Advanced Oncology Certified Nurse Practitioner (AOCNP) Certification Practice Test 2025 - Free AOCNP Practice Questions and Study Guide

The presence of neurological deficits in spinal cord compression primarily stems from the compression of the venous plexus and axonal swelling. When the spinal cord is compressed, it not only affects the neuronal structures directly but also disrupts the blood supply and drainage to the region, particularly through the venous plexus. This interruption leads to increased venous pressure and stasis of blood flow, causing neuronal edema and axonal swelling. The resulting swelling can impair the conduction of electrical signals along the neurons, leading to various neurological deficits, such as weakness, sensory changes, or autonomic dysfunction.

Furthermore, the cascading effects of this compression can result in ischemia of the spinal cord tissues due to the compromised blood supply. Understanding how the compression affects both blood flow and neuronal integrity is critical in managing patients with spinal cord compression, as it highlights the urgency of addressing the underlying cause to prevent permanent neurological damage.

While other factors like enlarged tumor cells, increased cerebrospinal fluid, and direct tumor invasion can also impact spinal cord function, they are less directly tied to the acute neurological deficits seen with compression. The primary mechanism of axonal swelling and venous compression provides a clearer pathway to understanding how these deficits arise in these clinical scenarios.