[1] The lack of fenestrations and endocytic vesicles reflects the restricted transcellular flow, while the increased number of mitochondria contributes to a high metabolic rate in these endothelial cells.
They release secretory compounds that influence the phenotype of endothelial cells and express aquaporin and potassium channels that help regulate ion concentration and fluid volume within the spinal cord.
[1][4] Research shows that the BSCB plays a significant role in the development and progression of neurodegenerative diseases, spinal cord injury, pain conditions, and other disorders that affect the CNS.
This impact disrupts the capillaries around the spinal cord and initiates many pathophysiological cascades by allowing the molecules and cells within the bloodstream to enter nervous tissue.
Because of this sudden infiltration of normally absent particles, an inflammatory response is triggered by astrocytes and microglia that extends the initial injury into previously uncompromised segments of cord.
[6] Because the disruption of the BSCB is a major exacerbating factor in SCIs, reestablishment of normal function is critical to reducing the severity of injury outcomes.
For example, if the initial injury includes excessive separation of the basement membrane from the blood vessels, a space is created that can accommodate more immune cells and thus propagate damaging inflammation.
[9] Inflammation, compromised tight junctions, and oxidative stress are all contributors to a severe complication of SCI called post-traumatic syringomyelia.
In post-traumatic syringomyelia, the structural and function loss of integrity of the BSCB encourages the development of fluid filled cysts within the spinal cord, causing pain and worsening disability.
[citation needed] Amyotrophic lateral sclerosis (ALS) is a chronic, progressive, and ultimately fatal neurodegenerative disease that is caused by the death of motor neurons in the brain and spinal cord.
[10] Regardless of whether the cause is idiopathic or genetic, ALS is associated with significant dysfunction of the endothelium and basement membrane of the CNS, with the BSCB being more effected than the BBB.
[10][12][13] Multiple sclerosis (MS), a neurodegenerative, autoimmune disease that deteriorates the myelin sheath coating axons and causes permanent damage to nerves, has also been associated with capillary and barrier dysfunction.
[14] Many studies support the idea that CNS barrier disruption precedes MS, particularly through altered tight junction protein expression.
Weakened tight junctions cause fragility in the barrier that can lead to immune system invasion, demyelination, and axonal damage.
[1] Many conditions can cause neuropathy, including diabetes, HIV, SCI, transverse myelitis, MS, amputation, peripheral nerve pain.
At its core, neuropathy occurs when the central excitatory and inhibitory nerves in the somatosensory system are altered in some way, as this leads to dysfunctional sensory signaling.
It results in increased BSCB permeability that allows white blood cells to migrate into the spinal cord, where they can release mediators that alter function.
[24] Most pharmaceutical research involving the BSCB aims to find efficient methods of overcoming its barrier mechanism to improve drug delivery.
However, hyperosmolarity may also be of use in drug delivery since it causes the membranes of endothelial cells to shrink, resulting in tight junctions stretching and paracellular gaps widening.