Study guidelines
- 1.
Describe the fate of immature neurons during embryonic development within the developing spinal cord (some send out ventral roots, others project along the marginal zone to form fibre tracts) and of the neural crest.
- 2.
Explain the clinical implications of the mature vertebral canal relationship between the spinal column and respective spinal cord level, for example a collapsed T11 vertebra would crush spinal cord segment L1.
- 3.
Contrast the clinical presentation of an injury to S2 to S4 ventral roots of the cauda equina (containing preganglionic parasympathetic fibres vital for bladder and bowel control) or the corresponding posterior roots (contain visceral afferents vital for reflexes).
- 4.
Provide an illustration of how the normal extradural venous plexus could facilitate the spread of an adjacent neoplasm.
- 5.
Discuss how the sense of numbness/tingling in the fingers in later life may result from compression of posterior nerve roots.
- 6.
Explain why for the most common and lowest two levels of disk prolapse, the next spinal nerve is the one likely to be caught.
- 7.
Be able to illustrate the structures traversed during, and the rationale for the site chosen to perform, a lumbar puncture (spinal tap).
Development of the spinal cord
The notochord
By day 17 of embryonic development a small aggregate of cells come together to form a thin rostral/caudal strip known as the notochord . This chord of cells induces the process of neurulation , in which a flattened region of the embryo known as the neural plate rolls up to form the neural tube . The notochord regresses in the adult except for a small portion contributing to the nucleus pulposus of the intervertebral disk.
Cellular differentiation
The neural tube of the embryo consists of a pseudostratified epithelium surrounding the neural canal ( Figure 14.1A ). Dorsal to the sulcus limitans the epithelium forms the alar plate ; ventral to the sulcus it forms the basal plate .
The neuroepithelium contains germinal cells that synthesise DNA before retracting to the innermost ventricular zone , where they divide. The daughter nuclei move outward, synthesise fresh DNA, then retreat and divide again. After several such cycles, postmitotic cells round up in the intermediate zone . Some of the postmitotic cells are immature neurons; the rest are glioblasts , which after further division become astrocytes or oligodendrocytes. Some of the glioblasts form an ependymal lining for the neural canal.
The microglial cells of the central nervous system (CNS) are derived from basophil cells of the blood.
Enlargement of the intermediate zone of the alar plate creates the dorsal horn of grey matter. The dorsal horn receives central processes of dorsal root ganglion cells ( Figure 14.1B ). As explained in Chapter 1 , the ganglion cells are derived from the neural crest.
Partial occlusion of the neural canal by the developing dorsal grey horn gives rise to the dorsal median septum and to the definitive central canal of the cord ( Figure 14.1C ).
Enlargement of the intermediate zone of the basal plate creates the ventral grey horn and the ventral median fissure ( Figure 14.1C ). Axons emerge from the ventral horn and form the ventral nerve roots.
In the outermost marginal zone of the cord, axons run to and from the spinal cord and brain.
Ascent of the spinal cord ( Figure 14.2 )
The spinal cord occupies the full length of the vertebral canal until the end of the twelfth postconceptual week. The sixth to eighth weeks are marked by the regression of the caudal end of the neural tube, to become a neuroglial thread, the filum terminale .
After the twelfth week, the vertebral column grows rapidly and drags the spinal cord upward. The tip of the spinal cord is at the second or third lumbar level (L2 or L3) at the time of birth. The adult level (L1 or L2) is attained 2 months postnatally.
As a consequence of the greater ascent of the lower part of the cord compared to the upper part, the spinal nerve roots show an increasing disparity between their segmental levels of attachment to the cord and the corresponding vertebral levels ( Figure 14.3 ).
Neural arches
During the fifth week, the mesenchymal vertebrae surrounding the notochord give rise to neural arches for the protection of the spinal cord ( Figure 14.4 ). The arches are initially bifid (split). Later, they fuse in the midline and form the vertebral spines.
Conditions where the two halves of the neural arches have failed to unite are collectively known as spina bifida ( Figures 14.5 and 14.6 , Clinical Panel 14.1 ).
Among the more common congenital malformations of the CNS are several conditions included under the general heading spina bifida . The ‘bifid’ effect is produced by failure of union of the two halves of the neural arches, usually in the lumbosacral region ( Figure 14.5 ).
Spina bifida occulta (A) is usually symptom-free, being detected incidentally in lumbosacral radiographs.
In spina bifida cystica a meningeal cyst protrudes through the vertebral defect. In 10% of these cases the cyst is a meningocele containing no nervous elements (B) . In 90%, unfortunately, the cyst is a meningomyelocele , containing either spinal cord or cauda equina (C) ; the lower limbs, bladder, and rectum are paralysed, as in the case illustrated in Figure 14.6 , and meningitis is likely to supervene sooner or later. To make matters worse an Arnold – Chiari malformation ( Chapter 4 ) is almost always present as well.
The most severe form of spina bifida is myelocele (D) , where the neural folds have remained open and CSF leaks on to the surrounding skin. The clinical outlook is very poor.
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