Motor deficits following cervical spinal injury most commonly manifest as bilateral weakness below the level of the lesion. However, when unilateral paresis develops, alternative mechanisms must be considered.

Opalski syndrome—a rare variant of lateral medullary (Wallenberg) syndrome—is distinguished by the addition of ipsilateral hemiparesis to the classic features of Wallenberg syndrome (trigeminal sensory loss, dysphagia, dysarthria, and Horner’s syndrome). While most reported cases arise from vertebral artery dissection or atherosclerotic disease, the occurrence of Opalski syndrome following traumatic cervical injury remains exceedingly rare.¹⁾

Here, we present a case of Opalski syndrome in a patient who sustained an unstable C4–C5 fracture with cervical spinal cord injury secondary to a motor vehicle collision, subsequently developing ipsilateral motor weakness. We aim to underscore the diagnostic clues for atypical brainstem ischemic lesions after traumatic cervical injury and to emphasize the importance of early recognition and appropriate management strategies in such cases.

60-year-old woman presented following a motor vehicle collision with notable upper extremity weakness. On examination, motor strength was 2/5 in the left arm and 3/5 in the right arm. Cervical spine radiographs revealed dislocation at the C4–C5 level (Fig. 1A). Computed tomography demonstrated locking of the left facet joint and subluxation of the right facet joint (Fig. 1B). Magnetic resonance imaging showed spinal cord compression at C4–C5 with corresponding intramedullary signal change (Fig. 1C).

To evaluate for vertebral artery injury secondary to facet dislocation, neck CT angiography was performed, confirming occlusion of the left vertebral artery at C4–C5 (Fig. 1D). As there were no acute posterior circulation symptoms, the patient underwent urgent anterior cervical discectomy and fusion (ACDF) at C4–C5 to relieve cord compression (Fig. 2A, B).

Postoperatively, her upper limb strength improved to 4/5 bilaterally, and sensory deficits resolved. Twelve hours after surgery, she developed new left facial numbness. Repeat neurologic examination showed right arm strength of 4/5 and near-intact strength on the left. Given the known vertebral artery occlusion, an urgent brain MRI was obtained; diffusion-weighted imaging revealed a high-signal lesion in the left lateral medulla (Fig. 3A), and MR angiography demonstrated dissection-related occlusion of the left vertebral artery (Fig. 3B). Aspirin therapy was initiated in consultation with the neurovascular team.

On postoperative day 2, she complained of severe left occipital headache. That afternoon, she reported subjective weakness of the left lower extremity and displayed gait ataxia with a leftward veer. Her previously restored left arm strength declined to 3/5. Considering her overall status, no additional endovascular procedures were performed. The patient was transferred to the department of physical medicine and rehabilitation for continued care.

At one-month follow-up, she was discharged with left arm strength recovered to 4/5, although gait ataxia persisted.

Opalski syndrome is a rare variant of lateral medullary (Wallenberg) syndrome characterized by the addition of ipsilateral hemiparesis to the classic medullary signs of trigeminal sensory loss, dysphagia, dysarthria, and Horner’s syndrome. While most reported cases arise from spontaneous vertebral artery occlusion or dissection, post-traumatic occurrences are exceptionally rare.¹⁾ Our case represents such an uncommon presentation following C4–C5 facet dislocation with subsequent vertebral artery dissection.

facet dislocation at C4–C5 imparted a shearing force to the adjacent vertebral artery, resulting in vessel wall dissection and luminal occlusion. Urgent anterior cervical decompression successfully relieved spinal cord compression and restored perfusion to the injured cord, but it did not address the dissected vertebral artery. Over the next 12 to 48 hours, the patient developed delayed lateral medullary infarction—most likely due to thromboembolic propagation from the injured segment or local reperfusion injury within the lateral medullary territory. This biphasic course underscores that surgical decompression of the spinal cord and management of vertebral artery injury represent distinct therapeutic priorities, and that vigilance for evolving brainstem ischemia must continue even after adequate cord decompression and reduction of dislocated facet joint.

unlike Brown–Séquard syndrome or isolated nerveroot injury—where ipsilateral deficits follow a predictable anatomic pattern—our patient exhibited pure ipsilateral hemiparesis without contralateral spinothalamic sensory loss. Moreover, her neurological signs emerged in a biphasic fashion: initial postoperative improvement of limb strength was followed by new facial numbness at 12 hours and lower limb weakness with gait ataxia at 48 hours. This temporal dissociation highlights the potential for evolving brainstem ischemia, rather than immediate compression, in cases of traumatic vertebral artery injury.

The management of vertebral artery dissection after recent spine surgery poses an antithrombotic dilemma. In our patient, aspirin monotherapy was initiated once medullary infarction was confirmed, while thrombolysis was deemed too high-risk given her fresh ACDF. Although intravenous thrombolysis has been reported to yield rapid improvement in spontaneous vertebral artery dissection, its safety and efficacy in the immediate postoperative setting remain undefined.²⁾

Spontaneous Opalski syndrome most often occurs in the setting of atherosclerosis or hypertension and typically presents acutely—within minutes to hours—after vessel injury.³⁾ Those patients frequently experience rapid neurological recovery following intravenous thrombolysis. In contrast, our patient’s syndrome arose from traumatic shear at C4–C5 due to facet dislocation, manifested in a delayed fashion 12 to 48 hours after surgery, and achieved only partial recovery with aspirin therapy. Furthermore, unlike spontaneous cases where spinal cord injury is absent, our patient’s neurological picture was complicated by a concomitant cervical cord lesion.

This case expands the etiologic spectrum of Opalski syndrome to include traumatic vertebral artery dissection. It emphasizes that in cervical spine trauma with facet dislocation, even in the absence of immediate posterior circulation symptoms, clinicians should remain vigilant for delayed brainstem ischemia. We propose that any new or worsening cranial nerve or limb deficits after decompression warrant prompt brainstem imaging. Finally, this report underscores the need for prospective studies to establish evidence-based antithrombotic guidelines in the postoperative management of vertebral artery dissection.

We report a rare case of Opalski syndrome following traumatic C4–C5 facet dislocation and vertebral artery dissection. This case underscores the potential for delayed lateral medullary infarction after cervical spine trauma and highlights the importance of early brainstem imaging and tailored antithrombotic management in such patients.

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