Abstract
Purpose:
This case report aims to describe remarkable neurological recovery in a patient presenting with AO type C L2 fracture-dislocation and initial ASIA grade A complete spinal cord injury (SCI).
Methods:
A 32-year-old male auto mechanic suffered L2 burst fracture-dislocation complicated by complete paraplegia and combined polytrauma. A full multidisciplinary care pathway was delivered, including targeted hemodynamic stabilization to maintain MAP 85–90 mmHg, delayed posterior spinal decompression and fusion, and long-term staged multimodal rehabilitation.
Results:
Neurological function recovered to ASIA grade D at the six-month follow-up. The patient achieved independent ambulation over 500 meters with a thoracolumbar brace and fully returned to his pre-injury heavy manual occupation. Irreparable left L1 nerve root avulsion caused permanent mild quadriceps and iliopsoas weakness, alongside slight hypoesthesia on the medial left thigh. Voluntary bladder function fully recovered, with only mild delayed defecation as a persistent minor complaint.
Conclusion:
Combined hemodynamic spinal neuroprotection, surgical decompression with primary dural reconstruction, and systematic rehabilitation enables meaningful functional recovery even for severe AO type C thoracolumbar trauma with initial ASIA A complete SCI. Serial neurological assessment is mandatory to differentiate transient spinal shock from irreversible anatomical spinal cord transection and avoid overly pessimistic early prognoses. Though concurrent traumatic nerve root avulsion limits full recovery to ASIA E, individualized timely surgery remains the core intervention to optimize long-term mobility and quality of life.
Introduction
Thoracolumbar fracture-dislocation classified as AO Spine type C corresponds to high-energy spinal injury with full three-column destruction, vertebral collapse and locked facet joints, which induces severe spinal instability and intramedullary spinal cord contusion, carrying poorer functional outcomes than simple compression fractures (, , ). Traditional clinical observations indicated patients with acute ASIA grade A complete SCI rarely regained walking ability, with most patients permanently wheelchair-bound ().
This pessimistic prognostic perspective has been updated with growing recognition of spinal shock, a temporary neurophysiological loss of distal spinal reflexes triggered immediately after severe spinal trauma. Kirshblum et al. confirmed that patients graded ASIA A solely due to spinal shock, rather than permanent spinal cord transection, have a far higher probability of recovering ambulatory function to ASIA D (). Multiple cohort studies further validated a positive linear relationship between thorough intraoperative spinal canal decompression and final neurological recovery potential (, ). Current international SCI guidelines consistently recommend strict targeted hemodynamic support to preserve perfusion of the spinal cord penumbra and reduce secondary ischemic neuronal damage ().
Compliant with all mandatory items of the CARE reporting checklist, this case report presents a rare polytrauma patient with L2 burst fracture-dislocation and initial ASIA A paralysis who regained brace-assisted independent walking six months after integrated treatment. We focus on the clinical value of sequential neurological monitoring to identify spinal shock, individualized delayed surgical timing for hemodynamically unstable multiple trauma patients, and synergistic effects of multidisciplinary staged rehabilitation for severe thoracolumbar SCI.
Case presentation
All identifiable personal information was anonymized to comply with clinical privacy regulations. The patient was a 32-year-old male auto mechanic without congenital spinal malformation, chronic low back pain, hypertension, diabetes, cerebrovascular lesions or hereditary neuromuscular disorders. He lived independently and undertook daily heavy physical labor before injury, with no history of mental illness, long-term alcohol, tobacco or illicit drug abuse, prior spinal surgery or spinal trauma, and regular chronic medication use. Pre-hospital emergency management including FAST ultrasound, chest radiography and crystalloid resuscitation was performed without adverse reactions.
The patient suffered vertical compressive waist trauma from a falling 2-ton metal crane component. At the scene, he complained of intractable lumbago, complete loss of voluntary motor function in bilateral lower limbs, and total disappearance of pain, light touch and temperature sensation below the hip folds, with no loss of consciousness or upper limb dysfunction. Upon emergency admission, vital signs were unstable with systolic blood pressure ranging 80–90 mmHg. Physical examination detected multiple perineal skin lacerations, bilateral rib fracture-related chest tenderness and bilateral pulmonary crackles suggestive of pulmonary contusion. Local spinal palpation showed obvious midline deviation of the L2 spinous process and diffuse lumbar percussion tenderness, with severe pain restricting passive spinal flexion and extension.
Standardized serial neurological examinations were conducted at admission (0 h), 6 h, 12 h, 24 h and 48 h post-trauma to track spinal shock progression. At admission, bilateral lower limb muscle strength was 0/5; cremasteric reflex disappeared, anal sphincter was lax, and all sacral dermatomal sensation (S1–S5) was completely absent, fully meeting ASIA A diagnostic criteria. Initial muscle tone was relatively normal, consistent with the incomplete early phase of spinal shock before generalized flaccidity developed. From 6 h to 24 h post-injury, muscle tone gradually diminished, knee and ankle deep tendon reflexes became increasingly difficult to elicit, and bilateral lower limb flaccidity worsened. Forty-eight hours before surgery, complete flaccid paralysis and total areflexia were detected with persistent S1–S5 sensory loss, confirming fully established spinal shock and sustained ASIA A neurological grade.
Two weeks after surgical intervention, the cremasteric reflex recovered and resting muscle tone returned to normal; bilateral deep tendon reflexes were present without pathological Babinski sign, marking complete resolution of spinal shock. At six-month follow-up, left iliopsoas and quadriceps strength was 4/5, while all other lower limb muscle groups recovered to grade 5/5. Only mild hypoesthesia remained over the medial cutaneous region of the left thigh; bilateral sacral sensation and voluntary micturition recovered completely, with merely mild delayed defecation as a persistent minor symptom.
Emergency bedside FAST ultrasound and portable chest radiography excluded life-threatening intrathoracic and intraperitoneal hemorrhage. Continuous invasive arterial blood pressure monitoring guided vasopressor infusion and blood transfusion throughout preoperative stabilization. Thoracolumbar multiplanar CT and T2-weighted MRI were performed after vital signs normalized at 48 h post-trauma, as lumbar plain radiography was delayed to prioritize hemorrhage control for the patient's critical hemodynamic instability and concurrent severe thoracic trauma. Preoperative CT verified L2 burst fracture-dislocation with >90% spinal canal stenosis, L1 wedge compression fracture and rupture of the posterior ligamentous complex; sagittal and coronal reconstructions demonstrated severe thoracolumbar kyphosis and retro-pulsed vertebral fragments occupying the spinal canal (Figure 1). Preoperative T2-weighted MRI showed anatomically intact spinal cord compressed by displaced bone fragments between the left L1 lamina and right L2 pedicle, with heterogeneous intramedullary T2 hyperintensity indicating spinal cord contusion and interstitial edema, alongside obvious compression of the conus medullaris and cauda equina (Figure 2).
Figure 1
Figure 2
The primary diagnostic difficulty lay in distinguishing transient spinal shock from irreversible spinal cord transection, which could only be clarified through serial neurological assessments and intraoperative direct visualization. Preoperative MRI failed to fully identify intradural injuries including L1 nerve root avulsion and localized dural laceration, both of which were confirmed intraoperatively. Differential diagnoses including permanent complete spinal cord transection, simple L1/L2 compression fracture without three-column injury, and isolated cauda equina syndrome without spinal cord contusion were all excluded based on imaging and serial neurological data. Favorable prognostic factors included intact spinal cord continuity on MRI, standardized MAP-targeted hemodynamic neuroprotection, complete intraoperative spinal canal decompression, repairable dural injury and long-term systematic rehabilitation. Unfavorable prognostic factors included irreparable traumatic left L1 nerve root avulsion, severe intramedullary edema at the conus medullaris, and initial ASIA A injury complicated by prolonged spinal shock.
Within three hours after trauma, intravenous methylprednisolone (30 mg/kg bolus followed by continuous infusion at 5.4 mg/kg/h for 24 h) was administered per institutional historical acute SCI protocol. We explicitly acknowledge current guideline controversies regarding high-dose steroid therapy, which elevates risks of infection, peptic ulcer bleeding and hyperglycemia; this regimen is only reported as the actual clinical intervention for this polytrauma patient and is not recommended for routine clinical application. Postoperative dexamethasone (10 mg intravenous daily for three days, followed by tapering over seven days) alleviated spinal cord and soft tissue edema, while mecobalamin (500 μg intramuscular injection daily for 14 days, then oral administration three times daily for three months) was prescribed to facilitate peripheral nerve repair for the left L1 nerve root injury.
Persistent hypotension induced by multiple traumatic hemorrhages required a 48-hour delay for definitive spinal decompression to avoid intraoperative hypoperfusion and secondary spinal cord ischemia. During stabilization, norepinephrine infusion (0.05–0.15 µg/kg/min) was titrated to maintain MAP 85–90 mmHg, combined with 2000mL crystalloid resuscitation within the first 24 h and packed red blood cell transfusion when hemoglobin dropped below 80 g/L. Continuous invasive arterial pressure monitoring adjusted vasopressor dosage to protect spinal cord penumbra perfusion, consistent with international SCI hemodynamic management standards.
Surgery was performed via posterior midline approach under general endotracheal anesthesia for L1–L2 fracture reduction. Incarcerated L2 bone fragments were resected first to eliminate mechanical traction on neural tissue during distraction reduction and prevent iatrogenic conus and nerve root injury. Long-segment pedicle screw fixation covering T11–L4 was applied to restore spinal stability, followed by controlled longitudinal distraction to reconstruct physiological thoracolumbar sagittal alignment and relieve spinal canal stenosis. A continuous running 5–0 Prolene suture was used for primary watertight dural repair to recover thecal sac integrity, reduce cerebrospinal fluid leakage and surgical infection risk, and stabilize intrathecal pressure; spontaneous spinal cord pulsation observed intraoperatively served as an immediate objective marker of complete neural decompression (Figure 3). Combined intracorporeal autologous vertebral bone graft and intertransverse process fusion was implemented to improve bony fusion rates and reduce late implant failure risk. Intraoperative observation confirmed complete non-repairable avulsion of the left L1 nerve root, the root cause of the patient's permanent partial lower-extremity sensory and motor deficit. Postoperative digital radiographs verified satisfactory fracture reduction and accurate pedicle screw placement across T11–L4 (Figure 4). Intraoperative photographs captured immediately after dural rupture were lost due to camera storage failure; only images taken after full dural repair are available for illustration.
Figure 3
Figure 4
A standardized three-stage rehabilitation program was delivered postoperatively. The early rehabilitation phase (postoperative day 3 to two weeks) contained bilateral lower limb passive range-of-motion training and neuromuscular electrical stimulation for paralyzed muscle groups, plus respiratory physiotherapy to prevent deep vein thrombosis, joint contracture and hypostatic pneumonia. The intermediate phase (two weeks to three months) focused on thoracolumbar orthosis-assisted standing and gait training, with electroacupuncture and hyperbaric oxygen therapy (HBOT) applied as secondary supportive adjuncts. Preclinical and small-scale clinical studies indicated these two modalities improve spinal microcirculation and suppress post-traumatic oxidative stress, though high-level prospective evidence supporting their independent efficacy for acute SCI remains limited. The late functional rehabilitation phase (three to six months) included unassisted overground walking training, daily living ability adaptation and vocational rehabilitation to support the patient's return to pre-injury heavy manual labor.
At two weeks post-operation, most bilateral superficial, pain and thermal sensation recovered, and lower limb muscle strength improved to grade 2/5; physiological deep tendon reflexes returned without pathological signs, and positive cremasteric reflex confirmed spinal shock resolution. Anal sphincter tone remained mildly lax, yet spontaneous voluntary urination was fully recovered with only mild delayed defecation. Six-month follow-up CT scans confirmed solid interbody and posterolateral bony fusion, intact T11–L4 pedicle screw constructs without loosening, migration or secondary loss of fracture reduction (Figure 5). The patient reached ASIA D neurological grade, capable of continuous independent walking over 500 meters with a thoracolumbar brace, and fully resumed his original occupation. He maintained full adherence to all medication, rehabilitation, acupuncture and HBOT regimens, without any drug-related adverse events or postoperative complications including cerebrospinal fluid leakage, surgical site infection, deep vein thrombosis or pulmonary embolism. Table 1 systematically summarizes the full clinical timeline covering diagnostic tests, therapeutic interventions and key recovery milestones at each time point.
Figure 5
Table 1
| Timepoint Post-Trauma | Neurological ASIA Grade | Key Diagnostic Tests | Therapeutic Interventions | Major Clinical Milestones |
|---|---|---|---|---|
| Admission (0 h) | A | FAST scan, chest x-ray, venous access, arterial line placement | Methylprednisolone bolus, crystalloid resuscitation, ICU admission | Total bilateral lower limb paralysis, S1–S5 sensory loss |
| 0–48 h | Serial A at 6/12/24/48 h | Thoracolumbar CT + MRI, serial blood gas/hemoglobin monitoring | Methylprednisolone 24 h infusion, norepinephrine (MAP 85–90 mmHg), 2 units packed RBC transfusion | Progressive spinal shock, complete flaccid paralysis by 48 h |
| 48 h (Surgery) | A | Intraoperative spinal fluoroscopy | Posterior open reduction, incarcerated L2 bone resection, T11–L4 pedicle screw fixation, 5–0 Prolene primary dural repair, intertransverse/intracorporeal bone grafting | Intraoperative visualization of restored spinal cord pulsation post-decompression |
| POD 1 | Improved sensory function | Postoperative lumbar DR | Dexamethasone tapering, mecobalamin IM initiation | Lower limb motor strength improved to grade 1/5 |
| POD 3–14 | Gradual sensory/motor gain | Daily neurological rounds | Early passive mobilization, neuromuscular electrical stimulation, pulmonary rehabilitation | Muscle strength increased to grade 2/5; cremasteric reflex recovered at 2 weeks (spinal shock resolved) |
| 2 weeks–3 months | Progressive improvement | Monthly clinical follow-up | Gait training with a thoracolumbar orthosis, adjuvant acupuncture, and HBOT, oral mecobalamin | Voluntary urination fully restored; residual mild defecatory delay persisted |
| 6 months | D | Thoracolumbar CT (Figure 5) | Continued functional vocational training | ASIA D grade; independent walking >500 m with a brace; return to full pre-injury work |
Structured timeline of clinical care, diagnostics, interventions, and follow-Up outcomes.
Discussion
This case illustrates that initial ASIA A complete SCI grading in the hyperacute trauma phase does not represent irreversible permanent paraplegia when neurological deficits are masked by transient spinal shock. The patient's excellent functional recovery was achieved through synergistic application of four core therapeutic strategies, analyzed systematically below with integrated high-level literature evidence to support clinical reasoning.
Spinal shock and the clinical value of serial neurological assessment
The patient's unique early presentation of ASIA A injury with preserved baseline muscle tone constituted a typical diagnostic pitfall, characteristic of the incomplete initial stage of spinal shock before diffuse lower limb flaccidity fully develops. Our sequential neurological assessments at 6, 12 and 24 h post-trauma documented progressive loss of deep tendon reflexes and muscle tone, objectively confirming the evolution of complete spinal shock. The reappearance of the cremasteric reflex two weeks after surgery acted as a definitive clinical marker of spinal shock resolution, which reliably ruled out permanent anatomical spinal cord transection. This case strongly highlights that single one-time neurological evaluation at emergency admission cannot deliver accurate early prognosis for acute SCI; repeated dynamic neurological monitoring is essential to avoid overly pessimistic clinical judgment, consistent with the cohort findings published by Kirshblum et al. ().
Surgical timing and targeted hemodynamic neuroprotection
Meta-analytic evidence recommends spinal decompression within 24 h post-injury to minimize secondary spinal cord ischemic damage (). However, this patient's life-threatening combined thoracic and perineal polytrauma with persistent hemodynamic instability necessitated a 48-hour surgical delay, consistent with consensus guidance that polytrauma patients require individualized surgical timing to avoid catastrophic intraoperative hypotension (). Kwon et al.'s 2024 international clinical practice guideline for acute SCI hemodynamic management systematically demonstrated that maintaining MAP at 85–90 mmHg effectively preserves microperfusion of the spinal cord penumbra and mitigates progressive neuronal ischemia (). During the 48-hour preoperative waiting period, we strictly titrated norepinephrine, balanced crystalloid resuscitation and blood transfusion to maintain this MAP target, and the patient obtained prominent neurological recovery despite delayed surgery. This real-world clinical observation provides direct supportive evidence for the guideline's hemodynamic optimization strategy as an effective bridging neuroprotective measure for unstable polytrauma patients unsuitable for ultra-early spinal decompression.
Operative strategy and complete intraoperative spinal canal decompression
The posterior midline surgical approach serves as the primary intervention for AO type C three-column thoracolumbar injuries, enabling direct visualization of injured neural structures and multi-level rigid fixation to restore spinal column stability (, ). Our stepwise surgical protocol — resecting incarcerated bone fragments before pedicle screw implantation and fracture distraction reduction — effectively prevented iatrogenic traction injury to the conus medullaris and traversing nerve roots. Aarabi and colleagues’ serial clinical studies confirmed a linear positive correlation between thorough spinal canal decompression and final neurological recovery potential in motor-complete traumatic SCI patients (, ). In this case, intraoperative spontaneous spinal cord pulsation after full decompression acted as an immediate objective marker of adequate neural release, which was further validated by the patient's significant six-month functional improvement. Primary watertight dural repair with continuous 5–0 Prolene sutures is another critical operative step: Taylor et al. verified that intact thecal sac reconstruction reduces postoperative cerebrospinal fluid leakage, surgical site infection risk and abnormal intrathecal pressure, constructing a favorable microenvironment for spinal cord tissue repair (). Intraoperatively confirmed irreparable left L1 nerve root avulsion independently limited full recovery to ASIA E grade, indicating concurrent traumatic nerve root injury as an unfavorable prognostic factor even after maximal surgical decompression.
Multimodal staged rehabilitation and adjunctive therapy
Surgical decompression alone cannot achieve optimal functional recovery; staged multidisciplinary rehabilitation translates anatomical spinal cord decompression into tangible motor and sensory gains. Early passive mobilization and neuromuscular electrical stimulation suppress disuse muscle atrophy and promote central nervous system neural plasticity, as validated by Henry et al. in their research on rehabilitation timing after incomplete SCI (). Electroacupuncture and HBOT were applied as secondary supportive adjuncts rather than core definitive therapies, corresponding to their limited high-quality prospective clinical trial evidence base for acute thoracolumbar SCI treatment (). Preclinical research by Chen et al. demonstrated electroacupuncture improves regional spinal microcirculation and inhibits post-traumatic neuronal apoptosis (), while Li et al.'s meta-analysis confirmed HBOT alleviates spinal cord hypoxia-ischemia and suppresses trauma-induced oxidative stress damage to neural tissue (, ). Combined multimodal rehabilitation accelerated the patient's motor and sensory recovery trajectory throughout the six-month follow-up period.
Strengths and limitations of this case report
The primary strength of this manuscript lies in full compliance with all mandatory items of the CARE case reporting checklist, including complete anonymized clinical data, serial standardized neurological documentation, structured diagnostic reasoning, detailed stepwise therapeutic protocols, objective imaging and functional follow-up outcomes, and patient subjective experience records. The precise quantitative documentation of perioperative hemodynamic parameters, vasopressor dosage, fluid and transfusion volume provides valuable reference data for clinicians managing polytrauma patients requiring delayed spinal surgery. Real-time intraoperative spinal cord pulsation as an objective decompression marker and standardized six-month imaging follow-up further enhance the clinical reference value of this report.
Several inherent limitations should be acknowledged. First, this is a single-center retrospective case report without matched control groups, restricting generalizability of the integrated treatment protocol to broader SCI populations. Second, intraoperative photographs capturing dural rupture and L1 nerve root avulsion were lost due to camera hardware failure; intraoperative intradural traumatic pathology can only be supported by operative notes without photographic corroboration, and preoperative MRI cannot fully delineate the severity of intradural soft tissue and nerve root injury. Third, high-dose methylprednisolone pulse therapy was administered following outdated institutional protocols; modern clinical guidelines discourage routine use of this regimen due to elevated systemic adverse event risks, and we only report its clinical application without advocating widespread routine steroid administration for acute SCI. Fourth, electroacupuncture and HBOT were used as adjunct rehabilitation modalities, yet large-scale high-quality prospective randomized controlled trials verifying their independent therapeutic efficacy in acute thoracolumbar SCI remain insufficient. Finally, follow-up duration is limited to six months postoperatively; long-term data (≥2 years) regarding progressive spinal degenerative changes, stability of permanent neurological deficits and late implant-related complications are unavailable, requiring extended follow-up to further validate long-term functional outcomes.
Conclusion
For young polytrauma patients with AO type C thoracolumbar burst fracture-dislocation and initial ASIA grade A complete SCI, an integrated full-spectrum care pathway consisting of standardized early hemodynamic spinal neuroprotection, delayed safe posterior spinal decompression combined with long-segment fixation, intraoperative primary watertight dural reconstruction, and sequential multidisciplinary staged rehabilitation can achieve substantial neurological recovery enabling brace-supported independent ambulation. Clinicians must recognize the confounding impact of spinal shock on hyperacute neurological grading and implement serial dynamic neurological assessments to avoid overly pessimistic early prognostic judgments. Concurrent traumatic spinal nerve root avulsion causes permanent partial neurological deficits and prevents complete ASIA grade E functional recovery; nevertheless, timely individualized surgical intervention remains the critical cornerstone to optimize long-term patient mobility and quality of life. This CARE-compliant case report provides detailed, reproducible clinical reference for managing comparable severe high-energy thoracolumbar spinal trauma complicated by initial complete paraplegia.
Statements
Data availability statement
The original contributions presented in the study are included in the article/Supplementary Material, further inquiries can be directed to the corresponding author.
Ethics statement
This retrospective case report complies with the ethical standards laid out in the 1964 Helsinki Declaration and all subsequent amendments. Institutional Review Board ethical approval was formally waived by the hospital ethics committee due to the fully anonymized, retrospective nature of the single-case analysis. Written informed consent was obtained from the individual(s) for the publication of any potentially identifiable images or data included in this article.
Author contributions
QT: Writing – original draft, Methodology, Investigation, Writing – review & editing. MF: Writing – review & editing, Methodology.
Funding
The author(s) declared that financial support was not received for this work and/or its publication.
Conflict of interest
The author(s) declared that this work was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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Summary
Keywords
AO type C lumbar fracture-dislocation, ASIA a spinal cord injury, multidisciplinary rehabilitation, posterior decompression, spinal shock
Citation
Tian Q and Feng M (2026) From ASIA A to D: substantial neurological recovery after surgical management of traumatic L2 burst fracture-dislocation – a case report. Front. Musculoskelet. Disord. 4:1872965. doi: 10.3389/fmscd.2026.1872965
Received
05 May 2026
Revised
05 July 2026
Accepted
13 July 2026
Published
07 August 2026
Volume
4 - 2026
Edited by
Carlos A. Bagley, Saint Luke’s Marion Bloch Neuroscience Institute, United States
Reviewed by
Ali Imran Ozmarasali, Bursa City Hospital, Türkiye
Sukhmin Singh, University of Delhi, India
Updates
Copyright
© 2026 Tian and Feng.
This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Mingxing Feng silence1900200@126.com
Disclaimer
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.