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Delayed Post-Traumatic Syringohydromyelia After an Uncomplicated Fracture of the Spine: Case Report and Literature Review

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Delayed Post-Traumatic Syringohydromyelia After an Uncomplicated Fracture of the Spine: Case Report and Literature Review Spinal Cord (1996) 34, 301- 304 © 1996 International Medical Society of Paraplegia All rights reserved 1362-4393/96 $12.00 Delayed post-traumatic syringohydromyelia after an uncomplicated fracture of the spine: Case report and literature review F Giiler-Uysall, S Orkun2, A Cila3 and N Ozgirgin1 I Specialist of PMR, Ankara Rehabilitation Center, Ankara; 2 Assoc. Prof in PMR, Ankara Rehabilitation Center, Ankara; 3 Assoc. Prof In Radiology, Dept. of Radiology, Hacettepe University, Faculty of Medicine, Ankara, Turkey A patient who had had a traffic accident resulting with a compression fracture of the Ll vertebra but with no neurological deficits, developed urinary incontinence and weakness in his lower extremities 25 years after the spinal injury. An MRI scan of the spine revealed gliosis of the conus medullaris at the level of the compression fracture, with syringohydromyelia extending from T6 to conus medullaris. The patient underwent a rehabilitation program at the end of which he was able to ambulate independently. Keywords: Syringomyelia; syringohydromyelia; spinal cord trauma; spinal cord injuries Introduction Case History Syringomyelia is a chronic disorder involving the spinal A 62 year old male presented in May 1994 with a 12 cord, characterized by the presence of longitudinally month history of bilateral progressive leg weakness and oriented cavities and gliosis. The term 'hydromyelia' is urinary incontinence. Twenty-five years previously he used to describe the appearance of dilatation of the had had a traffic accident which caused a crush central canal. Consequently, recent literature tends to fracture of Ll vertebra but with no transient or unite both terms as 'syringohydromyelia' or use only persistent neurological deficits. He had complete bed syringomyelia in order to define the spectrum of this rest for one month, during which he could again not disease. 1 The role of trauma in the pathogenesis of recall any neurological symptoms. He had had pain in syringomyelia has been known for a long time. Post the low back area lasting for a week after the accident traumatic syringomyelia is the most common cause of and no other pain or weakness until 25 years post neurological deterioration in patients who have injury. In 1993, he began to develop progressive sustained serious spinal cord trauma and who develop weakness of both the lower extremities accompanied progressive neurological deterioration months or years by urinary incontinence. Evaluation by a neurosurgeon after their injury. The overall incidence has been then revealed an incomplete paraplegia (Frankel D). A estimated to range from 1. 3% to 3. 2% of all spinal lumbar myelogram showed no block to the flow of cord injuries (SCI),2,3 but recent evidence from contrast around the level of the old vertebral fracture. magnetic resonance imaging (MRI) which is the most An MRI scan of the spine revealed a central cystic accurate modality for its diagnosis,I,4 has shown that cavity of the spinal cord extending from T6 to conus the incidence is actually higher. medullaris, indicating a hydromyelia (Figure 1). T2W Although delayed post-traumatic syringomyelia in sagittal images demonstrated hyperintensity of conus paraplegia or tetraplegia is a rather common entity, medullaris consistent with cord injury and gliosis at the patients presenting with delayed post-traumatic syr­ level of the old compression fracture (Figure 2). No ingomyelia several years after an uncomplicated spinal craniovertebral junction abnormalities such as the fracture with no neurological deficit is extremely rare Chiari malformation nor of arachnoiditis, which are and the significance of the past history of spinal common causes of syringomyelia, were observed on the 6 trauma may sometimes be overlooked.5, MRI. There was no family history of any neurological We report a patient with syringohydromyelia disease. He also did not have a pre-existing clinical presenting 25 years after a spinal injury that had abnormality other than the L 1 crush fracture that caused a vertebral fracture but absolutely no might be related to the development of the cavity neurological symptoms or signs, and draw attention within the spinal cord. Since the syrinx was too small to the subject. in diameter, and extended through T6 to conus medullaris, neurosurgical intervention was not consid­ ered and he was referred to Ankara Rehabilitation Center for rehabilitation. When the patient was referred to our center, he had Correspondence: F Giiler-Uysal lost motor power in the lower extremities within a Delayed post-traumatic syringa hydromyelia F Guler-Uysal et al 302 Figure 1 Midsagittal Tl W SE image shows Ll compression Figure 2 Midsagittal T2W SE image showing signal with posterior subluxation compressing conus medullaris. hyperintensity in conus medullaris (arrowhead) consistent Central syrinx cavity extending from conus to upper thoracal with cord injury and gliosis cord is seen as a thin black line (arrowheads) period of months and was wheelchair bound. He had and crutches. He gained a 'swing to' gait within 4 fairly good sitting balance but no standing balance. months and performed clean intermittent self cathe­ Cranial and upper extremity evaluation were comple­ terization for urinary excretion at discharge. tely normal. Wasting and weakness in the lower extremities were notable, the left side being worse Discussion than the right. The deep tendon reflexes in the lower extremities were abolished and the plantar responses Post-traumatic syringomyelia is a well recognized late could not be elicited. Pin prick, light touch, sequela to spinal trauma in spinal cord patients. The temperature sensation, joint position sense as well as clinical presentation is usually marked by pain, sweating were diminished below TIO level. Urody­ ascending sensory loss, increased muscle weakness namic studies revealed detrusor hyperreflexia and and depressed deep tendon reflexes in paraplegic or external sphincter dyssynergia. Control MRI was tetraplegic patients. Dissociated sensory loss, with loss performed and he was again evaluated by a of pain and temperature sensation and preservation of neurosurgeon. Surgical intervention was not consid­ light touch and proprioception is common.5,7 Although ered as there was no enlargement of the cyst cavity post-traumatic syringomyelia in paraplegic and tetra­ and no worsening of the neurological deficits. plegic patients has been known for a long time, Rehabilitation was first aimed to strengthen his syringomyelia occurring as a result of spinal injury in abdominal and back muscles through mat exercises to patients with no residual neurological deficit is a rather maintain good posture and standing balance. He was new entity, and the history of previous spinal trauma then treated within the parallel bars for posture and can easily be overlooked. balance with the aid of posterior shells. Meanwhile he Diagnostic studies show post-traumatic syrinxes to was given anticholinergic medication for his bladder originate at the level of the initial spinal cord trauma, dysfunction. After succeeding within the parallel bars, to be most frequently located in the dorsal region of he was prescribed bilateral KAFOs with pelvic belt the spinal cord, and to be variable in length, width and Delayed post-traumatic syringohydromyelia F Gliler-Uysal et at 303 position throughout the cord. Most often they extend eration and syringohydromyelia.lO A syrinx may proximally from the level of injury,3,5 just like our case develop after spinal cord trauma, either soon after in which the caudal end of the syrinx cavity resorption of an intramedullary hematoma or as a corresponded to the level of the previous fracture delayed phenomenon after cord contusion or (Figure 1). The relationship between the syrinx cavity compression with microcystic cavitation.6,11 Deficient and the vertebral fracture, the presence of gliosis of or altered blood supply in the region of trauma the conus medullaris indicating some previous intrinsic could also be blamed for the production of the cavity cord damage (Figure 2), together with the absence of within the cord.12 Microinfarcts as well as lysosomal Chiari malformations, arachnoiditis or tethered cord and other cellular enzymes may play an important determination by MRI, strongly suggests the role of role in the liquefaction process and cyst formation.7 previous spinal injury in the pathogenesis of syringo­ Cores of necrotic tissue may extend for several hydromyelia in our patient. segments from the level of injury and these could Barnett8 defined three categories of post-traumatic liquefy and form a cavity.7,IO,13 Cyst extension, syringomyelia: (I) following traumatic paraplegia and leading to the development of neurological symp­ tetraplegia, (2) following minor or moderate spinal toms and signs, has been thought to be due to the cord injury and (3) as a late complication of spinal transmission to the cyst cavity of cerebrospinal fluid trauma producing adhesive arachnoiditis. Four types pressure fluctuations occurring with flexion and 6 of trauma were suggested by Van den Bergh, to be extension of the spine and straining. Any local responsible for the development of syringomyelia: arachnoid adhesions tethering the spinal cord repeated microtrauma, trauma followed by arachnoi­ enhance the transmission of the cerebrospinal fluid ditis, severe single trauma followed by persistent para pressure fluctuations and cyst extension and may or tetraplegia and minor single trauma followed by contribute
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