B) cervical, (C) thoracic, and (D) lumbar spine showing no evidence of abnormality and with a Torg ratio >1.00 at levels C3 through C6.
32 male athletes 15 to 32 years old (29 were injured playing football and 3 by playing other sports) with age-matched "controls" who were not necessarily athletes. These (presumably skeletally larger) patients may have relatively larger vertebral bodies and an artificially lower ratio of spinal canal to vertebral body. Thus, the applicability of Torg's ratio to others, including female athletes, amateur athletes, participants in contact
Arch Phys Med Rehabil Vol 76, November 1995
sports other than football, and nonathletes, is unclear. Our case of transient traumatic quadriplegia in a nonathlete raises questions about the generalizability of Torg's ratio. The validity of the normal values of Torg ~is further questioned because of the control group, described as 49 male subjects whose ages were similar to those of the patients in our series but without mention of their level of athletic participation. Consequently,
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quadriplegia. All the patients in Torg's study reportedly had a cervical radiographic lesion other than a decreased Torg ratio; thus, the clinical validity and usefulness of Torg's ratio are unclear and its routine use theoretically could produce falsenegative diagnoses of spinal stenosis if used without other radiographic data. Torg's study I did not clearly define clinical features required for the diagnosis of transient quadriplegia. In particular, of the 32 cases of transient quadriplegia reported, there were no motor deficits in 7, motor deficits involving the upper extremities alone in 2, sensory deficits limited to both upper extremities in 6, sensory deficits limited to one upper extremity in 1, and sensory deficits limited to one hand in 1. These data suggest that Torg ~ may have classified as a distinct clinical entity what in fact is a spectrum of anatomic and pathophysiological disorders. Three of these patients had symptoms of extremely short duration (ranging from 5 to 60 seconds); thus, the findings probably were not documented by neurological examination. This is similar to a case of Funk and Wells is that Torg cited j° in which a patient noted numbness and paralysis for seconds after hyperextension; yet, the results of subsequent radiographic analysis and neurological examination were normal. Further studies might quantitate spinal stenosis through magnetic resonance imaging analysis of cerebrospinal fluid reserve by using published techniques] 9 Such a technique might help minimize errors resulting from differences in vertebral body size and radiographic magnification.
Fig 2. Spinal magnetic resonance imaging shows normal anatomy, with no evidence of developmental or traumatic abnormality of the cervical spine or cervical cord.
the demographics of the population used to construct normal values for this ratio may result in a high incidence of falsepositives (artificially low ratios ) when applied to a population of football players or to a high incidence of false-negatives (artificially high ratios) when applied to a population of nonfootball players. Although a decreased Torg ratio might be an indication to counsel a football player with a history of transient quadriplegia against subsequent activity, its implications in a routine preparticipation sports examination are less clear and a prospective study of such a ratio in a general population may be worthwhile. Such caution against overinterpretation of a decreased Torg ratio is further supported by the observation that of the 24 subjects Torg j reported who had a Torg ratio <0.8 at at least one measured cervical level, the published data show that less than half (11) met at even one anatomic level the classic definition for cervical stenosis of a spinal sagittal diameter < 14mm. 1°'t2-17 A further criticism of the earlier research of Torg I is that abnormal values of Torg's ratio were calculated on the basis of only 24 of the 32 subjects, because cervical spinal radiographs of the 8 other subjects were not available for review by Torg's colleagues. The study of Torg ~ does not explain whether these 8 subjects excluded from this analysis had a clinical history comparable to the 24 other subjects. Because Torg ~ guardedly counseled against future participation in contact sports for all subjects in their study, it is unclear whether this recommendation was made on the basis of a low Torg ratio, the presence of a congenital or developmental spinal abnormality, or a clinical history compatible with transient
CONCLUSION This unique case of transient traumatic quadriplegia without anatomic spinal abnormality raises significant concerns about the predictive value of a low Torg ratio in the absence of other radiographic findings. We continue to urge caution while interpreting evidence of any developmental spinal abnormality in a professional or amateur athlete. Although a Torg ratio <0.8 may be associated with an increased risk for initial or recurrent transient traumatic quadriplegia in a football player (it has not been shown to be associated with permanent neurological deficit), its applicability to other contact sports, female athletes, or amateur athletes is unclear. Moreover, although the positive predictive value of a low Torg ratio has been explored in relation to transient traumatic quadriplegia, the negative predictive value of a normal Torg ratio has yet to be elucidated. References
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