| Article Access Statistics|
| Viewed||4427 |
| Printed||90 |
| Emailed||3 |
| PDF Downloaded||85 |
| Comments ||[Add] |
Click on image for details.
|Year : 2014 | Volume
| Issue : 2 | Page : 192-194
Subacute post-traumatic ascending myelopathy (SPAM): Two cases of SPAM following surgical treatment of thoracolumbar fractures
Kamran Farooque1, Pankaj Kandwal2, Ankit Gupta1
1 Department of Orthopaedics, Jai Prakash Narayan Apex Trauma Centre, All India Institute of Medical Sciences, New Delhi, India
2 Department of Orthopaedics, All India Institute of Medical Sciences, Rishikesh, India
|Date of Submission||17-Feb-2014|
|Date of Decision||18-Mar-2014|
|Date of Acceptance||09-Apr-2014|
|Date of Web Publication||14-May-2014|
Department of Orthopaedics, All India Institute of Medical Sciences, Rishikesh - 249 201, Uttarakhand
Source of Support: None, Conflict of Interest: None
To report two cases of traumatic paraplegia who developed Sub-acute Post-Traumatic Ascending Myelopathy (SPAM) following surgical decompression.We hereby report two cases (both 35yr old male) with traumatic paraplegia that developed ascending weakness at 3rd and 5th Post-Op day respectively following surgical decompression. Both the patients experienced remarkable improvement in Neurology after treatment with steroids. The authors conclude by emphasizing on minimum cord handling during surgical decompression of the spinal cord to avoid this potentially life threatening complication.
Keywords: Subacute post-traumatic ascending myelopathy, thoracolumbar fractures, surgical decompression
|How to cite this article:|
Farooque K, Kandwal P, Gupta A. Subacute post-traumatic ascending myelopathy (SPAM): Two cases of SPAM following surgical treatment of thoracolumbar fractures. Neurol India 2014;62:192-4
|How to cite this URL:|
Farooque K, Kandwal P, Gupta A. Subacute post-traumatic ascending myelopathy (SPAM): Two cases of SPAM following surgical treatment of thoracolumbar fractures. Neurol India [serial online] 2014 [cited 2021 May 9];62:192-4. Available from: https://www.neurologyindia.com/text.asp?2014/62/2/192/132395
| » Introduction|| |
Secondary neurological deterioration following acute spinal cord injury is uncommon and is usually due to spinal column instability. The most common type of neurological deterioration is a rise in the level of the lesion by one and sometimes by two segments usually due to cord edema. This often occurs in the first four days and the deterioration is almost always temporary. 
A rare form of deterioration is when a spinal cord lesion corresponding to the bony injury ascends by several segments in the first three weeks after the original injury.  Sub-acute postoperative ascending myelopathy (SPAM) presents as neurological deterioration between day-1 to four weeks of initial spinal cord injury.  However, ascending weakness following surgical decompression for spinal trauma has not been documented in the literature.
| » Case Reports|| |
A 35-year-old male presented with paraplegia American Spinal Injury Association (ASIA A) following a motor vehicle accident. Spinal X-ray and computed tomography (CT) revealed L1-L2 fracture-dislocation with no other vertebral injury. Neurologic examination revealed paraplegia below level L1 with bladder and bowel involvement (ASIA A). Patient underwent posterolateral decompression, interbody fusion using local graft with posterior instrumented fusion from D12-L3. The cord was adequately decompressed without any adverse events. On postoperative day-5, patient developed weakness of both the upper limbs (2/5) with sensory loss below C6 dermatome. Magnetic resonance imaging (MRI) of whole spine showed bright cord signal in T2 and short tau inversion recovery (STIR) sequence extending upto C2-C3 cervical segments. Spinal cord expansion was noticed extending several levels above the original injured segment [Figure 1].
|Figure 1: Preoperative X-rays AP (a), Lateral views (b) and CT scan (c and d) indicating L1-L2 fracture dislocation. Postoperative X-rays AP (e) and lateral view (f) following decompression and instrumentation. Postoperative MRI: sagittal (e, g) and axial (f) showing cord edema extending up to cervical spine|
Click here to view
Patient was started on methyl prednisolone 30 mg/kg bolus followed by 5.4 mg/kg/hr in the next 23 hours (NASCIS II protocol). Later patient was started on tapering dose of prednisolone (10 mg) over a period of 3 weeks. Motor power in upper limbs improved (4/%) over a period of six weeks. Repeat magnetic resonance imaging (MRI) spine revealed reduction in the cord edema in the cervico-thoracic segment.
A 35-year-male presented with paraplegia (ASIA A) following fall from a height (20 meter height). Spine X-rays and CT revealed burst fracture of L1 vertebra with posterior retropulsion. Patient underwent anterior decompression using transthoracic, diaphragm cutting retroperitoneal approach. Partial corpectomy of L1 was done to ensure adequate decompression. Good decompression of the cord/thecal sac was achieved and the procedure was uneventful. Patient developed weakness in both the upper limbs on day-3 of post-operation. Neurologic examination revealed sensory loss for light touch and pin-prick below C4 dermatome and motor power of 2/5 in the elbow flexors. Whole spine MRI revealed ascending cord edema up to C8 [Figure 2]. Patient responded to steroids (NASCIS II protocol) and complete recovery of motor and sensory deficits in both the upper limbs was observed in three weeks.
|Figure 2: Burst fracture L1. Preoperative X-rays: AP (a) and lateral (b) view. CT scans: sagittal (c) and axial (d) sections showing posterior retropulsion. Postoperative x-rays: AP (e) and lateral (f) view following anterior decompression and anterior instrumentation. Postoperative MRI: sagittal (g) and axial (h) showing cord edema extending up to C3 vertebra|
Click here to view
| » Discussion|| |
The syndrome of delayed neurological deterioration by four or more cranial segments following spinal cord injury was first described by Frankel in 1968.  Patients typically present with an ascending neurological deficit within 3 weeks of the initial spinal cord insult. Sub-acute postoperative ascending myelopathy (SPAM) most commonly presents as neurological deterioration but may present with shoulder pain, respiratory involvement, or may be subclinical.  Most patients make a good recovery but there is a reported mortality of up to 10%, particularly, if the cord involvement ascends to the level of the brainstem. 
Delayed, sub-acute deterioration secondary to involvement of several segments cephalad to the original injury level is rare and its mechanism has not been fully elucidated. The various proposed pathophysiological mechanisms include: hypotension related ischemia, arterial thrombosis, venous thrombosis, venous congestion, inflammation and autoimmune mechanisms, and infections. ,, Potential role of apoptosis in the pathophysiology of SPAM has also been postulated.  It has been postulated that temporary changes in cerebro-spinal fluid (CSF) flow may contribute in the development of SPAM. ,,
Both our patients had thoracolumbar fracture with paraplegia; screening CT scan of whole spine did not reveal any concomitant fractures. Patient (case 1) with fracture-dislocation of L1 over L2, who underwent postero-lateral decompression, developed ascending weakness on fourth post-operative day; while the other patient (case 2) with burst fracture L1 who underwent anterior decompression, developed weakness of both upper limb on third post-operative day. The possible cause of SPAM, especially in postoperative cases could be due to inadvertent cord handling. Cord handling during decompression could trigger cascade of events leading to ascending myelopathy.
Characteristic MR imaging findings of SPAM include (i) a central area of hyperintense signal on T2-weighted sequences, which tapers at the rostral end of the lesion, (ii) heterogeneous intramedullary signal on T1-weighted sequences, and (iii) an expanded spinal cord. Syringes are absent, and on follow-up imaging the cord appears atrophic. , Both the patients in our study had characteristic MRI features of SPAM with cord edema (hyperintense on T2 sequences) extending several segments above the cord injury level.
A wide range of treatments have been proposed including anticoagulation, decompression, steroids  and mannitol. Few authors have described dural untethering and cordectomy for the treatment of SPAM. , Both the patients in our series responded to steroids, while one showed complete recovery; the other had some residual weakness in the upper limbs.
| » References|| |
|1.||Frankel HL. Ascending cord lesion in the early stages following spinal injury. Paraplegia 1969;7:111-8. |
|2.||Yablon IG, Ordia J, Mortara R, Reed J, Spatz E. Acute ascending myelopathy of the spine. Spine (Phila Pa 1976) 1989;14:1084-9. |
|3.||Planner AC, Pretorius PM, Graham A, Meagher TM. Subacute progressive ascending myelopathy following spinal cord injury: MRI appearances and clinical presentation. Spinal Cord 2008;46:140-4. |
|4.||Belanger E, Picard C, Lacerte D, Lavallee P, Levi AD. Subacute posttraumatic ascending myelopathy after spinal cord injury. Report of three cases. J Neurosurg 2000;93:294-9. |
|5.||Aito S, El Masry WS, Gerner HJ, Lorenzo ND, Pellicanò G, D′Andrea M, et al. Ascending myelopathy in the early stage of spinal cord injury. Spinal Cord 1999;37:617-23. |
|6.||Al-Ghatany M, Al-Shraim M, Levi AD, Midha R. Pathological features including apoptosis in subacute posttraumatic ascending myelopathy. Case report and review of the literature. J Neurosurg Spine 2005;2:619-23. |
|7.||Marshall LF, Knowlton S, Garfin SR, Klauber MR, Eisenberg HM, Kopaniky D, et al. Deterioration following spinal cord injury. A multicenter study. J Neurosurg 1987;66:400-4. |
|8.||Lee TT, Arias JM, Andrus HL, Quencer RM, Falcone SF, Green BA. Progressive posttraumatic myelomalacic myelopathy: Treatment with untethering and expansive duraplasty. J Neurosurg 1997;86:624-8. |
|9.||Meagher TM, Belci M, López de Heredia L, Ansorge O, Jamous A, Saif M, et al. Resolution of SPAM following cordectomy: implications for understanding pathophysiology. Spinal Cord 2012;50:638-40. |
[Figure 1], [Figure 2]