Spinal Cord - Introduction

Tutorial 15: Spinal Cord

Part 1: Image-Mapped Tutorial
Part 2: Matching Self-Test
Part 3: Multiple-Choice Self-Test

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The spinal cord was the first gross structure studied from a Western historical perspective, providing insights into the organization of functions within the central nervous system. It is a long cylindrical-like, structure with a diameter similar to that of the adult little finger. The spinal cord is located within the vertebral column or spinal column, and it relays information between structures found outside and inside the central nervous system. When looking down on a slice through the spinal cord (a cross-sectional view) one sees a greyish colored, H or butterfly-shaped region at the center of the cord surrounded by material of lighter color.

The spinal cord extends from the opening into the skull, called the foramen magnum, to the upper part of the lumbar region of the vertebral column. Along this length emerge 31 pairs of nerves that pass out between the vertebrae via holes called spinal foramens. Sensory (afferent or toward the brain) and motor information (efferent or away from the brain) pass to and from either side of the body through these spinal nerves. There are 8 cervical (located in the neck), 12 thoracic (located in the chest), 5 lumbar (located in the lower back), 5 sacral (located in the pelvic region), and 1 coccygeal (located in the inferior pelvic area) spinal nerves. The vertebrae at the sacral and coccygeal levels are fused. In addition to relaying sensory and motor control information between the peripheral and central nervous systems, the spinal cord contains the important neuronal connections that underlie our protective motor reflexes.

The spinal cord is approximately 2/3rds the length of the vertebral column. The space within the vertebral column below the inferior edge of the spinal cord is filled by a collection of spinal roots called the cauda equina, meaning "horse's tail". For certain surgical procedures involving the pelvic region and childbirth, an anesthetic is injected into the space surrounding the cauda equina, thus blocking the transmission of sensory and motor information of nerves composing the cauda equina. This procedure is called a caudal block.

Tutorial 15 illustrates and describes the basic structure and function of this important relay system.

Advanced

One of the first major discoveries about the nervous system was the observation that the dorsal region of the spinal cord carries sensory information, while the ventral region is related to motor function. This discovery is called the Bell-Magendie Law after the two men who were jointly responsible for this discovery (Gregory, 1987). Sir Charles Bell was a Scottish born anatomist and surgeon who practiced in London, England during the early 19th century. Bell's contemporary, Francois Magendie, was a French physiologist who studied and practiced medicine in Paris. It is generally thought that in 1822 Magendie provided the final proof and elaboration of the work originated by Bell. With the work of both of these scientists, the concept of localization of function in the nervous system emerged.

Injury to the spinal cord was once an irreversible condition. As mentioned elsewhere, the axons severed in the central nervous system do not have the capacity to regenerate effectively, as do the axons of peripheral neurons. Until recently, treatment of trauma to the spinal cord was limited to physically stabilizing the injured individual to prevent additional destruction, the treatment of secondary infections, and eventual physical therapy to maximize the capabilities that remained (Behar, Mizuno, Neumann & Woolf, 2000; Girardi, Khan, Cammisa, & Blanck, 2000).

The initial area of damage to the spinal cord may be small and limited to severed neurons and demyelination of axons (Kakulas, 1999). Secondary processes, however, extend the injury. Cysts, or fluid-filled sacs, form in the region of cell death and damage. These cysts block the migration of neurons under repair. Glial cells cluster about these cysts forming "scars" that release agents that inhibit the growth of axons. Research is underway to find therapies that may be effective in reducing the posttraumatic events that block effective repair and restoration of function following spinal cord damage. For example, damage following spinal cord trauma might be minimized when a steroid drug called methylprednisolone is administered within 8 hours following the damage (Bracken, 2000; Short, El Masry & Jones, 2000). Another approach being researched is the possibility of enhancing mechanisms that support cellular repair. These include the ability to compensate for the demyelination process (Shields, Schaecher, Hogan & Banik, 2000), promote regeneration of axons (Kakulas, 1999; Wroblewski, Roomans & Kozlova, 2000), guide regenerating axons to their appropriate targets (Butt & Berry, 2000), prevention of the spread of damage (Robertson, Crocker, Nicholson & Schulz, 2000), and the replacement of damaged cells (Behar, Mizuno, Neumann & Woolf, 2000). In addition, much effort has gone into the development of strategies to compensate for spinal cord damage. Electronic systems that can regulate motor movement by electrical stimulation of implanted wires have been used to restore some hand movements and bladder and bowel control. The ability to grasp objects with the hand has been restored in part by detaching the tendons of forearm muscles controlling finger movements and reattaching them to arm muscles regulated by undamaged regions of the spinal cord.

The incidence of sudden, traumatic spinal cord injury is quite high, approximately 1/4 of a million people in the United States are so affected, and the majority of these cases involve young adults. The cost is high worldwide.

References

Behar, O., Mizuno, K., Neumann, S. & Woolf, C.J. (2000). Putting the spinal cord together again. Neuron, 26(2), 291-293.

Bracken, M.B. (2000). Methylprednisolone and spinal cord injury. Journal of Neurosurgery, 93(1 Suppl.), 175-179.

Butt, A.M. & Berry, M. (2000). Oligodendrocytes and the control of myelination in vivo: new insights from the rat anterior medullary velum. Journal of Neuroscience Research, 59(4), 477-488.

Girardi, F.P., Khan, S.N., Cammisa, Jr., F.P. & Blanck, T.J. (2000). Advances and Strategies for Spinal Cord Regeneration. Orthopedic Clinics of North America, 31(3), 465-472.

Gregory, R.L. (1987). Bell, Megendie and Reflex Action. In The Oxford Companion to the Mind (pp. 77-79, 445, 676-677). New York: Oxford University Press.

Kakulas, B.A. (1999). A review of the neuropathology of human spinal cord injury with emphasis on special features. Journal of Spinal Cord Medicine, 22(2), 119-124.

Robertson, G.S., Crocker, S.J., Nicholson, D.W. & Schulz, J.B. (2000). Neuroprotection by the inhibition of apoptosis. Brain Pathology, 10(2), 283-292.

Shields, D.C., Schaecher, K.E., Hogan, E.L. & Banik, N.L. (2000). Calpain activity and expression increased in activated glial and inflammatory cells in penumbra of spinal cord injury lesion. Journal of Neuroscience Research, 61(2), 146-150.

Short, D.J., El Masry, W.S. & Jones, P.W. (2000). High dose methylprednisolone in the management of acute spinal cord injury - a systematic review from a clinical perspective. Spinal Cord, 38(5), 273-286.

Wroblewski, R., Roomans, G.M. & Kozlova, E.N. (2000). Effects of Dorsal Root Transection on Morphology and Chemical Composition of Degenerating Nerve Fibers and Reactive Astrocytes in the Dorsal Funiculus. Experimental Neurology, 164(1), 236-245.

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Tutorial 15: Spinal Cord

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