What Causes Paraplegia?

Paraplegia has a host of causes, ranging from the local to the cerebral. Most commonly, paraplegia is the result of accidents, which occur most often in the young adult male population, between 15 and 35 years, and cause traumatic injury to the spinal cord. This accounts for more than three-quarters of the total cases of spinal injury. The causes of paraplegia may be classified under the following headings:

Trauma to the spinal cord or brain

• Accidents may fall under vehicle accidents, sports accidents, gunshot or stab wounds, or suicide attempts.
• Workplace and household injuries are most commonly the result of falls, diving accidents, electrocution or blast injuries.
• Other accidents resulting in paraplegia include:
• Spinal injections of toxins which damage the nerves.
• Inflammation of the membranes surrounding the spinal nerves (arachnoiditis).
• Pathologic spinal fractures as in degenerative bone diseases.
• Surgical accidents.

Types of spinal injuries

• Hyperflexion, caused by blows to the back of the head, or forceful decelerations.
• Hyperflexion-rotation, caused by disruption to the posterior spinous ligament.
• Vertical compression, or axial loading, where the vertebral body is compressed, resulting in a range of conditions from decrease in height to complete fragmentation.
• Hyperextension, because of blows to the front of the head or whiplash injury. These are two times more common than hyperflexion.
• Extension-rotation, where both anterior and posterior spinal columns are disrupted, most commonly occurring in diving injuries.
• Lateral flexion, often seen along with flexion or extension injuries

Types of cerebral injuries include depressed skull fractures or subdural hematomas.

Medical

• Infections in and around the spinal cord, such as abscesses, tuberculous abscess or Pott’s disease, and parasitic infestations such as schistosomiasis or bilharziasis.
• Vascular lesions, including spinal cord infarction, extradural hematomas of the spine, arteriovenous malformations or aortic aneurysms.
• Tumors, due to primary or secondary growths of the spine, including myeloma, neurofibromatosis and neurilemmomas.
• Anesthetic accidents leading to spinal cord hypoxia.

Another useful classification of the causes of paraplegia is as focal, and systemic.

• Focal lesions
  • Focal compressive lesions
    • Vertebral  compression
      • Fracture or fracture-dislocation of vertebra
      • Pott’s disease
      • Disc herniation
      • Kyphoscoliosis
      • Tumors
    • Meningeal  compression
      • Intradural tumors, such as neurofibroma
      • Extradural tumor deposits, as in leukemia
      • Dural tumors, like meningiomas
    • Cord compression, as in syringomyelia
  • Focal inflammatory lesions, such as transverse myelitis.
  • Vascular lesions, such as hematomas, infarcts or hemangiomas of the spinal cord.
• Systemic lesions
  • Hereditary
• Hereditary spastic paraplegia
• Hereditary ataxias, such as Friedrich’s ataxia
  • Non-hereditary or nutritional
• Pellagra
• Subacute combined degeneration of the cord
  • Idiopathic
• motor neuron disease
• Disseminated disease, such as disseminated sclerosis
• Cerebral causes
  • Affecting the cerebrum, in the parasagittal region which regulates the voluntary movements of the lower limbs.
• Traumatic, as in subdural hematomas
• Inflammatory, as following meningoencephalitis
• Vascular, as superior sagittal sinus thrombosis
• Tumors of the parasagittal region
• Degenerative, as in cerebral palsy
  • Affecting the brainstem
• Midline tumors
• syringomyelia

Pathophysiology of acute spinal cord injury

Traumatic injury results from compression of the spinal cord against the neighboring bone-ligamentary complex. This leads to vascular injury, mainly of the tiny vessels inside the medulla of the bones, which produces hemorrhagic injury to the grey matter of the cord, as well as infarction due to spasm of the vessels.

The resulting fall in blood circulation inside the cord sets off the inflammatory cascade that leads to secondary injury by swelling, infarction and permanent loss of function of the cord. In addition to the release of pro-inflammatory mediators, other mechanisms that lead to the loss of blood flow include failure of autoregulation, hypotension, thrombosis, and impaired energy production by the damaged and shocked cells, and vasospasm.

The eventual result of this chain of events includes loss of nerve conduction through the cord, membrane disruption and the loss of structural integrity of the spinal cord.