What Happens in a Transected Spinal Cord Injury?

Damage to the spinal cord can have profound consequences, especially when it is completely transected. This type of injury disrupts communication between the brain and areas below the site of damage, leading to significant neurological impairments. Unlike partial injuries where some function may remain, a full transection results in a complete loss of motor and sensory function below the affected level.

Structural Disruption In A Transected Spinal Cord

A complete transection of the spinal cord results in an immediate and irreversible loss of structural integrity, severing all neural pathways that connect the brain to regions below the injury site. Both white and gray matter are affected, leading to anatomical and functional breakdowns. The white matter, composed of myelinated axons responsible for transmitting signals, is completely severed, halting communication between the central nervous system and peripheral structures. Simultaneously, the gray matter, which houses neuronal cell bodies and synaptic connections, undergoes extensive damage, impairing local processing and reflexive functions.

The loss of structural continuity also compromises the vascular network that supplies oxygen and nutrients to the spinal cord. Blood vessels are torn apart, leading to hemorrhaging and ischemia in the affected region. This deprivation of oxygen triggers widespread necrosis, particularly in the central gray matter, where metabolic demand is highest. As neurons and glial cells succumb to hypoxia, surrounding tissue becomes vulnerable to secondary degeneration, expanding the damage beyond the initial injury site.

Mechanical forces during transection also disrupt the extracellular matrix, a crucial scaffold providing structural support to neural tissue. The breakdown of this matrix destabilizes the remaining cellular architecture, making it difficult for surviving neurons to maintain connections. Severed axons retract from the injury site, forming dystrophic end bulbs that prevent reconnection. This structural disarray creates a physical barrier that impedes neural regeneration, reinforcing the permanence of functional loss.

Cellular And Molecular Responses To Injury

Following a complete transection, a series of cellular and molecular events unfold, shaping the progression of tissue degeneration and repair.

Inflammatory Cascade

The injury triggers a rapid inflammatory response, characterized by the activation of resident microglia and infiltration of peripheral immune cells. Within hours, microglia shift to a reactive state, releasing pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6). These molecules increase vascular permeability and recruit circulating monocytes, which differentiate into macrophages upon entering the damaged tissue.

Macrophages play a dual role. While they clear cellular debris through phagocytosis, they also release reactive oxygen species (ROS) and nitric oxide, exacerbating oxidative stress and secondary tissue damage. Studies published in The Journal of Neuroscience (2021) indicate that prolonged inflammation contributes to chronic neurodegeneration, as sustained cytokine release disrupts neuronal homeostasis. The breakdown of the blood-spinal cord barrier allows further immune cell infiltration, prolonging the inflammatory phase and hindering recovery.

Glial Scar Formation

As the inflammatory response progresses, astrocytes proliferate and migrate toward the injury site, forming a dense glial scar composed of hypertrophic astrocytes, chondroitin sulfate proteoglycans (CSPGs), and extracellular matrix components. The scar prevents the spread of further damage by isolating the lesion from surrounding healthy tissue but also presents a significant obstacle to axonal regeneration.

CSPGs, particularly neurocan and brevican, inhibit axonal growth by interacting with neuronal receptors such as protein tyrosine phosphatase sigma (PTPσ). Research published in Nature Neuroscience (2022) highlights that these inhibitory molecules disrupt severed axons’ ability to extend beyond the lesion site. While experimental strategies, such as enzymatic degradation of CSPGs using chondroitinase ABC, have shown promise in preclinical models, balancing scar formation with regenerative potential remains a challenge.

Axonal Degeneration

The severance of axons initiates Wallerian degeneration, where the distal segments of damaged axons break down due to the loss of connection with their cell bodies. This process is facilitated by calcium-dependent proteases, such as calpains, which degrade cytoskeletal components. Additionally, the myelin sheaths surrounding these axons disintegrate, releasing myelin-associated inhibitors like Nogo-A, MAG (myelin-associated glycoprotein), and OMgp (oligodendrocyte myelin glycoprotein), further suppressing axonal regrowth.

Oligodendrocytes, the myelinating cells of the central nervous system, undergo apoptosis in response to injury, exacerbating demyelination and impairing signal conduction in surviving axons. A study in The Journal of Neurotrauma (2023) demonstrated that oligodendrocyte loss contributes to chronic functional deficits, as remyelination is limited in the adult spinal cord. The combination of axonal fragmentation, myelin debris accumulation, and inhibitory signaling creates an environment highly resistant to regeneration, reinforcing the permanence of functional loss.

Neurological Consequences

A complete transection results in an irreversible loss of motor, sensory, and autonomic function below the site of injury. The extent of impairment depends entirely on the level of the spinal cord affected, as all neural pathways descending from the brain are interrupted. Cervical injuries lead to quadriplegia, affecting both upper and lower limbs, whereas thoracic or lumbar transections cause paraplegia, sparing the arms but leaving the lower body immobile.

Loss of motor function is immediate, as corticospinal tract fibers, which carry voluntary motor commands from the brain, are severed. Without these descending signals, muscles below the injury site become paralyzed, initially presenting with flaccidity due to spinal shock before transitioning to spasticity over time. This shift occurs as lower motor neurons, now disconnected from higher control centers, become hyperactive, leading to exaggerated reflexes and involuntary muscle contractions.

Disruption of the spinothalamic tract results in complete sensory loss below the lesion. Patients experience a sharp demarcation where sensation ceases, with no ability to perceive touch, pressure, or temperature in affected areas. This increases vulnerability to secondary complications, such as pressure ulcers and unnoticed injuries, as the body’s natural protective pain response is lost. Damage to autonomic pathways regulating vascular tone also leads to impaired blood pressure control, often causing hypotension and autonomic dysreflexia, a life-threatening condition where uncontrolled sympathetic activation results in dangerously high blood pressure.

Potential Secondary Effects On Bodily Functions

A transected spinal cord disrupts physiological processes regulated by the nervous system. One immediate concern is the loss of voluntary bladder and bowel control. Without descending neural input, the detrusor muscle of the bladder contracts unpredictably, leading to urinary retention or incontinence. Over time, this dysfunction increases the risk of recurrent urinary tract infections and kidney damage due to high intravesical pressures. Similarly, impaired colonic motility results in chronic constipation, requiring strict bowel management strategies to prevent complications such as fecal impaction or autonomic dysreflexia triggered by prolonged bowel distension.

Sexual function is also affected, with the degree of impairment depending on injury level. In men, reflexogenic erections may still occur if the sacral spinal cord remains intact, but psychogenic arousal, which relies on brain-spinal cord communication, is often lost. Ejaculatory dysfunction is common, with studies reporting fertility challenges due to impaired semen quality and emission mechanisms. Women experience reduced lubrication and altered genital sensation, though fertility remains largely unaffected. These changes necessitate specialized medical interventions, including assisted reproductive technologies and pharmacological management for sexual dysfunction.

Relevance Of Spinal Cord Level In Injury Severity

The level of a spinal cord transection dictates the extent of functional impairment, as different spinal segments control distinct motor, sensory, and autonomic functions. Higher injuries result in greater disabilities, while those in the thoracic or lumbar regions allow for some retained upper body function.

Cervical transections, particularly at C1-C4, eliminate voluntary control of all four limbs and often impair respiratory function by disrupting the phrenic nerve, which innervates the diaphragm. Individuals with such injuries typically require mechanical ventilation. Lower cervical injuries (C5-C8) preserve some arm and hand movement, allowing for limited independence with assistive devices. Thoracic transections lead to complete paralysis of the lower body and loss of trunk stability, depending on the precise vertebral level. Injuries at T6 and above disrupt autonomic regulation of blood pressure, increasing the risk of orthostatic hypotension and autonomic dysreflexia. Lumbar and sacral injuries primarily affect leg movement and bowel, bladder, and sexual function but leave upper body strength intact, allowing for greater mobility with rehabilitation and assistive technology.