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JMCR: Clinical Reasoning From Case Reports

Spontaneous Cervical Epidural Hemorrhage Presenting as Brown–Séquard Syndrome Source article: Li W, et al. Spontaneous hemorrhage in the spinal canal leading to Brown–Séquard syndrome: a case report and review of the literature. Journal of Medical Case Reports. 2026;20:284.

Richard Rison Jul 20, 2026

Case Presentation

A 56-year-old Han Chinese woman presented to the emergency department with abrupt onset of left-sided weakness that had developed one hour before admission. At first glance, this presentation strongly suggested an acute ischemic stroke. However, a more detailed history revealed that she had experienced progressive numbness involving all four extremities for nearly ten years. Her medical history was significant for hypertension treated with metoprolol and felodipine and previous resection of a breast fibroadenoma. Laboratory studies demonstrated mild anemia and thrombocytopenia, although coagulation parameters were within normal limits.

Neurological examination revealed severe weakness of the left upper and lower extremities, with muscle strength graded as 2/5. Strength on the right side was mildly reduced at 4/5. Sensory examination demonstrated bilateral hand numbness, diminished sensation involving the right side of the trunk below the sternal angle, and numbness extending into the right perineum and right lower extremity. Anal sphincter tone was reduced. Reflexes were decreased in the left upper extremity, whereas no pathologic reflexes were present.

Although unilateral weakness naturally raised concern for a cerebral infarction, several aspects of the examination did not fit comfortably within a cortical localization. The absence of aphasia, neglect, visual field deficits, or gaze deviation argued against a hemispheric lesion. More importantly, the presence of bowel dysfunction and a sensory level strongly suggested spinal cord involvement.

Diagnostic Reasoning

One of the cardinal principles of neurology is that localization precedes diagnosis. Before identifying the cause of a neurological syndrome, one must first determine where the lesion resides. In this patient, the pattern of deficits provided a powerful clue. The combination of ipsilateral weakness and contralateral sensory loss is highly characteristic of Brown–Séquard syndrome.

Brown–Séquard syndrome results from injury involving one side of the spinal cord. Damage to the corticospinal tract produces ipsilateral weakness because the fibers have already crossed within the lower medulla. In contrast, pain and temperature fibers ascend in the spinothalamic tract after crossing near their entry level within the spinal cord. Consequently, unilateral cord lesions produce contralateral sensory deficits. Although classical Brown–Séquard syndrome also includes ipsilateral loss of vibration and proprioception due to dorsal column involvement, many patients exhibit incomplete forms of the syndrome.

Recognition of this pattern immediately shifted attention away from the brain and toward the cervical spinal cord.

Differential Diagnosis

Several diagnostic possibilities required consideration.

An acute ischemic stroke was initially attractive because of the sudden onset of hemiparesis. However, bowel dysfunction, bilateral hand numbness, and contralateral sensory loss were atypical features. Furthermore, the absence of cortical signs argued strongly against a hemispheric lesion. Failure to recognize these inconsistencies could have resulted in administration of thrombolytic therapy with potentially disastrous consequences.

Cervical spondylotic myelopathy was another possibility. Chronic sensory symptoms and multilevel degenerative changes could explain the patient's long-standing complaints. However, the hyperacute development of severe weakness would be unusual.

Spinal cord infarction also deserved consideration. Acute spinal cord ischemia can produce rapidly evolving neurological deficits, although bilateral findings are more common. In addition, imaging would eventually demonstrate an extradural lesion rather than an intramedullary vascular insult.

Neoplasm represented another important possibility. Metastases, meningiomas, schwannomas, and lymphoma may present as extradural masses producing spinal cord compression. The patient's prolonged history of sensory symptoms made this diagnosis plausible.

Finally, spontaneous spinal epidural hematoma remained a critical consideration because it constitutes a neurosurgical emergency and may produce Brown–Séquard syndrome through asymmetric cord compression.

Imaging and Surgical Findings

Magnetic resonance imaging of the cervical spine demonstrated an extradural lesion extending from C4 through C6 with associated spinal cord edema. Because the lesion appeared mass-like, a neoplasm was initially suspected. Given the severity of spinal cord compression and profound neurological deficits, urgent surgical decompression was undertaken.

Following removal of the ligamentum flavum, surgeons unexpectedly encountered a large organized blood clot compressing the dura. Evacuation of the hematoma resulted in decompression of the spinal cord. Histopathological examination demonstrated blood clot without evidence of neoplasia.

The final diagnosis was spontaneous cervical epidural hematoma producing Brown–Séquard syndrome.

Pathophysiology

The precise mechanism of spontaneous spinal epidural hemorrhage often remains uncertain. Predisposing factors include hypertension, anticoagulant therapy, coagulopathies, thrombocytopenia, vascular malformations, and neoplasms. In this patient, longstanding hypertension and mild thrombocytopenia may have contributed to vascular fragility. Because spinal angiography was not performed, an underlying vascular malformation could not be entirely excluded.

As blood accumulates within the epidural space, progressive compression of the spinal cord occurs. Secondary ischemia, edema, and inflammatory responses further amplify tissue injury. The duration of compression becomes one of the most important determinants of neurological outcome.

Treatment

Because acute neurological deterioration and substantial spinal cord compression were present, urgent surgery represented the preferred therapeutic approach. Current evidence suggests that early decompression within the first 24 to 48 hours provides the greatest opportunity for neurological recovery. Delayed intervention allows irreversible ischemic injury and neuronal loss to develop.

Conservative management may be considered in selected patients who exhibit stable neurological findings and minimal cord compression. However, patients with progressive deficits generally require urgent surgical intervention.

Clinical Course and Outcome

Neurological improvement was apparent immediately after surgery. On postoperative day one, strength in the left extremities improved from 2/5 to 4/5, whereas right-sided strength normalized. Sensory deficits persisted but gradually improved.

Sixteen days after surgery, muscle strength had returned to normal in all four extremities. Continued rehabilitation produced progressive recovery. One year later, the patient reported no limitations in daily activities, stair climbing, or running. Only mild residual numbness involving the right buttock and lower extremity remained.

This favorable outcome highlights the remarkable capacity for neurological recovery when spinal cord compression is recognized and treated promptly.

Clinical Pearls

The localization of neurological deficits often provides the diagnosis before imaging studies are obtained.

Crossed motor and sensory findings should immediately suggest Brown–Séquard syndrome and spinal cord pathology.

Not every patient presenting with acute hemiparesis has a stroke.

Spontaneous spinal epidural hematoma is an important stroke mimic and a neurosurgical emergency.

Early surgical decompression substantially improves neurological outcome.

Clinical Pitfalls

Anchoring on the diagnosis of ischemic stroke.

Failing to recognize a sensory level.

Overlooking bowel or bladder dysfunction.

Delaying spinal imaging.

Administering thrombolytic therapy before excluding spinal pathology.

Thrombolytic therapy may worsen hemorrhage and increase hematoma expansion, potentially resulting in catastrophic neurological deterioration. For this reason, clinicians should remain vigilant for atypical features that suggest spinal cord disease rather than cerebral ischemia.

Clinical Take-Home Message

Spontaneous cervical epidural hematoma is an uncommon but important stroke mimic. The presence of crossed motor and sensory findings, bowel dysfunction, and a sensory level should immediately suggest Brown–Séquard syndrome and prompt urgent spinal imaging. Rapid recognition and timely decompression can lead to dramatic neurological recovery and prevent permanent disability.

Journal of Medical Case Reports is the world’s first international, PubMed-listed, medical journal devoted to publishing case reports from all medical disciplines and will consider any original case report that expands the field of general medical knowledge, and original research relating to case reports. The journal is open access, and strongly endorses the CARE guidelines for case reports, requiring authors to submit populated CARE checklists with submissions to improve transparency in reporting.