Physiology, Spinal Cord


Within the spinal column lies the spinal cord, a vital aspect of the central nervous system (CNS). The three primary roles of the spinal cord are to send motor commands from the brain to the body, send sensory information from the body to the brain, and coordinate reflexes. The spinal cord is organized segmentally, with thirty-one pairs of spinal nerves emanating from it. A spinal cord injury disrupts this conduit between the body and brain and can lead to deficits in sensation, movement, and autonomic regulation, as well as death.


The spinal cord is composed of gray and white matter, appearing in a cross-section as H-shaped gray matter surrounded by white matter. The gray matter consists of the cell bodies of motor and sensory neurons, interneurons, and neuropils (neuroglia cells and mostly unmyelinated axons). In contrast, the white matter is composed of interconnecting fiber tracts, which are primarily myelinated sensory and motor axons. The supports of the gray matter’s “H” make up the right dorsal, right ventral, left dorsal, and left ventral horns. Running longitudinally through the center of the spinal cord is the central canal, which is continuous with the brain’s ventricles and filled with cerebrospinal fluid (CSF).

The white matter is organized into tracts. Ascending tracts carry information from the sensory receptors to higher levels of the CNS, while descending tracts carry information from the CNS to the periphery. The major tracts and their most defining features are as follows:[1] 

Ascending Tracts

  • Dorsal column: contains the gracile fasciculus and cuneate fasciculus, which together form the dorsal funiculus. The dorsal column is responsible for pressure and vibration sensation, two-point discrimination, movement sense, and conscious proprioception. The dorsal column decussates at the superior portion of the medulla oblongata and forms the medial lemniscus. 
  • Lateral spinothalamic: carries pain and temperature information. The lateral spinothalamic tract decussates at the anterior commissure, two segments above the entry to the spinal cord.
  • Anterior spinothalamic: carries crude touch and pressure information. It decussates similar to the lateral spinothalamic tract.[2]
  • Dorsal and ventral spinocerebellar: transmit unconscious proprioception sensory information to the cerebellum. The ventral spinocerebellar tract does not decussate, while the dorsal spinocerebellar tract decussates twice, making them both ipsilateral.[3]

 Descending Tracts

  • Lateral and anterior corticospinal: involved in conscious control of the skeletal muscle. The majority of lateral corticospinal tract fibers decussate at the inferior portion of the medulla oblongata, while anterior corticospinal descends ipsilaterally in the spinal cord and decussates at the segmental level. The lateral corticospinal tract, also called the pyramidal tract, innervates primarily contralateral muscles of the limbs, while the anterior corticospinal tract innervates proximal muscles of the trunk. 
  • Vestibulospinal: carries information from the inner ear to control head positioning and is involved in modifying muscle tone to maintain posture and balance. The vestibulospinal tract does not decussate.
  • Rubrospinal: involved in the movement of the flexor and extensor muscles. The rubrospinal tract originates from the red nuclei in the midbrain and decussates at the start of its pathway.
  • Reticulospinal: originates from the reticular formation housed in the brainstem, and it facilitates, influences, and supplements the corticospinal tract.[4] The reticulospinal tract does not decussate. 

There is a laminar distribution of neurons in the gray matter, characterized by density and topography:

  • Lamina I is located at the tip of the dorsal horn and is composed of loosely packed neuropil along with neurons of low neuronal density.[5] The most abundant neuron in lamina I is the Waldeyer cell: large, fusiform, and with a disk-shaped dendritic domain.[6]
  • Lamina II is composed mainly of islet cells with rostrocaudal axes, which contain GABA and are thought to be inhibitory, and stalked cells with dorsoventral dendritic trees.
  • Lamina III has intermediate size cells, including antenna-like and radial neurons.[5] Many of these cells contain GABA or glycine and are also considered inhibitory.[7]
  • Lamina IV contains antenna-like and transverse cells, with dendrites that mainly go to Laminas II and III and whose axons are thought primarily to enter the spinothalamic tract. Lateral from lamina IV is the lateral spinal nucleus, which sends signals to lamina IV from the midbrain and brainstem.[5]
  • Lamina V and VI are composed of medium-sized multipolar neurons that can be fusiform or triangular. These neurons communicate with the reticular formation of the brainstem. 
  • Lamina VII is composed of homogenous medium-sized multipolar neurons and contains, in individual segments, well-defined nuclei, including the intermediolateral nucleus (T1-L1), which has autonomic functions, and the dorsal nucleus of Clarke (T1-L2), which make up the dorsal spinocerebellar tract.
  • Lamina VIII consists of neurons with dorsoventrally polarized dendritic trees.
  • Lamina IX has the cell bodies of motor neurons, with dendrites extending dorsally into laminas as far as VI. Lamina IX also has Renshaw cells, inhibitory interneurons, placed at the medial border of motor nuclei.
  • Lamina X is the substantia grisea centralis, or the gray matter that surrounds the central canal. In the distal portion, lamina X consists of bipolar cells with fan-shaped dendritic trees. In the ventral portion, lamina X consists of bipolar cells with poorly ramified longitudinal dendrites.[8] 


Neurulation begins in the trilaminar embryo when part of the mesoderm differentiates into the notochord. The formation of the notochord signals the overlying ectoderm to form the neural plate, the first structure that will become the nervous system. The neural plate folds in on itself, creating the neural tube, initially open at both ends and ultimately closed. From the neural tube comes the primitive brain and spinal cord.[9] The development of the nervous system begins seventeen days after gestation, and in the fifth week, myotomes start to form, allowing the development of rudimentary reflex circuitries. Myelination of the motor tracts begins in the first few months of life and continues into adolescence.

An interesting note is that reciprocal excitation changes to inhibition between nine and twelve months of age. Before that age, supraspinal descending fibers activate interneurons, resulting in extension or flexion. During this period of development, glycine and GABA are excitatory.[10]


The spinal cord is the conduit between the brain and the rest of the body. It sends motor commands from the motor cortex to the muscles of the body and sensory information from the afferent fibers to the sensory cortex. Additionally, the spinal cord can act without signals from the brain in certain instances. The spinal cord independently coordinates reflexes using reflex arcs. Reflex arcs allow the body to respond to sensory information without waiting for input from the brain. The reflex arc starts with a signal from a sensory receptor, which is carried to the spinal cord via a sensory nerve fiber, synapsed on an interneuron, carried over to the motor neuron, which stimulates an effector muscle or organ.[11] The spinal cord also has central pattern generators, which are interneurons that form the neural circuits, which control rhythmic movements. Although the existence of central pattern generators in humans is controversial, the lumbar spinal cord produces rhythmic muscle activation without volitional motor control or step-specific sensory feedback, suggesting their role in human movement.[12]


Three connective tissue layers, termed meninges, conceal the spinal cord. Directly lining the spinal cord is the pia mater, which also thickens to form the denticulate ligament, anchoring the spinal cord in the middle of the vertebral canal. The next layer of meninges is the arachnoid mater. Between the pia mater and arachnoid mater is the subarachnoid space, which contains CSF. On top of the arachnoid mater is the last layer of meninges, the dura mater, then the epidural space separating the meninges from the vertebral column.[13]

The spinal cord extends from the medulla oblongata of the brain stem at the level of the foramen magnum. In an adult human, the spinal cord gives rise to thirty-one pairs of spinal nerves, each of which originates from the adjacent spinal cord segment: 

  • Cervical nerves (C1-C8): there is an enlargement of the spinal cord here because spinal nerves from this area go to the upper extremities, which have more neural input and output.[14]
  • Thoracic nerves (T1-T12)
  • Lumbar nerves (L1-L5): there is an enlargement here as well, to account for the lower extremities.
  • Sacral nerves (S1-S5)
  • Coccygeal nerve (Co1)

Spinal nerves emerge from the spinal cord as rootlets, which join together to form two nerve roots. The anterior nerve roots contain motor fibers extending from the anterior horn to peripheral target organs. The motor neurons are multipolar, with at least two dendrites, a single axon, and one or more collateral branches. They control skeletal muscles and the autonomic nervous system. The posterior nerve roots contain sensory fibers and dorsal root ganglia. They contain sensory fibers transmitting sensory information from the periphery towards the CNS. The sensory neurons located at the dorsal root ganglia are pseudounipolar. The anterior and posterior nerve roots converge into spinal nerves, which split into dorsal and ventral rami. A dermatome is a skin area innervated by a single spinal nerve root (or spinal cord segment).

There are five spinal plexuses, which include sensory and motor nerves from the anterior rami:

  • Cervical plexus (C1-C5): the deep branches innervate neck muscles, and the superficial branches innervate the skin on the neck, head, and chest. The cranial plexus also has an autonomic function, including controlling the diaphragm and interactions with the vagus nerve.
  • Brachial (C5-T1): controls movement and sensation of the upper extremity.
  • Lumbar (L1-L4): controls movement and sensation of the abdominal wall, thigh, and external genitals.
  • Sacral (L4, L5, S1-S4): controls movement and sensation of the foot, leg, and thigh.
  • Coccygeal (S4, S5, Co): innervates the skin around the tailbone.

In adults, the spinal cord tapers to an end, termed the conus medullaris, at the second lumbar vertebra level. Past the conus medullaris, a bundle of spinal roots extends termed the cauda equina. The cauda equina and the subarachnoid space continue until S2 and is the target location for a lumbar puncture (spinal tap).

Related Testing

Electrophysiological Testing

Evoked potentials (EPs) measure electrical signals going to the brain and can determine whether there is motor or somatosensory impairment. The signal is detected by electroencephalography (EEG) or electromyography (EMG). Evoked potentials may be used to assess spinal cord damage in the setting of spinal cord injury and tumors, and measure functional impairment and predict disease progression in multiple sclerosis.[15] Somatosensory evoked potentials (SEPs) and motor evoked potentials (MEPs) are frequently used intra-operatively for monitoring and can be used post-operatively as surrogate endpoints to check muscle strength and sensory status.[16] 

Nerve conduction studies determine whether there has been an injury to a spinal nerve root, peripheral nerve, neuromuscular junction, muscle, cranial nerve, or spinal nerve. They can also be used to pinpoint spinal cord lesions. Nerve conduction studies work by stimulating nerves close to the skin or using a needle placed near a nerve or nerve root. Neurologists often use them with needle electromyograms.[17]

Lumbar Puncture 

A lumbar puncture, or spinal tap, samples the CSF from the subarachnoid space. The needle to obtain the sample should be inserted between lumbar spinal canal levels L3 and L4 to avoid contact with the spinal cord.[18] The CSF is then sent to a laboratory to establish whether any insult can be determined. For instance, a lumbar puncture can confirm or exclude bacterial meningitis, which will produce a cloudy fluid suggestive of a high leukocyte count. It is also important to know when not to use a lumbar puncture. Contraindications to lumbar puncture include signs of cerebral herniation, focal neurological signs, uncorrected coagulopathies, or cardiorespiratory compromise.[19]

Deep Tendon Testing 

One aspect of the neurological exam is a test of the deep tendon reflexes, which are involuntary motor responses to various stimuli that function via reflex arcs within the spinal cord. They can be used to test the function of the motor and sensory nerves at specific spinal cord levels. Reflex grading is on a scale of 0 (absent reflex) to 5+ (sustained clonus).[20] Some commonly tested reflexes are as follows: 

  • Biceps reflex: C5/C6
  • Brachioradialis reflex: C6
  • Triceps reflex: C7
  • Patellar reflex: L2/L3/L4
  • Achilles reflex: S1 

Additionally, the Babinski reflex, or the extensor plantar reflex, can be seen in newborns but is an abnormal response after six to twelve months of age. If the Babinski reflex is seen after 12 months of age, it may indicate an abnormality in the corticospinal system.[21]


Spinal Cord Injury

Primary spinal cord injury occurs due to local deformation of the spine, such as direct compression. Secondary spinal cord injury occurs following primary damage and involves cascades of biochemical and cellular processes, including electrolyte disturbances, free radical damage, edema, ischemia, and inflammation.[22] Secondary spinal cord injury has several phases: acute, subacute, and chronic. During the acute phase (up to 48 hours after the primary injury), hemorrhage and ischemia lead to ion balance disruption, excitotoxicity, and inflammation. During the subacute phase (up to two weeks following primary injury), there is a phagocytic response and a reactive proliferation of astrocytes, which leads to a glial scar in the chronic phase. The thinking is that scarification is the critical component to permanent disability because it prevents axonal regeneration; axons otherwise could regenerate, but their growth is blocked. However, that notion has been subject to challenge, and there are suggestions that astrocyte scar formation could aid in regeneration.[23] In the chronic phase (over six months after the primary injury), the scarification process is complete.[24]


Open neural tube defects occur when there is a failure of the neural tube to close. If it fails to close at the cranial end, the fetus may develop anencephaly. If the failure is at the caudal end, the fetus may have myelomeningocele or open spina bifida. Craniorachischisis can also occur if the entire neural tube remains open. Closed neural tube defects are spinal cord development problems that are skin-covered, such as occult spina bifida. Folic acid supplements lower the risk of neural tube defects, although severe folate deficiency in mouse models does not lead to neural tube defects unless there is already a genetic predisposition. Suggestions are that folate can overcome a genetic predisposition for adverse effects, potentially leading to neural tube defects.[25]

Clinical Significance

A spinal cord injury can be classified as complete or incomplete. A complete injury, based on the International Standard Neurological Classification of Spinal Cord Injury (ISNCSCI) examination, developed by the American Spinal Cord Injury Association (ASIA), implies that there is no sensation at the inferior segments of the spinal cord (S4-S5); no deep anal pressure (DAP) or voluntary anal contraction (VAC) is present. If no perianal sensation is present and DAP and VAC are absent, the present function below the level of injury is a zone of partial preservation.[26]

An injury in the cervical region often results in quadriplegia if both sides of the spinal cord are affected and hemiplegia if only one side is affected. Nerves from C3, C4, and C5 stimulate the phrenic nerve, which controls the diaphragm, so injury to C4 and above may result in a permanent need for a ventilator. An injury to the thoracic region often limits the function of nerves related to the lower torso and lower extremities. Usually, it does not affect the upper torso and upper extremities, except in rare cases such as subacute posttraumatic ascending myelopathy (SPAM).[27] Injury to the spinal cord often causes loss of bowel and bladder control, loss of sexual function, and blood pressure dysregulation, as the spinal cord relays autonomic and somatic information.


Several syndromes correlate with spinal cord injury. Central cord syndrome usually occurs in individuals who suffer a hyperextension injury, and it often leads to incomplete injury with weakness predominantly affecting the upper limbs. The reason for this phenomenon is the organization of the fibers in the spinal cord: the fibers running to the lower extremities are longer than those running to the upper extremities; the longer fibers are located more laterally in the spinal cord (“L-L rule”). As the central portion of the spinal cord is injured, there is a sparing of the fibers running to the lower extremities. Brown-Sequard syndrome is due to a spinal cord hemisection, leading to a complete loss of sensation at the level of the lesion, as well as deficits below the lesion – loss of proprioception, vibration, and motor control, ipsilaterally, and a loss of pain and temperature sensation, contralaterally. Anterior cord syndrome is due to a compromised blood supply to the anterior two-thirds of the spinal cord, damaging the corticospinal and spinothalamic tracts. This syndrome is associated with several deficits at and below the lesion, including motor loss and a loss of pain and temperature sensation. However, light touch and joint position sense from the dorsal columns are left intact.[26] Injury to T12-L2 segments may result in conus medullaris syndrome, while injury to L3-L5 segments can lead to cauda equina syndrome. Usually, these syndromes present as incomplete injuries and result in neurogenic bladder and/or bowel, loss of sexual function, and perianal loss of sensation.[28]

Article Details

Article Author

Vamsi Reddy

Article Editor:

George Jimsheleishvili


1/29/2022 5:52:13 PM



Bican O,Minagar A,Pruitt AA, The spinal cord: a review of functional neuroanatomy. Neurologic clinics. 2013 Feb;     [PubMed PMID: 23186894]


Honey CM,Ivanishvili Z,Honey CR,Heran MKS, Somatotopic organization of the human spinothalamic tract: in vivo computed tomography-guided mapping in awake patients undergoing cordotomy. Journal of neurosurgery. Spine. 2019 Feb 15     [PubMed PMID: 30771779]


Sakai N,Insolera R,Sillitoe RV,Shi SH,Kaprielian Z, Axon sorting within the spinal cord marginal zone via Robo-mediated inhibition of N-cadherin controls spinocerebellar tract formation. The Journal of neuroscience : the official journal of the Society for Neuroscience. 2012 Oct 31     [PubMed PMID: 23115176]


Chen YT,Li S,Zhou P,Li S, A startling acoustic stimulation (SAS)-TMS approach to assess the reticulospinal system in healthy and stroke subjects. Journal of the neurological sciences. 2019 Apr 15     [PubMed PMID: 30782527]


Schoenen J, The dendritic organization of the human spinal cord: the dorsal horn. Neuroscience. 1982;     [PubMed PMID: 7145088]


Puskár Z,Polgár E,Todd AJ, A population of large lamina I projection neurons with selective inhibitory input in rat spinal cord. Neuroscience. 2001     [PubMed PMID: 11226680]


Todd AJ,Sullivan AC, Light microscope study of the coexistence of GABA-like and glycine-like immunoreactivities in the spinal cord of the rat. The Journal of comparative neurology. 1990 Jun 15;     [PubMed PMID: 2358549]


Honda CN,Lee CL, Immunohistochemistry of synaptic input and functional characterizations of neurons near the spinal central canal. Brain research. 1985 Sep 16;     [PubMed PMID: 2412642]


Colas JF,Schoenwolf GC, Towards a cellular and molecular understanding of neurulation. Developmental dynamics : an official publication of the American Association of Anatomists. 2001 Jun;     [PubMed PMID: 11376482]


Geertsen SS,Willerslev-Olsen M,Lorentzen J,Nielsen JB, Development and aging of human spinal cord circuitries. Journal of neurophysiology. 2017 Aug 1;     [PubMed PMID: 28566459]


PERL ER, A comparison of monosynaptic and polysynaptic reflex responses from individual flexor motoneurones. The Journal of physiology. 1962 Dec;     [PubMed PMID: 13942459]


Minassian K,Hofstoetter US,Dzeladini F,Guertin PA,Ijspeert A, The Human Central Pattern Generator for Locomotion: Does It Exist and Contribute to Walking? The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry. 2017 Dec;     [PubMed PMID: 28351197]


Sakka L,Gabrillargues J,Coll G, Anatomy of the Spinal Meninges. Operative neurosurgery (Hagerstown, Md.). 2016 Jun 1     [PubMed PMID: 29506096]


Ko HY,Park JH,Shin YB,Baek SY, Gross quantitative measurements of spinal cord segments in human. Spinal cord. 2004 Jan     [PubMed PMID: 14713942]


Kraft GH, Evoked potentials in multiple sclerosis. Physical medicine and rehabilitation clinics of North America. 2013 Nov;     [PubMed PMID: 24314688]


Holdefer RN,MacDonald DB,Skinner SA, Somatosensory and motor evoked potentials as biomarkers for post-operative neurological status. Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology. 2015 May;     [PubMed PMID: 25499613]


Mallik A,Weir AI, Nerve conduction studies: essentials and pitfalls in practice. Journal of neurology, neurosurgery, and psychiatry. 2005 Jun;     [PubMed PMID: 15961865]


Doherty CM,Forbes RB, Diagnostic Lumbar Puncture. The Ulster medical journal. 2014 May;     [PubMed PMID: 25075138]


Riordan FA,Cant AJ, When to do a lumbar puncture. Archives of disease in childhood. 2002 Sep;     [PubMed PMID: 12193440]


Clark A,M Das J,Mesfin FB, Trauma Neurological Exam StatPearls. 2021 Jan     [PubMed PMID: 29939692]


Walker HK, The Plantar Reflex 1990;     [PubMed PMID: 21250238]


Ambrozaitis KV,Kontautas E,Spakauskas B,Vaitkaitis D, [Pathophysiology of acute spinal cord injury]. Medicina (Kaunas, Lithuania). 2006;     [PubMed PMID: 16607070]


Tanie Y,Tanabe N,Kuboyama T,Tohda C, Extracellular Neuroleukin Enhances Neuroleukin Secretion From Astrocytes and Promotes Axonal Growth {i}in vitro{/i} and {i}in vivo{/i}. Frontiers in pharmacology. 2018     [PubMed PMID: 30459611]


Kim YH,Ha KY,Kim SI, Spinal Cord Injury and Related Clinical Trials. Clinics in orthopedic surgery. 2017 Mar;     [PubMed PMID: 28261421]


Copp AJ,Greene ND, Neural tube defects--disorders of neurulation and related embryonic processes. Wiley interdisciplinary reviews. Developmental biology. 2013 Mar-Apr;     [PubMed PMID: 24009034]


Kirshblum SC,Burns SP,Biering-Sorensen F,Donovan W,Graves DE,Jha A,Johansen M,Jones L,Krassioukov A,Mulcahey MJ,Schmidt-Read M,Waring W, International standards for neurological classification of spinal cord injury (revised 2011). The journal of spinal cord medicine. 2011 Nov;     [PubMed PMID: 22330108]


Al-Ghatany M,Al-Shraim M,Levi AD,Midha R, Pathological features including apoptosis in subacute posttraumatic ascending myelopathy. Case report and review of the literature. Journal of neurosurgery. Spine. 2005 May     [PubMed PMID: 15945441]


Brouwers E,van de Meent H,Curt A,Starremans B,Hosman A,Bartels R, Definitions of traumatic conus medullaris and cauda equina syndrome: a systematic literature review. Spinal cord. 2017 Oct     [PubMed PMID: 28534496]