The simplest way to divide the cortex is into the frontal and posterior cortex. The frontal cortex (frontal lobe) specializes in action, ranging from cognition, emotion, and autonomic control to movements and speech. The posterior cortex (parietal, temporal, and occipital lobes) is concerned with perception and memory. The frontal and posterior cortex, along with subcortical structures and the peripheral nervous system, provide the hierarchically arranged feedback loops that allow us to interact with our environment to achieve goals successfully.
The prefrontal cortex (PFC) (cortex rostral to the motor association cortex) directs the cognitive and emotional processes, called perception-action cycles, that adapt (and preadapt) us to our environment. The PFC predicts and creates the future. Working in cooperation with networked brain structures, the PFC marshals its executive functions of planning, attention, working memory, and decision making to develop innovative and sophisticated actions to pursue future goals (Fuster, 2015).
This unit addresses II. Basic Neurophysiology and Neuroanatomy - B. Neuroanatomy.
This unit covers Basic Neuroanatomy of Ascending Sensory Pathways to the Cortex, Thalamic, Cortical, and Subcortical Generators of the EEG, General Cortical and Subcortical Anatomy, Major Functions of Cortical Lobes and Major Subcortical Structures and Brodmann Areas, and Overview of Connectivity, Phase, and Coherence Concepts Related to EEG Networks and Tracts.
Please click on the podcast icon below to hear a full-length lecture.
BASIC ANATOMY OF ASCENDING SENSORY PATHWAYS TO THE CORTEX
Sensory input produced by activities like reading a novel and listening to music can desynchronize cortical
activity resulting in lower-amplitude, higher-frequency EEG waveforms (Neumann, Strehl, & Birbaumer, 2003).
Arousal and specific forms of cognitive activity may reduce alpha amplitude or eliminate it, a
phenomenon called alpha blocking, while increasing EEG power in the beta range
(Andreassi, 2007).
The classical routes for EEG activation consist of ascending sensory pathways that
distribute information to specialized thalamic nuclei and then project the results of thalamic processing to
the appropriate cortical regions. A hallmark of these pathways is their hierarchical structure that preserves the location from which signals arise, with specialized thalamic nuclei serving as critical relay points for sensory information. The exception to this rule is olfaction (smell), which goes directly to the
primary olfactory cortex.
The old-school view is that these ascending sensory pathways exercise bottom-up control of perception as feedforward circuits. This overlooks the fact that ten times more cortical efferent neurons target the sensory thalamus as thalamic afferent neurons project to the cortex.
The new-school view is that there are extensive interconnections between the thalamus and cortex, which permit a degree of top-down cortical control over perception (Kandel et al., 2021). Subcortical areas (midbrain, thalamus, cerebellum) also participate in ascending and descending transmission and processing of neural messages.
We will examine the visual, auditory, and somatosensory
systems to better understand the ascending sensory pathways to the cortex.
Visual System
Retinal ganglion cells, which comprise the optic nerves, ascend to the midline optic chiasm where the two optic nerves meet. Here, temporal axons (toward the side of the head) continue as part of their own side's optic tract, and the nasal halves cross over to join the opposite side's optic tract. Most optic tract axons project information to the lateral geniculate nucleus of the thalamus.
While the
lateral geniculate nucleus (LGN) relays visual information to the cortex, brainstem, and cortical neurons modulate its activity. Brainstem neurons that mediate alertness and attention can adjust the LGN's response to visual input. Moreover, the cortex can exert a top-down selection of visual input to increase attention to a salient region of the visual field at the expense of others (Bear, Connors, & Paradiso, 2020).
LGN neurons form the optic radiations and project to the primary visual cortex (V1) in the occipital lobe in cortical layer IV. A minority of retinal ganglion cell axons target the dorsal midbrain superior colliculus, which is concerned with visual gaze direction and attention to selected visual objects (Breedlove & Watson, 2023).
The cortex contains many specialist regions to process
visual properties like color, shape, location, motion, and orientation. Evolution has organized these visual areas into dorsal and ventral streams that begin in the primary visual cortex. The dorsal stream, which projects from V1 to the parietal lobe, helps us localize objects and guide movements. There are neurons with visual and motor properties in the adjacent motor association cortex, called mirror neurons. Networks of mirror neurons may play a role in learning how to perform actions by observing others' movements, understanding others' actions and intentions, and empathy.
The cochlea's inner hair cells within the organ of Corti send 30,000 to 50,000 auditory fibers to several destinations: the midbrain superior olivary nuclei and inferior colliculi, and the medial geniculate nucleus of the thalamus. The superior olivary nuclei process binaural (two-ear) information to localize sound. All ascending auditory neurons innervate the inferior colliculi, some via intermediate relays.
The auditory cortex processes auditory
information within dorsal and ventral streams. The dorsal stream, which extends to the parietal lobe, helps us spatially localize sounds. The lower ventral stream, which projects to the temporal lobe, appears to analyze sound components, perhaps including speech sounds (Breedlove & Watson, 2023).
As with the visual pathways, the auditory system involves extensive feedback. Neurons in the brainstem innervate the outer hair cells that adjust the sensitivity of the basilar membrane within the organ of Corti to specific frequencies. Also, auditory cortex axons innervate both the inferior colliculi and MGN to exercise top-down control (Bear, Connors, & Paradiso, 2020).
As with the visual and auditory systems,
the ascending pathways do far more than relay information. These networks process and alter sensory information at each successive synapse. The cortex exercises top-down control over neurons in the dorsal column and VPN to dynamically adjust cortical inputs (Bear, Connors, & Paradiso, 2020).
THALAMIC, CORTICAL, AND SUBCORTICAL GENERATORS OF THE EEG
Thalamic Generators
Anderson and Anderson (1968) advanced the facultative pacemaker theory that thalamic neurons activate cortical neurons and thalamic inhibitory interneurons via recurrent collaterals. While these thalamocortical neurons only excite a limited number of cortical neurons, thalamic interneurons inhibit a large pool of thalamocortical relay neurons. When the inhibition ends after one-tenth of a second, the thalamocortical neurons experience rebound excitation. This synchronized depolarization excites both cortical neurons and thalamic inhibitory interneurons, which will inhibit a more extensive pool of thalamocortical relay neurons and initiate another cycle of excitation and inhibition that produces EEG rhythms (Fisch, 1999). Graphic courtesy of Zachary Barry and featured in Wikipedia's article Recurrent ThalamoCortical Resonance.
The networking of excitatory and inhibitory thalamic neurons imposes a group rhythm on its members that is transmitted to cortical macrocolumns by thalamocortical neurons (Bear, Connors, & Paradiso, 2020).
The nucleus reticularis of the thalamus may function as a pacemaker by releasing the inhibitory transmitter GABA at synapses with thalamocortical neurons. These neurons depolarize cortical neurons and thalamic inhibitory interneurons via burst discharges when their inhibition ends.
As discussed in the Neurophysiology unit, oscillatory activity may involve an interaction between thalamocortical relay neurons (TCR), nucleus reticularis neurons (RE), and interneurons. These interactions are mediated by diverse neurotransmitters, including acetylcholine and GABA.
The thalamus is the dominant pacemaker for rhythmic EEG activity, including theta (3-8 Hz), alpha (8-12 Hz), and SMR (13-15 Hz) (Amzica & Lopes da Silva, 2018).
Vertical cortical macrocolumns contain hundreds of pyramidal neurons and supporting stellate and basket cells (Thompson & Thompson, 2016). Each pyramidal neuron may receive more than 100,000 synapses. These macrocolumns are positioned side by side and perpendicular to the cortical surface. Since neighboring macrocolumns often receive the same afferent messages, this increases the probability that they will fire together and generate a potential that we can detect from the scalp. A reliable scalp EEG requires a minimum of 6 cm² of synchronized cortex (Dyro, 1989).
Although thalamic pacemakers generate EEG rhythms, resonant loops between cortical macrocolumns may be another source (Traub et al., 1989). Over 97 percent of the conversations within the brain are cortical-to-cortical (Thompson & Thompson, 2016). This communication is primarily confined within the same hemisphere. A resonant loop develops when macrocolumns that share afferent input fire synchronously to generate an electrical potential. The distance between the cortical macrocolumns that participate in a resonant loop is one determinant of EEG frequency. The closer the macrocolumns in a resonant loop, the higher the frequency they can generate (Lubar, 1997).
There are three types of resonant loops driven by afferent input or thalamic pacemakers: local, regional, and global. Local loops couple neighboring macrocolumns and may generate frequencies above 30 Hz in the high-beta and gamma ranges.
Regional loops couple macrocolumns separated by several centimeters and may produce alpha and beta rhythms. Finally, global loops couple macrocolumns as distant as 7 cm (for example, between the frontal and parietal lobes) and may create delta and theta rhythms.
While only 3 percent of these linkages are thalamocortical, they greatly influence the EEG by subcortically connecting distant cortical regions and producing most synchronous activity (Steriade, 1990). Lubar (1997) proposed a violin analogy where the thalamic pacemakers that fire at varying frequencies are the strings, and the resonant loops that introduce different time delays are the instrument's resonant cavity.
Different spindle frequencies are due to corresponding durations of thalamocortical neuron hyperpolarization. For example, longer hyperpolarizations associated with EEG synchronized states produce 7-Hz or lower-frequency spindles. In contrast, relatively short hyperpolarizations result in 14 Hz spindles (Steriade, 2005).
The electrical potentials generated by the thalamus can volume conduct near the speed of light through cerebrospinal fluid (CSF), brain tissue, the skull, and the scalp so that nearly identical waveforms can simultaneously appear at distant sites (Fisch, 1999; Thompson & Thompson, 2016).
The Locus Coeruleus Inhibits Thalamic Alpha Generators
When we are inattentive, thalamic pacemakers generate the alpha rhythm. When we need to focus attention, we activate the brainstem noradrenergic locus coeruleus. The increased release of norepinephrine by this 15-millimeter network focuses attention and abolishes alpha oscillations. The locus coeruleus enhances the brain's sensory information processing by suppressing thalamic alpha generators. This may be an underlying mechanism of the phenomenon of alpha blocking.
Although researchers cannot noninvasively monitor locus coeruleus activity in human participants, it is correlated with pupil dilation. In human studies, the greater the alpha blocking response and pupil dilation, the better the performance on demanding attention tasks (Dahl et al., 2020; Dahl et al., 2022).
Ascending projections from the basal forebrain, reticular formation, locus coeruleus, and raphe systems disrupt brain rhythms.These neurons receive information from most sensory systems and cortical regions and directly desynchronize the EEG through synapses on cortical neurons and indirectly through innervation of thalamic pacemakers. Desynchronization shifts pyramidal neurons from burst firing to more continuous firing or the generation of single spikes (Fisch, 1999).
The reticular activating system (RAS) includes a network of 90 nuclei within the central brainstem
from the lower medulla through the thalamus that activates the brain to promote attention, consciousness, and wakefulness. This network receives input from ascending sensory tracts (auditory, olfactory, somatosensory, and visual systems). The RAS projects to the thalamus and diffusely to the cortex. The RAS also has diffuse cortical projections that bypass the thalamus. Reticular formation graphic redrawn by minaanandag on Fiverr.com.
Cortical and Subcortical Generators of Specific EEG Rhythms
Slow Cortical Potentials (0-1 Hz)
Slow cortical potentials (SCPs) have been identified in cortical
neurons, the thalamus, and glial cells. Cortical neurons in layers II to VI generate slow oscillations when the
thalamus is removed or when cortical tissue is studied in vitro (in an artificial environment) or in
vivo (within a living organism). Thalamic reticular neurons exhibit similar slow spontaneous oscillations
when studied in vitro, and synchronized intracortical oscillations may depend on a corticothalamic network that targets these thalamic neurons.
Glial cells generate slow SCPs when they burn sugar, producing negatively charged bicarbonate ions. Unlike EEG
rhythms like delta, SCPs are not the summation of dendritic potentials. SCPs are associated with glial cells and gap junctions. Glial cells chemically communicate among themselves and with neurons. The slow oscillations of glial cells may influence the timing of neuronal firing through their control of potassium ion outflow
(Steriade, 2005). These slow oscillations appear to organize the generation of other brain rhythms.
"The concept of a unified corticothalamic network that generates diverse types of brain rhythms grouped by the cortical slow oscillation (Steriade, 2001a,b) is supported by EEG studies in humans" (Molle et al., 2002).
Caton (1875) observed that the cortex's direct current baseline becomes negative whenever it is more active. The voltage gradients range from 150-200 μV. Underlying "tone" or valence factors determine the firing characteristics of neurons within a network. When SCPs are more positive, there is reduced firing of cortical neurons due to hypopolarization. When SCPs are more negative, there is increased firing due to depolarization.
While frequency band labels are helpful descriptors, they can also be misleading. Classification of an EEG rhythm is based on context (measurement conditions and EEG activity during the specific epoch), frequency, and waveform morphology.
The process of up-training or down-training signal amplitude in one or more of the EEG bands using an EEG is called EEG biofeedback or neurofeedback. Minimum EEG voltages of 20-30 μV are seen in children and adults (Kraus et al., 2011).
Brainwaves Reflect Behavior
The ratio of slow (theta) to faster (beta)
brainwaves shows how alert you are. This is the theta/beta ratio.
In the next section, we will examine delta, theta, rhythmic slow-wave, alpha, mu, synchronous "alpha," SMR, beta, high or fast beta, and gamma activity.
Local Versus Global Decision-making
The short time windows of fast oscillators facilitate local integration and decision-making, primarily because of the limitations of the axon conduction delays. The long time windows of slow oscillators can involve many neurons in large or distant brain areas and favor complex, global decisions.
Delta (0.5-3 Hz)
There are two delta rhythms, a slow oscillation under 1 Hz and a traditional 1-4 Hz oscillation. The slow 0.3-0.4 Hz oscillation originates in the neocortex and persists when the thalamus is removed. Thalamo-cortical neurons generate the 1-4 Hz oscillations observed during human stage-3 sleep. Slow neocortical oscillations may synchronize the thalamic delta rhythm (Steriade, 2005).
Delta activity is generated by cortical neurons when other connections do not activate them and is found predominantly in frontal areas. Delta is associated with sleep and infancy. During stage-3 sleep, delta allows astrocytes to rebuild their stores of glycogen. Clinicians observe delta in clients diagnosed with ADHD, brain tumors, learning disorders, and traumatic brain injury (TBI). Rhythmic high-amplitude delta is associated with TBI, mainly if localized. Diffuse delta may be found in ADHD and learning disorders.
Delta waves are the main EEG activity during infancy, reflecting the immature brain's low-frequency cortical activity. As neural networks develop and mature, faster rhythms like alpha and beta replace delta dominance in waking states. In adults, waking delta activity is minimal but may transiently appear during states of drowsiness or relaxation.
Normal Amplitudes
Delta should not be present in significant amounts in the awake adult EEG. "Apparent" delta is usually an eye movement artifact. Some delta activity probably occurs in the waking adult EEG.
The mechanisms that generate the theta rhythm are poorly understood. Theta differs depending on location and source. Amzica and Lopes da Silva (2011) consider the classic septal/diagonal band pacemaker model incomplete. Hippocampal interneurons, which innervate the hypothetical medial septum pacemaker, exercise top-down control. The hypothalamic supramammillary nucleus, with extensive connections to the brainstem, diencephalon, and medial septum, may also pace and modulate hippocampal theta. Further, a non-cholinergic theta source has been found within the entorhinal cortex of the hippocampus.
Theta is associated with creativity, global synchronization, memory formation, and recall. Increased theta amplitudes correspond with hypo-perfusion and decreased glucose metabolism.
Excessive frontal theta is linked with depression, daydreaming, distractibility, and inattention. A theta/beta (T/B) ratio of 3.0 may indicate ADHD depending on age, as T/B ratios are developmentally mediated (Monastra et al., 1999).
Normal Amplitudes
Theta voltage is age-related in the awake EEG. Voltage diminishes from age 8-30 with minimal amounts over age 30. A typical 6-7 Hz rhythm in the frontal midline (FCz) is associated with mental activity such as problem-solving and a wide variety of other functions. This rhythm appears to be limbic in origin. It is higher in amplitude and more synchronous when processing the feedback that an error has occurred. The 4-Hz rhythm is associated with childhood pleasurable experiences and memory searches in adults.
Rhythmic Slow Wave (RSW or Theta)
Inhibit theta to remediate symptoms. Reward posterior RSW in alpha/theta training for addictions, global synchronization, optimal performance, and PTSD. RSW is generally not increased frontally. Clinicians may train for increases or decreases in phase synchrony. RSW is mainly seen in the frontal-midline (FCz) when awake with eyes open. The limbic system and thalamus generate RSW. Depending on location, RSW may be slowed-alpha as thalamic output slows.
Researchers have correlated the alpha rhythm with
relaxed wakefulness. There are age- and function-related differences. Spindle waves, in contrast, originate in the thalamus and occur during
unconsciousness and stage 2 sleep (Steriade, 2005).
Alpha is the dominant rhythm in adults and is located posteriorly. The 8-10 Hz range is associated with ADHD, daydreaming, fogginess, OCD, and TBI. Frontal asymmetry is associated with depression. The 10-12 Hz range is seen with inner calm (calm and alert) and meditation. Clinicians train alpha amplitude and phase synchrony up or down for remediation of symptoms, depending on location.
Posterior Dominant Rhythm (PDR)
The posterior alpha rhythm is visible at about 4 months with a frequency of around 4 Hz. Between 3-5 years, this rhythm is approximately 8 Hz with amplitudes as high as 100 μV. From 6-15 years, this rhythm is 9 Hz by age 7 and 10 Hz by ages 10-15 with a mean amplitude of 50-60 μV. Girls show a statistically faster acceleration of posterior alpha frequency than boys. From 13-21 years, the mean alpha frequency is 10 Hz, and amplitudes decline throughout this period. Faster alpha frequencies are associated with higher IQ and better memory performance.
The typical adult alpha frequency ranges from 9.5-10.5 Hz. Alpha below 8 Hz is considered abnormal. There are age-related differences. Alpha frequency declines after age 70. Adult amplitudes are 50 μV or less:
60% have ~ 20-60
μV
28% have < 25
μV
6% have > 60
μV
Higher alpha amplitudes are observed over the non-dominant (right) hemisphere (alpha asymmetry). Most studies show no effect of handedness. Asymmetry is generally no more than 20 μV or 20% of the greater of the two amplitudes (Amzica & Lopes da Silva, 2018).
Causes of Excessive Alpha Amplitudes
Sleep deprivation or metabolic exhaustion can result in high amplitude and slowing of the peak frequency and persistent alpha during an eyes-open condition. Meditation practices can cause increased amplitudes and slowing, a faster alpha response to an eyes-closed condition, and persistent alpha in an eyes-open condition. Marijuana use and abuse can cause increased amplitudes and slowing, persistent alpha in an eyes-open condition, depending on the type of marijuana. These effects can persist for many years following abstinence.
While the 7-11-Hz mu rhythm usually overlaps with the alpha range. The mu rhythm has a different shape from the alpha waveform as one end is pointed. The mu rhythm can be recorded at C3 and C4 in a minority of subjects and may represent suppression of hand movement or imagining hand movement (Thompson & Thompson, 2016).
Mu rhythms appear to regulate motor cortex activities via prefrontal cortical mirror neurons. These circuits may play a critical role in imitation learning and our ability to understand the actions of others. Mu rhythms facilitate the conversion of visual and auditory input into integrated skill-building functions. Attenuation of the mu rhythm appears to be associated with the activation of this function (Pineda, n.d.). The mu rhythm is highlighted below.
This second example of the mu rhythm shows a classic 10-11 Hz and
19-20 Hz "Owl Eye" presentation.
Synchronous "Alpha"
Various sensory systems such as our auditory, somatosensory, and visual systems produce localized and semi-independent "alpha" activity. Synchronous, distributed alpha integrates perception and facilitates action. Synchronous "alpha" appears to block the localized alpha-like patterns such as mu and the posterior rhythm in favor of more broadly distributed network integration during tasks requiring global processing.
Sensorimotor Rhythm (13-15 Hz)
The sensorimotor rhythm (SMR) is beta 1 located on the sensorimotor strip (C3, Cz, C4). SMR amplitude increases when the motor circuitry is idle. SMR increases with stillness and decreases with movement. Deficient SMR may be observed in movement spectrum complaints like hyperactivity and tics. SMR appears as sleep spindles during stage-2 sleep. SMR is associated with neutral blood perfusion of the brain and resting levels of glucose metabolism. Clinicians typically reward increased SMR amplitude to calm hyperactivity and during theta/beta ratio training.
Beta consists of rhythmic activity between 13-38 Hz. There are four beta ranges: beta 1 (12-15 Hz), beta 2 (15-18 Hz), beta 3 (18-25 Hz), and beta 4 (25-38 Hz). Beta is located mainly in the frontal lobes. Beta is associated with focus, analysis, and relaxed thinking (Thompson & Thompson, 2015).
Excessive beta is observed in anxiety, depression (asymmetry), insomnia, OCD, and sleep disorders. Deficient beta is seen in ADHD, cognitive decline, and learning disorders.
Since beta overlaps with the EMG range, clinicians must be careful when up-training this rhythm and use an EMG inhibit. Beta is generated by the brainstem and cortex and is associated with hyper-perfusion and increased glucose metabolism.
Fast 20-35-Hz oscillations are generated by activation of the mesencephalic reticular formation. Thalamocortical, rostral thalamic intralaminar, and cortical neurons spontaneously oscillate in this range. This activity is primarily seen in the frontal lobes and is associated with hyper-perfusion and increased glucose metabolism. Persistent excessive activity can lead to metabolic exhaustion.
This activity may be associated with peak performance and cognitive processing and related to specificity and precision in information processing. Excessive high beta is associated with alcoholism, anxiety, OCD, rumination, and worry.
Clinicians often inhibit high beta activity but rarely reward it.
Amzica and Lopes da Silva (2011)
concluded that gamma oscillations might speed information distribution and processing. Gamma bursts occur during problem-solving, and the absence of gamma is associated with cognitive deficits and learning disorders. Gamma synchrony is related to cognitive processing and is essential in coding by contributing specificity and precision to information processing. Gamma is theorized to serve as a "binding rhythm" that integrates sensory inputs into perception and consciousness.
Nerves are bundles of axons that lie outside of the central nervous system. Motor nerves distribute instructions from the CNS to the rest of the body. Sensory nerves transmit information from sensory receptors to the CNS.
The autonomic nervous
system regulates cardiac and smooth muscle and glands, transmits sensory
information to the CNS, and innervates muscle spindles. The autonomic nervous system is the brain’s main system for monitoring and controlling major organs.
While we normally do not exercise very much intentional, conscious autonomic control, self-regulation disciplines like yoga and animal and human research in biofeedback have shown that we can teach voluntary autonomic control of heart rate variability, blood flow to our fingers, toes, and scalp, and finger sweat gland activity to treat disorders and achieve optimal performance.
The autonomic nervous system is divided into three main systems: sympathetic, parasympathetic, and enteric. Check out the YouTube video, The Autonomic Nervous System.
We activate the sympathetic nervous system when we encounter a threat that we can fight or flee. However, we also activate this branch when we get up from our couch and when we exercise.
The parasympathetic system can oppose or complement sympathetic activity. When we feel safe, the parasympathetic branch allows us to self-regulate (meditate or use neurofeedback skills), socially engage with others, and engage in executive functions like planning. When we feel endangered and cannot fight or flee, this system produces freezing (think mouse in the jaws of a cat), fainting responses, or dissociation responses.
The enteric system consists of over 100 million neurons that release over 30 neurotransmitters to control the gut under CNS control. This system helps to maintain fluid and nutrient balance.
Three customary planes for viewing the body and brain are sagittal, coronal, and horizontal.
Please click on the podcast icon below to hear a lecture over the second half of this unit.
The sagittal plane divides the body into right and left halves. The coronal plane separates the body into front and back parts. Finally, the horizontal (transverse) plane divides the brain into upper and lower parts (Breedlove & Watson, 2023).
Graphic courtesy of Blausen.com staff "Blausen gallery 2014," Wikiversity Journal of Medicine.
Directional Terms
Important directional terms include medial (toward the middle) and lateral (toward the side), ipsilateral (same side) and contralateral (opposite side), superior (above) and inferior (below), anterior/rostral (toward the head), and caudal (toward the tail), proximal (near the center) and distal (toward the periphery, and dorsal (toward or at the back) and ventral (toward the belly) (Breedlove & Watson, 2023). Graphic courtesy of Blausen.com staff "Blausen gallery 2014," Wikiversity Journal of Medicine.
Cortical Features
The adult human brain has a volume of about 1100 cm2 and requires convolutions to fit within the skull (Bear, Connors, & Paradiso, 2020). If the cortex were flattened into a sheet, its surface area would be almost one square meter (2.5 square feet). Two-thirds of the cortical surface lies within these folds (Breedlove & Watson, 2023). Anatomists distinguish three topographical features of the cerebral cortex: gyrus, sulcus, and fissure.
A gyrus is a ridged area of the brain. The precentral gyrus, which is anterior to the central sulcus, is the primary motor cortex (controls muscles and movements). The postcentral gyrus, which is posterior to the central sulcus, is the primary somatosensory cortex (receives somatosensory information).
A sulcus is a groove in the cortical surface. As we just observed, the central sulcus separates the primary motor cortex from the primary somatosensory cortex. A fissure is a deep groove. The Sylvian fissure (also called the lateral
fissure or lateral sulcus) is the upper boundary of the temporal lobe (Breedlove & Watson, 2023).
Graphic courtesy of Blausen.com staff "Blausen gallery 2014," Wikiversity Journal of Medicine.
The Unfixed Brain
This video was produced by Suzanne Stensaas, PhD, Department of Neurobiology and Anatomy, and the Spencer S. Eccles Health Sciences Library, University of Utah.
Dissecting Brains
This video is courtesy of the Wellcome Collection.
The hindbrain contains the metencephalon and myelencephalon. The metencephalon is comprised of the cerebellum and pons. The cerebellum plays a role in higher-level functions like emotional and cognitive regulation, speed, capacity, consistency, and appropriateness of cognitive and emotional processes. Damage to the cerebellum can reduce general intelligence.
Comprising 22 bones, the skull is divided into the cranium, which houses the brain, and the facial bones. The cranium itself is composed of several major bones, including the frontal, parietal, temporal, and occipital bones, which are fused together by sutures. This intricate bony framework provides a rigid protective case for the brain while also serving as an anchor for the meninges and other protective layers (Niedermeyer & da Silva, 2004).
The skull's primary function is to protect the brain from physical damage. The bones of the skull are dense and have a thickness that varies across different regions, with an average thickness of about 6.5 mm in adults. This density and thickness can significantly impact the transmission of electrical signals, such as those measured by EEG. The skull acts as a low-pass filter, attenuating high-frequency components of the brain's electrical activity while allowing lower-frequency components to pass through. The skull can reduce signal amplitude by approximately 85% (He & Li, 2010). This attenuation is primarily due to the skull's low conductivity compared to the brain and scalp tissuesThis filtering effect is a crucial consideration in EEG signal analysis, as it can affect the accuracy and interpretation of the recorded data (Sanei & Chambers, 2013).
The attenuation of EEG signals by the skull occurs due to several factors. Firstly, the skull's high impedance compared to the soft tissues of the brain and scalp means that much of the electrical activity generated by neurons is dissipated before it reaches the electrodes on the scalp. This leads to a reduction in the amplitude of the recorded signals, making it more challenging to detect subtle neural oscillations. Additionally, the varying thickness and composition of the skull bones can introduce spatial distortions in the EEG signals, complicating the localization of neural activity sources (Lopes da Silva, 2010).
Furthermore, the skull's heterogeneous structure, which includes both dense cortical bone and less dense cancellous bone, contributes to the complexity of EEG signal attenuation. The cortical bone is particularly effective at blocking electrical signals due to its high density, whereas the cancellous bone, which contains more porous and less dense material, offers slightly less resistance. This variation in bone density can cause anisotropic attenuation, meaning that the degree of signal reduction can vary depending on the direction of the electrical currents. This anisotropy must be accounted for in advanced EEG analysis techniques, such as source localization and brain connectivity studies (Nunez & Srinivasan, 2006).
In addition to the bones themselves, the skull's sutures and foramina (openings) also influence EEG signal propagation. Sutures, the fibrous joints between the bones, can act as additional barriers or channels for electrical signals. Foramina (holes), which allow the passage of nerves and blood vessels, can create localized points where signals might be less attenuated. These anatomical features add further complexity to the interpretation of EEG data, requiring sophisticated modeling and analysis techniques to accurately account for the skull's impact on signal transmission (He & Li, 2010).
Another aspect to consider is the individual variability in skull anatomy, which can significantly influence EEG signal attenuation. Factors such as age, sex, and developmental conditions can lead to differences in skull thickness and density. For instance, children's skulls are generally thinner and less dense than those of adults, potentially resulting in less signal attenuation. This variability necessitates personalized approaches in EEG analysis, particularly in clinical settings where accurate brain activity measurement is critical for diagnosis and treatment planning (Schoffelen & Gross, 2009).
Moreover, the presence of soft tissues, including the scalp and meninges, also affects EEG signal transmission. The scalp, composed of skin, connective tissue, and muscle, adds another layer of impedance that electrical signals must traverse. The meninges, consisting of the dura mater, arachnoid mater, and pia mater, further complicate the signal path. Each of these layers has distinct electrical properties that contribute to the overall attenuation and distortion of EEG signals. Understanding the combined effect of these tissues alongside the skull is essential for accurate EEG interpretation (Lopes da Silva, 2010).
Overall, the anatomy of the human skull is a critical factor in the study of EEG. Understanding how the skull attenuates EEG signals is essential for accurate brain signal interpretation and for the development of advanced EEG techniques. The skull's protective role, its variable thickness, heterogeneous composition, and anatomical features like sutures and foramina all contribute to the complex interplay between neural activity and its measurable manifestations on the scalp. Accurate modeling of these factors is paramount for improving the reliability and precision of EEG-based diagnostics and research (Niedermeyer & da Silva, 2004).
Caption: Also known as the glymphatic clearance pathway or the paravascular system, this system clears waste and fluid from the vertebrate central nervous system (CNS). Interstitial fluid is removed via the cerebrospinal fluid (CSF). It is similar to the lymphatic system, but functions to remove waste products from the brain and spinal cord. This view shows the subarachnoid space (across top) between the brain and its membranes. The blue arrows show the movement of interstitial fluid and solutes.
By removing harmful substances such as the amyloid and tau proteins implicated in Alzheimer’s and Parkinson's disease, the glymphatic flow may protect us from various neurological disorders (Breedlove & Watson, 2023). The glymphatic system removes most of its waste during stage 3 sleep, called slow-wave sleep.
The frontal lobes (F7, F3, Fz, F8, F4) consist of the cortex anterior to the central sulcus and consist of the primary motor cortex, motor association cortex, Broca's area, and prefrontal cortex.
Essential left frontal lobe functions include working memory, concentration, planning, and positive emotion. The main clinical concern is Major Depressive Disorder (MDD).
Critical right frontal lobe functions include declarative memory, social awareness, and negative emotions. The main clinical concerns include Generalized Anxiety Disorder (GAD), fear, and impaired executive functioning.
The primary motor cortex is located in the precentral gyrus (Brodmann area 4, BA 4). It organizes the opposite side of the body's muscles and movements required for the fine motor
coordination required by tasks like writing. Lesions can result in loss of motor control, including rigid paralysis.The graphic below, which shows the motor and sensory homunculi, was retrieved from the nccpbwikiproject.
The motor association cortex (premotor cortex) is rostral to the primary motor cortex (BA 6) and helps program and execute movements. The motor association cortex is the piano player, and the primary motor cortex is the piano keyboard (Carlson & Birkett, 2016).The primary and motor association cortex collectively appear to map behaviors instead of specific muscles or movements (Breedlove & Watson, 2020).
Broca's area, which is located in the inferior frontal gyrus (BA 44 and 45) of the dominant hemisphere (F7-T3 in the left hemisphere), is concerned with speech production, grammar, language comprehension, and sequencing (Caplan, 2006). Lesions to Broca's area can produce dyslexia, deficits in grammar, spelling, and reading, and Broca's aphasia. Broca's area receives input from Wernicke's area via the arcuate fasciculus (Breedlove & Watson, 2023). Graphic courtesy of Blausen.com staff "Blausen gallery 2014," Wikiversity Journal of Medicine.
The prefrontal cortex (PFC) is rostral to the motor association area (BA 9, 10, 11, 12, 46, 47). It is responsible for executive functions, which involve attention, working memory, prediction of the outcomes of current and hypothetical actions, working toward goals, problem-solving, planning, and the ability to suppress actions that could lead to unwanted outcomes (Diamond, 2013). The PFC integrates emotion and reward in decision-making (Fuster, 2015).
Important subdivisions of the
PFC include the orbitofrontal cortex, ventromedial, and dorsolateral PFC.
The orbitofrontal cortex (OFC) consists of Brodmann area (BA 10, 11, and 47) (Kringelbach, 2005). The OFC may aid planning by evaluating the consequences
(rewards and punishments) of our actions and helping to generate the motivation to ingest drugs. Phineas Gage's profound personality changes were produced by damage to this subdivision and the
ventromedial PFC (VMPFC). The OFC appears to adjust decision-making based on the stakes involved and enables us to
switch between significant (investments) and trivial (snacks) choices. Finally, the OFC compares our current options with recent ones, while the anterior cingulate cortex
registers our predictions and prediction errors (Kennerley et al., 2011).
The ventromedial prefrontal cortex (VMPFC) corresponds to the ventromedial reward network (Ongur & Price, 2000) and includes BA 10, 14, 25, 32, and parts of 11, 12, and 13. The VMPFC is implicated in making decisions, where the outcomes are uncertain and moral values must be applied to actual situations. Patients with damage to the VMPFC choose outputs that lead to immediate reward, regardless of their future cost. They do not learn from their mistakes. Since they have difficulty understanding social cues, they may not recognize deception, irony, or sarcasm (Zaid & Andreotti, 2010). Likewise, they may not control their emotional reactions in social situations, particularly anger and violence (Carlson & Birkett, 2016).
The dorsolateral prefrontal cortex (DLPFC) is located in the middle frontal gyrus and includes BA 9 and 46. The DLPFC shares responsibility with cortical and subcortical networks for executive functions like abstract reasoning, cognitive flexibility, decision-making, inhibition, planning, and working memory (Miller & Cummings, 2007). It exercises the highest cortical level of motor control (Hale & Fiorello, 2004).
The left DLPFC is concerned with approach behavior and
positive affect. It helps us select positive goals and organizes and implements behavior to achieve these goals.
The right DLPFC organizes withdrawal-related behavior and
negative affect and mediates threat-related vigilance. It plays a role in working memory for object location. In
unipolar depression and premenstrual dysphoric disorder, the right DLPFC may be more
active than the left (alpha asymmetry). The prefrontal cortex graphic redrawn by minaanandag at fiverr.com.
Anterior Cingulate Cortex (ACC)
The cingulate cortex has reciprocal connections with the parahippocampal gyri, integrates limbic functions, and is part of the salience network. Cingulate cortical functions include child nurturing, grooming, play, and organization and managing input/output functions.
The anterior cingulate cortex (ACC) (Fpz, Fz, Cz, Pz) lies above the corpus callosum (BA 24, 32, 33). The dorsal ACC is connected to both the PFC and parietal cortex. The ACC plays a vital role in attention and is
activated during working memory. The ACC mediates emotional and physical pain, and has cognitive (dorsal anterior
cingulate) and affective (ventral anterior cingulate) conflict-monitoring components. Graphic courtesy of Geoff B. Hall in Wikimedia Commons.
The Stroop test illustrates a cognitive monitoring task where color and names
conflict. Discrepancies between facial and vocal cues show an affective conflict. The anterior cingulate
recruits other brain areas to resolve these conflicts.
The anterior cingulate gyrus helps us allocate attention to focusing on a target and then disengaging, perceiving options, and making adaptive choices. The anterior cingulate gyrus, the prefrontal cortex, and the caudate
function abnormally in children diagnosed with ADHD during selective attention tasks. fMRI evaluation showed
that neurofeedback could teach children to normalize activity in these structures (Beauregard & Levesque,
2006).
The anterior cingulate gyrus is involved in motivation and the perception of emotional and physical pain. Eisenberger, Lieberman, and Williams (2003) used an fMRI to study the
brains of subjects who believed that two companions playing an on-line baseball simulation suddenly
dropped them from the game. Their emotional distress activated the anterior cingulate cortex, which evaluates
the unpleasantness of physical pain. de Charms and colleagues (2005) provided real-time fMRI feedback
from the anterior cingulate to subjects. They learned to reduce its metabolism and the intensity of experimental
pain.
Lesions to the cingulate can produce akinetic mutism, in which a
person cannot produce orienting responses. Cingulate malfunction can result in addictive behaviors (alcohol or
drug abuse, eating disorders, chronic pain), obsessive-compulsive disorder and OCD spectrum disorders,
and “road rage.”
Parahippocampal Gyri
The parahippocampal gyri are located within the medial temporal lobe. The parahippocampal gyri form spatial and nonspatial contextual associations, which serve as building blocks for contextual processing, episodic memory, navigation, and scene processing (Aminoff, Kveraga, & Bar, 2013). They may also play a role in emotional responsiveness. Polygon data were generated by Database Center for Life Science(DBCLS). Creative Commons Attribution-Share Alike 2.1 jp.
Parietal Lobes
The parietal lobes (Pz, P3, P4) are posterior to the frontal lobes (BA 1, 2, 3, 5, 7, 39, 40) and are divided
into the primary somatosensory cortex and secondary somatosensory cortex. Their main function
is to process somatosensory information like pain and touch.
The primary somatosensory cortex (S1) is located in the parietal lobe's postcentral gyrus posterior to the central sulcus (BA 3, 1, and 2). S1 maps touch and pain information from the opposite side of the body. The secondary somatosensory cortex (S2) is adjacent to S1 (BA 40 and 43), receives projections from it, and maps touch and pain from both sides of the body (Breedlove & Watson, 2023). Graphic by Paskari from Wikimedia Commons.
The primary function of the parietal lobes is to process somatosensory information like pain and touch. The parietal cortex monitors
our preparation for a movement and is responsible for our subjective feeling of intending to move (Sirigu et
al., 2004).
Major left hemisphere functions include attention, association, complex grammar, math,
object names, and somatosensation.
Major right hemisphere functions include body boundary,
geometry, guiding reaching with the hands, somatosensation, and spatial perception (Demos, 2019).
Temporal Lobes
The temporal lobes (T3, T4, T5, T6) are separated from the rest of the cortical
lobes by the Sylvian fissure (BA 15, 20, 21, 22, 37, 38, 39, 40, 52). The temporal lobes process hearing, smell, and taste information and help us
understand spoken language and recognize visual objects and faces (Breedlove & Watson, 2023).
Wernicke's area, located in the temporoparietal cortex (BA 22) of the dominant hemisphere, is specialized for speech perception and production. Damage can result in an inability to understand the meaning of speech and to construct intelligible sentences. Graphic courtesy of Blausen.com staff "Blausen gallery 2014," Wikiversity Journal of Medicine.
Major left hemisphere functions include
affect, declarative memories, language comprehension, perception of movement, reading, and word recognition.
Important right hemisphere functions include face and object recognition, music, and social cues (Demos, 2019).
Their primary functions are visual and include the analysis of orientation, color, spatial frequency, illusory contours, and complex patterns like concentric and radial stimuli (Breedlove & Watson, 2023).
Insular Cortex
The insular cortex lies deep within the lateral sulcus that divides the temporal and parietal lobes (BA 13). The insula is involved in emotional and autonomic responses to external stimuli and is part of the salience network. The insula detects salient events via afferent pathways and switches between other large-scale networks when such events are identified, affecting attention and working memory. The anterior and poster insulae interact to regulate autonomic responses to salient stimuli. Interactive communication between the insula and anterior cingulate cortex facilitates motor control (Menon & Uddin, 2010). The right insula mediates awareness of our body, empathy, and understanding others’ points of view (Khazan, 2019).
Increased heart rate variability strengthens the connectivity between the ACC and the insula for empathy and the ability to understand others’ emotions, feel gratitude, socially connect, understand our own psychophysiological states, and restore nervous system balance. Mindfulness meditation increases insula gray matter and activation.
The insula functions as an integrative and organizational hub for the salience network. The insula integrates interoceptive awareness, emotional experience, and external perception to facilitate our global perception of the world and relationship with it. The insula directs specific networks in the processing of salient stimuli and in generating appropriate behavioral responses to these stimuli (Wiebking & Northoff, 2014).
The insula is the primary taste cortex and is activated when you see something
that disgusts you (a fraternity bathroom) or see another person’s expression of disgust. Pictures of lovers also activate the anterior insula as opposed to friends. When the anterior insula was activated in neuroeconomic studies, subjects chose risk-avoidant financial strategies (choosing bonds instead of stocks). In the Prisoner’s Dilemma game, mutually cooperative decisions also resulted in the activation of this region. Insular cortex graphic redrawn by minaanandag at fiverr.com.
Antonio Damasio has proposed that this region helps map visceral
states associated with emotional experience and generate conscious feelings. This could provide the basis of
somatic markers like the discomfort produced by a risky decision.
The insular cortex has been implicated in the
experience of pain and basic emotions, including anger, disgust, fear, happiness, and sadness. The insular
cortex receives reports of internal states, like hunger and drug craving, and motivates individuals to engage in
consummatory behavior.
The insular cortex plays a crucial role in craving and impulse control. This region is stimulated by drug-related cues and may activate memories of
pleasurable drug-related experiences. Stroke damage to the insular cortex (see red area below) can eliminate nicotine addiction.
National Institute of Drug Abuse graphic retrieved from Wikimedia Commons.
Mirror Neuron System
Researchers have proposed that the human neocortex contains a mirror neuron system that is selectively activated
when we perform movements or observe the actions of others. In humans, this system may encompass Broca's area, the
inferior frontal gyrus, inferior parietal cortex, insular cortex, occipital cortex, premotor cortex, and superior
temporal sulcus.
Molenberghs et al. (2011) unexpectedly found neurons with
mirroring properties in the cerebellum, limbic system, and primary visual cortex. Graphic courtesy of
Wikimedia Commons.
The authors proposed that a core network is responsible for observing and executing movements. The
nervous system recruits additional areas to perform non-motor affective, auditory, and somatosensory
functions.
Mirror neurons look like other neurons when examined using a microscope. Their mirror properties emerge from their sensory, motor, and emotional systems connections. Perhaps most mirror neurons may be tuned by experience (Catmur, Walsh, & Heyes, 2007).
The mirror neuron system appears to encode the goal of a motor act and its component movements, whether a model
manipulates an object or mimes the action. The mirror neuron system encodes the actions of others and stores them to
predict their future actions (Rajmohan & Mohandas, 2007).
Soon after birth, an immature mirror neuron system may allow babies to imitate their parents' mouth movements, like thrusting out the tongue. Graphic courtesy of Wikimedia Commons.
Ramachandran (2011) has called the mirror neurons activated when
they observe others' movements "monkey see—monkey do neurons." He calls mirror neurons activated by others' emotional displays "Gandhi neurons."
Rizzolatti and Sinigaglia (2008) hypothesized that the primary role
of the mirror neuron system is to help us understand others’ intentions, which allows us to achieve
empathy. When we observe others’ facial expressions of emotion, visual information may be directly
transmitted to mirror neurons in the insula, producing the visceral changes that color our emotions.
In autism, mirror neurons may not fire when observing other individuals performing actions. This may help
explain deficits in empathy, social skills, language, and the development of a theory of mind (Enticott et al.,
2011).
Cortical and Subcortical Connections
Neocortical zones are connected with cortical and subcortical regions by specialized fiber tracts: association bundles, projection fibers, and commissural bundles. A meta-networking model proposes that the dynamic interaction of "distributed but relatively specialized networks" mediates brain functions like language (Herbet & Duffau, 2020, p. 1181).
Association Bundles
Association bundles link cortical regions located in the same hemisphere using U-shaped white matter tracts. These include the arcuate fasciculus (AF), frontal aslant tract (FAT), inferior fronto-occipital fasciculus (IFOF), inferior longitudinal fascicle (ILF), middle longtitudinal fasciculus (MdLF), superior longitudinal fasciculus (SLF), and uncinate fasciculus (UF).
Projection Fibers
Projection fibers connect the cortex with structures deep in the brain, the brainstem, and spinal cord. The frontostriatal tract (FST) connects the premotor cortex with the caudate nucleus and putamen, thalamocortical, optic, and pyramidal tracts. Tractography animation Alfred Anwander, CC BY-SA 4.0, via Wikimedia Commons.
The anterior commissure, shown above the third ventricle at the bottom of the diagram,
is considerably smaller than the corpus callosum and connects the left and right temporal lobes and the
hippocampus and amygdala. Anterior commissure graphic Winter, T. J. & Franz, E. A., CC BY 3.0, via Wikimedia Commons.
Subcortical regions, including the thalamus, basal ganglia, and limbic system, regulate fundamental functions like sensory processing and, movement, and emotion. Sometimes, the cerebellum is included in the list of subcortical structures. These structures also contribute to regulation of various qualities of thinking and emotion.
Thalamus
The thalamus consists of specialized nuclei that process and relay data to and from the telencephalon (cerebral cortex, basal ganglia, and limbic system). The thalamus analyzes
all sensory data except olfaction before distributing this information to the cortex via thalamocortical afferent
fibers (Breedlove & Watson, 2023). The cortex also sends information
to the thalamus to adjust its information processing via corticothalamic fibers. This two-way conversation creates
feedback loops that are crucial generating several EEG rhythms. The thalamus helps regulate arousal, sleep, and wakefulness (Steriade & Llinás, 1988). Through its functional connection to the hippocampus, it plays a crucial role in episodic memory (Aggleton et al., 2010).
The hippocampus is a seahorse-shaped limbic structure. The hippocampus is required to
form declarative memories and plays a vital role in emotion, navigation, and spatial memory, and dampening the endocrine stress
response. The hippocampus simultaneously integrates emotional, auditory, and visuospatial information to create episodic memories. The hippocampus also contains leukocyte receptors, making it part of the feedback loop for immune system regulation. Hippocampal neurons and networks that include it are sources of the theta rhythm (Amzica & Lopes da Silva, 2011).
Hippocampal Brainwaves Travel in Two Directions
The old-school view was that hippocampal brainwaves travel in one direction. This model could not explain how the hippocampus integrates information from various interconnected specialized systems. The new-school view, based on recording from human participants undergoing brain surgery, is that brainwaves travel through the hippocampus in both directions: from the back to the front and from the front to the back (Kleen et al., 2021). Moreover, cognitive activity differentially influences the direction of movement for low (e.g., 1.9 Hz) and high (e.g., 13.8 Hz) frequency waveforms.
The amygdala, a collection of nuclei, is an essential limbic structure located deep within the medial temporal lobes at the end of the hippocampus. The amygdala comprises many nuclei, including the lateral nucleus and the central nucleus. Rotating limbic system graphic lifesciencedb, CC BY-SA 2.1 JP, via Wikimedia Commons.
Brodmann areas are regions of the cerebral cortex defined based on their distinct cytoarchitectonic characteristics, first delineated by German neurologist Korbinian Brodmann in the early twentieth century. Using Nissl staining techniques, Brodmann examined the organization, density, and layering of neurons across different regions of the cerebral cortex. His classification was based on systematic observations made from the brains of multiple mammalian species, including humans.
The Functional Significance of Specific Brodmann Areas
The Brodmann map remains a widely used anatomical reference in both clinical and research neuroanatomy. For example, Brodmann area 4 corresponds to the primary motor cortex, located in the precentral gyrus, and is critical for voluntary motor control (Penfield & Boldrey, 1937). Similarly, area 17, also known as the primary visual cortex, is located in the occipital lobe and is the initial cortical recipient of visual input from the lateral geniculate nucleus (Zeki, 1993). The use of Brodmann areas facilitates the identification of functional zones during neurosurgical procedures and functional imaging studies, aiding in the interpretation of brain activity and lesions.
Language Processing and Brodmann Areas
The Brodmann map remains a widely used anatomical reference in both clinical and research neuroanatomy. For example, Brodmann area 4 corresponds to the primary motor cortex, located in the precentral gyrus, and is critical for voluntary motor control (Penfield & Boldrey, 1937). Similarly, area 17, also known as the primary visual cortex, is located in the occipital lobe and is the initial cortical recipient of visual input from the lateral geniculate nucleus (Zeki, 1993). The use of Brodmann areas facilitates the identification of functional zones during neurosurgical procedures and functional imaging studies, aiding in the interpretation of brain activity and lesions.
Neuroimaging and Cortical Mapping
Recent advancements in neuroimaging techniques, such as fMRI and PET, have enabled researchers to refine the functional mapping of Brodmann areas with greater precision. Moreover, probabilistic cytoarchitectonic atlases, such as those developed by the Jülich Brain Atlas project, have supplemented Brodmann’s static classification with data derived from multiple brains, allowing for population-level variability in cortical organization (Eickhoff et al., 2005). This evolution reflects the growing recognition that while Brodmann's map provides a valuable framework, individual differences in cortical morphology and function necessitate more dynamic and data-driven mapping approaches.
Relevance and Limitations
Brodmann areas continue to serve as a foundational framework for understanding cortical organization and function. Their relevance persists in both clinical and research contexts, from neurosurgical planning to the study of cognitive processes and neuropsychiatric disorders. However, ongoing advances in neuroimaging and connectomics are gradually supplementing this early anatomical schema with more detailed and individualized models of brain organization. These developments reflect a broader shift toward integrating structural and functional data to achieve a more comprehensive understanding of cerebral cortex architecture.
Researchers have revised the Brodmann maps and correlated areas with their functions. The Brodmann maps below were contributed by Mark Dow, Research Assistant at the Brain Development Lab, the University of Oregon to Wikimedia Commons.
Brodmann Area Involvement in Clinical Disorders
The clinical correlations between various psychiatric and neurological disorders and specific Brodmann areas provide valuable insights into the underlying neural mechanisms of these conditions. Brodmann areas, defined by their distinct cytoarchitectonic characteristics, have been extensively studied in relation to numerous mental health and neurological disorders. Understanding the abnormalities in these regions can offer critical information for diagnosis, treatment, and the development of targeted therapies. This post explores the associations between specific Brodmann areas and disorders such as ADHD, autism spectrum disorder, bipolar disorder, major depressive disorder, panic disorder, PTSD, schizophrenia, and substance use disorder.
Attention-Deficit Hyperactivity Disorder (ADHD)
ADHD is associated with abnormalities in multiple Brodmann areas, including BAs 44/45 (Broca's area), 8/9, 10, 11, 46 (frontal regions), 7, 39, 40 (parietal regions), 4 (motor cortex), 30 (cingulate gyrus), 21, 38 (temporal regions), and 6 (premotor cortex). These abnormalities contribute to the diverse cognitive, attentional, and motor deficits observed in individuals with ADHD.
In individuals with ADHD, various brain regions show notable abnormalities. Broca's area, which includes Brodmann Areas 44 and 45, exhibits functional disturbances, particularly a lower fractional amplitude of low-frequency fluctuations (fALFF). This dysfunction is linked to language deficits, with different subtypes of ADHD affecting distinct parts of Broca's area: Area 44 in the inattentive subtype and Area 45 in the combined subtype (Pikusa & Jończyk, 2015; Silk et al, 2005).
In the frontal regions, children with ADHD display grey matter deficits in the right superior frontal gyrus (Brodmann Areas 8 and 9), suggesting disruptions in attentional networks (Overmeyer et al., 2001). Adolescents with ADHD show decreased activation in the middle frontal gyrus (Area 10) and the dorsolateral prefrontal cortex (Area 46), indicating widespread frontal lobe dysfunction (Silk et al., 2005). Furthermore, abnormalities in the ventromedial orbitofrontal cortex (Area 11) are linked to motivational deficits in adults with ADHD (Farré-Colomés et al., 2021).
The parietal regions, including the superior parietal lobe (Area 7) and the inferior parietal lobule (Areas 39 and 40), also show decreased activation in those with ADHD, implicating these areas in attentional and action-attentional systems (Silk et al., 2005). Additionally, children with ADHD exhibit decreased activation in the primary motor cortex (Area 4) during motor tasks, suggesting anomalies in motor development (Gaddis et al., 2015; Gilbert et al., 2011, 2019).
The right posterior cingulate gyrus (Area 30) shows grey matter deficits in children with ADHD, which may contribute to difficulties in attentional control (Overmeyer et al., 2001). Structural alterations are also observed in the temporal regions, with lower cortical thickness in the fusiform gyrus and temporal pole (Areas 21 and 38) in children with ADHD (Hoogman et al., 2019; Karalok et al., 2019; Lake et al., 2019; McLaughlin et al., 2014). Lastly, increased connectivity in the premotor cortex (Area 6) in individuals with ADHD may be associated with challenges in motor planning and execution (Hoshi & Tanji, 2007; Oldehinkel et al., 2016; Sörös et al., 2019; Suskauer et al., 2008).
Autism Spectrum Disorder (ASD)
Research indicates that abnormalities in Brodmann areas 24, 44, 45, and 10 are associated with Autism Spectrum Disorder. These abnormalities include changes in neuron size and density, gray matter volume, and functional connectivity, which are linked to the social and communication deficits characteristic of ASD. Further studies on these areas could enhance our understanding of the neural underpinnings of autism. In the anterior cingulate cortex (ACC), particularly in Brodmann Area 24, there is a notable reduction in cell size and cell packing density, specifically in layers 24b and 24c. Additionally, this region shows elevated levels of glial fibrillary acidic protein (GFAP) in the white matter, indicating increased astrocyte activation. During verbal memory tasks, a decrease in glucose metabolism is observed in BA24. Furthermore, there are dysregulated DNA methylation patterns in this area, impacting genes related to immune functions and synaptic membranes.
In the inferior frontal cortex, encompassing Brodmann Areas 44 and 45, there is a decrease in the size of pyramidal neurons, which play crucial roles in language processing and social behaviors (Jacot-Descombes et al., 2012). There is also reduced gray matter volume in the pars opercularis (BA44) and pars triangularis (BA45), which is linked to difficulties in social communication (Yamasaki et al., 2010).
The anterior prefrontal cortex, specifically Brodmann Area 10, exhibits abnormal functional connectivity between the right and left hemispheres. This abnormality correlates with the severity of social deficits (Kikuchi et al., 2013). Similar to BA24, BA10 also shows dysregulated DNA methylation, affecting genes involved in immune response and synaptic function (Nardone et al., 2014).
Other areas affected include the medial/cingulate regions (BAs 32, 24, and 25), where lower glucose metabolism is observed during verbal memory tasks (Deery et al., 2022; Hazlett et al., 2004, 2010). Additionally, there is a reduction in white matter volumes in the posterior frontal lobe and along the cingulate arch (Aalst et al., 2021; Gardener et al., 2016).
Bipolar Disorder (BD)
Research indicates that abnormalities in several Brodmann areas, including BAs 9, 24, 38, 41, 42, 46, and 10, are associated with bipolar disorder. These abnormalities span structural changes, such as reduced glial numbers and cortical volume, as well as functional and molecular disruptions, including altered gene expression and DNA methylation. Understanding these abnormalities can provide insights into the pathophysiology of BD and aid in the development of targeted treatments. In Brodmann Area 9, part of the dorsolateral prefrontal cortex, there are abnormalities in DNA methylation and gene expression, indicating its role in the pathophysiology of bipolar disorder (BD). Additionally, this area shows decreased numbers and density of glial cells, suggesting potential disruptions in neurochemical regulation.
The subgenual prefrontal cortex, specifically Brodmann Area 24, exhibits reduced volume and fewer glial cells, which have been associated with familial forms of BD. This area is significant for mood regulation and reflects neurobiological changes linked to the disorder (Öngür et al., 1998; Scarr et al., 2019).
In the temporal pole, Brodmann Area 38 displays notable differences in DNA methylation, which are associated with BD, indicating its involvement in the molecular mechanisms underlying the disorder (Ho et al., 2019).
In the primary auditory cortex, comprising Brodmann Areas 41 and 42, decreased BOLD signals in response to auditory stimuli have been identified as potential biomarkers for BD, pointing to functional abnormalities in auditory processing (Okamoto et al., 2022).
Brodmann Area 46, another region of the dorsolateral prefrontal cortex, shows altered gene expression, with specific genes exhibiting differential expression in BD, suggesting disruptions in neuronal network functions (Nakatani et al., 2006; Visueta et al., 2012).
Finally, the prefrontal cortex, particularly Brodmann Area 10, also presents changes in gene expression in BD. These alterations highlight the complex regional-specific changes in cortical gene expression associated with the disorder (Scarr et al., 2019; Vizueta et al., 2012).
Major Depressive Disorder (MDD)
Research consistently implicates several Brodmann areas in the pathology of major depressive disorder. Key areas include the anterior cingulate cortex (BA 24 and BA 32), dorsolateral prefrontal cortex (BA 9 and BA 46), ventromedial prefrontal cortex (BA 10), orbitofrontal cortex (BA 13 and BA 47/12), and subgenual cingulate cortex (BA 25). These regions are associated with structural and functional abnormalities, altered connectivity, and changes in inflammatory markers, all contributing to the complex neurobiology of MDD. In the anterior cingulate cortex, particularly in Brodmann Areas 24 and 32, structural abnormalities and reduced volume in the subgenual part of BA 24 are linked to familial forms of major depressive disorder (MDD). Elevated levels of tumor necrosis factor (TNF) have been observed in BA 24 among MDD patients, suggesting the involvement of pro-inflammatory pathways. Furthermore, abnormalities in BA 32 have been associated with antidepressant treatment.
In the dorsolateral prefrontal cortex, including Brodmann Areas 9 and 46, both structural and functional abnormalities have been connected to MDD. In BA 9, changes in connectivity and increased fractional amplitude of low-frequency fluctuation (fALFF) are noted (Gao et al., 2021; Lai & Wu, 2015; Ye et al., 2012; Vasic et al. 2008; Zhukovsky et al., 2020). Additionally, elevated TNF levels in BA 46 indicate a role in the disorder's pathophysiology (Dean et al., 2010).
The ventromedial prefrontal cortex (BA 10) shows abnormal functional connectivity, which is linked to emotional regulation deficits in MDD patients (Almeida et al., 20111; Johnstone et al., 2007; Wackerhagen et al., 2017; Young et al., 2016). Epigenetic modifications, such as methylation changes, have also been identified in BA 9 and BA 38 (Ho et al., 2019).
In the orbitofrontal cortex, including Brodmann Areas 13 and 47/12, reduced functional connectivity in BA 13, a region involved in reward processing, is associated with depressive symptoms (Cheng et al., 2016). Conversely, increased functional connectivity in BA 47/12, related to non-reward and punishment, correlates with negative self-perception in MDD (Cheng et al., 2016).
The subgenual cingulate cortex (BA 25) exhibits reduced functional connectivity with regions involved in emotional regulation in MDD patients (Peng et al., 2020). Methylation changes in BA 25 have been consistently found in independent brain samples, highlighting its significance in the etiology of MDD (Åberg et al., 2018).
Panic Disorder
Research indicates that abnormalities in Brodmann areas 11, 25, 32, and 15, as well as regions within the prefrontal cortex and parahippocampal gyrus, are associated with panic disorder. These areas show altered activity and connectivity, contributing to the pathophysiology of PD. The findings highlight the involvement of the prefronto-limbic network and suggest that both hyperactivation and hypoactivation patterns in these regions play a role in the disorder. During panic attacks, there is a noticeable decrease in regional cerebral blood flow (rCBF) in the right orbitofrontal cortex (BA 11) and the prelimbic cortex (BA 25). This reduction is also observed in the anterior cingulate cortex (BA 32), where panic attacks lead to decreased rCBF. In the context of emotional processing in patients with panic disorder (PD), the anterior cingulate cortex (BA 32) exhibits mixed patterns of hyperactivation and hypoactivation.
The parahippocampal gyrus in PD patients shows significant abnormal asymmetry in cerebral blood flow. Similarly, the anterior temporal cortex (BA 15) experiences decreased rCBF during panic attacks (Hasler et al., 2007). Key regions within the prefronto-limbic network, particularly areas within the prefrontal cortex (PFC), show selective deficits in emotional processing among PD patients (Hasler et al., 2007; Shang et al., 2014). Additionally, dysfunctional communication within frontotemporal structures, including areas in the prefrontal cortex, is indicated by decreased coherence imaging values (Shang et al., 2014; Speer et al., 2003).
Increased resting-state functional connectivity between the thalamus and insula suggests excessive sensitivity to external information in PD patients. This heightened connectivity highlights a potential neural mechanism underlying the heightened responsiveness to stimuli often experienced by individuals with panic disorder (Feldker et al., 2016, 2019; Zhou et al., 2022).
Post-Traumatic Stress Disorder (PTSD)
PTSD is associated with abnormalities in several Brodmann areas, including the anterior cingulate cortex (BA 32 and BA 24), medial prefrontal cortex (BA 10 and BA 11), dorsolateral prefrontal cortex (BA 46), insula (BA 13), orbitofrontal cortex (BA 25), and sensorimotor areas (BA 4/6). These regions are involved in emotional regulation, memory processing, and response to trauma-related stimuli, highlighting the complex neural underpinnings of PTSD. In individuals with PTSD, the dorsolateral prefrontal cortex (DLPFC), specifically Brodmann area 46, shows decreased activity and signs of mitochondrial dysfunction. The anterior cingulate gyrus, located in Brodmann area 32, also exhibits less activation in PTSD subjects compared to those without PTSD. There are notable differences in functional connectivity in this region, suggesting its involvement in the recall of traumatic events.
The medial prefrontal cortex, encompassing Brodmann areas 10 and 11, shows reduced activation in PTSD subjects (Etkin & Wager, 2007; Herringa et al., 2012; Manthey et al., 2021; Sartory et al, 2013). The activation levels in BA 10, in particular, correlate with PTSD symptoms during threat processing. The insula, specifically Brodmann area 13, demonstrates increased delta slow waves, which are linked to worsening PTSD symptoms over time (Harricharan et al., 2019; Herringa et al., 2012; Rabinak et al., 2011). Additionally, differences in functional connectivity in the insula are observed between PTSD and non-PTSD individuals (Rabinak et al., 20111; Sripada et al., 2012; Zhang et al., 2016).
During symptom provocation in PTSD patients, there is increased regional cerebral blood flow (rCBF) in the right sensorimotor areas, specifically Brodmann areas 4 and 6 (Pissiota et al., 2000). Conversely, lowered rCBF is observed in the right retrosplenial cortex, which includes Brodmann areas 26, 29, and 30 (Pissiota et al., 2000).
Structural and functional changes in the hippocampus and amygdala are consistently observed in PTSD, highlighting their crucial roles in memory and emotional processing (Chen et al., 2018; Hull, 2002).
Schizophrenia
Research indicates that abnormalities in specific Brodmann areas, particularly in the frontal (BAs 4, 6, 8, 9, 10, 44, 46, 47), temporal (BAs 24, 25, 29, 30, 31), and cingulate (BAs 24, 25, 29, 30, 31) cortices, are associated with schizophrenia. These abnormalities include disrupted intercorrelations, altered receptor binding, gene expression changes, and structural deficits. The findings suggest that these regions play critical roles in the cognitive and functional impairments observed in schizophrenia, and they may serve as potential biomarkers for the disorder. Research has highlighted several key insights into the brain abnormalities associated with schizophrenia. Notably, significant reductions in gray matter volume have been observed in the left anterior hippocampus-amygdala, left parahippocampal gyrus, and left superior temporal gyrus. These reductions are particularly linked to thought disorders, with a correlation found between the volume of the left posterior superior temporal gyrus and the severity of these disorders.
Additionally, disruptions in D2 dopamine receptor patterns have been identified in specific regions of the temporal lobe, including the perirhinal, superior, and inferior temporal cortices (Goldsmith et al., 1997; Joyce et al., 1997). These areas correspond to Brodmann areas 20, 22, 37, 39, and 42. The observed disruptions are distinct to the temporal lobe and are not attributable to long-term antipsychotic treatment, suggesting a specific role in the manifestation of auditory hallucinations and other positive symptoms of schizophrenia.
In the context of schizotypal personality disorder, which shares some features with schizophrenia, lower fractional anisotropy (FA) has been observed in the left temporal lobe, particularly within Brodmann areas 20, 21, and 22 (Chan et al., 2018; Ellison-Wright & Bullmore, 2009; Hazlett et al., 2011; Lee et al., 2016). This finding indicates alterations in the white matter microstructure (Szeszko et al., 2008).
Moreover, schizophrenia is associated with a thinner cortex and reduced surface area in the temporal lobe, with the most significant reductions in cortical thickness observed at the temporal pole (Kaur et al., 2020; McCarley et al., 1999; Shenton et al., 1992) . There is also evidence of progressive volumetric changes over time, particularly a decrease in temporal white matter volume, indicating ongoing structural abnormalities in the brains of individuals with schizophrenia (Kaur et al., 2020; Mathew et al., 2014; Olabi et al., 2011).
Finally, enhanced functional connectivity between the left dorsolateral prefrontal cortex (DLPFC) and the left mid-posterior temporal lobe has been identified in patients experiencing their first episode of schizophrenia (Zhou et al., 2007). This altered connectivity pattern may play a role in the cognitive and perceptual disturbances characteristic of the disorder.
Substance Use Disorder (SUD)
Abnormalities in specific Brodmann areas, particularly BA 10, BA 24, BA 30, BA 18, BA 21/22, and BA 19, are associated with substance use disorder. These areas are involved in critical functions such as self-reflection, emotional regulation, memory, and executive function, which are often impaired in individuals with SUD.
In adolescents with substance use disorder (SUD), there is reduced activity in Brodmann Area 10, located in the superior, medial, and middle frontal gyrus (Dalwani et al., 2014). This reduction suggests difficulties in self-referential evaluation and future planning. The anterior cingulate cortex, specifically Brodmann Area 24, shows abnormal activity, impacting emotional behavior and executive function in individuals with SUD.
Conclusion
The examination of specific Brodmann areas reveals significant correlations with various psychiatric and neurological disorders, highlighting the importance of these brain regions in disease pathology. ADHD features disruptions in regions related to attention and executive function. Autism spectrum disorder is characterized by changes in areas affecting social and communication skills. Bipolar disorder involves alterations in areas associated with mood regulation.
Panic disorder and PTSD both involve the prefronto-limbic network, impacting emotional and stress responses. Schizophrenia is associated with widespread disruptions in areas affecting cognition and perception, and substance use disorder involves regions critical for executive function and emotional regulation. Understanding these specific brain region abnormalities offers insights into the mechanisms underlying these disorders and aids in developing targeted treatments.
CONNECTIVITY, PHASE, AND COHERENCE
Neural networks are systems of interconnected ensembles of neurons that collaborate to achieve a goal (Thompson & Thompson, 2016).
Networks communicate and perform functions via hub- or node-based communication systems. Dorsal and lateral views of the connectivity backbone of human brain. Labels indicating anatomical subregions are placed at their respective centers of mass. Nodes (individual ROIs) are coded according to strength and edges are coded according to connection weight (see legend).
Hagmann, P., Cammoun, L., Gigandet, X., Meuli, R., Honey, C. J,, Wedeen, V. J., & Sporns, O. (2008) Mapping the structural core of human cerebral cortex. PLoS Biology, 6(7), e159, Wikimedia Commons, licensed under the Creative Commons Attribution 3.0 Unported license.
Connectivity
Networks like the Affect, Attention, Default, Executive, and Salience systems synchronize the activity of cortical and subcortical regions to perform functions. Connectivity is the degree of synchrony between the oscillations of specialized brain regions (nodes) within a network (Bastos & Schoffelen, 2016). Strongly connected brain regions are called hubs. Hubs can be
primarily connected to nodes (vertices) within their local modules (sets of interconnected nodes) or nodes in more distant modules
(Bullmore & Sporns, 2009).
Neurofeedback training can increase or decrease connectivity using a normative database. For example, BrainMaster's BrainAvatar software allows clinicians to train specific networks, like the Default Mode Network (DMN).
See the Assumptions unit for an in-depth discussion of the Affective, Default Mode, Executive, Motor, Network, Oculomotor, Salience, and Social Networks.
Phase reset (PR) is defined by a sudden change in phase difference (phase shift duration or SD) followed by a period of phase locking (lock duration or LD). PR = SD + LD (Thatcher et al., 2009). Gap junction coupling explains phase locking and phase shifting (Hughes & Crunelli, 2007).
Resetting the phase of ongoing oscillatory activity to endogenous (internal) or exogenous (environmental) cues facilitates coordinated information transfer within circuits and between distributed brain areas. Phase resetting is a critical marker of dynamic state changes within functional networks (Voloh & Womelsdorf, 2016).
Phase rests create a neural context, a narrow band of frequencies that uniquely characterize the activated circuits. They impose coherent low-frequency phases to which high-frequency activations can synchronize. These are identifiable as cross-frequency correlations that span large distances. Phase rests are critical for neural coding models that depend on phase, increasing the informational content of neural representations. They likely originate from the dynamics of canonical E-I circuits that are anatomically ubiquitous.
Phase resets reorganize oscillations in diverse task contexts: attentional stimulus selection, classical conditioning, cross-modal integration, sensory perception, and spatial navigation. Phase resets can drive changes in ensemble organization, functional networks, neural excitability, and overt behavior.
Networks of neurons generating the EEG activity at different sites can
produce signals that are identical in amplitude, frequency, and phase or that are entirely
unrelated.
Synchrony means that the firing of pools of neurons is coordinated. EEG
signals can display local synchrony, frequency synchrony, and phase
synchrony.
Local synchrony occurs when the coordinated firing of cortical neurons produces high-amplitude EEG signals. For example, an alpha amplitude
of 20-60 μV detected at O1-A1 is produced by
the synchronous firing of pools of neurons. This site's beta activity amplitude is lower due to desynchronized firing. This is
analogous to the volume generated by a choir. When performers sing in
unison, they produce a louder sound than singing separately.
Frequency synchrony occurs when identical EEG frequencies are detected at
two or more electrode sites. For example, 12 Hz may be simultaneously
detected at O1-A1 and O2-A2.
Phase synchrony reflects the degree of alignment of oscillatory activity across regions. For example, if the peaks of theta waves occur at the same instant in time at two cortical regions, then there is zero phase lag between the two regions.
The phase alignment of two EEG signals of the same frequency between two cortical locations reflects the speed of information transmission, with lower phase lag (greater synchrony) reflecting faster communication between sites. High synchrony within frequency bands, such as alpha or beta, supports efficient communication. Cross-frequency synchrony, between different EEG bands, plays a role in the integration of brain functions.
In some cases increased phase synchrony simply reflects two areas receiving input from the same rhythmic generators and doesn’t necessarily mean that the two areas are communicating. Increased phase synchrony can also be the result of damage to the interactive communication generally. This is particularly true in the case of delta activity, which can occur in cases of TBI, resulting in damaged regions independently producing delta oscillations due to a lack of other input, sometimes with increased synchrony.
EEG training may produce phase-synchronous 12-Hz alpha waves at O1-A1 and
O2-A2.
Coherence
Coherence represents the degree of coupling between separate cortical
regions and reflects neural network connectivity and dynamics
(Bullmore & Sporns, 2009). Coherence evaluates the linear association or correlation between the EEG waveforms recording from two different scalp locations (two referential montages). A two-channel referential montage is shown below.
Coherence measures the degree to which two areas have consistent phase relationships at a designated frequency. When the phase difference between two signals is constant, coherence = 1. When the phase difference is random, coherence = 0.
Hyper-coherence means too much coupling and involves a failure to activate cortical regions selectively and may interfere with multitasking and rapid decision-making. Hypo-coherence, which often results from traumatic brain injuries, means too little coupling and involves a breakdown in
communication between regions that should normally communicate with each other (Wilson et al., 2011).
Coherence is a correlation coefficient (squared) that estimates relative amplitude and phase consistency between any pair of signals in each frequency band (Bendat & Piersol, 2000).
The key component of that explanation is the word consistency. Coherence is based on phase, and phase measures the relationship between two signals (two separate electrode locations), generally relating to a specific EEG frequency band when discussing EEG phase and coherence. Phase measures the timing relationship of the two waveforms.
The image below shows five identical wave patterns that are shifted in time compared to each other. If we start with the first waveform at the bottom of the image, the subsequent waves are shifted in time. This is known as phase shift or phase angle. The angle is represented as degrees, so a wave that begins one-fourth of the way through the original wave’s cycle is said to have a 90-degree phase angle (example B). The same waveform beginning at the halfway point has a phase angle of 180 degrees, which means the waves are exactly opposite (example C). When the original wave is in the upward part of its cycle, the 180 degrees out of phase wave is in the downward part of its cycle. Graphic redrawn by minaanandag on Fiverr.com.
As previously noted, coherence is a measure of the consistency of these phase relationships. Wave patterns do not have to be in phase (zero phase angle – A compared to E above to be coherent. They only need to be in the same phase relationship consistently to be highly coherent.
Coherence values range from 0-1, with zero representing a random relationship between the two signals and 1 representing the signals remaining in the same phase relationship for the entire period being measured (usually a minimum of 2 seconds).
Because signals can be out of phase and remain coherent, the term coherence should not be confused with phase synchrony, which describes two waves oscillating with the same time value (zero phase angle). For example, coherence is often incorrectly applied to heart rate and respiration. Generally, one of the goals for heart rate variability training (HRV) is to synchronize the respiration and heart rate waveforms. This is an example of phase synchrony.
When this is consistently the case, the two waves are highly coherent. However, suppose a true coherence calculation is used. In that case, the two waveforms could be significantly offset from one another and still show a high degree of coherence, as long as they remained consistently in the same phase relationship. This may confuse the outcome measures.
In truth, all HRV measures use a calculation of phase angle, the Pearson’s correlation coefficient, to determine their relative phase synchrony rather than the more complex coherence calculation, which is a combination of the cross-spectral density and the auto-spectral density between the two signals.
EEG coherence estimates interaction between neural systems, measured by amplitude and phase consistency in each EEG frequency band between two distinct scalp sensor locations. This is not the same as a synchrony measure between locations. However, as noted above, high coherence can correspond to increased phase synchrony between two locations at a given EEG frequency. The key factor in the coherence measure is consistency.
Two signals can be asynchronous but can have high coherence if consistently in the same asynchronous relationship. This consistency implies that there is some coordinating mechanism between the two locations that is related to communication and/or the interaction between the two locations (Nunez, 2006).
The history of coherence measures being applied to the EEG began with Donald Walter (Walter, 1963), and since that time, there have been many studies published regarding the use of EEG coherence to identify factors in cognition, brain maturation, heritability, gender differences, and a variety of clinical disorders (Thatcher, 2012).
There are a variety of methods for estimating coherence. Typically coherence was measured using the linked ears montage or a common reference.
Thatcher (2012) states that this approach is necessary to correctly calculate phase differences because other montage arraignments distort the original time series and thus the relationships between individual sensor locations. Thatcher (2004) claims that the reliability of coherence measures using common average reference or Laplacian montages, though generally quite high, is irrelevant because these montaging methods render the resulting calculations uninterpretable.
He argues that these montages involve the “mixing” of signals from multiple electrodes (all 19 channels in the case of common average and the electrodes immediately surrounding the electrode of interest in Laplacian). He provides examples using artificially-generated signals and compares the accuracy and sensitivity of response of the various montages, and determines that only the linked-ear or common reference (such as Cz or Fcz) correctly represents the changes occurring in the source signals as greater amounts of noise are added.
Unfortunately, the linked ear and common references in this study were necessarily neutral, without signal content, and therefore do not reflect real-world examples.> On the other hand, Nunez and Srinivasan (2006) demonstrate that coherence using a common reference (such as a linked-ear or linked-mastoid sensors) elevates all coherence measures for all frequencies and electrode combinations because this method adds a common signal to each channel.
The idea of a “neutral” reference without any EEG or other electrical activity is not valid in real-world examples. Ear and mastoid reference channels frequently show rhythmic alpha activity, particularly in the eyes-closed condition, and are also often contaminated by EMG artifacts from masseter muscle contractions.
Similarly, a common reference such as Cz or Fcz would add real EEG signal characteristics to the resulting calculation. These factors influence the phase and coherence calculations, particularly for frontal electrode locations when using the linked ear or linked mastoid references, because of the function of the differential amplifier.
For a complete discussion of differential amplifier functions, please see the Instrumentation and Electronics section. For our purposes in this discussion, it is sufficient to understand the concept of common-mode rejection.
Common-mode rejection eliminates those common or similar signals between two inputs, often called the active and reference but more correctly known as positive and negative. The initial purpose of this method was to eliminate “mains” artifact, commonly known as 60 Hz artifact in North America, and 50 Hz artifacts in most of the rest of the world, due to the standard oscillating frequency of the alternating current in electrical wiring.
Common mode rejection also rejects any other electrical signal, including EEG, from active/reference pairs when the signals are the same in frequency and, to a lesser extent, amplitude. However, if the active and the reference inputs contain signals that are different, then those different signals are retained in the resulting signal.
When the “reference” channel derived from the ear or mastoid references that contain substantial EEG activity, such as alpha, is compared to the frontal “active” channels that generally do not contain substantial alpha activity, even in the eyes closed condition, the resulting signal will retain the alpha activity from the reference channel. This creates the appearance of rhythmic, highly synchronous alpha activity in frontal sensors and therefore results in high alpha coherence values in comparisons of those sensor pairs.
Compared to a normative database, these high coherence values will generate falsely elevated z-score values compared to the normative population, and neurofeedback training may be implemented to “correct” this high coherence.
Nunez and Srinivasan (2006) suggest that the common average reference method shows coherence results more similar to experimental, reference-independent coherence calculations. However, they note that many sensors are needed to generate an effective average reference value. Their example used 111 scalp electrode locations rather than the typical 19 electrode locations used in most normative databases.>
Another method for calculating coherence is the use of the surface Laplacian method. This method removes some of the issues associated with reference contamination though it does tend to increase noise at each electrode location (Nunez & Srinivasan, 2006). It also removes the problem of volume conduction.
Volume conduction represents the conduction of bioelectric signals (brainwaves) through neural tissues. They show up in adjacent sensor locations that are not directly above the signal generator in the cortex. Volume conduction decreases with distance, so closely spaced electrode pairs can be expected to be more coherent, and the greater coherence will be disproportionally affected by common sources and volume conduction.
In contrast, widely spaced electrode pairs can be expected to reflect actual communication variables between the two areas more accurately. Because the Laplacian operator utilizes the average of the immediately surrounding electrodes as the reference, the common signals are minimized, and the coherence may provide a more accurate reflection of coherence in closely spaced electrode pairs.
The eventual answer to which coherence measure is better must await further studies, ideally using real-world models. Current practice utilizing either method will produce results that require an understanding of the benefits and limitations of each approach.
Excess frontal alpha coherence derived from linked ear reference data should be reviewed cautiously. The raw EEG signal should always be viewed using multiple montages to determine the accuracy of the frontal alpha activity displays.
Two examples of the same recording are shown below. The top example shows the linked ears montage with clear frontal alpha activity. Note the alpha activity present in the A1 and A2 electrode tracings at the bottom of the image and also note the alpha activity at T5 and T6, which are adjacent to the ears. The second image shows the longitudinal bipolar montage with a more typical posterior distribution of alpha activity and very little frontal alpha. The electrode locations and/or derivations (comparisons) are shown on the left side of each image. Note also the elevated global alpha coherence derived from the linked ears montage. No coherence calculation is possible for the longitudinal bipolar montage.
Other factors that can influence coherence measures include pervasive EMG artifacts that could not be removed with typical artifact removal methods. Sometimes this type of EMG artifact is not evident, particularly to beginning practitioners, and may be allowed to contaminate the record. When this happens, excessive hypercoherence in the beta and fast beta frequencies is sometimes seen in the example below. Note the excess beta and fast beta in the absolute power and relative power topographic maps and the global hypercoherence in the same frequency bands. This example also shows frontal delta and theta activity due to lateral eye movement artifact and the resulting hypercoherence in those frequencies in frontal comparisons.
With these cautions in mind, coherence remains a useful tool, as it can be quite revealing, particularly in cases of traumatic brain injury, stroke, lesion, and other evaluations. With experience, it is usually possible to identify which coherence values represent actual findings and, more importantly, to correlate those findings with client history and presenting symptoms.
On the other hand, simple phase measurements alone are not particularly useful. For one thing, they are not directional. They simply show the timing relationship between two sensor locations. Even with statistical analysis, this does not reveal which location may be dysfunctional or what the causal factors may be (Nunez, 2006).
Additionally, a common reference distorts the phase in the same way mentioned in the coherence discussion because the phase is the source of the coherence calculation. Nunez (1974) shows that using a bipolar montage for phase calculation eliminates the problem of closely spaced electrodes (volume conduction) and the addition of the common signal (reference contamination). However, this isn’t suggested as a viable montage for the subsequent coherence calculation.
Values represent the measure of phase from -1 to +1, and statistical calculations can be made based on normative samples. However, experimental data (Nunez, 1995; Silberstein et al., 1993) show that only about 8% of the phase data collected could be identified as associated with traveling waves. The rest was too complex to identify source relationships. The data may represent valuable information, but interpretation using simple phase measures is not possible due to the complex nature of cortical communication systems. More recent work has examined phase slope, however, which provides a measure of effective connectivity, the directionality of influence between two EEG sources.
Co-Modulation
Co-modulation is the degree of association in the magnitude of signals detected from two sources (sites). Co-modulation, which can be measured using the Pearson Product-Moment Correlation Coefficient, shows the degree to which signals strengthen and weaken in a correlated manner (Collura, 2009). Co-modulation does not measure phase or coherence, although it may reflect phase effects (Sterman & Kaiser, 2001).
Glossary
acetylcholine: an amine neurotransmitter that binds to nicotinic and muscarinic
ACh receptors.
acetylcholine esterase (AChE): the enzyme that deactivates ACh.
AChE-R: an abnormal form of acetylcholine esterase (AChE), which may render
dendrites with acetylcholine receptors more excitable when stressed.
action potential: a propagated electrical signal that usually starts at a neuron’s
axon hillock and travels to presynaptic axon terminals.
adenylate cyclase: at a metabotropic receptor, an enzyme that transforms ATP
into the second messenger cyclic AMP.
afferent: a neuron that transmits sensory information towards the central
nervous system, or from one region to another.
all-or-none law: once an action potential is triggered in an axon, it is
propagated, without decrement, to the end of the axon. The amplitude of the action potential is unrelated to the
intensity of the stimulus that triggers it.
alpha blocking: arousal and specific forms of cognitive activity may reduce
alpha amplitude or eliminate it entirely while increasing EEG power in the beta range.
alpha rhythm: 8-12-Hz activity that depends on the interaction between rhythmic burst firing by a subset of thalamocortical (TC) neurons linked by gap junctions and rhythmic inhibition by widely distributed reticular nucleus neurons. Researchers have correlated the alpha rhythm with "relaxed wakefulness." Alpha is the dominant rhythm in adults and is located posteriorly. The alpha rhythm may be divided into alpha 1 (8-10 Hz) and alpha 2 (10-12 Hz).
alpha spindles: regular bursts of alpha activity.
alpha-subunit: a subunit of a G protein associated with the neuron membrane that breaks away to activate enzymes within the neuron when a ligand binds to a metabotropic receptor.
amino acid neurotransmitters: the oldest family of transmitters. These molecules bind to ionotropic and metabotropic receptors, transmitting information and modulating neuronal activity. Most synaptic communication is accomplished in the brain by glutamate (generally excitatory) and GABA (generally inhibitory).
AMPA (glutamate) receptors: ionotropic receptors which open sodium channels,
depolarizing the neuron's membrane (producing an EPSP), and dislodging a Mg+ ion that blocks an adjacent NMDA
(glutamate) receptor's calcium channel. AMPA receptors are responsible for most activity at glutamatergic
synapses.
amplitude: the energy or power contained within the EEG signal measured in
microvolts or picowatts.
amygdala: a limbic system structure plays a crucial role in learning about the consequences of our actions and creating declarative memories for events with emotional significance.
angular gyrus: located in the parietal lobe near the junction of the temporal and occipital lobes, the angular gyrus corresponds to Brodmann area 39. It plays a role in language processing, attention, spatial cognition, and integration of sensory information.
anisotropic attenuation: the variation in the degree of signal attenuation depending on the direction of the electrical currents. This phenomenon occurs due to the heterogeneous nature of the skull's structure.
anion: negative ion, for example, chloride (Cl-).
anterior: near or toward the front of the head, for example, the anterior
cingulate.
anterior cingulate cortex (ACC): a division of the prefrontal cortex (Fpz, Fz, Cz, Pz) that plays a vital
role in attention and is activated during working memory. The ACC mediates emotional and physical pain and has cognitive (dorsal anterior cingulate) and affective (ventral anterior cingulate) conflict-monitoring components.
anterior commissure: a bundle of nerve fibers that crosses the midline and connects the left and right temporal lobes, hippocampus, and amygdala.
anterior prefrontal cortex (APFC): found in the most anterior region of the prefrontal cortex, the anterior prefrontal cortex includes Brodmann areas 10 and 11. It involves complex cognitive processes such as planning, decision-making, working memory, and abstract reasoning.
apical dendrite: a dendrite that arises from the top of the pyramid and extends
vertically to layer 1 of the neocortex.
arousal: a process that combines alertness and wakefulness, produced by at least
five neurotransmitters, including acetylcholine, histamine, hypocretin, norepinephrine, and serotonin.
astrocytes: star-shaped glial cells that communicate with and support neurons
and help determine whether synapses will form.
asynchronous waves: voltages produced when neurons depolarize and hyperpolarize independently.
ATP: the energy source for a neuron’s sodium-potassium transporters.
Attention-Deficit Hyperactivity Disorder (ADHD): a neurodevelopmental disorder characterized by inattention, hyperactivity, and impulsivity. It is associated with abnormalities in brain regions such as the prefrontal cortex and basal ganglia.
auditory cortex: temporal cortex that processes auditory information within the dorsal and ventral streams.
autism spectrum disorder (ASD): a neurodevelopmental disorder characterized by deficits in social communication and interaction, along with restricted and repetitive behaviors. It involves atypical brain development and connectivity, particularly in areas such as the temporal lobes and frontal cortex.
autonomic nervous system: a subdivision of the peripheral nervous system that innervates glands and internal organ smooth muscles and includes enteric, parasympathetic, and sympathetic divisions.
autoreceptors: metabotropic receptors that can be located on the membrane of
any part of a neuron. They detect neurotransmitters released the neuron releases, generate IPSPs that inhibit the
neuron from reaching the excitation threshold, and regulate internal processes like transmitter synthesis and release through the
second messenger system.
axoaxonic synapses: junctions between two axons that do not affect the
generation of an action potential, only the amount of neurotransmitter distributed.
axodendritic synapses: junctions between axons and dendrites determine
whether the axon hillock will initiate an action potential.
axon: long, cylindrical structures that convey information from the soma to
the terminal buttons. An axon also transports molecules in both directions along the outer surface of protein
bundles called microtubules.
axon hillock: a swelling in the cell body where a neuron integrates the
messages it has received from other neurons and decides whether to fire an action potential.
axonal varicosity: a swelling in an axon wall allowing neurotransmitter release through the wall via volume transmission.
axoplasmic transport: the movement of molecules in both directions along the outer
surface of protein bundles called microtubules.
basal dendrite: dendrite that horizontally branches out from the 30-μm base of the pyramid through the layer where the neuron resides.
basal forebrain: a cholinergic network located in the ventral frontal lobe and anterior hypothalamus that influences cerebral blood flow and cognitive activity.
basal ganglia: these forebrain structures consist of an egg-shaped nucleus
that contains the putamen and globus pallidus and a tail-shaped structure called the caudate,
which together are responsible for the production of movement. The basal ganglia have also been implicated in
obsessive-compulsive disorder, Parkinson’s disease, and Huntington’s chorea.
benzodiazepine receptor agonist (BZRA) hypnotics: nonbenzodiazepines like zolpidem (Ambien).
beta rhythm: 12-38-Hz activity associated with arousal and attention generated by brainstem mesencephalic reticular stimulation that depolarizes neurons in both the thalamus and cortex. The beta rhythm can be divided into multiple ranges: beta 1 (12-15 Hz), beta 2 (15-18 Hz), beta 3 (18-25 Hz), and beta 4 (25-38 Hz).
bilateral synchronous slow waves: a pathological sign observed in drowsy
children. When detected in alert adults, intermittent bursts of high amplitude slow waves may signify gray
matter lesions in deep midline structures.
bipolar disorder (BD): a mental health disorder characterized by extreme mood swings, including manic and depressive episodes. It is associated with abnormalities in brain regions involved in mood regulation, such as the prefrontal cortex and amygdala.
brain connectivity studies: research focused on understanding how different regions of the brain communicate with each other. These studies often use EEG data to map functional connections and require accurate signal interpretation to account for the effects of the skull and other tissues.
Broca's area: area located inferior frontal gyrus (BA 44 and 45) of the dominant hemisphere (F7-T3 in the left hemisphere) concerned with speech production, grammar, language comprehension, and sequencing.
Brodmann areas: 47 numbered cytoarchitectural zones of the cerebral cortex based on Nissl staining.
brain connectivity studies: research focused on understanding how different regions of the brain communicate with each other. These studies often use EEG data to map functional connections and require accurate signal interpretation to account for the effects of the skull and other tissues.
cancellous bone: also known as trabecular or spongy bone, it is found inside bones and is less dense and more porous than cortical bone. It offers slightly less resistance to electrical signals than cortical bone.
cation: a positive ion, for example, sodium (Na+).
caudal: away from the front of the head.
cell body or soma: contains machinery for cell life processes and receives and integrates EPSPs and IPSPs from axons generated by axosomatic synapses (junctions between axons and somas). The cell body of a typical neuron is 20 μm in diameter, and its spherical nucleus, which contains
chromosomes comprised of DNA, is 5-10 μm across.
central nervous system (CNS): the division of the nervous system that includes the brain, spinal cord, and retina.
central nucleus of the amygdala: the nucleus that orchestrates the nervous
system's response to essential stimuli by activating circuits in the brainstem (autonomic arousal) and the basal
ganglia and periaqueductal gray (defensive behavior).
central sulcus: fissure that separates the frontal and parietal lobes.
cerebral cortex: the layer of gray matter that covers the cerebral
hemispheres. The cerebral cortex consists of gray matter and white matter.
cerebral ventricles: a network of fluid-filled chambers that protects the brain from trauma due to abrupt head movements and facilitates the exchange of nutrients and wastes between blood vessels and the brain.
cerebrospinal fluid (CSF): fluid produced by the choroid plexus membrane of the lateral ventricles that fills the ventricular system.
chemical synapses: junctions between neurons that transmit molecules across
gaps of less than 300 angstroms. Neurons use chemical synapses to produce short-duration (milliseconds) and long-duration
(seconds to hours) changes in the nervous system. Chemical synapses are capable of more extensive communication and initiate more diverse and long-lasting changes than electrical synapses.
cingulate cortex: va part of the limbic system, the cingulate cortex is situated in the medial aspects of the frontal and parietal lobes, covering Brodmann areas 23, 24, 30, 31, and 33. It involves emotion processing, memory, attention, and cognitive control.
circle of Willis: vascular network located at the base of the brain comprised of the carotid and basilar arteries. This structure may provide another route for delivering blood when a major artery is compromised by disease or traumatic injury.
classical routes for EEG activation: specific sensory pathways like the visual
(retina to the visual cortex), auditory (cochlea to the auditory cortex), and somatosensory (chemoreceptors and
mechanoreceptors to the somatosensory cortex) systems. Increased transmission of information through these
pathways desynchronizes EEG activity in the cortical regions to which these afferent neurons project, as
specialized circuits of neurons independently process this information.
coherence: the degree of coupling between separate cortical regions and reflects neural network connectivity and dynamics. Coherence evaluates the linear association or correlation between the EEG waveforms recording from two different scalp locations (two referential montages).
commissures: axon tracts. The left and right hemispheres communicate using the
corpus callosum, anterior commissure, and posterior commissure.
co-modulation: the degree of association in the magnitude of signals detected from two different sources (sites). Co-modulation, which can be measured using the Pearson Product-Moment Correlation Coefficient, shows the degree to which signals strengthen and weak in a correlated manner.
complex: a sequence of waves.
COMT: a degrading enzyme that only targets the catecholamines dopamine and
norepinephrine.
connectivity: the degree of synchrony between the oscillations of specialized brain regions (nodes) within a network.
contingent negative variation (CNV): a steady, negative shift in potential (15
μV in young adults) detected at the vertex. This slow cortical potential may reflect expectancy,
motivation, intention to act, or attention. The CNV appears 200-400 ms after a warning signal (S1), peaks within
400-900 ms, and sharply declines after a second stimulus that requires the performance of a response (S2).
continuous irregular delta: slow waves produced by white matter lesions seen
in disorders like multiple sclerosis.
contralateral: structures that are located on opposite sides of the body. For
example, neurons in the left primary motor cortex control muscles on the right side of the body.
coronal plane: the plane that separates the body into front and back parts.
corpus callosum: the largest commissure that connects the left and right
frontal, parietal, and occipital lobes.
cortical bone: the dense, outer surface layer of bone that provides strength and rigidity. It is one of the two types of bone found in the skull and has high resistance to electrical signals.
corticothalamic network: a unified network that generates diverse types of brain
rhythms grouped by slow cortical oscillations.
cranial nerves: 12 pairs of nerves connected to the brain and are part of the sensory and motor systems of the head and neck.
cranium: the part of the skull that encloses the brain, composed of several bones fused together, including the frontal, parietal, temporal, and occipital bones.
cyclic AMP: a second messenger that moves about the neuron, activating other
enzymes. Protein kinase A, which controls the excitability of ion channels, is a crucial enzyme target of
cyclic AMP. Cyclic AMP also travels to the nucleus to regulate gene expression.
Dale's principle: the incorrect view that a neuron can only release one
neurotransmitter. They often release two to four.
delta rhythm: 0.05-3-Hz oscillationsgenerated by thalamocortical neurons during stage-3 sleep.
dendrite: a branched structure designed to receive messages from other neurons via axodendritic synapses (junctions between axons and dendrites), determining whether the axon hillock will initiate an action potential.
dendritic spines: protrusions on the dendrite shaft where axons typically form
axodendritic synapses.
dendrodendritic synapses: junctions between dendrites that communicate
chemically across synapses and electrically across gap junctions.
depolarize: to make the membrane potential more positive by making the inside
of the neuron more positive with respect to its outside.
desynchronization: the absence or loss of coordinated neuronal firing and synchronization of brain waves.
diencephalon: the posterior forebrain subdivision that contains the thalamus and hypothalamus.
diffusion: the distribution of molecules from areas of high concentration to
low concentration.
diphasic wave: a wave that contains both a negative and positive deflection from
the baseline.
dipole: the electrical field generated between the sink (where current enters the neuron) and the source (place at the other end of the neuron where current leaves) may be located anywhere along the dendrite.
distal: toward the periphery.
dominant frequency: EEG frequency with the greatest amplitude.
dopamine: a monoamine neurotransmitter that exerts its postsynaptic effects on at least six receptors linked to G proteins. This means that dopamine functions as a neuromodulator. The two major families include D1 (D1 and D5) and D2 (D2A, D2B, D3, and D4).
dorsal: toward the upper back or head.
dorsal anterior cingulate cortex (dACC): located in the dorsal region of the anterior cingulate cortex, the dorsal anterior cingulate cortex includes Brodmann areas 24 and 32. It plays a role in cognitive control, decision-making, and conflict monitoring.
dorsal entorhinal cortex (DEC): situated in the medial temporal lobe, the dorsal entorhinal cortex comprises parts of Brodmann area 28. It is involved in spatial memory and navigation.
dorsal stream (auditory): the pathway from the temporal to the parietal lobes that helps spatially localize sounds.
dorsal stream (visual): the pathway from the primary visual cortex (V1) to the parietal lobe that helps to localize objects and guide movements towards them.
dorsolateral prefrontal cortex (DLPFC): the region of the middle frontal gyrus (BA 9 and 4) that shares responsibility with cortical and subcortical networks for executive functions like abstract reasoning, cognitive flexibility, decision-making, inhibition, planning, and working memory (Miller & Cummings, 2007) and exercises the highest cortical level of motor control.
D-serine: a neurotransmitter that binds to the glycine site on the NMDA receptor
to trigger calcium entry into a dendritic spine when glutamate binds to its site, resulting in a large, prolonged
increase in intracellular calcium.
dual-action antidepressants: medications that activate 5-HT1 receptors to
produce antidepressant and anxiolytic effects, while they blockade 5-HT2 (agitation, restlessness, and sexual
dysfunction) and 5-HT3 (nausea, headache, and vomiting) receptors to minimize their side effects.
ectosplenial cerebral cortex: part of the retrosplenial cortex, the ectosplenial cerebral cortex is situated within the cingulate cortex and covers Brodmann area 29. It plays a role in spatial memory, navigation, and contextual processing.
EEG activity: a single wave or successive waves.
EEG power: the signal energy in the EEG spectrum. Most EEG power falls
within the 0-20 Hz frequency range. EEG power is measured in microvolts or picowatts.
efferent: a motoneuron that transmits information towards the periphery.
electrical synapse: a symmetrical synapse where neurons communicate information
bidirectionally across gap junctions between adjacent membranes using ions. Transmission across electrical
synapses is instantaneous, compared with the 10 ms or longer delay in chemical synapses. The rapid information
transmission that characterizes electrical synapses enables large circuits of distant neurons to synchronize their
activity and simultaneously fire.
electroencephalogram (EEG): the voltage difference between at least two
electrodes, where at least one electrode is located on the scalp or inside the brain. The EEG is a recording of
both EPSPs and IPSPs that occur primarily in dendrites in pyramidal cells located in macrocolumns, several mm in
diameter, in the upper cortical layers.
electrostatic pressure: the attractive or repulsive force between ions that
moves them from one region to another.
entorhinal cortex: a structure located in the caudal region of the temporal lobe and that receives pre-processed sensory information from all modalities and reports on cognitive operations. The entorhinal cortex provides the main input to the hippocampus, is involved in memory consolidation and spatial localization, and provides input into the septohippocampal system that may generate the 4-7 Hz theta rhythm.
enzymatic deactivation: the process in which an enzyme breaks a neurotransmitter
apart into inactive fragments. For example, acetylcholine transmission is ended by the enzyme acetylcholine
esterase (AChE). Deactivating enzymes located in the synaptic cleft degrade a neurotransmitter molecule when it detaches from its binding site.
evoked potential: an event-related potential (ERP) elicited by external sensory
stimuli (auditory, olfactory, somatosensory, and visual). An evoked potential has a negative peak at 80-90 ms and
a positive peak around 170 ms following stimulus onset. The orienting response ("What is it?") is a sensory
ERP. The N1-P2 complex in the auditory cortex of the temporal cortex reveals whether an uncommunicative person can
hear a stimulus.
excitatory postsynaptic potential (EPSP): a brief positive shift in a
postsynaptic neuron's potential produced when neurotransmitters bind to receptors and cause positive
sodium ions to enter the cell. An EPSP pushes the neuron towards the excitation threshold when it can initiate
an action potential.
executive functions: a set of cognitive processes, including working memory, flexible thinking, and self-control, that enable goal-directed behavior.
exocytosis: the process of neurotransmitter release. When an action potential
arrives and depolarizes the terminal button, calcium ions enter the terminal button from the extracellular fluid. Calcium binds with clusters of protein molecules that join the vesicles with the presynaptic membrane. The
clusters move apart, forming a hole through both membranes called a fusion pore, and the neurotransmitter leaves the
terminal button for the synaptic cleft or extracellular fluid.
exogenous ERP: an event-related potential (ERP) elicited by external sensory
stimuli (auditory, olfactory, somatosensory, and visual).
explicit learning: behavioral changes that occur with our conscious awareness
that require processing by the hippocampus.
extracellular dipole layers: macrocolumns of pyramidal cells, which lie
parallel to the surface of the cortex, send opposite charges towards the surface and the deepest of the 5-7 layers
of cortical neurons.
extracellular fluid: the fluid surrounding a neuron.
facultative pacemaker theory: Anderson and Anderson's (1968) theory that thalamic neurons activate cortical neurons and thalamic inhibitory interneurons via recurrent collaterals.
fast cortical potentials: EEG rhythms that range from 0.5 Hz-100 Hz. The main
frequency ranges include delta, theta, alpha, sensorimotor rhythm, and beta.
feature binding: the process of linking information to perceptual objects
(linking an apple's color to its shape) that may involve the 40-Hz rhythm.
fissures: deep grooves, for example, the lateral fissure.
focal waves: EEG waves detected within a limited area of the scalp,
cerebral cortex, or brain.
foramina: openings or holes in the skull that allow for the passage of nerves and blood vessels. These structures can create localized points where electrical signals might experience less attenuation.
forebrain: the anterior brain subdivision that consists of the cerebral hemispheres (telencephalon) and the thalamus and hypothalamus (diencephalon), also called the prosencephalon.
frequency: the number of cycles completed each second expressed in hertz (Hz).
frequency synchrony: when identical EEG frequencies are detected at two or
more electrode sites. For example, 12 Hz may be simultaneously detected at O1-A1 and O2-A2.
frontal lobes: the most anterior cortical lobes of the brain (F7, F3, Fz, F8, F4) that are divided
into the primary motor cortex, motor association cortex, Broca's area, and prefrontal cortex.
fusion pore: a hole through a vesicle and presynaptic membrane that allows
neurotransmitters to leave the terminal button for the synaptic cleft or extracellular fluid.
G protein: a protein located inside a neuron’s membrane next to a
metabotropic receptor, activated when the receptor binds a ligand. An alpha-subunit of the G protein then
breaks away to perform actions within the cell.
GABA: an amino acid that is often inhibitory. GABA may be the most
important inhibitory neurotransmitter in the brain. There are several types of GABA receptors, each producing inhibition differently.
gamma rhythms: a 28-80 Hz rhythm that includes the 38-42 Hz Sheer rhythm and is associated with learning and problem-solving, meditation, mental acuity, and peak brain function in children and adults.
gap junction: an electrical synapse, which is a symmetrical synapse where neurons communicate information bidirectionally across gap junctions between adjacent membranes using ions. Transmission across electrical synapses is instantaneous, compared with the 10-ms or longer delay in chemical synapses. The rapid information transmission that characterizes electrical synapses enables large circuits of distant neurons to synchronize their activity and simultaneously fire.
generalized asynchronous slow waves: waves seen in sleepy children
and those with elevated temperatures. This may indicate degenerative disease, dementia, encephalopathy, head injury, high fever, migraine, and Parkinson's disease in adults.
glial cells: nonneural cells that guide, insulate, and repair neurons and
provide structural, nutritional, and information-processing support. Glial cells generate slow cortical
potentials (SCPs). Glial cells include astrocytes, microglia, oligodendrocytes, radial glial cells, and Schwann
cells.
global loops: cortical macrocolumns separated by as much as 7 cm and receive shared input fire synchronously to generate delta and theta rhythms.
glutamate: an amino acid that is often excitatory and that may be the primary
excitatory neurotransmitter in the brain. Its receptors are found on the surface of almost all neurons. There are
at least 13 different receptors for glutamate, 5 ionotropic and 8 metabotropic. Most presynaptic neurons in the
brain excite postsynaptic neurons via ionotropic glutamate receptors in the postsynaptic membrane. Metabotropic
glutamate receptors may play a regulatory function, either augmenting or suppressing the activation of ionotropic
glutamate receptors.
glycine: an amino acid that is often inhibitory and has a binding
site on the NMDA receptor.
gray matter: brain tissue that looks grayish brown and comprises cell
bodies, dendrites, unmyelinated axons, glial cells, and capillaries.
gyrus: ridge of cortex demarcated by sulci or fissures, for example, the
precentral gyrus.
hertz (Hz): unit of frequency, an abbreviation for cycles per second.
high alpha (alpha 2): 10-12-Hz alpha associated with open awareness.
high beta (beta 4): 25-38-Hz activity mostly seen in the frontal lobes and is associated with hyper-perfusion and increased glucose metabolism. High or fast beta activity may be related to peak performance and cognitive processing and related to specificity and precision in information processing. Excessive high beta is associated with alcoholism, anxiety, OCD, rumination, and worry.
hindbrain: posterior brain division that consists of the cerebellum, pons, and medulla.
hippocampus: a seahorse-shaped limbic structure. The hippocampus is required to form declarative memories and plays a vital role in emotion, navigation, spatial memory, and dampening the endocrine stress response. The hippocampus also contains leukocyte receptors, making it part of the feedback loop for immune system regulation. Hippocampal neurons and networks that include it are sources of the theta rhythm.
horizontal (transverse) plane: the plane that divides the brain into upper and lower parts.
hubs: highly centralized nodes through which other node pairs communicate;
hubs allow efficient communication.
hyper-coherence: excessive coupling due to a failure to selectively activate cortical regions. Hyper-coherence may interfere with multitasking and rapid decision-making.
hypo-coherence: deficient coupling due to a breakdown in communication between regions that should generally communicate with each other. Hypo-coherence often results from traumatic brain injuries.
hyperpolarize: a negative shift in membrane potential (the inside becomes more
negative with respect to the outside) due to the loss of positive ions or gain of negative ions.
impedance: a measure of the opposition that a circuit presents to the passage of a current when a voltage is applied. In the context of EEG, the skull's impedance affects the transmission of electrical signals from the brain to the electrodes on the scalp.
inferior colliculi: midbrain structures that integrate information about spatial localization and multiple sensory modalities, including somatosensory information.
inhibitory postsynaptic potential (IPSP): a brief negative shift in a
postsynaptic neuron's potential produced when cations like potassium leave a neuron or anions (negative
ions) like chloride enter a neuron, which hyperpolarizes the cell. An IPSP pushes the neuron away from the
threshold of excitation.
insular cortex: cortex that lies deep within the lateral sulcus that divides the temporal and parietal lobes (BA 13). The insula is involved in emotional and autonomic responses to external stimuli and is part of the salience network.
integration: the addition of EPSPs and IPSPs at the axon hillock. Neurons sum
EPSPs and IPSPs over their surface in spatial integration and over ms of time in temporal
integration to raise the membrane from its resting potential to the excitation threshold. EPSPs and IPSPs
last from 15-200 ms, while action potentials occur in 1-2 ms.
internal carotid artery: a major paired artery that supplies blood to nearly two-thirds of the cerebral hemispheres.
interneurons: neurons that receive input from and distribute output to other
neurons. They have short processes and are confined to the central nervous system. They provide the integration
required for decisions, learning and memory, perception, planning, and movement.
intracellular fluid: the watery cytoplasm contained within a neuron.
ion: a charged atom or molecule with a positive or negative charge. Positive
ions are called cations, and negative ions are called anions.
ionotropic receptor: receptor protein that contains a binding site for a
ligand and an ion channel that opens when the neurotransmitter attaches to this site.
ipsilateral: structures that are located on the same side of the body. For
example, the left olfactory bulb distributes axons to the left hemisphere.
irregular waves: successive waves that constantly alter their shape and
duration.
kappa rhythm: bursts of alpha or theta and is detected over the temporal lobes
of subjects during cognitive activity.
lambda waves: saw-toothed transient waves from 20-50 mV in amplitude and
100-250 ms in duration detected over the occipital cortex during wakefulness. These positive deflections are
time-locked to saccadic movements and observed during visual scanning, as during reading.
lateral: to the side, away from the center, as in the lateral geniculate
nucleus.
lateral geniculate nucleus (LGN): thalamic nucleus that relays visual information to the cortex.
lateral nucleus of the amygdala: a nucleus that processes sensory information
and distributes it throughout the amygdala.
lateralized waves: waves that are primarily detected on one side of the scalp
and may indicate pathology.
Layers I-III: cortical layers that receive corticocortical afferent fibers
that connect the left and right hemispheres.
Layer III: the cortical layer that is the primary source of efferent
corticocortical fibers.
Layer IV: the cortical layer that is the primary destination of
thalamocortical afferents and intra-hemispheric corticocortical afferents.
Layer V: the cortical layer that is the primary origin of efferent fibers that
target subcortical structures that have motor functions.
Layer VI: the cortical layer that projects cortico-thalamic efferent fibers to
the thalamus, which, together with the thalamocortical afferents, creates a dynamic and reciprocal relationship
between these two structures.
left dorsolateral prefrontal cortex: the division of the prefrontal cortex
concerned with approach behavior and positive affect. It helps us select positive goals and organizes and
implements behavior to achieve these goals.
limbic system: a poorly-defined widespread network of nuclei involved in emotion, motivation, learning, memory, and navigation. Three important limbic structures are the hippocampus, amygdala, and septal nuclei.
local loops: neighboring cortical macrocolumns that share input generate frequencies above 30 Hz in the high-beta and gamma ranges.
local synchrony: synchrony that occurs when the coordinated firing of cortical neurons produces high-amplitude EEG signals.
localized slow waves: waves that may indicate a transient ischemic attack
(TIA) or stroke, migraine, mild head injury, or tumors above the tentorium. Deep lesions result in bilateral or
unilateral delta.
locus coeruleus system: the noradrenergic branch of the ascending reticular activating system that projects to the thalamus, limbic system, and cerebral cortex, and contributes to wakefulness and vigilance for salient stimuli. Subnormal norepinephrine transmission may contribute to ADHD.
long-latency potentials: potentials that have extended latencies following
stimulus onset, for example, P300 and N400 ERPs.
long-term depression (LTD): a persistent decrease in synaptic strength
following low-frequency stimulation.
long-term potentiation (LTP): a persistent increase in synaptic strength
following high-frequency stimulation.
low alpha (alpha 1): 8-10-Hz alpha below a client's peak alpha frequency when eyes are closed.
low-pass filter: a filter that allows signals with a frequency lower than a certain cutoff frequency to pass through and attenuates signals with frequencies higher than the cutoff frequency. The skull acts as a natural low-pass filter for EEG signals.
macrocolumns: circuits of cortical pyramidal neurons several millimeters in diameter
that create extracellular dipole layers parallel to the surface of the cortex, that send opposite charges towards
the surface and the deepest of the 5-7 layers of cortical neurons. Since the pyramidal neurons are all
aligned with the cortical surface, the postsynaptic potentials at cells within the same macrocolumn add together
because they have the same positive or negative charge. The macrocolumns fire synchronously.
Major Depressive Disorder (MDD): a psychological disorder characterized by persistent feelings of sadness, loss of interest, and other cognitive and physical symptoms. It is associated with abnormalities in brain regions such as the prefrontal cortex, amygdala, and hippocampus.
medial: toward the center of the body, away from the side. For example, the
medial geniculate nucleus.
medial geniculate nucleus (MGN): thalamic nucleus that projects to several cortical auditory areas using two separate pathways. The MGN mainly relays frequency, amplitude, and binaural information to the auditory cortex in the temporal lobe.
medial prefrontal cortex: the division of the prefrontal cortex that integrates
cognitive-affective information and helps control the hypothalamic–pituitary–adrenal (HPA) axis during
emotional stress.
membrane potential: a neuron’s electrical charge created by a difference
in ion distribution within and outside the neuron. A typical resting potential is about -70 mV
(thousandths of a volt) since the inside of a resting axon is more negatively charged than the outside.
meninges: three protective layers (dura mater, pia mater, and arachnoid) that enclose the brain and spinal cord.
mesocortical neurons: dopaminergic neurons that project from the ventral
tegmental area of the midbrain to the prefrontal cortex and excite prefrontal cortical neurons that control
working memory, planning, and strategy preparation for problem solving. Underactivity in this pathway is
associated with the negative symptoms of schizophrenia-like attentional deficits.
metabotropic receptors: include all G protein-linked receptors located on
neurons, including autoreceptors. Neurotransmitters that bind to G protein-linked receptors are often called
neuromodulators. Metabotropic receptors, which indirectly control the cell's operations, expend energy, and
produce slower, longer-lasting, and more diverse changes than ionotropic receptors. Their effects can last several
seconds, instead of milliseconds, because of the long-lived activity of G proteins and cyclic AMP.
metencephalon: the hindbrain subdivision that consists of the cerebellum and pons.
microtubules: hollow cylindrical protein bundles that are involved in
axoplasmic transport.
midbrain: the middle division called the mesencephalon, which includes the inferior colliculi, superior colliculi, and substantia nigra.
mirror neurons: neurons activated when we perform a movement or observe others perform the same activity. Mirror neurons may facilitate observational learning, understanding others' actions and intentions, and empathy.
modulating effects: neuromodulators like the monoamines alter the performance
of diffuse networks of target neurons by indirectly controlling cellular operations when they bind to metabotropic
receptors.
module: a set of interconnected nodes in a neural network.
monoamine neurotransmitters: amine neurotransmitters that include
dopamine, norepinephrine, epinephrine (catecholamines), and serotonin (indoleamine). These neurotransmitters
are released using volume transmission and generally have modulating effects, altering the performance of diffuse
networks of target neurons.
monoamine oxidase (MAO): an enzyme that degrades and inactivates the monoamine
neurotransmitters dopamine, norepinephrine, and serotonin.
monoamine oxidase inhibitors (MAOIs): antidepressant drugs that interfere with
MAO's breakdown of monoamines and increase monoamine availability to treat clinical depression.
monophasic wave: either a single negative (upward) or positive (downward)
deflection from baseline.
motor cortex: a subdivision of the frontal lobe located in the
precentral gyrus and guides fine motor coordination (like writing).
motor ERPs: event-related potentials detected over the primary motor cortex
(precentral gyrus) during movement. Their amplitude is proportional to the force and rate of skeletal muscle
contraction.
motor nerves: efferent neurons that convey commands to glands, muscles, and
other neurons.
movement-related potentials (MRPs): slow cortical potentials that occur at 1
second as subjects prepare for unilateral voluntary movements. MRPs are distributed bilaterally with maximum
amplitude at Cz. The supplementary motor area and primary motor and somatosensory cortices primarily generate
these potentials.
mu rhythm: 7-11-Hz waves resemble wickets and appear as several-second trains over central or centroparietal sites (C3 and C4).
multiple spike-and-slow-wave complex: multiple spikes associated with at least
one slow wave.
muscarinic receptors: metabotropic ACh receptors that are stimulated by
muscarine and blocked by atropine. Muscarinic receptors control smooth muscle and predominate in the CNS. In the
CNS, muscarinic receptors help mediate learning, memory, attention, arousal, EEG, and postural control.
myelencephalon: the hindbrain subdivision that consists of the medulla.
myelinated axons: axons insulated by myelin by oligodendrocytes in
the central nervous system and Schwann cells in the peripheral nervous system.
N1-P2: a sensory event-related potential in the auditory cortex of the
temporal cortex that reveals whether an uncommunicative person can hear a stimulus.
N400 potential: an event-related potential (ERP) elicited when we encounter
semantic violations like ending a sentence with a semantically incongruent word ("The handsome prince married
the beautiful fish"), or when the second word of a pair is unrelated to the first (BATTLE/GIRL).
negative SCPs: slow cortical potentials produced by glial cells that increase
the probability of neuron firing.
nerve: bundled axons outside of the central nervous system.
neural network: a system of interconnected ensembles of neurons that collaborate to achieve a goal. These networks communicate and perform functions via hub- or node-based communication systems.
neuroaxis: an imaginary line that runs centrally through the central nervous
system (CNS) from the front of the prefrontal cortex to the base of the spinal cord.
neuromodulator: neurochemical that modifies the effect of neurotransmitters
through mechanisms like binding to metabotropic receptors.
neuron: a nerve cell that is the fundamental anatomical unit of the nervous
system.
nicotinic ACh receptor: an ionotropic receptor that is stimulated by nicotine and
blocked by curare. They are mainly found in the PNS on skeletal muscles. At CNS axoaxonic synapses, they produce
presynaptic facilitation (increase neurotransmitter release). In the CNS, nicotinic receptors help regulate
cortical blood flow, anxiety reduction, and decision-making.
nigrostriatal pathway: a dopaminergic pathway from the substantia nigra to the
basal ganglia (caudate nucleus and putamen) that controls movement. The nigrostriatal pathway is progressively
destroyed in Parkinson’s disease.
nitric oxide: a gaseous retrograde transmitter that is involved in long-term
potentiation (LTP).
NMDA (glutamate) receptors: ligand-gated and voltage-gated glutamate receptors
that bind the glutamate agonist NMDA. NMDA receptors play an important role in long-term potentiation (LTP).
node: a vertex within a neural network.
nodes of Ranvier: gaps between myelinated axon segments where the axon
membrane is exposed to extracellular fluid and action potentials are regenerated by sodium ion entry.
norepinephrine: a monoamine neurotransmitter that exerts postsynaptic effects at
alpha and beta receptors, each with two subtypes. All norepinephrine receptors are G protein-linked. The
cell bodies of the most critical noradrenergic system are located in the locus coeruleus, a nucleus found in the
dorsal pons.
nucleus accumbens: a limbic structure that receives dopamine released by
the mesolimbic pathway. The nucleus accumbens plays a critical role in reinforcing diverse activities,
including ingestion of drugs like central nervous system stimulants.
nucleus reticularis: a thalamic nucleus that may function as a pacemaker by releasing the inhibitory transmitter GABA at synapses with thalamocortical neurons.
occipital lobes: cortical lobes (Oz, O1, O2) posterior to the parietal lobes. The primary visual cortex (VI) is located within the calcarine sulcus (BA 17). They
process visual information from the eyes in collaboration with the frontal, parietal, and temporal
lobes.
odd-ball stimulus: a meaningful stimulus that is different from others in a
series used to elicit the P300 potential. For example, a colored playing card is presented in a series of monochrome
cards.
open awareness: the ability to adaptively respond to various environmental changes.
orbitofrontal cortex (OFC): the frontal lobe subdivision (BA 10, 11, and 47) that may aid planning by evaluating the consequences (rewards and punishments) of our actions and helping to generate the motivation to ingest drugs. The OFC appears to adjust decision-making based on the stakes involved and enables us to switch between substantial (investments) and trivial (snacks) choices.
orienting response: Pavlov’s "What is it?" reaction to stimuli
like the sound of a vase crashing that includes (1) increased sensory sensitivity, (2) head (and ear) turning
toward the stimulus, (3) increased muscle tone (reduced movement), (4) EEG desynchrony, (5) peripheral
constriction and cephalic vasodilation, (6) a rise in skin conductance, (7) heart rate slowing, and (8) slower,
deeper breathing.
P300 potential: an event-related potential (ERP) with a 300-900 ms latency and
greatest positive peaks located over parietal lobe sites. The P300 potential may reflect an event’s
subjective probability, meaning, and transmission of information.
panic disorder (PD): an anxiety disorder characterized by recurrent, unexpected panic attacks and persistent concern about future attacks. It involves dysfunction in brain regions such as the amygdala and prefrontal cortex.
parahippocampal gyri: structures located within the medial temporal lobe that form spatial and nonspatial contextual associations, which serve as building blocks for contextual processing, episodic memory, navigation, and scene processing. They may also play a role in emotional responsiveness.
parietal lobes: cortical lobes (Pz, P3, P4) posterior to the frontal lobes divided
into the primary somatosensory cortex (postcentral gyrus) and secondary somatosensory cortex. Their primary function
is to process somatosensory information like pain and touch.
perception-action cycles: cognitive and emotional processes that adapt (and preadapt) us to our environment.
peripheral nervous system (PNS): autonomic and somatic nervous system neurons and nerves outside the skull and spinal cord.
phase: the degree to which the peaks and valleys of EEG waveforms
coincide. Phase measures the time shift between EEG activity in two brain regions.
phase reset: a sudden change in phase difference (phase shift duration or SD) followed by a period of phase locking (lock duration or LD). PR = SD + LDs.
phase synchrony: synchrony when identical EEG frequencies are detected at two
or more electrode sites, and the peaks and valleys of the EEG waveforms coincide. This is also called global
synchrony. For example, EEG training may produce phase-synchronous 12-Hz alpha waves at O1-A1 and O2-A2.
polyphasic (multiphasic) wave: a wave that contains two or more deflections of
opposite polarity from baseline.
positive SCPs: slow cortical potentials produced by glial cells that
decrease the probability of neuron firing.
Post-Traumatic Stress Disorder (PTSD): a psychological condition triggered by experiencing or witnessing a traumatic event. It involves dysfunction in brain regions such as the amygdala, hippocampus, and prefrontal cortex.
postcentral gyrus: primary somatosensory cortex, posterior to the central sulcus.
posterior: near or toward the back of the head.
posterior basic rhythm: posterior alpha rhythm associated with IQ and memory performance.
posterior cerebral arteries: the left and right posterior arterial branches of the basilar artery that supply blood to the posterior cerebral hemispheres, cerebellum, and brainstem.
posterior commissure: axon tracts located below the corpus callosum
connect the right and left diencephalon and mesencephalon.
posterior cortex: parietal, temporal, and occipital cortical areas concerned with perception and memory.
precentral gyrus: primary motor cortex, anterior to the central sulcus.
prefrontal cortex (PFC): the most anterior frontal lobe division (BA 9, 10, 11, 12, 46, 47) that is subdivided
into dorsolateral, medial, orbitofrontal, and anterior cingulate regions and is responsible for executive
functions like attention, working memory, prediction of the outcomes of current and hypothetical actions, the ability to work toward goals, problem-solving, planning, and the ability to suppress actions that could lead to unwanted outcomes.
premotor cortex (motor association cortex): the frontal lobe subdivision (BA 6) that is anterior to the motor cortex
and helps to program and execute head, trunk, and limb movements.
presynaptic facilitation: a modulatory process in which a neuron increases the
presynaptic neuron's neurotransmitter release by delivering a neurotransmitter that increases calcium ion entry
into its terminal button.
presynaptic inhibition: a modulatory process in which a neuron decreases
neurotransmitter release by reducing calcium ion entry.
primary motor cortex: the frontal lobe region located along the precentral gyrus (BA 4) that organizes the opposite side of the body's muscles and movements required for fine motor coordination in tasks like writing. Lesions can result in loss of motor control, including rigid paralysis.
primary somatosensory cortex (S1): parietal lobe subdivision located in the parietal lobe's postcentral gyrus posterior to the central sulcus (BA 3, 1, and 2). S1 maps touch and pain information from the opposite side of the body.
primary visual cortex (V1): the occipital lobe region (also called striate cortex) which receives most visual information from the lateral geniculate nucleus of the thalamus.
protein kinase A: an intracellular enzyme that controls the excitability of
ion channels and is a vital enzyme target of cyclic AMP.
raphe system: the midline network of cell bodies within the brainstem and midbrain that may influence alertness and vigilance through reciprocal connections with the suprachiasmatic nucleus of the hypothalamus.
rate law: the principle that neurons represent the intensity of a stimulus by
variation in the rate of axon firing.
readiness potential: slow-rising, negative potential (10-15 μV)
detected at the vertex before voluntary and spontaneous movement. This slow cortical potential precedes voluntary
action by 0.5 to 1 s and peaks when the subject responds.
regional loops: cortical macrocolumns that share input and are separated by several centimeters generate alpha and beta rhythms.
regular or monomorphic waves: successive waves with identical shapes.
Regular waves may resemble sine waves (sinusoidal) or maybe arched (resembling wickets), or saw-toothed
(asymmetrical and triangular).
resonant loop: the synchronous firing by macrocolumns that share afferent input to generate an electrical potential.
resting potential: the membrane potential of a neuron when it is not influenced by
messages from other neurons.
reticular activating system (RAS): a network of 90 nuclei within the central brainstem from
the lower medulla to the upper midbrain. The reticular formation sends axons to the spinal cord, thalamus, and cortex, contributing to diverse functions like neurological reflexes, muscle tone and movement, attention, arousal, and sleep.
reuptake: the primary method that neurons terminate the action of
neurotransmitters. Reuptake transporters located in terminal buttons and astrocytes remove neurotransmitters from
the synaptic cleft.
reward deficiency syndrome: Blum’s hypothesis that an abnormal form of
the A1 allele is present in most severe alcoholics and results in defective D2 receptors. Reduced D2 receptor
activity may reduce the activation of the nucleus accumbens and hypothalamus and result in dysphoria, drug
craving, and compulsive drug-seeking and abuse.
rhythmic slow wave activity: a posterior waveform generated by the limbic system and thalamus that is mostly seen in the frontal-midline (FCz) when awake with eyes open.
right dorsolateral prefrontal cortex: division of the prefrontal cortex that
organizes withdrawal-related behavior and negative affect and mediates threat-related vigilance. It plays a role
in working memory for object location.
rostral: toward the front of the head.
sagittal plane: the plane that divides the body into right and left halves.
saltatory conduction: action potential conduction in myelinated axons in which
action potentials jump from node to node for 200 times greater speed.
secondary somatosensory cortex (S2): the region of the parietal lobe adjacent to S1 (BA 40 and 43), receives projections from it and maps touch and pain from both sides of the body.
sensorimotor rhythm (SMR): 13-15 Hz (beta 1) rhythm that is located
over the sensorimotor strip (C3, Cz, C4). The waves are synchronous. SMR increases with stillness and decreases with movement. Deficient SMR may be observed in movement spectrum complaints like hyperactivity and tics.
sensorimotor system: in Sterman’s model, ascending pathways that convey
information about touch and proprioception to the thalamus, the thalamus and its thalamic projections to the
sensorimotor cortex, and the sensorimotor cortex, and its efferent fibers.
sensory event-related potentials (ERPs): event-related potentials evoked by external sensory
stimuli (auditory, olfactory, somatosensory, and visual). These evoked potentials or exogenous ERPs have a
negative peak around 80-90 ms and a positive peak about 170 ms following stimulus onset. These changes in brain activity in response to
specific stimuli. ERPs can be detected throughout the cortex. Investigators monitor
ERPs by placing electrodes at locations like the midline (Fz, Cz, and Pz). A computer analyzes a subject's EEG
responses to the same stimulus or task over many trials to subtract random EEG activity. ERPs always have the same
waveform morphology. Their negative and positive peaks occur at regular intervals following the stimulus.
sensory nerves: neurons specialized for sensory intake. They are called
afferent because they transmit sensory information towards the central nervous system.
septal nuclei: a limbic structure that contains several nuclei involved in emotion, control of aggressive behavior, reward, and addiction. The septohippocampal system contributes to the theta rhythm.
septohippocampal system: a subcortical circuit from the septum to the hippocampus
that contributes to 4-7 Hz theta activity.
septum: a limbic structure that contains several nuclei involved in emotion and
addiction and control of aggressive behavior.
sharp transients: a sequence that contains several sharp waves.
sharp waves: waves that resemble spikes with a pointed peak with a longer
70-200-ms duration.
sink: a site where current enters the neuron. Positive sodium ion entry into a
neuron creates an active sink, represented by -ve.
slow cortical potentials (SCPs): gradual changes in the membrane potentials of
cortical dendrites that last from 300 ms to several seconds. These potentials include the contingent negative
variation (CNV), readiness potential, movement-related potentials (MRPs), and P300 and N400 potentials. SCPs
modulate the firing rate of cortical pyramidal neurons by exciting or inhibiting their apical dendrites. They
group the classical EEG rhythms using these synchronizing mechanisms.
sodium (Na+) ions: positive ions that enter a neuron during EPSPs
and action potentials.
sodium-potassium transporters: pumps that are powered by ATP and that exchange
three sodium for two potassium ions.
soma or cell body: the part of a neuron that contains machinery for cell life processes and receives and integrates EPSPs and IPSPs from axons generated by axosomatic synapses (junctions between axons and somas). The cell body of a typical neuron is 20
μm in diameter, and its spherical nucleus, which contains chromosomes comprised of DNA, is 5-10 μm
across.
somatic nervous system: spinal nerves that innervate somatosensory receptors in the skin, joints, and skeletal muscles.
source: the place at the end of the neuron opposite of the sink where current
leaves. The source is symbolized by +ve. The extracellular area surrounding the source becomes electrically
positive.
source localization: a method used in EEG analysis to determine the origin of electrical activity within the brain. Accurate source localization requires accounting for the attenuation and distortion of signals caused by the skull and other tissues.
spatial summation: the addition of EPSPs and IPSPs over a neuron’s
surface.
spike: a negative transient with a pointed peak at conventional paper speeds,
20-70 ms duration, and 40-100 μV amplitude.
spike-and-slow-wave complex: a spike followed by a higher amplitude
slow wave at 3 Hz. In an absence seizure, the amplitudes are very high (e.g., 160 μV).
spinal cord: the column of neurons and glial cells within the vertebral canal that extend from the brainstem to the lumbar vertebrae. The spinal cord distributes sensory information from the body to the brain, and CNS commands from the brain to the body. The spinal cord also contains networks that control reflexes and central pattern generators.
spinal nerve: 31 pairs of nerves that exit the spinal cord.
spindle waves: waves that originate in the thalamus and occur during
unconsciousness and stage-2 sleep.
striatal: basal ganglia (caudate nucleus and putamen).
stroke: cerebrovascular accident (CVA) involves the destruction of brain tissue (infarction) due to cerebral hemorrhage and cerebral ischemia affecting blood vessels that supply the brain. CVAs show abrupt onset and involve temporary or permanent neurological symptoms like aphasia, paralysis, or loss of sensation.
Stroop test: cognitive monitoring task where color and names conflict.
substance use disorder (SUD): a condition characterized by the harmful or hazardous use of psychoactive substances, including alcohol and illicit drugs. It involves dysregulation in reward pathways and prefrontal cortex functioning.
substantia nigra: the midbrain structure that projects to the basal ganglia (caudate nucleus and putamen) to control movement and is progressively destroyed in Parkinson’s disease.
sulcus: a shallow groove in the surface of the cerebral hemisphere, for
example, the central sulcus.
superior colliculus: the dorsal midbrain structure that receives visual information and directs visual gaze and attention to selected stimuli.
superior olivary nuclei: midbrain structures that process binaural information to localize sound.
sutures: fibrous joints that connect the bones of the skull. These joints are immovable and allow for the growth of the skull in children and adolescents.
Sylvian fissure: deep fissure that serves as the upper boundary of the temporal lobe.
synapse-associated polyribosome complexes (SPRCs): organelles with dendrites
that can produce proteins that allow rapid remodeling of synapses. A polyribosome complex consists of several
ribosomes bound to messenger RNA (mRNA). SPRCs represent one mechanism underlying synaptic plasticity.
synaptic cleft: 20-40 nm fluid-filled gap between presynaptic and postsynaptic
structures.
synchronous: adverb meaning that groups of neurons depolarize and
hyperpolarize simultaneously.
synchronous "alpha": network-wide "alpha" that integrates perception and facilitates action. This distributed activity appears to block localized alpha-like patterns such as mu and the posterior rhythm in favor of more broadly distributed network integration.
synchrony: the coordinated firing of pools of neurons. EEG signals can display
local synchrony, frequency synchrony, and phase synchrony.
telencephalon: the frontal forebrain subdivision that consists of the
cerebral cortex, basal ganglia, and limbic system.
temporal summation: the addition of EPSPs and IPSPs over time. Summation is
more effective when postsynaptic potentials are generated more closely in time.
temporal lobes: lobes separated from the rest of the cortical lobes by the Sylvian fissure (BA 15, 20, 21, 22, 37, 38, 39, 40, 52). The temporal lobes process hearing, smell, and taste information and help us understand spoken language and recognize visual objects and faces.
terminal buttons: buds located on the ends of axon branches that form synapses
and release neurochemicals to other neurons. They contain vesicles that store neurotransmitters for release when
an action potential arrives. A terminal button’s presynaptic membrane may have reuptake transporters that
return neurotransmitters from the synapse or extracellular space for repackaging.
thalamus: the forebrain structure above the hypothalamus that consists of specialized nuclei that process and relay data to and from the telencephalon (cerebral cortex, basal ganglia, and limbic system). The thalamus analyzes all sensory data except olfaction before distributing this information to the cortex via thalamocortical afferent fibers. The thalamus contributes to SCPs, delta, theta, alpha, SMR activity, and beta-gamma activity.
theta rhythm: 4-8-Hz rhythms generated a cholinergic septohippocampal system that receives input from the ascending reticular formation and a noncholinergic system that originates in the entorhinal cortex, which corresponds to Brodmann areas 28 and 34 at the caudal region of the temporal lobe.
threshold of excitation: the membrane potential at which an axon initiates an
action potential, nominally -40 mV.
transient: a single wave or sequence of regular waves, called a complex,
distinguishable from background EEG activity.
triphasic wave: a wave that contains three deflections from baseline.
unmyelinated axons: smaller-diameter axons without fatty insulation that
conduct more slowly than myelinated axons.
+ve: The source is the place at the other end of the neuron where the current
leaves. The source is symbolized by +ve.
-ve: A sink is where the current enters the neuron. Positive sodium ion entry into
a neuron creates an active sink, symbolized by -ve.
ventral: toward the base of the skull or front of the body.
ventral posterior nucleus (VPN): a thalamic nucleus that receives somatosensory information following crossover at the medulla and projects to the primary somatosensory cortex (S1).
ventral stream (auditory): the subcortical auditory pathway to the auditory cortex that appears to analyze sound components, including speech sounds.
ventral stream (visual): the pathway from the primary visual cortex (V1) to the inferior temporal and frontal areas that allows us to identify objects and faces.
ventral striatum: the olfactory tubercle and nucleus accumbens.
ventral tegmental area: the midbrain structure that distributes dopaminergic axons
to the nucleus accumbens. Serotonin receptors on endorphin-releasing neurons in the hypothalamus may increase the
activity of dopaminergic reward pathways by inhibiting the release of GABA at receptors on cell bodies of the
ventral tegmental area neurons.
ventromedial prefrontal cortex (VMPFC): the ventromedial reward network (BA 10, 14, 25, 32, and parts of 11, 12, and 13) implicated in making decisions where the outcomes are uncertain and where moral values must be applied to actual situations.
vigilance system: in Sterman’s model, a system that consists of both
specific brainstem nuclei (e.g., locus coeruleus and raphe nuclei) and their diffuse connections with the
thalamus and other subcortical structures, and the cortex. Several neurotransmitter systems mediate vigilance,
including cholinergic/glutamatergic (reticular formation), noradrenergic (locus coeruleus), and serotonergic
(raphe) neurons.
volume conduction: the movement of the EEG through body tissues and interstitial fluid to the scalp.
volume transmission: extrasynaptic neurotransmitter release from axonal
varicosities, dendrites, and terminal button into the extracellular space. Monoamines like norepinephrine and
serotonin are released outside the synaptic cleft.
waveform: the shape and form of an EEG signal.
Wernicke's area: area of the temporoparietal cortex (BA 22) of the dominant hemisphere specialized for speech perception and production. Damage can result in an inability to understand the meaning of speech and construct intelligible sentences.
white matter: the layer beneath the cortex that mainly consists of myelinated
axons.
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