The spinal cord is a long, thin, tubular bundle of nerves that is an extension of the central nervous system from the brain and is enclosed in and protected by the bony vertebral column. The main function of the spinal cord is transmission of neural inputs between the periphery and the brain.
It is about 45 cm long in men and 43 cm long in women, ovoid-shaped, and is enlarged in the cervical and lumbar regions. In cross-section, the peripheral region of the cord contains neuronal white matter tracts containing sensory and motor neurons. Internal to this peripheral region is the gray, butterfly shaped central region made up of nerve cell bodies. This central region surrounds the central canal, which is an anatomic extension of the spaces in the brain known as the ventricles and, like the ventricles, contains cerebrospinal fluid.
The three meninges that cover the spinal cord -- the outer dura mater, the arachnoid mater, and the innermost pia mater -- are continuous with that in the brainstem and cerebral hemispheres. Similarly, cerebrospinal fluid is found in the subarachnoid space. The cord is stabilized within the dura mater by the connecting denticulate ligaments which extend from the enveloping pia mater laterally between the dorsal and ventral roots. The dural sac ends at the vertebral level of the second sacral vertebra.
There are 31 spinal cord nerve segments in a human spinal cord:
Because the vertebral column grows longer than the spinal cord, spinal cord segments do not correspond to vertebral segments in adults, especially in the lower spinal cord. In the fetus, vertebral segments do correspond with spinal cord segments. In the adult, however, the spinal cord ends around the L1/L2 vertebral level, forming a structure known as the conus medullaris. For example, lumbar and sacral spinal cord segments are found between vertebral levels T9 and L2.
Although the spinal cord cell bodies end around the L1/L2 vertebral level, the spinal nerves for each segment exit at the level of the corresponding vertebra. For the nerves of the lower spinal cord, this means that they exit the vertebral column much lower (more caudally) than their roots. As these nerves travel from their respective roots to their point of exit from the vertebral column, the nerves of the lower spinal segments form a bundle called the cauda equina.
There are two regions where the spinal cord enlarges:
Additionally, the floor plate will also secrete netrins. The netrins act as chemoattractants to decussation of pain and temperature sensory neurons in the alar plate across the anterior white commissure where they will then ascend towards the thalamus.
Lastly it is important to note that the past studies of Viktor Hamburger and Rita Levi-Montalcini in the chick embryo have been further proven by more recent studies which demonstrated that the elimination of neuronal cells by programmed cell death (PCD) is necessary for the correct assembly of the nervous system.
Overall, spontaneous embryonic activity has been shown to play a role in neuron and muscle development, but is probably not involved in the initial formation of connections between spinal neurons.
In the dorsal column-medial leminiscus tract, a primary neuron's axon enters the spinal cord and then enters the dorsal column. If the primary axon enters below spinal level T6, the axon travels in the fasciculus gracilis, the medial part of the column. If the axon enters above level T6, then it travels in the fasciculus cuneatus, which is lateral to the fasiculus gracilis.
Either way, the primary axon ascends to the lower medulla, where it leaves its fasiculus and synapses with a secondary neuron in one of the dorsal column nuclei: either the nucleus gracilis or the nucleus cuneatus, depending on the pathway it took.
At this point, the secondary axon leaves its nucleus and passes anteriorly and medially. The collection of secondary axons that do this are known as internal arctuate fibers.. The internal arcuate fibers decussate and continue ascending as the contralateral medial leminiscus.
Secondary axons from the medial leminiscus finally terminate in the ventral posterolateral nucleus (VPL) of the thalamus, where they synapse with tertiary neurons. From there, tertiary neurons ascend via the posterior limb of the internal capsule, and end in the primary sensory cortex.
The anterolateral system works somewhat differently. Its primary neurons enter the spinal cord and then ascend one to two levels before synapsing in the substantia gelatinosa. The tract that ascends before synapsing is known as Lissauer's tract. After synapsing, secondary axons decussate and ascend in the anterior lateral portion of the spinal cord as the spinothalamic tract.
This tract ascends all the way to the VPL where it synapses on tertiary neurons. Tertiary neuronal axons then travel to the primary sensory cortex via the posterior limb of the internal capsule.
It should be noted that some of the "pain fibers" in the ALS deviate from their pathway towards the VPL. In one such deviation, axons travel towards the reticular formation in the midbrain. The reticular formation then projects to a number of places including the hippocampus (to create memories about the pain), to the centromedian nucleus (to cause diffuse, non-specific pain) and various parts of the cortex. Additionally, some ALS axons project to the periaqueductal gray in the pons, and the axons forming the periaqueductal gray then project to the nucleus raphe magnus, which projects back down to where the pain signal is coming from and inhibits it. This helps control the sensation of pain to some degree.
Cortical upper motor neurons originate from Brodmann areas 1, 2, 3, 4, and 6 and then descend in the posterior limb of the internal capsule, through the crus cerebri, down through the pons, and to the medullary pyramids, where about 90% of the axons cross to the contralateral side at the decussation of the pyramids. They then descend as the lateral corticospinal tract. These axons synapse with lower motor neurons in the ventral horns of all levels of the spinal cord. The remaining 10% of axons descend on the ipsilateral side as the ventral corticospinal tract. These axons also synapse with lower motor neurons in the ventral horns. Most of them will cross to the contralateral side of the cord right before synapsing.
The midbrain nuclei include four motor tracts that send upper motor neuronal axons down the spinal cord to lower motor neurons. These are the rubrospinal tract, the vestibulospinal tract, the tectospinal tract and the reticulospinal tract. The rubrospinal tract descends with the lateral corticospinal tract and the remaining three descend with the anterior corticospinal tract.
The function of lower motor neurons can be divided into two different groups: the lateral corticospinal tract and the anterior cortical spinal tract. The lateral tract contains upper motor neuronal axons which synapse on dorsal lateral (DL) lower motor neurons. The DL neurons are involved in distal limb control. Therefore, these DL neurons are found specifically only in the cervical and lumbosaccral enlargements within the spinal cord. There is no decussation in the lateral corticospinal tract after the decussation at the medullary pyramids.
The anterior corticospinal tract descends ipsilaterally in the anterior column where the axons emerge and either synapse on lower ventromedial (VM) motor neurons in the ventral horn ipsilaterally or descussate at the anterior white commissure where they synapse on VM lower motor neurons contralaterally . The tectospinal, vestibulospinal and reticulospinal descend ipsilaterally in the anterior column, but do not synapse across the anterior white commissure. Rather, they only synapse on VM lower motor neurons ipsilaterally. The VM lower motor neurons control the large, postural muscles of the axial skeleton. These lower motor neurons, unlike those of the DL, are located in the ventral horn all the way throughout the spinal cord.
From the levels of L2 to T1, proprioceptive information enters the spinal cord and ascends ipsilaterally, where it synapses in Clarke's nucleus. The secondary neuronal axons continue to ascend ipsilaterally and then pass into the cerebellum via the inferior cerebellar peduncle. This tract is known as the dorsal spinocerebellar tract.
From above T1, proprioceptive primary axons enter the spinal cord and ascend ipsilaterally until reaching the accessory cuneate nucleus, where they synapse. The secondary axons pass into the cerebellum via the inferior cerebellar peduncle where again, these axons synapse on cerebellar deep nuclei. This tract is known as the cuneocerebellar tract.
Spinal cord injuries can be caused by trauma to the spinal column (stretching, bruising, applying pressure, severing, etc... the spinal cord). The vertebral bones or intervertebral disks can shatter, causing the spinal cord to be punctured by a sharp fragment of bone. Usually victims of spinal cord injuries will suffer loss of feeling in certain parts of their body. In milder cases a victim might only suffer loss of hand or foot function. More severe injury may result in paraplegia, tetraplegia, or full body paralysis below the site of injury to the spinal cord.
Damage to upper motor neurons axons in the spinal cord results in a characteristic pattern of ipsilateral deficits. These include hyperreflexia, hypertonia and muscle weakness. Lower motor neuronal damage results in its own characteristic pattern of deficits. Rather than an entire side of deficits, there is a pattern relating to the myotome affected by the damage. Additionally, lower motor neurons are characterized by muscle weakness, hypotonia, hyporeflexia and muscle atrophy.
The two areas of the spinal cord most commonly injured are the cervical spine (C1-C7) and the lumbar spine (L1-L5). (The notation C1, C7, L1, L5 refer to the location of a specific vertebra in either the cervical, thoracic, or lumbar region of the spine.)