Abstract

Degenerative cervical myelopathy is the leading cause of non-traumatic spinal cord dysfunction in older adults and may occasionally present with rapid neurological deterioration. A 78-year-old man presented with rapidly progressive cervical myelopathy characterized by bilateral upper-limb weakness and acute urinary retention. Neurological evaluation demonstrated advanced myelopathy with a modified Japanese Orthopaedic Association (mJOA) score of 6/18. Magnetic resonance imaging revealed cervical canal stenosis with dominant anterior compression at C3–C4 and multilevel degenerative changes. Given comorbidities and high perioperative risk, a focused short-segment anterior cervical decompression and fusion at C3–C4 was performed using a lordotic interbody cage to restore sagittal alignment and facilitate indirect decompression of adjacent levels. Operative time was 85 min with an estimated blood loss of 120 ml. At 1-year follow-up, the mJOA improved to 15/18 (75% recovery), indicating that limited anterior decompression with restoration of cervical lordosis can provide neurological recovery in high-risk elderly patients.

Introduction

Degenerative cervical myelopathy (DCM), most commonly caused by cervical spondylotic myelopathy (CSM), is the leading cause of non-traumatic spinal cord dysfunction in adults over 50 years [1–3]. Progressive degenerative changes—including disc collapse, osteophyte formation, ligamentum flavum hypertrophy, and ossification of the posterior longitudinal ligament (OPLL)—lead to spinal canal narrowing and chronic cord compression. A congenitally narrow canal reduces physiologic reserve and predisposes to symptomatic myelopathy [1, 2].

DCM typically follows a gradual or stepwise course; approximately 75% of patients show episodic deterioration, 20% steady progression, and only a minority experience rapid neurological decline [2]. Nevertheless, acute non-traumatic deterioration has been reported, particularly in association with disc herniation or OPLL [2–4]. Clinically, DCM presents with upper motor neuron signs, gait disturbance, hand clumsiness, and sensory deficits. Advanced disease may include autonomic dysfunction such as urinary retention, indicating severe cord compromise [1, 5].

Magnetic resonance imaging (MRI) is the gold standard for evaluating cord compression and signal change, while computed tomography better defines osseous pathology and OPLL [3]. Surgical decompression is recommended for moderate to severe or progressive cases, with approach selection determined by compression morphology and patient factors [1, 6–8].

Case presentation

A 78-year-old male presented with rapidly progressive cervical myelopathy characterized by severe neck pain, bilateral upper limb weakness (right greater than left), and acute urinary retention requiring Foley catheterization. He had significant cardiovascular and metabolic comorbidities, placing him at high perioperative risk. There was no trauma history.

Neurological examination revealed advanced myelopathy. Motor strength was 2/5 in the right upper limb and 3/5 in the left upper limb (Medical Research Council scale). The patient was non-ambulatory 3 days ago. Hyperreflexia and positive upper motor neuron signs were present. Severe right-sided and moderate left-sided radiculopathy were noted. Neurogenic bladder dysfunction was confirmed. The preoperative modified Japanese Orthopaedic Association (mJOA) score was 6/18, indicating severe myelopathy.

Preoperative laboratory values were within acceptable surgical limits: hemoglobin 12.4 g/dl (13.0–17.0), WBC 7.8 × 109/L (4.0–11.0), platelets 230 × 109/L (150–400), creatinine 1.1 mg/dl (0.7–1.3), sodium 138 mmol/L (135–145), potassium 4.2 mmol/L (3.5–5.0), CRP 3 mg/L (<5), and INR 1.0 (0.9–1.2). Intravenous corticosteroids were administered per protocol.

MRI demonstrated severe cervical canal stenosis with dominant anterior compression at C3–C4 and multilevel degenerative changes at C5–C6 and C6–C7, with cord signal changes consistent with myelopathy. The principal pathological level was C3–C4 (Fig. 1).

Two-panel preoperative T2-weighted cervical MRI. Panel A shows severe multilevel cervical canal stenosis, greatest at C3-C4, with dominant anterior spinal cord compression and additional degenerative narrowing at C5-C6 and C6-C7. Panel B shows marked ventral spinal cord compression at C3-C4 caused by a disc-osteophyte complex.
Figure 1

Preoperative cervical MRI. (A) Sagittal T2-weighted image demonstrating severe cervical canal stenosis with dominant anterior compression at C3–C4 and multilevel degenerative changes. (B) Axial T2-weighted image at C3–C4 showing marked ventral spinal cord compression from a disc–osteophyte complex.

Given the patient’s age and comorbidities, minimizing operative time and physiological stress was prioritized. A combined anterior–posterior procedure was deemed high risk. A focused short-segment anterior cervical decompression and fusion at C3–C4, C4–C5 was performed.

Adequate decompression was achieved through a standard anterior approach. A lordotic interbody cage was inserted to restore cervical alignment, facilitating indirect decompression at C5–C6 and C6–C7. Operative time was 85 minutes with estimated blood loss of 120 ml. No intraoperative complications occurred.

Postoperative radiographs confirmed appropriate cage positioning and restoration of physiological lordosis without subsidence or malalignment (Fig. 2). Postoperative cervical MRI further demonstrated improved sagittal alignment, restoration of cervical lordosis, and adequate spinal cord decompression, with relief of central canal compression at C3–C4 and maintained canal decompression at C4–C5 (Fig. 3). These radiological findings were consistent with the marked clinical improvement observed after surgery. Postoperative labs remained stable (hemoglobin 11.8 g/dl; WBC 8.5 × 109/L; creatinine 1.0 mg/dl; CRP 6 mg/L).

Two-panel postoperative cervical radiographs following anterior cervical discectomy and fusion at C3-C4 and C4-C5. Panel A shows the anteroposterior view with appropriately positioned anterior instrumentation and satisfactory cervical alignment. Panel B shows the lateral view with interbody cages and anterior fixation, demonstrating restoration of cervical lordosis.
Figure 2

Postoperative cervical radiographs. (A) Anteroposterior view demonstrating anterior cervical instrumentation at C3–C4 and C4–C5 with satisfactory alignment. (B) Lateral view demonstrating ACDF with interbody cages and fixation with restoration of cervical lordosis.

Two-panel postoperative cervical radiographs following anterior cervical discectomy and fusion at C3-C4 and C4-C5. Panel A shows an anteroposterior view with appropriately positioned anterior instrumentation and satisfactory cervical alignment. Panel B shows a lateral view with interbody cages and anterior fixation, demonstrating restoration of cervical lordosis.
Figure 3

Postoperative cervical spine MRI. (A) Sagittal T2-weighted MRI showing improvement of cervical alignment with restoration of cervical lordosis and adequate decompression of the spinal cord. (B) Axial T2-weighted MRI at the C3–C4 level demonstrating relief of central canal compression after surgery. (C) Axial T2-weighted MRI at the C4–C5 level showing maintained canal decompression postoperatively.

Neurological improvement was observed early after surgery. Motor strength improved to 4/5 bilaterally, radicular symptoms decreased, ambulation became independent, and urinary retention resolved after Foley catheter removal.

At one-year follow-up, the patient remained independently ambulatory with normal bladder function. The mJOA score improved from 6/18 to 15/18, corresponding to a 75% recovery rate using the Hirabayashi formula. Follow-up imaging confirmed maintained lordosis, stable fusion, and sustained postoperative decompression (Figs 2 and 3).

Discussion

DCM results from chronic cervical canal narrowing and is typically characterized by gradual neurological decline [1–3]. However, acute deterioration has been documented, including sudden tetraplegia and rapidly progressive myelopathy in degenerative conditions [2, 3]. These reports demonstrate that DCM may unpredictably evolve into a surgical emergency.

Rahyussalim et al. described urinary retention in CSM treated with laminoplasty, demonstrating neurological recovery after posterior decompression [1]. Young et al. reported sudden non-traumatic tetraplegia during sleep secondary to cervical spondylosis [2]. Westwick et al. and Brogna et al. emphasized the importance of anterior decompression in cases involving ventral pathology and OPLL [3, 4]. Other reports highlight diagnostic delay and atypical presentations contributing to advanced neurological deficits before intervention [5–8].

In contrast to these cases, our patient was a medically fragile elderly individual deemed high risk for extensive multilevel or combined surgery. Rather than performing circumferential decompression, we targeted the dominant compressive level and restored sagittal alignment using a lordotic cage to achieve indirect decompression of adjacent segments. This strategy minimized operative time and blood loss while achieving meaningful neurological recovery.

The postoperative MRI supported this clinical improvement by demonstrating restored cervical lordosis and adequate decompression of the spinal cord.

The clinical outcome in this case resolution of bladder dysfunction, restoration of ambulation, and a 75% mJOA recovery rate at 1 year demonstrates that carefully selected short-segment anterior decompression with sagittal realignment can provide substantial functional recovery even in high-risk elderly patients. This approach may represent a pragmatic alternative when extensive reconstructive surgery is contraindicated.

Conclusion

Short-segment anterior decompression with restoration of cervical lordosis can achieve significant neurological recovery in elderly high-risk patients with severe DCM. Strategic sagittal realignment may allow indirect multilevel decompression while limiting operative burden. Individualized surgical planning is essential to optimize outcomes in medically fragile populations.

Acknowledgements

The authors would like to thank all the staff who provided administrative and technical support for this work.

Conflicts of interest

The authors declare that they have no conflict of interest.

Funding

No external funding sources are related to this work.

Ethics approval and consent to participate

This study has been reviewed and approved by the relevant ethics committee. All participants provided informed consent prior to participation.

Consent to publication

All authors accept to transmit the authors’ right to the publishing journal upon acceptance.

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