Biology:Frontal lobe

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Short description: Part of the brain
Frontal lobe
Template:Cerebrum labelled map
Principal fissures and lobes of the cerebrum viewed laterally (Frontal lobe is shown in blue.).
Part ofCerebrum
ArteryAnterior cerebral
Middle cerebral
Latinlobus frontalis
Anatomical terms of neuroanatomy

The frontal lobe is the largest of the four major lobes of the brain in mammals, and is located at the front of each cerebral hemisphere (in front of the parietal lobe and the temporal lobe). It is parted 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.[2] The frontal cortex includes the premotor cortex and the primary motor cortex – parts of the motor cortex. The front part of the frontal cortex is covered by the prefrontal cortex. The nonprimary motor cortex is a functionally defined portion of the frontal lobe.

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.[3]

The frontal lobe contains most of the dopaminergic 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 coming from the thalamus to the forebrain.[4]


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 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:

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 only after the 20s—the prefrontal cortex, in particular, continues in maturing till the second and third decades of life—[5] which, thereafter, marks 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.[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]


The entirety of the frontal cortex can be considered the "action cortex", much as the posterior 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, the prefrontal cortex (PFC), is responsible for internal, purposeful mental action, commonly called reasoning or prefrontal 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's limbic system. The frontal lobe modifies those emotions, generally to 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, numeracy skills[8] and decision making[9] which are all controlled by frontal lobe.

Clinical significance

Main page: Medicine:Frontal lobe disorder
Main page: Medicine:Frontal lobe injury


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 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).[10] Very often, frontal lobe damage is recognized in those with prenatal alcohol exposure.


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".[10] Those who are close to the person who has experienced the damage may notice changes in behavior.[11] 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.[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 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.[10][13]

DNA damage

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 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.[14]

Individuals with HIV associated neurocognitive disorders accumulate nuclear and mitochondrial DNA damage in the frontal cortex.[15]


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.[16]



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,[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 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"[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. 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

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

See also


  1. Muzio, Bruno Di. "Frontal pole | Radiology Reference Article |" (in en). 
  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" (in en), Prefrontal Cortex (InTech), doi:10.5772/intechopen.79571, ISBN 978-1-78923-903-4,, retrieved 2023-06-24 
  3. 3.0 3.1 Carpenter, Malcolm (1985). Core text of neuroanatomy (3rd ed.). Williams & Wilkins. pp. 22–23. ISBN 978-0683014556. 
  4. "Incoming Sensory Information - an overview | ScienceDirect Topics". 
  5. Kolk, Sharon M.; Rakic, Pasko (January 2022). "Development of prefrontal cortex" (in en). Neuropsychopharmacology 47 (1): 41–57. doi:10.1038/s41386-021-01137-9. ISSN 1740-634X. PMID 34645980. 
  6. "One-year brain atrophy evident in healthy aging". The Journal of Neuroscience 29 (48): 15223–31. December 2009. doi:10.1523/JNEUROSCI.3252-09.2009. PMID 19955375. 
  7. "Quantitative cerebral anatomy of the aging human brain: a cross-sectional study using magnetic resonance imaging". Neurology 42 (3 Pt 1): 527–36. March 1992. doi:10.1212/wnl.42.3.527. PMID 1549213. 
  8. "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. December 1993. doi:10.1037/0096-3445.122.4.411. PMID 8263463. 
  9. "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. 2017. doi:10.3389/fpsyg.2017.01417. PMID 28878714. 
  10. 10.0 10.1 10.2 10.3 10.4 ""No longer Gage": frontal lobe dysfunction and emotional changes". Journal of Consulting and Clinical Psychology 60 (3): 349–59. June 1992. doi:10.1037/0022-006X.60.3.349. PMID 1619089. 
  11. ""Theory of mind" impairments and their relationship to executive functioning following frontal lobe excisions". Brain 124 (Pt 3): 600–16. March 2001. doi:10.1093/brain/124.3.600. PMID 11222459. 
  12. "Mood disorders in stroke patients. Importance of location of lesion". Brain 107 ( Pt 1) (1): 81–93. March 1984. doi:10.1093/brain/107.1.81. PMID 6697163. 
  13. "Capgras syndrome associated with a frontal lobe tumour". Irish Journal of Psychological Medicine 8 (2): 135–6. September 1991. doi:10.1017/S0790966700015093. 
  14. 14.0 14.1 "Gene regulation and DNA damage in the ageing human brain". Nature 429 (6994): 883–91. June 2004. doi:10.1038/nature02661. PMID 15190254. Bibcode2004Natur.429..883L. 
  15. "Accumulation of nuclear and mitochondrial DNA damage in the frontal cortex cells of patients with HIV-associated neurocognitive disorders". Brain Research 1458: 1–11. June 2012. doi:10.1016/j.brainres.2012.04.001. PMID 22554480. 
  16. "Gene Slows Frontal Lobes, Boosts Schizophrenia Risk". National Institute of Mental Health. May 29, 2001. 
  17. "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. 2007. doi:10.1080/08039480701643498. PMID 17990197. 
  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. 22.0 22.1 "Humans and great apes share a large frontal cortex". Nature Neuroscience 5 (3): 272–6. March 2002. doi:10.1038/nn814. PMID 11850633. 
  23. "Pathways to language: fiber tracts in the human brain". Trends in Cognitive Sciences 13 (4): 175–81. April 2009. doi:10.1016/j.tics.2009.01.001. PMID 19223226. 

Further reading

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

External links