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Gi Jeong Park, Do Yun Kwon, Kwang-Ryeol Kim, Brown-Séquard syndrome caused by cervical disc herniation with associated Horner’s syndrome: a case report, Journal of Surgical Case Reports, Volume 2026, Issue 8, August 2026, rjag513, https://doi.org/10.1093/jscr/rjag513
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Abstract
Brown-Séquard Syndrome (BSS) is a rare incomplete spinal cord injury. Its association with Horner syndrome (HS) secondary to cervical disc herniation is exceptionally rare, presenting a significant diagnostic and therapeutic challenge. A 37-year-old man presented with neck pain, right shoulder pain, and progressive right upper limb motor weakness. The patient also exhibited gait disturbances and ipsilateral facial signs of HS, including ptosis, miosis, and anhidrosis. Cervical magnetic resonance imaging revealed a large right-sided disc extrusion at the C3–4 level, which resulted in severe spinal cord compression. The patient underwent anterior cervical discectomy and fusion. The extruded disc fragment was completely removed. After surgery, his right upper limb motor strength fully recovered and the gait disturbance resolved. Signs of HS also resolved completely. This case highlights that cervical disc herniation, although uncommon, should be considered in the differential diagnosis of BSS, particularly when associated with HS.
Introduction
Brown-Séquard syndrome (BSS) is a rare type of incomplete spinal cord syndrome that results from a unilateral injury to the spinal cord [1]. Although BSS is most commonly associated with traumatic injuries such as penetrating wounds and vertebral fractures, it may also arise from non-traumatic causes, including autoimmune diseases or epidural hematomas [1, 2]. There are rare case reports of BSS caused by decompression sickness or cervical synovial cysts [3, 4].
BSS typically presents with an ipsilateral loss of motor function and proprioception, contralateral loss of pain and temperature sensation. These clinical features result from involvement of the corticospinal tract, spinothalamic tract, and dorsal column pathway [1, 5]. When the lesion is located at a high cervical level, additional clinical findings such as Horner syndrome (HS) may manifest due to disruption of the oculosympathetic pathway [6, 7].
Although some studies and case reports suggest that early decompression has a favorable prognosis, there is no established general consensus regarding the optimal treatment for BSS [8–10]. Here, we report a case of BSS associated with HS following cervical disc herniation.
Case report
A 37-year-old man with no significant past medical history presented with neck pain and progressive weakness of the right upper limb. Motor strength in the right upper limb was graded as 3/5 on manual muscle testing. Sensory examination demonstrated ipsilateral loss of light touch and proprioception with contralateral loss of pain and temperature sensation, consistent with BSS. In addition to these symptoms, anhidrosis, miosis, and ptosis were observed on the face (Fig. 1). Magnetic resonance imaging (MRI) performed at an outside hospital revealed a right-sided C3–4 disc extrusion causing severe spinal cord compression with associated intramedullary signal changes (Fig. 2). To objectively assess motor impairment, bilateral handgrip strength was measured using an electronic dynamometer (Fig. 3), and bilateral motor and sensory nerve tests were performed according to the ASIA scale grade C.

Preoperative right-sided ptosis (a) and anhidrosis observed using an oil-control film (b), secondary to Horner syndrome. Postoperative photograph showing complete resolution of right-sided ptosis (c).

Preoperative sagittal (a) and axial (b) T2-weighted MRI showing herniated disc at the C3–4 level with associated cord edema (white arrow), compressing the right lateral half of the spinal cord (dashed arrow).

(a) Measurement of handgrip strength using a digital dynamometer. (b) Changes in grip strength of the right (affected) and left (normal) sides at baseline, 1 month, 3 months, and 6 months after surgery.
Nerve conduction studies (NCS) and somatosensory evoked potentials (SSEP) of the upper extremities were within normal limits. However, the tibial nerve SSEP and motor evoked potentials revealed prolonged latency. Electromyography (EMG) demonstrated abnormal spontaneous activity in the right cervical paraspinal and right upper limb muscles, consistent with cervical myelopathy combined with right cervical radiculopathy (Table 1).
| Before operation . | After operation . | |||||||||
|---|---|---|---|---|---|---|---|---|---|---|
| SSEP | P37 (ms) | Amp P37 (μV) | P37 (ms) | Amp P37 (μV) | ||||||
| Lt. Tibial | 46.67 | 1.4 | 47.08 | 1.0 | ||||||
| Rt. Tibial | 50.10 | 0.53 | 47.81 | 0.54 | ||||||
| MEP | Latency (ms) | Amp (mV) | Latency (ms) | Amp (mV) | ||||||
| Lt. cortex – Rt. TA | 30.42 | 0.2 | 30.27 | 0.1 | ||||||
| Rt. Cortex – Lt. TA | 28.60 | 0.6 | 28.31 | 0.7 | ||||||
| Needle EMG | Spontaneous | MUAP | Spontaneous | MUAP | ||||||
| Fib | PSW | Amp | Dur | PPP | Fib | PSW | Amp | Dur | PPP | |
| Rt. Cervical PSP | 1+ | 1+ | Normal | Normal | Normal | 1+ | 1+ | Normal | Normal | Normal |
| Rt. Triceps | 1+ | 1+ | Normal | Normal | Normal | 1+ | 1+ | Normal | Increase | Poly |
| Rt. FCR | 1+ | 1+ | Normal | Normal | Normal | 1+ | 1+ | Normal | Increase | Poly |
| Rt. FDI | 1+ | 1+ | Normal | Normal | Normal | 1+ | 1+ | Normal | Increase | Poly |
| Rt. APB | 1+ | 1+ | Normal | Normal | Normal | 1+ | 1+ | Normal | Increase | Poly |
| Before operation | After operation | |||||||||
|---|---|---|---|---|---|---|---|---|---|---|
| SSEP | P37 (ms) | Amp P37 (μV) | P37 (ms) | Amp P37 (μV) | ||||||
| Lt. Tibial | 46.67 | 1.4 | 47.08 | 1.0 | ||||||
| Rt. Tibial | 50.10 | 0.53 | 47.81 | 0.54 | ||||||
| MEP | Latency (ms) | Amp (mV) | Latency (ms) | Amp (mV) | ||||||
| Lt. cortex – Rt. TA | 30.42 | 0.2 | 30.27 | 0.1 | ||||||
| Rt. Cortex – Lt. TA | 28.60 | 0.6 | 28.31 | 0.7 | ||||||
| Needle EMG | Spontaneous | MUAP | Spontaneous | MUAP | ||||||
| Fib | PSW | Amp | Dur | PPP | Fib | PSW | Amp | Dur | PPP | |
| Rt. Cervical PSP | 1+ | 1+ | Normal | Normal | Normal | 1+ | 1+ | Normal | Normal | Normal |
| Rt. Triceps | 1+ | 1+ | Normal | Normal | Normal | 1+ | 1+ | Normal | Increase | Poly |
| Rt. FCR | 1+ | 1+ | Normal | Normal | Normal | 1+ | 1+ | Normal | Increase | Poly |
| Rt. FDI | 1+ | 1+ | Normal | Normal | Normal | 1+ | 1+ | Normal | Increase | Poly |
| Rt. APB | 1+ | 1+ | Normal | Normal | Normal | 1+ | 1+ | Normal | Increase | Poly |
*Values in bold represent abnormal findings.
Abbreviation: SSEP, somatosensory evoked potential; MEP, motor evoked potential; EMG, electromyogram; TA, tibialis anterior; PSP, paraspinalis; FCR, flexor carpi radialis; FDI, first dorsal interosseous; APB, abductor pollicis brevis; MUAP, motor unit action potential; Fib, fibrillation; PSW, positive sharp wave; Amp, amplitude; Dur, duration; PPP, polyphasic potentials
Under general anesthesia, anterior cervical discectomy and fusion at C3/4 was performed using the Smith–Robinson technique [11]. A massive ruptured disc fragment compressing the spinal cord was identified and removed on the right side at C3/4. Subsequently, inter-body fusion was performed (Fig. 4).

Postoperative radiograph (a), sagittal (b), and axial (c) T2-weighted MRI findings. Lateral cervical radiograph showing stable fixation with an allobone cage and anterior plate following anterior cervical discectomy and fusion (ACDF). Sagittal and axial T2-weighted MRI demonstrating resolution of the herniated disc (C3–4 level) with complete de-compression of the spinal cord.
Postoperatively, the patient's symptoms improved significantly. Long-tract signs, including gait disturbances, resolved completely. Right upper limb motor power improved to grade 4 immediately after surgery, with further improvement to grade 5 within a few days, achieving symmetrical strength (Fig. 3). Sensory deficits, including the ipsilateral loss of light touch and contralateral loss of pain and temperature sensation, also improved. Upon discharge, the patient’s condition was classified as ASIA grade E. The signs of HS, including ptosis, miosis, and anhidrosis, resolved (Fig. 1).
On follow-up NCS and EMG after 3 months, there were no interval changes in the NCS. However, EMG revealed polyphasic potentials in the right upper limb muscles, suggesting peripheral nerve regeneration (Table 1).
Discussion
BSS is characterized by a well-defined pattern of neurological impairment, which can aid in its clinical diagnosis [1–3]. The hallmark findings of ipsilateral motor weakness and loss of proprioception, along with contralateral loss of pain and temperature sensation, occur because of the anatomical arrangement of the spinal cord tracts [10]. The corticospinal tract, which governs motor function, and the dorsal columns, which transmit proprioceptive and fine-touch information, ascends ipsilaterally through the spinal cord and cross the medulla. Conversely, the spinothalamic tract crosses a few segments of its entry into the spinal cord and ascends contralaterally, explaining the dissociation of sensory and motor deficits observed in BSS [8–10]. Differential diagnoses such as intramedullary tumors, epidural abscesses, or demyelinating disorders should also be considered while evaluating patients with BSS-like symptoms, underscoring the diagnostic value of MRI in identifying disc herniation as the primary etiology [2–5].
HS is characterized by ipsilateral ptosis, miosis, and anhidrosis and can be classified into central, preganglionic, and postganglionic types [7, 12]. Cases of cervical disc herniation causing HS are rare, and few case reports have documented that disc herniations at the C4–5 and C5–6 levels may compress the sympathetic pathway, thereby producing these symptoms [5, 6]. The coexistence of BSS and HS can be explained by the anatomical proximity of the corticospinal and spinothalamic tracts to the descending sympathetic fibers within the lateral funiculus of the cervical spinal cord. Therefore, compression at the C3–4 level may simultaneously disrupt both the sensorimotor and autonomic pathways, resulting in the combined manifestation of BSS and HS. In the present case, the patient exhibited typical manifestations of HS, including ptosis, miosis, and anhidrosis, all of which resolved completely after surgical decompression.
Management of BSS depends on the underlying cause and severity of neurological impairment and includes analgesics, cervical soft collar, and surgical treatments [2, 13]. Although conservative management may be an option for patients with mild or improving symptoms, surgical intervention is often necessary for those with significant or progressive neurological deficits, particularly when there is clear evidence of spinal cord compression [13–15].
The optimal timing of surgical intervention in cases of acute spinal cord injury remains a topic of significant clinical discussion [8, 9]. However, a growing body of evidence suggests that early surgical decompression improves neurological outcomes [8, 10]. Several reports have documented complete or near-complete neurological recovery after surgical decompression in patients with BSS caused by cervical disc herniation, supporting an aggressive approach [13, 14]. Although BSS caused by disc herniation is not identical to that caused by traumatic spinal cord injury, the underlying principle of alleviating mechanical compression to prevent secondary injury cascades is similar [8, 13]. Early decompression may reduce secondary injury cascades and improve neurological recovery. This case highlights the importance of early intervention before irreversible myelopathic changes occur.
The prognosis of BSS tends to be more favorable than that of other forms of spinal cord injury because of the partial preservation of neurological function. Many patients regain significant motor function after intensive rehabilitation, even though sensory deficits may persist [13, 14, 16]. The prognosis of BSS resulting from cervical disc herniation is particularly good, with high rates of functional recovery after surgery [14].
Conclusion
BSS with HS caused by cervical disc herniation is rare and should be diagnosed rapidly and accurately. Surgical decompression of the spinal cord may be crucial for improving patient outcomes.
Author contributions
Conceptualization: G.J.P., D.Y.K., K.R.K.; Methodology: D.Y.K., K.R.K.; Data curation: G.J.P.; Formal analysis: G.J.P., K.R.K.; Investigation: G.J.P., D.Y.K., K.R.K.; Writing—original draft: G.J.P., D.Y.K., K.R.K.; Writing—review & editing: All authors; Supervision: K.R.K. All authors have read and approved the final manuscript.
Conflicts of interest
None declared.
Funding
None declared.
Data availability
The data that support the findings of this study are available from the corresponding author upon reasonable request. The data are not publicly available due to institutional and patient privacy restrictions.
Consent
Written informed consent was obtained from the patient for publication of this case report and any accompanying images.