1.1 Spinal cord segments
2 Sensory Organization
3 Motor Organization
4 Spinocerebellar Tracts
6 Additional images
8 See also
9 External links
The spinal cord is the main pathway for information connecting the brain and peripheral nervous system. The length of the spinal cord is much shorter than the length of the bony spinal column. The human spinal cord extends from the medulla oblongata and continues through the conus medullaris near the first or second lumbar vertebrae, terminating in a fibrous extension known as the filum terminale.
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.
Spinal cord segments
The human spinal cord is divided into 31 different segments, with motor nerve roots exiting in the ventral aspects and sensory nerve roots entering in the dorsal aspects. The ventral and dorsal roots later join to form paired spinal nerves, one on each side of the spinal cord.
There are 31 spinal cord nerve segments in a human spinal cord:
8 cervical segments (cervical nerves exit spinal column above C1 and below C1-C7)
12 thoracic segments (thoracic nerves exit spinal column below T1-T12)
5 lumbar segments (lumbar nerves exit spinal column below L1-L5)
5 sacral segments (sacral nerves exit spinal column below S1-S5)
1 coccygeal segment (coccygeal nerves exit spinal column at coccyx)
Because the vertebral column grows longer than the spinal cord, spinal cord segments become higher than the corresponding vertebra, especially in the lower spinal cord segments in adults. In a fetus, the vertebral levels originally correspond with the spinal cord segments. In the adult, the cord ends around the L1/L2 vertebral level at the conus medullaris, with all of the spinal cord segments located superiorly to this. For example, the segments for the lumbar and sacral regions are found between the vertebral levels of T9 and L2. The S4 spinal nerve roots arise from the cord around the upper lumbar/lower thoracic vertebral region, and descend in the vertebral canal. After they pass the end of the spinal cord, they are considered to be part of the cauda equina. The roots for S4 finally leave the vertebral canal in the sacrum.
There are two regions where the spinal cord enlarges:
Cervical enlargement – corresponds roughly to the brachial plexus nerves, which innervate the upper limb. It includes spinal cord segments from about C4 to T1. The vertebral levels of the enlargement are roughly the same (C4 to T1).
Lumbosacral enlargement – corresponds to the lumbosacral plexus nerves, which innervate the lower limb. It comprises the spinal cord segments from L2 to S3, and is found about the vertebral levels of T9 to T12.
The spinal cord is made from part of the neural tube during development. As the neural tube begins to develop, the notochord begins to secrete a factor known as Sonic hedgehog or SHH. As a result, the floor plate then also begins to secrete SHH and this will induce the basal plate to develop motor neurons. Meanwhile, the overlying ectoderm secretes bone morphogenetic protein (BMP). This will induce the roof plate to begin to also secrete BMP which will induce the alar plate to develop sensory neurons. The alar plate and the basal plate are separated by the sulcus limitans.
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.
Somatosensory organization is divided into the dorsal column-medial lemniscus tract (the touch/proprioception/vibration sensory pathway) and the spinothalamic tract (the pain/temperature sensory pathway).
Each of these sensory pathways utilizes three different neurons to get information from the sensory receptors to the cerebral cortex. These neurons are designated primary, secondary and tertiary sensory neurons. The primary neuron has its cell body in the dorsal root ganglia and its axon projects into the spinal cord.
In the case of the touch/proprioception/vibration sensory pathway, the primary neuron enters the spinal cord and travels in the dorsal column. Below level T6, the neuron travels in the fasciculus gracilis – the most medial part of the column. Above level T6, the neuron enters the fasciculus cuneatus – lateral to the fasiculus gracilis.
As the primary axons reach the caudal medulla, they leave their respective fasiculi and enter and synapse on secondary neurons within the nucleus gracilis and the nucleus cuneatus, respectively. At this point, the secondary neuronal axons decussate and continue to ascend as the medial leminiscus. They run up to the VPL nucleus of the thalamus,and synapse there on the tertiary neurons. From there, the tertiary neurons ascend via the posterior limb of the internal capsule to the post central gyrus, or Brodmann area 3,1,2.
The pain/temperature sensory pathway differs from that of the touch/proprioception/vibration pathway. The pain neurons enter as primary neurons and ascend 1-2 levels before synapsing in the substantia gelatinosa. The tract that ascends those 1-2 levels before synapsing is known as Lissauer’s tract. After synapsing, the secondary neurons decussate and ascend as the spinothalamic tract in the anterior lateral portion of the spinal cord. Hence, the spinothalamic tract is also known as the anterior lateral system (ALS). The tract ascends all the way to the VPL of the thalamus where it synapses on the tertiary neurons. The tertiary neuronal axons then project via the posterior limb of the internal capsule to the post-central gyrus or Broadmann area 3,1,2.
It should be noted that the pain fibers in the ALS can also deviate in their pathway towards the VPL. In one pathway, the axons project 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 places in the cortex. Additionally, neurons project to the periaqueductal gray in the pons. The neurons form 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 reduces the pain sensation to some degree.
Upper motor neuronal input comes from the cerebral cortex and from primitive brain stem nuclei. Cortical upper motor neurons originate in Brodmann areas 4, 6, 3, 1 and 2. They then descend through the genu and the posterior limb of the internal capsule. This pathway is known as the corticospinal tract. After passing through the internal capsule, the tract descends through the cerebral peduncles, down through the pons and to the medullary pyramids. At this point, ~85% of these upper motor neuronal axons decussate. These fibers then descend as the lateral corticospinal tract. The remaining ~15% descend as the anterior corticospinal tract.
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.
Proprioceptive information in the body travels up the spinal cord via three tracts. Below L2 the proprioceptive information travels up the spinal cord in the ventral spinocerebellar tract. Also known as the anterior spinocerebellar tract, sensory receptors take in the information and travel into the spinal cord. The cell bodies of these primary neurons are located in the dorsal root ganglia. In the spinal cord, the axons synapse and the secondary neuronal axons decussate and then travel up to the superior cerebellar peduncle where they decussate again. From here, the information is brought to deep nuclei of the cerebellum including the fastigial and interposed nuclei.
From the levels of L2 to T1, the proprioceptive information enters the spinal cord and ascends ipsilaterally where it synapses in the Dorsal Nucleus of Clark. The secondary neuronal axons continue to ascend ispilaterally and enter the pass into the cerebellum via the inferior cerebellar peduncle. This tract is known as the dorsal spinocerebellar tract and also as the posterior 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.
Main article: Spinal cord injury
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.)