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Frontal lobe

From Wikipedia, the free encyclopedia
Part of the brain
Not to be confused withPrefrontal cortex.
Frontal lobe
Principal fissures and lobes of thecerebrum viewed laterally (Frontal lobe is shown in blue.).
Details
Part ofCerebrum
ArteryAnterior cerebral
Middle cerebral
Identifiers
Latinlobus frontalis
AcronymFL
MeSHD005625
NeuroNames56
NeuroLex IDbirnlex_928
TA98A14.1.09.110
TA25445
FMA61824
Anatomical terms of neuroanatomy

Thefrontal lobe is the largestlobe of the vertebrate brain and the most anterior lobe of thecerebral hemispheres. The anatomicalgroove known as thecentral sulcus separates the frontal lobe from theparietal lobe, and the deeper anatomical groove called thelateral sulcus separates the frontal lobe from thetemporal lobe. The most anterior ventral, orbital end of the frontal lobe is known as the frontal pole, which is one of the three so-calledpoles of the cerebrum.[1]

The outer, multifurrowed surface of the frontal lobe is called thefrontal cortex.[2] Like all cortical tissue, the frontal cortex is a thin layer of gray matter making up the outer portion of the brain. The frontal cortex is further subdivided into several anatomical and functional structures, including those of themotor cortex (thepremotor cortex, thenonprimary motor cortex, theprimary motor cortex) and theprefrontal cortex (e.g., thedorsolateral prefrontal cortex).

Located in the frontal lobe are also four principalgyri. Theprecentral gyrus is directly anterior to thecentral sulcus, running parallel to it and containing theprimary motor cortex, which controls voluntary movements ofspecific body parts. Three other frontal gyri, horizontally arranged, are thesuperior frontal gyrus, themiddle frontal gyrus, and theinferior frontal gyrus. The inferior frontal gyrus is further subdivided into theorbital part, thetriangular part, and theopercular part,[3] and it is functionally known as theventrolateral prefrontal cortex.

The frontal lobe further contains most of thedopaminergic neurons in thecerebral cortex.Dopaminergic pathways are associated withreward,attention,short-term memory,planning, andmotivation.Dopamine tends to limit and selectsensory information coming from thethalamus to theforebrain.[4]

Structure

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Frontal lobe (red) of left cerebral hemisphere

The frontal lobe is the largest lobe of the brain and makes up about a third of the surface area of eachhemisphere.[3] On the dorsal surface of each hemisphere, thecentral sulcus separates the frontal lobe from the parietal lobe. Thelateral sulcus separates the frontal lobe from thetemporal lobe.

The frontal lobe can be divided into a lateral, polar, orbital (above theorbit; also called basal orventral), andmedial part. Each of these parts consists of a particulargyrus:

The gyri are separated bysulci. For example, the precentral gyrus is in front of the central sulcus, and behind theprecentral sulcus. The superior and middle frontal gyri are divided by thesuperior frontal sulcus. The middle and inferior frontal gyri are divided by theinferior frontal sulcus.

The human frontal lobe reaches full maturity only at mid to late 20s (25-30 years of age)—in fact, the prefrontal cortex, in particular, continues to mature well into the third decade.[5] A small amount ofatrophy, however, is normal in the aging person's frontal lobe. Fjell et al. (2009), studying the rate of brain atrophy over time among 142 healthy adults aged 60–91 years compared with 122 patients withAlzheimer's disease, showed that there was a marked volumetric decline in those with Alzheimer's and a much smaller decline (averaging 0.5%) in the healthy group at the 1-yearfollow-up.[6] These findings replicate those of Coffey et al. (1992), whose results also showed that the frontal lobe decreases in volume approximately 0.5–1% per year.[7]

Function

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The frontal lobe, which comprises several anatomical and functional structures, supports, among other things, goal-directed behavior and abstract mental representations (e.g., the phenomenal, human ability to transcend the immediate spatiotemporal context by imagining oneself in the future).[8][9] It is a mistake to believe that the primary function of the frontal lobe isaction—that it is wholly committed, for instance, to reasoning and thus the regulation of sensory phenomena such asemotion oraffect.[10][11][12][13][14]

Psychological tests that measure the functional integrity of the structures belonging to the frontal lobe includefinger tapping, theWisconsin Card Sorting Test, and measures oflanguage,numeracy skills,[15] and decision making.[16]

Clinical significance

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Main article:Frontal lobe disorder
Main article:Frontal lobe injury

Damage

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Damage to the frontal lobe can occur in a number of ways and result in many different consequences.Transient ischemic attacks (TIAs) also known as mini-strokes, andstrokes are common causes of frontal lobe damage in older adults (65 and over). These strokes and mini-strokes can occur due to the blockage ofblood flow to the brain or as a result of the rupturing of ananeurysm in acerebral artery. Other ways in which injury can occur includetraumatic brain injuries incurred following accidents, diagnoses such asAlzheimer's disease orParkinson's disease (which causedementia symptoms), andfrontal lobe epilepsy (which can occur at any age).[17] Very often, frontal lobe damage is recognized in those withprenatal alcohol exposure.

Symptoms

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Common effects of damage to the frontal lobe are varied. Patients who have experienced frontal lobe trauma may know the appropriate response to a situation but display inappropriate responses to those same situations in real life[citation needed]. Similarly, emotions that are felt may not be expressed in the face or voice. For example, someone who is feeling happy would not smile, and the voice would be devoid of emotion. Along the same lines, though, the person may also exhibit excessive, unwarranted displays of emotion. Depression is common in stroke patients. Also common is a loss of or decrease in motivation. Someone might not want to carry out normal daily activities and would not feel "up to it".[17] Those who are close to the person who has experienced the damage may notice changes in behavior.[18] The case ofPhineas Gage was long considered exemplary of these symptoms, though morerecent research has suggested that accounts of his personality change have been poorly evidenced. The frontal lobe is the same part of the brain that is responsible forexecutive functions such as planning for the future, judgment, decision-making skills,attention span, and inhibition. These functions can decrease in someone whose frontal lobe is damaged.[17]

Consequences that are seen less frequently are also varied.Confabulation may be the most frequently indicated "less common" effect. In the case of confabulation, someone gives false information while maintaining the belief that it is the truth. In a small number of patients, uncharacteristic cheerfulness can be noted. This effect is seen mostly in patients with lesions to the right frontal portion of the brain.[17][19]

Another infrequent effect is that ofreduplicative paramnesia, in which patients believe that the location in which they currently reside is a replica of one located somewhere else. Similarly, those who experienceCapgras syndrome after frontal lobe damage believe that an identical "replacement" has taken the identity of a close friend, relative, or other person and is posing as that person. This last effect is seen mostly in schizophrenic patients who also have a neurological disorder in the frontal lobe.[17][20]

DNA damage

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In the human frontal cortex, a set of genes undergo reduced expression after age 40 and especially after age 70.[21] This set includes genes that have key functions insynaptic plasticity important in learning and memory,vesicular transport andmitochondrial function. Duringaging,DNA damage is markedly increased in thepromoters of the genes displaying reduced expression in the frontal cortex. In cultured human neurons, these promoters are selectively damaged byoxidative stress.[21]

Individuals withHIV associated neurocognitive disorders accumulate nuclear andmitochondrial DNA damage in the frontal cortex.[22]

Genetic

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A report from theNational Institute of Mental Health says agene variant of(COMT) that reduces dopamine activity in theprefrontal cortex is related to poorer performance and inefficient functioning of that brain region during working memory, tasks, and to a slightly increased risk forschizophrenia.[23]

History

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Psychosurgery

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In the early 20th century, a medical treatment formental illness, first developed byPortugueseneurologistEgas Moniz, involved damaging the pathways connecting the frontal lobe to thelimbic system. A frontallobotomy (sometimes called frontal leucotomy) successfully reduced distress but at the cost of often blunting the subject's emotions, volition andpersonality. The indiscriminate use of thispsychosurgical procedure, combined with its severe side effects and amortality rate of 7.4 to 17 per cent,[24] earned it a bad reputation. The frontal lobotomy has largely died out as a psychiatric treatment. More precise psychosurgical procedures are still used, although rarely. They may include anterior capsulotomy (bilateral thermal lesions of the anterior limbs of theinternal capsule) or thebilateral cingulotomy (involving lesions of the anteriorcingulate gyri) and might be used to treat otherwise untreatableobsessional disorders orclinical depression.

Theories of function

[edit]

Theories of frontal lobe function can be separated into four categories:

  • Single-process theories, which propose that "damage to a single process or system is responsible for a number of differentdysexecutive symptoms"[25]
  • Multi-process theories, which propose "that the frontal lobe executive system consists of a number of components that typically work together in everyday actions (heterogeneity of function)"[26]
  • Construct-led theories, which propose that "most if not all frontal functions can be explained by one construct (homogeneity of function) such as working memory or inhibition"[27]
  • Single-symptom theories, which propose that a specific dysexecutive symptom (e.g., confabulation) is related to the processes and construct of the underlying structures.[28]

Other theories include:

  • Stuss (1999) suggests a differentiation into two categories according to homogeneity and heterogeneity of function.[full citation needed]
  • Grafman's managerial knowledge units (MKU) / structured event complex (SEC) approach (cf. Wood & Grafman, 2003)[full citation needed]
  • Miller & Cohen's integrative theory of prefrontal functioning (e.g. Miller & Cohen, 2001)
  • Rolls's stimulus-reward approach and Stuss's anterior attentional functions (Burgess & Simons, 2005; Burgess, 2003; Burke, 2007).[full citation needed]

It may be highlighted that the theories described above differ in their focus on certain processes/systems or construct-lets.[clarification needed] Stuss (1999) remarks that the question of homogeneity (single construct) or heterogeneity (multiple processes/systems) of function "may represent a problem of semantics and/or incomplete functional analysis rather than an unresolvable dichotomy" (p. 348). However, further research will show if a unified theory of frontal lobe function that fully accounts for the diversity of functions will be available.

Other primates

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Many scientists had thought that the frontal lobe was disproportionately enlarged in humans compared to other primates. This was thought to be an important feature of human evolution and seen as the primary reason why human cognition differs from that of other primates. However, this view in relation to great apes has since been challenged byneuroimaging studies. Usingmagnetic resonance imaging to determine the volume of the frontal cortex in humans, all extant ape species, and severalmonkey species, it was found that the human frontal cortex was not relatively larger than the cortex of othergreat apes, but was relatively larger than the frontal cortex oflesser apes and the monkeys.[29] The higher cognition of the humans is instead seen to relate to a greater connectedness given byneural tracts that do not affect the cortical volume.[29] This is also evident in thepathways of thelanguage network connecting the frontal and temporal lobes.[30]

See also

[edit]
This article usesanatomical terminology.

References

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  1. ^Muzio, Bruno Di."Frontal pole | Radiology Reference Article | Radiopaedia.org".radiopaedia.org.
  2. ^João, Rafael Batista; Filgueiras, Raquel Mattos (2018). "Frontal Lobe: Functional Neuroanatomy of Its Circuitry and Related Disconnection Syndromes".Prefrontal Cortex.doi:10.5772/intechopen.79571.ISBN 978-1-78923-903-4.
  3. ^abCarpenter, Malcolm (1985).Core text of neuroanatomy (3rd ed.). Williams & Wilkins. pp. 22–23.ISBN 978-0683014556.
  4. ^McAlonan, Kerry; Brown, Verity J.; Bowman, Eric M. (2000-12-01)."Thalamic Reticular Nucleus Activation Reflects Attentional Gating during Classical Conditioning".Journal of Neuroscience.20 (23):8897–8901.doi:10.1523/JNEUROSCI.20-23-08897.2000.ISSN 0270-6474.PMC 6773087.PMID 11102499.
  5. ^Kolk, Sharon M.; Rakic, Pasko (January 2022)."Development of prefrontal cortex".Neuropsychopharmacology.47 (1):41–57.doi:10.1038/s41386-021-01137-9.ISSN 1740-634X.PMC 8511863.PMID 34645980.
  6. ^Fjell AM, Walhovd KB, Fennema-Notestine C, McEvoy LK, Hagler DJ, Holland D, Brewer JB, Dale AM (December 2009)."One-year brain atrophy evident in healthy aging".The Journal of Neuroscience.29 (48):15223–31.doi:10.1523/JNEUROSCI.3252-09.2009.PMC 2827793.PMID 19955375.
  7. ^Coffey, C. E.; Wilkinson, W. E.; Parashos, La.; Soady, S.A.R.; Sullivan, R. J.; Patterson, L. J.; Figiel, G. S.; Webb, M. C.; Spritzer, C. E.; Djang, W. T. (March 1992). "Quantitative cerebral anatomy of the aging human brain: A cross-sectional study using magnetic resonance imaging".Neurology.42 (3):527–536.doi:10.1212/wnl.42.3.527.PMID 1549213.
  8. ^Stuss, D. T. (2001-02-01)."The frontal lobes are necessary for 'theory of mind'".Brain.124 (2):279–286.doi:10.1093/brain/124.2.279.PMID 11157555.
  9. ^Badre, David; D'Esposito, Mark (September 2009)."Is the rostro-caudal axis of the frontal lobe hierarchical?".Nature Reviews Neuroscience.10 (9):659–669.doi:10.1038/nrn2667.ISSN 1471-0048.PMC 3258028.PMID 19672274.
  10. ^Dixon, Matthew L.; Thiruchselvam, Ravi; Todd, Rebecca; Christoff, Kalina (October 2017)."Emotion and the prefrontal cortex: An integrative review".Psychological Bulletin.143 (10):1033–1081.doi:10.1037/bul0000096.ISSN 1939-1455.PMID 28616997.
  11. ^Koban, Leonie; Gianaros, Peter J.; Kober, Hedy; Wager, Tor D. (May 2021)."The self in context: brain systems linking mental and physical health".Nature Reviews Neuroscience.22 (5):309–322.doi:10.1038/s41583-021-00446-8.ISSN 1471-003X.PMC 8447265.PMID 33790441.
  12. ^Binder, Jeffrey R. (August 2016)."In defense of abstract conceptual representations".Psychonomic Bulletin & Review.23 (4):1096–1108.doi:10.3758/s13423-015-0909-1.ISSN 1069-9384.PMID 27294428.
  13. ^Buckner, Randy L.; DiNicola, Lauren M. (October 2019)."The brain's default network: updated anatomy, physiology and evolving insights".Nature Reviews Neuroscience.20 (10):593–608.doi:10.1038/s41583-019-0212-7.ISSN 1471-003X.PMID 31492945.
  14. ^Fedorenko, Evelina; Blank, Idan A. (2020-04-01)."Broca's Area Is Not a Natural Kind".Trends in Cognitive Sciences.24 (4):270–284.doi:10.1016/j.tics.2020.01.001.ISSN 1364-6613.PMC 7211504.PMID 32160565.
  15. ^Kimberg DY, Farah MJ (December 1993). "A unified account of cognitive impairments following frontal lobe damage: the role of working memory in complex, organized behavior".Journal of Experimental Psychology. General.122 (4):411–28.doi:10.1037/0096-3445.122.4.411.PMID 8263463.
  16. ^Yang X, Gao M, Shi J, Ye H, Chen S (2017)."Modulating the Activity of the DLPFC and OFC Has Distinct Effects on Risk and Ambiguity Decision-Making: A tDCS Study".Frontiers in Psychology.8 1417.doi:10.3389/fpsyg.2017.01417.PMC 5572270.PMID 28878714.
  17. ^abcdeStuss DT, Gow CA, Hetherington CR (June 1992). ""No longer Gage": frontal lobe dysfunction and emotional changes".Journal of Consulting and Clinical Psychology.60 (3):349–59.doi:10.1037/0022-006X.60.3.349.PMID 1619089.
  18. ^Rowe AD, Bullock PR, Polkey CE, Morris RG (March 2001).""Theory of mind" impairments and their relationship to executive functioning following frontal lobe excisions".Brain.124 (Pt 3):600–16.doi:10.1093/brain/124.3.600.PMID 11222459.
  19. ^Robinson RG, Kubos KL, Starr LB, Rao K, Price TR (March 1984). "Mood disorders in stroke patients. Importance of location of lesion".Brain. 107 ( Pt 1) (1):81–93.doi:10.1093/brain/107.1.81.PMID 6697163.
  20. ^Durani SK, Ford R, Sajjad SH (September 1991). "Capgras syndrome associated with a frontal lobe tumour".Irish Journal of Psychological Medicine.8 (2):135–6.doi:10.1017/S0790966700015093.
  21. ^abLu T, Pan Y, Kao SY, Li C, Kohane I, Chan J, Yankner BA (June 2004). "Gene regulation and DNA damage in the ageing human brain".Nature.429 (6994):883–91.Bibcode:2004Natur.429..883L.doi:10.1038/nature02661.PMID 15190254.
  22. ^Zhang Y, Wang M, Li H, Zhang H, Shi Y, Wei F, Liu D, Liu K, Chen D (June 2012). "Accumulation of nuclear and mitochondrial DNA damage in the frontal cortex cells of patients with HIV-associated neurocognitive disorders".Brain Research.1458:1–11.doi:10.1016/j.brainres.2012.04.001.PMID 22554480.
  23. ^"Gene Slows Frontal Lobes, Boosts Schizophrenia Risk". National Institute of Mental Health. May 29, 2001. Archived fromthe original on 2015-04-04. Retrieved2013-06-20.
  24. ^Ogren K, Sandlund M (2007). "Lobotomy at a state mental hospital in Sweden. A survey of patients operated on during the period 1947–1958".Nordic Journal of Psychiatry.61 (5):355–62.doi:10.1080/08039480701643498.PMID 17990197.
  25. ^(Burgess, 2003, p. 309).[full citation needed]
  26. ^(Burgess, 2003, p. 310).[full citation needed]
  27. ^(Stuss, 1999, p. 348; cf. Burgess & Simons, 2005).[full citation needed]
  28. ^(cf. Burgess & Simons, 2005).[full citation needed]
  29. ^abSemendeferi K, Lu A, Schenker N, Damasio H (March 2002). "Humans and great apes share a large frontal cortex".Nature Neuroscience.5 (3):272–6.doi:10.1038/nn814.PMID 11850633.
  30. ^Friederici AD (April 2009). "Pathways to language: fiber tracts in the human brain".Trends in Cognitive Sciences.13 (4):175–81.doi:10.1016/j.tics.2009.01.001.PMID 19223226.

Further reading

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  • Donald T. Stuss and Robert T. Knight (Eds.),Principles of Frontal Lobe Function, Second Edition, Oxford University Press, New York, 2013.

External links

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Anatomy of thecerebral cortex of thehuman brain
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Prefrontal
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