A transected spinal cord results from a complete severance or functional discontinuity of the neural tissue. This disruption breaks the communication lines between the brain and the body below the injury site. The inability of the adult human spinal cord to naturally restore these connections is the central challenge in neuroscience and clinical medicine. Understanding the biological reasons for its permanence and the current medical responses provides a framework for appreciating the intensive research aimed at repair.
Defining Complete Spinal Cord Transection
A complete spinal cord injury (SCI) is defined as the total loss of all motor and sensory function below the level of the lesion. This is distinct from an incomplete injury, where some function is preserved. The concept of “transection” refers to a functional or anatomical severing.
The effects of a complete injury are determined by the neurological level along the spine. An injury in the cervical spine (neck) can lead to tetraplegia, affecting the arms, trunk, and legs. A lesion in the thoracic or lumbar spine results in paraplegia, affecting the trunk and legs. Following trauma, the spinal cord enters spinal shock, where reflexes below the injury are temporarily lost. A complete transection eliminates motor control, sensation, and autonomic functions like bladder and bowel control below the injury level.
Biological Roadblocks to Healing
The reason a transected spinal cord does not heal is the hostile, inhibitory environment created in the central nervous system after injury. Mature CNS neurons have a limited intrinsic capacity for axonal regeneration. The injury triggers a cascade of events that actively prevent the regrowth of severed nerve fibers.
The most significant barrier is the formation of the glial scar, composed primarily of reactive astrocytes. While the scar initially limits inflammation, its chronic persistence creates a dense physical and chemical obstacle to regeneration. Within this scar, inhibitory molecules called chondroitin sulfate proteoglycans (CSPGs) are upregulated. These CSPGs suppress axonal growth cones, preventing nerve endings from navigating across the lesion site. The scar tissue also lacks the necessary neurotrophic support that encourages axonal sprouting and elongation. This combination of physical obstruction and chemical inhibition prevents spontaneous functional reconnection.
Current Stabilization and Rehabilitation
The initial medical response focuses on immediate stabilization to prevent further damage. This involves surgical stabilization of the spine, where fractured or dislocated vertebrae are fused to create a rigid column. Careful management of blood pressure and oxygenation is also maintained to ensure adequate perfusion to the injured cord to minimize secondary injury.
Once the patient is stable, the focus shifts to comprehensive, long-term rehabilitation. This interdisciplinary process begins early and includes physical and occupational therapy. Physical therapy strengthens preserved muscle groups and maintains joint flexibility to prevent contractures. Occupational therapy helps individuals adapt to daily living tasks, often utilizing assistive devices. Ongoing care involves managing secondary complications, such as establishing regular bowel and bladder management programs, addressing respiratory concerns, and preventing pressure sores that result from immobility. This long-term supportive care is the current standard of treatment.
Promising Avenues in Spinal Cord Repair
Research efforts are focused on several experimental approaches showing promise in preclinical and early clinical trials. One major strategy involves cellular therapies using stem cells to promote repair, including Neural stem cells, Mesenchymal stem cells (MSCs) from sources like bone marrow, and Olfactory ensheathing cells (OECs).
These cells are transplanted into the injury site, where they may differentiate into new neurons or glial cells, or secrete neurotrophic factors that support the survival and growth of existing neurons. Another approach targets the inhibitory molecules in the glial scar, such as using enzymes like chondroitinase ABC to degrade the inhibitory CSPGs. This creates a more permissive environment for axonal regrowth.
A third strategy involves using biomaterials and tissue engineering to physically bridge the gap created by the transection. Researchers are developing scaffolds, often made of biodegradable hydrogels, that can be implanted into the lesion site. These scaffolds guide the direction of regenerating axons and can be engineered to slowly release beneficial factors, like neurotrophic factors or anti-inflammatory agents, to create a favorable microenvironment for nerve fiber extension.