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Pyramidal tracts

From Wikipedia, the free encyclopedia
Central nervous system pathways
Pyramidal tracts
Deep dissection of brain-stem. Lateral view. ("pyramidal tract" visible in red, and "pyramidal decussation" labeled at lower right.)
Spinal cord tracts, withpyramidal tracts labeled at upper left
Details
DecussationMany fibres in themedullary pyramids
FromCerebral cortex
ToSpinal cord (corticospinal) orbrainstem (corticobulbar)
Identifiers
Latintractus pyramidalis
tractus corticospinalis
MeSHD011712
NeuroNames1320
NeuroLex IDbirnlex_1464
TA98A14.1.04.102
A14.1.06.102
TA26040
FMA72634
Anatomical terms of neuroanatomy

Thepyramidal tracts include both thecorticobulbar tract and thecorticospinal tract. These are aggregations ofefferent nerve fibers from theupper motor neurons that travel from thecerebral cortex and terminate either in thebrainstem (corticobulbar) orspinal cord (corticospinal) and are involved in thecontrol of motor functions of the body.

The corticobulbar tract conductsimpulses from thebrain to thecranial nerves.[1] These nerves control the muscles of the face and neck and are involved in facial expression, mastication, swallowing, and other motor functions.

Thecorticospinal tract conducts impulses from the brain to the spinal cord. It is made up of alateral andanterior tract. The corticospinal tract is involved in voluntary movement. The majority of fibres of the corticospinal tractcross over in themedulla oblongata, resulting in muscles being controlled by the opposite side of the brain. The corticospinal tract contains theaxons of the pyramidal cells, the largest of which are theBetz cells, located in theprimary motor cortex.

The pyramidal tracts are named because they pass through thepyramids of themedulla oblongata. The corticospinal fibers converge to a point when descending from theinternal capsule to the brain stem from multiple directions, giving the impression of an inverted pyramid. Involvement of the pyramidal tract at any level leads topyramidal signs.

Themyelination of the pyramidal fibres is incomplete at birth and gradually progresses in cranio-caudal direction and thereby progressivelygaining functionality. Most of the myelination is complete by two years of age and thereafter it progresses very slowly in cranio-caudal direction up to twelve years of age.

Structure

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Pyramidal tracts

The termpyramidal tracts refers toupper motor neurons that originate in thecerebral cortex and terminate in thespinal cord (corticospinal) orbrainstem (corticobulbar). Nerves emerge in thecerebral cortex, pass down and maycross sides in themedulla oblongata, and travel as part of thespinal cord until theysynapse withinterneurons in thegrey column of the spinal cord.[2]

There is some variation in terminology. Thepyramidal tracts definitively encompass thecorticospinal tracts, and many authors also include thecorticobulbar tracts.[3]

Corticospinal tract

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Further information:Corticospinal tract

Nerve fibres in the corticospinal tract originate frompyramidal cells in layer V of thecerebral cortex. Fibres arise from theprimary motor cortex (about 30%),supplementary motor area and thepremotor cortex (together also about 30%), and thesomatosensory cortex,parietal lobe, andcingulate gyrus supplies the rest.[2] The cells have theirbodies in the cerebral cortex, and theaxons form the bulk of the pyramidal tracts.[4] The nerve axons travel from the cortex through theposterior limb of internal capsule, through thecerebral peduncle and into thebrainstem and anteriormedulla oblongata. Here they form two prominences called themedulla oblongatary pyramids. Below the prominences, the majority of axons cross over to the opposite side from which they originated, known asdecussation. The axons that cross over move to the outer part of the medulla oblongata and form thelateral corticospinal tract, whereas the fibres that remain form theanterior corticospinal tract.[2] About 80% of axons cross over and form the lateral corticospinal tract; 10% do not cross over and join the tract, and 10% of fibres travel in the anterior corticospinal tract.[citation needed]

The nerve axons traveling down the tract are theefferent nerve fibers of theupper motor neurons. These axons travel down the tracts in thewhite matter of the spinal cord until they reach thevertebral level of the muscle that they will innervate.[5] At this point, the axonssynapse withlower motor neurons. The majority of axons do not directly synapse with lower motor neurons, but instead synapse with aninterneuron that then synapses with a lower motor neuron. This generally occurs in theanterior grey column.[2] Nerve axons of the lateral corticospinal tract that did not cross over in the medulla oblongata do so at the level of the spinal cord they terminate in.[6]

These tracts contain more than 1 million axons and the majority of the axons are myelinated. The corticospinal tracts myelinate largely during the first and second years after birth. The majority of nerve axons are small (<4μm) in diameter. About 3% of nerve axons have a much larger diameter (16μm) and arise fromBetz cells, mostly in the leg area of the primary motor cortex. These cells are notable because of their rapid conduction rate, over 70m/sec, the fastest conduction of any signals from the brain to the spinal cord.[2]

Horizontal section through the lower part of the pons, showing the fibers of the corticospinal tract (#19) passing through the pontine nuclei

Corticobulbar tract

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Further information:Corticobulbar tract

Fibres from theventralmotor cortex travel with the corticospinal tract through the internal capsule, but terminate in a number of locations in themidbrain (cortico-mesencephalic tract),pons (Corticopontine tract), andmedulla oblongata (cortico-bulbar tract).[6] Theupper motor neurons of the corticobulbar tract synapse with interneurons or directly with the lower motor neurons located in the motorcranial nerve nuclei, namelyoculomotor,trochlear, motor nucleus of thetrigeminal nerve,abducens,facial nerve andaccessory and in thenucleus ambiguus to thehypoglossal,vagus andaccessory nerves.[6] These nuclei are supplied by nerves from both sides of the brain, with the exception of the parts of the facial nerve that control muscles of the lower face. These muscles are only innervated by nerves from the contralateral (opposite) side of the cortex.[6]

Function

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The nerves within the corticospinal tract are involved inmovement ofmuscles of the body. Because of the crossing-over of fibres, muscles are supplied by the side of the brain opposite to that of the muscle.[2] The nerves within the corticobulbar tract are involved in movement in muscles of the head. They are involved in swallowing,phonation, and movements of the tongue.[6] By virtue of involvement with thefacial nerve, the corticobulbar tract is also responsible for transmittingfacial expression.[5] With the exception of lower muscles of facial expression, all functions of the corticobulbar tract involve inputs from both sides of the brain.[5]

Theextrapyramidal system refers to tracts within the spinal cord involved in involuntary movement but not part of the pyramidal tracts.[2] Their functions include the control of posture andmuscle tone.[citation needed]

Clinical significance

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Further information:Pyramidal signs
  1. Damage to the fibres of the corticospinal tracts, anywhere along their course from the cerebral cortex to the lower end of the spinal cord, can cause anupper motor neuron syndrome.
  2. A few days after the injury to the upper motor neurons, a pattern of motor signs and symptoms appears, includingspasticity, hyperactive reflexes, a loss of the ability to performfine movements, and anextensorplantar response known as theBabinski sign.[7]
  3. Symptoms generally occur alongside other sensory problems.
  4. Causes may include disorders such asstrokes,[8]cerebral palsy,[9][10]subdural hemorrhage,abscesses andtumours, neurodegenerative diseases such asmultiple system atrophy, inflammation such asmeningitis andmultiple sclerosis, and trauma to the spinal cord, including fromslipped discs.[4]
  5. If thecorticobulbar tract is damaged on only one side, then only the lower face will be affected, however if there is involvement of both the left and right tracts, then the result ispseudobulbar palsy. This causes problems with swallowing, speaking, andemotional lability.[4]
  6. Severe disabling involuntary movements such ashemiballismus or severechorea might exhaust the patient and become a life-threatening situation.
  7. In the past, this condition was treated by partial section of the pyramidal tract either at theprimary motor cortex or at thecerebral crus (pedunculotomy).[11]

Additional images

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  • Dissection of brain-stem. Lateral view.
    Dissection of brain-stem. Lateral view.
  • Superficial dissection of brain-stem. Ventral view.
    Superficial dissection of brain-stem. Ventral view.
  • The motor tract.
    The motor tract.
  • Diagram of the principal fasciculi of the spinal cord, from Gray's anatomy
    Diagram of the principal fasciculi of the spinal cord, fromGray's anatomy

In popular culture

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InNational Lampoon's European Vacation, the Griswold family wins a vacation on a game show calledPig in a Poke when their opponents fail to correctly answer a question about the pyramidal tracts, despite Clark Griswold (played by Chevy Chase) mistakenly answering that they are a housing development outside Cairo.[12]

References

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  1. ^Chapter 9 of "Principles of Physiology" (3rd edition) by Robert M. Berne and Mathew N. Levy. Published by Mosby, Inc. (2000)ISBN 0-323-00813-5.
  2. ^abcdefgHall, Arthur C. Guyton, John E. (2005).Textbook of medical physiology (11th ed.). Philadelphia: W.B. Saunders. pp. 687–690.ISBN 978-0-7216-0240-0.{{cite book}}: CS1 maint: multiple names: authors list (link)
  3. ^Anthoney, Terence R. (1994).Neuroanatomy and the neurologic exam: a thesaurus of synonyms, similar-sounding non-synonyms, and terms of variable meaning. Boca Raton: CRC Press. pp. 458–460.ISBN 978-0-8493-8631-2.Archived from the original on 2018-05-03.
  4. ^abcFauci, Anthony S.; Harrison, T. R., eds. (2008).Harrison's principles of internal medicine (17th ed.). New York: McGraw-Hill Medical. pp. 147–149.ISBN 978-0-07-147692-8.
  5. ^abcArslan, Orhan (2001).Neuroanatomical Basis of Clinical Neurology. CRC Press. p. 368.ISBN 1-4398-0613-6.Archived from the original on 2018-05-03.
  6. ^abcdeYoung, Paul A. (2007).Basic clinical neuroscience (2nd ed.). Philadelphia, Pa.: Lippincott Williams & Wilkins. pp. 69–70.ISBN 978-0-7817-5319-7.Archived from the original on 2017-03-13.
  7. ^Neuroscience (2. ed.). Sunderland, Mass: Sinauer Assoc. 2001. pp. Damage to Descending Motor Pathways: The Upper Motor Neuron Syndrome.ISBN 0-87893-742-0.Archived from the original on 2018-05-03.
  8. ^Topcuoglu, MA; Saka, E; Silverman, SB; Schwamm, LH; Singhal, AB (1 September 2017)."Recrudescence of Deficits After Stroke: Clinical and Imaging Phenotype, Triggers, and Risk Factors".JAMA Neurology.74 (9):1048–1055.doi:10.1001/jamaneurol.2017.1668.PMC 5710180.PMID 28783808.
  9. ^Vitrikas, K; Dalton, H; Breish, D (15 February 2020). "Cerebral Palsy: An Overview".American Family Physician.101 (4):213–220.PMID 32053326.
  10. ^Farag, Sara M.; Mohammed, Manal O.; EL-Sobky, Tamer A.; ElKadery, Nadia A.; ElZohiery, Abeer K. (March 2020)."Botulinum Toxin A Injection in Treatment of Upper Limb Spasticity in Children with Cerebral Palsy".JBJS Reviews.8 (3) e0119.doi:10.2106/JBJS.RVW.19.00119.PMC 7161716.PMID 32224633.
  11. ^DeMyer, William (1998).Neuroanatomy. Williams & Wilkins.ISBN 978-0-683-30075-8.Archived from the original on 2018-03-03.
  12. ^"Quotes from "National Lampoon's European Vacation"".Archived from the original on 25 March 2017. Retrieved3 May 2018 – via www.imdb.com.

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