请输入您要查询的百科知识:

 

词条 Frontal lobe
释义

  1. Structure

  2. Function

  3. Clinical significance

     Damage  Symptoms  DNA damage  Genetic 

  4. History

      Psychosurgery    Theories of function  

  5. Other animals

  6. See also

  7. References

  8. External links

{{Infobox brain
| Name = Frontal lobe
| Latin = Lobus Frontalis
|
| Image = LobesCaptsLateral.png
| Caption = Principal fissures and lobes of the cerebrum viewed laterally. (Frontal lobe is shown in pale green.)
| Image2 = Gray729.png
| IsPartOf = Cerebrum
| Components =
| Artery = Anterior cerebral
Middle cerebral
| Vein =
| Acronym = FL
}}{{confused | Prefrontal cortex}}

The frontal lobe is the largest of the four major lobes of the brain in mammals, and is located at the front of each hemisphere (in front of the parietal lobe and the temporal lobe). It is separated from the parietal lobe by a groove between tissues called the central sulcus, and from the temporal lobe by a deeper groove called the lateral 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 three poles of the cerebrum.[1]

The frontal lobe is covered by the frontal cortex. The frontal cortex includes the premotor cortex, and the primary motor cortex – cortical parts of the motor cortex. The front part of the frontal lobe is covered by the prefrontal cortex.

There are four principal gyri in the frontal lobe. The precentral gyrus, is directly anterior to the central sulcus, running parallel to it and contains the primary motor cortex, which controls voluntary movements of specific body parts. Three horizontally arranged subsections of the frontal gyrus are the superior frontal gyrus, the middle frontal gyrus, and the inferior frontal gyrus. The inferior frontal gyrus is divided into three parts – the orbital part, the triangular part, and the opercular part.[2]

The frontal lobe contains most of the dopamine neurons in the cerebral cortex. The dopaminergic pathways are associated with reward, attention, short-term memory tasks, planning, and motivation. Dopamine tends to limit and select sensory information arriving from the thalamus to the forebrain.

Structure

The frontal lobe is the largest lobe of the brain and makes up about a third of the surface area of each hemisphere.[2] On the lateral surface of each hemisphere, the central sulcus separates the frontal lobe from the parietal lobe. The lateral sulcus separates the frontal lobe from the temporal lobe.

The frontal lobe can be divided into a lateral, polar, orbital (above the orbit; also called basal or ventral), and medial part. Each of these parts consists of a particular gyrus:

  • Lateral part: lateral part of the superior frontal gyrus, middle frontal gyrus, inferior frontal gyrus.
  • Polar part: Transverse frontopolar gyri, frontomarginal gyrus.
  • Orbital part: Lateral orbital gyrus, anterior orbital gyrus, posterior orbital gyrus, medial orbital gyrus, gyrus rectus.
  • Medial part: Medial part of the superior frontal gyrus, cingulate gyrus.

The gyri are separated by sulci. E.g., the precentral gyrus is in front of the central sulcus, and behind the precentral sulcus. The superior and middle frontal gyri are divided by the superior frontal sulcus. The middle and inferior frontal gyri are divided by the inferior frontal sulcus.

In humans, the frontal lobe reaches full maturity around the late 20s,[3] marking the cognitive maturity associated with adulthood. A small amount of atrophy, 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 using MRI. Their results were compared to those of 122 participants with Alzheimer's disease. A follow-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.[4] These findings corroborate those of Coffey, who in 1992 indicated that the frontal lobe decreases in volume approximately 0.5%–1% per year.[5]

Function

The frontal lobe plays a large role in voluntary movement. It houses the primary motor cortex which regulates activities like walking.

The function of the frontal lobe involves the ability to project future consequences resulting from current actions. Frontal lobe functions also include override and suppression of socially unacceptable response as well as differentiation tasks.

The frontal lobe 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's limbic system. The frontal lobe modifies those emotions to generally fit socially acceptable norms.

Psychological tests that measure frontal lobe function include finger tapping (as the frontal lobe controls voluntary movement), the Wisconsin Card Sorting Test, and measures of language and numeracy skills.[6]

Clinical significance

Damage

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, and strokes are common causes of frontal lobe damage in older adults (65 and over). These strokes and mini-strokes can occur due to the blockage of blood flow to the brain or as a result of the rupturing of an aneurysm in a cerebral artery. Other ways in which injury can occur include head injuries such as traumatic brain injuries incurred following accidents, diagnoses such as Alzheimer's disease or Parkinson's disease (which cause dementia symptoms), and frontal lobe epilepsy (which can occur at any age).[7]

Symptoms

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". 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".[7] Those who are close to the person who has experienced the damage may notice changes in behavior.[8] This personality change is characteristic of damage to the frontal lobe and was exemplified in the case of Phineas Gage. The frontal lobe is the same part of the brain that is responsible for executive functions such as planning for the future, judgment, decision-making skills, attention span, and inhibition. These functions can decrease drastically in someone whose frontal lobe is damaged.[7]

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.[7][9]

Another infrequent effect is that of reduplicative paramnesia, in which patients believe that the location in which they currently reside is a replica of one located somewhere else. Similarly, those who experience Capgras 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.[7][10]

DNA damage

In the human frontal cortex, a set of genes undergo reduced expression after age 40 and especially after age 70.[11] This set includes genes that have key functions in synaptic plasticity important in learning and memory, vesicular transport and mitochondrial function. During aging, DNA damage is markedly increased in the promoters of the genes displaying reduced expression in the frontal cortex. In cultured human neurons, these promoters are selectively damaged by oxidative stress.[11]

Individuals with HIV associated neurocognitive disorders, accumulate nuclear and mitochondrial DNA damage in the frontal cortex.[12]

Genetic

A report from the National Institute of Mental Health says a gene variant of (COMT) that reduces dopamine activity in the prefrontal cortex is related to poorer performance and inefficient functioning of that brain region during working memory tasks, and to a slightly increased risk for schizophrenia.[13]

History

Psychosurgery

In the early 20th century, a medical treatment for mental illness, first developed by Portuguese neurologist Egas Moniz, involved damaging the pathways connecting the frontal lobe to the limbic system. A frontal lobotomy (sometimes called frontal leucotomy) successfully reduced distress but at the cost of often blunting the subject's emotions, volition and personality. The indiscriminate use of this psychosurgical procedure, combined with its severe side effects and a mortality rate of 7.4 to 17 per cent,[14] gained 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 the internal capsule) or the bilateral cingulotomy (involving lesions of the anterior cingulate gyri) and might be used to treat otherwise untreatable obsessional disorders or clinical depression.

Theories of function

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 different dysexecutive symptoms” [15]
  • 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)" [16]
  • 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" [17]
  • Single-symptom theories, which propose that a specific dysexecutive symptom (e.g., confabulation) is related to the processes and construct of the underlying structures.[18]

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. 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 animals

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 has since been challenged by neuroimaging studies. Using magnetic resonance imaging to determine the volume of the frontal cortex in humans, all extant ape species and several monkey species, it was found that the human frontal cortex was not relatively larger than the cortex of other great apes but was relatively larger than the frontal cortex of lesser apes and the monkeys.[19] The higher cognition of the humans is instead seen to relate to a greater connectedness given by neural tracts that do not affect the cortical volume.[19] This is also evident in the pathways of the language network connecting the frontal and temporal lobes.[20]

See also

{{Anatomy-terms}}
  • Broca's area
  • Limen insulae
  • Regions in the human brain

References

1. ^{{cite web|last1=Muzio|first1=Bruno Di|title=Frontal pole {{!}} Radiology Reference Article {{!}} Radiopaedia.org|url=https://radiopaedia.org/articles/frontal-pole|website=radiopaedia.org|language=en}}
2. ^{{cite book |last1=Carpenter |first1=Malcolm |title=Core text of neuroanatomy |date=1985 |publisher=Williams & Wilkins |isbn=0683014552 |pages=22-23 |edition=3rd}}
3. ^{{cite journal |vauthors=Giedd JN, Blumenthal J, Jeffries NO |title=Brain development during childhood and adolescence: a longitudinal MRI study |journal=Nature Neuroscience |volume=2 |issue=10 |pages=861–3 |date=October 1999 |pmid=10491603 |doi=10.1038/13158|display-authors=etal}}
4. ^{{cite journal |vauthors=Fjell AM, Walhovd KB, Fennema-Notestine C |title=One-year brain atrophy evident in healthy aging |journal=The Journal of Neuroscience |volume=29 |issue=48 |pages=15223–31 |date=December 2009 |pmid=19955375 |pmc=2827793 |doi=10.1523/JNEUROSCI.3252-09.2009|display-authors=etal}}
5. ^{{cite journal |vauthors=Coffey CE, Wilkinson WE, Parashos IA |title=Quantitative cerebral anatomy of the aging human brain: a cross-sectional study using magnetic resonance imaging |journal=Neurology |volume=42 |issue=3 Pt 1 |pages=527–36 |date=March 1992 |pmid=1549213|doi=10.1212/wnl.42.3.527 |display-authors=etal}}
6. ^{{cite journal |vauthors=Kimberg DY, Farah MJ |title=A unified account of cognitive impairments following frontal lobe damage: the role of working memory in complex, organized behavior |journal=Journal of Experimental Psychology. General |volume=122 |issue=4 |pages=411–28 |date=December 1993 |pmid=8263463 |url=http://content.apa.org/journals/xge/122/4/411 |doi=10.1037/0096-3445.122.4.411}}
7. ^{{cite journal |vauthors=Stuss DT, Gow CA, Hetherington CR |title='No longer Gage': frontal lobe dysfunction and emotional changes |journal=Journal of Consulting and Clinical Psychology |volume=60 |issue=3 |pages=349–59 |date=June 1992 |pmid=1619089 |doi=10.1037/0022-006X.60.3.349}}
8. ^{{cite journal |vauthors=Rowe AD, Bullock PR, Polkey CE, Morris RG |title='Theory of mind' impairments and their relationship to executive functioning following frontal lobe excisions |journal=Brain |volume=124 |issue=Pt 3 |pages=600–16 |date=March 2001 |pmid=11222459 |url=http://brain.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=11222459 |doi=10.1093/brain/124.3.600}}
9. ^{{cite journal |vauthors=Robinson RG, Kubos KL, Starr LB, Rao K, Price TR |title=Mood disorders in stroke patients. Importance of location of lesion |journal=Brain |volume=107 |issue=1 |pages=81–93 |date=March 1984 |pmid=6697163 |url=http://brain.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=6697163 |doi=10.1093/brain/107.1.81}}
10. ^{{cite journal |last1=Durani |first1=Shiban K. |last2=Ford |first2=Rodney |last3=Sajjad |first3=S. H. |date=September 1991 |title=Capgras syndrome associated with a frontal lobe tumour |journal=Irish Journal of Psychological Medicine |volume=8 |issue=2 |pages=135–6 |doi=10.1017/S0790966700015093}}
11. ^{{cite journal |vauthors=Lu T, Pan Y, Kao SY, Li C, Kohane I, Chan J, Yankner BA |title=Gene regulation and DNA damage in the ageing human brain |journal=Nature |volume=429 |issue=6994 |pages=883–91 |date=June 2004 |pmid=15190254 |doi=10.1038/nature02661 |url=}}
12. ^{{cite journal |vauthors=Zhang Y, Wang M, Li H, Zhang H, Shi Y, Wei F, Liu D, Liu K, Chen D |title=Accumulation of nuclear and mitochondrial DNA damage in the frontal cortex cells of patients with HIV-associated neurocognitive disorders |journal=Brain Res. |volume=1458 |issue= |pages=1–11 |date=June 2012 |pmid=22554480 |doi=10.1016/j.brainres.2012.04.001 |url=}}
13. ^{{cite web | url=http://www.nih.gov/news/pr/may2001/nimh-29.htm | title=Gene Slows Frontal Lobes, Boosts Schizophrenia Risk | publisher=National Institute of Mental Health | date=May 29, 2001 | accessdate=2013-06-20|archiveurl=https://web.archive.org/web/20150404205032/http://www.nih.gov/news/pr/may2001/nimh-29.htm|archivedate=2015-04-04|deadurl=yes}}
14. ^{{cite journal |vauthors=Ogren K, Sandlund M |title=Lobotomy at a state mental hospital in Sweden. A survey of patients operated on during the period 1947-1958 |journal=Nordic Journal of Psychiatry |volume=61 |issue=5 |pages=355–62 |year=2007 |pmid=17990197 |doi=10.1080/08039480701643498}}
15. ^(Burgess, 2003, p. 309).
16. ^(Burgess, 2003, p. 310).
17. ^(Stuss, 1999, p. 348; cf. Burgess & Simons, 2005).
18. ^(cf. Burgess & Simons, 2005).
19. ^{{cite journal |last1=Semendeferi |first1=K |last2=Lu |first2=A |last3=Schenker |first3=N |last4=Damasio |first4=H |title=Humans and great apes share a large frontal cortex |journal=Nature Neuroscience |date=March 2002 |volume=5 |issue=3 |pages=272–6 |doi=10.1038/nn814 |pmid=11850633}}
20. ^{{cite journal |last1=Friederici |first1=AD |title=Pathways to language: fiber tracts in the human brain |journal=Trends in Cognitive Sciences |date=April 2009 |volume=13 |issue=4 |pages=175–81 |doi=10.1016/j.tics.2009.01.001 |pmid=19223226}}

External links

{{Commons category|Frontal lobe}}
  • [https://www.neuinfo.org/mynif/search.php?q=Frontal%20Lobe&t=data&s=cover&b=0&r=20 NIF Search - Frontal Lobe] via the Neuroscience Information Framework
{{Prosencephalon}}{{Authority control}}{{DEFAULTSORT:Frontal Lobe}}

2 : Cerebrum|Frontal lobe

随便看

 

开放百科全书收录14589846条英语、德语、日语等多语种百科知识,基本涵盖了大多数领域的百科知识,是一部内容自由、开放的电子版国际百科全书。

 

Copyright © 2023 OENC.NET All Rights Reserved
京ICP备2021023879号 更新时间:2024/9/24 5:27:07