Spinal Cord Syndromes — Brown-Séquard, Central Cord and Tract Localisation

Begin with motor function, pain and temperature, vibration and position sense, and bladder symptoms. Decide whether findings are unilateral or bilateral and whether they occur at the lesion level or below it. A spinal cord lesion can damage a local segment and long pathways passing through that segment. Those two effects explain why the same patient can have different signs in different regions.

A sensory level, long-tract weakness and bladder dysfunction support a cord process. In a traumatic presentation, the priority is safe assessment and prevention of further injury, while the examination establishes the neurological pattern. The name of a syndrome describes a distribution of deficits; it does not replace imaging, identify every cause or determine treatment by itself.

Use the sequence modality → pathway → crossing → side of deficit. Motor and dorsal-column findings generally remain ipsilateral to a cord hemilesion, whereas pain-temperature loss appears contralaterally below it. Central and anterior patterns then follow from the pathways involved. Understanding the crossings lets you reconstruct the syndromes when a stem changes the side or level.

The dorsal columns carry sensory information upward before crossing in the medulla. A hemicord injury therefore interrupts information from the same side. Descending corticospinal fibres have already crossed above the spinal cord, so their interruption also produces weakness on the side of the lesion. Pain-temperature fibres cross within the cord and then ascend on the opposite side.

Do not apply the side rule from one pathway to every modality. A question may deliberately pair normal vibration with absent pinprick, or ipsilateral weakness with contralateral loss of temperature. Treat each finding as evidence about a different tract. Light touch alone is less useful for a simple three-pathway matching exercise than a clearly stated vibration or pain-temperature deficit.

Brown-Séquard syndrome is the clinical pattern of a hemicord lesion. Below the lesion, there is ipsilateral motor weakness and impaired vibration/proprioception, with contralateral loss of pain and temperature. A perfectly clean anatomical hemisection is uncommon in real injuries, so patients may show an incomplete or mixed pattern rather than every textbook feature.

For example, a left-sided hemicord lesion produces left-sided weakness and impaired position sense below the lesion, with right-sided pain-temperature loss. The side of the motor deficit is therefore a useful starting point. Confirm it with the dorsal-column findings, then check that the pain-temperature deficit is on the opposite side rather than forcing all deficits into one half of the body.

At the injured segment, damage to anterior horn cells or their outgoing motor fibres can produce lower motor neuron signs: reduced tone, reduced reflexes, weakness and eventual muscle wasting. Below the lesion, interruption of descending control produces upper motor neuron signs once acute spinal shock resolves. These are effects at different anatomical locations, not contradictory descriptions of one examination finding.

Acute cord injury may initially produce flaccidity and reduced reflexes below the lesion through spinal shock. The later long-tract signs can therefore be masked early. An immediate post-trauma examination with weak, areflexic limbs does not prove that the lesion is exclusively a peripheral nerve disorder. Document the initial examination and reassess the evolving neurological findings.

This distinction also matters in syringomyelia. Expansion into anterior horn cells can cause hand muscle wasting at the affected cervical segments, while extension towards corticospinal pathways can produce spastic lower-limb findings. Local damage and descending-pathway interruption belong in the same anatomical explanation. Identify which muscles are supplied by the affected segment before interpreting the reflexes.

The hallmark of central cord syndrome is disproportionately greater weakness in the upper limbs than in the lower limbs, often most marked in the hands. Sensory deficits vary, and urinary retention may accompany the syndrome. The pattern commonly follows a cervical hyperextension injury in an older person with pre-existing canal stenosis or spondylosis.

A classic stem describes a fall with neck extension followed by poor grip and difficulty moving the arms, with less severe leg weakness. The patient may still be able to move or use the legs despite substantial hand dysfunction. Preserved sacral sensation can occur. These findings indicate an incomplete cervical cord pattern rather than proving that the spinal cord is normal because leg function remains.

The traditional explanation relied heavily on a neat arrangement of arm and leg corticospinal fibres. Contemporary evidence questions that simple somatotopic account. Compression, oedema and broader white-matter or interneuronal dysfunction can contribute. For an exam, recognise the arm-predominant phenotype, but avoid presenting a central-arm/peripheral-leg cartoon as a firmly established explanation of every traumatic case.

Anterior cord syndrome impairs motor function and pain-temperature pathways while relatively preserving vibration and proprioception carried by the dorsal columns. When caused by anterior spinal artery ischaemia, the distribution reflects the arterial territory. This selective preservation is the decisive clue in a stem describing acute bilateral weakness and absent pinprick sensation.

The anterior spinal artery supplies much of the cord outside the posterior-column territory. The posterior spinal arteries help maintain the dorsal sensory pathways. This explains why an anterior vascular lesion can damage motor and pain-temperature function while sparing posterior-column sensation. The syndrome is a localisation pattern; the history establishes whether ischaemia, compression or another injury is responsible.

Aortic surgery, aortic pathology and severe perfusion disturbance are important clinical settings for anterior spinal artery injury. An abrupt deficit in such a setting should prompt urgent assessment. Do not turn a named vascular territory into a reason to overlook potentially treatable compression; neurological localisation and investigation of the cause must proceed together.

A syrinx is a fluid-filled cavity within the spinal cord. An early central cavity can interrupt crossing pain-temperature fibres in the anterior white commissure, while more distant dorsal columns remain intact. The result is dissociated sensory loss: pain and temperature are impaired, while touch and vibration may be preserved at the affected segments.

In a cervical syrinx, the distribution can be cape-like across the shoulders and upper limbs. The loss is segmental rather than a blanket loss of every modality throughout the body below a transverse level. The patient may fail to notice painful or hot stimuli in affected areas despite being able to detect other sensations. The split between modalities is what makes the pattern memorable.

As the cavity expands, it can affect anterior horn cells and produce hand weakness or wasting, then involve nearby corticospinal pathways. Syringomyelia is often associated with Chiari malformation, but trauma, tumours and other disturbances of cerebrospinal-fluid flow can also be involved. The association should not be treated as the only possible cause.

The table works because it compares which pathways are affected and which remain functional. A preserved modality is active localisation evidence. If pain and temperature are lost while vibration remains, think of selective anterolateral or crossing-fibre involvement. If vibration and position are lost without the corresponding motor pattern, consider a posterior-column process rather than naming a hemicord syndrome automatically.

Sacral sensation and motor function require explicit assessment in suspected injury. Sparing supports an incomplete injury pattern and is not equivalent to absence of serious cord damage. Central cord syndrome can retain distal function while substantially impairing the arms. Conversely, broad bilateral deficits should not be called complete from a casual limb examination without evaluating the relevant sacral findings.

1. In trauma, support airway, breathing and circulation while restricting spinal motion.
2. Prevent hypoxia and hypotension, which can worsen secondary cord injury.
3. Record a structured motor, sensory and sacral examination and repeat it as the clinical state changes.
4. Use appropriate imaging and obtain urgent spinal or neurosurgical assessment when compression, instability or neurological deterioration is suspected.
5. Plan bladder care, prevention of immobility complications and rehabilitation alongside treatment of the cause.

CT helps assess fractures and alignment in traumatic injury, while MRI shows the spinal cord, soft tissues and compression more directly. A reassuring plain structural assessment does not negate a persisting neurological deficit. Imaging should answer the clinical question raised by the examination and mechanism, with specialist input when urgent decompression or stabilisation may be needed.

High-dose methylprednisolone in acute traumatic spinal cord injury is controversial and should not be taught as an automatic treatment for every cord syndrome. A label such as central cord or Brown-Séquard does not replace an individual treatment plan. Current care focuses on preventing secondary injury and identifying mechanical or other treatable causes while supporting recovery.