which brain structure primarily controls judgment decision making and problem solving

Cerebral Cortex: What It Is, Function & Location

Olivia Guy-Evans, MSc

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BSc (Hons) Psychology, MSc Psychology of Education

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In psychology, the cerebral cortex is defined as the outermost layer of the brain , composed of folded gray matter, playing a crucial role in various complex cognitive processes. It is responsible for functions like thought, perception, language, memory, attention, consciousness, and advanced motor functions.

The cerebral cortex is the brain’s outermost layer on top of the cerebrum and is associated with our highest mental capabilities.

The cerebral cortex is primarily constructed of grey matter (neural tissue made up of neurons ), with between 14 and 16 billion neurons found here.

Although the cerebral cortex is only a few millimeters thick, it consists of approximately half the weight of the total brain mass. The cerebral cortex has a wrinkled appearance, consisting of bulges, also known as gyri, and deep furrows, known as sulci.

The many folds and wrinkles of the cerebral cortex allow for a wider surface area for an increased number of neurons to live there, permitting large amounts of information to be processed.

The cortex is also divided into two hemispheres, the right and left, which are separated by a large sulcus called the medial longitudinal fissure.

The two hemispheres are connected via bundles of nerve fibers called the corpus callosum to allow both hemispheres of the cerebral cortex to communicate and make further connections.

The cerebral cortex controls a vast array of functions through the use of the lobes, which are divided based on the location of gyri and sulci . These lobes are called the frontal lobes , temporal lobes, parietal lobes , and occipital lobes .

The cerebral cortex has a layered structure, with 6 layers numbered from the outer surface (Layer 1) to the innermost layer (Layer 6).

• Layer 1 is the molecular layer, containing few neuronal cell bodies but many dendrites and axons.
• Layer 2 is the external granular layer, containing small pyramidal neurons and numerous small granule cells.
• Layer 3 is the external pyramidal layer, with predominantly small and medium pyramidal neurons.
• Layer 4 is the internal granular layer, with mainly stellate and pyramidal neurons.
• Layer 5 is the internal pyramidal layer, containing large pyramidal neurons that give rise to major output pathways.
• Layer 6 is the multiform layer, with few large pyramidal neurons among many smaller types.

The cerebral cortex can be divided into 3 main regions:

• Neocortex: The evolutionarily newest part, with 6 layers. Makes up about 90% of the human cerebral cortex. Responsible for higher cognitive functions like sensory perception, generation of motor commands, spatial reasoning, language, and conscious thought.
• Allocortex: The older part with fewer than 6 layers. Includes the olfactory cortex and hippocampus. Plays a role in olfaction and memory.
• Archicortex: The oldest part with only 3 cortical layers. Forms the hippocampus. Involved in memory and spatial navigation.

The cortex also contains many different types of neurons and neuroglial cells that support cortical function:

• Pyramidal cells: The primary projection neurons shaped like pyramids. Located in layers 3, 5, and 6. Transmit signals from one region of the cortex to another.
• Stellate cells: Found in layer 4. Receive and integrate inputs from the thalamus.
• Basket cells: Inhibitory interneurons found in layers 2-6. Help regulate cortical excitability.
• Astrocytes: Star-shaped glial cells that provide structural and metabolic support to neurons. Help regulate neurotransmitter levels.
• Oligodendrocytes: Produce myelin to insulate neuron axons, speeding up signal transmission.
• Microglia: Act as the immune cells of the brain, responding to pathogens and brain injuries.

Cerebral Cortex Function

The cerebral cortex, which is the outer surface of the brain, is associated with higher level processes such as consciousness, thought, emotion, reasoning, language, and memory. Each cerebral hemisphere can be subdivided into four lobes, each associated with different functions.

Together, the lobes serve many conscious and unconscious functions, such as being responsible for movement, processing sensory information from the senses, processing language, intelligence , and personality.

Frontal Lobes

The frontal lobes are the largest part of the cerebral cortex, located at the front of the brain behind the forehead. 

The frontal lobes are highly developed in humans and critical for many higher-order cognitive functions.

Specific regions and functions of the frontal lobe include:

• Prefrontal cortex: Involved in planning complex cognitive behaviors, personality expression, decision-making, and moderating social behavior. 
• Primary motor cortex: Located in the precentral gyrus. Initiates voluntary movements and contains a motor homunculus. Damage can cause contralateral paralysis.
• Premotor cortex: Plays a role in the selection and control of voluntary motor movements, especially learned sequences of movements. Damage can cause issues with coordinated motor planning.
• Frontal eye fields: Guide eye movement and visual attention.
• Broca’s area: Critical for speech production and language expression. Located in the left inferior frontal gyrus. Damage causes expressive aphasia.
• Dorsolateral prefrontal cortex: Involved in working memory, executive function , and attention regulation. Damage impairs cognition.
• Orbitofrontal cortex: Plays a key role in decision-making, impulse control, and socially appropriate behaviors.

The frontal lobes are highly interconnected with other cortical and subcortical regions, including the limbic system . They are critically involved in higher cognitive functions, executive control, emotional regulation, and social cognition.

Damage can cause personality changes, impaired judgment, memory loss, and reduced motor control and language expression, depending on the specific region affected.

Occipital Lobes

The occipital lobes are located at the very back of the brain. This region processes visual information received from the eyes.

The main functions of the occipital lobes include:

• Vision – The primary visual cortex in the occipital lobe interprets visual signals from the retinas of the eyes. This area handles basic visual functions like perceiving color, motion, and shape.
• Recognition – Additional visual association areas help identify objects, faces, words, and scenes that you see.
• Imagery – The occipital lobes contribute to visual imagery and picturing images in your mind.
• Communication – This region connects with other parts of the brain to integrate visual perceptions with memories, sounds, and more.

Damage to the occipital lobes can cause issues like blindness, difficulty recognizing objects or words, and problems with visual processing. Overall, this area is essential for interpreting visual stimuli.

Parietal Lobes

The parietal lobes are located near the top of the brain behind the frontal lobes. This area integrates sensory information from different parts of the body.

Key functions of the parietal lobes include:

• Touch – The primary somatosensory cortex receives information about touch, temperature, pain, and the body’s position.
• Integration – It combines input from the senses to represent the body and its location in space.
• Motion – The parietal lobes guide actions and movements in response to sensory stimuli.
• Attention – It plays a role in selective attention and focusing on relevant stimuli.
• Spatial orientation – This region helps construct a sensory map of the environment and understand spatial relationships.

Injury to the parietal lobes can cause issues with coordinating movement, directing attention, and processing sensory information from the body and surroundings. Overall, it integrates sensory signals to guide behavior.

Temporal Lobes

The temporal lobes are located on the sides of the brain above the ears. This part of the brain helps with processing sounds, understanding language, forming memories, and regulating emotions.

The main roles of the temporal lobes include:

• Hearing – The temporal lobes receive auditory information from the ears and help interpret sounds and words. A small area called the primary auditory cortex processes the basic aspects of hearing.
• Memory – An important structure called the hippocampus is located in the temporal lobes. The hippocampus helps form new memories about events, facts, places, and experiences.
• Language – A region called Wernicke’s area in the left temporal lobe is important for understanding spoken and written language.
• Emotion – The amygdala, found deep in the temporal lobes, regulates emotions like fear, anger, and aggression. It also links memories to emotional reactions.

The temporal lobes work with other parts of the brain to help us recognize words, speak, form memories of life events, perceive emotional cues, and understand language.

Damage to this area can cause issues with hearing, memory, emotions, or comprehending language.

In summary, the temporal lobes are involved in sound processing, memory, emotional control, and language functions.

They allow us to understand speech, form memories, regulate moods, and interpret auditory stimuli. Damage can disrupt these important abilities.

Areas of the Cerebral Cortex

The cerebral cortex can be characterized as being made up of three types of divisions, which serve different purposes: sensory, motor, and association areas.

The combination of these three areas accounts for most of human cognition and behavior.

Sensory Areas

The sensory areas of the cerebral cortex receive sensory information from the senses and environmental stimuli. This information is also processed by the sensory areas to give meaning to this information.

The sensory areas include the visual cortex, the somatosensory cortex, the auditory cortex, and the gustatory cortex. The visual cortex is an area within the occipital lobes that is essential to the conscious processing of visual stimuli.

There are two visual cortices in the brain: the cortex in the left hemisphere receives signals from the right visual field, whereas the cortex in the right hemisphere receives signals from the left visual field.

The visual cortex is important for making sense of visual information and plays a role in object recognition and representation.

The somatosensory cortex is located within the parietal lobe and receives tactile information from the body. This information can include temperature, touch, and pain, all of which are then integrated into the somatosensory cortex to produce a ‘map’ of the body.

The auditory cortex is an area within the temporal lobes which is responsible for processing auditory information. This cortex can perform basic and higher functions relating to hearing, including the ability for some people to language switch.

Finally, the gustatory cortex is a region in the frontal lobe that is responsible for the perception of taste and flavor.

Motor Areas

The motor areas of the cerebral cortex are involved in the regulation and initiation of voluntary movement. These areas are primarily found within the frontal lobes and include the primary motor cortex , premotor cortex, and the supplementary cortex.

The primary motor cortex is associated with the coordination and initiation of motor movements. Each cerebral hemisphere of the primary motor cortex contains a motor-related representation of the opposite side of the body.

There is also a representational map of the body with the primary motor cortex, called a motor homunculus. The premotor cortex is involved in preparing and executing limb movements, as well as using information from other regions of the cortex to select appropriate movements.

The premotor cortex is also necessary for learning, especially through imitation and social cognition, specifically empathy .

The supplementary cortex is responsible for the planning of complex movements and contributes to the control of movement.

Association Areas

The association areas are spread throughout the cerebral cortex in the four lobes. These areas act by integrating information from these brain regions, often adding more complexity to their functions.

These association areas can also form connections to sensory and motor areas to give meaning to and organize information in these areas. Association areas within the frontal lobes are involved in key processes such as planning, thinking, and feeling.

These areas also play a role in personality and controlling emotional behaviors. Association areas within the parietal lobe are involved in spatial skills such as spatial awareness and reasoning, as well as being responsible for paying attention to visual stimuli in the environment.

In the temporal lobes, association areas function primarily in memory processes, such as helping to process procedural and episodic memories .

These areas also communicate with other lobes of the cortex so they can complete memory-related processes.

Occipital lobe association areas help to facilitate memories associated with visuals to be retained, as well as enable us to think in a visual manner.

These areas in the occipital lobes also communicate with other lobes of the cortex to assimilate visual information with memories, sounds, and language to understand visual stimuli.

Brodmann Areas

Brodmann Areas, named after German neurologist Korbinian Brodmann, are a system for mapping and categorizing regions of the human cerebral cortex based on their distinct cellular architecture and functions.

These numbered areas, which range from 1 to 52, provide a structural framework for understanding different brain functions, such as sensory processing, motor control, and higher cognitive processes, contributing to our knowledge of brain organization and function.

Clinical Relevance

• A literature review investigated the frontal lobe’s association with schizophrenia and found that many patients had differences in grey matter volumes and functional activity in their frontal lobes compared to those without the disorder (Mubarik & Tohid, 2016), suggesting that the frontal lobes are associated with this disorder. 
• It has been found that there was reduced grey matter volume of the parietal lobes in those diagnosed with schizophrenia (Zhou et al., 2007). This suggests that structural abnormalities or atrophy in the parietal lobes may contribute to some of the symptoms of schizophrenia, implying that treatments targeting this brain region could potentially help manage the disorder.
• Children with ADHD showed altered functional connectivity and reduced network efficiency in the frontal and occipital lobes when viewing facial emotions, indicating differences in emotional processing compared to neurotypical children (Nasab et al., 2021).
• Researchers found that impairments with attention within the temporal lobes are associated with developmental dyslexia (Voldois et al., 2019).
• A review of brain imaging studies found differences in the development of frontal lobe volume in children with autism spectrum disorder compared to typically developing children. Frontal lobe volume was greater between ages 2-4 years in autistic children, suggesting altered brain development in regions important for cognitive skills (Crucitti et al., 2022).
• It has also been suggested that early signs of Alzheimer’s disease may be noticed within the temporal lobes (Lowndes & Savage, 2007).
• A brain imaging study found people with depression had differences in the temporal lobe, including less volume and surface area compared to healthy individuals. Connections between the temporal lobe and visual processing areas were also reduced in depression. These differences may act as biomarkers to identify depression (Zhang et al., 2023). 

Crucitti, J., Hyde, C., Enticott, P., & Stokes, M. (2022). A systematic review of frontal lobe volume in autism spectrum disorder revealing distinct trajectories.

FlintRehab. (2021, January 11). Cerebral Cortex Damage: Definition, Symptoms, and Recovery . https://www.flintrehab.com/cerebral-cortex-damage/#:~:text=Parietal%20Lobe%20Damage,problems%20with%20sensation%20and%20perception.

Huang, J. (2020, September). Brain Dysfunction by Location. MSD Manual . https://www.msdmanuals.com/en-gb/home/brain,-spinal-cord,-and-nerve-disorders/brain-dysfunction/brain-dysfunction-by-location

Lowndes, G., & Savage, G. (2007). Early detection of memory impairment in Alzheimer’s disease: a neurocognitive perspective on assessment. Neuropsychology Review, 17 (3), 193-202.

Mubarik, A., & Tohid, H. (2016). Frontal lobe alterations in schizophrenia: a review. Trends in Psychiatry and Psychotherapy, 38(4), 198-206.

Nasab, A. S., Panahi, S., Ghassemi, F., Jafari, S., Rajagopal, K., Ghosh, D., & Perc, M. (2021). Functional neuronal networks reveal emotional processing differences in children with ADHD. Cognitive Neurodynamics , 1-10.

Onitsuka, T., McCarley, R. W., Kuroki, N., Dickey, C. C., Kubicki, M., Demeo, S. S., Frumin, M., Kikinis, R., Jolesz, F. A. & Shenton, M. E. (2007). Occipital lobe gray matter volume in male patients with chronic schizophrenia: A quantitative MRI study. Schizophrenia Research, 92 (1-3), 197-206.

Valdois, S., Lassus-Sangosse, D., Lallier, M., Moreaud, O., & Pisella, L. (2019). What bilateral damage of the superior parietal lobes tells us about visual attention disorders in developmental dyslexia. Neuropsychologia, 130 , 78-91.

Zhang, S., She, S., Qiu, Y., Li, Z., Wu, X., Hu, H., … & Wu, H. (2023). Multi-modal MRI measures reveal sensory abnormalities in major depressive disorder patients: A surface-based study.  NeuroImage: Clinical ,  39 , 103468.

Zhou, S. Y., Suzuki, M., Takahashi, T., Hagino, H., Kawasaki, Y., Matsui, M., Seto, H. & Kurachi, M. (2007). Parietal lobe volume deficits in schizophrenia spectrum disorders. Schizophrenia Research, 89 (1-3), 35-48.

Further Information

• Kniermin J. Neuroscience online: an electronic textbook for the neurosciences. Chapter 5: Cerebellum. University of Texas Health Science Center at Houston.
• Stoodley, C. J. (2016). The cerebellum and neurodevelopmental disorders. The Cerebellum, 15(1), 34-37.
• D”Angelo, E. (2019). The cerebellum gets social. Science, 363(6424), 229-229.

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• Published: 18 August 2021

The role of prefrontal cortex in cognitive control and executive function

• Naomi P. Friedman   ORCID: orcid.org/0000-0002-4901-808X 1 &
• Trevor W. Robbins   ORCID: orcid.org/0000-0003-0642-5977 2  

Neuropsychopharmacology volume  47 ,  pages 72–89 ( 2022 ) Cite this article

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• Cognitive control
• Human behaviour
• Psychiatric disorders

Concepts of cognitive control (CC) and executive function (EF) are defined in terms of their relationships with goal-directed behavior versus habits and controlled versus automatic processing, and related to the functions of the prefrontal cortex (PFC) and related regions and networks. A psychometric approach shows unity and diversity in CC constructs, with 3 components in the most commonly studied constructs: general or common CC and components specific to mental set shifting and working memory updating. These constructs are considered against the cellular and systems neurobiology of PFC and what is known of its functional neuroanatomical or network organization based on lesioning, neurochemical, and neuroimaging approaches across species. CC is also considered in the context of motivation, as “cool” and “hot” forms. Its Common CC component is shown to be distinct from general intelligence ( g ) and closely related to response inhibition. Impairments in CC are considered as possible causes of psychiatric symptoms and consequences of disorders. The relationships of CC with the general factor of psychopathology (p) and dimensional constructs such as impulsivity in large scale developmental and adult populations are considered, as well as implications for genetic studies and RDoC approaches to psychiatric classification.

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Introduction.

Many psychiatric disorders and neurological conditions are associated with deficits in cognitive control (CC) and/or dysfunction of the prefrontal cortex (PFC) and its associated circuitry [ 1 , 2 , 3 , 4 ]. Consequently, there is a considerable premium on elucidating the basic psychological and neuronal mechanisms underlying the PFC’s role within the neural networks that regulate behavior and cognition.

CC is a term usually associated with the healthy functioning of the PFC and related regions such as the cingulate cortex [ 5 ]. Deriving from a cybernetic and cognitive neuroscience perspective, CC has often been considered synonymous with the earlier notion of executive function (EF), which has its roots in studies of clinical neuropsychology. In both cases, a core process of behavioral regulation is envisaged that optimises goal-directed behavior and counters automaticity. This process has many similarities with the distinction between controlled and automatic responding [ 6 ], which approximately aligns with the learning theory distinction between goal-directed and habitual responding [ 7 ]. One would expect the absence of CC to produce automatic behavior; controlled responding is goal-directed and flexible.

Miller and Cohen (2001) [ 8 ] proposed that “[CC] stems from the active maintenance of patterns of activity in the PFC that represent goals and the means to achieve them. They provide bias signals to other brain structures whose net effect is to guide the flow of activity along neural pathways that establish the proper mappings between inputs, internal states, and outputs needed to perform a given task” (p. 167). This seminal account of the role of PFC in CC essentially consists of the contextual biasing of attention (for example, via instructions) to resolve conflicts and exert attentional control. The typical example is the much-used Stroop interference paradigm (see Fig.  1 ), in which participants are required to name the color (e.g., green) of the ink used to print words whose meaning is incongruent with that color (e.g, RED). The greater pre-potency of reading words over-reporting color causes interference, manifested as a slowing of decisional latency and activation of the anterior cingulate cortex (ACC) [ 9 ]. The conflict can be resolved by focusing attention on the color of the ink, associated with control (or bias) exerted by PFC regions. The theory was supported by an fMRI study showing that ACC activation was accompanied by activations of the dorsolateral (dl)PFC associated with top-down adjustments of response control [ 10 ]. Hence, in the simple model proposed by Miller and Cohen [ 8 ], the ACC detects conflict that is resolved by top-down biasing of response options from the dlPFC [ 9 ]. This theoretical scheme has provided one of the first demonstrations of a CC process to be mediated by specific, interactive PFC circuitry.

When relevant, text above each schematic indicates different conditions, and text below indicates correct responses. The faces included in the emotional n -back illustration are taken from the NimStim set of models who have granted permission to publish their images in scientific journals [ 246 ].

One question to be considered here is whether CC is best considered as a unitary construct, a set of component processes, or a hybrid product of these extremes. If CC is best characterized as a set of distinct component processes, another question is how many of these can be identified and can they be further defined? The possible fractionation of CC can be related broadly to the heterogeneous nature of the PFC itself, which comprises, across species, many distinctive sub-regions, characterized by their cytoarchitectonic characteristics and by their connectivity with other brain regions. A related question then arises as to whether the PFC’s role in CC is that of a unitary entity or “multiple demand” (MD) system [ 11 ]. The MD system appeals to the enormous neural plasticity shown to be inherent within the PFC, so that the same neuronal ensembles can be recruited for superficially different tasks using “adaptive coding” [ 12 , 13 , 14 ]. However, an alternative viewpoint would be that the PFC sub-regions have somewhat different functions, potentially mediating the specific domains of CC. A more sophisticated version conceives specific PFC subregions of having multiple functions, as a consequence of the network-like nature of brain organization that has been revealed by brain imaging (see Haber et al., this issue, and Menon & D’Esposito, this issue [ 15 , 16 ]). Yet a further view would argue that CC is emergent from network processing in the brain, and there is no particular network area that mediates control (see [ 17 , 18 ]).

This article will consider these fundamental questions, beginning with the key issues of how CC is measured and how its unity and possible diversity have been evaluated at both the behavioral and neurobiological levels. In considering the neural substrates of CC, we draw upon the human neuropsychological and neuroimaging literature, as well as basic neuroscience studies in experimental animals. Clearly, these studies are well poised to address the question of dissociation of component processes, for example, via interventional techniques including lesions and neuropharmacological manipulations. A particular issue is how CC operates in different states of the internal or external environment, for example, following stress, that may alter the neurochemical ambience and functioning of the PFC and produce curvilinear, “inverted U-shaped,” functions of performance efficacy [ 19 ]. CC or EF in the past has also been related to other unitary constructs such as general intelligence, or g [ 11 ]. To what extent, therefore, are these entities the same, also entailing presumably similar neural substrates? In fact, we will discuss evidence that although these unitary neurocognitive constructs overlap to some extent, they are different.

Finally, we will consider clinical implications, particularly how CC or EF functions relate to personality traits or dimensions relevant to psychopathology, such as impulsivity and compulsivity, as well as the general psychopathological factor p , which captures covariance across a range of mental health disorders [ 20 ]. We will conclude with future research priorities, with an ultimate aim of determining how CC can be optimized for dealing with behavioral problems and mental health disorders.

Psychological organization of CC

The neuroanatomical connectivity of the PFC to most parts of the cortical and subcortical brain makes it well suited for participating in a number of neural networks and carrying out CC operations in different functional domains (e.g., spatial, visual, and verbal). Moreover, PFC functions probably depend on specializations of dendritic branching and spine density of pyramidal cells, especially in the cycloarchitectonically distinct regions of the granular PFC (Fig.  2 ) [ 21 , 22 , 23 ]. The cellular physiology of these regions is characterized by rapid firing and properties of neural plasticity that may enable such functions as goal maintenance in working memory and the flexible functioning of an MD network [ 24 , 25 , 26 , 27 ].

The top panel depicts a lateral view, and the bottom panel depicts a medial view. Numbers indicate Brodmann Areas (BA). Note that the commonly described “ventromedial prefrontal cortex” potentially subsumes several BAs: 25, 32, 14, and possibly 11 and 13.

However, it is a major challenge to deduce how the PFC is organized to mediate the range of cognitive processes referred to as CC/EF, which include stopping automatic or dominant responses, controlling interference, switching between tasks, coordinating multiple tasks, updating working memory, monitoring, and planning [ 28 , 29 , 30 ] (see Fig.  1 for illustrations of some example tasks used to assess these cognitive processes). The term “unity and diversity” was first used in 1972 to describe the relationships among such diverse frontal lobe processes: Teuber [ 31 ] observed a “bewildering variety in man’s reaction even to fairly restricted and non-progressive [prefrontal] lesions” (p. 637), that nevertheless, could be described broadly in terms of levels of “compulsiveness” or “abnormally stimulus-bound behavior” (p. 640). Similarly, Duncan and colleagues [ 32 ] reiterated this unity and diversity term to describe frontal lobe deficits after head injury: They observed uniformly low correlations among frontal lobe tests, yet a common element of “goal neglect, or disregard of a known task requirement” (p. 713).

The term “unity and diversity” has also been used to describe the pattern of correlations among laboratory CC tests in individuals without brain lesions. Specifically, Miyake et al. [ 33 ] investigated the structure of CC in college students by administering a battery of tasks, each designed to tap one of three CC abilities: inhibiting a prepotent response (stopping an automatic response, sometimes in order to make an alternative response), updating working memory (continuously replacing no-longer relevant information in working memory with newly relevant information when it is detected in the environment), or shifting between mental sets (switching between two alternative tasks). They administered multiple tasks to assess each of these three functions so that they could estimate a latent variable (a statistical extraction of the common variance in a set of tasks) for each function. They then examined the relationships among these functions at the level of these latent variables, rather than at the level of individual tasks. The basic model they examined is shown in Fig.  3a , along with alternative models examined in later studies (Fig.  3b, c ).

Proposed CC functions are represented as latent variables (depicted with ellipses) that predict variation in performance on specific tasks (rectangles) chosen to measure those abilities. Factor loadings are depicted with single-headed arrows between the factors and nine measured tasks. The short arrows indicate residual variances, the unique variance in each task that is unrelated to the CC factors, attributable to measurement error as well as reliable task-specific variation. a In a correlated factors model, tasks are predicted by CC factors that are allowed to be correlated, and unity and diversity are represented in the correlations between factors (represented with curved double-headed arrows). The numbers shown are the average correlations and the range of correlations from six studies using a similar battery ( N s = 137–786). b A higher-order “Common” CC factor can also be used to model the correlations among the factors [ 39 , 158 ]. This higher-order factor predicts the lower-order factors, and they correlate to the extent to which they are jointly predicted by the common factor. In such models, the diversity is captured by the residuals of these factors after the variance due to the common factor is removed (inhibiting-specific, updating-specific, and shifting-specific variances). The numbers shown indicate the average and range of factor loadings for the Common CC factor, and the corresponding averages and ranges for the residual variances for inhibiting, updating, and shifting factors (i.e., the variance not explained by the common factor), derived from the correlations in panel a . *indicates the standardized loadings were bound at 1, and the residual variances bound at zero. c Alternative model structures (called nested factors models or bifactor models) can be used to capture unity and diversity factors more directly. In these models, all tasks load on a common factor, but also load on orthogonal specific factors. These models thus partition each factor into variance that is common across all tasks and variance that is unique to tasks assessing particular processes. Although these alternative parameterizations typically do not result in appreciably different fits to the data, they can make it more convenient to examine relationships to other constructs of interest: Because the unity and diversity components are represented with orthogonal latent variables rather than in the correlations between factors or with residual variances, it is straightforward to discern whether a construct is related to the unity vs. diversity components.

This approach was motivated by the recognition that the low correlations observed in prior studies might reflect “task impurity” of CC measures. That is, CC is by definition control of other cognitive processes, and so performance in CC tasks may reflect variation in those other processes as well as the CC process of interest. Evaluating a CC ability in multiple contexts and statistically extracting what is common enables purer measures that are also free of random measurement error. Indeed, Miyake et al. [ 33 ] found that although the individual tasks showed relatively low correlations ( r  = –0.05 to 0.34), consistent with much prior research, the latent variable correlations were stronger ( r  = 0.42–0.63). These correlations were all significantly greater than zero, indicating that these three CC processes indeed shared something in common (they showed some “unity”). However, these three factors were also somewhat separable (they also showed some “diversity”): A model in which these nine tasks were explained by three correlated factors was superior to models that used fewer factors. Since that initial study, this psychometric latent variable approach has been used in a large number of studies to show that unity and diversity of CC is evident across samples and ages (e.g., [ 34 , 35 , 36 , 37 , 38 , 39 , 40 , 41 ]), although there are some studies that suggest more unity (higher correlations between factors) in early childhood [ 35 , 42 , 43 , 44 ].

Although latent variable studies often focus on the same three constructs selected by Miyake et al. [ 33 ], their model was never intended to be comprehensive. Other candidate components of CC and taxonomies are considered in Box  1 . Miyake et al. also recognized that commonly examined CC processes might comprise multiple components. For example, measures of working memory capacity and updating can include separable sub-functions like maintenance and removal of items in working memory [ 45 ]. Mental set-shifting tasks may require multiple sub-processes, including interference control, retrieval of task sets, and task-set reconfiguration [ 46 ]. And these intermediate levels may be combined with other functions (e.g., sequencing subgoals) to result in more complex postulated CC functions like planning [ 33 ].

Finally, goal-directed behavior or associated outcomes have motivational and value-based elements in decision-making cognition that raise the issue of whether CC can be distinguished from motivational control and value-based processes. Thus, for example, Koechlin [ 47 ] firmly distinguishes between CC and “motivational control.” Most models of CC focus on so-called “cool” tasks that use non-emotional stimuli, such as the color-word Stroop task or the n -back task with letters or neutral words. “Hot” CC can be measured with similar paradigms but using emotional stimuli (Fig.  1 ), thus assessing control over motivational or emotional information. For example, hot Stroop tasks might require naming the font color of emotionally salient words (e.g., “failure”) [ 48 ] or categorizing the emotional valence of words (e.g., “miserable”) in the context of faces with emotional expressions that conflict with those words (e.g., [ 49 ]). Hot CC can also be measured with tasks that do not have a cool analogue, such as gambling tasks and delay of gratification tasks [ 50 , 51 ] (Fig.  1 ). Research with children suggests separability of hot and cool CC in terms of their relations with each other and with other measures [ 50 , 52 , 53 , 54 , 55 , 56 , 57 ]. However, neuroimaging studies comparing CC tasks with non-emotional and emotional stimuli find that they involve similar CC regions [ 58 , 59 ] (dorsal ACC, anterior insula, and lateral and medial PFC), but tasks with emotional conflict also recruit distinct neural regions related to salience and emotional processing (amygdala, more rostral areas of the ACC and medial PFC, and orbitofrontal cortex) [ 60 , 61 , 62 , 63 , 64 , 65 , 66 ]. Such patterns suggest that there may be common CC processes across hot and cool tasks.

Box 1 Alternative candidate components (or taxonomies) of CC

Miyake et al.’s [ 33 ] model recognized that there could be other potential, separable CC constructs, besides the traditional triad of working memory, cognitive flexibility, and inhibition. How other candidate processes such as (attentional) monitoring; dual-tasking; strategic retrieval and generativity (including e.g., verbal fluency and episodic memory) [ 233 , 247 , 248 ]; “compositionality” [ 70 ]; self-report (e.g., impulsiveness); and metacognition [ 249 ] including social aspects (e.g., “theory of mind”), might relate to or derive from the original triad is unclear. Studies that have tested the relations of some of these candidate CC components have found that they are correlated with the more commonly examined CC processes but also show some separability [ 233 , 247 , 248 ]. Thus, the notion of unity and diversity is likely to apply to models that include more than the most typically examined three constructs.

One rough parcellation of alternative CC components has been achieved by anatomical localization in a large number of patients with frontal injuries [ 250 , 251 , 252 ]. The tasks included requirements to attend, switch, be vigilant, tap rhythmically, and respond quickly. Superior medial deficits were associated with “energization” (initiating and sustaining a response, problems with which were related to slower reaction times). Right lateral lesions were associated with “monitoring” (checking performance and adjusting behavior when necessary). Left lateral lesions were associated with “task setting” (setting up a stimulus-response relationship and organizing the processes necessary to complete a task), especially their acquisition and flexible use; and, for the inferior medial group, a problem of maintaining task set (possibly related to distractibility). These proposed CC components have only an approximate relationship with those discussed earlier (typically examined in latent variable models), and intriguingly do not appeal at all to any construct of “inhibition.” Rather, Stuss and Alexander [ 250 ] proposed that inhibition emerged as a combination of these three processes.

Fractionation and integration of CC within PFC

The main methodologies employed for examining how PFC mediates CC have been (i) the anatomical localization of specific aspects of CC/EF, based for example on evidence of lesions in conjunction with correlative neurophysiological or neuroimaging methods; and (ii) the analysis of task performance using the mapping of neural network methodology aimed at elucidating the sequencing and overall integration of CC processes. With respect to the latter, resting state and functional connectivity data suggest several distinct configurations (networks) of PFC and other brain regions, reviewed by Menon and D’Esposito (this issue) [ 16 ]: the lateral “fronto-parietal” (or “central executive”) network (FPN), anchored in the dorsolateral (dl) and dorsomedial PFC and posterior parietal cortex; the “cingulo-opercular” network (CON), which overlaps with a “salience” network and includes the ACC, the insula, and subcortical regions; the “ventral attention” network, which includes inferior frontal gyrus, regions of the insula, and the temporoparietal junction; the “dorsal attention” network, which includes the frontal eye fields and intraparietal sulcus; and the “default mode network” (DMN) comprising medial PFC regions interacting with certain posterior cortical regions (Haber et al., this issue; Menon & d’Esposito, this issue [ 15 , 16 ]). The DMN typically shows inverse levels of activity in relation to the other networks during external task performance, with the DMN being more active at rest, and consequently associated with “internal” control processes (Menon & D’Esposito, this issue [ 16 ]).

With respect to the neurobiological substrates of unity and diversity, one view would emphasize the participation of the PFC as a hub of an MD network that mediates all of the common facets of CC. Another would point to the cytoarchitectonic heterogeneity of the PFC (Fig.  2 ) and ask how the various components of CC were coordinated and integrated in different tasks by different PFC regions, and their specific roles as functional nodes within networks. The relevant circuitries include connectivity of the PFC to posterior cortical regions such as the parietal lobes and to subcortical regions, such as the striatum. Hybrid models of organization may incorporate MD characteristics in certain PFC regions, but also allow for specificity of neural connectivity, to mediate, for example, specific aspects of response inhibition, updating, or cognitive flexibility, as well as other forms of CC that putatively involve, for example, interactions with language systems and autobiographical episodic memory. An important consideration is the extent to which hierarchical CC processing maps onto a hierarchical lateral PFC system and how motivational processes interact with it to achieve integration of these dual forms of control [ 67 ]. The following sections selectively survey findings from the enormous literature on these issues (see also reviews by Tanji & Hoshi [ 68 ] and Badre [ 69 ]).

Fractionation of CC

Evidence from the double dissociation of component CC processes is relevant to the question of whether PFC’s role in CC is unitary. By the time of the classic edited book, The Frontal Granular Cortex and Behavior [ 70 ], lesion studies in non-human primates had already shown, via the double dissociation strategy, considerable apparent localization of function within the frontal lobes. For example, whereas impairments in working memory test paradigms such as spatial delayed response were produced by lesions of the sulcus principalis (dlPFC), damage to more ventrolateral and orbitofrontal regions produced impairments in tests apparently measuring inhibition and cognitive flexibility, such as reversal learning and Go/No-Go responding. These findings apparently provided strong evidence against a unitary system.

In the case of working memory , the lateral frontal cortex in primates, already implicated in the spatial delayed response task, was known to contain cells that exhibited activity in delay periods [ 24 ] in response to stimuli in a number of sensory modalities. Goldman-Rakic [ 71 ] in particular suggested that the dlPFC (BA-46 /sulcus principalis) mediated the maintenance of spatial information in memory in preparation for action. Subsequent work queried whether the maintenance of information per se was a critical PFC function. Thus, it was shown from other electrophysiological evidence as well as human functional imaging that the anterior inferotemporal/perirhinal and parietal cortex also exhibited maintenance operations [ 72 ], although the dlPFC did appear to have important roles in resisting interference (e.g., distraction) in working memory [ 73 ]. Moreover, other investigators (e.g., [ 74 ]) have interpreted the role of the “mid-dorsal” (BA-9/46) PFC to mediate CC processes, such as the monitoring or tagging of recently selected items, as in self-ordered or n -back tasks, rather than the passive maintenance of information (see also [ 75 ] for a meta-analysis). By contrast, damage to a different sector of more posterior dlPFC (BA-8) impaired selection of motor responses to particular stimuli (conditional learning of task sets) but such performance was not affected by BA-9/46 damage. This type of double dissociation further supports the hypothesis that distinct processes of CC in lateral PFC are mediated by different regions and is relevant to hierarchical theories of CC, considered below.

There are also distinct functions within nodes of the FPN, where some of the “manipulation” sub-processes of working memory are mediated by parietal cortex, for example, including representations and operations relevant for mental arithmetic [ 76 ] and mental rotation [ 77 ]. By combining fMRI methods with the measurement of evoked response potentials (ERP), it is possible to track the time-course of FPN control processes: Frontal dipoles contributed prior to parietal dipoles in a task involving updating working memory to bias processing of stimulus-response mappings mediated by the parietal cortex [ 78 ].

Theories relating basic processing of external stimulus features for immediate action to future planning functions involving working memory for sequential actions or branching rule contingencies have suggested a linear hierarchy of control operations in the FPN, with the most abstract levels represented by the most anterior PFC structures, i.e., in fronto-polar regions [ 67 , 79 ]. This hierarchical scheme, supported by evidence from functional neuroimaging and dynamic causal modeling, postulates the caudal lateral PFC to be responsive to external stimulus features, the mid-lateral PFC to contextual rules for attention, and the most rostral parts of lateral PFC to implement rules from working memory. However, causal analyses employing theta-burst transcranial magnetic stimulation (TMS) to reduce cortical excitability of infra-PFC connections have suggested that the “hub” or “apex” where these control influences over attention to the present, external world and the future, “internal” one, are integrated in mid-lateral, not rostral PFC [ 80 ].

With respect to cognitive flexibility , one of the classical tests in humans, the Wisconsin Card Sort Task (WCST; see Fig.  1 ), originally implicated both OFC and dlPFC [ 81 ], on the basis of lesion studies in humans and monkeys. A modern lesion study [ 82 ] in the marmoset showed that excitotoxic, cell body (i.e., fiber-sparing) lesions to the OFC (BA-13) and to the lateral PFC, BA-12/47) produced a clear double dissociation between two distinct tests commonly associated with cognitive flexibility (or inhibitory control): Reversal learning was robustly impaired by the OFC lesion (BA-11), and extra-dimensional set-shifting (as occurs in the WCST) by ventrolateral (vl)PFC (BA-12/47) lesions. (An apparently similar neural dissociation of these deficits has subsequently also been shown in both rats and mice, as well as in humans [ 83 ]). Moreover, other studies revealed that the set-shifting deficit occurred in the absence of any obvious “on-line” working memory impairments [ 84 ].

These studies suggest dissociation, not only between elements of CC, but also even within the domain of cognitive flexibility. The findings are also compatible with the hypothetically hierarchical organization of PFC function by which reversing contingencies for objects based on changes in value are at a lower level than flexibly attending to perceptual dimensions or categories. There is also evident task impurity in the former case; impairments in reversal learning could have resulted from deficits in the processing of negative feedback or the value of objects rather than cognitive flexibility per se.

Functional neuroimaging studies in humans confirm that these two tests of cognitive flexibility implicate different PFC regions, lateral PFC in the case of set-shifting (compared with intra-dimensional shifts) and OFC regions in the case of reversal learning occurring after negative feedback [ 85 ]. Additional analyses in that study suggested that the parietal activations occurred when previous stimulus-reward mappings needed to be overwritten and dlPFC activation at all phases of the task involving new solutions, thus providing a fractionation of the neural regions implicated in attentional control. Another, resting state, study of patients with OCD and healthy controls showed that the ability to perform the extra-dimensional shift task was related to functional connectivity between the ventrolateral PFC and the caudate nucleus, whereas performance of a visuospatial planning task implicated activity in a distinct fronto-striatal pathway [ 86 ]).

Whereas set-shifting and reversal learning may depend on learning from reinforcing feedback, switching rapidly between established stimulus-response mappings or task sets may produce switch costs. The latter are caused by the required reconfiguration of task sets and interference between them, and exaggerated by damage to PFC regions, especially to the right and left inferior frontal cortex [ 87 ]. Functional neuroimaging studies with several forms of task set switching that isolated perceptual versus response-related aspects of switching highlighted the right inferior junction and posterior parietal cortex as domain general zones for switching [ 88 , 89 ]. dlPFC was more implicated specifically in response switching, and posterior frontal regions (e.g., premotor cortex) in perceptual switching, with a familiar caudal-rostral PFC gradient of increasingly abstract switching rules [ 89 ]. Thus, mechanisms underlying cognitive flexibility overlap anatomically with those of updating working memory to some extent, but likely also depend on some specialized circuitry [ 90 ].

To examine response inhibition , Aron et al. [ 91 ] applied the lesion approach method to a single paradigm, the stop-signal task [ 92 ], in group of patients with variable volumes of damage to different sectors of the PFC. They showed that the only sector correlating with stop-signal reaction time was the right inferior frontal gyrus (RIFG; including BA-44 and BA-45, especially pars opercularis). Go reaction time, for example, was more related to damage to other PFC regions. This result was of theoretical significance, as the stop-signal task can readily be considered to measure response inhibition, although, like virtually all other tests of CC, it is impure and also incorporates attentional components. A good deal of evidence from a variety of methodologies, including fMRI and disruptive TMS, has supported this general correlation of RIFG dysfunction with impaired response inhibition [ 93 ], but the question has remained whether this region specifically mediates response inhibition or other aspects of performance (e.g., [ 94 , 95 , 96 , 97 ]). It is notable, for example, that patients with lesions in this area also exhibit deficits in spatial working memory performance [ 98 ], consistent with the MD model of lateral PFC function.

The issue of anatomical specificity matching cognitive specificity for stopping inhibition has been addressed from a variety of perspectives. A meta-analysis of the large number of relevant fMRI studies has shown two main peak BOLD activations, one within the insular cortex, apparently coincident with initial processing of the STOP signal, and a subsequent peak focused more in the RIFG, and plausibly associated with the production of the response. A possible solution of the issue may depend on sophisticated network analyses [ 99 ]. Early on, Aron and Poldrack [ 100 ] proposed a specific circuit for response braking that included the hyperdirect projection from RIFG to the subthalamic nucleus (STN), so it could perhaps be argued that among its various functions, via part of its extensive pattern of connections, the “hub” that is the RIFG has specific “spokes” that mediate relatively specific components of CC. An analysis of effective connectivity among PFC regions during stop-signal task performance revealed that the best selected Bayesian model allowed the RIFG to modulate an excitatory influence of the pre-SMA on the STN, thereby amplifying downstream polysynaptic inhibition from the STN to the motor cortex. Diffusion tensor imaging of the white fiber connectivity of these structures validated these conclusions and predicted individual differences in stopping efficiency [ 101 ]. To show CC specificity would require double dissociations of the dynamics of network action of this type, but this analysis clearly identifies highly specific interactions among frontal regions and an important modulatory role for the RIFG “hub.”

In the stop-signal task there is also a right frontal electrophysiological signature of increased beta power for successful versus stop trials, which is matched by a similar signal during a requirement to stop an unwanted thought coming to mind [ 102 ]. This match raises the possibility that the right lateral frontal cortex controls a general inhibitory mechanism that does not simply brake actions, but can also inhibit cognitive and emotional outputs [ 103 ]. The latter study [ 103 ] found that the right medial gyrus contained three nodes of activation that mediated cognitive and emotional inhibitory effects at the more anterior sites and motor inhibition more posteriorly, interacting with the RIFG. The emotional inhibition task engaged the OFC and amygdala, whereas a think-no-think task involved the hippocampus, congruent with the work of Anderson [ 104 , 105 ], who has consistently shown that memory retrieval can be inhibited by a dlPFC pathway to the hippocampus, via relays in the mid-temporal lobe or retrosplenial cortex (see Anderson & Floresco, this issue [ 106 ]). Overall, there is increasing evidence for parallel, top-down inhibitory systems over a range of behavioral and cognitive responses, somewhat lateralised to the right hemisphere. The reasons for this lateralization are not currently clear, but could relate to the lateralization of language to the left hemisphere, or possibly to lateralization of some emotional functions to the right. Existing evidence suggests that the complementary left inferior frontal cortex regions play a role in semantic memory retrieval [ 107 ], as well as constituting Broca’s area (BA-44/45).

In the case of motivational control (“hot” vs “cool” CC) , perhaps the most striking dissociations for human patients with frontal lobe injury were cases of everyday decision-making in the absence of obvious impairment in IQ or conventional neuropsychological testing of classical “frontal” deficits [ 108 ]. Subsequent work established that such deficits were caused by extensive damage to the orbitofrontal and ventromedial (vm)PFC, extending into the frontal pole (BA-10) [ 109 , 110 ]. Such patterns may indicate a clear division between “hot” and “cool” cognition, the latter comprising what could be termed as CC. By contrast, the vmPFC, an often ill-defined area potentially comprising several distinct cytoarchitectonic regions (Fig.  2 ), is commonly associated with a “goal-directed” system [ 7 ].

Although working memory components incorporate such notions as “goal maintenance,” it is important to consider how PFC circuits mediate the associative learning and monitoring of instrumental behavior, leading to such goals or response outcomes, including their valuation. Such motivational and evaluation functions are the province of PFC regions including the OFC (BA 11,12,13,14) and ACC (BA 24 and 32) ([ 7 ]; see also reviews by Monosov & Rushworth, this issue, and Rudebek & Izquierdo, this issue [ 111 , 112 ]), as well as the neuromodulatory influences of the ascending monoaminergic systems (Cools & Arnsten, this issue [ 113 ]).

Early notions of a role for the ACC in inhibition of prepotent dispositions and error monitoring in CC theory have more recently been supplanted by considerations of effort, choice difficulty, and adaptive coding of response outcomes, relevant to flexible foraging behavior and the exploration of alternative choices [ 114 ]. ACC activity is enhanced under conditions not only of conflict, but also cognitive effort and choice difficulty [ 115 ]. Moreover, studies using fMRI and electrophysiological (error-related negativity) methods in humans, as well as single-unit electrophysiology in experimental animals, have identified the ACC to be a site of computation of prediction errors encoding the difference between expected and obtained outcomes of responding [ 115 , 116 , 117 ].

It has proven to be a difficult task to accommodate all of these empirical phenomena in one computational model; how therefore can such a diversity of functions most parsimoniously be explained? Notable have been attempts to incorporate effortful and cost-benefit factors, as in the Expected Value of Control model [ 118 ] and the extension of the conflict monitoring notion to decision-making between options of similar value in the Choice Difficulty model [ 119 ] (see also Collins & Shenhav, this issue [ 120 ]). By contrast, the Predicted Response Outcome model [ 117 ] uses as its basis unsigned prediction errors of any type, whether appetitive or aversive outcomes, and whether negative (unexpected omission of expected outcome) or positive (unexpected occurrence of outcome) “surprise,” over multiple time-scales to directly affect actions (and not stimulus representations). This model thus accommodates observations of multiple signals in this region concerning outcomes of actions based on appetitive reward as well as aversive pain [ 114 ] and explains non-prepotent responses on the Stroop and errors as being less expected events. Further extensions to the model explain how this information can lead to behavioral adaptation during decision-making and to both proactive and reactive CC [ 121 ], in terms of anticipatory adjustments to responding on one hand, as in risk-avoidance and foraging behavior, and to error-induced slowing caused by negative surprise and the temporary invigoration of responding (“hot-hand”) of repeated positive surprise in association with rewarding feedback [ 122 ] on the other. The latter computational model has recently been suggested to capture the most important functions of the entire PFC [ 122 ].

A recent fMRI test of speeded value-based decision-making that could distinguish amongst the predictions made by the various models has favored the Predicted Response Outcome model over the Expected Value of Control and Choice Difficulty alternatives [ 123 ]. However, the Predicted Response Outcome model has a characteristic signature in several other brain regions, including the lateral PFC and parietal cortex, that pose questions about how signals from the ACC are relayed to other regions of the brain, including to the fronto-parietal axis, the striosomes of the striatum, and the noradrenergic locus coeruleus, with diverse applications. Moreover, it is possible that the differing strengths of the models may be reflected by anatomical differentiation within what is a large, quite heterogeneous anatomical region. Thus, choice difficulty has been related to a more dorsomedial region close to the pre-supplementary motor area and pain to more ventral regions of the ACC [ 114 , 122 ].

Neurochemical modulation of CC

CC has to occur in the context and history of different motivational states including those produced by prior stress and learning, mediated in part by phasic and tonic changes in the ascending monoaminergic and cholinergic neurotransmitter systems. For example, dopamine receptors in the PFC have been related hypothetically to three main elements of CC: gating; maintaining and relaying motor commands; and producing error learning signals [ 116 , 124 , 125 ].

An extensive literature in human and experimental animals has shown that CC is susceptible to pharmacological intervention and hence to neuromodulation by the ascending monoaminergic and cholinergic systems [ 126 , 127 ] (see also Cools & Arnsten, this issue [ 113 ]). For example, catecholaminergic drugs such as methylphenidate and atomoxetine, or manipulations affecting the dopaminergic and noradrenergic neurotransmitter systems, can affect several aspects of CC, including working memory, cognitive flexibility, and response inhibition. However, drug effects are generally dose-dependent and conform to a familiar inverted U-shaped function. Moreover, different tasks reflecting different components of CC may be affected in dissociable ways. For example, dopamine depletion in the marmoset PFC impaired spatial delayed response whilst enhancing extra-dimensional shifting [ 128 ]. Floresco [ 129 ] reviews data suggesting that dopamine D1 receptors are more implicated in working memory, whereas D2 receptors promote cognitive flexibility in rodents. In patients with Parkinson’s disease, therapeutic doses of L-Dopa appear to improve working memory and task-set switching but impair reversal learning and decision-making [ 130 ].

On the other hand, serotonin depletion of the OFC in marmosets impaired reversal learning without affecting extra-dimensional set-shifting [ 131 ]. In human studies, the noradrenergic reuptake inhibitor atomoxetine enhanced stop-signal performance but had no effect on probabilistic learning known to engage OFC mechanisms, whereas the selective serotonin reuptake inhibitor citalopram had the reverse pattern of effects [ 132 ]. These findings indicate a degree of specificity in how these ascending transmitter systems interact with PFC–striatal networks and also raise the possibility that the motivational states mediated by activity in these systems may differentially prime different aspects of CC. The possibility of “top-down” or local control of the cholinergic system [ 133 ] or the catecholamine system [ 134 ] by PFC circuitry may also provide mechanisms for the allocation of “cognitive effort”.

Integration of CC

Despite the evidence for fractionation (“diversity”) of CC, there is also considerable evidence for overlap (“unity”) across separable CC/EF processes. As described earlier, at the behavioral level, this unity can be observed in the correlations among EF latent factors, which enables estimation of a “Common” CC factor (Fig.  3 ). At the neurobiological level, this unity can be seen in the overall patterns of neural activations during CC tasks [ 135 , 136 , 137 ]: Neuroimaging studies suggest that individuals performing these kinds of tasks generally activate some of the same brain regions across multiple tasks, although they also activate some regions that are unique to a particular task.

Conjunction maps of activation during different tasks (e.g., during inhibiting, updating, and shifting tasks), either with data estimated within one study [ 135 , 138 , 139 ] or with meta-analytic techniques [ 137 , 140 , 141 ], suggest that both children and adults recruit a common set of regions within the FPN and CON during diverse EF tasks. The FPN and CON are functionally separable brain networks that enable flexible adaptive control and sustained task-set maintenance [ 142 ]; together, they form the MD network [ 143 ], a set of brain regions that is active during a range of tasks that require goal-directed behavior [ 139 ]. For example, Niendam et al.‘s [ 137 ] meta-analytic study of 193 neuroimaging fMRI studies of EF showed broad patterns of activation across the lateral and medial PFC, including regions BA-9 and BA-46 (dlPFC) and BA-32 (rostral ACC), as well as both superior and inferior regions of the parietal lobes for tasks with predominantly working memory, flexibility, or inhibitory components.

However, despite overall conjunctions of activation, there may be subtle differences among tasks that also account for diversity. In Niendam et al.‘s [ 137 ] meta-analysis, flexibility tasks alone activated BA 11 and a sub-class of tasks involving initiation did not activate parietal regions. A similar conclusion was arrived at by Fedorenko et al. [ 139 ] using a more refined design by which individual subjects were shown to exhibit overlapping activation in a variety of tasks including verbal and spatial working memory, arithmetic, Stroop, and attentional tasks. The concept of diversity as well as unity of PFC functions can be illustrated in a typical fMRI study [ 144 ] which had defined task components of response inhibition and cognitive flexibility, finding increased BOLD activity in the FPN including both the RIFG region and in the parietal cortex. However, whereas the response control-related activity was greatest in the RIFG, the opposite was the case for attentional shifting; hence the different nodes of the FPN as well as functioning as part of a network, evidently had different roles within that network. The FPN can be regarded in some sense as a domain-general system that flexibly connects with other networks depending on the nature of the task, but the various dissociations reviewed also highlight how CC can be deployed in specific ways, perhaps capturing diversity as well as unity of PFC function.

Although there are clearly common neural areas recruited by diverse CC tasks, an open question is whether these same areas are involved in individual differences in performance of these tasks. That is, most people activate the FPN during demanding tasks, but do performance differences across tasks systematically relate to how strongly individuals activate the FPN or its nodes during these tasks? Few studies have looked at conjunction maps of areas related to individual differences in performance, but one study that did so did not find areas of significant overlap across three CC tasks, despite significant areas of mean activation across those tasks [ 138 ].

Studies that have correlated individual differences in Common CC ability with a neural measure, such as functional activation of a particular region during a task, functional or structural connectivity, or gray matter volume, often find that areas within but also outside of the MD network contribute to performance [ 145 , 146 , 147 , 148 ]. A meta-analysis of healthy adults [ 149 ] found that better performance on individual CC tasks was associated with larger PFC volume and greater PFC thickness, particularly for lateral PFC, although there was significant heterogeneity in the strength of association that was related to the particular tasks examined as well as sample age variability. Examining a group of healthy college-aged young adults, Smolker et al. [ 147 ] found that a Common CC factor was related to changes in gray matter and cortical folding in the broad vmPFC area, typically associated with the goal-directed system, whereas the specific aspects of updating of working memory and cognitive shifting were related specifically to dlPFC and vlPFC, respectively. However, it is notable that using a latent factor analysis in concert with structural imaging, there was only limited evidence of a major involvement of fronto-parietal activity for the Common CC factor.

A later study [ 148 ] in a large group ( N  = 251) of healthy adults approximately a decade older, and employing a larger test battery, did not confirm all of these associations, possibly because of an important developmental factor. In this study, Common CC was related to greater volume of the right middle frontal gyrus/frontal pole and to fractional anisotropy of the right superior longitudinal fasciculus, connecting the frontal lobes to other regions of posterior neocortex, including the parietal lobes. Updating-specific ability was linked to gray matter changes in regions both within and outside the fronto-parietal axis. In contrast, Shifting-specific ability implicated widespread white matter changes, as measured by mean, radial and axial diffusivity measures. In a similarly aged sample (ages 22–35) from the Human Connectome Project, Lerman-Sinkoff et al. [ 150 ] examined correlates of a Common CC composite using a data-driven approach (independent components analysis) to reduce multimodal imaging data. They found that CC was related to two components, one of which included variation related to visual network activity and insular gray matter volume, and the other of which included activity of the FPN and gray matter thickness in the CON [ 150 ].

Taken together, these results suggest that individual differences in Common CC are linked to structural and functional characteristics of the brain that include the FPN and CON, but also networks related to lower-level processes such as the visual network. Stronger global or specific connectivity of the dlPFC to other regions throughout the brain has been associated with better performance on diverse CC tasks or factors [ 151 , 152 ]. As such, dlPFC seems to affect individual differences in performance through its influence on other areas within and outside of the FPN.

Finally, a number of recent studies that have examined variations in structural and functional connectivity also suggest that more large-scale properties (as opposed to region-specific or even network-specific properties) may relate to Common CC. A large study of participants aged 8–22 years [ 153 ] found that higher scores on a CC factor were related to higher modularity of white matter brain networks (stronger connections within networks and weaker connections between networks), particularly the FPN, and modularity mediated age-related increases in CC scores. More modular, segregated networks may allow for more specialization and less interference across brain networks. CC scores were also positively associated with global efficiency, a measure of how quickly information can flow across networks. These results suggest that higher Common CC is associated with brain structures characterized by both more specialization of networks but also greater coordination across networks. Moreover, the extent to which brain network connectivity changes in response to cognitive demands is associated with better performance on different CC tasks [ 154 , 155 ], suggesting that task-based neural flexibility may facilitate Common CC through adaptive control [ 156 ].

The robust evidence for shared variance and common patterns of neural activations across CC tasks begs the key question of what cognitive process(es) comprise the “unity” of CC. There are a number of proposed mechanisms for the Common CC factor, which have both informed and been informed by the neuropsychological literature.

One proposed mechanism for the Common CC factor is inhibition , a mechanism apparently consistent with a strong relationship between the Common CC factor and the response inhibition factor that has been observed in several studies: When a higher-order common factor is used to model the correlations among response inhibition, working memory updating, and mental set shifting (see Fig.  3b ), that common factor almost perfectly predicts the inhibition factor [ 37 , 38 , 157 , 158 ], but there is significant variance in the updating and shifting factors that is not related to the common factor. Similarly, when the correlated factors model is re-parameterized into a bifactor model (see Fig.  3c ), there are updating-specific and shifting-specific factors, but there is no evidence for a response inhibition-specific factor [ 37 , 38 , 157 ]. In other words, the variance that is shared across response inhibition tasks is the same variance shared across all tasks (response inhibition, working memory updating, and mental set shifting). Broadly speaking, this pattern suggests that, at the level of individual differences, unity (what is common to CC processes) may be isomorphic with response inhibition, whereas diversity is evident in additional processes associated with updating working memory and mental set shifting.

This pattern of little inhibition-specific variance could be interpreted as indicating that what is common to CC abilities is inhibition. That is, one could describe most if not all CC processes as requiring some sort of inhibition [ 159 ]. For example, updating working memory tasks could be characterized as requiring inhibition both to stop irrelevant information from entering working memory and to remove no-longer-relevant information from working memory when appropriate [ 160 ]. Similarly, mental set shifting tasks could be characterized as requiring inhibition to ignore information irrelevant to the current task set [ 161 ], as well as to suppress the no-longer-relevant task set when switching sets [ 162 ].

However, this characterization relies on the assumption that processes described with similar terms (such as “inhibition”) are in fact similar, an assumption that may not be valid [ 163 ]. Even though the same inhibition term is used to describe these requirements, those processes may be dissociable [ 161 , 164 ], and in some cases, may not involve inhibition (i.e., neural inhibition) at all [ 165 , 166 ].

An alternative proposal is that the unity component reflects individual differences in the ability to actively maintain goals and use those goals to bias ongoing processing [ 29 , 97 , 167 ]. To perform well in all CC tasks, participants must have accurate representations of the task goals that can be used to direct attention to task-relevant information, particularly when there is conflicting task-irrelevant information. In some cases, participants must also monitor the environment for conditions that signal that the goal is relevant. For example, in stop-signal tasks, the stop goal is only relevant on a subset of trials in which a signal occurs, so performance may partially depend on being able to quickly recognize the relevance of the signal and stop the response [ 95 ]. According to this proposal, individual differences in response inhibition tasks may be particularly related to this ability because if a goal is inactive or ineffective, then more automatic or prepotent responses will take over, leading to poor performance on these tasks. If response-inhibition-specific neural processes, such as global motor suppression [ 93 , 168 ], do not show large individual differences, then task performance may be more driven by whether those processes are triggered in the first place. To the extent that keeping goals highly active and proactively biasing ongoing processing influences stopping, performance may be more determined by these global processes rather than inhibition-specific ones [ 29 , 97 , 169 ].

This proposal that unity captures goal maintenance and biasing [ 29 ] is in fact a classic conception of CC and frontal lobe function [ 8 , 170 , 171 ]. In addition to proposing that CC involves the active maintenance of goals in the PFC that bias processing elsewhere in the brain, Miller and Cohen [ 8 ] argued that this key function of PFC is responsible for various aspects of CC, such as selective attention, response inhibition, and working memory. Seen from an individual differences perspective, they essentially proposed a “common” CC ability that depended on such goal maintenance and bias.

Specifically, building on Desimone and Duncan’s [ 170 ] model of such competitive dynamics during visual attention, Miller and Cohen argued that prefrontal goal representations enable weak stimulus-response mappings to out-compete more habitual ones when appropriate: Goal representations bias competition by boosting activation for task-relevant processing, which, by virtue of lateral inhibition, suppress activity of competing representations. In this sense, “inhibition” could be seen as fundamental to common CC ability. Yet, this goal maintenance and biasing account of common CC ability is conceptually different from accounts that invoke a broader inhibition mechanism, discussed earlier.

The goal maintenance/biasing perspective is incorporated into several other CC frameworks, such as the executive attention framework [ 172 ] and the dual mechanisms of CC framework [ 121 ]. Duncan and colleagues’ MD framework also prominently incorporates a goal-maintenance/biasing perspective. They characterized the unity of frontal lobe functions in terms of goal-related processes, specifically the ability to form and carry out goals at multiple levels of abstraction [ 32 ]. Failures in this ability can manifest as goal neglect, a phenomenon commonly observed with head injury, as also noted by Teuber [ 31 ]. Duncan et al. [ 32 ] found that goal neglect was more related to general brain atrophy than focal frontal lesions, and Duncan [ 11 ] later linked these general goal-related processes to the MD network a network of frontal and parietal regions that is commonly activated across tasks.

Duncan and colleagues [ 11 , 32 ] have also linked goal neglect and the activity of the MD network with general fluid intelligence, leading to the last interpretation of the unity component we consider here: that it recapitulates intelligence or Spearman’s g . Indeed, a large body of work has documented moderate to large correlations between intelligence measures, particularly measures of fluid intelligence (such as reasoning) with measures of CC. Perhaps most relevant, studies that have measured a common CC latent factor have reported correlations with intelligence ranging from r  = 0.53–0.91 [ 41 , 158 , 173 , 174 ]. Such correlations suggest that the unity of CC is related to intelligence or g . However, at least in adult samples, this correlation is only moderate, and is significantly lower than 1 ( r  = 0.53–0.68 [ 41 , 158 ]), indicating that these constructs cannot be considered identical, even when examined with latent variables. Moreover, CC and intelligence seem to show discriminant predictive validity of behavior, in that CC is associated with problems related to attention-deficit/hyperactivity disorder (e.g., [ 175 , 176 ]) or lack of self-restraint [ 177 ], even when controlling for intelligence.

In addition to correlating with common CC, intelligence also significantly correlates with the variance that is unique to working memory processes (working memory updating and/or capacity) [ 41 , 158 ]. Such results suggest that although the CC unity component may reflect some of the same processes tapped by intelligence measures, common CC is not equivalent to intelligence. Rather, intelligence may be related to both common CC and working memory-specific processes, consistent with earlier research showing that intelligence and particularly reasoning ability are strongly related to working memory capacity [ 178 , 179 ].

Clinical implications

Many psychiatric and neurological disorders are associated with specific symptoms that may be at least partly a product of impaired CC, or with more general cognitive deficits that accompany the specific symptoms. For example, Attention-Deficit Hyperactivity Disorder (ADHD) has major EF/CC impairments in attentional control, working memory, and response inhibition that contribute to DSM-5 symptoms of distractibility and impulsivity. Similarly, some symptoms of major depressive disorder include problems of decision-making and concentration, which appear to entail primary CC impairments. In schizophrenia, negative symptoms have been related to impaired goal-directed behavior [ 180 ] and positive symptoms such as delusions and hallucinations to deficits in reality monitoring [ 181 ], although there is an additional domain of symptoms in schizophrenia of cognitive impairment that includes major working memory deficits and impedes rehabilitation [ 182 ].

One hypothesis concerning addiction is that it results from a general impairment in goal-directed behavior, leading to more pronounced habitual tendencies, and exacerbated by a loss of top-down control, to contribute to compulsive drug-seeking [ 183 ]. An analogous mechanism has been proposed to account for other forms of compulsive behavior, such as checking or washing in obsessive-compulsive disorder [ 184 ]. However, it should also be recognized that hyperactivity in medial PFC regions in such disorders (Ahmari & Rauch, this issue [ 185 ]) could potentially be associated with specific compulsive behaviors that retain their goal-directness. Moreover, it is possible that a simple dichotomy between goal-directed and habitual behavior is too simple. A recent computational formulation [ 186 ] has suggested an intermediate type of control mode relying on model-based and model-free computations guided by “successor representations’“ that enable behavior to be both flexibly goal-directed but also efficiently model free.

Although the precise contribution of dysfunctional CC mechanisms to psychiatric and neurological symptoms, perhaps in combination with altered perceptual and motivational processes, remains to be determined, at a general level, it is clear that CC deficits are characteristic of a wide range of disorders. Indeed, meta-analyses suggest transdiagnostic associations of CC deficits with psychiatric disorders, including major depressive disorder, post-traumatic stress disorder [ 187 ], obsessive-compulsive disorder [ 188 ], bipolar disorder [ 189 ], schizophrenia [ 190 ], ADHD [ 191 , 192 ], conduct disorder and antisocial personality disorder [ 193 ], and substance use disorders [ 194 ].

Unity and diversity of psychopathology in relation to CC

Although such psychiatric and neurological disorders are often treated as distinct entities, a growing body of work has focused on the observation that these disorders share considerable variance [ 195 ]. That is, whether treated as dimensional or categorical constructs, different disorders are often comorbid, either concurrently or sequentially across the lifespan [ 20 , 195 ]. This common variance occurs at multiple levels of specificity. At one level, particular disorders can be clustered into internalizing (depression and anxiety), externalizing (antisocial behavior and substance use), and thought disorder (schizophrenia, bipolar disorder, obsessive-compulsive disorder) factors. At a higher-order level, these internalizing, externalizing, and thought disorder factors correlate with each other, and these correlations can be modeled with a general psychopathology factor [ 20 , 195 , 196 ]. This hierarchical general factor has been dubbed the “ p factor” in recognition of its parallel to the g factor for cognitive abilities [ 197 ]. The p factor has been modeled in a number of datasets, and shows longitudinal stability and criterion validity, in that it predicts a number of clinical outcomes [ 195 , 196 ].

However, like any statistical factor, it describes a pattern of correlations but not an explanation of those correlations. That is, its neurobiological underpinnings are not well understood and its psychological interpretation varies [ 20 , 195 ]. For example, the p factor has been proposed to reflect negative emotionality, disordered thinking, and/or poor CC, particularly impulse control (inhibitory control) over positive and negative emotions [ 2 , 20 , 195 , 198 ].

With respect to CC, the transdiagnostic associations of CC with psychopathology support the notion that the p factor may partly reflect CC deficits [ 1 , 2 , 197 ], although there may also be specific CC deficits associated with particular disorders or clusters of disorders (e.g., [ 197 , 199 ]). Moreover, within many disorders, it appears that multiple aspects of CC (inhibition, shifting or flexibility, and working memory processes) are impaired [ 1 ], though possibly to different extents. These patterns suggest that CC impairments associated with psychopathology may be general, reflecting variance that is shared across multiple CC constructs [ 1 ]. Indeed, several studies have examined this hypothesis directly, finding that a common CC factor is associated with a p factor ( r  = –0.16 to –0.56) [ 174 , 200 , 201 , 202 , 203 ].

Studies of neural correlates of psychopathology also suggest the importance of CC-related regions of interest and networks. In particular, multiple psychiatric disorders are associated with hypoactivation of the FPN and CON during CC tasks [ 2 , 204 ], alterations in functional connectivity of these networks at rest [ 3 , 205 ], and alterations in gray matter volume in nodes of these networks, including the dorsal ACC, insula, and dorsomedial and vmPFC [ 2 , 3 , 206 ]. When integrated with findings that these same patterns are associated with poorer performance on CC tasks [ 2 , 3 ], these results are consistent with the conclusion that CC and mental health share neural substrates, and that disruptions of these neural substrates may account for increased p and decreased common CC functioning [ 2 , 3 ].

Links between impulse control, CC, and psychopathology

Many PFC areas are particularly associated with control over emotionally relevant information (hot CC) [ 60 , 61 , 62 , 63 , 64 , 66 ], which, as discussed earlier, show some dissociations from cool CC. These associations are consistent with interpretations of the p factor that focus on emotional regulation, particularly impulse control in the context of high arousal (both positive and negative emotion) [ 198 ]. At the behavioral level, such emotional impulse control is often measured with self-report measures of impulsivity and emotional urgency, such as those assessed with the UPPS-P impulsivity scale [ 207 ].

Although such emotional impulse control is thought to be enabled by general processes and neural correlates of CC [ 198 ], and urgency measures are correlated with CC, these correlations are generally weak ( r  = ~0.10 to 0.20), as are correlations between laboratory CC tasks and more general self-control and EF questionnaires [ 157 , 208 , 209 , 210 , 211 , 212 ]. These weak relationships could indicate that there is no great dependency of impulse control on CC processes or the PFC, or indicate that subjective report of impulse control represents a domain of EF outside classical CC function, or it could simply reflect methodological differences. For example, the self-report questionnaires measure subjective aspects of performance whereas laboratory tests such as the Stroop measure objective aspects. However, some evidence suggests that task-based and self-report measures of CC may best be considered separable constructs that are both relevant to mental health [ 209 , 213 ], because they independently predict psychopathology in multiple regressions [ 157 , 214 , 215 ]. This conclusion is consistent with the possibility that these different aspects of CC may depend on different PFC regions: e.g., self-report measures have been correlated with medial PFC morphology, whereas CC tasks typically activate more lateral PFC [ 216 ].

Whether other-dimensional measures of performance, such as apathy (e.g., as measured by the Apathy Motivation Index [ 217 ]) or compulsivity (as measured by the Obsessive-Compulsive Inventory, OCI [ 218 ]) will be beset by similar issues is as yet unclear. One potentially important approach has been to combine computational paradigms such as the two-stage Markov decision-making task with latent factors including compulsivity from an analysis of multiple questionnaires used in impulsive-compulsive disorders [ 219 ]. This study showed that a factor of compulsivity was related to a bias to “model-free” responding, over “model-based” responding, which is commonly associated with goal-directed behavior. Participants in the “model-free” mode tend to respond according to the “win-stay/lose-shift” heuristics of Thorndike’s Law of Effect underlying reinforcement learning, whereas “model-based” responding entails developing a “mental model” of the task, which may involve higher-order processes of CC to optimize performance (e.g., switching away from win-stay when it is ultimately advantageous to do so).

Causal direction of associations between CC and psychopathology and substance use

Although it is clear that CC deficits are behaviorally associated with psychopathology, the causal origin of these relationships are often unclear. Are CC deficits a cause or consequence of emotional and behavioral problems, or perhaps both (i.e., is there a bidirectional relationship)? And if CC deficits are a consequence of the psychopathology, do they produce exacerbation of those symptoms, or other distinct problems that require rehabilitation? An obvious example is substance use disorders, where pre-existing deficits in CC may predispose to drug taking, but drug taking may also cause CC deficits by producing neuropathology, for example in the PFC and related circuitry. Cause-effect relationships regarding other forms of psychiatric morbidity can plausibly operate in a similar fashion. However, it is also possible that these relationships reflect common associations with other variables (e.g., correlated genetic or environmental risk factors).

Quasi-experimental observational designs such as family studies provide some evidence that these associations are at least partly due to correlated genetic risk. For example, stimulant drug abusers and their first degree relatives both have deficits in response inhibition on the Stop task, correlated with reductions in white matter in the RIFG [ 220 ]. Whilst this can be interpreted as showing that PFC-related response inhibition deficits promote vulnerability to stimulants, this influence of impaired response inhibition could theoretically arise from family-related environmental, as well as genetic, influences. Twin studies suggest that associations between psychopathology/substance use and CC are attributable largely to shared genetic influences [ 157 , 221 ]. However, there is some evidence for correlated environmental influences in addition to correlated genetic influences for a common CC factor with depression symptoms in a middle-aged male twin sample [ 222 ] and for a common CC factor with a p factor in children and adolescents [ 200 ].

Several co-twin control studies, which examine relationships controlling for shared familial risk factors, generally suggest that associations of lower cognitive ability with substance use, particularly cannabis, are not consistent with causal models in which substance use causes cognitive impairment. Specifically, the twin who used cannabis more often or began using earlier did not have lower cognitive ability or brain volume than their co-twins, which is inconsistent with a causal effect of the drug [ 223 , 224 , 225 , 226 ]. However, a recent co-twin-control study of young adults [ 227 ] found that the association of alcohol, but not cannabis, misuse with reduced cortical thickness of central executive and salience networks was consistent with causal effects of alcohol exposure as well as pre-existing genetic associations of cortical thickness with the propensity to misuse alcohol. Specifically, causal effects of alcohol misuse were present for lateral PFC, medial frontal and parietal areas, and the frontal operculum (BA 44). These results are thus consistent with a model in which reduced cortical thickness in areas that enable CC, particularly those related to response inhibition, may increase risk for alcohol misuse, and subsequent misuse further impacts those cortical areas (see also [ 228 ]).

Summary and future research directions

Lesion studies and psychometric models both suggest unity and diversity of CC. CC tasks that assess processes such as response inhibition, interference control, working memory maintenance and updating, and mental set shifting show unique variances, but also exhibit some overlap. This overlap (the “unity” of CC) can be characterized in multiple ways, but most characterizations include goal-related processes, such as active goal maintenance and the use of such goals to bias ongoing processing. It appears that there are CC processes that distinguish working memory updating, mental set shifting, and potentially other functions (dual-tasking ability and generativity, as in verbal fluency) from the common CC factor. It is also clear that hot CC can be distinguished from cool CC, and that CC as measured by laboratory tasks is quite different from constructs like impulsivity, which are typically measured with self-reports but can also be measured with laboratory paradigms. Given that different “objective” measures of impulsivity often fail to inter-correlate themselves [ 229 ], and there is also neural evidence of dissociation [ 230 ], it is likely that impulsivity, like CC and inhibition, is a multi-dimensional construct that includes a family of related but separable processes and underlying neural systems. Both CC and self-reported dimensions such as impulsivity may independently relate to psychiatric dysfunction, perhaps at different levels (i.e., at the level of individual disorders or factors that capture variance common across disorders).

Our understanding of the “unity and diversity” of PFC function at the neural level is necessarily incomplete, but suggests some congruency with the evidence at psychometric levels. There is evidence, for example, that networks involving the PFC, for example, the FPN, can mediate superficially different types of cognitive performance, suggesting the operation of an MD system of CC. Nevertheless, the existence of functional dissociations following different types of intervention is also compelling and may suggest that there is specialization of circuitry conferred by the flexible networking of its “hubs” with other neural circuitry. In particular, different PFC nodes within the network, as well their interactions with other neural circuitry, presumably have distinct contributions to information processing, and elucidation of such dynamic transactions in real time will be an important future focus of research. Finally, it appears likely that CC will have to be understood in the context of complementary motivational control networks, including subcortical influences of chemical neuromodulatory systems. Thus, the heterogeneous, but also overlapping, nature of psychiatric symptoms across different DSM5 categories presumably reflects the unity and diversity of CC.

The PFC and its associated networks will thus continue to be a major factor in understanding psychiatric and neurological disorders and developing new treatments. We can foresee future research priorities in several areas. The unity and diversity model of CC/EF needs to be developed further to explore other possible constructs related to PFC networks, perhaps especially hot CC, which may be of greatest significance to mental health disorders. It may also prove necessary to decompose some of its existing constructs, e.g., working memory updating and cognitive flexibility (e.g., set shifting), into their components in order to relate them to distinctive psychiatric symptoms and neural dysfunction.

There is also a need to compare different theoretical positions, such as the cognitive, learning theory, and computational modeling approaches, to optimize our descriptions of phenotypes for mapping onto PFC networks. Such refinements could perhaps enhance genetic studies, as well as improve new nosological systems such as United States’ National Institute of Mental Health’s Research Domain Criteria (RDoC) [ 231 ], a research framework that advocates examining mental disorders from the perspective of basic dimensions of functioning, each examined at multiple levels of analysis (genes to circuits to behavior) that may apply to multiple diagnostic categories. Most relevant to this review, the RDoC includes cognitive systems, with CC and working memory constructs, but their dysfunctioning in mental health disorders has ultimately to be related to their neural substrates and pathophysiology.

Understanding the unity and diversity of genetic influences on CC and how they map onto associated PFC development and structure is another priority for future research. Structurally, there is evidence of differential genetic regulation of different PFC regions; for example, development of the mouse dorsal (and not ventral) PFC is especially sensitive to the fibroblast growth factor family of genes [ 232 ]. Several independent twin studies [ 36 , 39 , 41 , 157 , 233 ] have yielded evidence that at the latent variable level, CC constructs are moderately to highly heritable and, importantly, that the separability of working memory updating and mental set shifting from the common CC factor is largely attributable to different genetic influences.

However, the specific genes that account for these patterns, presumably in part via expression in the PFC, have yet to be identified. Most genome-wide association studies (GWAS) to date have focused on intelligence or g [ 234 , 235 , 236 , 237 ], and suggest that hundreds to thousands of genes additively influence variation in intelligence, with the effect of any one gene being very small (typically in GWAS, a variant has r 2  < 0.05% [ 238 ]). The largest GWAS of CC to date [ 239 ] included individual CC tests such as the Stroop task with samples smaller than 11,000 individuals, and did not yield any significant associations. Clearly, more work is needed with sufficiently large samples to enable GWAS. However, acquiring detailed cognitive task data on such large samples ( N  = 10’s to 100’s of thousands) is no easy feat and will most certainly require harmonization across multiple samples and/or online testing. Though resulting measures are typically crude compared to the measures included in smaller studies [ 240 ], the trade-off between phenotype depth and sample size may be effective for gene discovery [ 241 ], as demonstrated by a recent preliminary report [ 242 ] of a GWAS for the Common CC factor.

Once such variants are identified, bioinformatic follow-up analyses can be used to identify genetic pathways that influence CC-related neural differences. For example, a recent GWAS [ 243 ] suggested that global measures of cortical surface area and thickness were related to distinct genetic influences associated with different developmental mechanisms (i.e., associated with regulatory elements present during fetal development and in adults, respectively); and total surface area was bidirectionally causally related to general cognitive ability and educational attainment. Similar analyses applied to more nuanced CC phenotypes could confirm hypothesized pathways and suggest new avenues of research for understanding behavioral and neural variation related to CC variation and associated clinical outcomes.

As developmental studies are also likely to be of increasing importance for determining the factors influencing the etiology of mental disorders, large scale longitudinal studies of CC/EF, combined with sensitive clinical scales, trait questionnaires, neuroimaging, and genotyping, as for example, in the National Institutes’ of Health Adolescent Brain Cognitive Development (ABCD) study [ 244 ], will be invaluable. Such an ambitious project may well have to involve increasingly sophisticated ways of obtaining this information via on-line testing.

Deficits in neural networks, including the PFC, are increasingly being used to determine the neural substrates of CC/EF. However, more analysis is required of the underlying pathophysiology of these networks (e.g., at the circuit and molecular levels), because a network abnormality could arise in many different ways that may have significance for diagnosis, drug discovery, and neuromodulation strategies. Finally, if experimental animals are to be used to model genetic and molecular deficits in the developing brain, new research needs to be done to test whether the “unity and diversity” approach applies across species and fits what is known of PFC homology (Preuss & Wise, this issue [ 245 ]).

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NPF is currently supported by NIH grants DA046064, DA046413, DA042742, DA051018, MH117131, AG046938, and HD078532. This research was funded in part, by the Wellcome Trust (Grant 104631/Z/14/Z to TWR). For the purpose of open access, the author has applied a CC BY public copyright licence to any Author Accepted Manuscript version arising from this submission. TWR also acknowledges a National Research Foundation (Singapore) CREATE Grant to the University of Cambridge and Nanyang Technological University for the Centre of Lifelong Learning and Individualised Cognition (CLIC). He discloses consultancy and royalties from Cambridge Cognition, consultancy with Arcadia, Greenfield Bioventures, Takeda, Merck Sharp & Dohne, Lundbeck, and research grants from Shionogi and GlaxoSmithKline.

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Friedman, N.P., Robbins, T.W. The role of prefrontal cortex in cognitive control and executive function. Neuropsychopharmacol. 47 , 72–89 (2022). https://doi.org/10.1038/s41386-021-01132-0

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Brain Anatomy and How the Brain Works

What is the brain.

The brain is a complex organ that controls thought, memory, emotion, touch, motor skills, vision, breathing, temperature, hunger and every process that regulates our body. Together, the brain and spinal cord that extends from it make up the central nervous system, or CNS.

What is the brain made of?

Weighing about 3 pounds in the average adult, the brain is about 60% fat. The remaining 40% is a combination of water, protein, carbohydrates and salts. The brain itself is a not a muscle. It contains blood vessels and nerves, including neurons and glial cells.

What is the gray matter and white matter?

Gray and white matter are two different regions of the central nervous system. In the brain, gray matter refers to the darker, outer portion, while white matter describes the lighter, inner section underneath. In the spinal cord, this order is reversed: The white matter is on the outside, and the gray matter sits within.

Gray matter is primarily composed of neuron somas (the round central cell bodies), and white matter is mostly made of axons (the long stems that connects neurons together) wrapped in myelin (a protective coating). The different composition of neuron parts is why the two appear as separate shades on certain scans.

Each region serves a different role. Gray matter is primarily responsible for processing and interpreting information, while white matter transmits that information to other parts of the nervous system.

How does the brain work?

The brain sends and receives chemical and electrical signals throughout the body. Different signals control different processes, and your brain interprets each. Some make you feel tired, for example, while others make you feel pain.

Some messages are kept within the brain, while others are relayed through the spine and across the body’s vast network of nerves to distant extremities. To do this, the central nervous system relies on billions of neurons (nerve cells).

Main Parts of the Brain and Their Functions

At a high level, the brain can be divided into the cerebrum, brainstem and cerebellum.

The cerebrum (front of brain) comprises gray matter (the cerebral cortex) and white matter at its center. The largest part of the brain, the cerebrum initiates and coordinates movement and regulates temperature. Other areas of the cerebrum enable speech, judgment, thinking and reasoning, problem-solving, emotions and learning. Other functions relate to vision, hearing, touch and other senses.

Cerebral Cortex

Cortex is Latin for “bark,” and describes the outer gray matter covering of the cerebrum. The cortex has a large surface area due to its folds, and comprises about half of the brain’s weight.

The cerebral cortex is divided into two halves, or hemispheres. It is covered with ridges (gyri) and folds (sulci). The two halves join at a large, deep sulcus (the interhemispheric fissure, AKA the medial longitudinal fissure) that runs from the front of the head to the back. The right hemisphere controls the left side of the body, and the left half controls the right side of the body. The two halves communicate with one another through a large, C-shaped structure of white matter and nerve pathways called the corpus callosum. The corpus callosum is in the center of the cerebrum.

The brainstem (middle of brain) connects the cerebrum with the spinal cord. The brainstem includes the midbrain, the pons and the medulla.

• Midbrain. The midbrain (or mesencephalon) is a very complex structure with a range of different neuron clusters (nuclei and colliculi), neural pathways and other structures. These features facilitate various functions, from hearing and movement to calculating responses and environmental changes. The midbrain also contains the substantia nigra, an area affected by Parkinson’s disease that is rich in dopamine neurons and part of the basal ganglia, which enables movement and coordination.
• Pons. The pons is the origin for four of the 12 cranial nerves, which enable a range of activities such as tear production, chewing, blinking, focusing vision, balance, hearing and facial expression. Named for the Latin word for “bridge,” the pons is the connection between the midbrain and the medulla.
• Medulla. At the bottom of the brainstem, the medulla is where the brain meets the spinal cord. The medulla is essential to survival. Functions of the medulla regulate many bodily activities, including heart rhythm, breathing, blood flow, and oxygen and carbon dioxide levels. The medulla produces reflexive activities such as sneezing, vomiting, coughing and swallowing.

The spinal cord extends from the bottom of the medulla and through a large opening in the bottom of the skull. Supported by the vertebrae, the spinal cord carries messages to and from the brain and the rest of the body.

The cerebellum (“little brain”) is a fist-sized portion of the brain located at the back of the head, below the temporal and occipital lobes and above the brainstem. Like the cerebral cortex, it has two hemispheres. The outer portion contains neurons, and the inner area communicates with the cerebral cortex. Its function is to coordinate voluntary muscle movements and to maintain posture, balance and equilibrium. New studies are exploring the cerebellum’s roles in thought, emotions and social behavior, as well as its possible involvement in addiction, autism and schizophrenia.

Brain Coverings: Meninges

Three layers of protective covering called meninges surround the brain and the spinal cord.

• The outermost layer, the dura mater , is thick and tough. It includes two layers: The periosteal layer of the dura mater lines the inner dome of the skull (cranium) and the meningeal layer is below that. Spaces between the layers allow for the passage of veins and arteries that supply blood flow to the brain.
• The arachnoid mater is a thin, weblike layer of connective tissue that does not contain nerves or blood vessels. Below the arachnoid mater is the cerebrospinal fluid, or CSF. This fluid cushions the entire central nervous system (brain and spinal cord) and continually circulates around these structures to remove impurities.
• The pia mater is a thin membrane that hugs the surface of the brain and follows its contours. The pia mater is rich with veins and arteries.

Lobes of the Brain and What They Control

Each brain hemisphere (parts of the cerebrum) has four sections, called lobes: frontal, parietal, temporal and occipital. Each lobe controls specific functions.

• Frontal lobe. The largest lobe of the brain, located in the front of the head, the frontal lobe is involved in personality characteristics, decision-making and movement. Recognition of smell usually involves parts of the frontal lobe. The frontal lobe contains Broca’s area, which is associated with speech ability.
• Parietal lobe. The middle part of the brain, the parietal lobe helps a person identify objects and understand spatial relationships (where one’s body is compared with objects around the person). The parietal lobe is also involved in interpreting pain and touch in the body. The parietal lobe houses Wernicke’s area, which helps the brain understand spoken language.
• Occipital lobe. The occipital lobe is the back part of the brain that is involved with vision.
• Temporal lobe. The sides of the brain, temporal lobes are involved in short-term memory, speech, musical rhythm and some degree of smell recognition.

Deeper Structures Within the Brain

Pituitary gland.

Sometimes called the “master gland,” the pituitary gland is a pea-sized structure found deep in the brain behind the bridge of the nose. The pituitary gland governs the function of other glands in the body, regulating the flow of hormones from the thyroid, adrenals, ovaries and testicles. It receives chemical signals from the hypothalamus through its stalk and blood supply.

Hypothalamus

The hypothalamus is located above the pituitary gland and sends it chemical messages that control its function. It regulates body temperature, synchronizes sleep patterns, controls hunger and thirst and also plays a role in some aspects of memory and emotion.

Small, almond-shaped structures, an amygdala is located under each half (hemisphere) of the brain. Included in the limbic system, the amygdalae regulate emotion and memory and are associated with the brain’s reward system, stress, and the “fight or flight” response when someone perceives a threat.

Hippocampus

A curved seahorse-shaped organ on the underside of each temporal lobe, the hippocampus is part of a larger structure called the hippocampal formation. It supports memory, learning, navigation and perception of space. It receives information from the cerebral cortex and may play a role in Alzheimer’s disease.

Pineal Gland

The pineal gland is located deep in the brain and attached by a stalk to the top of the third ventricle. The pineal gland responds to light and dark and secretes melatonin, which regulates circadian rhythms and the sleep-wake cycle.

Ventricles and Cerebrospinal Fluid

Deep in the brain are four open areas with passageways between them. They also open into the central spinal canal and the area beneath arachnoid layer of the meninges.

The ventricles manufacture cerebrospinal fluid , or CSF, a watery fluid that circulates in and around the ventricles and the spinal cord, and between the meninges. CSF surrounds and cushions the spinal cord and brain, washes out waste and impurities, and delivers nutrients.

Blood Supply to the Brain

Two sets of blood vessels supply blood and oxygen to the brain: the vertebral arteries and the carotid arteries.

The external carotid arteries extend up the sides of your neck, and are where you can feel your pulse when you touch the area with your fingertips. The internal carotid arteries branch into the skull and circulate blood to the front part of the brain.

The vertebral arteries follow the spinal column into the skull, where they join together at the brainstem and form the basilar artery , which supplies blood to the rear portions of the brain.

The circle of Willis , a loop of blood vessels near the bottom of the brain that connects major arteries, circulates blood from the front of the brain to the back and helps the arterial systems communicate with one another.

Cranial Nerves

Inside the cranium (the dome of the skull), there are 12 nerves, called cranial nerves:

• Cranial nerve 1: The first is the olfactory nerve, which allows for your sense of smell.
• Cranial nerve 2: The optic nerve governs eyesight.
• Cranial nerve 3: The oculomotor nerve controls pupil response and other motions of the eye, and branches out from the area in the brainstem where the midbrain meets the pons.
• Cranial nerve 4: The trochlear nerve controls muscles in the eye. It emerges from the back of the midbrain part of the brainstem.
• Cranial nerve 5: The trigeminal nerve is the largest and most complex of the cranial nerves, with both sensory and motor function. It originates from the pons and conveys sensation from the scalp, teeth, jaw, sinuses, parts of the mouth and face to the brain, allows the function of chewing muscles, and much more.
• Cranial nerve 6: The abducens nerve innervates some of the muscles in the eye.
• Cranial nerve 7: The facial nerve supports face movement, taste, glandular and other functions.
• Cranial nerve 8: The vestibulocochlear nerve facilitates balance and hearing.
• Cranial nerve 9: The glossopharyngeal nerve allows taste, ear and throat movement, and has many more functions.
• Cranial nerve 10: The vagus nerve allows sensation around the ear and the digestive system and controls motor activity in the heart, throat and digestive system.
• Cranial nerve 11: The accessory nerve innervates specific muscles in the head, neck and shoulder.
• Cranial nerve 12: The hypoglossal nerve supplies motor activity to the tongue.

The first two nerves originate in the cerebrum, and the remaining 10 cranial nerves emerge from the brainstem, which has three parts: the midbrain, the pons and the medulla.

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Parts of the Brain and Their Functions

The human brain is the epicenter of our nervous system and plays a pivotal role in virtually every aspect of our lives. It’s a complex, highly organized organ responsible for thoughts, feelings, actions, and interactions with the world around us. Here is a look at the intricate anatomy of the brain, its functions, and the consequences of damage to different areas.

Introduction to the Brain and Its Functions

The brain is an organ of soft nervous tissue that is protected within the skull of vertebrates. It functions as the coordinating center of sensation and intellectual and nervous activity. The brain consists of billions of neurons (nerve cells) that communicate through intricate networks. The primary functions of the brain include processing sensory information, regulating bodily functions, forming thoughts and emotions, and storing memories.

Main Parts of the Brain – Anatomy

The three main parts of the brain are the cerebrum, cerebellum, and brainstem.

1. Cerebrum

• Location: The cerebellum occupies the upper part of the cranial cavity and is the largest part of the human brain.
• Functions: It’s responsible for higher brain functions, including thought, action, emotion, and interpretation of sensory data.
• Effects of Damage: Depending on the area affected, damage leads to memory loss, impaired cognitive skills, changes in personality, and loss of motor control.

2. Cerebellum

• Location: The cerebellum is at the back of the brain, below the cerebrum.
• Functions: It coordinates voluntary movements such as posture, balance, coordination, and speech.
• Effects of Damage: Damage causes problems with balance, movement, and muscle coordination (ataxia).

3. Brainstem

• Location: The brainstem is lower extension of the brain, connecting to the spinal cord. It includes the midbrain, pons, and medulla oblongata.
• Functions: This part of the brain controls many basic life-sustaining functions, including heart rate, breathing, sleeping, and eating.
• Effects of Damage: Damage results in life-threatening conditions like breathing difficulties, heart problems, and loss of consciousness.

Lobes of the Brain

The four lobes of the brain are regions of the cerebrum:

• Location: This is the anterior or front part of the brain.
• Functions: Decision making, problem solving, control of purposeful behaviors, consciousness, and emotions.
• Location: Sits behind the frontal lobe.
• Functions: Processes sensory information it receives from the outside world, mainly relating to spatial sense and navigation (proprioception).
• Location: Below the lateral fissure, on both cerebral hemispheres.
• Functions: Mainly revolves around auditory perception and is also important for the processing of both speech and vision (reading).
• Location: At the back of the brain.
• Functions: Main center for visual processing.

Left vs. Right Brain Hemispheres

The cerebrum has two halves, called hemispheres. Each half controls functions on the opposite side of the body. So, the left hemisphere controls muscles on the right side of the body, and vice versa. But, the functions of the two hemispheres are not entirely identical:

• Left Hemisphere: It’s dominant in language and speech and plays roles in logical thinking, analysis, and accuracy. .
• Right Hemisphere: This hemisphere is more visual and intuitive and functions in creative and imaginative tasks.

The corpus callosum is a band of nerves that connect the two hemispheres and allow communication between them.

Detailed List of Parts of the Brain

While knowing the three key parts of the brain is a good start, the anatomy is quite a bit more complex. In addition to nervous tissues, the brain also contains key glands:

• Cerebrum: The cerebrum is the largest part of the brain. Divided into lobes, it coordinates thought, movement, memory, senses, speech, and temperature.
• Corpus Callosum : A broad band of nerve fibers joining the two hemispheres of the brain, facilitating interhemispheric communication.
• Cerebellum : Coordinates movement and balance and aids in eye movement.
• Pons : Controls voluntary actions, including swallowing, bladder function, facial expression, posture, and sleep.
• Medulla oblongata : Regulates involuntary actions, including breathing, heart rhythm, as well as oxygen and carbon dioxide levels.
• Limbic System : Includes the amygdala, hippocampus, and parts of the thalamus and hypothalamus.
• Amygdala: Plays a key role in emotional responses, hormonal secretions, and memory formation.
• Hippocampus: Plays a vital role in memory formation and spatial navigation.
• Thalamus : Acts as the brain’s relay station, channeling sensory and motor signals to the cerebral cortex, and regulating consciousness, sleep, and alertness.
• Basal Ganglia : A group of structures involved in processing information related to movement, emotions, and reward. Key structures include the striatum, globus pallidus, substantia nigra, and subthalamic nucleus.
• Ventral Tegmental Area (VTA) : Plays a role in the reward circuit of the brain, releasing dopamine in response to stimuli indicating a reward.
• Optic tectum : Also known as the superior colliculus, it directs eye movements.
• Substantia Nigra : Involved in motor control and contains a large concentration of dopamine-producing neurons.
• Cingulate Gyrus : Plays a role in processing emotions and behavior regulation. It also helps regulate autonomic motor function.
• Olfactory Bulb : Involved in the sense of smell and the integration of olfactory information.
• Mammillary Bodies : Plays a role in recollective memory.
• Function: Regulates emotions, memory, and arousal.

Glands in the Brain

The hypothalamus, pineal gland, and pituitary gland are the three endocrine glands within the brain:

• Hypothalamus : The hypothalamus links the nervous and endocrine systems. It contains many small nuclei. In addition to participating in eating and drinking, sleeping and waking, it regulates the endocrine system via the pituitary gland. It maintains the body’s homeostasis, regulating hunger, thirst, response to pain, levels of pleasure, sexual satisfaction, anger, and aggressive behavior.
• Pituitary Gland : Known as the “master gland,” it controls various other hormone glands in the body, such as the thyroid and adrenals, as well as regulating growth, metabolism, and reproductive processes.
• Pineal Gland : The pineal gland produces and regulates some hormones, including melatonin, which is crucial in regulating sleep patterns and circadian rhythms.

Gray Matter vs. White Matter

The brain and spinal cord consist of gray matter (substantia grisea) and white matter (substantia alba).

• White Matter: Consists mainly of axons and myelin sheaths that send signals between different brain regions and between the brain and spinal cord.
• Gray Matter: Consists of neuronal cell bodies, dendrites, and axon terminals. Gray matter processes information and directs stimuli for muscle control, sensory perception, decision making, and self-control.

Frequently Asked Questions (FAQs) About the Human Brain

• The human brain contains approximately 86 billion neurons. Additionally, it has a similar or slightly higher number of non-neuronal cells (glial cells), making the total number of cells in the brain close to 170 billion.
• There are about 86 billion neurons in the human brain. These neurons are connected by trillions of synapses, forming a complex networks.
• The average adult human brain weighs about 1.3 to 1.4 kilograms (about 3 pounds). This weight represents about 2% of the total body weight.
• The brain is about 73% water.
• The myth that humans only use 10% of their brain is false. Virtually every part gets use, and most of the brain is active all the time, even during sleep.
• The average size of the adult human brain is about 15 centimeters (6 inches) in length, 14 centimeters (5.5 inches) in width, and 9 centimeters (3.5 inches) in height.
• Brain signal speeds vary depending on the type of neuron and the nature of the signal. They travel anywhere from 1 meter per second to over 100 meters per second in the fastest neurons.
• With age, the brain’s volume and/or weight decrease, synaptic connections reduce, and there can be a decline in cognitive functions. However, the brain to continues adapting and forming new connections throughout life.
• The brain has a limited ability to repair itself. Neuroplasticity aids recovery by allowing other parts of the brain to take over functions of the damaged areas.
• The brain consumes about 20% of the body’s total energy , despite only making up about 2% of the body’s total weight . It requires a constant supply of glucose and oxygen.
• Sleep is crucial for brain health. It aids in memory consolidation, learning, brain detoxification, and the regulation of mood and cognitive functions.
• Douglas Fields, R. (2008). “White Matter Matters”. Scientific American . 298 (3): 54–61. doi: 10.1038/scientificamerican0308-54
• Kandel, Eric R.; Schwartz, James Harris; Jessell, Thomas M. (2000). Principles of Neural Science (4th ed.). New York: McGraw-Hill. ISBN 978-0-8385-7701-1.
• Kolb, B.; Whishaw, I.Q. (2003). Fundamentals of Human Neuropsychology (5th ed.). New York: Worth Publishing. ISBN 978-0-7167-5300-1.
• Rajmohan, V.; Mohandas, E. (2007). “The limbic system”. Indian Journal of Psychiatry . 49 (2): 132–139. doi: 10.4103/0019-5545.33264
• Shepherd, G.M. (1994). Neurobiology . Oxford University Press. ISBN 978-0-19-508843-4.

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The Anatomy of the Brain

The brain controls your thoughts, feelings, and physical movements

Associated Conditions

The brain is a unique organ that is responsible for many functions such as problem-solving, thinking, emotions, controlling physical movements, and mediating the perception and responses related to the five senses. The many nerve cells of the brain communicate with each other to control this activity.

Each area of the brain has one or more functions. The skull, which is composed of bone, protects the brain. A number of different health conditions can affect the brain, including headaches , seizures , strokes , multiple sclerosis , and more. These conditions can often be managed with medical or surgical care.

The brain is primarily composed of nerve cells, which are also called neurons. Blood vessels supply oxygen and nutrients to the neurons of the brain. Cerebrospinal fluid (CSF), a fluid that provides nourishment and immune protection to the brain, flows around the brain and within the ventricular system (spaces between the regions of the brain).

The brain and the CSF are protected by the meninges, composed of three layers of connective tissue: the pia, arachnoid, and dura layers. The skull surrounds the meninges.

The brain has many important regions, such as the cerebral cortex, brainstem, and cerebellum. The areas of the brain all interact with each other through hormones and nerve stimulation.

The regions of the brain include:

• Cerebral cortex : This is the largest portion of the brain. It includes two hemispheres (halves), which are connected to each other—physically and functionally—by the corpus callosum. The corpus callosum runs from the front of the cerebral cortex to the back of the cerebral cortex. The outer part of the cerebral cortex is often described as gray matter, and the deeper areas are often described as white matter due to their microscopic appearance.
• Lobes of the cerebral cortex : Each hemisphere of the cerebral cortex is composed of four lobes. The frontal lobes are the largest, and they are located at the front of the brain. The temporal lobes are located on the sides of the brain, near and above the ears. The parietal lobes are at the top middle section of the brain. And the occipital lobes, which are the smallest lobes, are located in the back of the cerebral cortex.
• Limbic system : The limbic system is located deep in the brain and is composed of several small structures, including the hippocampus, amygdala, thalamus, and hypothalamus .
• Internal capsule : This area is located deep in the brain and is considered white matter. The frontal regions of the cerebral cortex surround the left and right internal capsules. The internal capsule is located near the lateral ventricles.
• Thalamus : The left and right thalami are below the internal capsule, above the brainstem, and near the lateral ventricles.
• Hypothalamus and pituitary gland : The hypothalamus is a tiny region of the brain located directly above the pituitary gland. The pituitary gland is a structure that extends directly above the optic chiasm, where the optic nerves meet.
• Brainstem : The brainstem is the lowest region of the brain and is continuous with the spinal cord. It is composed of three sections: the midbrain, pons, and medulla. The cranial nerves emerge from the brainstem.
• Cerebellum : The cerebellum is located at the lower back of the brain, under the occipital lobe and behind the brainstem. It has two hemispheres (left and right) that are connected by a middle structure called the vermis.
• Blood vessels : The blood vessels that supply your brain include the anterior cerebral arteries , middle cerebral arteries , posterior cerebral arteries, basilar artery , and vertebral arteries . These blood vessels and the blood vessels that connect them to each other compose a collection of blood vessels described as the circle of Willis .
• Ventricular system : CSF flows in the right and left lateral ventricles, the third ventricle, the cerebral aqueduct, the fourth ventricle, and down into the central canal in the spinal cord.

The brain has a number of functions, including motor function (controlling the body’s movements), coordination, sensory functions (being aware of sensations), hormone control, regulation of the heart and lungs, emotions, memory, behavior, and creativity.

These functions often rely on and interact with each other. For example, you might experience an emotion based on something that you see and/or hear. Or you might try to solve a problem with the help of your memory. Messages travel very quickly between the different regions in the brain, which makes the interactions almost instantaneous.

Functions of the brain include:

• Motor function : Motor function is initiated in an area at the back of the frontal lobe called the motor homunculus. This region controls movement on the opposite side of the body by sending messages through the internal capsule to the brainstem, then to the spinal cord, and finally to a spinal nerve through a pathway described as the corticospinal tract.
• Coordination and balance : Your body maintains balance and coordination through a number of pathways in the cerebral cortex, cerebellum, and brainstem.
• Sensation : The brain receives sensory messages through a pathway that travels from the nerves in the skin and organs to the spine, then to the brainstem, up through the thalamus, and finally to an area of the parietal lobe called the sensory homunculus, which is directly behind the motor homunculus. Each hemisphere receives sensory input from the opposite side of the body. This pathway is called the spinothalamic tract.
• Vision : Your optic nerves in your eyes can detect whatever you see, sending messages through your optic tract (pathway) to your occipital lobes. The occipital lobes put those messages together so that you can perceive what you are seeing in the world around you.
• Taste and smell : Your olfactory nerve detects smell, while several of your cranial nerves work together to detect taste. These nerves send messages to your brain. The sensations of smell and taste often interact, as smell amplifies your experience of taste.
• Hearing : You can detect sounds when a series of vibrations in your ear stimulate your vestibulocochlear nerve. The message is sent to your brainstem and then to your temporal cortex so that you can make sense of the sounds that you hear.
• Language : Speaking and understanding language is a specialized brain function that involves several regions of your dominant hemisphere (the side of the brain opposite your dominant hand). The two major areas that control speech are Wernicke’s area , which controls the understanding of speech, and Broca’s area, which controls the fluency of your speech.
• Emotions and memory : Your amygdala and hippocampus play important roles in storing memory and associating certain memories with emotion.
• Hormones : Your hypothalamus, pituitary gland, and medulla all respond to the conditions of your body, such as your temperature, carbon dioxide level, and hormone levels, by releasing hormones and other chemicals that help regulate your body’s functions. Emotions such as fear can also have an influence on these functions.
• Behavior and judgment : The frontal lobes control reasoning, planning, and maintaining social interactions. This area of the brain is also involved in judgment and maintaining appropriate behavior.
• Analytical thinking : Mathematical problem solving is located in the dominant hemisphere. Often, this type of reasoning involves interaction with the decision-making regions of the frontal lobes.
• Creativity : There are many types of creativity, including the production of visual art, music, and creative writing. These skills can involve three-dimensional thinking, also described as visual-spatial skills. Creativity also involves analytical reasoning and usually requires a balance between traditional ways of thinking (which occurs in the frontal lobes) and "thinking outside the box."

There are many conditions that can affect the brain. You may experience self-limited issues, such as the pain of a headache, or more lasting effects of brain disease, such as paralysis due to a stroke. The diagnosis of brain illnesses may be complex and can involve a variety of medical examinations and tests, including a physical examination, imaging tests, neuropsychological testing, electroencephalography (EEG) , and/or lumbar puncture .

Common conditions that involve the brain include:

• Headaches : Head pain can occur due to chronic migraines or tension headaches. You can also have a headache when you feel sleepy, stressed, or due to an infection like meningitis (an infection of the meninges).
• Traumatic brain injury : An injury to the head can cause damage such as bleeding in the brain, a skull fracture, a bruise in the brain, or, in severe cases, death. These injuries may cause vision loss, paralysis, or severe cognitive (thinking) problems.
• Concussion : Head trauma can cause issues like loss of consciousness, memory impairment, and mood changes. These problems may develop even in the absence of bleeding or a skull fracture. Often, symptoms of a concussion resolve over time, but recurrent head trauma can cause serious and persistent problems with brain function, described as chronic traumatic encephalopathy (CTE).
• Transient ischemic attack (TIA) : A temporary interruption in the blood supply to the brain can cause the affected areas to temporarily lose function. This can happen due to a blood clot, usually coming from the heart or carotid arteries. If the interruption in blood flow resolves before permanent brain damage occurs, this is called a TIA . Generally, a TIA is considered a warning that a person is at risk of having a stroke, so a search for stroke causes is usually necessary—and stroke prevention often needs to be initiated.
• Stroke : A stroke is brain damage that occurs due to an interruption of blood flow to the brain. This can occur due to a blood clot (ischemic stroke) or a bleed in the brain (hemorrhagic stroke) . There are a number of causes of ischemic and hemorrhagic stroke, including heart disease, hypertension, and brain aneurysms.
• Brain aneurysm : An aneurysm is an outpouching of a blood vessel. A brain aneurysm can cause symptoms due to pressure on nearby structures. An aneurysm can also bleed or rupture, causing a hemorrhage in the brain. Sometimes an aneurysm can be surgically repaired before it ruptures, preventing serious consequences.
• Dementia : Degenerative disease of the regions in the brain that control memory and behavior can cause a loss of independence. This can occur in several conditions, such as Alzheimer’s disease , Lewy body dementia, Pick’s disease, and vascular dementia (caused by having many small strokes).
• Multiple sclerosis (MS) : This is a condition characterized by demyelination (loss of the protective fatty coating around nerves) in the brain and spine. MS can cause a variety of effects, such as vision loss, muscle weakness, and sensory changes. The disease course can be characterized by exacerbations and remissions, a progressive decline, or a combination of these processes.
• Parkinson’s disease : This condition is a progressive movement disorder that causes tremors of the body (especially the arms), stiffness of movements, and a slow, shuffling pattern of walking. There are treatments for this condition, but it is not curable.
• Epilepsy : Recurrent seizures can occur due to brain damage or congenital (from birth) epilepsy. These episodes may involve involuntary movements, diminished consciousness, or both. Seizures usually last for a few seconds at a time, but prolonged seizures (status epilepticus) can occur as well. Anti-epileptic medications can help prevent seizures, and some emergency anti-epileptic medications can be used to stop a seizure while it is happening.
• Meningitis or encephalitis : An infection or inflammation of the meninges (meningitis) or the brain (encephalitis) can cause symptoms such as fever, stiff neck, headache, or seizures. With treatment, meningitis usually improves without lasting effects, but encephalitis can cause brain damage, with long-term neurological impairment.
• Brain tumors : A primary brain tumor starts in the brain, and brain tumors from the body can metastasize (spread) to the brain as well. These tumors can cause symptoms that correlate to the affected area of the brain. Brain tumors also may cause swelling in the brain and hydrocephalus (a disruption of the CSF flow in the ventricular system). Treatments include surgery, chemotherapy, and radiation therapy.

If you have a condition that could be affecting your brain, there are a number of complex tests that your medical team may use to identify the problem. Most important, a physical exam and mental status examination can determine whether there is any impairment of brain function and pinpoint the deficits. For example, you may have weakness of one part of the body, vision loss, trouble walking, personality or memory changes, or a combination of these issues. Other signs, such as rash or fever, which are not part of the neurological physical examination, can also help identify systemic issues that could be causing your symptoms.

Diagnostic tests include brain imaging tests such as computerized tomography (CT), magnetic resonance imaging (MRI), or functional magnetic resonance imaging (fMRI). These tests can identify structural and functional abnormalities. And sometimes, tests such as CT angiography (CTA), MRI angiography (MRA), or interventional cerebral angiography are needed to visualize the blood vessels in the brain.

Another test, an evoked potential test, can be used to identify hearing or vision problems in some circumstances. And a lumbar puncture may be used to evaluate the CSF surrounding the brain. This test can detect evidence of infection, inflammation, or cancer. Rarely, a brain biopsy is used to sample a tiny area of the brain to assess the abnormalities.

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Cognitive Function

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Cognition ; Cognitive abilities ; Intelligence ; Mental functioning ; Neuropsychological function ; Thought

Cognitive function is a broad term that refers to mental processes involved in the acquisition of knowledge, manipulation of information, and reasoning. Cognitive functions include the domains of perception, memory, learning, attention, decision making, and language abilities.

Description

Classical models of human cognition have been conceptualized by cognitive scientists within an information processing paradigm. This approach is grounded by a computational metaphor which draws an analogy between mental operations with the functioning of a computer. Although the central nervous system is recognized as the mechanism underpinning cognition under this approach, a distinction between the brain and cognition is likened to the relation between computer hardware (often referred to as “wetware”) and computer software. Historically, two competing information processing...

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Baltes, P. B., Staudinger, U. M., & Lindenberger, U. (1999). Lifespan psychology: Theory and application to intellectual functioning. Annual Review of Psychology, 50 , 471–507.

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Kiely, K.M. (2014). Cognitive Function. In: Michalos, A.C. (eds) Encyclopedia of Quality of Life and Well-Being Research. Springer, Dordrecht. https://doi.org/10.1007/978-94-007-0753-5_426

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7.1 What Is Cognition?

Learning objectives.

By the end of this section, you will be able to:

• Describe cognition
• Distinguish concepts and prototypes
• Explain the difference between natural and artificial concepts
• Describe how schemata are organized and constructed

Imagine all of your thoughts as if they were physical entities, swirling rapidly inside your mind. How is it possible that the brain is able to move from one thought to the next in an organized, orderly fashion? The brain is endlessly perceiving, processing, planning, organizing, and remembering—it is always active. Yet, you don’t notice most of your brain’s activity as you move throughout your daily routine. This is only one facet of the complex processes involved in cognition. Simply put, cognition is thinking, and it encompasses the processes associated with perception, knowledge, problem solving, judgment, language, and memory. Scientists who study cognition are searching for ways to understand how we integrate, organize, and utilize our conscious cognitive experiences without being aware of all of the unconscious work that our brains are doing (for example, Kahneman, 2011).

Upon waking each morning, you begin thinking—contemplating the tasks that you must complete that day. In what order should you run your errands? Should you go to the bank, the cleaners, or the grocery store first? Can you get these things done before you head to class or will they need to wait until school is done? These thoughts are one example of cognition at work. Exceptionally complex, cognition is an essential feature of human consciousness, yet not all aspects of cognition are consciously experienced.

Cognitive psychology is the field of psychology dedicated to examining how people think. It attempts to explain how and why we think the way we do by studying the interactions among human thinking, emotion, creativity, language, and problem solving, in addition to other cognitive processes. Cognitive psychologists strive to determine and measure different types of intelligence, why some people are better at problem solving than others, and how emotional intelligence affects success in the workplace, among countless other topics. They also sometimes focus on how we organize thoughts and information gathered from our environments into meaningful categories of thought, which will be discussed later.

Concepts and Prototypes

The human nervous system is capable of handling endless streams of information. The senses serve as the interface between the mind and the external environment, receiving stimuli and translating it into nervous impulses that are transmitted to the brain. The brain then processes this information and uses the relevant pieces to create thoughts, which can then be expressed through language or stored in memory for future use. To make this process more complex, the brain does not gather information from external environments only. When thoughts are formed, the mind synthesizes information from emotions and memories ( Figure 7.2 ). Emotion and memory are powerful influences on both our thoughts and behaviors.

In order to organize this staggering amount of information, the mind has developed a "file cabinet" of sorts. The different files stored in the file cabinet are called concepts. Concepts are categories or groupings of linguistic information, images, ideas, or memories, such as life experiences. Concepts are, in many ways, big ideas that are generated by observing details, and categorizing and combining these details into cognitive structures. You use concepts to see the relationships among the different elements of your experiences and to keep the information in your mind organized and accessible.

Concepts are informed by our semantic memory (you will learn more about semantic memory in a later chapter) and are present in every aspect of our lives; however, one of the easiest places to notice concepts is inside a classroom, where they are discussed explicitly. When you study United States history, for example, you learn about more than just individual events that have happened in America’s past. You absorb a large quantity of information by listening to and participating in discussions, examining maps, and reading first-hand accounts of people’s lives. Your brain analyzes these details and develops an overall understanding of American history. In the process, your brain gathers details that inform and refine your understanding of related concepts such as war, the judicial system, and voting rights and laws.

Concepts can be complex and abstract, like justice, or more concrete, like types of birds. In psychology, for example, Piaget’s stages of development are abstract concepts. Some concepts, like tolerance, are agreed upon by many people, because they have been used in various ways over many years. Other concepts, like the characteristics of your ideal friend or your family’s birthday traditions, are personal and individualized. In this way, concepts touch every aspect of our lives, from our many daily routines to the guiding principles behind the way governments function.

Another technique used by your brain to organize information is the identification of prototypes for the concepts you have developed. A prototype is the best example or representation of a concept. For example, what comes to your mind when you think of a dog? Most likely your early experiences with dogs will shape what you imagine. If your first pet was a Golden Retriever, there is a good chance that this would be your prototype for the category of dogs.

Natural and Artificial Concepts

In psychology, concepts can be divided into two categories, natural and artificial. Natural concepts are created “naturally” through your experiences and can be developed from either direct or indirect experiences. For example, if you live in Essex Junction, Vermont, you have probably had a lot of direct experience with snow. You’ve watched it fall from the sky, you’ve seen lightly falling snow that barely covers the windshield of your car, and you’ve shoveled out 18 inches of fluffy white snow as you’ve thought, “This is perfect for skiing.” You’ve thrown snowballs at your best friend and gone sledding down the steepest hill in town. In short, you know snow. You know what it looks like, smells like, tastes like, and feels like. If, however, you’ve lived your whole life on the island of Saint Vincent in the Caribbean, you may never actually have seen snow, much less tasted, smelled, or touched it. You know snow from the indirect experience of seeing pictures of falling snow—or from watching films that feature snow as part of the setting. Either way, snow is a natural concept because you can construct an understanding of it through direct observations, experiences with snow, or indirect knowledge (such as from films or books) ( Figure 7.3 ).

An artificial concept , on the other hand, is a concept that is defined by a specific set of characteristics. Various properties of geometric shapes, like squares and triangles, serve as useful examples of artificial concepts. A triangle always has three angles and three sides. A square always has four equal sides and four right angles. Mathematical formulas, like the equation for area (length × width) are artificial concepts defined by specific sets of characteristics that are always the same. Artificial concepts can enhance the understanding of a topic by building on one another. For example, before learning the concept of “area of a square” (and the formula to find it), you must understand what a square is. Once the concept of “area of a square” is understood, an understanding of area for other geometric shapes can be built upon the original understanding of area. The use of artificial concepts to define an idea is crucial to communicating with others and engaging in complex thought. According to Goldstone and Kersten (2003), concepts act as building blocks and can be connected in countless combinations to create complex thoughts.

A schema is a mental construct consisting of a cluster or collection of related concepts (Bartlett, 1932). There are many different types of schemata, and they all have one thing in common: schemata are a method of organizing information that allows the brain to work more efficiently. When a schema is activated, the brain makes immediate assumptions about the person or object being observed.

There are several types of schemata. A role schema makes assumptions about how individuals in certain roles will behave (Callero, 1994). For example, imagine you meet someone who introduces himself as a firefighter. When this happens, your brain automatically activates the “firefighter schema” and begins making assumptions that this person is brave, selfless, and community-oriented. Despite not knowing this person, already you have unknowingly made judgments about them. Schemata also help you fill in gaps in the information you receive from the world around you. While schemata allow for more efficient information processing, there can be problems with schemata, regardless of whether they are accurate: Perhaps this particular firefighter is not brave, they just work as a firefighter to pay the bills while studying to become a children’s librarian.

An event schema , also known as a cognitive script , is a set of behaviors that can feel like a routine. Think about what you do when you walk into an elevator ( Figure 7.4 ). First, the doors open and you wait to let exiting passengers leave the elevator car. Then, you step into the elevator and turn around to face the doors, looking for the correct button to push. You never face the back of the elevator, do you? And when you’re riding in a crowded elevator and you can’t face the front, it feels uncomfortable, doesn’t it? Interestingly, event schemata can vary widely among different cultures and countries. For example, while it is quite common for people to greet one another with a handshake in the United States, in Tibet, you greet someone by sticking your tongue out at them, and in Belize, you bump fists (Cairns Regional Council, n.d.)

Because event schemata are automatic, they can be difficult to change. Imagine that you are driving home from work or school. This event schema involves getting in the car, shutting the door, and buckling your seatbelt before putting the key in the ignition. You might perform this script two or three times each day. As you drive home, you hear your phone’s ring tone. Typically, the event schema that occurs when you hear your phone ringing involves locating the phone and answering it or responding to your latest text message. So without thinking, you reach for your phone, which could be in your pocket, in your bag, or on the passenger seat of the car. This powerful event schema is informed by your pattern of behavior and the pleasurable stimulation that a phone call or text message gives your brain. Because it is a schema, it is extremely challenging for us to stop reaching for the phone, even though we know that we endanger our own lives and the lives of others while we do it (Neyfakh, 2013) ( Figure 7.5 ).

Remember the elevator? It feels almost impossible to walk in and not face the door. Our powerful event schema dictates our behavior in the elevator, and it is no different with our phones. Current research suggests that it is the habit, or event schema, of checking our phones in many different situations that makes refraining from checking them while driving especially difficult (Bayer & Campbell, 2012). Because texting and driving has become a dangerous epidemic in recent years, psychologists are looking at ways to help people interrupt the “phone schema” while driving. Event schemata like these are the reason why many habits are difficult to break once they have been acquired. As we continue to examine thinking, keep in mind how powerful the forces of concepts and schemata are to our understanding of the world.

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Lobes of the brain

Author: Sophie Stewart • Reviewer: Gordana Sendić, MD Last reviewed: October 30, 2023 Reading time: 20 minutes

The brain, along with the spinal cord, is the main organ of the central nervous system. It is the most complex organ of the body, with many layers and components that play their roles in almost every function performed by the body. The brain is composed of the cerebrum , cerebellum and brainstem . The cerebrum is the largest part of the brain, and is divided into a left and right hemisphere. Although the cerebrum appears to be a uniform structure, it can actually be broken down into separate regions based on their embryological origins, structure and function. 

Each hemisphere of the cerebrum is composed of the cerebral cortex  and various structures that lie beneath it, also called subcortical structures . The cerebral cortex is a highly convoluted gray matter structure consisting of many gyri and sulci. The lobes of the cerebrum are actually divisions of the cerebral cortex based on the locations of the major gyri and sulci. 

The cerebral cortex is divided into six lobes: the frontal , temporal , parietal , occipital ,  insular and limbic lobes . Each lobe of the cerebrum exhibits characteristic surface features that each have their own functions. These lobes are not anatomically separated from one another by any barriers, but are physically continuous with each other, or interconnected via neural pathways in order to work together to process and synthesize information.

This article will discuss the anatomy and function of the cerebral lobes.

Components and function

Composition and function, broca's aphasia, wernicke's aphasia, clinical case, frontal lobe.

The frontal lobe is the largest lobe of the brain comprising almost one-third of the hemispheric surface. It lies largely in the anterior cranial fossa of the skull , leaning on the orbital plate of the frontal bone . 

The frontal lobe forms the most anterior portion of the cerebral hemisphere and is separated from the parietal lobe posteriorly by the central sulcus , and from the temporal lobe posteroinferiorly by the lateral sulcus (Sylvian fissure). The most anterior portion of the frontal lobe is known as the frontal pole .

The frontal lobe is made up of three cortical surfaces: a lateral, medial and inferior surface. 

• The lateral surface of the frontal lobe contains four principal gyri: the precentral, superior frontal, middle frontal, and the inferior frontal gyri. 
• The medial (interhemispheric) surface extends down to the cingulate sulcus and consists mainly of the paracentral lobule (an extension of the precentral and postcentral gyri), and the medial extension of the superior frontal gyrus.
• The inferior surface contains the olfactory tract and olfactory bulb , the straight gyrus and the four orbital gyri.

Functionally, the entire frontal cortex of the frontal lobe is divided into three parts: the prefrontal cortex, motor cortex and Broca’s area.

Prefrontal cortex

The most rostral portion of the frontal cortex is known as the prefrontal cortex , which encompasses the superior, middle and inferior frontal gyri of the frontal lobe. It plays a crucial role in the processing of intellectual and emotional information, including aggression, and facilitates judgement and decision-making.

Motor cortex

The motor cortex corresponds to the precentral gyrus of the frontal lobe. The precentral gyrus contains the primary motor cortex (Brodmann area 4), which is responsible for integrating signals from different brain regions to modulate motor function. The primary motor cortex is where the corticospinal tract originates. 

Anterior to the primary motor cortex of the precentral gyrus is the premotor area , or premotor cortex (Brodmann area 6), and the supplemental motor cortex . These regions of the cortex occupy the anterior part of the precentral gyrus and the posterior parts of the superior, middle, and inferior frontal gyri. Collectively, they function to assist in organizing movements and actions.

Encompassing part of the middle and inferior frontal gyri, just rostral to the premotor region, is an area called the frontal eye fields (Brodmann area 6,8,9), which is responsible for voluntary control of conjugate (horizontal) eye movements.

Broca's area

The inferior frontal gyrus is divided into three parts: i) the pars opercularis , ii) the pars triangularis , and iii) the pars orbitalis . Pars opercularis refers to the most dorsal part of the gyrus, pars triangularis is the middle triangularly-shaped part, while the pars orbitalis represents the most ventral part of the gyrus.

Functionally, the pars opercularis and triangularis in the dominant hemisphere are referred to as  Broca’s speech area (Brodmann area 44 and 45). Broca’s area is responsible for producing the motor component of speech, which includes verbal fluency, phonological processing, grammar processing and attention during speech.

Parietal lobe

The parietal lobe is located just underneath the parietal bone, lying posterior to the frontal lobe and anterior and superior to the temporal and occipital lobes. 

The anterior border of the parietal lobe is demarcated by the central sulcus , and the posterior border is formed by an imaginary line that extends between the parietooccipital sulcus (superiorly) and the preoccipital notch (inferiorly). The inferior border is formed by the lateral sulcus (Sylvian fissure), while the superior boundary of the parietal lobe ​​is formed by the medial longitudinal fissure that separates the two cerebral hemispheres.

The parietal lobe can be divided into three regions. The most anterior portion of the parietal lobe is the postcentral gyrus which runs parallel to the central sulcus. Functionally, this area is known as the primary somatosensory cortex (Brodmann areas 1,2 and 3). This region receives sensory information from all sensory receptors that provide information related to temperature, pain ( spinothalamic pathway ), vibration, proprioception and fine touch ( dorsal column pathway ). Thus, the postcentral gyrus of the frontal lobe is mainly involved in processing various types of sensory information.

The remainder of the parietal lobe can be divided into two main regions: the superior and inferior parietal lobules , which are separated anatomically by the intraparietal sulcus . The superior parietal lobule contributes to sensorimotor integration while the inferior parietal lobule contributes to auditory and language functions.

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Temporal lobe

The temporal lobe largely occupies the middle cranial fossa, and its name relates to its proximity to the temporal region/bone of the skull. The temporal lobe is separated from the frontal and parietal lobes superiorly by the lateral sulcus (Sylvian fissure). It extends ventrally from this fissure to the inferior surface of the cerebral cortex. Dorsally, it extends to an arbitrary line running between the parietooccipital sulcus and the preoccipital notch. 

The temporal lobe contains the cortical areas that process hearing, as well as sensory aspects of speech and memory.

The temporal lobe consists of three main gyri, the superior, middle and inferior temporal gyri , which are visible on the lateral surface. The superior temporal sulcus separates the superior and middle temporal gyri, while the inferior temporal sulcus separates the middle and inferior temporal gyri. The inferomedial aspect of the temporal lobe forms the hippocampus. 

The primary auditory area ( Brodmann area 41), also known as the transverse gyri of Heschl, is located on the internal, superior part of the superior temporal gyrus. It is a specialized region of cortex primarily responsible for the reception of auditory information. 

Auditory information is further processed within the secondary auditory area . The secondary auditory area (Brodmann area 42) lies posterior to the primary auditory area in the superior temporal gyrus, at the parietotemporal junction (Wernicke’s region in the dominant hemisphere), and receives impulses from the primary auditory area and thalamus. 

Unlike the superior temporal gyrus, the middle and inferior temporal gyri are responsible for visual perception. The middle temporal gyrus is associated with the perception of movement within the visual field; whereas the inferior temporal gyrus contains the fusiform face area (FFA) , which is necessary for face recognition.

Now that you are becoming more familiar with identifying structures of the brain from a lateral view. Test your knowledge on the lobes of the brain from a lateral perspective in the quiz below. 

Occipital lobe

The occipital lobe lies just underneath the occipital bone. It forms the most posterior portion of the brain and is found behind both the parietal and temporal lobes. The occipital lobe lies over the tentorium cerebelli , while its medial surface faces the falx cerebri . 

The occipital lobe is separated superiorly from the parietal lobe by the parietoocccipital sulcus . Anteriorly, it is separated from the temporal lobe by an imaginary line called the lateral parietotemporal line , that extends from the termination of the parietooccipital sulcus superiorly, and to the preoccipital notch inferiorly.

There is significant anatomic variability in the sulci and gyri of this lobe. The superolateral aspect of the occipital lobe presents with three notable gyri: the superior, middle and inferior occipital gyri . The superior occipital gyrus is the clearly defined gyrus on the lateral surface of the occipital lobe. The middle and inferior occipital gyri are often indistinct and may be absent. The intraoccipital sulcus, which is formed as an extension of the intraparietal sulcus, separates the superior and middle gyri (if present). The lateral occipital sulcus (also known as the inferior occipital sulcus) separates the inferior occipital gyrus from the superior, or the middle occipital gyrus (if present). 

The surface anatomy of the medial aspect of the occipital lobe is more consistent and clearly defined. A fissure known as the calcarine sulcus begins slightly above the occipital pole just behind the parietooccipital sulcus. The calcarine sulcus divides the medial aspect of the occipital lobe into the cuneate gyrus (cuneus) superiorly and the lingual gyrus inferiorly. 

The calcarine sulcus also marks the location of the primary visual cortex (Brodmann area 17) which is responsible for visual perception. 

The visual association cortex (Brodmann area 18 and 19) constitutes the remaining regions of the occipital lobe and is also known as the extrastriate visual cortex. The visual association cortex functions to interpret visual images. 

The occipital lobe is identified as the main visual processing centre . It is associated with color determination, facial recognition, depth perception, visuospatial processing and even plays a role in memory formation. The occipital lobe not only enables visual perception but allows us to process and interpret visual information.

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Insular lobe

Deep within the lateral sulcus (Sylvian fissure) is the fifth lobe of the brain, the insular lobe. This lobe is not clearly visible from the outside, but can be viewed when the temporal lobe is retracted from the cortex. The parts of the frontal, parietal and temporal lobes that overlie the insula are known as the opercula .

When the insular operculum is opened, the first structure to be seen is the central sulcus of the insula that divides it into an anterior and a posterior part .

The anterior portion of the insular lobe is formed by three short gyri (anterior, middle and posterior short gyri) and an accessory gyrus . The posterior portion of the insular lobe is formed by two long gyri (anterior and posterior long gyri). 

The insula is associated with processing and integration of various types of information, including taste sensation, visceral sensation, pain sensation, and vestibular function.

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Limbic lobe 

The limbic lobe refers to a region of the cerebral cortex that borders the corpus callosum on the medial aspect of each hemisphere. This medially located lobe surrounds the rim of the ventricles of the brain and can be found just deep to the frontal, parietal and temporal lobes. 

Structures in this region play influential roles in the modulation of emotions, visceral functions, autonomic functions, hormonal functions, and in learning and memory.

The structures which comprise the limbic lobe are the paraterminal (subcallosal), cingulate , and parahippocampal gyri , as well as the hippocampal formation. 

The paraterminal gyrus is a small gyrus which sits inferior to the rostrum of the corpus callosum. This gyrus is thought to be involved in depression. 

The cingulate gyrus is a ‘C’ shaped structure that is divided into a prelimbic and an infralimbic cortex , an anterior cingulate and a retrosplenial cortex . It is believed that the cingulate gyrus is strongly associated with the perception of neuropathic pain and nociception.

The parahippocampal gyri can be better appreciated on the inferior surface of the temporal lobe of the cerebrum. This area corresponds with several Brodmann areas such as the entorhinal cortex (Brodmann area 27, 28), and areas 35, 36, 48 and 49. Part of the anterior end of the parahippocampal gyrus projects medially, forming a structure called the uncus . 

The parahippocampal gyrus provides a path of communication between the hippocampus and all cortical association areas through which afferent impulses enter the hippocampus.

Now that you have mastered the 6 lobes of the brain, why not test your knowledge with the quiz below: 

Clinical notes 

Broca’s aphasia, otherwise known as motor aphasia, is associated with damage to Broca’s area in the inferior frontal gyrus of the dominant cerebral hemisphere. It is called “motor” aphasia because affected persons can comprehend language, but they have difficulty with language output, or expression: they struggle with speech production, particularly word repetition and object naming.

Wernicke’s aphasia, also known as sensory aphasia, is associated with damage to Wernicke’s area in the temporal lobe of the dominant cerebral hemisphere. It is called “sensory” aphasia because affected persons cannot make sense of language input: they cannot comprehend spoken language, and cannot repeat what is spoken to them. Although their speech remains fluent, it tends to be irrelevant and nonsensical.

In 1848, a young railroad worker in Vermont by the name of Phineas Gage experienced a horrific accident: premature detonation of explosive powder sent a tamping iron upward into his cheek, through his brain, and right out the top of his skull . Shockingly, for the most part he recovered physically (although he was left blind in one eye); but his personality changed dramatically after the accident. Once a very capable foreman, after the accident he became disorganized, irritable, and even hostile at times.

In its upward trajectory through his skull, the tamping iron damaged the prefrontal cortex of Phineas Gage’s frontal lobes. The changes observed in Phineas Gage after his accident provided the first evidence of the role of the prefrontal cortex in modulating emotion, aggression, judgment and decision-making, linking the prefrontal cortex with personality.

• Crossman AR. Cerebral hemispheres. In: Gray’s Anatomy: The Anatomical Basis of Clinical Practice. 41st ed. 2016. 
• Crossman AR, Neary D. Neuroanatomy: An illustrated colour text. 4th ed. Churchill Livingston Elsevier; 2010. 
• Patestas MA, Gartner LP. A textbook of neuroanatomy. 1st ed. Blackwell Science Ltd.; 2006. 
• Moore KL, Dalley AF, Agur AMR. Clinically oriented anatomy. 7th ed. 2014. 
• Haines, D: Neuroanatomy in Clinical Context, Ninth Ed., Wolters Kluwer Health (2015), p. 210-13.
• Purves, D., Augustine, G.J., Fitzpatrick, D: “The Limbic System” in Neuroscience, Second Ed., Sinauer Associates (2001)

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