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Spinal cord
The spinal cord shown in yellow extends through most of the length of the vertebral column to connect the brain with peripheral nerves.
Details
Part ofCentral nervous system
ArterySpinal artery
VeinSpinal vein
Identifiers
Latinmedulla spinalis
MeSHD013116
NeuroNames22
TA98A14.1.02.001
TA26049
FMA7647
Anatomical terminology

The spinal cord is a long, thin, tubular structure made up of nervous tissue that extends from the medulla oblongata in the lower brainstem to the lumbar region of the vertebral column (backbone) of vertebrate animals. The center of the spinal cord is hollow and contains a structure called the central canal, which contains cerebrospinal fluid. The spinal cord is also covered by meninges and enclosed by the neural arches. Together, the brain and spinal cord make up the central nervous system.

In humans, the spinal cord is a continuation of the brainstem and anatomically begins at the occipital bone, passing out of the foramen magnum and then enters the spinal canal at the beginning of the cervical vertebrae. The spinal cord extends down to between the first and second lumbar vertebrae, where it tapers to become the cauda equina. The enclosing bony vertebral column protects the relatively shorter spinal cord. It is around 45 cm (18 in) long in adult men and around 43 cm (17 in) long in adult women. The diameter of the spinal cord ranges from 13 mm (1⁄2 in) in the cervical and lumbar regions to 6.4 mm (1⁄4 in) in the thoracic area.

The spinal cord functions primarily in the transmission of nerve signals from the motor cortex to the body, and from the afferent fibers of the sensory neurons to the sensory cortex. It is also a center for coordinating many reflexes and contains reflex arcs that can independently control reflexes.[1] It is also the location of groups of spinal interneurons that make up the neural circuits known as central pattern generators. These circuits are responsible for controlling motor instructions for rhythmic movements such as walking.[2]

Structure

[edit]
Parts of human spinal cord
1 central canal
2 posterior median sulcus
3 gray matter
4 white matter
5 dorsal root (left),
dorsal root ganglion (right)
6 ventral root
7 fascicles
8 anterior spinal artery
9 arachnoid mater
10 dura mater
Sectional organization of spinal cord

The spinal cord is the main pathway for information connecting the brain and peripheral nervous system.[3][4] Much shorter than its protecting spinal column, the human spinal cord originates in the brainstem, passes through the foramen magnum, and continues through to the conus medullaris near the second lumbar vertebra before terminating in a fibrous extension known as the filum terminale.

The human spinal cord is an estimated 45 centimetres (18 inches) long in average-height males and about 43 cm (17 in) in average-height females.[citation needed] It is ovoid-shaped and is enlarged in the cervical and lumbar regions. The cervical enlargement, stretching from the C4 to T1 vertebrae, is where sensory input comes from and motor output goes to the arms and trunk. The lumbar enlargement, located between T10 and L1, handles sensory input and motor output coming from and going to the legs.

The spinal cord is continuous with the caudal portion of the medulla, running from the base of the skull to the body of the first lumbar vertebra. It does not run the full length of the vertebral column in adults. It is made of 31 segments from which branch one pair of sensory nerve roots and one pair of motor nerve roots. The nerve roots then merge into bilaterally symmetrical pairs of spinal nerves. The peripheral nervous system is made up of these spinal roots, nerves, and ganglia.

The dorsal roots are afferent fascicles, receiving sensory information from the skin, muscles, and visceral organs to be relayed to the brain. The roots terminate in dorsal root ganglia, which are composed of the cell bodies of the corresponding neurons. Ventral roots consist of efferent fibers that arise from motor neurons whose cell bodies are found in the ventral (or anterior) gray horns of the spinal cord.[5]

The spinal cord (and brain) are protected by three layers of tissue or membranes called meninges, that surround the canal. The dura mater is the outermost layer, and it forms a tough protective coating. Between the dura mater and the surrounding bone of the vertebrae is a space called the epidural space. The epidural space is filled with adipose tissue, and it contains a network of blood vessels. The arachnoid mater, the middle protective layer, is named for its open, spiderweb-like appearance. The space between the arachnoid and the underlying pia mater is called the subarachnoid space. The subarachnoid space contains cerebrospinal fluid, which can be sampled with a lumbar puncture, or "spinal tap" procedure. The delicate pia mater, the innermost protective layer, is tightly associated with the surface of the spinal cord. 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.

In cross-section, the peripheral region of the cord contains neuronal white matter tracts containing sensory and motor axons. Internal to this peripheral region is the grey matter, which contains the nerve cell bodies arranged in the three grey columns that give the region its butterfly-shape. This central region surrounds the central canal, which is an extension of the fourth ventricle and contains cerebrospinal fluid.

The spinal cord is elliptical in cross section, being compressed dorsolaterally. Two prominent grooves, or sulci, run along its length. The posterior median sulcus is the groove in the dorsal side, and the anterior median fissure is the groove in the ventral side.

Segments

[edit]
Diagram of the spinal cord showing segments
Spinal cord segments and spinal nerves, spinal cord detail, and spinal meninges and conus medullaris

The human spinal cord is divided into segments where pairs of spinal nerves (mixed; sensory and motor) form. Six to eight motor nerve rootlets branch out of right and left ventrolateral sulci in a very orderly manner. Nerve rootlets combine to form nerve roots. Likewise, sensory nerve rootlets form off right and left dorsal lateral sulci and form sensory nerve roots. The ventral (motor) and dorsal (sensory) roots combine to form spinal nerves (mixed; motor and sensory), one on each side of the spinal cord. Spinal nerves, with the exception of C1 and C2, form inside the intervertebral foramen. These rootlets form the demarcation between the central and peripheral nervous systems.[6]

Generally, the spinal cord segments do not correspond to bony vertebra levels. As the spinal cord terminates at the L1–L2 level, other segments of the spinal cord would be positioned superior to their corresponding bony vertebral body. For example, the T11 spinal segment is located higher than the T11 bony vertebra, and the sacral spinal cord segment is higher than the L1 vertebral body.[7]

The grey columns, (three regions of grey matter) in the center of the cord, is shaped like a butterfly and consists of cell bodies of interneurons, motor neurons, neuroglia cells and unmyelinated axons. The anterior and posterior grey columns present as projections of grey matter and are also known as the horns of the spinal cord.

The white matter is located outside of the grey matter and consists almost totally of myelinated motor and sensory axons. Columns of white matter known as funiculi carry information either up or down the spinal cord.

The spinal cord proper terminates in a region called the conus medullaris, while the pia mater continues as an extension called the filum terminale, which anchors the spinal cord to the coccyx. The cauda equina ("horse's tail") is a collection of nerves inferior to the conus medullaris that continue to travel through the vertebral column to the coccyx. The cauda equina forms because the spinal cord stops growing in length at about age four, even though the vertebral column continues to lengthen until adulthood. This results in sacral spinal nerves originating in the upper lumbar region. For that reason, the spinal cord occupies only two-thirds of the vertebral canal. The inferior part of the vertebral canal is filled with cerebrospinal fluid and the space is called the lumbar cistern.[8]

Within the central nervous system (CNS), nerve cell bodies are generally organized into functional clusters, called nuclei, their axons are grouped into tracts.

There are 31 spinal cord nerve segments in a human spinal cord:

  • 8 cervical segments forming 8 pairs of cervical nerves (C1 spinal nerves exit the spinal column between the foramen magnum and the C1 vertebra; C2 nerves exit between the posterior arch of the C1 vertebra and the lamina of C2; C3–C8 spinal nerves pass through the intervertebral foramen above their corresponding cervical vertebrae, with the exception of the C8 pair which exit between the C7 and T1 vertebrae)
  • 12 thoracic segments forming 12 pairs of thoracic nerves
  • 5 lumbar segments forming 5 pairs of lumbar nerves
  • 5 sacral segments forming 5 pairs of sacral nerves
  • 1 coccygeal segment
Spinal cord segments in some common species[9]
Species Cervical Thoracic Lumbar Sacral Caudal/Coccygeal Total
Dog 8 13 7 3 5 36
Cat 8 13 7 3 5 36
Cow 8 13 6 5 5 37
Horse 8 18 6 5 5 42
Pig 8 15/14 6/7 4 5 38
Human 8 12 5 5 1 31
Mouse[10] 8 13 6 4 3 35

In the fetus, vertebral segments correspond with spinal cord segments. However, because the vertebral column grows longer than the spinal cord, spinal cord segments do not correspond to vertebral segments in the adult, particularly in the lower spinal cord. For example, lumbar and sacral spinal cord segments are found between vertebral levels T9 and L2, and the spinal cord ends around the L1/L2 vertebral level, forming a structure known as the conus medullaris.

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.

Spinal cord enlargements

Enlargements

[edit]

There are two regions where the spinal cord enlarges:

Blood supply

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The spinal cord is supplied with blood by three arteries that run along its length starting in the brain, and many arteries that approach it through the sides of the spinal column. The three longitudinal arteries are the anterior spinal artery, and the right and left posterior spinal arteries.[11] These travel in the subarachnoid space and send branches into the spinal cord. They form anastomoses (connections) via the anterior and posterior segmental medullary arteries, which enter the spinal cord at various points along its length.[11] The actual blood flow caudally through these arteries, derived from the posterior cerebral circulation, is inadequate to maintain the spinal cord beyond the cervical segments.

The major contribution to the arterial blood supply of the spinal cord below the cervical region comes from the radially arranged posterior and anterior radicular arteries, which run into the spinal cord alongside the dorsal and ventral nerve roots, but with one exception do not connect directly with any of the three longitudinal arteries.[11] These intercostal and lumbar radicular arteries arise from the aorta, provide major anastomoses and supplement the blood flow to the spinal cord. In humans the largest of the anterior radicular arteries is known as the artery of Adamkiewicz, or anterior radicularis magna (ARM) artery, which usually arises between L1 and L2, but can arise anywhere from T9 to L5.[12] Impaired blood flow through these critical radicular arteries, especially during surgical procedures that involve abrupt disruption of blood flow through the aorta for example during aortic aneurysm repair, can result in spinal cord infarction and paraplegia.

Development

[edit]
Spinal cord seen in a midsection of a five-week-old embryo
Spinal cord seen in a midsection of a three-month-old fetus

The spinal cord is made from part of the neural tube during development. There are four stages of the spinal cord that arises from the neural tube: The neural plate, neural fold, neural tube, and the spinal cord. Neural differentiation occurs within the spinal cord portion of the tube.[13] As the neural tube begins to develop, the notochord begins to secrete a factor known as Sonic hedgehog (SHH). As a result, the floor plate then also begins to secrete SHH, and this will induce the basal plate to develop motor neurons. During the maturation of the neural tube, its lateral walls thicken and form a longitudinal groove called the sulcus limitans. This extends the length of the spinal cord into dorsal and ventral portions as well.[14] Meanwhile, the overlying ectoderm secretes bone morphogenetic protein (BMP). This induces the roof plate to begin to secrete BMP, which will induce the alar plate to develop sensory neurons. Opposing gradients of such morphogens as BMP and SHH form different domains of dividing cells along the dorsal ventral axis.[15] Dorsal root ganglion neurons differentiate from neural crest progenitors. As the dorsal and ventral column cells proliferate, the lumen of the neural tube narrows to form the small central canal of the spinal cord.[16] The alar plate and the basal plate are separated by the sulcus limitans. Additionally, the floor plate also secretes 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 then ascend towards the thalamus. Following the closure of the caudal neuropore and formation of the brain's ventricles that contain the choroid plexus tissue, the central canal of the caudal spinal cord is filled with cerebrospinal fluid.

Earlier findings by Viktor Hamburger and Rita Levi-Montalcini in the chick embryo have been confirmed by more recent studies which have demonstrated that the elimination of neuronal cells by programmed cell death is necessary for the correct assembly of the nervous system.[17]

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.

Spinal cord tracts

[edit]

The spinal cord mainly functions to carry information to and from the brain, in ascending and descending tracts.

Ascending tracts

[edit]

Spinal cord tracts ascending tracts shown in blue

There are two ascending somatosensory pathways in the spinal cord. The dorsal column–medial lemniscus pathway (DCML pathway), and the anterolateral system (ALS).[18]

DCML

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In the dorsal column-medial lemniscus pathway, a primary neuron's axon enters the spinal cord and then enters the dorsal column. Here the dorsal column connects to the axon of the nerve cell. If the primary axon enters below spinal level T6, the axon travels in the gracile fasciculus, the medial part of the column. If the axon enters above level T6, then it travels in the cuneate fasciculus, which is lateral to the fasciculus gracilis. Either way, the primary axon ascends to the lower medulla, where it leaves its fasciculus 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 arcuate fibers. The internal arcuate fibers decussate and continue ascending as the contralateral medial lemniscus. Secondary axons from the medial lemniscus finally terminate in the ventral posterolateral nucleus (VPLN) 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 proprioception of the lower limbs differs from the upper limbs and upper trunk. There is a four-neuron pathway for lower limb proprioception. This pathway initially follows the dorsal spino-cerebellar pathway. It is arranged as follows: proprioceptive receptors of lower limb → peripheral process → dorsal root ganglion → central process → Clarke's column → 2nd order neuron → spinocerebellar tract →cerebellum.

Anterolateral system

[edit]

The anterolateral system (ALS) works somewhat differently. Its primary neurons axons 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 VPLN, where it synapses on tertiary neurons. Tertiary neuronal axons then travel to the primary sensory cortex via the posterior limb of the internal capsule.

Some of the "pain fibers" in the ALS deviate from their pathway towards the VPLN. 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), the centromedian nucleus (to cause diffuse, non-specific pain) and various parts of the cortex. Additionally, some ALS axons from the spinomesencephalic pathway project to the periaqueductal gray in the pons, and the axons forming the periaqueductal gray then project to the nucleus raphes 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.

Spinocerebellar tracts

[edit]

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 decussates 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, 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.

Descending tracts

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Actions of the spinal nerves
Level Motor function
C1–C6 Neck flexors
C1–T1 Neck extensors
C3, C4, C5 Supply diaphragm (mostly C4)
C5, C6 Move shoulder, raise arm (deltoid); flex elbow (biceps)
C6 externally rotate (supinate) the arm
C6, C7 Extend elbow and wrist (triceps and wrist extensors); pronate wrist
C7, C8 Flex wrist; supply small muscles of the hand
T1–T6 Intercostals and trunk above the waist
T7–L1 Abdominal muscles
L1–L4 Flex hip joint
L2, L3, L4 Adduct thigh; Extend leg at the knee (quadriceps femoris)
L4, L5, S1 abduct thigh; Flex leg at the knee (hamstrings); Dorsiflex foot (tibialis anterior); Extend toes
L5, S1, S2 Extend leg at the hip (gluteus maximus); flex foot and flex toes

The descending tracts are of motor information. Descending tracts involve two neurons: the upper motor neuron, and lower motor neuron.[19] A nerve signal travels down the upper motor neuron until it synapses with the lower motor neuron in the spinal cord. Then, the lower motor neuron conducts the nerve signal to the spinal root where efferent nerve fibers carry the motor signal toward the target muscle. The descending tracts are composed of white matter. There are several descending tracts serving different functions. The corticospinal tracts (lateral and anterior) are responsible for coordinated limb movements.[19]

The corticospinal tract serves as the motor pathway for upper motor neuronal signals coming from the cerebral cortex and from primitive brainstem motor nuclei.

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 (via the anterior white commissure) 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 lumbosacral 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.

Other functions

[edit]

The spinal cord is a center for coordinating many reflexes and contains reflex arcs that can independently control reflexes.[1] It is also the location of groups of spinal interneurons that make up the neural circuits known as central pattern generators. These circuits are responsible for controlling motor instructions for rhythmic movements such as walking.[2]

In mice, a projection exists from primary and secondary somatosensory cortex to interneurons in laminae III-V of the lumbar spinal cord that aids the detection of light touch.[20] In humans, research finds prior knowledge about when sensory input will happens top-down modulates spinal activity and does so with responses as early at 13 to 16 ms after stimulation.[21]

Clinical significance

[edit]

A congenital disorder is diastematomyelia in which part of the spinal cord is split usually at the level of the upper lumbar vertebrae. Sometimes the split can be along the length of the spinal cord.

Injury

[edit]
Main article: Spinal cord injury

Spinal cord injuries can be caused by trauma to the spinal column (stretching, bruising, applying pressure, severing, laceration, etc.). 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 injuries may result in paraplegia, tetraplegia (also known as quadriplegia), or full body paralysis below the site of injury to the spinal cord.

Damage to upper motor neuron 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.

Spinal shock and neurogenic shock can occur from a spinal injury. Spinal shock is usually temporary, lasting only for 24–48 hours, and is a temporary absence of sensory and motor functions. Neurogenic shock lasts for weeks and can lead to a loss of muscle tone due to disuse of the muscles below the injured site.

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.) Spinal cord injury can also be non-traumatic and caused by disease (transverse myelitis, polio, spina bifida, Friedreich's ataxia, spinal cord tumor, spinal stenosis etc.)[22]

Globally, it is expected there are around 40 to 80 cases of spinal cord injury per million population, and approximately 90% of these cases result from traumatic events.[23]

Real or suspected spinal cord injuries need immediate immobilisation including that of the head. Scans will be needed to assess the injury. A steroid, methylprednisolone, can be of help as can physical therapy and possibly antioxidants.[citation needed] Treatments need to focus on limiting post-injury cell death, promoting cell regeneration, and replacing lost cells. Regeneration is facilitated by maintaining electric transmission in neural elements.

Stenosis

[edit]
Main article: Spinal stenosis

Spinal stenoses at the lumbar region are usually due to disc herniation, hypertrophy of the facet joint and ligamentum flavum, osteophyte, and spondylolisthesis. An uncommon cause of lumbar spinal stenosis is spinal epidural lipomatosis, a condition where there is excessive deposit of fat in the epidural space, causing compression of nerve root and spinal cord. The epidural fat can be seen as low density on CT scan and high intensity on T2-weighted fast spin echo MRI images.[24]

Tumors

[edit]
Main article: Spinal tumor

Spinal tumors can occur in the spinal cord and these can be either inside (intradural) or outside (extradural) the dura mater.

Procedures

[edit]

The spinal cord ends at the level of vertebrae L1–L2, while the subarachnoid space – the compartment that contains cerebrospinal fluid – extends down to the lower border of S2.[22] Lumbar punctures in adults are usually performed between L3–L5 (cauda equina level) in order to avoid damage to the spinal cord.[22] In the fetus, the spinal cord extends the full length of the spine and regresses as the body grows.

Additional images

[edit]
  • Spinal cord in the nervous system
    Spinal cord in the nervous system
  • Diagrams of the spinal cord
    Diagrams of the spinal cord
  • Cross-section through the spinal cord at the mid-thoracic level
    Cross-section through the spinal cord at the mid-thoracic level
  • Cross-sections of the spinal cord at varying levels
    Cross-sections of the spinal cord at varying levels
  • Cervical vertebra
    Cervical vertebra
  • A portion of the spinal cord, showing its right lateral surface. The dura is opened and arranged to show the nerve roots.
    A portion of the spinal cord, showing its right lateral surface. The dura is opened and arranged to show the nerve roots.
  • The spinal cord with dura cut open, showing the exits of the spinal nerves
    The spinal cord with dura cut open, showing the exits of the spinal nerves
  • The spinal cord showing how the anterior and posterior roots join in the spinal nerves
    The spinal cord showing how the anterior and posterior roots join in the spinal nerves
  • The spinal cord showing how the anterior and posterior roots join in the spinal nerves
    The spinal cord showing how the anterior and posterior roots join in the spinal nerves
  • A longer view of the spinal cord
    A longer view of the spinal cord
  • Projections of the spinal cord into the nerves (red motor, blue sensory)
    Projections of the spinal cord into the nerves (red motor, blue sensory)
  • Projections of the spinal cord into the nerves (red motor, blue sensory)
    Projections of the spinal cord into the nerves (red motor, blue sensory)
  • Cross-section of rabbit spinal cord
    Cross-section of rabbit spinal cord
  • Cross section of adult rat spinal cord stained using Cajal method
    Cross section of adult rat spinal cord stained using Cajal method
  • Spinal nerves exit the spinal cord between each pair of vertebrae.
    Spinal nerves exit the spinal cord between each pair of vertebrae.

See also

[edit]
This article uses anatomical terminology.

References

[edit]
[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Spinal cord

View on Grokipedia
from Grokipedia
The spinal cord is a long, cylindrical extension of the central nervous system that originates from the medulla oblongata in the brainstem and extends caudally through the vertebral canal to the level of the first or second lumbar vertebra in adults, where it tapers into the conus medullaris. It measures approximately 42 to 45 cm in length in adults, with a diameter ranging from 0.64 cm in the thoracic region to 1.33 cm in the cervical and lumbar enlargements, and is divided into 31 segments: 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 1 coccygeal. These segments correspond to the 31 pairs of spinal nerves that emerge from the cord, facilitating communication between the brain and the rest of the body. Structurally, the spinal cord consists of an inner core of gray matter arranged in an H- or butterfly-shaped configuration, which contains neuronal cell bodies, dendrites, and synapses, surrounded by an outer layer of white matter composed of myelinated axons organized into ascending and descending tracts. The gray matter is subdivided into Rexed laminae I through X, with the dorsal horns processing sensory input, the ventral horns housing motor neurons, and the lateral horns in the thoracic and upper lumbar regions containing preganglionic sympathetic neurons. A central canal lined with ependymal cells runs through the gray matter, filled with cerebrospinal fluid that provides buoyancy and nutrient exchange. Below the conus medullaris, the cord gives rise to the cauda equina, a bundle of lumbar and sacral nerve roots that extend to their respective foramina. The primary functions of the spinal cord include relaying sensory and motor information between the brain and periphery, coordinating spinal reflexes, and modulating autonomic activities. Ascending tracts, such as the dorsal column-medial lemniscus and spinothalamic pathways, transmit sensory signals like touch, proprioception, pain, and temperature to the brain, while descending tracts, including the corticospinal and vestibulospinal pathways, convey motor commands for voluntary and involuntary movements. Reflex arcs within the cord enable rapid, local responses—such as the knee-jerk reflex—independent of brain input, involving a sensory neuron directly synapsing onto a motor neuron in a two-neuron, monosynaptic circuit. Additionally, the spinal cord houses central pattern generators that control rhythmic activities like locomotion. The spinal cord is protected by the bony vertebral column, three layers of meninges—dura mater (outermost, tough fibrous layer), arachnoid mater (middle, web-like with subarachnoid space containing cerebrospinal fluid), and pia mater (innermost, adhering closely to the cord)—and a cushioning layer of cerebrospinal fluid. Its blood supply is provided by the anterior spinal artery (supplying the anterior two-thirds, including motor tracts) and paired posterior spinal arteries (supplying the dorsal columns), with the great radicular artery (artery of Adamkiewicz) reinforcing the lower thoracic and lumbar regions to prevent ischemia. Embryologically, the spinal cord develops from the neural tube during the third week of gestation, with the basal plate forming ventral motor regions and the alar plate forming dorsal sensory regions, a process vulnerable to disruptions leading to conditions like spina bifida.

Anatomy

Gross structure

The spinal cord is a long, cylindrical structure that extends from the foramen magnum at the base of the skull to the conus medullaris, typically located at the level of the L1-L2 vertebrae in adults. It measures approximately 42 to 45 cm in length in adults, with slight variations between males (about 45 cm) and females (about 42 cm). The cord tapers gradually toward its caudal end, forming a conical tip known as the conus medullaris, and it occupies the upper two-thirds of the vertebral canal while being suspended and protected within it. The spinal cord is segmented into 31 distinct regions, corresponding to the points of emergence of spinal nerves: 8 cervical (C1-C8), 12 thoracic (T1-T12), 5 lumbar (L1-L5), 5 sacral (S1-S5), and 1 coccygeal (Co1). Each segment features a pair of dorsal roots, which carry sensory information into the cord, and ventral roots, which convey motor signals outward; these roots unite to form the 31 pairs of spinal nerves that innervate the body. Regionally, the cord exhibits two enlargements due to increased gray matter volume for limb innervation: the cervical enlargement, spanning segments C4 to T1 and giving rise to the brachial plexus for upper limb nerves, and the lumbar enlargement, spanning segments L1 to S3 and forming the lumbosacral plexus for lower limb innervation. Distal to the conus medullaris, the lumbar and sacral nerve roots extend inferiorly as a bundle resembling a horse's tail, termed the cauda equina, which travels through the lumbar cistern filled with cerebrospinal fluid. The entire spinal cord is enveloped by three protective meninges: the tough outer dura mater, the delicate middle arachnoid mater, and the vascular inner pia mater, which adheres closely to the cord's surface and extends along the roots. The spinal cord is further suspended within the dural sac by the denticulate ligaments, paired triangular extensions of the pia mater that attach laterally to the dura mater between the dorsal and ventral roots, and anchored caudally by the filum terminale, a non-neural filamentous extension of the pia mater that attaches to the dorsal surface of the coccyx, helping to prevent excessive movement.

Internal organization

In cross-section, the spinal cord displays a central region of gray matter shaped like the letter H or butterfly, consisting of anterior (ventral) horns, posterior (dorsal) horns, and, in the thoracic and upper lumbar segments, lateral horns; this gray matter is encircled by white matter. The gray matter primarily comprises neuronal cell bodies, dendrites, and synapses, serving as the site for local neural processing. Within the gray matter, the anterior horns house lower motor neurons that innervate skeletal muscles, the posterior horns contain sensory neurons receiving input from peripheral afferents, and the intermediate zone, including the lateral horns, is populated by interneurons and autonomic preganglionic neurons, respectively. The surrounding white matter consists of myelinated and unmyelinated axons organized into three major columns, or funiculi—anterior, lateral, and posterior—that facilitate long-distance signal transmission between the spinal cord and brain. At the center of the H-shaped gray matter lies the central canal, a narrow, fluid-filled channel lined by ependymal cells that contributes to the circulation of cerebrospinal fluid (CSF) within the ventricular system. For finer functional organization, the gray matter is subdivided into ten Rexed laminae (I through X), based on cytoarchitecture and neuronal types; for example, lamina I in the posterior horn is involved in processing nociceptive (pain) signals. These laminae provide a layered framework for integrating sensory and motor information. Variations in internal organization occur across spinal segments to accommodate regional demands; notably, the anterior horns are enlarged in the cervical and lumbosacral regions, reflecting the greater number of motor neurons required for upper and lower limb innervation. In contrast, thoracic segments exhibit relatively smaller gray matter volumes, with prominent lateral horns for sympathetic outflow.

Vascular supply

The spinal cord's arterial supply is derived from three main longitudinal arteries: the single anterior spinal artery and the paired posterior spinal arteries. The anterior spinal artery originates from the union of branches from the vertebral arteries at the level of the medulla and descends along the anterior median fissure, supplying approximately two-thirds of the cord's cross-sectional area, including the anterior and lateral white matter columns as well as the anterior horns of the gray matter. The two posterior spinal arteries arise either directly from the vertebral arteries or from the posterior inferior cerebellar arteries and course along the posterolateral sulci, primarily perfusing the dorsal columns and posterior horns. These longitudinal arteries are reinforced by segmental radicular arteries that enter the spinal canal via the intervertebral foramina; among these, the artery of Adamkiewicz (also known as the great anterior radiculomedullary artery) is the largest, typically arising from an intercostal or lumbar artery between T9 and L2 levels on the left side, and it provides the dominant blood flow to the lower thoracic, lumbar, and sacral segments via anastomosis with the anterior spinal artery. Venous drainage of the spinal cord follows a similar anterior-posterior organization but lacks valves, enabling free communication and potential retrograde flow. Intrinsic veins within the cord include the anterior median vein along the anterior median fissure and posterior median veins in the posterior median sulcus, which drain into a superficial pial venous plexus on the cord's surface. This plexus converges into longitudinal anterior and posterior spinal veins that run parallel to the arteries and exit via radicular veins accompanying the spinal nerve roots to join the internal vertebral venous plexus (also called the epidural plexus) surrounding the dura mater. The valveless nature of this system facilitates the spread of infections or metastases from distant sites to the spinal cord via hematogenous routes. Watershed zones in the spinal cord occur where arterial territories meet with limited anastomoses, rendering certain regions particularly susceptible to ischemic injury during systemic hypoperfusion. The midthoracic cord, especially between T4 and T8, constitutes a primary watershed area due to sparse radicular feeder contributions and tenuous collateral circulation in this segment, increasing vulnerability to infarction under conditions of hypotension or aortic compromise. Lymphatic drainage of the spinal cord is limited, as the central nervous system parenchyma lacks conventional lymphatic vessels; instead, meningeal lymphatics along the dura and perineural spaces facilitate clearance of interstitial fluid and antigens, ultimately draining into prevertebral lymph nodes via cervical and thoracic pathways. The vasculature of the spinal cord is under autonomic control, primarily through sympathetic innervation originating from preganglionic neurons in the intermediolateral cell column of the thoracic spinal segments (T1 to L2), which postganglionically influence vasomotor tone to regulate blood flow and maintain perfusion stability.

Embryonic development

Early formation

The early formation of the spinal cord originates during gastrulation in the third week of human embryonic development, when the bilaminar embryonic disc transforms into a trilaminar structure through the migration of epiblast cells via the primitive streak to form mesoderm and endoderm layers. The notochord, arising from the axial mesoderm as the notochordal process, emerges as a critical signaling center that induces the overlying ectoderm to differentiate into the neural plate. This induction is primarily mediated by the secretion of Sonic hedgehog (Shh) protein from the notochord, which establishes a ventral-to-dorsal gradient that promotes neuroectodermal fate and ventralizes the neural tissue. Neural tube formation, or primary neurulation, occurs during weeks 3 and 4, beginning with the induction of the neural plate from the ectoderm adjacent to the notochord and primitive streak. The neural plate thickens and its lateral edges elevate as neural folds, mediated by differential cell shape changes driven by Shh signaling and interactions with the overlying surface ectoderm. Fusion of the neural folds proceeds bidirectionally from the hindbrain-spinal cord junction (around the fourth somite), forming the neural tube; the anterior neuropore closes on approximately day 25 at the 18- to 20-somite stage, while the posterior neuropore closes on day 27 to 28 at the 25- to 29-somite stage, completing the enclosure of the central nervous system primordium. Defects in neurulation arise from disruptions in these processes, often due to genetic, environmental, or multifactorial causes affecting neural tube closure. Spina bifida results from incomplete closure of the posterior neuropore, leading to a defect in the vertebral arches and potential protrusion or tethering of the spinal cord meninges, with varying severity from occult to myelomeningocele. Anencephaly, conversely, stems from failure of anterior neuropore closure, resulting in the absence of the cranial vault and cerebral hemispheres while the spinal cord typically forms normally. These conditions underscore the narrow temporal window for successful neurulation, with incidence rates influenced by folate status and other teratogenic factors. Parallel to neural tube formation, the paraxial mesoderm on either side of the neural tube segments into approximately 42 to 44 pairs of somites starting around day 20, in a process called somitogenesis that proceeds craniocaudally at a rate of 3 to 4 somites per day. Each somite differentiates into distinct regions, with the ventral sclerotome component undergoing epithelial-to-mesenchymal transition and migrating medially to surround the neural tube, contributing mesenchymal cells that form the vertebral bodies, intervertebral discs, and neural arches of the axial skeleton. This segmentation ensures the metameric organization that aligns vertebrae with spinal cord segments. Rostrocaudal patterning of the nascent spinal cord is initiated early by Hox transcription factor genes, clustered in four genomic complexes (HoxA-D) and expressed in collinear, nested domains along the embryonic axis from the hindbrain transition to the caudal spinal cord. Hox genes establish positional identity by regulating downstream targets that specify segmental domains, such as HoxC6 for upper cervical levels or HoxD10 for lumbar regions, thereby coordinating the alignment of neural segments with somites and ensuring proper topographic organization. Disruptions in Hox expression can alter spinal cord patterning, as evidenced by experimental models showing shifts in segmental identity.

Maturation and myelination

Following neural tube closure, the central lumen undergoes cavitation to form the ependymal-lined central canal of the spinal cord, which persists as a narrow cerebrospinal fluid-filled channel throughout life. Subsequently, neuroblasts proliferate within the ventricular zone of the neural tube and migrate radially to establish the alar plate dorsally, which differentiates into sensory structures, and the basal plate ventrally, which forms motor components; these plates are separated by the sulcus limitans. Neuroblasts in the alar plate give rise to interneurons and relay neurons for sensory input, while those in the basal plate develop into somatic and visceral motor neurons that populate the ventral and lateral horns. The caudal portion of the spinal cord, extending to the sacral and coccygeal levels, forms through secondary neurulation after posterior neuropore closure. This process involves the formation of a secondary neural tube from the caudal eminence (tail bud) through cavitation and mesenchymal-to-epithelial transition, integrating with the primary neural tube. Defects in secondary neurulation can contribute to caudal spinal dysraphisms, such as terminal myelocystocele. The spinal cord achieves its segmental organization through differential growth patterns, reducing from an initial 42-44 somite pairs (including 4 occipital, 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 8-10 coccygeal) to 31 functional segments (8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 1 coccygeal), as caudal somites contribute to the tail and fuse while the vertebral column elongates faster than the cord. This process ensures precise alignment of spinal nerves with vertebral levels via resegmentation of somitic sclerotomes. Myelination in the spinal cord begins with oligodendrocytes in the central nervous system around 10-12 weeks of gestation, when precursor cells differentiate and extend processes to ensheath axons, with the process peaking during the first two postnatal years as myelin sheaths thicken to support rapid conduction. In contrast, Schwann cells myelinate the peripheral roots starting in the fifth fetal month, providing insulation for spinal nerve entry and exit points outside the cord. Glial development parallels neuronal maturation, with astrocytes emerging from radial glia to provide structural support, regulate the extracellular matrix, and guide axonal growth in the developing spinal cord. Microglia, derived from yolk sac progenitors, play supportive roles by phagocytosing debris, pruning excess synapses, and acting as guideposts for neuronal and axonal migration during early spinal cord circuit formation. Apoptosis, or programmed cell death, occurs extensively during this period to refine neuron populations, eliminating up to 50% of generated neurons through caspase-mediated pathways and thereby shaping the final architecture and connectivity of spinal cord circuits. This process is most active in the perinatal phase, ensuring balanced sensory and motor neuron numbers without disrupting overall functionality.

Functions

Sensory processing

The spinal cord serves as the primary conduit for ascending sensory pathways, transmitting information from peripheral receptors to higher brain centers for processing. These pathways, composed of first-, second-, and third-order neurons, enable conscious perception of touch, proprioception, pain, and temperature, as well as unconscious coordination via cerebellar inputs. Sensory signals enter the spinal cord through dorsal roots, where primary afferents from dorsal root ganglia synapse in the dorsal horn gray matter. The dorsal column-medial lemniscus (DCML) pathway conveys fine touch, vibration, and proprioception from mechanoreceptors in the skin, muscles, and joints. First-order neurons, with cell bodies in the dorsal root ganglia, ascend ipsilaterally in the dorsal columns: the fasciculus gracilis carries information from the lower body (below T6), while the fasciculus cuneatus handles upper body inputs (above T6). These fibers remain uncrossed until synapsing in the medulla's nucleus gracilis and cuneatus, where second-order neurons decussate in the sensory decussation and project via the medial lemniscus to the thalamus's ventral posterolateral nucleus. Third-order thalamic neurons then relay to the somatosensory cortex. This pathway supports discriminative tactile sensations and body position awareness. In contrast, the anterolateral system, including the spinothalamic tract, transmits pain, temperature, and crude touch. Primary afferents enter via dorsal roots and synapse quickly in the dorsal horn's substantia gelatinosa (laminae I-II) or deeper layers (laminae V-VI). Second-order neurons decussate within one or two segments in the anterior white commissure and ascend contralaterally in the lateral and anterior spinothalamic tracts: the lateral tract primarily carries pain and temperature, while the anterior tract conveys crude touch and pressure. These project to the thalamus's posterolateral and intralaminar nuclei, with onward connections to the somatosensory and insular cortices for emotional and perceptual aspects of sensation. This system allows rapid relay of potentially harmful stimuli. The spinocerebellar tracts provide unconscious proprioceptive feedback to the cerebellum for motor coordination, bypassing conscious awareness. The posterior (dorsal) spinocerebellar tract originates from Clarke's column (lamina VII) in the thoracic and upper lumbar cord, carrying ipsilateral information from lower limb muscle spindles and Golgi tendon organs; it ascends laterally without decussation and enters the cerebellum via the inferior cerebellar peduncle. The anterior (ventral) spinocerebellar tract, from lumbar and sacral levels, conveys bilateral inputs from the lower body, crossing twice (once in the cord and again in the pons) before entering via the superior cerebellar peduncle. These tracts ensure fine-tuned adjustments to posture and movement. Sensory neuron types are classified by fiber diameter, myelination, and conduction velocity, influencing the modalities they carry. Large, myelinated A-beta fibers (6-12 μm diameter, 30-70 m/s conduction) mediate touch and vibration, entering via dorsal roots and projecting directly to the dorsal column nuclei or synapse in deeper dorsal horn layers. Smaller, thinly myelinated A-delta fibers (1-5 μm, 5-30 m/s) transmit sharp, initial pain and cold, synapsing in laminae I and V of the dorsal horn. Unmyelinated C fibers (0.2-1.5 μm, 0.5-2 m/s) carry dull, aching pain, warmth, and itch, also terminating in the substantia gelatinosa. All originate from pseudounipolar neurons in dorsal root ganglia. Ascending tracts exhibit somatotopic organization, preserving the spatial mapping of body regions along their course. In the dorsal columns, fibers are layered with sacral inputs most medial, progressing laterally to lumbar, thoracic, and cervical, forming a "laminated" arrangement that maintains peripheral receptive field order. The spinothalamic tract shows a similar posterolateral-to-anteromedial gradient in the spinal cord, with sacral fibers dorsolateral and cervical ventromedial, though partial somatotopy is retained up to the thalamus. Spinocerebellar tracts follow segmental ordering, with lower body fibers positioned laterally. This organization facilitates precise cortical representation in the somatosensory homunculus.

Motor control

The motor control functions of the spinal cord are primarily mediated by descending pathways that transmit signals from the brain to coordinate voluntary and involuntary movements. These pathways originate from upper motor neurons in the cerebral cortex and brainstem, which project through the white matter columns of the spinal cord to influence lower motor neurons in the anterior horn. The corticospinal tract is the principal pathway for voluntary skilled movements, consisting of the lateral corticospinal tract, which controls distal limb muscles and carries over 90% of the fibers after decussation in the medullary pyramids, and the anterior corticospinal tract, which remains mostly ipsilateral and innervates axial and proximal muscles. Other key descending tracts include the rubrospinal tract, originating from the red nucleus in the midbrain, which facilitates flexor muscles and inhibits extensors to support fine motor adjustments in the upper limbs; the vestibulospinal tract, arising from vestibular nuclei, which maintains balance and posture by modulating extensor tone in antigravity muscles; and the reticulospinal tract, from the reticular formation in the pons and medulla, which regulates locomotion, posture, and overall muscle tone through bilateral projections. Upper motor neurons, located in layer V of the primary motor cortex or in brainstem nuclei, send long axons that descend via these tracts and synapse directly or indirectly with interneurons and lower motor neurons in the ventral horn of the spinal cord gray matter. These neurons integrate cortical commands for precise voluntary actions with brainstem inputs for automatic adjustments, ensuring coordinated output to skeletal muscles. Lower motor neurons, comprising alpha motor neurons that directly innervate extrafusal muscle fibers for contraction and gamma motor neurons that regulate muscle spindle sensitivity for proprioception, reside in the anterior horn and exit the spinal cord through the ventral roots to form peripheral nerves. The descending tracts exhibit somatotopic organization within the spinal cord's lateral and anterior funiculi, with lateral regions of the columns dedicated to distal limb musculature for fractionated movements and medial regions targeting proximal and axial muscles for gross postural control. This mapping allows for efficient spatial segregation of motor signals along the cord's length. Additionally, descending inputs achieve balanced motor control through interactions with spinal interneurons, which provide inhibition to antagonist muscles and facilitation to agonists, preventing excessive activation and enabling smooth reciprocal movements.

Reflex and autonomic roles

The spinal cord mediates local reflexes through segmental circuits that enable rapid, automatic responses to stimuli, independent of higher brain centers. A reflex arc, the fundamental pathway for these responses, consists of five key components: a sensory receptor that detects the stimulus, an afferent neuron that transmits the signal to the spinal cord, an integration center within the cord where the signal is processed, an efferent neuron that carries the response signal away, and an effector such as a muscle or gland that produces the action. These arcs are primarily organized in the dorsal and ventral horns of the spinal gray matter, allowing for efficient local processing. Monosynaptic reflexes represent the simplest form, involving a direct connection between afferent and efferent neurons without interneurons. The stretch reflex, exemplified by the knee-jerk response, occurs when muscle spindles detect rapid lengthening of the muscle, activating Ia afferent fibers that synapse directly onto alpha motor neurons in the ventral horn, prompting contraction to resist the stretch. This reflex maintains muscle tone and posture by providing immediate feedback to proprioceptive changes. In contrast, polysynaptic reflexes incorporate interneurons for more complex coordination, allowing integration of multiple inputs. The withdrawal reflex, triggered by painful stimuli to the skin, involves nociceptive afferents synapsing onto interneurons in the dorsal horn, which then excite flexor motor neurons to retract the limb while inhibiting extensors. The crossed extensor reflex complements this by activating contralateral extensor muscles via interneurons, providing stability during withdrawal, such as extending the opposite leg when one foot encounters a sharp object. Interneurons in these circuits enable reciprocal inhibition, ensuring antagonist muscles relax while agonists contract. The spinal cord also integrates autonomic functions, regulating visceral activities through preganglionic neurons housed in specific gray matter regions. Sympathetic preganglionic neurons originate in the intermediolateral column of the thoracic and upper lumbar segments (T1-L2), projecting to sympathetic ganglia for responses like increased heart rate during stress. Parasympathetic preganglionic neurons, conversely, are located in similar lateral positions but in the sacral segments (S2-S4), innervating pelvic organs to promote rest-and-digest activities such as digestion. In the sacral cord, specialized centers coordinate micturition and defecation, integrating sensory input from bladder and bowel distension with motor outputs to sphincters and smooth muscles. The sacral micturition center (S2-S4) facilitates bladder emptying by relaxing the urethral sphincter and contracting detrusor muscle via parasympathetic efferents, while interneurons modulate reciprocal inhibition of somatic sphincters. Similarly, the defecation center (S2-S4) synchronizes rectal contraction, internal anal sphincter relaxation, and external sphincter control, ensuring coordinated expulsion of waste. These reflexes maintain continence during filling and promote efficient voiding or evacuation when thresholds are met. Following acute spinal cord injury, spinal shock manifests as a transient phase of flaccid paralysis and areflexia below the lesion level, resulting from disrupted neural excitability and temporary loss of reflex activity due to ionic imbalances and neurotransmitter depletion. This state typically resolves over hours to weeks, allowing gradual return of segmental reflexes as spinal circuits recover.

Clinical aspects

Traumatic injuries

Traumatic spinal cord injuries (TSCI) occur annually at a global rate of approximately 500,000 to 600,000 new cases (as of 2021 estimates), with the majority resulting from external mechanical forces. The most common causes include falls (leading globally, especially among older adults), motor vehicle collisions (MVCs; approximately 20-40% depending on region), and sports-related incidents (5-10%). These etiologies often involve high-impact forces leading to immediate structural damage to the spinal cord. TSCI mechanisms are classified into primary and secondary injury phases. Primary injury arises directly from mechanical disruption, including contusion (bruising from compression by displaced vertebrae or hematoma), laceration (tearing by sharp bone fragments or penetrating objects), and transection (severing of the cord, which can be complete—total disconnection—or incomplete—partial severance allowing some fiber preservation). Secondary injury follows within minutes to weeks, involving cascading pathophysiological processes such as ischemia due to vascular compression, inflammation from glial activation, and excitotoxicity from excessive neurotransmitter release, exacerbating neuronal death. The spinal cord's limited vascular redundancy heightens susceptibility to ischemic damage during these secondary events. The level of injury determines the extent of neurological deficits. Cervical injuries (C1-C8) typically cause tetraplegia, impairing all four limbs, trunk, and respiratory function due to disruption of descending motor pathways. Thoracic injuries (T1-T12) result in paraplegia, affecting the lower limbs and trunk while sparing upper body function. Lumbar and sacral injuries (L1-S5) produce variable effects, often limited to lower limb weakness, bowel, bladder, and sexual dysfunction, as higher pathways remain intact. Specific incomplete injury patterns include Brown-Séquard syndrome, resulting from hemisection of the cord, which produces ipsilateral loss of motor function and proprioception below the lesion (due to corticospinal and dorsal column tract damage) and contralateral loss of pain and temperature sensation (from spinothalamic tract involvement, which decussates). Central cord syndrome, often from cervical hyperextension in patients with preexisting spondylosis, manifests as greater weakness in the upper extremities than lower ones, with variable sensory deficits and bladder dysfunction, stemming from selective damage to central cord regions rich in upper limb motor fibers. Severity is standardized using the ASIA Impairment Scale (AIS), ranging from A (complete injury: no sensory or motor function preserved in sacral segments S4-S5) to E (normal neurological function, used in follow-up for recovery). Grades B (sensory incomplete: sacral sensory preservation without motor) and C/D (motor incomplete: motor function below the level, with C indicating <3/5 strength in >50% of key muscles and D ≥3/5) guide prognosis and management of immediate consequences like spinal shock and autonomic instability.

Non-traumatic disorders

Non-traumatic disorders of the spinal cord include degenerative, inflammatory, and vascular conditions that progressively impair neurological function through mechanisms such as compression, demyelination, or ischemia, without acute mechanical injury. These pathologies often manifest with symptoms like weakness, sensory alterations, gait disturbances, and autonomic dysfunction, varying by the specific disorder and spinal level affected. Diagnosis typically relies on clinical presentation combined with magnetic resonance imaging (MRI) to visualize cord changes, and management focuses on symptom relief and slowing progression, though outcomes depend on early intervention. Spinal stenosis involves narrowing of the spinal canal, which can be congenital—present at birth due to developmental anomalies like achondroplasia—or acquired through degenerative processes such as osteoarthritis, ligamentum flavum hypertrophy, or disc herniation. This narrowing compresses the spinal cord, leading to myelopathy characterized by gait instability, loss of hand dexterity, upper and lower extremity weakness, sensory deficits, and in severe cases, bowel or bladder dysfunction. In the lumbar region, symptoms often include neurogenic claudication with leg pain, weakness, or numbness exacerbated by walking and relieved by flexion. Cervical spinal stenosis is more likely to cause myelopathy than lumbar stenosis, as the latter more commonly affects nerve roots rather than the cord directly, making cervical involvement the leading cause of non-traumatic myelopathy in adults over 55. Multiple sclerosis (MS) is a chronic autoimmune demyelinating disease featuring multifocal plaques of inflammation and myelin loss in the central nervous system, including the spinal cord, which shows involvement in approximately 80% of patients on MRI. Spinal cord lesions are typically short (less than two vertebral segments), peripheral, and asymmetric, contributing to symptoms like spasticity, sensory disturbances, and motor weakness, particularly in the relapsing-remitting form that affects most individuals at onset. These plaques disrupt saltatory conduction, leading to episodic exacerbations followed by partial or full remissions, with spinal involvement often correlating with greater disability than brain lesions alone due to the cord's limited compensatory capacity. Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder characterized by selective degeneration of upper motor neurons in the corticospinal tracts and lower motor neurons in the anterior horn cells of the spinal cord, resulting in combined upper and lower motor neuron signs such as muscle weakness, atrophy, fasciculations, spasticity, and hyperreflexia. Spinal cord pathology focuses on the anterior horns, where motor neuron loss leads to denervation and muscle wasting, typically starting in the limbs and progressing to respiratory failure; the disease spares sensory and autonomic functions. Pathological hallmarks include TDP-43 protein aggregates and gliosis, with onset usually between ages 50 and 70 and a median survival of 3-5 years. Vascular disorders of the spinal cord, such as anterior spinal artery syndrome, arise from ischemia due to occlusion or hypoperfusion of the anterior spinal artery, often from atherosclerosis, embolism, aortic surgery, or hypotension. This syndrome presents with acute onset of severe back pain at the lesion level, followed by bilateral flaccid paralysis and loss of pain and temperature sensation below the affected segment, while proprioception and vibration sense remain preserved due to intact posterior columns. Autonomic features like urinary retention and hypotension may occur, and the thoracic cord is most vulnerable given the artery's watershed zones; recovery is limited, with persistent motor deficits in most cases. Transverse myelitis is an acute inflammatory disorder causing focal spinal cord dysfunction across multiple segments, often triggered by post-infectious immune responses (e.g., after viral illnesses like herpes zoster) or autoimmune conditions such as systemic lupus erythematosus. Symptoms develop rapidly over hours to days, including bilateral weakness, sensory level deficits, paresthesias, and autonomic issues like bladder dysfunction or bowel incontinence, with MRI showing T2 hyperintensities and possible gadolinium enhancement indicating active inflammation. It predominantly affects the thoracic cord and can be monophasic or recurrent, with about one-third of cases progressing to significant disability if untreated. Syringomyelia involves the formation of a fluid-filled syrinx within the spinal cord parenchyma, often associated with Chiari malformation or prior arachnoiditis, leading to gradual expansion that disrupts crossing spinothalamic tracts. This results in dissociative sensory loss—impaired pain and temperature sensation with preserved light touch, proprioception, and vibration—in a cape-like distribution over the shoulders and arms, alongside potential motor weakness, atrophy (especially in hand intrinsics), and scoliosis. The syrinx typically extends longitudinally over several segments, starting in the cervical region, and symptoms progress insidiously unless complicated by syrinx expansion or hemorrhage.

Neoplastic conditions

Neoplastic conditions of the spinal cord encompass a range of primary and secondary tumors that arise within or adjacent to the spinal cord parenchyma, leading to compression, infiltration, or disruption of neural function. These tumors are classified based on their anatomical location relative to the dura mater and spinal cord: intramedullary (within the cord), extramedullary-intradural (within the dura but outside the cord), and extradural (outside the dura). Primary spinal tumors are rare, accounting for approximately 15% of all central nervous system neoplasms, with an annual incidence of about 0.5 to 1 per 100,000 individuals. Intramedullary tumors originate within the spinal cord tissue and represent 20-40% of primary intraspinal neoplasms. Ependymomas are the most common intramedullary tumors in adults, comprising ~60% of cases and typically classified as World Health Organization (WHO) grade II, arising from ependymal cells lining the central canal. These tumors often present with gradual onset of sensory disturbances, motor weakness, and back pain due to progressive cord compression. Astrocytomas, more prevalent in pediatric populations, account for about 60% of intramedullary tumors in children and are frequently low-grade (WHO grade I-II) but can infiltrate diffusely. Extramedullary-intradural tumors develop within the dural sac but external to the spinal cord, often involving the meninges or nerve roots. Meningiomas, which are benign (WHO grade I) and predominantly affect the thoracic spine, constitute around 25-30% of spinal tumors in this category and arise from arachnoid cap cells. Schwannomas, originating from Schwann cells of the nerve sheath, are another common type, typically benign (WHO grade I), and frequently occur in the cervical or lumbar regions, causing radicular pain or myelopathy through mass effect. Extradural tumors, the most frequent overall, comprise 55-60% of all spinal neoplasms and are predominantly metastatic, originating from primary cancers such as breast, lung, or prostate. These lesions often lead to epidural compression syndrome, characterized by acute back pain, motor deficits, and sensory loss due to vertebral involvement and cord compression. Primary extradural tumors are less common but include chordomas or sarcomas. The WHO classification system grades central nervous system tumors, including those of the spinal cord, from I (least aggressive) to IV (most malignant), based on histological features, molecular markers, and behavior. For spinal tumors, grades I-II are typically benign or low-grade (e.g., ependymoma, meningioma), while grades III-IV indicate high-grade malignancies like anaplastic astrocytoma or glioblastoma. Paraneoplastic syndromes associated with spinal cord involvement, though rare, can mimic neoplastic compression; for instance, subacute motor neuronopathy presents as painless lower motor neuron weakness in extremities and is linked to Hodgkin lymphoma. Prognosis varies by tumor type and grade, with complete resection being a key factor; spinal ependymomas, for example, achieve a 5-year overall survival rate exceeding 80% following gross total resection.

Interventional procedures

Interventional procedures for spinal cord conditions encompass a range of diagnostic, surgical, and therapeutic approaches aimed at assessing, alleviating, and potentially restoring function. Diagnostic imaging plays a central role in evaluating spinal cord pathology, with magnetic resonance imaging (MRI) serving as the gold standard for visualizing cord compression, edema, and lesions due to its non-invasive multiplanar capabilities and high soft-tissue contrast. Computed tomography (CT) myelography is employed when MRI is contraindicated, involving intrathecal contrast to delineate cord anatomy and identify compressive lesions. Advanced techniques like diffusion tensor imaging (DTI) assess white matter tract integrity by quantifying fractional anisotropy and mean diffusivity, aiding in prognosis and surgical planning for conditions such as degenerative myelopathy. Invasive electrophysiological diagnostics provide functional insights into neural pathways. Electromyography (EMG) evaluates motor root and peripheral nerve integrity by recording muscle electrical activity in response to stimulation, helping localize lesions in spinal cord disorders. Somatosensory evoked potentials (SSEPs) measure sensory conduction from periphery to cortex, detecting disruptions in dorsal column pathways during intraoperative monitoring or preoperative assessment of cord viability. Surgical interventions focus on decompression, resection, and stabilization to mitigate cord damage. Laminectomy decompresses the spinal canal in cases of stenosis, removing bone to relieve pressure on the cord while preserving stability in select patients. For intramedullary tumors like ependymoma, en bloc resection aims for complete removal to minimize recurrence, often combined with neuromonitoring to protect adjacent tracts. In traumatic injuries, spinal fusion stabilizes fractured vertebrae using instrumentation and grafts, preventing further cord impingement and promoting alignment. Pharmacological therapies target acute neuroprotection, though efficacy varies. Although the National Acute Spinal Cord Injury Studies (NASCIS II and III) suggested modest motor recovery benefits from high-dose methylprednisolone within 8 hours, current guidelines recommend against its routine use due to insufficient evidence and significant risks including infection and gastrointestinal complications. Neuroprotective agents, such as riluzole or minocycline, are under investigation to reduce secondary injury cascades like excitotoxicity and inflammation, with ongoing trials assessing their role in limiting cord damage. Rehabilitative interventions emphasize activity-based recovery. Functional electrical stimulation (FES) activates paralyzed muscles during gait training, enhancing circulation, muscle strength, and potentially neuroplasticity in incomplete injuries. Locomotor training, often body-weight-supported, promotes stepping patterns to retrain central pattern generators, improving overground walking ability and cardiovascular fitness. Emerging therapies include stem cell interventions, with phase II trials as of 2024 demonstrating preliminary safety and functional gains in chronic spinal cord injury through intrathecal or intramedullary delivery of mesenchymal stem cells to promote regeneration and reduce inflammation. As of 2025, phase 1 trials such as a world-first study at Griffith University for chronic SCI have commenced, alongside ongoing phase II evaluations showing preliminary safety.

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