Spinal Cord Compressions


Surgical lesions impacting the spinal cord can be classified as either extradural or intradural. Intradural lesions can be extramedullary or intramedullary. Spinal cord compression can be secondary or primary. The cause of primary spinal cord compressions includes meningeal, nerve root, developmental, or neuroectodermal whereas secondary compressions typically result from carcinomas of the breast, lung, thyroid, and prostate. Other causes of cord compression include neuroblastoma, multiple myeloma, and lymphomas. According to Fortin et al., (2015), the occurrence of spinal cord compression is 3-10 people out of a population of 100,000. This paper presents an analysis of Susan Kennedy, a 65-year old female who was diagnosed and confirmed to have spinal cord compression disorder that occurred because of osteoporotic vertebral fractures of T5-T6.

How the patient’s risk factors are linked to the diagnosed disease’s pathophysiological

Progressive spondylosis is the overall term for progressive alterations that happen in the spine and the main source of non-specific back and neck pain in the older people. When progressive changes cause the spinal canal to narrow, neurologic deficits linked to spinal cord compression, or myelopathy may occur. Stenotic injury on the spinal cord occurs as a result of two activities that’s ischemia associated with damage of venous and arterial components surrounding the spinal cord, and direct compression of the neural elements (Chen & Wang, 2013). Eventually, an increase in vertebral mass causes compression the thecal sac, spinal cord, and spinal vasculature causing neurologic deficits and pain. Besides, the vertebral body damage may lead to a compression abnormality of direct solidity of bony parts of the spinal cord. The most affected part in MSCC is the thoracic spine, then the cervical and lumbar vertebral levels. Thus, the risk factors of spinal cord compression for Susan Kennedy make up an exceptional proportion of spinal malignancy.

How the disease’s pathophysiology manifests to produce all of the patient’s clinical manifestations

Spinal cord compression happens due to a sudden disruption of descending supraspinal pathways. According to Qiao et al., (2017), spinal cord compression involves an occurrence when ischemia, trauma inflammation, or hemorrhage causes abrupt damage of neurological functions under the extent of the damage. Clinically, reduction in the reflex activities and transient loss below the degree of damage, disturbance of motor, hypotonia, autonomic and sensory functions preponderate. To explain the mechanism for the spinal cord compression and ensuing hyperreflexia or return of reflex activity in the patience, some changes took place in motor neurons below the degree of damage.

The changes comprise three key stages, which include a decrease in reflex activity because of reduced spinal motor neuron excitability, voluntary movement or resumption of reflex activity associated with hyperreflexia, and denervation hypersensitivity that result from new synaptic development (Qiao et al., 2017). Subsequently, the motor neuron below the extent of damage is mainly because of either reflex or voluntary control. Consequently, different spasticity levels grow or, in the event of a partial compression, voluntary movement may be recuperated, dependent of the degree of spinal cord damage.

Justification of the diagnostic investigations and treatment modalities listed in the concept map

Spinal cord compression is a disorder that, unless treated promptly or detected early, can result in lasting neurologic damage and may extremely impact Susan Kennedy’s quality of life. Views concerning the assertiveness of the approaches to be employed in the palliative framework are divergent. According to D?nciulescu & Lungulescu (2019), the most commonly applied therapeutic modalities for the treatment of Susan Kennedy’s situation include radiotherapy, surgery, and corticotherapy. The key goal of using corticotherapy is to minimize inflammation and edema in the areas affected by the spinal cord compression. The patient has manifested pain caused directly by tumor intrusion into nearby structures and organs or as a result of the growth of peritumoral edema. The effectiveness of corticotherapy in the treatment of spinal cord compression can be revealed in regards to motor function and pain relief (D?nciulescu & Lungulescu, 2019). Usage of adjuvant high-dose steroid alongside normal radiotherapy can be seen as beneficial; however, it is linked to increasing incidences of severe effects.


Conclusively, spinal cord compression is as an oncologic emergency is capable of adversely affecting the remainder of Susan Kennedy’s life. The disorder developed in the patent due to falling from a seat and as a result pressure was exerted on the spinal cord by a collapsed vertebral body. However, when the disease is detected and managed early, Susan can regain her ambulatory eminence; but, if the diagnosis is done late when neurologic damage has happened already, the likelihood of the patient to regain the impaired functions is very minimal. The treatment for spinal cord compression includes occasional surgery as well as radiation therapy and dexamethasone. Therefore, nursing care is a vital factor in the management of this disorder.


Chen, H., & Wang, X. (2013). Heparin for venous thromboembolism prophylaxis in patients with acute spinal cord injury: a systematic review and meta-analysis. Spinal Cord, 51(8), 596-602. https://doi.org/10.1038/sc.2013.48

D?nciulescu, M., & Lungulescu, C. (2019). Corticotherapy – an important therapeutic method in cancer treatment. Oncolog-Hematolog.Ro, 4(49), 7. https://doi.org/10.26416/onhe.49.4.2019.2736

Fortin, C., Voth, J., Jaglal, S., & Craven, B. (2015). Inpatient rehabilitation outcomes in patients with malignant spinal cord compression compared to another non-traumatic spinal cord injury: A population-based study. The Journal Of Spinal Cord Medicine, 38(6), 754-764. https://doi.org/10.1179/2045772314y.0000000278

Qiao, Y., Peng, C., Li, J., Wu, D., & Wang, X. (2017). Spinal cord ischemia-reperfusion causes the damage of neurocytes by inhibiting RAP2C. Neurological Research, 39(10), 877-884. https://doi.org/10.1080/01616412.2017.1352120

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