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Neurology · Neuro

Spinal Cord Syndromes

A localization-first tour of the classic spinal cord syndromes, using the crossing rules of the dorsal columns, corticospinal, and spinothalamic tracts to explain Brown-Séquard, anterior cord, central cord/syringomyelia, subacute combined degeneration, and tabes dorsalis. Includes board-style next-best-step decisions for cord compression, cauda equina, and epidural abscess.

13 min readHigh yield

The three tracts and their crossing rules

Every classic cord syndrome is decoded from three long tracts and where each crosses. The dorsal columns (fasciculus gracilis = legs/medial, cuneatus = arms/lateral) carry vibration, proprioception, and fine touch; they ascend ipsilaterally and decussate in the caudal medulla. The lateral corticospinal tract carries motor output and has already crossed at the pyramids, so a cord lesion causes ipsilateral upper-motor-neuron (UMN) weakness below it. The spinothalamic tract carries pain and temperature; second-order fibers cross in the anterior white commissure within ~1–2 levels of entry, then ascend contralaterally. Anterior horn cells produce lower-motor-neuron (LMN) signs at the level. Because these tracts cross at different points, one lesion can dissociate sensation from motor and left from right — the anatomic basis of localization.

Localization pearls
  • Dorsal columns cross in the medulla → deficit is ipsilateral below the lesion (vibration, proprioception, fine touch)
  • Lateral corticospinal crossed at the pyramids → ipsilateral UMN weakness below (spastic, hyperreflexic, up-going toe)
  • Spinothalamic crosses within 1–2 levels → contralateral pain/temperature loss, starting ~2 levels below
  • Anterior horn/ventral rootipsilateral LMN signs at the level (flaccid, atrophy, fasciculations, areflexia)
  • UMN vs LMN: UMN = spastic, hyperreflexic, Babinski; LMN = flaccid, atrophic, fasciculations, absent reflexes
  • A sensory level on the trunk (dermatomal cutoff) = transverse cord lesion
  • Sacral sparing points to an intramedullary/central lesion (spinothalamic lamination: sacral fibers most lateral, spared by lesions expanding from the center)
Labeled transverse section of the spinal cord showing the dorsal columns, lateral corticospinal tract, and spinothalamic tract
Cord cross-section: locate the dorsal columns (posterior), lateral corticospinal tract, and anterolateral spinothalamic tract to predict every syndrome's deficit. · Wikimedia Commons — User:Polarlys — CC BY 2.5, via Wikimedia Commons

Incomplete cord syndromes at a glance

SyndromeTracts hitHallmark deficitClassic cause
Brown-Séquard (hemisection)Ipsi dorsal column + corticospinal; contra STTIpsi motor + vibration loss; contra pain/temp ~2 levels belowPenetrating trauma, lateral tumor
Anterior cordCorticospinal + STT (dorsal columns spared)Bilateral motor + pain/temp loss; vibration/proprioception intactASA infarct (aortic surgery, hypotension)
Central cord / syrinxCrossing STT fibers ± anterior hornsCape-like pain/temp loss; arms > legs weaknessSyringomyelia (Chiari I); elderly hyperextension
SCD (posterolateral)Dorsal columns + corticospinal + spinocerebellarSensory ataxia, +Romberg, spastic paresisB12 (also copper, N₂O)
Tabes dorsalisDorsal columns / dorsal rootsSensory ataxia, lancinating pain, Argyll Robertson pupilTertiary syphilis
Vignette — the split lesion

Vignette: A 24-year-old man is stabbed in the right back at T10. Exam shows right leg spastic weakness with hyperreflexia and an up-going toe, right-sided loss of vibration/proprioception, and left-sided loss of pain and temperature beginning a few dermatomes below the wound.

  • Diagnosis: Brown-Séquard (cord hemisection).
  • Why the split: corticospinal + dorsal columns are ipsilateral; spinothalamic already crossed → pain/temp loss is contralateral and starts ~2 levels below.
  • Next best step: MRI of the spine (plus trauma survey) and neurosurgical evaluation for decompression/stabilization. Routine high-dose steroids are not recommended in penetrating SCI.
Vignette — sensory ataxia + macrocytosis

Vignette: A 60-year-old with prior gastric bypass (or strict vegan diet / chronic metformin) reports progressive gait unsteadiness and tingling feet. Exam: reduced vibration/proprioception, a positive Romberg, spastic legs with hyperreflexia yet paradoxically absent ankle jerks; conjunctivae are pale and MCV is elevated.

  • Diagnosis: Subacute combined degeneration from B12 deficiency (dorsal columns + lateral corticospinal ± spinocerebellar). The mixed picture — extensor plantars with absent ankle jerks — is the classic exam clue.
  • Workup: low B12; elevated methylmalonic acid + homocysteine (most sensitive early); smear with macro-ovalocytes and hypersegmented neutrophils.
  • Next best step: start parenteral B12 promptly; evaluate for pernicious anemia (anti-intrinsic-factor Ab). Do not give folate alone — it corrects the anemia but can worsen the neuro deficit.
Syringomyelia & traumatic central cord
  • Syringomyelia: a fluid-filled cavity (syrinx) expanding from the central canal, typically C8–T1
  • Hits crossing spinothalamic fibers first → cape/suspended dissociated sensory loss (pain/temp lost, touch & vibration preserved)
  • Expansion into anterior horns → LMN wasting of the hands; lateral horns → Horner syndrome
  • Strongly linked to Chiari I; also post-traumatic or intramedullary tumor
  • Classic clue: painless burns or cuts on the hands
  • Acute traumatic central cord (elderly, cervical spondylosis, hyperextension): arms > legs weakness — the most common incomplete SCI
  • Next step: MRI; treat the cause (e.g., posterior fossa decompression for Chiari-related syrinx)
Argyll Robertson pupil

Argyll Robertson pupil (tabes dorsalis / neurosyphilis): small, irregular pupils with light–near dissociationAccommodation Reflex Present (ARP), Pupillary (light) Reflex Absent (PRA). In one line: it accommodates but does not react to light. Pair it with the tabes triad of sensory ataxia, lancinating pains, and a positive Romberg.

  • Testing (get the categories right): VDRL/RPR are nontreponemal serum screens — confirm a reactive result with a treponemal test (FTA-ABS or TP-PA).
  • Neurosyphilis is documented on CSF: CSF-VDRL is specific but insensitive, alongside lymphocytic pleocytosis and elevated protein.

Conus medullaris vs cauda equina

FeatureConus medullarisCauda equina
Lesion siteCord tip (~L1–L2)Lumbosacral nerve roots below L2
Neuron typeMixed UMN + LMNLMN only
SymmetrySymmetricAsymmetric
PainLess prominentSevere, radicular
Bladder/bowelEarly, prominent retentionLate, variable
ReflexesUp-going toes possibleAreflexia
SensorySymmetric perianalSaddle anesthesia
Next-best-step: cord emergencies
  • Acute cord compression (trauma, epidural metastasis/abscess, hematoma) → immediate MRI; do not wait for plain films
  • Metastatic epidural compression (breast/lung/prostate; back pain worse lying down/at night): give IV dexamethasone immediately and get emergent MRI of the whole spine + rad-onc/neurosurgery
  • Cauda equina syndrome (saddle anesthesia, urinary retention, bilateral sciatica): urgent MRI → surgical decompression, ideally <48 h
  • Spinal epidural abscess (fever + focal spine pain, IVDU/diabetes, ↑ESR/CRP): MRI + blood cultures → drainage + antibiotics covering *S. aureus* (empiric MRSA coverage)
  • Acute traumatic SCI: ABCs + immobilize; routine high-dose methylprednisolone is no longer standard
  • ALS: combined UMN + LMN with NO sensory loss; disease-modifying riluzole (± edaravone)

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