Brown-Séquard Syndrome: Tracts, Findings & Lesion Level

Brown-Séquard syndrome is a hemisection of the spinal cord. Below the lesion it causes ipsilateral spastic weakness (corticospinal tract) and ipsilateral loss of vibration and proprioception (dorsal columns), plus contralateral loss of pain and temperature (spinothalamic tract) starting about 1–2 segments below the lesion. At the lesion level there are ipsilateral lower motor neuron signs and segmental sensory loss, and a cervical or upper thoracic lesion can add an ipsilateral Horner syndrome.

Brown-Séquard findings at a glance

Touch is split too: fine touch is lost on the lesion side with the dorsal columns, while crude touch, carried by the anterior spinothalamic tract, is lost on the opposite side. A pure hemisection is rare; most real cases are partial patterns that still show the ipsilateral-motor, contralateral-pain split. These incomplete, asymmetric forms are often called Brown-Séquard-plus syndrome, a label some sources also apply when eye, bowel or bladder deficits are added.

Why the findings split: three tracts, two crossing points

One-line rule: of the three tested tracts, only pain and temperature have already crossed inside the cord. Motor and dorsal column fibers still serve their own side, so the lesion side is the weak side.

For a tract-by-tract review with diagrams, see spinal cord tracts.

Finding the lesion level

• Go up from the pain line. Pain and temperature fibers run up or down for one or two segments in Lissauer's tract before they synapse and cross, so the contralateral sensory level sits about 1–2 segments below the true lesion. Pinprick lost from the umbilicus (T10) on the right means a left-sided lesion around T8–T9.
• The at-level signs pin it down. Ipsilateral segmental sensory loss and LMN weakness (for example, wasting of the hand muscles in a lower cervical lesion) mark the exact segment.
• Know the landmark dermatomes:

• Beware spinal shock. In the first days after trauma, the limb below the lesion can be flaccid and areflexic; spasticity, hyperreflexia and the Babinski sign appear later.

Causes

• Penetrating trauma is the classic cause, and knife wounds are the most common traumatic mechanism; gunshot wounds, motor vehicle collisions, blunt trauma and falls with vertebral fracture can also produce it. Brown-Séquard syndrome accounts for about 1–4% of traumatic spinal cord injuries, most often at cervical or thoracic levels.
• Nontraumatic causes: disc herniation, cysts, cervical spondylosis, tumors, multiple sclerosis, radiation myelopathy, spinal hemorrhage or ischemia, decompression sickness and infections such as tuberculosis, plus transverse myelitis.

Workup and acute management (Step 2 CK)

1. Spinal precautions until the injury's extent and stability are known.
2. Imaging: CT of the spine (and of other injured regions) to define bony and penetrating injury; MRI of the spinal cord at the level of injury gives the most detail on the cord and the cause.
3. Blood pressure: after acute traumatic spinal cord injury, the 2024 AO Spine/Praxis guideline suggests augmenting mean arterial pressure to at least 75–80 mm Hg but not actively beyond 90–95 mm Hg, for 3–7 days, to protect cord perfusion (a weak recommendation from very low-quality evidence). This revised the 2013 AANS/CNS target of MAP 85–90 mm Hg for the first 7 days, which some older resources, including StatPearls' neurogenic shock chapter, still give.
4. Decompression: when the cord is compressed, the same guideline group recommends offering early surgery within 24 hours of injury as the preferred option for adults; patients decompressed early were about twice as likely to improve by 2 or more ASIA grades.
5. Steroids: high-dose IV methylprednisolone is controversial: the 2013 AANS/CNS guideline does not recommend it, while the 2017 AO Spine guideline suggests a 24-hour infusion only as an option when started within 8 hours of injury, so it is not a routine answer.
6. Rehabilitation begins once the patient is medically stable; earlier mobilization is increasingly favored.

Spinal shock vs neurogenic shock

Both terms appear in trauma stems, and they are different problems.

Grading the injury: the ASIA Impairment Scale

Neurologic recovery after cord injury is tracked with the ASIA Impairment Scale (AIS), the grading used in the surgical timing data above.

Sacral sparing (light touch or pinprick sensation at S4–S5, deep anal pressure, or voluntary anal contraction) separates complete from incomplete injury. Brown-Séquard, central cord, anterior cord and posterior cord syndromes are all incomplete patterns.

Prognosis

Brown-Séquard syndrome has a better outlook than anterior or central cord syndrome. More than half of patients recover well, most post-traumatic patients regain motor function, and up to about 90% walk without assistive devices after rehabilitation. Recovery slows after 3–6 months but can continue for up to 2 years. Because autonomic damage is one-sided, bladder and bowel sphincter function is usually preserved.

Brown-Séquard vs other spinal cord syndromes

Central cord syndrome is the most common incomplete spinal cord injury. The key to all of these: only Brown-Séquard puts motor loss and pain loss on opposite sides. The neighbors each have their own page: anterior cord syndrome and syringomyelia.

Exam traps and look-alikes

• Picking the wrong side. The lesion is on the side of the weakness and vibration loss, not the side of the pain loss.
• Reading the pain level as the lesion level. The contralateral pain/temperature level is 1–2 segments too low; move up.
• Confusing it with a stroke. A cortical or internal capsule infarct puts weakness and sensory loss on the same side of the body, opposite the lesion, with no dissociated split; see stroke localization by artery. Crossed findings plus cranial nerve signs point to the brainstem instead.
• Missing the Horner clue. Ptosis and miosis on the weak side place a hemisection in the cervical or upper thoracic cord.
• Calling early flaccidity an LMN lesion. Below-level flaccidity in the first days is spinal shock; LMN signs belong only to the injured segment.
• Choosing steroids. High-dose methylprednisolone is not the expected answer for acute cord injury; blood pressure support and early decompression are.

How USMLE tests Brown-Séquard

• Step 1 asks for the tract: name the damaged pathway behind one deficit (for example, contralateral pinprick loss = spinothalamic tract on the lesion side), or where a pathway decussates.
• Step 1 asks for the side and level: the weak side is the lesion side; the pain level sits 1–2 segments below the lesion.
• Step 2 CK asks for the next step: spinal precautions, CT and MRI, blood pressure support, early decompression of a compressive lesion, and not high-dose steroids.
• Both exams test the look-alikes: anterior cord (bilateral, dorsal columns spared), central cord (hands worst) and syringomyelia (cape-like pain loss).

Worked examples

Vignette 1. A 27-year-old man is stabbed in the back just left of the midline. His left leg is weak, with brisk reflexes and an upgoing toe, and he cannot feel a tuning fork or sense passive toe movement on the left. On the right, pinprick and cold are lost from the umbilicus down. Damage to which structure explains the right-sided deficit, and where is the lesion?

Answer: The left lateral spinothalamic tract, in a left hemisection at about T8–T9.

Reasoning: Pain and temperature fibers from the right body cross in the anterior white commissure within 1–2 segments of entry, so they travel in the left cord; a T10 (umbilicus) sensory level places the lesion 1–2 segments higher.

Vignette 2. A 34-year-old woman has a right-sided neck stab wound. Her right leg is weak, the small muscles of her right hand are weak and flaccid, and her right pupil is small with mild ptosis. Vibration and position sense are lost in the right leg, and pinprick is lost on the left from the upper chest down. Where is the lesion?

Answer: A right hemisection of the lower cervical cord (around C8).

Reasoning: Ipsilateral weakness and vibration loss with contralateral pain loss define Brown-Séquard; at-level LMN signs in the hand localize the segment, and the ipsilateral Horner syndrome fits a lesion that interrupts the descending sympathetic fibers at or above the ciliospinal center (C8–T2).

Vignette 3. A 72-year-old man wakes after repair of a thoracoabdominal aortic aneurysm unable to move either leg. Pinprick and temperature are lost in both legs, but he feels a tuning fork at both ankles and knows the position of his toes. Which syndrome is this, and why is it not Brown-Séquard?

Answer: Anterior cord syndrome from anterior spinal artery ischemia.

Reasoning: Bilateral weakness and bilateral pain and temperature loss with preserved dorsal column function is the anterior cord pattern; Brown-Séquard is one-sided, with motor and dorsal column loss on one side and pain loss on the other.

Key takeaways

• Hemisection = ipsilateral weakness and vibration/proprioception loss, contralateral pain and temperature loss, below the lesion.
• Only the spinothalamic tract has crossed within the cord; corticospinal and dorsal column fibers cross in the medulla.
• The contralateral pain level sits 1–2 segments below the lesion; at-level LMN signs and segmental sensory loss mark the true level.
• A cervical or upper thoracic lesion can add an ipsilateral Horner syndrome.
• Knife wounds are the classic cause; manage with spinal precautions, MRI, MAP support (lower limit 75–80, up to 90–95 mm Hg for 3–7 days) and early decompression when compressive.
• The prognosis is better than for anterior or central cord syndrome: up to about 90% walk again.

More neuroanatomy reviews are on the neurology topic hub.

Sources

• Brown-Séquard Syndrome — StatPearls, NCBI Bookshelf
• Neuroanatomy, Spinothalamic Tract — StatPearls, NCBI Bookshelf
• Central Pain Pathways: The Spinothalamic Tract — Neuroscience (Purves et al.), NCBI Bookshelf
• Central Cord Syndrome — StatPearls, NCBI Bookshelf
• Spinal Cord Injuries — StatPearls, NCBI Bookshelf
• Neurogenic Shock — StatPearls, NCBI Bookshelf
• Anterior Cord Syndrome (Ventral Cord Syndrome) — StatPearls, NCBI Bookshelf
• Syringomyelia — StatPearls, NCBI Bookshelf
• Spinal Cord Subacute Combined Degeneration — StatPearls, NCBI Bookshelf
• Kwon BK, et al. A Clinical Practice Guideline for the Management of Patients With Acute Spinal Cord Injury: Recommendations on Hemodynamic Management. Global Spine J. 2024 (PubMed)
• Fehlings MG, et al. An Update of a Clinical Practice Guideline for the Management of Patients With Acute Spinal Cord Injury: Recommendations on the Role and Timing of Decompressive Surgery. Global Spine J. 2024 (PubMed)