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]
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]
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]
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]
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 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]
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.
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]
^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.PMID1549213.
^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.PMID8263463.
^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.PMID6697163.
^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.
^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.PMID22554480.
^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.PMID17990197.
^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.PMID11850633.
^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.PMID19223226.