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Frontal lobe

From Wikipedia, the free encyclopedia
(Redirected fromFrontal cortex)
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
Acronym(s)FL
MeSHD005625
NeuroNames56
NeuroLex IDbirnlex_928
TA98A14.1.09.110
TA25445
FMA61824
Anatomical terms of neuroanatomy

Thefrontal lobe is the largest of the four majorlobes of the brain inmammals, and is located at the front of eachcerebral hemisphere (in front of theparietal lobe and thetemporal lobe). It is parted from the parietal lobe by agroove between tissues called thecentral sulcus and from the temporal lobe by a deeper groove called thelateral sulcus (Sylvian fissure). The most anterior rounded part of the frontal lobe (though not well-defined) is known as the frontal pole, one of the threepoles of the cerebrum.[1]

The frontal lobe is covered by thefrontal cortex.[2] The frontal cortex includes thepremotor cortex and theprimary motor cortex – parts of themotor cortex. The front part of the frontal cortex is covered by theprefrontal cortex. Thenonprimary motor cortex is a functionally defined portion of the frontal lobe.

There are four principalgyri in the frontal lobe. Theprecentral gyrus is directly anterior to thecentral sulcus, running parallel to it and contains the primary motor cortex, which controls voluntary movements of specific body parts. Three horizontally arranged subsections of thefrontal gyrus are thesuperior frontal gyrus, themiddle frontal gyrus, and theinferior frontal gyrus. The inferior frontal gyrus is divided into three parts – theorbital part, thetriangular part and theopercular part.[3]

The frontal lobe contains most of thedopaminergic neurons in thecerebral cortex. Thedopaminergic pathways are associated withreward,attention,short-term memory tasks,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 each hemisphere.[3] On thelateral 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. E.g., 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.

In humans the frontal lobe reaches full maturity only after the 20s—the prefrontal cortex, in particular, continues in maturing 'til the second and third decades of life[5]—which, thereafter, marks the cognitive maturity associated with adulthood. A small amount ofatrophy, however, is normal in the aging person's frontal lobe. Fjell, in 2009, studied atrophy of the brain in people aged 60–91 years. The 142 healthy participants were scanned usingMRI. Their results were compared to those of 122 participants withAlzheimer's disease. Afollow-up one year later showed there to have been a marked volumetric decline in those with Alzheimer's and a much smaller decline (averaging 0.5%) in the healthy group.[6] These findings corroborate those of Coffey, who in 1992 indicated that the frontal lobe decreases in volume approximately 0.5–1% per year.[7]

Function

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The entirety of the frontal cortex can be considered the "action cortex", much as theposterior cortex is considered the "sensory cortex". It is devoted to action of one kind or another: skeletal movement, ocular movement, speech control, and the expression of emotions. In humans, the largest part of the frontal cortex, theprefrontal cortex (PFC), is responsible for internal, purposeful mental action, commonly called reasoning orprefrontal synthesis.

The function of the PFC involves the ability to project future consequences that result from current actions. PFC functions also include override and suppression of socially unacceptable responses as well as differentiation of tasks.

The PFC also plays an important part in integrating longer non-task based memories stored across the brain. These are often memories associated with emotions derived from input from the brain'slimbic system. The frontal lobe modifies those emotions, generally to fit socially acceptable norms.[citation needed]

Psychological tests that measure frontal lobe function includefinger tapping (as the frontal lobe controls voluntary movement), theWisconsin Card Sorting Test, and measures oflanguage,numeracy skills,[8] and decision making,[9] all of which are controlled by the frontal lobe.

Clinical significance

[edit]
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).[10] 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".[10] Those who are close to the person who has experienced the damage may notice changes in behavior.[11] 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.[10]

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.[10][12]

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.[10][13]

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.[14] 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 by oxidative stress.[14]

Individuals withHIV associated neurocognitive disorders accumulate nuclear andmitochondrial DNA damage in the frontal cortex.[15]

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.[16]

History

[edit]

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,[17] 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"[18]
  • 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)"[19]
  • 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"[20]
  • Single-symptom theories, which propose that a specific dysexecutive symptom (e.g., confabulation) is related to the processes and construct of the underlying structures.[21]

Other theories include:

  • Stuss (1999) suggests a differentiation into two categories according to homogeneity and heterogeneity of function.
  • Grafman's managerial knowledge units (MKU) / structured event complex (SEC) approach (cf. Wood & Grafman, 2003)
  • 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).

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

[edit]

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.[22] 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.[22] This is also evident in thepathways of thelanguage network connecting the frontal and temporal lobes.[23]

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 (2018-10-03), Starcevic, Ana; Filipovic, Branislav (eds.),"Frontal Lobe: Functional Neuroanatomy of Its Circuitry and Related Disconnection Syndromes",Prefrontal Cortex, InTech,doi:10.5772/intechopen.79571,ISBN 978-1-78923-903-4,S2CID 149544570, retrieved2023-06-24
  3. ^abCarpenter, Malcolm (1985).Core text of neuroanatomy (3rd ed.). Williams & Wilkins. pp. 22–23.ISBN 978-0683014556.
  4. ^"Incoming Sensory Information - an overview | ScienceDirect Topics".www.sciencedirect.com. Retrieved2023-03-31.
  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 CE, Wilkinson WE, Parashos IA, Soady SA, Sullivan RJ, Patterson LJ, Figiel GS, Webb MC, Spritzer CE, Djang WT (March 1992). "Quantitative cerebral anatomy of the aging human brain: a cross-sectional study using magnetic resonance imaging".Neurology.42 (3 Pt 1):527–36.doi:10.1212/wnl.42.3.527.PMID 1549213.S2CID 20481757.
  8. ^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.
  9. ^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.
  10. ^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.
  11. ^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.
  12. ^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.
  13. ^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.S2CID 74081936.
  14. ^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.S2CID 1867993.
  15. ^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.S2CID 23744888.
  16. ^"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.
  17. ^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.S2CID 26307989.
  18. ^(Burgess, 2003, p. 309).
  19. ^(Burgess, 2003, p. 310).
  20. ^(Stuss, 1999, p. 348; cf. Burgess & Simons, 2005).
  21. ^(cf. Burgess & Simons, 2005).
  22. ^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.S2CID 5921065.
  23. ^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.S2CID 15609709.

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
Frontal lobe
Superolateral
Prefrontal
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Parietal lobe
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Occipital lobe
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sulci/fissures
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Limbic lobe
Parahippocampal gyrus
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Insular cortex
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