The Facts on Spinal Cord Injuries
Spinal cord injuries (SCI) involve different cellular elements, blood networks and membranes present in the cord itself. If disruption in the integrity of the cord occurs, the body encounters serious complications that have fatality risks.
Anatomically, the spinal cord extends from the opening of the foramen magnum to the first two lumbar columns of the backbone (L1 to L2). The spinal cord is composed of several neurologic pathways and cellular elements (e.g. preganglionic sympathetic neurons, somatomotor neurons, etc.) most expressed in its white and gray matter. By structure and consistency, spinal cord is a delicate branch of neural fibers controlling mainly the motor sympathetic and parasympathetic functions of the body, and with its soft structural property, spinal cord is indeed at risk of several traumatic injuries. Trauma, malformations and diseases are some of the most common physiological conditions that cause SCI. According to Lobato, Gravenstein and Kirby (2007), the average age of the patient that can possess high risk of SCI occurrences is 32.3 years of age, and the typical causes are usually traumatic accidents (e.g. vehicular accidents, physical trauma, etc.). SCI result from vertebral shearing or stretching of the neural elements involving any of the cervical vertebrae 5, 6 and 7; thoracic vertebra 12 and the lumbar vertebra (Madara and Pomarico-Deniro, 2008 p.137). Neural damages during traumatic cases of SCI can affect motor and sensory function, reflex activity and muscle control. The discussion centers in the pathophysiological concepts involving cellular mechanisms, spinal cord recovery and protective mechanisms utilized by the cord itself.
Spinal Cord Injury
Statistically, there are approximately 10,000 to 20,000 severe cases of SCI occurring each year only in the United States (Madara and Pomarico-Deniro, 2008 p.134). SCI cases are usually triggered by compressed blood flow in the spine, slipped-disks, columnar trauma directed to the cord, over stretching of the back and ligament injuries. According to Lobato, Gravenstein and Kirby (2007), non-traumatic SCIs among older aged individuals (60 years old and above) result from degenerative spice conditions, ischemia, demyelination, inflammation and extrinsic neoplastic, hemorrhagic or pyogenic masses (p.387). Madara and Pomarico-Deniro (2008), the most common complications of SCI include spinal shock, autonomic hyperreflexia and respiratory failure (p.134). According to Lobato, Gravenstein and Kirby (2007), the most commonly affected area of the spinal cord is on the weakest columnar area present in the neck region (C5 to C6) (p.134).
Considering the different traumatic insults directed to the cord of an SCI patient (e.g. transaction, compression, distraction, stretching, etc.), Vaccaro () emphasizes the value of determining (1) the amount of impact energy applied to the cord, (2) the pre-injury space available for the cord, and (3) medical comorbidities associated to the impact, which all provide basis in understanding the pattern and assessing the degree of neurological trauma following the insult (p.15). According to the WHO, SCIs are commonly caused by traumatic injuries such as motor vehicle accidents (55%), sports injuries (18%), and penetrating injuries from either stab or gunshots (15%) (Madara and Pomarico-Deniro, 2008 p.134).
Types of Cells in the Spinal Cord
Cellular responses are the immediate action utilized by the body to counter the progressive effects of SCI. According to Seeley, Stephens and Tate (2004), the body comprises of different cells found most prominently in the CNS’ brain centers and spinal cord (p.200). The following cells present in the spinal cord are (1) astrocytes – the star shaped cells that provide structural support in the blood-brain barrier and neural cord fibers, (2) ependymal cells – squamous epithelial that facilitate the circulation of cerebrospinal fluid (CSF) in the cord, (3) Microglia – the antibody centers of the spinal cord acting against foreign materials and sites of infection, and (4) oligodendrocytes – forms myelin sheaths to insulate neural pathways (Seeley, Stephens and Tate, 2004 p.201). Maintenance cells, such as astrocytes, ependymal and oligodendrocytes, form part in the homeostasis and nerve exchange of both sensory and motor nerve fibers in the spinal cord.
According to Selzer and Cohen (2006), SCI initially inflicts its damage towards these surfacing oligodendrocytes and astrocytes since these are the membranous external layers initially affected prior to internal nerve damage (p.11). Lobato, Gravenstein and Kirby (2007) mention three significant phases of SCI damage infliction: (a) initial injury – mechanical trauma is directed to the cord through shearing, stretching, compression, hemorrhage, etc, (b) secondary injury – triggering bodily responses against the injury (e.g. Ischemic calcium release, inflammatory symptoms due to microglial action, and exicito-toxic cellular response, etc.), and (c) lastly, apoptosis or cell death (p.388). Selzer and Cohen (2006) add that membrane-producing cells, especially oligodendrocytes, degenerate in response to SCI demyelinating axon fibers of nerve cells and eventually causing serious neural complications of the body (p.11). Inflammatory responses brought by the systemic leukocytes and microglial macrophages prevent further spread of infection in the surrounding areas of the wound site (Seeley, Stephens and Tate, 2004 p.201). Meanwhile, according to Kalb and Strittmatter (1999), astrocytes – the reactive inhibitory cells – proliferate and hypertrophy around the injured site (process known as astrogliosis) in order to strengthen immunoreactivity increasing the potency of immunologic response directed to the wound site (p.121). Even so, damages directed by SCI to these cells are still reversible, but injuries on the spinal nerves themselves are considered irreversible due to the ultimately slow-phased nerve regeneration process (Vacarro, 2002 p.16). Apoptotic spinal cells brought by SCI are usually replaced by extensive myelination produced by oligodendrocytes during recovery process.
The Pathophysiology behind the Damaged Neural Systems
Pathophysiological events occurring prior, during and after the occurrence of SCI are crucial in planning health care interventions for the patient. Lobato, Gravenstein and Kirby (2007) mention, “ at the time of injury, the initial disruption of spinal cord blood vessels causes a loss of autoregulation and altered autonomic tone” (p.387). During the initial phase of injury, the body first detects the affected motor or sensory areas branching from the injured spinal area. The usual symptoms manifested in this scenario are subsequent hypotension, neuronal hypoxia (due to calcium release directed to the neurons), vasospasms, and activation of membrane phospholipases (Lobato, Gravenstein and Kirby, 2007 p.387). Due to the local release of these biochemicals, cellular membrane in the affected area breaks down to form free radicals.
Due to this physiological formation, autoimmune responses are triggered by the body enacting against the impending infection brought by the infection site. Considering the developing pressure in the wound site, the pressure centers of the hypothalamus trigger bodily responses to decrease blood pressure minimizing eventually blood-CSF compressions (Madara and Pomarico-Deniro, 2008 p.135). In the process of body compromised coping mechanisms and response to the wound site, cellular mediated cells are the most immediate buffers available to counter the effects of infection and progressive damage. According to Kalb and Strittmatter (1999), astrocytes act as the emergency cellular buffer that initiates the build-up of neural surface area countering the potential effects of chemical activation (e.g. phospholipases, interleukin inflammatory responses, etc.) (p.121). Meanwhile, oligodendrocytes increase demyelination of damaged axon fibers to prevent further damage in the neural networks. Microglial cells, together with leukocyte macrophages, engulf foreign microbodies preventing further contamination in the surrounding wound area. Cellular-mediated response during SCI cases is indeed an important component in providing emergency life-saving support for the body of the wounded individual.
SCI case is a serious condition that can be fatal at any point following its occurrence. However, due to the bodies’ cellular mediated response, an emergency bodily mechanism targets the progressing infection, increasing inflammatory response and contamination of the surrounding wound area. Physiologically, blood centers of the body (e.g. hypotension response, etc.), neural networks (e.g. myelination of neural pathways, etc.) and antibodies in the cord exist to prevent the fatal damages of SCI.
Kalb, R. G., & Strittmatter, S. M. (1999). Neurobiology of Spinal Cord Injury. Cambridge, U.K: Humana Press.
Lobato, E. B., Gravenstein, N., & Kirby, R. R. (2007). Complications in Anesthesiology. New York, U.S.A: Lippincott Williams & Wilkins.
Madarra, B., & Pomarico-Denino, V. (2008). Pathophysiology: Pathophysiology. New York, U.S.A: Jones & Bartlett Publishers.
Seeley, R. R., Stephens, T. D., & Tate, P. (2004). Essentials of Anatomy and Physiology: Essentials of Anatomy & Physiology. New York, U.S.A: McGraw-Hill Higher Education.
Selzer, M., & Cohen, L. (2006). Textbook of Neural Repair and Rehabilitation: V.1 Neural Repair and Plasticity, V.2 Medical Neurorehabilitation. Cambridge, U.K: Cambridge University Press.
Vacarro, A. R. (2002). Fractures of the Cervical, Thoracic, and Lumbar Spine. New York, U.S.A: Informa Health Care.