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This injury to the spinal cord would result in several different consequences to the cells and functioning of the spinal cord. For example, the severing of the axons of the neurons in the affected region would greatly impact the communication between the brain and the muscles. Thus, this will impede the transmission of sensory signals to the brain, as well as motor signals coming from the brain. Also, the death of oligodendrocytes would result in a lack of myelination in any pathways that did remain. This would greatly impede the function of any remaining connections, as action potentials cannot be conducted as efficiently in the absence of myelin. Therefore, signals will move slower and will of often not reach their targets. Astrocytes would also be impacted by this injury. In response to the damage astrocytes would extend their processes and divide to form a protective barrier referred to as a glial scar around the site of the injury. This inhibits the ability of the neurons to regenerate. Microglia would function to remove dead cells and debris from the site following an injury.
The corticospinal tract and the spinothalamic tract would be impacted by this injury. The dorsal column medial lemniscus pathway would not be affected by this injury, as the dorsal white matter remains intact. You would want to access the patient on their ability to move their limbs as well as their sensation to touch and pain at areas below the site of the injury. You could do this by testing fine touch on their arm by presenting a nonpainful stimuli. You could then test pain perception with a painful stimulus such as a prick. Motor function can be assessed by asking the patient to raise their shoulders. Based on this particular injury, I would predict that the patient would have a loss of pain sensation on both sides of the body as well as the inability to move parts of the body below the site of the injury. This is because the areas of the spinal cord in which the spinothalamic tract, which conveys pain and temperature signals, and the corticospinal tract, which carries motor signals from the brain to the muscles, are located would both be impaired on both sides of the spinal cord.
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As the dorsal column lemniscus pathway appears to be undamaged I would imagine that the patient would not experience any loss of touch sensation. The damage is to C4 which corresponds to the neck, C5 which corresponds to the upper arms, and C6 which corresponds to the lateral forearm and the thumb. Each of these levels also correspond to a specific myotome which is the group of muscles that is innervated by that specific nerve root. C4 contains muscles responsible for shoulder innervation including the diaphragm, trapezius, levator scapula, scalenus anterior & medius. C5 is responsible for shoulder abduction and contains the Rhomboid major & minor, deltoid, supraspinatus, infraspinatus, teres minor, biceps, scalene anterior & medius. C6 is responsible the wrist extension and the flexing of the elbow, it includes the serratus anterior, latissiumus dorsi, subscapularis, teres major, pectoralis major (clavicular head) biceps brachii, coracobrachialis, brachioradialis, supinator, extensor carpi radialis longus, scalenus anterior, medius & posterior. Therefore, this injury would result in the loss of pain perception and paralysis of the muscles at any point below C4. Meaning the patient would not feel any pain below the neck and would be unable to move any muscles below the shoulder. The paralysis is likely to be flaccid from C4 to C6 and spastic below C6.
Immediately following a spinal cord injury, there is likelihood of bleeding and spinal shock, and there may also be immediate cell death depending on the extent of the injury. As the injury progresses a series of biochemical events is triggered in which the damage becomes more extensive and more cell death occurs. This includes a reduction of blood flow to the spinal cord which can directly result in additional cell death. There is also an excess of neurotransmitters, such as glutamate and aspartate, released, which causes additional damage by overstimulating the cells. Additionally, there is an overproduction of free radicals that occurs, that have the potential to damage structures including the cell membranes of neurons. There is also an immune response that occurs. As a result of damage to the blood brain barrier, white blood cells have the ability to enter the central nervous system at the site of the injury, which can then trigger an inflammatory response that results in even more cell death. The associated immune response can also result in programmed cell death by apoptosis, specifically in the oligodendrocytes. Loss of these cells results in loss of myelination on any remaining axons at the injury site. Finally, astrocytes proliferate and extend in order to form a physical barrier around the injury known as a glial scar. The glial scar also acts as a chemical barrier and releases inhibiters such as CSPGs, which makes axon regeneration even more difficult.
My strategy would target the inhibitory activity of chondroitin sulfate proteoglycans (CSPGs) that are released from astrocytes at the glial scar. As CSPGs released by astrocytes at the glial scar have been proven to have an inhibitory impact on axonal regeneration, my proposed strategy would involve the injection of some drug, containing an active ingredient that would target and neutralize the impact of this inhibitor. The best way to accomplish this would be to use an enzyme that could break down CSPGs to an inactive form. For example, studies have shown that the enzyme chondroitinase ABC breaks down the side chains of CPSGs rendering it inactive, and therefore helping to promote the regeneration of axons in the CNS (Bradbury et al., 2002). When injected into mice with spinal cord damage at C4, this treatment showed to be effective at promoting axonal growth and restoring functional connections in the spinal cord CNS (Bradbury et al., 2002).
I would use this therapy immediately after the injury occurred, or as soon as it is possible to do so. Other studies demonstrated the most success when injecting the enzyme directly to the lesion every other day for approximately 10 days following the injury. When using this therapy, I would follow this model. The patient would remain hospitalized for the duration of the treatment and would receive the injected enzyme directly into the spinal cord every other day for 10 days following the injury.
This strategy involves preventing the apoptotic cell death that occurs as part of the immune response in the secondary phases of a spinal cord injury. The apoptotic cell death that occur after a spinal cord injury has been proven to be associated with the function of the protein caspase 3, a member of the cysteine-aspartic acid protease family. It has been previously demonstrated that caspase 3 is activated by the immune response that occurs following a spinal cord, specifically cytokines. This protein sets off a cascade of biochemical events that results in programmed cell death of additional neurons and especially of oligodendrocytes. Therefore, by injecting the patient with an inhibitor of caspase 3, you can prevent the additional cell death and limit the damage of the injury. Previous studies have had success using the caspase inhibitor z-DEVD-fmk, which is a cell permeable fluoromethyl ketone (Zhao, Wei, et al, 2019). In rats with lesioned spinal cords this treatment demonstrated a significant decrease in apoptosis and helped to improve functional recovery (Zhao, Wei, et al, 2019).
I would recommend this treatment as close to the time of the injury as possible in order to maintain as many functioning cells as possible. This treatment should be done in a hospital and would consist of the injection of this caspase 3 inhibitor directly into the spinal cord at the injury.
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