Frontal lobe

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.

Frontal lobe
Principal fissures and lobes of the cerebrum viewed laterally. (Frontal lobe is shown in pale green.)
Part ofCerebrum
ArteryAnterior cerebral
Middle cerebral
LatinLobus Frontalis
NeuroLex IDbirnlex_928
Anatomical terms of neuroanatomy


Frontal lobe animation
Animation. 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.[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:

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]


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 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]


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]


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]



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


  1. ^ Muzio, Bruno Di. "Frontal pole | Radiology Reference Article |".
  2. ^ a b Carpenter, Malcolm (1985). Core text of neuroanatomy (3rd ed.). Williams & Wilkins. pp. 22–23. ISBN 0683014552.
  3. ^ Giedd JN, Blumenthal J, Jeffries NO, et al. (October 1999). "Brain development during childhood and adolescence: a longitudinal MRI study". Nature Neuroscience. 2 (10): 861–3. doi:10.1038/13158. PMID 10491603.
  4. ^ Fjell AM, Walhovd KB, Fennema-Notestine C, et al. (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.
  5. ^ Coffey CE, Wilkinson WE, Parashos IA, et al. (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.
  6. ^ 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.
  7. ^ a b c d e Stuss 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.
  8. ^ 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.
  9. ^ Robinson RG, Kubos KL, Starr LB, Rao K, Price TR (March 1984). "Mood disorders in stroke patients. Importance of location of lesion". Brain. 107 (1): 81–93. doi:10.1093/brain/107.1.81. PMID 6697163.
  10. ^ Durani, Shiban K.; Ford, Rodney; Sajjad, S. H. (September 1991). "Capgras syndrome associated with a frontal lobe tumour". Irish Journal of Psychological Medicine. 8 (2): 135–6. doi:10.1017/S0790966700015093.
  11. ^ a b Lu 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. doi:10.1038/nature02661. PMID 15190254.
  12. ^ 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 Res. 1458: 1–11. doi:10.1016/j.brainres.2012.04.001. PMID 22554480.
  13. ^ "Gene Slows Frontal Lobes, Boosts Schizophrenia Risk". National Institute of Mental Health. May 29, 2001. Archived from the original on 2015-04-04. Retrieved 2013-06-20.
  14. ^ 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.
  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. ^ a b Semendeferi, 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.
  20. ^ 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.

External links

Brodmann area 4

Brodmann area 4 refers to the primary motor cortex of the human brain. It is located in the posterior portion of the frontal lobe.

Brodmann area 4 is part of the precentral gyrus. The borders of this area are: the precentral sulcus in front (anteriorly), the medial longitudinal fissure at the top (medially), the central sulcus in back (posteriorly), and the lateral sulcus along the bottom (laterally).

This area of cortex, as shown by Wilder Penfield and others, has the pattern of a homunculus. That is, the legs and trunk fold over the midline; the arms and hands are along the middle of the area shown here; and the face is near the bottom of the figure. Because Brodmann area 4 is in the same general location as primary motor cortex, the homunculus here is called the motor homunculus.

The term area 4 of Brodmann-1909 refers to a cytoarchitecturally defined portion of the frontal lobe of the guenon. It is located predominantly in the precentral gyrus. Brodmann-1909 regarded it as topographically and cytoarchitecturally homologous to the human gigantopyramidal area 4 and noted that it occupies a much greater fraction of the frontal lobe in the monkey than in the human. Distinctive features (Brodmann-1905): the cortex is unusually thick; the layers are not distinct; the cells are relatively sparsely distributed; giant pyramidal (Betz) cells are present in the internal pyramidal layer (V); lack of an internal granular layer (IV) such that the boundary between the external pyramidal layer (III) and the internal pyramidal layer (V) is indistinct; lack of a distinct external granular layer (II); a gradual transition from the multiform layer (VI) to the subcortical white matter.

Brodmann area 47

Brodmann area 47, or BA47, is part of the frontal cortex in the human brain. Curving from the lateral surface of the frontal lobe into the ventral (orbital) frontal cortex. It is below areas BA10 and BA45, and beside BA11. This cytoarchitectonic region most closely corresponds to the gyral region the orbital part of inferior frontal gyrus, although these regions are not equivalent. Pars orbitalis is not based on cytoarchitectonic distinctions, and rather is defined according to gross anatomical landmarks. Despite a clear distinction, these two terms are often used liberally in peer-reviewed research journals.

BA47 is also known as orbital area 47. In the human, on the orbital surface it surrounds the caudal portion of the orbital sulcus (H) from which it extends laterally into the orbital part of inferior frontal gyrus (H). Cytoarchitectonically it is bounded caudally by the triangular area 45, medially by the prefrontal area 11 of Brodmann-1909, and rostrally by the frontopolar area 10 (Brodmann-1909).

It incorporates the region that Brodmann identified as "Area 12" in the monkey, and therefore, following the suggestion of Michael Petrides, some contemporary neuroscientists refer to the region as "BA47/12".

BA47 has been implicated in the processing of syntax in oral and sign languages, musical syntax, and semantic aspects of language.

Brodmann area 8

Brodmann area 8 is one of Brodmann's cytologically defined regions of the brain. It is involved in planning complex movements.

Corticobulbar tract

The corticobulbar (or corticonuclear) tract is a two-neuron white matter motor pathway connecting the motor cortex in the cerebral cortex to the medullary pyramids, which are part of the brainstem's medulla oblongata (also called "bulbar") region, and are primarily involved in carrying the motor function of the non-oculomotor cranial nerves. The corticobulbar tract is one of the pyramidal tracts, the other being the corticospinal tract.

Frontal lobe disorder

Frontal lobe disorder is an impairment of the frontal lobe that occurs due to disease or head trauma. The frontal lobe of the brain plays a key role in higher mental functions such as motivation, planning, social behaviour, and speech production. A frontal lobe syndrome can be caused by a range of conditions including head trauma, tumours, degenerative diseases, neurosurgery and cerebrovascular disease. Frontal lobe impairment can be detected by recognition of typical clinical signs, use of simple screening tests, and specialist neurological testing.

Frontal lobe epilepsy

Frontal lobe epilepsy, or FLE, is a neurological disorder that is characterized by brief, recurring seizures that arise in the frontal lobes of the brain, often while the patient is sleeping. It is the second most common type of epilepsy after temporal lobe epilepsy (TLE), and is related to the temporal form by the fact that both forms are characterized by the occurrence of partial (focal) seizures. Partial seizures occurring in the frontal lobes can occur in one of two different forms: either simple partial seizures (that do not affect awareness or memory) or complex partial seizures (that affect awareness or memory either before, during or after a seizure). The symptoms and clinical manifestations of frontal lobe epilepsy can differ depending on which specific area of the frontal lobe is affected.The onset of a seizure may be hard to detect since the frontal lobes contain and regulate many structures and functions about which relatively little is known. Due to the lack of knowledge surrounding the functions associated with the frontal lobes, seizures occurring in these regions of the brain may produce unusual symptoms which can often be misdiagnosed as a psychiatric disorder, non-epileptic seizure or a sleep disorder.During the onset of a seizure, the patient may exhibit abnormal body posturing, sensorimotor tics, or other abnormalities in motor skills. In some cases, uncontrollable laughing or crying may occur during a seizure. Afflicted persons may or may not be aware that they are behaving in an abnormal manner, depending on the patient and type of seizure. A brief period of confusion known as a postictal state may sometimes follow a seizure occurring in the frontal lobes. However, these postictal states are often undetectable and generally do not last as long as the periods of confusion following seizures that occur in the temporal lobes.

There are many different causes of frontal lobe epilepsy ranging from genetics to head trauma that result in lesions in the frontal lobes. Although frontal lobe epilepsy is often misdiagnosed, tests such as prolonged EEG monitoring and/or a MRI scan of the frontal lobes can be administered in order to reveal the presence of a tumor or vascular malformation. Unlike most epileptic EEGs, the abnormalities in FLE EEGs precede the physical onset of the seizure and aid in localization of the seizure's origin. Medications such as anti-epileptic drugs can typically control the onset of seizures, however, if medications are ineffective the patient may undergo surgery to have focal areas of the frontal lobe removed.

Frontal lobe injury

The frontal lobe of the human brain is both relatively large in mass and less restricted in movement than the posterior portion of the brain. It is a component of the cerebral system, which supports goal directed behavior. This lobe is often cited as the part of the brain responsible for the ability to decide between good and bad choices, as well as recognize the consequences of different actions. Because of its location in the anterior part of the head, the frontal lobe is arguably more susceptible to injuries. Following a frontal lobe injury, an individual’s abilities to make good choices and recognize consequences are often impaired. Memory impairment is another common effect associated with frontal lobe injuries, but this effect is less documented and may or may not be the result of flawed testing. Damage to the frontal lobe can cause increased irritability, which may include a change in mood and an inability to regulate behavior. Particularly, an injury of the frontal lobe could lead to deficits in executive function, such as anticipation, goal selection, planning, initiation, sequencing, monitoring (detecting errors), and self-correction (initiating novel responses). A widely reported case of frontal lobe injury was that of Phineas Gage, a railroad worker whose left frontal lobe was damaged by a large iron rod in 1848 (though Gage's subsequent personality changes are almost always grossly exaggerated).

Frontotemporal dementia

The frontotemporal dementias (FTD) encompass six types of dementia involving the frontal or temporal lobes. They are: behavioral variant of FTD, semantic variant primary progressive aphasia, nonfluent agrammatic variant primary progressive aphasia, corticobasal syndrome, progressive supranuclear palsy, and FTD associated with motor neuron disease.One variant is the clinical presentation of frontotemporal lobar degeneration, which is characterized by progressive neuronal loss predominantly involving the frontal or temporal lobes, and typical loss of over 70% of spindle neurons, while other neuron types remain intact.It was first described by Arnold Pick in 1892 and was originally called "Pick's disease", a term now reserved for Pick disease, one specific type of frontotemporal dementia. Second only to Alzheimer's disease (AD) in prevalence, FTD accounts for 20% of young-onset dementia cases. Signs and symptoms typically manifest in late adulthood, more commonly between the ages of 45 and 65, approximately equally affecting men and women.Common signs and symptoms include significant changes in social and personal behavior, apathy, blunting of emotions, and deficits in both expressive and receptive language. Currently, there is no cure for FTD, but there are treatments that help alleviate symptoms.

Inferior frontal gyrus

The inferior frontal gyrus (IFG), (gyrus frontalis inferior), is the lowest positioned gyrus of the frontal gyri, of the frontal lobe, and is part of the prefrontal cortex.

Its superior border is the inferior frontal sulcus (which divides it from the middle frontal gyrus), its inferior border is the lateral sulcus (which divides it from the superior temporal gyrus) and its posterior border is the inferior precentral sulcus. Above it is the middle frontal gyrus, behind it is the precentral gyrus.The inferior frontal gyrus is the location of Broca's area involved in language processing and speech production.

Inferior frontal sulcus

The inferior frontal sulcus is a sulcus between the middle frontal gyrus and the inferior frontal gyrus.

Medial frontal gyrus

The superior frontal gyrus is situated above the superior frontal sulcus and is continued on to the medial surface of the hemisphere, the medial frontal gyrus. The medial and superior frontal gyri are two of the frontal gyri of the frontal lobe. The portion on the lateral surface of the hemisphere is usually more or less completely subdivided into an upper and a lower part by an antero-posterior sulcus, the paramedial sulcus, which, however, is frequently interrupted by bridging gyri.

There is some evidence that it plays a role in executive mechanisms.

Middle frontal gyrus

The middle frontal gyrus makes up about one-third of the frontal lobe of the human brain. (A gyrus is one of the prominent "bumps" or "ridges" on the surface of the human brain.)

The middle frontal gyrus, like the inferior frontal gyrus and the superior frontal gyrus, is more of a region in the frontal gyrus than a true gyrus.

The borders of the middle frontal gyrus are the inferior frontal sulcus below; the superior frontal sulcus above; and the precentral sulcus behind.

Orbital gyri

The inferior or orbital surface of the frontal lobe is concave, and rests on the orbital plate of the frontal bone. It is divided into four orbital gyri by a well-marked H-shaped orbital sulcus. These are named, from their position, the medial, anterior, lateral, and posterior, orbital gyri. The medial orbital gyrus presents a well-marked antero-posterior sulcus, the olfactory sulcus, for the olfactory tract; the portion medial to this is named the straight gyrus, and is continuous with the superior frontal gyrus on the medial surface.

Orbital sulcus

The inferior or orbital surface of the frontal lobe is concave, and rests on the orbital plate of the frontal bone. It is divided into four orbital gyri by a well-marked H-shaped orbital sulcus

Paracentral lobule

Paracentral lobule is on the medial surface of the hemisphere and is the continuation of the precentral and postcentral gyri. The paracentral lobule controls motor and sensory innervations of the contralateral lower extremity. It is also responsible for control of defecation and urination.

It includes portions of the frontal and parietal lobes:

The anterior portion of the paracentral lobule is part of the frontal lobe and is often referred to as the supplementary motor area.

The posterior portion is considered part of the parietal lobe and deals with somatosensory of the distal limbs.While the boundary between the lobes, the central sulcus, is easy to locate on the lateral surface of the cerebral hemispheres, this boundary is often discerned in a cytoarchetectonic manner in cases where the central sulcus is not visible on the medial surface.

Precentral gyrus

The precentral gyrus is a prominent gyrus on the surface of the posterior frontal lobe of the brain. It is the site of the primary motor cortex that in humans is cytoarchitecturally defined as Brodmann area 4.

Precentral sulcus

The precentral sulcus lies parallel to, and in front of, the central sulcus. (A sulcus is one of the prominent grooves on the surface of the human brain.)

The precentral sulcus divides the inferior, middle and superior frontal gyri from the precentral gyrus. In most brains, the precentral sulcus is divided into two parts: the inferior precentral sulcus and the superior precentral sulcus. However, the precentral sulcus may sometimes be divided into three parts or form one continuous sulcus.

Superior frontal gyrus

The superior frontal gyrus (SFG) also marginal gyrus, makes up about one third of the frontal lobe of the human brain. It is bounded laterally by the superior frontal sulcus.The superior frontal gyrus is one of the frontal gyri.

Superior frontal sulcus

The superior frontal sulcus is a sulcus between the superior frontal gyrus and the middle frontal gyrus.

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