Acute Spinal Cord Syndromes

Acute Spinal Cord Syndromes

Natalie R. Weathered

Noam Y. Harel


Patients presenting with acute spinal cord syndromes represent true neurologic emergencies. Pathologic damage to the cord is usually incomplete. Therefore, there is opportunity to salvage (and peril of losing) vital cord tissue and function over the ensuing minutes and hours after presentation. As with other neurologic presentations, clinicians must first localize and then differentiate the type of damage in order to initiate the most effective interventions.


To aid with localization, recall that the caudal spinal cord segments do not align with the vertebrae bearing the same names. The spinal cord ends around L1, with the roots of the cauda equina below that vertebral level. Additionally, within the cervical cord, the spinal roots exit the spinal canal above the associated vertebral level except for root C8, which exits between C7 and T1. Thereafter, each spinal root exits below the corresponding vertebral body.


The majority of the corticospinal tract, mediating a large proportion of our volitional limb movements, decussates in the medulla before descending in the contralateral lateral corticospinal tract. The minority of motor axons that do not decussate within the medulla form the anterior corticospinal tract. The lower motor neurons, receiving input from corticospinal fibers as well as segmental interneurons, reside within the ventral horn (Fig. 16.1).


Afferent sensory fibers from the dorsal root ganglia enter the spinal cord at the dorsal horn. From there, their course depends on the type of modality being transmitted.

Pain and Temperature

These fibers travel rostrally within Lissauer tract for one or two spinal segments before synapsing within the dorsal horn and crossing to the contralateral anterolateral system. The anterolateral system is composed of the anterior spinothalamic tract, which carries crude touch sensory fibers, and the lateral spinothalamic tract, which carries pain and temperature fibers.

TABLE 16.1 Differential Diagnosis for Acute Spinal Syndromes



Disk herniation

Epidural abscess

Epidural hematoma

Epidural neoplasm/metastasis

Vertebral compression fracture


Ischemic stroke

Dural arteriovenous fistula

Arteriovenous malformation

Cavernous malformation


Multiple sclerosis

Neuromyelitis optica

Transverse myelitis

Acute disseminated encephalomyelitis (ADEM)



Systemic lupus erythematosus (SLE)

Antiphospholipid antibody syndrome (APS)

Sjögren syndrome

Mixed connective tissue disease (MCTD)

Behçet disease




Arachnoiditis after angiographic/myelographic contrast agents

Methotrexate toxicity

Cytarabine toxicity

Amphotericin B toxicity



Viral gray matter/acute flaccid paralysis



Coxsackieviruses A & B

West Nile virus (WNV)

Japanese encephalitis (JE)

Tick-borne encephalitis

Viral white matter/longitudinal myelitis

Herpes simplex virus (HSV)

Varicella-zoster virus (VZV)

Cytomegalovirus (CMV)

Epstein-Barr virus (EBV)



Mycoplasma pneumoniae





Cryptococcus neoformans

Coccidioides immitis

Blastomycetes dermatitides

Histoplasma capsulatum

Candida species

Aspergillus species



Schistosoma species

Toxoplasma gondii

Taenia solium (cysticercosis)

TABLE 16.2 Classic Spinal Cord Syndromes


Typical Causes

Clinical Characteristics

Central cord syndrome (syringomyelia)

Underlying cervical spondylosis with hyperextension injury; damage relatively greater to gray than white matter

Weakness in upper extremities > in lower extremities; may have neurogenic bladder dysfunction and varying degrees of sensory loss at or below the lesion (often in a “cape-like” distribution).

Brown-Séquard syndrome

Penetrating trauma (many nonpenetrating injuries show partial asymmetric syndromes)

Ipsilateral motor and vibration/proprioception loss below the lesion, contralateral pain/temperature loss two levels below the lesion

Anterior cord syndrome

Hypotensive event leading to infarct within the midthoracic region, or hyperflexion injury leading to compression of the anterior spinal artery

Bilateral loss of motor, pain/temperature sensation below the lesion with preservation of vibration/proprioception/two-point discrimination

Posterior cord syndrome

B12 deficiency, MS, vascular malformations, atlantoaxial subluxation

Bilateral loss of vibration/proprioception/two-point discrimination with preservation of motor, pain/temperature sensation below the lesion

Cauda equina syndrome

Disk herniation, tumor

Asymmetric lower extremity weakness, patchy impaired sensation to all modalities, loss of deep tendon reflexes as well as bulbocavernosus reflex and anal wink, often with low back and radicular pain

Conus medullaris syndrome

Disk herniation, trauma, tumor

Symmetric sacral > lumbar weakness (may have normal leg strength), saddle anesthesia, bowel/bladder dysfunction

MS, multiple sclerosis.

Vibration, Proprioception, and Two-Point Discrimination

These fibers travel within the ipsilateral dorsal columns to the gracilis and cuneatus nuclei of the lower medulla. Axons from the legs (fasciculus gracilis) are pushed medially by entering axons from the arms (fasciculus cuneatus) (see Fig. 16.1).



Sympathetic preganglionic neurons are located within the inter-mediolateral nucleus of the thoracic and upper lumbar (L1-L2) spinal cord. Their axons exit via the ventral roots and synapse on the postganglionic sympathetic neurons in the paravertebral ganglia (the “sympathetic chain ganglia”) or the prevertebral ganglia.

FIGURE 16.1 Anatomy of the spinal cord (cross-section). Tract lamination: S, sacral segments; L, lumbar segments; Th, thoracic segments; C, cervical segments. (From Brazis PW, Masdeu JC, Biller J. Localization in Clinical Neurology. 5th ed. Philadelphia: Lippincott Williams and Wilkins; 2007.)

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Jul 27, 2016 | Posted by in NEUROLOGY | Comments Off on Acute Spinal Cord Syndromes
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