A spinal cord injury (SCI) involves damage to any part of the spinal cord or the nerves at its end, known as the cauda equina. The spinal cord acts as the primary communication pathway, relaying signals between the brain and the rest of the body. While SCIs are often associated with affecting motor and sensory functions below the injury site, they also have substantial effects on the brain itself. The brain and spinal cord form a continuous central nervous system, meaning damage to one directly impacts the other.
Immediate Brain Responses to Spinal Cord Injury
Immediately following a spinal cord injury, the brain undergoes rapid, acute changes. One such phenomenon is neurogenic shock, a severe medical emergency affecting the body’s ability to regulate heart rate, blood pressure, and temperature due to nervous system damage. Occurring in an estimated 19% to 31% of SCI cases, it results from a disruption of sympathetic control over vascular tone, causing excessive blood vessel dilation. This leads to low blood pressure and reduced blood flow, meaning organs, including the brain, do not receive adequate oxygen and nutrients.
Beyond neurogenic shock, the direct disruption of ascending and descending neural pathways that connect the brain to the body occurs instantaneously. This interruption leads to an immediate change in the state of large cortical networks within minutes of the injury. For instance, a complete thoracic spinal cord transection can immediately increase cortical responses to stimuli from areas above the lesion, such as the forepaws, while eliminating responses from below the lesion. These immediate cortical changes are accompanied by slower, more silent spontaneous cortical activity, resembling a state of slow-wave sleep.
Spinal cord injury also triggers early inflammatory signals that can influence brain regions. Neutrophils, a type of immune cell, infiltrate the injury site within hours. These cells release destructive enzymes and pro-inflammatory cytokines, contributing to secondary injury at the spinal cord site and potentially affecting brain tissue. The breakdown of the blood-brain barrier allows inflammatory mediators to cross into the central nervous system, impacting brain health.
Structural and Functional Reorganization of the Brain
Following the initial acute phase, spinal cord injury leads to long-term physical and functional alterations in the brain. Grey matter atrophy, or shrinkage of brain regions, is a common consequence. This atrophy is particularly observed in areas like the primary somatosensory cortex and motor cortex, which lose sensory input or motor output from the spinal cord. However, atrophy can also extend to non-sensorimotor areas, such as the anterior cingulate cortex and insular cortex.
White matter degeneration also occurs, involving changes or damage to the myelin sheaths and axons in pathways connecting the brain to the spinal cord or other brain regions. This process, often referred to as Wallerian degeneration, spreads from the injury site. Imaging studies indicate demyelination and axonal disruption in cerebral white matter following SCI.
Neural networks and communication pathways within the brain and between the brain and body are significantly altered. This disruption can manifest as reduced connectivity in affected areas, while other regions may show increased connectivity as the brain attempts to compensate. For example, the integrity of the corticospinal tract, a major motor pathway, is a predictor of natural functional recovery after SCI in humans.
Cortical reorganization is a notable long-term adaptation where brain maps for body parts below the injury may change or be influenced by other sensory inputs. Studies have shown that cortical representation for spared forelimb stimulation can enlarge and invade adjacent, sensory-deprived hindlimb territory in the primary somatosensory cortex. This brain plasticity, while sometimes beneficial for functional recovery, can also contribute to pathological consequences like phantom sensations or neuropathic pain.
Cognitive and Emotional Impacts
Spinal cord injuries have observable effects on an individual’s mental abilities and emotional state, stemming from the brain changes discussed earlier. Cognitive deficits are common, with many individuals with SCI experiencing some form of cognitive impairment. These deficits often include memory impairment, difficulties with attention and concentration, and problems with executive functions like planning, problem-solving, and decision-making.
The incidence of emotional and mood disorders is also elevated in individuals with SCI. Studies show a higher incidence of anxiety and depressive disorders in adults with SCI. This increased prevalence can be linked to both the psychological impact of the injury and neurobiological changes in the brain, such as altered neurotransmitter systems and changes in limbic system activity.
Chronic fatigue is another significant challenge experienced by individuals with SCI. This type of fatigue is a mental and physical state characterized by excessive tiredness, exhaustion, and lowered mood. Central nervous system changes can contribute to this fatigue, as the brain may fail to adequately drive spinal motor neurons, leading to “central fatigue”. Many adults with SCI report substantial problems with fatigue.
Neurobiological Mechanisms Driving Brain Changes
Several underlying cellular and molecular processes contribute to the observed brain changes after a spinal cord injury. Neuroinflammation plays a significant role, with chronic inflammation originating from the spinal cord injury site. Inflammatory mediators can cross the blood-brain barrier, affecting brain tissue and contributing to neurodegeneration in regions linked to memory and emotions. Microglia, the brain’s resident immune cells, become activated and release cytokines, contributing to inflammation and potentially causing neuronal damage.
Excitotoxicity, the damage to neurons due to overstimulation by neurotransmitters, is another mechanism. After SCI, damaged neural cells can release excessive glutamate, which overstimulates receptors, leading to neuronal cell death. This process can also contribute to delayed white matter degeneration.
Deafferentation, the impact of reduced sensory input from the body below the injury, also influences brain areas that normally receive these signals. This loss of afferent information can lead to reorganization of the nervous system, potentially contributing to conditions like chronic pain. Brain regions like the somatosensory cortex, cingulate cortex, and thalamus are implicated in these changes.
Secondary degeneration refers to the cascade of events triggered by the initial injury that leads to further cell death and damage in connected brain regions over time. This process can expand outwards from the immediate injury site, contributing to progressive degenerative events in the spinal cord and subsequently affecting the brain. These secondary injury processes explain many of the cognitive deficits observed in patients with SCI.