Incomplete spinal cord syndromes

Incomplete spinal cord syndromes are caused by lesions of the ascending or descending spinal tracts that result from trauma, spinal compression, or occlusion of spinal arteries. Central cord syndrome is the most common type; other examples include anterior cord syndrome, posterior cord syndrome, Brown-Séquard syndrome, cauda equina syndrome, and conus medullaris syndrome. In contrast to complete spinal cord injuries, lesions only affect part of the cord, and affected individuals present with dissociated sensory loss. Clinical features depend on the affected sensory and motor pathways in the spinal cord. MRI of the spine is the diagnostic modality of choice to assess the level, extent, and underlying cause of the lesion, which determine the treatment. In some patients, surgery may be necessary to treat the underlying cause and improve outcome.

For more information, see “Treatment of spinal cord injuries.”

For more information on cauda equina syndrome and conus medullaris syndrome, see “Compressive spinal emergencies.”

Basic neuroanatomy and function

• Lateral and anterior corticospinal tracts
  • Descending tracts that originate in the cerebral cortex and extend to the alpha motor neuron in the ventral horn of the spinal cord
  • About 90% of pyramidal nerve fibers decussate as they pass through the medulla and descend further, forming the lateral corticospinal tract.
  • The remaining 10% comprise the anterior corticospinal tract and decussate at the segmental level.
  • Function: controls motor function
• Dorsal column
  • Neuronal fibers decussate at the medulla oblongata.
  • Remains ipsilateral in the spinal cord
  • Function: conveys epicritic sensation and proprioception
• Spinothalamic tract
  • Neuronal fibers decussate only at the segmental level or shortly above.
  • Function: conveys protopathic sensation
• For more information, see ''Spinal cord tracts.''

Overview of incomplete spinal cord syndromes

• Definition: a syndrome caused by injury to the central region of the spinal cord, which includes the central corticospinal tracts and decussating fibers of the lateral spinothalamic tract
• Epidemiology ^[3]
  • Most common type of incomplete cord syndrome
  • More common in individuals > 50 years old because of age-related degeneration of the cervical spine
• Etiology
  • Hyperextension injury (e.g., whiplash injury with chronic cervical spondylosis)
  • Cervical spondylosis
  • Degenerative spine disease
  • Traumatic disk herniation
  • Syringomyelia
• Clinical features
  • Bilateral motor paresis (upper > lower extremities; distally > proximally)
  • Loss of bladder control
  • Variable sensory impairment
    • Burning pain in the arms
    • Loss of pain and temperature sensation in the arms
  • Sacral sparing
• Diagnostics
  • CT or x-ray of the spine: findings of cervical spondylosis, spinal canal stenosis, or vertebral fractures
  • MRI of the spine: diagnostic modality of choice for evaluating spinal cord pathology
• Treatment: See “Treatment of spinal cord injuries.”

• Definition: a syndrome caused by injury to the anterior two-thirds of the spinal cord ^[4]
• Epidemiology
  • Approx. 5% of incomplete spinal cord syndromes ^[5]
  • Approx. 6% of acute myelopathies ^[6]
  • Most common type of spinal cord infarction ^[7]
• Etiology ^[8]
  • Anterior spinal artery syndrome (∼ 95% of cases): reduced blood flow or occlusion of the anterior spinal artery (ASA)
  • Systemic hypoperfusion (e.g., heart failure)
  • Iatrogenic injury (e.g., during aortic surgery, spinal angiography, or spinal anesthesia)
    • Aortic repairs may result in lesions of the artery of Adamkiewicz: a thoracic radicular artery (branch of the intercostal vasculature) that supplies the lower two-thirds of the spinal cord.
    • The midthoracic region of the ASA is a watershed area because the artery of Adamkiewicz is the only major vessel that supplies the spinal cord below spinal level T8/T9. ^[9]
  • Trauma; (e.g., burst fracture, penetrating injury, and hyperflexion injury with vertebral instability) ^[8]
  • Arteriosclerosis, vasculitis (e.g., due to diabetes)
  • Thrombosis, embolic occlusion
  • Aortic dissection, aneurysm
  • Severe hypotension (e.g., following hemorrhage)
  • Pathological compression (e.g., tumors, cervical spondylosis)
• Clinical features
  • Acute (within hours)
    • Back or chest pain
    • Bilateral loss of temperature and pain sensation below the level of the lesion due to damage of the spinothalamic tracts
    • Lower motor neuron deficits (flaccid paralysis) at the level of and below the lesion
    • Autonomic dysfunction (spastic bladder, neurogenic bowel, erectile dysfunction, orthostatic hypotension)
    • Absent bulbocavernosus reflex
  • Late (within days or weeks)
    • Upper motor neuron dysfunction (spastic paraparesis or quadriparesis) below the level of the lesion due to damage to the corticospinal tracts
    • Lower motor neuron deficits (flaccid paralysis) at the level of the lesion due to damage to the anterior horn
    • Continued sensory and autonomic dysfunction
    • Hyperreflexia
• Diagnostics
  • MRI of the spine (diagnostic modality of choice)
    • Findings: spinal cord parenchyma abnormalities (e.g., infarction) in the anterior part of the spinal cord
    • Excludes soft tissue lesions (e.g., tumors, hematomas) and vascular malformations
• Treatment: See “Treatment of spinal cord injuries.”

Vibration and proprioception are typically spared because of an intact dorsal column.

• Definition: a syndrome caused by injury to the posterior spinal cord affecting the dorsal columns (bilateral loss of fine touch, vibration, pressure, and proprioception below the level of the lesion). In larger lesions, the lateral corticospinal tracts (CSTs) and autonomic tracts may be affected.
• Epidemiology: very rare ^[6]
• Etiology ^[1]
  • Occlusion of the posterior spinal artery
  • Subacute combined degeneration
  • Multiple sclerosis
  • Tabes dorsalis
  • Friedreich ataxia
• Clinical features ^[1]
  • Bilateral loss of vibration, fine touch, and proprioceptive sensation below the level of the lesion
  • Frequent falls
  • Sensory ataxia, positive Romberg sign
  • Muscle weakness and subsequent spasticity
  • Autonomic dysfunction (spastic bladder, neurogenic bowel, erectile dysfunction, orthostatic hypotension)
• Diagnostics
  • MRI of the spine: findings consistent with underlying cause (e.g., infarction of the dorsal columns in posterior spinal artery occlusion, demyelinating plaques in MS)
  • VDRL or RPR if syphilis is suspected
• Treatment: See “Treatment of spinal cord injuries.”

• Definition: : a syndrome involving hemisection of the spinal cord (often in the cervical cord)
• Epidemiology: approx. 1–4% of all traumatic SCIs ^[5]
• Etiology ^[10][11]
  • Unilateral compression or trauma of the spinal cord (e.g., penetrating injuries, motor vehicle crashes, crush injuries)
  • Less commonly: disk herniations, spinal epidural hematomas, spinal epidural abscesses, spinal tumors, multiple sclerosis, complication of decompression sickness
• Clinical features
  • Ipsilateral
    • Loss of all sensation at the level of the lesion
    • Segmental flaccid paralysis at the level of the lesion due to damage of lower motor neurons
    • Loss of proprioception, vibration, and tactile discrimination (fine touch) below the level of the lesion due to an interrupted dorsal column
    • Spastic paresis and Babinski sign below the level of the lesion due to damage of upper motor neuron axons in the lateral corticospinal tracts
    • In lesions above T1, Horner syndrome occurs because of damage to ipsilateral sympathetic fibers (oculosympathetic pathway).
  • Contralateral: loss of pain, temperature, and nondiscriminative touch (crude touch) one or two levels below the level of the lesion due to an interrupted spinothalamic tract
• Diagnostics
  • Clinical diagnosis
  • Imaging studies can help identify the underlying pathology.
    • CT of the spine: for bone abnormalities, vertebral fractures, trauma
    • MRI of the spine
      • Diagnostic modality of choice for spinal cord pathology
      • Findings: unilateral abnormal signal in the spinal cord at the level of the lesion, surrounding injuries of soft tissues or ligaments (e.g., epidural hematoma)
• Treatment: See “Treatment of spinal cord injuries.”

Autonomic symptoms are usually absent in Brown-Séquard syndrome because of unilateral involvement of the descending autonomic fibers.