The Operating System of the Brain

Siegfried Othmer, Ph.D., Chief Scientist, EEG Spectrum
Copyright, 2002, The EEG Institute

Sometimes the issue in science is more fundamental than answering certain questions about which we are ignorant. The more basic issue may be framing the question. One remaining crucial enigma can be summed up, in the idiom of the day, as figuring out the brain's operating system.
How does the brain accomplish its tasks from moment to moment? How does it communicate internally?
How does it combine inputs from sensory modalities into our coherent experience of the world?
How does it combine sensory experience with top-level judgments and intention into motor output?
How do emotions and feelings get into the act?
How does the brain organize hierarchies, like the hierarchy of attention? What in the brain allows us to distinguish figure from ground?

More specifically, one might ask:
How does the brain use discontinuous events, the action potentials, to give us the subjective experience of seamless continuity?
How does the image of our world stay stable and organized in our heads even as we move our heads, and let our eyes dart around?
How does the brain organize sequencing, the remembrance of a sequence of numbers or words?
How does the brain organize "working memory", where we hold a thought live in our brain in order to elaborate on it at greater length?
How does the brain record into memory even a single event in our lives?
How does the brain keep track of it all, particularly if it even remembers what you had for lunch yesterday?
And how does it access such arcane information at will?

The importance of timing

It is now clear that information encoding in the brain cannot rely simply on the firing rate of neurons, where the brain listens in on a neuron firing away over time and judges the level of input on that basis. That process does happen, but it is insufficient to explain our ability to appraise events quickly and react to them promptly. To keep us alive, our brain has to do a lot of parallel computing. This means that information is encoded not in individual neurons, but rather in what we call "ensembles." In other words, a nugget of information requires a whole raft of neurons to represent it. That, in turn, places a burden of coordination on the brain, which must have a mechanism for preserving the integrity of that ensemble throughout the signal processing chain. This problem should not be underestimated, because a moment later another volley of information comes down the pike, and it also has to be organized unto itself. Not only that, it has to be integrated with what came before, and with what follows.

Recent discoveries in the neurosciences highlight the centrality of that process, and postulate that the brain, in some generality, distinguishes different ensembles, or cohorts, by subleties of timing. This model is called "time binding."

Some crucial aspects of neuronal function lead naturally to such a model, although these things are always much clearer in retrospect than in prospect. When a neuron is stimulated by an excitatory input, a single such input is never sufficient by itself to cause the neuron to generate an action potential and continue the propagation of the signal. Hence, successful activation of a neuron is always a conspiracy of events. If a neuron is considered as a voting machine, there are always at least two people in the voting booth pulling the levers at the same time in order for the vote to be counted. Neurons, in other words, are coincidence detectors. This brings brain timing front and center.

We can talk about this economically by saying that the input of interest, say from some sensory modality, is always gated, or modulated, at the synaptic junction by another signal, which we can simply say represents the rest of the nervous system. So, at every synaptic junction, and in every signal transfer event, the central nervous system gets a vote! This may be a subtle modulation, but the effect is go/no-go. This sharpens contrast down the information processing chain, and it also sharpens the information in the timing domain. The gating signal has a very narrow window of opportunity in which it is able to "pass" the incoming signal.

What emerges is the realization that one of the key functions of the brain is to coordinate timing both locally and globally, in order to facilitate communication between different brain regions. The implication is that disruption of timing integrity can wreak either subtle or gross malfunction of the brain. Unfortunately, such timing is not rendered visible on all of the fancy brain imaging techniques we have developed over the last few decades.

A second key problem mentioned above is to understand how the brain organizes continuity of experience, continuity of its own state, and working memory, with discrete and transient events (the action potentials). It apparently does so by organizing repetition. This repetition is crucial for the organization of sensory experience. It is also crucial for those functions that the brain uses to maintain itself from moment to moment, a problem we may call "state management." Perhaps a kind of economy is operative in nature, by which the same process operative in managing sensory information and cognitive events is also used by the brain to regulate its own affairs in considerable generality.

The Brain's Got Rhythm

The repetition of brain events imposes a requirement for a kind of strobing or reference signal that serves as a template by means of which information is shaped in the time domain. This template may have a local organization, concomitant with the localization of certain information processing, or it may have a more global character, when it is governing relationships and interactions between different brain regions. The analogy to an orchestra comes to mind, where individual instruments have their own locality and frequency characteristics, but each has to fit into an overall pattern of timing and rhythmicity. An overall harmonic structure must prevail in which the whole ensemble is coordinated. Something along the same lines must be going on in the brain, in which case we can assign a major role to what we may call the "virtual conductor," the self-organizing functions in the brain that serve to manage and coordinate this overall timing. If we must localize this virtual conductor somewhere in the brain, it would be at the thalamus, the grand organizer of brain timing.

It is now proposed that high-frequency repetitions organize the very transient events of sensory experience, nuggets of cognitive activity, and specific motor acts. And it is surmised that low frequency repetitions organize those aspects of brain function which have longer persistence over time, such as states of activation and arousal, the sleep-wake cycle, and perhaps even states of our immune system and of the endocrine system.

This more global role of brain timing is gradually coming to be realized. In a treatise on how consciousness might be understood in brain terms, Rodolfo Llinas posited some years ago:

" Attempting to understand how the brain, as a whole, might be organized seems, for the first time, to be a serious topic of inquiry. One aspect of its neuronal organization that seems particularly central to global function is the rich thalamocortical interconnectivity, and most particularly the reciprocal nature of the thalamocortical neuronal loop function. Moreover, the interaction between the specific and nonspecific thalamic loops suggest that rather than a gate into the brain, the thalamus represents a hub from which any site in the cortex can communicate with any other such site or sites".

"The neuronal basis for consciousness," Rodolfo Llinas, Philos Trans R Soc Lond B Biol Sci 1998 Nov 29; 353 (1377): 1841-9.
Dissonance

What happens when brain timing is disturbed? We have experienced an instructive experiment of nature when Japanese children suffered seizures, nausea, and unconsciousness following a mere five-second exposure to a rhythmically flashing light on a TV screen. About one in 5000 children was affected. On the one hand, scientists were not seriously shaken. They have known about "photic epilepsy" for years. But the significance of this event-of why we are subject to photic epilepsy-received essentially no attention. This is because the context for that information was entirely lacking within the field of clinical neurology. In view of what we have said above, it is quite clear that in these fragile cases, the rhythmic stimulus could not be stabilized by the brain, and instead it escalated into higher and higher amplitudes until a seizure developed or consciousness was lost.

This is a clear demonstration of how utterly dependent we are on the integrity of our own brain rhythms. When that mechanism fails, it can fail gloriously! Such failures must be a rare phenomenon, or we would not survive as a species. Subtle failures of timing can have effects that are somewhat less dramatic. Antonio Damasio speculated in his book, Descartes' Error, as follows: "Any malfunction of the timing mechanism would be likely to create spurious integration and disintegration. This may indeed be what happens in states of confusion caused by head injury, or in some symptoms of schizophrenia and other diseases." (p.95)

Most recently, David McCormick, who has studied the interaction between the cortex and the thalamus with his research group for many years, asserted:
Recent evidence indicates that "dysrhythmias" cause alterations in the normal function of the thalamocortical loop and lead to various types of neurological disorders. Will decoding this rhythm help us to understand the basis for movement disorders, chronic pain, and even neuropsychological dysfunction?

A New Model for Psychopathologies

These considerations may be the opening foray into an entirely new model for psychopathologies, a model based on deficiencies in the brain as an operating system, and as a control system. This emerging model has much greater richness than the present pharmacologically driven model, where the brain is treated almost like an endocrine gland, and where the failures are attributed to either too much or too little of one or another neuromodulator substance. In the future, such one-dimensional models of brain function, in which something so complex as Tourette Syndrome or addictions is attributed to a dopamine receptor deficit, and something so multi-faceted as depression is reduced to a serotonin deficiency, will be displaced with models that match the complexity of the phenomenology they are trying to explain.

Already it is becoming clear that these one-dimensional models serve the marketing interests of the pharmaceutical companies more than they do scientific understanding. One physiologist said he has given up thinking that a person's well-being is determined by the amount of dopamine floating around in his brain. And a professor of neurophysiology, in trying to understand the role of Prozac in the brain, said that the best analogy he can come up with is that of kicking his ancient clock radio, which had some chance of provoking the radio into a more functional state. In other words, the role of Prozac is not as a remedy in its own right, but as a means of provoking the brain into a more functional state. In order to understand this, we have to understand more than the neurochemistry of serotonin in the brain. We have to understand the brain in its timing and bio-electrical function.

The failure of the brain as a regulatory and control system is referred to as disregulation. This model suits the data in that it provides for a continuum of severity, and it does not involve discrete boundaries between disorders. The underlying ideas can already be found in various places in the literature. Progress has also been made on the clinical side in understanding psychopathologies in terms of the disregulation model. Surprisingly, this model is even getting support from a psychiatrist in the psychoanalytical tradition. Says James Grotstein:

One certainly must view disorders on the anxiety spectrum, such as the disorders of anxiety, panic, phobias, hypochondria, and such trait-state disorders as borderline personality, the obsessive-compulsive disorders, schizophrenia, and many others as being deeply rooted in one or another form of a neurobiologically induced disorder of disregulation.
-- James S. Grotstein, in the Preface to Alan Schore's "Affect Regulation and the Origin of the Self."

A Remedy Matched to the Model

Even though there is now some recognition of the need to understand regulatory systems in their temporal properties, researchers are currently tempted to conclude that this information will simply allow us to do better pharmacology and more targeted surgeries. However, there is a technique that precisely matches the problem of disregulation, and that is simply training the brain toward improved self-regulation. We take advantage of the fact that most of the mechanisms underlying the dysfunctions are typically functioning at some level. We are not usually talking about an all-or-nothing situation. If there is function at all, then it can be discerned, and challenged to function better over the long term. This is what neurofeedback is all about. We observe the brain in its regulatory activities with the EEG, and we challenge the brain to change the EEG in particular ways.

By rewarding a person whenever the brain chances to move into a more favorable state, we enhance the probability that this happenstance will be repeated. This is known as Thorndike's "Law of Effect," which has been a staple of biological psychology for the last century. Over time, the brain learns the new behavior, and concomitantly we observe more regulated organismic behavior. Clinical evidence for the effectiveness of this approach has now been found for a large variety of clinical categories that in many instances don't appear to have much in common. The capacity of the brain to respond to EEG-training challenges seems, therefore, to have a broad reach over the domain of psychopathology. Such clinical efficacy is the final link in the chain of argument that it is time to reframe the discussion of psychopathology as primarily an issue of brain self-regulation, and to adopt a remedy that is attuned to the problem.

Our understanding of the brain's operating system, of the brain's software, will lead to the opening of new possibilities for entirely software-based, self-regulation-based solutions to some of our society's most intractable mental health concerns.
Conditions for which evidence of efficacy of neurofeedback exists

Clinical evidence for the effectiveness of this approach has now been found for over 80 different clinical categories. The capacity of the brain to respond to self-regulation strategies in general, and to EEG-training challenges in particular, seems to have a broad reach over the domain of psychopathology. Such clinical efficacy is the final link in the chain of argument that it is time to reframe the discussion of psychopathology as primarily an issue of brain disregulation, and to adopt a remedy that is attuned to the problem: The direct training and support of brain self-regulation.

The growing list:

ADHD
Absence Seizures
Addictions
Alcoholism
Allergies
Anxiety
Anorexia
Appetite Disregulation
Articulation problems
Asperger's Syndrome
Asthma
Attachment Disorder
Autism spectrum
Bipolar Disorder
Birth injury
Blepharospasm
Brain Injury
Bruxism
Bulimia
Chemical and Environmental Sensitivities
Chronic Fatigue Syndrome
Cognitive decline
Cognitive dysfunction
Complex-partial Seizures
Complex Regional Pain Syndrome
Compulsive Behavior
Conduct Disorder
Coprolalia
Crohn's Disease
Dementia
Depression
Developmental Delay
Diabetes
Diffuse Cortical Atrophy
Distractibility
Drug babies
Dyscalculia
Dysgraphia
Dyslexia
Eating Disorders
Emotional Disturbance
Encopresis
Enuresis
Epilepsy
Episodic Dyscontrol
Executive Function Deficit
Fear Conditioning
Fetal Alcohol Syndrome
Fetal Alcohol Effect
Fibromyalgia
Headaches
Hot flashes
Hypomania
Hypotonia
Hyperactivity
Hypertension
Hypoglycemia, Dysglycemia
Impulse Control Disorders
Inattention
Incontinence
Insomnia
Intermittent Explosive Disorder
Irritable Bowel Syndrome
Late Luteal Phase Dysphoric Disorder
Learning Disabilities
Lupus
Mania
Memory function
Menopausal symptoms
Migraines, classic and common
Motor and vocal tics
Motor Seizures
Multiple Sclerosis
Nausea
Nightmares
Night Terrors
Nocturnal Bruxism
Nocturnal Myoclonus
Obsessive behavior
Oppositionality
Optimum mental fitness
Paranoia
Parkinson's
Perfectionist behavior
Performance anxiety
Peripheral Neuropathy Pain
Pervasive Developmental Delay
Polydipsia
Post-Traumatic Stress Disorder
Rage behavior
Reflex Sympathetic Dystrophy
Restless leg syndrome
PMS
Seizures
Sleep Disorders
Sleep talking
Sleep walking
Social anxiety
Sociopathy, Psychopathy
Spasticity
Speech and language problems
Stroke recovery
Suicidal behavior
Temper tantrums
Thrill-seeking behavior
Tinnitus
Tremor
Tourette Syndrome
Traumatic Brain Injury
Vertigo
Working memory
Worry

See also:

Grotstein, J.S. (1986). The psychology of powerlessness. Disorders of self-regulation and interactional regulation as a new paradigm for psychopathology. Psychoanalytic Inquiry, 6, 93-118
For David McCormick: www.mccormicklab.org