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Cervical spinal cord injury without radiological abnormality in adults.
Correspondence Address:
Spinal cord injury occurring without concomitant radiologically demonstrable trauma to the skeletal elements of the spinal canal rim, or compromise of the spinal canal rim without fracture, is a rare event. Though documented in children, the injury is not very well reported in adults. We present seventeen adult patients with spinal cord injury without accompanying fracture of the spinal canal rim, or vertebral dislocation, seen over seven years. None had preexisting spinal canal stenosis or cervical spondylosis. Following trauma, these patients had weakness of all four limbs. They were evaluated by MRI (CT scan in one patient), which showed hypo / isointense lesion in the cord on T1 weighted images, and hyperintensity on T2 weighted images, suggesting cord contusion or oedema. MRI was normal in two patients. With conservative management, fifteen patients showed neurological improvement, one remained quadriplegic and one died. With increasing use of MRI in the evaluation of traumatic myelopathy, such injuries will be diagnosed more often. The mechanism of injury is probably acute stretching of the cord as in flexion and torsional strain. Management is essentially conservative and prognosis is better than that seen in patients with fracture or dislocation of cervical spine.
Spinal cord injury without radiological abnormality (SCIWORA) is a syndrome of cervical spinal cord trauma, describing post traumatic myelopathy without evidence of vertebral fracture or mal-alignment on plain radiographs or on computed tomography. The injury is documented in children, probably due to increased elasticity of the paediatric spine. It is not described very well in adults with normal spinal canals, although the elderly patients with osteoarthrotic spines and stenosed cervical canals can suffer traumatic spinal cord damage without accompanying vertebral injury.[1] We present 17 young adults with isolated cervical cord injury, without accompanying vertebral dislocation or fracture involving the spinal canal rim. Relevant literature is briefly reviewed.
Over a period of seven years (1992-98), we managed 17 young adults with traumatic cervical myelopathy. None of these patients had features of preexisting cervical spondylosis. Only those patients with traumatic cervical myelopathy were included who did not have (a) radiologically demonstrable fracture or dislocation corresponding to the clinical level of myelopathy (b) radiologically demonstrable fracture of the spinal canal rim at clinical level of myelopathy. It meant that patients with fractures of spinous or transverse process, but with intact spinal canal, could be included in the study.
17 adult patients with traumatic cervical myelopathy who met the criteria mentioned above were included in the study. There were sixteen males and one female. All the patients were below 40 years of age, the youngest being a 17-year-old male. There was no previous history pertaining to the cervical spine. History of neck hyperflexion was available in [eight] patients, hyperextension in three, and torsional strain in four patients. Two patients sustained gunshot wound involving only the soft tissues of the neck. Neurological deficit was noticed immediately after the injury. Myelopathy was present in all the patients at the time of admission. The pattern of deficits was recorded according to Benzel and Larson neurological grading[2] on admission [Table I] and [Table II]. There were two patients with features of cervicomedullary involvement (nystagmus, quadriparesis with predominant weakness of upper limbs). Two patients had unilateral Horner's syndrome (including one with gunshot wound to his neck). Ten patients complained of dysaesthesia. Twelve patients had neurogenic bladder dysfunction (retention of urine, uninhibited bladder). Imaging : Cervical spine radiographs showed straightening of the lordotic curve in one and no abnormality in fourteen patients. One patient had chip fracture of anteroinferior part of C4 vertebral body and two had fractures of tips of spinous processes. MRI study was done in 16 cases and computed tomography (CT) is one. MRI could be done within 24 hours in one and within 10 days in 15 patients. Results of these imaging procedures are given in [Table III]. Commonest finding on T1WI was isointense or hypointense spinal cord swelling at the site of lesion [Figure. 1], which appeared hyperintense on T2WI. Three patients had diffuse hyperintensity involving two cord segments [Figure. 2],3). MRI was normal in two patients, including one with gunshot wound to his neck. No correlation could be made between the direction of the injuring force and MRI appearance of the injured spinal cord. None of the patients had cervical canal stenosis. Patients with compressive lesions like spinal epidural haematoma and ruptured cervical disc with myelopathy were excluded from the study. Management : All patients were managed conservatively with care of back, administration of corticosteroids, care of bladder functions and physiotherapy. Ambulation was encouraged at the earliest, which was usually by 7 to 14 days after injury. Clinical Course and Outcome : One patient died seventy two hours after the injury and autopsy showed extensive intramedullary haemorrhage at C4-C5, with intact spine [Figure. 4]. Two patients (with normal MRI) had complete neurological recovery within 96 hours of injury. All other patients improved in their functional neurological grades, except one patient who remained quadriplegic.
Cervical spinal cord can rarely be injured without a concomitant injury to either discocorporeal or discoligamentous structures. Such an injury is described in children, in whom the cervical spine has increased range of movements, including hyperflexion, hyperextension and distraction. Pang and Wilberger[3] coined the term spinal cord injury without radiographic abnormality (SCIWORA) to distinguish this injury from traumatic myelopathy with disruption of skeletal elements of the cervical spine. This injury is not described very well in young adults with normal spinal canals. Patients may have distant unrelated fractures of the cervical spine such as chip fracture of the anterior part of the vertebral body, or that of spinous and transverse processes while retaining the integrity of the bony rim of the normal spinal canal. The injury has to be distinguished from central cord syndrome following trauma in the elderly, who often have osteoarthritic spines, and hyperextension may cause the cervical spinal cord to be pinched between the posterior longitudinal ligament (PLL) and hypertrophied ligamentum flavum, leading to intramedullary haemorrhage and central infarction of the spinal cord.[1] Pathogenesis of Spinal Cord Injury : Spinomedullary Dynamics : Spinal cord is a viscoelastic tissue exhibiting adaptive properties according to the time distribution following stretch or compression of the cord. Equally important is the reciprocal behavioral adaptation of the meninges to neutralize the stretching of the cord. The spinal canal lengthens between 5 and 9.7 cm depending on individual variation, during extension to maximum flexion[4] The osteoligamentous sheath represented by the spinal canal is deformable in normal mechanics of movement. The requirements of movements are thus naturally and passively sustained by the spinal cord and nerve roots. During non physiological movements of excessive amplitudes, the nervous structures can be subjected to strain which exceeds their capacity to adapt. It is thus likely that SCIWORA represents those cases where the force was sufficient to cause cord damage but was unable to damage the discocorporeal or discoligamentous structures. Although the exact mechanism of injury to the cervical spinal cord in adults with normal spinal canal is uncertain, some analogy to similar injuries seen in children may be derived. The spinal cord can get damaged while the spine remains intact during non physiological conditions with excessive amplitude, even if for a short time. Such non physiological movement may involve hyperextension or hyperflexion of the spine, torsional strain, distraction along the longitudinal axis or concussive wave as in missile injuries of the neck. Hyperflexion causes the maximum stretching of the cord.[5] Prolonged neck flexion under anaesthesia, or Cervical Spinal Cord Injury acute hyperflexion may also result in impairment of blood flow to the cord. Tethering of the cord by the dentate ligament further worsens the condition.[6] Likewise, chiropractic manipulation of the neck has been reported to cause vertebrobasilar insufficiency or occlusion, leading to cord infarction and quadriplegia.[7],[8] Hyperextension of the neck can damage the cervical cord.[9],[10] Greatest cord compression occurs between C3 and C6 due to pinching of the cord between the ligamentum flavum and PLL.[9] Rotatory acceleration may result in spinal cord damage in a manner similar to diffuse axonal injury (DAI) in the brain, since the shearing forces are generated in the spinal cord where the pia is restrained more than the rest of the cord by the dentate ligament and spinal nerve roots; grey matter in the spinal cord gets damaged by rotatory acceleration.[11] Gunshot wounds of the soft tissues of the neck can damage the spinal cord either by avulsing the nerve roots from the cord and producing haematomyelia, or by concussion wave. Blast or concussive forces cause temporary neurological impairment, as seen in high velocity missile injuries, and support the concept of concussive theory. Shock waves can be followed by spinal cord oedema. Concussive forces are less with low velocity civilian injuries, which are more likely to damage the cord by avulsing the root and causing intramedullary haemorrhage.[12] It has been hypothesised that there are two mechanisms for damage to the spinal cord after injury the primary mechanical injury to the axons andmicrovasculature, and a secondary injury due to one or more additional damaging processes initiated by the primary injury.[13],[14] Secondary cord injury occurs due to thrombosis, platelet aggregation or vasospasm of arterioles traversing the grey matter to supply the white matter.[15] The ischaemic insult is compounded by impairment of autoregulation in the injured spinal cord, especially in the presence of systemic hypotension.[16] Since there is no continuing or unrelieved compression of the spinal cord or vertebral instability in SCIWORA, the role of secondary factors is debatable. Clinical Picture : It is unusual to have a picture of complete cord transection. An incomplete cord lesion-whether central cord syndrome,anterior cord syndrome or myelopathy with sensory and motor involvement - is usually seen. The classical findings of quadriparesis with upper limbs affected more than the lower limbs may not always be seen.[17] There may be dysaesthesiae over the trunk and limbs, Horner's syndrome, and neurogenic bladder dysfunction. Dysaesthesiae often persist even after neurological recovery. Imaging : The cervical spine radiographs usually do not show any abnormality. Flexion and extension views are essential to exclude instability. MRI is being increasingly used in the evaluation of post traumatic myelopathy. Its importance lies in not only in its ability to image the injured cord, but also to prognosticate the outcome.[7],[18] Significant changes in signal intensity, whether due to haemorrhage, contusion or oedema, are best seen in T2WI. The term SCIWORA has been rendered inaccurate by MRI. The temporal profile of appearances of the injured cord has been well documented.[19],[20] It is now established in animal models that the extent of signal change shown on MRI is related to the severity of injury.[21] Clinical studies also have shown a general association between the extent of signal change on MRI and functional outcome.[7],[18],[22],[23] Marciello et al,[24] after analysing 24 cases of acute spinal cord injury with MRI, stressed the prognostic significance of the finding of intramedullary haemorrhage. While a normal looking cord had the best prognosis, the outcome progressively worsened with the findings of intramedullary oedema involving one or more segment of cord segment, and was worst with intramedullary haemorrhage. Inspite of having clear-cut features of cervical myelopathy following trauma, MRI may occasionally show a normal spinal cord, as in two of our patients (including one with gunshot wound to the neck). Such patients have features of mild cord dysfunction, which usually recover within a short period. They have been diagnosed as having spinal cord concussion (SCC). It was hypothesised that SCC occurred due to functional disturbances of axonal membrane without disruption of structural integrity.[11] Zwimpfer and Bernstein[25] diagnose SCC when there is (a) no evidence of cervical canal stenosis, (b) spinal trauma precedes the onset of deficit, (c) neurological deficit is consistent with spinal cord involvement at the level of injury and (d) there is complete recovery within 72 hours. Subtle cord changes of oedema can be missed due to relatively poor spatial resolution and signal-to-noise ratio, and limited minimum slice thickness.[26],[27] Management : Management of spinal cord injury without associated fracture or dislocation is essentially conservative. There is no role for traction. In the three cases of such injury with quadriplegia reported by Laud and Ramani[28] where diffuse hyperintensity was seen on T2WI, wide laminectomy resulted in significant improvement in neurological grades. All, except one, patient in the present study showed improvement with conservative management. Recovery is good and most of the patients improve their neurological deficit over 4-12 weeks.
Cervical cord injury without associated vertebral fracture or dislocation is rare in adults with normal spinal canals. The concept of cord injury by skeletal displacement in hyperflexion with spontaneous recoil is untenable. It appears that strain of the cervical spine in any direction can injure the cord. In hyperextension, the cord gets damaged due to compression, while in hyperflexion, rotatory acceleration and distraction, injury occurs due to a combination of stretching, tethering and vascular compromise. With increasing utilization of MRI in the evaluation of traumatic myelopathy, more cases of spine injury without radiological abnormality can be discovered and their natural history studied. Management is conservative and outcome is not as dismal as seen in injuries with cervical fracture or dislocations.
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