Progressive Hemiparesis Due to Cervical Ossification of the Ligamentum Flavum Resembling Stroke: A Case Report

Abstract

Ossification of the ligamentum flavum (OLF) predominantly affects the thoracic spine; cervical involvement is rare and often underrecognized, typically progressing slowly with motor or sensory symptoms. Here, the authors present a 70-year-old male who has experienced a subacute progression of hemiparesis, which is atypical for OLF and could easily be misdiagnosed as a stroke attack, attributed to OLF that resolved following a laminectomy. A 70-year-old man with diabetes mellitus developed initial bilateral upper limb numbness, followed by progressive left upper and lower extremity weakness over 1 month. Initial stroke suspicion was negated by normal brain imaging. A cervical magnetic resonance imaging revealed ossified lesions at C5–C6 with posterior spinal cord compression. Cervical laminectomy was performed, and pathological examination confirmed OLF. Neurological symptoms improved steadily following surgery and rehabilitation. Cervical OLF may cause severe hemiparesis in such a short period of time, presenting in an atypical manner for its nature and may resemble cerebrovascular disease. Accurate and timely diagnosis is essential to prevent permanent neurological deficit through appropriate surgical decompression, such as laminectomy.

 

MissingLinkText

Keywords

cervical lesion - hemiparesis - laminectomy - ligamentum flavum - ossification

Introduction

Ossification of the ligamentum flavum (OLF) is a rare cause of cervical myelopathy, as it is more common in thoracic region.[1] Radiological characteristics of OLF in general include ossified masses, tram tack and comma signs,[2] local kyphosis,[3] and hypertrophy of the facets and laminae.[4] OLF frequently coexists with ossification of the posterior longitudinal ligament (OPLL) and, in some cases, with diffuse idiopathic skeletal hyperostosis.[1] Surgical intervention, typically via posterior decompression procedures such as laminectomy, has been reported to yield immediate symptom relief and measurable neurological recovery, although complications such as cerebrospinal fluid leaks may occur.[5]

In this report, we present a unique case of cervical OLF characterized by rapid progression of hemiparesis. Unlike typical insidious course of OLF, this case exhibited an accelerated deterioration over a short period without any previous trauma, mimicking a cerebrovascular event.

 

MissingLinkText

Case Description

A 70-year-old man with a history of diabetes mellitus visited his neighborhood physician complaining of mild numbness in both upper extremities, beginning with the left hand. The patient's symptoms progressed rapidly, with a loss of muscle strength in the left upper extremity, followed by weakness in the left lower extremity, and about a month later, the patient had difficulty in walking. A stroke was ruled out since magnetic resonance (MR) imaging of the brain and MR angiography of the brain revealed no significant abnormality. The patient was referred to our hospital for further evaluation. The patient did not recall any recent trauma.

The patient reported spontaneous neck pain, which worsened with neck extension. Neurological examination revealed mild weakness (manual muscle testing [MMT] score of 4) in the flexor muscles of the left upper and lower limbs, while the extensor muscles remained intact. No weakness was observed on the right side. Sensory examination demonstrated hypoesthesia to pain and temperature in the left C4–C8 dermatome and bilateral deep sensory impairment in the L1–S1 regions. Hoffmann's sign, Trömner's sign, and Babinski's sign were absent. The brachioradialis reflex was absent, while the biceps, triceps, patellar, and Achilles tendon reflexes were normal. No bladder or bowel dysfunction was observed. The cervical spondylotic Japanese Orthopaedic Association (JOA) score was 9, indicating moderate to severe impairment.

Laboratory findings showed a slightly elevated HbA1c level of 6.6%, but diabetes had been well controlled. Blood count, coagulation tests, and electrolyte levels, including calcium and phosphate, were within normal range. Cervical spine radiographs revealed a high-density lesion ventral to the C5–C6 lamina ([Fig. 1]). No cervical alignment instability was observed, and dynamic flexion–extension view showed no significant cervical instability ([Fig. 2]). Computed tomography (CT) scans confirmed multiple high-density nodules posteriorly at the C5–C6 level compressing the cord ventrally consistent with ossification of ligamentum flavum, measuring 8 mm in its longest diameter ([Fig. 3]). These nodules were distinct from the medial edge of the pedicle. Similar but smaller high-density lesions were observed at other cervical levels. There was no ossification of the posterior longitudinal ligament. MR imaging also showed low signal intensity on both T1- and T2-weighted images (WIs) consistent with OLF, similarly contributing to dorsal cord intrusion ([Fig. 4]).

Fig. 1 A cervical spine radiograph, left anterior oblique image, showing a high-density mass (arrow) on the anterior aspect of the lamina at the C5–C6 level.

Fig. 2 Cervical spine radiographs in flexion (A) and extension (B) views demonstrate that there is no instability of the cervical spine.

Fig. 3 Computed tomography (CT) scans of the cervical spine. (A) Sagittal CT image demonstrating a highly dense calcified nodule protruding posteriorly and medially into the spinal canal at the C5–C6 level, causing severe spinal cord compression. (B) Axial CT image at the C5–C6 level, showing the largest ossified lesion of the ligamentum flavum (OLF) predominantly on the left side, which significantly impinges upon the spinal cord. (C) Axial CT image at the C4–C5 level, revealing a smaller, but clearly identifiable, ossified lesion on the right posterior side of the spinal canal. These images clearly delineate the extent and location of the ossified lesions, providing critical anatomical detail for surgical planning.

Fig. 4 Magnetic resonance (MR) images of the cervical spine. (A) Sagittal T1-weighted image (WI) and (B) sagittal T2WI both reveal a lesion at the C5–C6 level, exhibiting low signal intensity, consistent with ossification. This lesion causes severe posterior spinal cord compression. Importantly, the sagittal T2WI (B) demonstrates a focal area of high signal intensity within the compressed spinal cord parenchyma at C5–C6, indicative of myelopathic changes such as edema or gliosis. (C) Axial T2WI at the C5–C6 level (note: distorted by susceptibility artifact from the ossified lesion). Despite the artifact, it clearly shows significant posterior and predominantly left-sided compression of the spinal cord (arrow).

Surgery and Postoperative Course

The patient underwent C5–C6 laminectomy under somatosensory evoked potential (SEP) monitoring. Under general anesthesia, the patient's head was fixed with a Mayfield skull clamp, with the neck positioned in slight flexion to maintain cervical lordosis. A midline incision was made, exposing the laminae, and the spinous processes of C5 and C6 were resected. Laminectomy was performed from the superior border of C5 to the inferior border of C6, within the medial edges of both pedicles. Firm masses of OLF were adherent to the dura but most of them were easily separated from the surroundings. Macroscopically, the resected lesion contained yellowish powdery deposits in addition to a hard ossified mass within the ligamentum flavum.

Postoperative recovery was uneventful. Early ambulation and rehabilitation were initiated, and the patient was able to walk independently upon discharge after approximately 10 days, with mild residual gait disturbance. By 4 weeks postoperatively, both sensory disturbances and gait impairment had significantly improved, with a JOA score of 14 points. Pathological diagnosis confirmed OLF ([Fig. 5]).

Fig. 5 Hematoxylin and eosin staining of excised lesions (x100). The left side of the figure shows an ossified ligamentum flavum with an extracellular matrix stained bright pink. In contrast, the right side of the figure shows a normal ligamentum flavum with elastic fibers appearing as wavy structures with interspersed fibroblasts.

 

MissingLinkText

 

MissingLinkText

Discussion

In our case, the patient presented with progressive hemiparesis over 1 month. As shown in [Table 1], hemiparesis is an unusual presentation of cervical OLF,[6] [7] [8] as most cases exhibit bilateral motor deficits due to the central location of spinal cord compression.[6] The rarity of hemiparesis in cervical OLF may be explained by asymmetrical ossification, leading to lateralized compression of the corticospinal tract. Previous reports suggest that unilateral motor deficits in cervical OLF are often associated with more focal and eccentric ossification patterns, which selectively affect one side of the spinal cord.[8]

Table 1 Previously published case reports and ours that present hemiparesis in OLF patients

Author	Age/Sex	Symptom	Laterality and level of OLF	Timing of surgery	Surgical treatment	Outcome
Kobayashi et al[7] (1991)	61/M	Left hemiparesis	Left C3–C4	5 years	C3–C5 wide laminectomy	Improvement
Mizuno and Nakagawa[6] (2002)	64/M	Left hemiparesis	Left C6–C7	5 years	C6–C7 unilateral osteoplastic laminectomy	Improvement
Ishikawa et al[8] (2021)	70/M	Left hemiparesis	Left C2–C4	6 months	C2–C3 laminectomy and C4–C7 laminoplasty	Improvement
Our case (2025)	70/M	Left hemiparesis	Left C5–C6	1 month	C5–C6 laminectomy	Improvement

Abbreviation: OLF, ossification of the ligamentum flavum.

Radiological findings revealed severe spinal cord compression at the C5–C6 level, which likely played a central role in the patient's neurological decline. The rapid neurological deterioration in this case, despite the typically slow progression of OLF, warrants a deeper discussion into potential contributing factors. Increased mechanical stress on the preexisting ossified ligament may have abruptly worsened the compression. Even if ossification had been progressing slowly, a triggering event—such as forceful neck movement, prolonged static posture, or minor trauma—could have precipitated acute clinical deterioration.[9] This concept is supported by studies analyzing the biomechanical effects of cervical dynamic activities on the spinal cord in OLF, indicating that certain movements can increase compression.[10] Furthermore, microvascular compromise within the compressed spinal cord segment may also have contributed to the acute functional decline, potentially exacerbated by heightened spinal cord vulnerability. Chronic compression can impair local blood supply, making the cord more susceptible to transient ischemic events even with minor changes in posture or blood pressure.[11] Moreover, transient inflammatory changes in or around the ossified ligament cannot be excluded as an additional factor worsening the symptoms via inflammation-induced edema or irritation. The patient's history of diabetes mellitus, although relatively well controlled (HbA1c 6.6%), may have played a role in disease progression by rendering the spinal cord more susceptible to ischemic or inflammatory injury, thereby accelerating the onset and progression of neurological symptoms even under mild compression. Similar associations between diabetes mellitus and other spinal ligamentous ossifications, such as ossification of the OPLL, have been reported, suggesting a systemic predisposition to ectopic ossification.[12]

Given the overlap in clinical presentation between cervical OLF and cerebrovascular diseases, distinguishing between these conditions is essential. Brain MR imaging is a crucial diagnostic tool to exclude stroke,[13] as was performed in this case. Moreover, the presence of neck pain, progressive motor decline without abrupt onset, and MRI findings of focal spinal cord compression should raise suspicion for a spinal pathology rather than a cerebrovascular event.[14] In our case, the absence of facial weakness, combined with the specific pattern of sensory (pain and temperature hypoesthesia in left C4–C8 and bilateral deep sensory impairment in L1–S1) and motor deficits (left-sided flexor weakness but preserved extensors), further pointed away from a typical cerebrovascular event. Electrophysiological studies such as SEP may also provide additional diagnostic insights by identifying conduction abnormalities specific to spinal cord compression. Although the differential diagnosis of progressive hemiparesis includes intracranial pathologies such as neoplasms or degenerative disorders, stroke remains the most immediate and common consideration. Consequently, spinal causes like cervical OLF can be overlooked, particularly when the presentation closely resembles a stroke.

Early surgical decompression remains the cornerstone of treatment for symptomatic cervical OLF.[5] In this case, timely laminectomy at the C5–C6 level successfully alleviated spinal cord compression, leading to significant neurological recovery. The combination of early diagnosis, surgical intervention, and rehabilitation played a critical role in optimizing the patient's prognosis.

 

MissingLinkText

Conclusion

This case demonstrates that cervical OLF can present with rapidly progressive hemiparesis, mimicking a cerebrovascular event. Early laminectomy effectively reversed neurological deficits, highlighting its therapeutic value.

 

MissingLinkText

 

MissingLinkText

Conflict of Interest

None declared.

Authors' Contributions

M.S. served as the main author of the manuscript. K.Y. contributed to revisions and acted as a supervisor. T.T., H.A., S.H., and N.S. provided advisory support throughout the process. E.I. was involved in both revisions and supervision, in addition to serving as an advisor.

• References

• 1 Kawaguchi Y, Nakano M, Yasuda T. et al. Characteristics of ossification of the spinal ligament; incidence of ossification of the ligamentum flavum in patients with cervical ossification of the posterior longitudinal ligament—analysis of the whole spine using multidetector CT. J Orthop Sci 2016; 21 (04) 439-445
• 2 Li B, Qiu G, Guo S. et al. Dural ossification associated with ossification of ligamentum flavum in the thoracic spine: a retrospective analysis. BMJ Open 2016; 6 (12) e013887
• 3 Erdani D, Topolovec M, Hero N, Brumat P. Ossification of ligamentum flavum related to progressive thoracic myelopathy and acute paraplegia in a Central-European male with a thoracic kyphoscoliosis. J Surg Case Rep 2023; 2023 (02) rjad070
• 4 Singhal U, Jain M, Jaiswal AK, Behari S. Unilateral ossified ligamentum flavum in the high cervical spine causing myelopathy. Indian J Orthop 2009; 43 (03) 305-308
• 5 Kubota M, Baba I, Sumida T. Myelopathy due to ossification of the ligamentum flavum of the cervical spine. A report of two cases. Spine 1981; 6 (06) 553-559
• 6 Mizuno J, Nakagawa H. Unilateral ossification of the ligamentum flavum in the cervical spine with atypical radiological appearance. J Clin Neurosci 2002; 9 (04) 462-464
• 7 Kobayashi S, Okada K, Onoda K, Horikoshi S. Ossification of the cervical ligamentum flavum. Surg Neurol 1991; 35 (03) 234-238
• 8 Ishikawa Y, Miyakoshi N, Hongo M. et al. Thin cervical spinal cord between ossifications of the ligamentum flavum and the posterior longitudinal ligament: case report and literature review. World Neurosurg 2021; 145: 83-88
• 9 Yang YT, Zhu SJ, Xu ML. et al. The biomechanical effect of different types of ossification of the ligamentum flavum on the spinal cord during cervical dynamic activities. Med Eng Phys 2023; 121: 104062
• 10 Xu ML, Zeng HZ, Zheng LD. et al. Effect of degenerative factors on cervical spinal cord during flexion and extension: a dynamic finite element analysis. Biomech Model Mechanobiol 2022; 21 (06) 1743-1759
• 11 Ren ZX, Xu JH, Cheng X, Xu GX, Long HQ. Pathophysiological mechanisms of chronic compressive spinal cord injury due to vascular events. Neural Regen Res 2023; 18 (04) 790-796
• 12 Kobashi G, Washio M, Okamoto K. et al; Japan Collaborative Epidemiological Study Group for Evaluation of Ossification of the Posterior Longitudinal Ligament of the Spine Risk. High body mass index after age 20 and diabetes mellitus are independent risk factors for ossification of the posterior longitudinal ligament of the spine in Japanese subjects: a case-control study in multiple hospitals. Spine 2004; 29 (09) 1006-1010
• 13 Fernandes PM, Whiteley WN, Hart SR, Al-Shahi Salman R. Strokes: mimics and chameleons. Pract Neurol 2013; 13 (01) 21-28
• 14 Zhou LL, Zhu SG, Fang Y. et al. Neck pain and absence of cranial nerve symptom are clues of cervical myelopathy mimicking stroke: two case reports. World J Clin Cases 2022; 10 (32) 11835-11844

Publikationsverlauf

Artikel online veröffentlicht:
18. August 2025