Central cord syndrome

Central cord syndrome is the most common type of incomplete spinal cord syndrome, usually, the result of trauma, accounting for ~10% of all spinal cord injuries. As the name implies, this syndrome is the result of damage to the central portion spinal cord and in the setting of trauma most commonly affects the cervical cord. 

Epidemiology

Most often central cord syndrome occurs in the setting of trauma, and most often in older individuals with underlying cervical spondylosis. However, it may also be seen in younger persons who sustain substantial trauma to the cervical spine, for example during forceful football tackling when a player "spears" another with their head. 

Central cord syndrome is also seen in spinal cord tumours and other non-traumatic conditions (see below), and the epidemiology will match that of the underlying condition. 

Clinical presentation

The pattern of neurological deficit in patients with central cord syndrome depends on the size of the injury which in turn affects which parts of the spinal cord are involved.

In smaller central lesions, the spinothalamic tract fibersfibres that cross the anterior white matter commissure are interrupted resulting in bilateral pain and temperature loss at the affected levels ¹². Below these levels, cord function is intact. As the cervical region is most commonly affected, the neurological defect described as affecting a "cape" distribution (both arms and shoulders and upper chest but sparing the rest of the body) ¹². 

In larger lesions, other parts of the cord are involved, including the corticospinal tracts, spinothalamic tracts, dorsal columns, and spinal grey matter. The result is an upper motor neuronneurone pattern of a deficit below the level of injury (due to interruption of descending corticospinal tracts), with spastic paralysis and urinary retention, and a lower motor neuronneurone pattern of deficit at the levels of injury (due to damage to the anterior horn cells) ¹². The upper extremities are classically more affected than the lower extremities (due to upper limb fibres being located more centrally) with motor function more severely impaired than sensory function ¹².

Pathology

Central cord syndrome is most often the result of trauma but can also be seen in a variety of non-traumatic cord pathologies including: 

• intramedullary spinal cord tumours (e.g. spinal ependymoma)
• syringohydromyelia  (e.g. Chiari I malformation)

These are discussed separately, in their respective articles. 

Trauma

A hyperextension cervical injury in individuals with degenerative canal stenosis is the most common mechanism for central cord syndrome, and in such cases, the cord is pinched between disc and/or osteophytes anteriorly and ligamentum flavum hypertrophy posteriorly ¹². Hyperextension teardrop fracture has associated acute traumatic central cord syndrome in ~80% of cases ⁷.

Other mechanisms including flexion, fracture-dislocation and acute disc herniation can also result in a central cord syndrome and these are seen more frequently in younger individuals ¹². 

Radiographic features

Plain radiograph and CT

Osseous imaging may be normal, show spondylosis, acquired/congenital canal stenosis, or fracture. 

The presence of an extension teardrop fracture should be a warning sign.

MRI

Findings depend upon the severity of trauma and presence of pre-existing canal stenosis, following features can be seen ¹¹:

• cord compression
• cord oedema
• cord haematoma: associated with poor prognosis

Typically the cord will demonstrate the following signal characteristics: 

• T1
  • the affected region is usually of isointense signal compared to rest of cord or slightly hypointense
  • haemorrhagic contusion may have areas of high T1 signal
• T2
  • increased signal centrally within the cord at the affected level (oedema/contusion)
  • haemorrhagic contusions will have variable signal with areas of low T2 eventually becoming apparent
• T2* - SWI/GE: will show low signal and blooming if blood product 

History and etymology

Central cord syndrome was first described by R C Schneider et et al. in 1954 ¹.