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Default mode network

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Default mode network
 
fMRI scan showing regions of the default mode network; the dorsal medial prefrontal cortex, the posterior cingulate cortex, the precuneus and the angular gyrus
Anatomical terminology
 
Default mode network connectivity. This image shows main regions of the default mode network (yellow) and connectivity between the regions color-coded by structural traversing direction (xyz → rgb).[1][2]

In neuroscience, the default mode network (DMN), also known as the default network, default state network, or anatomically the medial frontoparietal network (M-FPN), is a large-scale brain network primarily composed of the dorsal medial prefrontal cortex, posterior cingulate cortex, precuneus and angular gyrus. It is best known for being active when a person is not focused on the outside world and the brain is at wakeful rest, such as during daydreaming and mind-wandering. It can also be active during detailed thoughts related to external task performance.[3] Other times that the DMN is active include when the individual is thinking about others, thinking about themselves, remembering the past, and planning for the future.[4][5] The DMN creates a coherent "internal narrative" control to the construction of a sense of self.[6]

The DMN was originally noticed to be deactivated in certain goal-oriented tasks and was sometimes referred to as the task-negative network,[7] in contrast with the task-positive network. This nomenclature is now widely considered misleading, because the network can be active in internal goal-oriented and conceptual cognitive tasks.[8][9][10][11] The DMN has been shown to be negatively correlated with other networks in the brain such as attention networks.[12]

Evidence has pointed to disruptions in the DMN of people with Alzheimer's disease and autism spectrum disorder.[4] Psilocybin produces the largest changes in areas of the DMN associated with neuropsychiatric disorders.[13]

History

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Hans Berger, the inventor of the electroencephalogram, was the first to propose the idea that the brain is constantly busy. In a series of papers published in 1929, he showed that the electrical oscillations detected by his device do not cease even when the subject is at rest. However, his ideas were not taken seriously, and a general perception formed among neurologists that only when a focused activity is performed does the brain (or a part of the brain) become active.[14]

But in the 1950s, Louis Sokoloff and his colleagues noticed that metabolism in the brain stayed the same when a person went from a resting state to performing effortful math problems, suggesting active metabolism in the brain must also be happening during rest.[4] In the 1970s, David H. Ingvar and colleagues observed blood flow in the front part of the brain became the highest when a person is at rest.[4] Around the same time, intrinsic oscillatory behavior in vertebrate neurons was observed in cerebellar Purkinje cells, inferior olivary nucleus and thalamus.[15]

In the 1990s, with the advent of positron emission tomography (PET) scans, researchers began to notice that when a person is involved in perception, language, and attention tasks, the same brain areas become less active compared to passive rest, and labeled these areas as becoming "deactivated".[4]

In 1995, Bharat Biswal, a graduate student at the Medical College of Wisconsin in Milwaukee, discovered that the human sensorimotor system displayed "resting-state connectivity," exhibiting synchronicity in functional magnetic resonance imaging (fMRI) scans while not engaged in any task.[16][17]

Later, experiments by neurologist Marcus E. Raichle's lab at Washington University School of Medicine and other groups[18] showed that the brain's energy consumption is increased by less than 5% of its baseline energy consumption while performing a focused mental task. These experiments showed that the brain is constantly active with a high level of activity even when the person is not engaged in focused mental work. Research thereafter focused on finding the regions responsible for this constant background activity level.[14]

Raichle coined the term "default mode" in 2001 to describe resting state brain function;[19] the concept rapidly became a central theme in neuroscience.[20] Around this time the idea was developed that this network of brain areas is involved in internally directed thoughts and is suspended during specific goal-directed behaviors. In 2003, Greicius and colleagues examined resting state fMRI scans and looked at how correlated different sections in the brain are to each other. Their correlation maps highlighted the same areas already identified by the other researchers.[21] This was important because it demonstrated a convergence of methods all leading to the same areas being involved in the DMN. Since then other networks have been identified, such as visual, auditory, and attention networks. Some of them are often anti-correlated with the default mode network.[12]

Until the mid-2000s, researchers labeled the default mode network as the "task-negative network" because it was deactivated when participants had to perform external goal-directed tasks.[7] DMN was thought to only be active during passive rest and inactive during tasks. However, more recent studies have demonstrated the DMN to be active in certain internal goal-directed tasks such as social working memory and autobiographical tasks.[8]

Around 2007, the number of papers referencing the default mode network skyrocketed.[22] In all years prior to 2007, there were 12 papers published that referenced "default mode network" or "default network" in the title; however, between 2007 and 2014 the number increased to 1,384 papers. One reason for the increase in papers was the robust effect of finding the DMN with resting-state scans and independent component analysis (ICA).[18][23] Another reason was that the DMN could be measured with short and effortless resting-state scans, meaning they could be performed on any population including young children, clinical populations, and nonhuman primates.[4] A third reason was that the role of the DMN had been expanded to more than just a passive brain network.[4]

Anatomy

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Graphs of the dynamic development of correlations between brain networks. (A) In children the regions are largely local and are organized by their physical location; the frontal regions are highlighted in light blue. (B) In adults the networks become highly correlated despite their physical distance; the default network is highlighted in light red.[24] This result is now believed to have been confounded by artifactual processes attributable to the tendency of younger subjects to move more during image acquisition, which preferentially inflates estimates of connectivity between physically proximal regions (Power 2012, Satterthwaite 2012).

The default mode network is an interconnected and anatomically defined[4] set of brain regions. The network can be separated into hubs and subsections:

Functional hubs:[25] Information regarding the self

  • Posterior cingulate cortex (PCC) & precuneus: Combines bottom-up (not controlled) attention with information from memory and perception. The ventral (lower) part of PCC activates in all tasks which involve the DMN including those related to the self, related to others, remembering the past, thinking about the future, and processing concepts plus spatial navigation. The dorsal (upper) part of PCC involves involuntary awareness and arousal. The precuneus is involved in visual, sensorimotor, and attentional information.
  • Medial prefrontal cortex (mPFC): Decisions about self-processing such as personal information, autobiographical memories, future goals and events, and decision making regarding those personally very close such as family. The ventral (lower) part is involved in positive emotional information and internally valued reward.
  • Angular gyrus: Connects perception, attention, spatial cognition, and action and helps with parts of recall of episodic memories.

Dorsal medial subsystem:[25] Thinking about others

Medial temporal subsystem:[25] Autobiographical memory and future simulations

The default mode network is most commonly defined with resting state data by putting a seed in the posterior cingulate cortex and examining which other brain areas most correlate with this area.[21] The DMN can also be defined by the areas deactivated during external directed tasks compared to rest.[19] Independent component analysis (ICA) robustly finds the DMN for individuals and across groups, and has become the standard tool for mapping the default network.[18][23]

It has been shown that the default mode network exhibits the highest overlap in its structural and functional connectivity, which suggests that the structural architecture of the brain may be built in such a way that this particular network is activated by default.[1] Recent evidence from a population brain-imaging study of 10,000 UK Biobank participants further suggests that each DMN node can be decomposed into subregions with complementary structural and functional properties. It has been a widespread practice in DMN research to treat its constituent nodes to be functionally homogeneous, but the distinction between subnodes within each major DMN node has mostly been neglected. However, the close proximity of subnodes that propagate hippocampal space-time outputs and subnodes that describe the global network architecture may enable default functions, such as autobiographical recall or internally-orientated thinking.[27]

In the infant's brain, there is limited evidence of the default network, but default network connectivity is more consistent in children aged 9–12 years, suggesting that the default network undergoes developmental change.[12]

Functional connectivity analysis in monkeys shows a similar network of regions to the default mode network seen in humans.[4] The PCC is also a key hub in monkeys; however, the mPFC is smaller and less well connected to other brain regions, largely because human's mPFC is much larger and well developed.[4]

Diffusion MRI imaging shows white matter tracts connecting different areas of the DMN together.[22] The structural connections found from diffusion MRI imaging and the functional correlations from resting state fMRI show the highest level of overlap and agreement within the DMN areas.[1] This provides evidence that neurons in the DMN regions are linked to each other through large tracts of axons and this causes activity in these areas to be correlated with one another. From the point of view of effective connectivity, many studies have attempted to shed some light using dynamic causal modeling, with inconsistent results. However, directionality from the medial prefrontal cortex towards the posterior cingulate gyrus seems confirmed in multiple studies, and the inconsistent results appear to be related to small sample size analysis.[28]

Function

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The default mode network is thought to be involved in several different functions:

It is potentially the neurological basis for the self:[22]

  • Autobiographical information: Memories of collection of events and facts about one's self
  • Self-reference: Referring to traits and descriptions of one's self
  • Emotion of one's self: Reflecting about one's own emotional state

Thinking about others:[22]

  • Theory of mind: Thinking about the thoughts of others and what they might or might not know
  • Emotions of others: Understanding the emotions of other people and empathizing with their feelings
  • Moral reasoning: Determining a just and an unjust result of an action
  • Social evaluations: Good-bad attitude judgements about social concepts
  • Social categories: Reflecting on important social characteristics and status of a group
  • Social isolation: A perceived lack of social interaction[29]

Remembering the past and thinking about the future:[22]

  • Remembering the past: Recalling events that happened in the past
  • Imagining the future: Envisioning events that might happen in the future
  • Episodic memory: Detailed memory related to specific events in time
  • Story comprehension: Understanding and remembering a narrative
  • Replay: Consolidating recently acquired memory traces[30]

The default mode network is active during passive rest and mind-wandering[4] which usually involves thinking about others, thinking about one's self, remembering the past, and envisioning the future rather than the task being performed.[22] Recent work, however, has challenged a specific mapping between the default mode network and mind-wandering, given that the system is important in maintaining detailed representations of task information during working memory encoding.[31] Electrocorticography studies (which involve placing electrodes on the surface of a subject's cerebral cortex) have shown the default mode network becomes activated within a fraction of a second after participants finish a task.[32] Additionally, during attention demanding tasks, sufficient deactivation of the default mode network at the time of memory encoding has been shown to result in more successful long-term memory consolidation.[33]

Studies have shown that when people watch a movie,[34] listen to a story,[35][36] or read a story,[37] their DMNs are highly correlated with each other. DMNs are not correlated if the stories are scrambled or are in a language the person does not understand, suggesting that the network is highly involved in the comprehension and the subsequent memory formation of that story.[36] The DMN is shown to even be correlated if the same story is presented to different people in different languages,[38] further suggesting the DMN is truly involved in the comprehension aspect of the story and not the auditory or language aspect.

The default mode network is deactivated during some external goal-oriented tasks such as visual attention or cognitive working memory tasks.[7] However, with internal goal-oriented tasks, such as social working memory or autobiographical tasks, the DMN is positively activated with the task and correlates with other networks such as the network involved in executive function.[8] Regions of the DMN are also activated during cognitively demanding tasks that require higher-order conceptual representations.[10] The DMN shows higher activation when behavioral responses are stable, and this activation is independent of self-reported mind wandering.[39] Meditation, which involves focusing the mind on breathing and relaxation, is associated with reduced activity of the DMN.[40]

Tsoukalas (2017) links theory of mind to immobilization, and suggests that the default network is activated by the immobilization inherent in the testing procedure (the patient is strapped supine on a stretcher and inserted by a narrow tunnel into a massive metallic structure). This procedure creates a sense of entrapment and, not surprisingly, the most commonly reported side-effect is claustrophobia.[41]

Gabrielle et al. (2019) suggests that the DMN is related to the perception of beauty, in which the network becomes activated in a generalized way to aesthetically moving domains such as artworks, landscapes, and architecture. This would explain a deep inner feeling of pleasure related to aesthetics, interconnected with the sense of personal identity, due to the network functions related to the self.[42]

Clinical significance

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The default mode network has been hypothesized to be relevant to disorders including Alzheimer's disease, autism, schizophrenia, major depressive disorder (MDD), chronic pain, post-traumatic stress disorder (PTSD) and others.[4][43] In particular, the DMN has also been reported to show overlapping yet distinct neural activity patterns across different mental health conditions, such as when directly comparing attention deficit hyperactivity disorder (ADHD) and autism.[44]

People with Alzheimer's disease show a reduction in glucose (energy use) within the areas of the default mode network.[4] These reductions start off as slight decreases in patients with mild symptoms and continue to large reductions in those with severe symptoms. Surprisingly, disruptions in the DMN begin even before individuals show signs of Alzheimer's disease.[4] Plots of the peptide amyloid-beta, which is thought to cause Alzheimer's disease, show the buildup of the peptide is within the DMN.[4] This prompted Randy Buckner and colleagues to propose the high metabolic rate from continuous activation of DMN causes more amyloid-beta peptide to accumulate in these DMN areas.[4] These amyloid-beta peptides disrupt the DMN and because the DMN is heavily involved in memory formation and retrieval, this disruption leads to the symptoms of Alzheimer's disease.

DMN is thought to be disrupted in individuals with autism spectrum disorder.[4][45] These individuals are impaired in social interaction and communication which are tasks central to this network. Studies have shown worse connections between areas of the DMN in individuals with autism, especially between the mPFC (involved in thinking about the self and others) and the PCC (the central core of the DMN).[46][47] The more severe the autism, the less connected these areas are to each other.[46][47] It is not clear if this is a cause or a result of autism, or if a third factor is causing both (confounding).

Although it is not clear whether the DMN connectivity is increased or decreased in psychotic bipolar disorder and schizophrenia, several genes correlated with altered DMN connectivity are also risk genes for mood and psychosis disorders.[48]

Rumination, one of the main symptoms of major depressive disorder, is associated with increased DMN connectivity and dominance over other networks during rest.[49][50] Such DMN hyperconnectivity has been observed in first-episode depression[51] and chronic pain.[52] Altered DMN connectivity may change the way a person perceives events and their social and moral reasoning, thus increasing their susceptibility to depressive symptoms.[53]

Lower connectivity between brain regions was found across the default network in people who have experienced long-term trauma, such as childhood abuse or neglect, and is associated with dysfunctional attachment patterns. Among people experiencing PTSD, lower activation was found in the posterior cingulate gyrus compared to controls, and severe PTSD was characterized by lower connectivity within the DMN.[43][54]

Adults and children with ADHD show reduced anticorrelation between the DMN and other brain networks.[55][56] The cause may be a lag in brain maturation.[57] More generally, competing activation between the DMN and other networks during memory encoding may result in poor long-term memory consolidation, which is a symptom of not only ADHD but also depression, anxiety, autism, and schizophrenia.[33]

Modulation

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The default mode network (DMN) may be modulated by the following interventions and processes:

  • Acupuncture – Deactivation of the limbic brain areas and the DMN.[58] It has been suggested that this is due to the pain response.[59]
  • Antidepressants – Abnormalities in DMN connectivity are reduced following treatment with antidepressant medications in PTSD.[60]
  • Attention Training Technique - Research shows that even a single session of Attention Training Technique changes functional connectivity of the DMN.[61]
  • Deep brain stimulation – Alterations in brain activity with deep brain stimulation may be used to balance resting state networks.[62]
  • Meditation – Structural changes in areas of the DMN such as the temporoparietal junction, posterior cingulate cortex, and precuneus have been found in meditation practitioners.[63] There is reduced activation and reduced functional connectivity of the DMN in long-term practitioners.[63] Various forms of nondirective meditation, including Transcendental Meditation[64] and Acem Meditation,[65] have been found to activate the DMN.
  • Physical Activity and Exercise – Physical Activity, and more likely Aerobic Training, may alter the DMN. In addition, sports experts are showing networks differences, notably of the DMN.[66][67][68]
  • Psychedelic drugs – Reduced blood flow to the PCC and mPFC was observed under the administration of psilocybin. These two areas are considered to be the main nodes of the DMN.[69] One study on the effects of LSD demonstrated that the drug desynchronizes brain activity within the DMN; the activity of the brain regions that constitute the DMN becomes less correlated.[70]
  • Psychotherapy – In PTSD, the abnormalities in the default mode network normalize in individuals who respond to psychotherapy interventions.[71][60]
  • Sleep deprivation – Functional connectivity between nodes of the DMN in their resting-state is usually strong, but sleep deprivation results in a decrease in connectivity within the DMN.[72] Recent studies suggest a decrease in connectivity between the DMN and the task-positive network as a result of sleep loss.[73]
  • Sleeping and resting wakefulness
    • Onset of sleep – Increase in connectivity between the DMN and the task-positive network.[74]
    • REM sleep – Possible increase in connectivity between nodes of the DMN.[74]
    • Resting wakefulness – Functional connectivity between nodes of the DMN is strong.[74]
    • Stage N2 of NREM sleep – Decrease in connectivity between the posterior cingulate cortex and medial prefrontal cortex.[74]
    • Stage N3 of NREM sleep – Further decrease in connectivity between the PCC and MPFC.[74]

Criticism

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Some have argued the brain areas in the default mode network only show up together because of the vascular coupling of large arteries and veins in the brain near these areas, not because these areas are actually functionally connected to each other. Support for this argument comes from studies that show changing in breathing alters oxygen levels in the blood which in turn affects DMN the most.[4] These studies however do not explain why the DMN can also be identified using PET scans by measuring glucose metabolism which is independent of vascular coupling[4] and in electrocorticography studies[75] measuring electrical activity on the surface of the brain, and in MEG by measuring magnetic fields associated with electrophysiological brain activity that bypasses the hemodynamic response.[76]

The idea of a "default network" is not universally accepted.[77] In 2007 the concept of the default mode was criticized as not being useful for understanding brain function, on the grounds that a simpler hypothesis is that a resting brain actually does more processing than a brain doing certain "demanding" tasks, and that there is no special significance to the intrinsic activity of the resting brain.[78]

Nomenclature

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The default mode network has also been called the language network, semantic system, or limbic network.[11] Even though the dichotomy is misleading,[8] the term task-negative network is still sometimes used to contrast it against other more externally-oriented brain networks.[56]

In 2019, Uddin et al. proposed that medial frontoparietal network (M-FPN) be used as a standard anatomical name for this network.[11]

See also

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References

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Electrocorticography

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Not to be confused with ECOG as electrocochleography.


Electrocorticography
 
Intracranial electrode grid for electrocorticography.
SynonymsIntracranial electroencephalography
Purposerecord electrical activity from the cerebral cortex.(invasive)

Electrocorticography (ECoG), a type of intracranial electroencephalography (iEEG), is a type of electrophysiological monitoring that uses electrodes placed directly on the exposed surface of the brain to record electrical activity from the cerebral cortex. In contrast, conventional electroencephalography (EEG) electrodes monitor this activity from outside the skull. ECoG may be performed either in the operating room during surgery (intraoperative ECoG) or outside of surgery (extraoperative ECoG). Because a craniotomy (a surgical incision into the skull) is required to implant the electrode grid, ECoG is an invasive procedure.

History

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ECoG was pioneered in the early 1950s by Wilder Penfield and Herbert Jasper, neurosurgeons at the Montreal Neurological Institute.[1] The two developed ECoG as part of their groundbreaking Montreal procedure, a surgical protocol used to treat patients with severe epilepsy. The cortical potentials recorded by ECoG were used to identify epileptogenic zones – regions of the cortex that generate epileptic seizures. These zones would then be surgically removed from the cortex during resectioning, thus destroying the brain tissue where epileptic seizures had originated. Penfield and Jasper also used electrical stimulation during ECoG recordings in patients undergoing epilepsy surgery under local anesthesia.[2] This procedure was used to explore the functional anatomy of the brain, mapping speech areas and identifying the somatosensory and somatomotor cortex areas to be excluded from surgical removal. A doctor named Robert Galbraith Heath was also an early researcher of the brain at the Tulane University School of Medicine.[3][4]

Electrophysiological basis

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ECoG signals are composed of synchronized postsynaptic potentials (local field potentials), recorded directly from the exposed surface of the cortex. The potentials occur primarily in cortical pyramidal cells, and thus must be conducted through several layers of the cerebral cortex, cerebrospinal fluid (CSF), pia mater, and arachnoid mater before reaching subdural recording electrodes placed just below the dura mater (outer cranial membrane). However, to reach the scalp electrodes of a conventional electroencephalogram (EEG), electrical signals must also be conducted through the skull, where potentials rapidly attenuate due to the low conductivity of bone. For this reason, the spatial resolution of ECoG is much higher than EEG, a critical imaging advantage for presurgical planning.[5] ECoG offers a temporal resolution of approximately 5 ms and spatial resolution as low as 1-100 μm.[6]

Using depth electrodes, the local field potential gives a measure of a neural population in a sphere with a radius of 0.5–3 mm around the tip of the electrode.[7] With a sufficiently high sampling rate (more than about 10 kHz), depth electrodes can also measure action potentials.[8] In which case the spatial resolution is down to individual neurons, and the field of view of an individual electrode is approximately 0.05–0.35 mm.[7]

Procedure

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The ECoG recording is performed from electrodes placed on the exposed cortex. In order to access the cortex, a surgeon must first perform a craniotomy, removing a part of the skull to expose the brain surface. This procedure may be performed either under general anesthesia or under local anesthesia if patient interaction is required for functional cortical mapping. Electrodes are then surgically implanted on the surface of the cortex, with placement guided by the results of preoperative EEG and magnetic resonance imaging (MRI). Electrodes may either be placed outside the dura mater (epidural) or under the dura mater (subdural). ECoG electrode arrays typically consist of sixteen sterile, disposable stainless steel, carbon tip, platinum, Platinum-iridium alloy or gold ball electrodes, each mounted on a ball and socket joint for ease in positioning. These electrodes are attached to an overlying frame in a "crown" or "halo" configuration.[9] Subdural strip and grid electrodes are also widely used in various dimensions, having anywhere from 4 to 256[10] electrode contacts. The grids are transparent, flexible, and numbered at each electrode contact. Standard spacing between grid electrodes is 1 cm; individual electrodes are typically 5 mm in diameter. The electrodes sit lightly on the cortical surface, and are designed with enough flexibility to ensure that normal movements of the brain do not cause injury. A key advantage of strip and grid electrode arrays is that they may be slid underneath the dura mater into cortical regions not exposed by the craniotomy. Strip electrodes and crown arrays may be used in any combination desired. Depth electrodes may also be used to record activity from deeper structures such as the hippocampus.

DCES

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Direct cortical electrical stimulation (DCES), also known as cortical stimulation mapping, is frequently performed in concurrence with ECoG recording for functional mapping of the cortex and identification of critical cortical structures.[9] When using a crown configuration, a handheld wand bipolar stimulator may be used at any location along the electrode array. However, when using a subdural strip, stimulation must be applied between pairs of adjacent electrodes due to the nonconductive material connecting the electrodes on the grid. Electrical stimulating currents applied to the cortex are relatively low, between 2 and 4 mA for somatosensory stimulation, and near 15 mA for cognitive stimulation.[9] The stimulation frequency is usually 60 Hz in North America and 50 Hz in Europe, and any charge density more than 150 μC/cm2 causes tissue damage.[11][12]

The functions most commonly mapped through DCES are primary motor, primary sensory, and language. The patient must be alert and interactive for mapping procedures, though patient involvement varies with each mapping procedure. Language mapping may involve naming, reading aloud, repetition, and oral comprehension; somatosensory mapping requires that the patient describe sensations experienced across the face and extremities as the surgeon stimulates different cortical regions.[9]

Clinical applications

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Since its development in the 1950s, ECoG has been used to localize epileptogenic zones during presurgical planning, map out cortical functions, and to predict the success of epileptic surgical resectioning. ECoG offers several advantages over alternative diagnostic modalities:

  • Flexible placement of recording and stimulating electrodes[2]
  • Can be performed at any stage before, during, and after a surgery
  • Allows for direct electrical stimulation of the brain, identifying critical regions of the cortex to be avoided during surgery
  • Greater precision and sensitivity than an EEG scalp recording – spatial resolution is higher and signal-to-noise ratio is superior due to closer proximity to neural activity

Limitations of ECoG include:

  • Limited sampling time – seizures (ictal events) may not be recorded during the ECoG recording period
  • Limited field of view – electrode placement is limited by the area of exposed cortex and surgery time, sampling errors may occur
  • Recording is subject to the influence of anesthetics, narcotic analgesics, and the surgery itself[2]

Intractable epilepsy

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Epilepsy is currently ranked as the third most commonly diagnosed neurological disorder, afflicting approximately 2.5 million people in the United States alone.[13] Epileptic seizures are chronic and unrelated to any immediately treatable causes, such as toxins or infectious diseases, and may vary widely based on etiology, clinical symptoms, and site of origin within the brain. For patients with intractable epilepsy – epilepsy that is unresponsive to anticonvulsants – surgical treatment may be a viable treatment option. Partial epilepsy[14] is the common intractable epilepsy and the partial seizure is difficult to locate.Treatment for such epilepsy is limited to attachment of vagus nerve stimulator. Epilepsy surgery is the cure for partial epilepsy provided that the brain region generating seizure is carefully and accurately removed.

Extraoperative ECoG

Before a patient can be identified as a candidate for resectioning surgery, MRI must be performed to demonstrate the presence of a structural lesion within the cortex, supported by EEG evidence of epileptogenic tissue.[2] Once a lesion has been identified, ECoG may be performed to determine the location and extent of the lesion and surrounding irritative region. The scalp EEG, while a valuable diagnostic tool, lacks the precision necessary to localize the epileptogenic region. ECoG is considered to be the gold standard for assessing neuronal activity in patients with epilepsy, and is widely used for presurgical planning to guide surgical resection of the lesion and epileptogenic zone.[15][16] The success of the surgery depends on accurate localization and removal of the epileptogenic zone. ECoG data is assessed with regard to ictal spike activity – "diffuse fast wave activity" recorded during a seizure – and interictal epileptiform activity (IEA), brief bursts of neuronal activity recorded between epileptic events. ECoG is also performed following the resectioning surgery to detect any remaining epileptiform activity, and to determine the success of the surgery. Residual spikes on the ECoG, unaltered by the resection, indicate poor seizure control, and incomplete neutralization of the epileptogenic cortical zone. Additional surgery may be necessary to completely eradicate seizure activity. Extraoperative ECoG is also used to localize functionally-important areas (also known as eloquent cortex) to be preserved during epilepsy surgery. [17] Motor, sensory, cognitive tasks during extraoperative ECoG are reported to increase the amplitude of high-frequency activity at 70–110 Hz in areas involved in execution of given tasks.[17][18][19] Task-related high-frequency activity can animate 'when' and 'where' cerebral cortex is activated and inhibited in a 4D manner with a temporal resolution of 10 milliseconds or below and a spatial resolution of 10 mm or below.[18][19]

Intraoperative ECoG

The objective of the resectioning surgery is to remove the epileptogenic tissue without causing unacceptable neurological consequences. In addition to identifying and localizing the extent of epileptogenic zones, ECoG used in conjunction with DCES is also a valuable tool for functional cortical mapping. It is vital to precisely localize critical brain structures, identifying which regions the surgeon must spare during resectioning (the "eloquent cortex") in order to preserve sensory processing, motor coordination, and speech. Functional mapping requires that the patient be able to interact with the surgeon, and thus is performed under local rather than general anesthesia. Electrical stimulation using cortical and acute depth electrodes is used to probe distinct regions of the cortex in order to identify centers of speech, somatosensory integration, and somatomotor processing. During the resectioning surgery, intraoperative ECoG may also be performed to monitor the epileptic activity of the tissue and ensure that the entire epileptogenic zone is resectioned.

Although the use of extraoperative and intraoperative ECoG in resectioning surgery has been an accepted clinical practice for several decades, recent studies have shown that the usefulness of this technique may vary based on the type of epilepsy a patient exhibits. Kuruvilla and Flink reported that while intraoperative ECoG plays a critical role in tailored temporal lobectomies, in multiple subpial transections (MST), and in the removal of malformations of cortical development (MCDs), it has been found impractical in standard resection of medial temporal lobe epilepsy (TLE) with MRI evidence of mesial temporal sclerosis (MTS).[2] A study performed by Wennberg, Quesney, and Rasmussen demonstrated the presurgical significance of ECoG in frontal lobe epilepsy (FLE) cases.[20]

Research applications

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ECoG has recently emerged as a promising recording technique for use in brain-computer interfaces (BCI).[21] BCIs are direct neural interfaces that provide control of prosthetic, electronic, or communication devices via direct use of the individual's brain signals. Brain signals may be recorded either invasively, with recording devices implanted directly into the cortex, or noninvasively, using EEG scalp electrodes. ECoG serves to provide a partially invasive compromise between the two modalities – while ECoG does not penetrate the blood–brain barrier like invasive recording devices, it features a higher spatial resolution and higher signal-to-noise ratio than EEG.[21] ECoG has gained attention recently for decoding imagined speech or music, which could lead to "literal" BCIs[22] in which users simply imagine words, sentences, or music that the BCI can directly interpret.[23][24]

In addition to clinical applications to localize functional regions to support neurosurgery, real-time functional brain mapping with ECoG has gained attention to support research into fundamental questions in neuroscience. For example, a 2017 study explored regions within face and color processing areas and found that these subregions made highly specific contributions to different aspects of vision.[25] Another study found that high-frequency activity from 70 to 200 Hz reflected processes associated with both transient and sustained decision-making.[26] Other work based on ECoG presented a new approach to interpreting brain activity, suggesting that both power and phase jointly influence instantaneous voltage potential, which directly regulates cortical excitability.[27] Like the work toward decoding imagined speech and music, these research directions involving real-time functional brain mapping also have implications for clinical practice, including both neurosurgery and BCI systems. The system that was used in most of these real-time functional mapping publications, "CortiQ". has been used for both research and clinical applications.

Recent advances

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The electrocorticogram is still considered to be the "gold standard" for defining epileptogenic zones; however, this procedure is risky and highly invasive. Recent studies have explored the development of a noninvasive cortical imaging technique for presurgical planning that may provide similar information and resolution of the invasive ECoG.

In one novel approach, Lei Ding et al.[28] seek to integrate the information provided by a structural MRI and scalp EEG to provide a noninvasive alternative to ECoG. This study investigated a high-resolution subspace source localization approach, FINE (first principle vectors) to image the locations and estimate the extents of current sources from the scalp EEG. A thresholding technique was applied to the resulting tomography of subspace correlation values in order to identify epileptogenic sources. This method was tested in three pediatric patients with intractable epilepsy, with encouraging clinical results. Each patient was evaluated using structural MRI, long-term video EEG monitoring with scalp electrodes, and subsequently with subdural electrodes. The ECoG data were then recorded from implanted subdural electrode grids placed directly on the surface of the cortex. MRI and computed tomography images were also obtained for each subject.

The epileptogenic zones identified from preoperative EEG data were validated by observations from postoperative ECoG data in all three patients. These preliminary results suggest that it is possible to direct surgical planning and locate epileptogenic zones noninvasively using the described imaging and integrating methods. EEG findings were further validated by the surgical outcomes of all three patients. After surgical resectioning, two patients are seizure-free and the third has experienced a significant reduction in seizures. Due to its clinical success, FINE offers a promising alternative to preoperative ECoG, providing information about both the location and extent of epileptogenic sources through a noninvasive imaging procedure.

See also

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References

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