Thursday, June 27, 2019

Rehabilitating Your Laughter Will Make It Much More Pleasurable

The muscles involved in laughing have been traumatized by life-stress and it is well worth the effort to rehab them. As an infant your laugh was genuine and primordial. Combining anxiety with fake laughing, and worrying that your laugh is too aggressive has damaged your instinctual laughing pattern. As you might expect, people that are depressed or anxious have the least convincing laughs. Extremely dominant people laugh loudly, without hesitating, at whatever they like. But most people stifle their laugh in the same way that they stifle their posture, and breathing. This is why the laughs of most adults are eccentric, and largely deviated from the innate laughing reflex. Most adult laughs hardly activate the pleasure system at all. Laughing should be intensely pleasurable and highly beneficial for your health. This entry will help you make this a reality.
Baby’s laughs are healthy and natural. Infants don’t stifle their laughs. To relearn to laugh genuinely it is helpful to watch infants and toddlers laughing. Please take some time, and search for videos of “babies laughing” on the internet and mimic them. The video below is an excellent example. Pay attention to how the baby laughs at 22 seconds into the video. This is how you want to laugh, but before you can, you need to practice emulating it.

A hearty and progressive emptying of the lungs applies a significant load to the diaphragm and the muscles of the chest wall triggering the endorphin system (Dunbar, 2017). After years of stifling laughter we have forgotten how to laugh in a genuine way that produces this response. The role of the diaphragm in laughter has been weakened so much that laughter no longer recruits the endorphin response and is draining rather than exhilarating.
The respiratory diaphragm is the main muscle responsible for natural laughter. Fake and nervous laughter comes from the throat and often results in increasing tension rather that relieving it. By training yourself to laugh through deep contractions of the diaphragm and abdominals you can rebuild an authentic laugh. These muscles should reach exhaustion and start to fail during a good laugh. If your diaphragm and abdominals start to burn like they did when you were a child, you know that you are doing it right. The next exercise will show you exactly how to retrain your diaphragm to cooperate in the laugh.
Composed Kindness #3: Diaphragmatic Laughing
Practice laughing while exhaling completely. This is an uninterrupted emptying of the lungs with no intervening inhalations. Inhale completely only after you laugh/exhale completely. Try to make a long series of laughing sounds punctuated by vocal (glottal) closure. The brief closing of the vocal tract against the exhalation allows pressure to build and makes the laugh sound like a series of rapid-fire punches. Practice this as an exercise, and attempt to make the laugh last for at least 5 seconds, but shoot for 10 to 20 seconds. Laugh all the way to the bottom of your range of exhalation. Complete 10 to 20 such laughs a day. Try the following variations:
1)      Focus on and coordinate the laughs so that they proceed at a smooth and steady rate.
2)      Notice inadvertent irregularities in timing, and the tendency to gulp, choke or falter and iron these out.
3)      Cause the punctuated exhalations to roll out as fast as possible while maintaining a fixed rythm. After speeding them up, try slowing them down.
4)      Do this using your voice in different ranges, but focus on using a deep voice to create a deep laugh.
5)      Explore your preferred ways of laughing (melody, inflection, and timing) and while doing so, modulate each.
6)      Laugh authoritatively, compellingly, boldly, forcefully, mightily.
7)      Employ different melodies and model other people’s laughs.
8)      Watch videos of babies laughing and simulate their laughs.
9)      Try laughing while exhaling completely until it turns into a wheeze, and you feel you don’t have a cubic centimeter of air left in your lungs. Ensure that the laughing pattern remains coordinated even at the bottom of your exhalation. This will greatly strengthen the muscles involved.
10)  Don't raise your shoulders when you laugh, and focus on keeping them pushed toward the floor. Try to induce paroxysms of laughter without raising the eyebrows, squinting, sneering or tensing any other muscles.
11)  Try to do this with a relaxed face, this will make it so that you can laugh heartily without intense facial constriction.

Because the muscles are strained, stagnant and uncoordinated, at first this will sound like the laugh of an insane villain, but with practice it will become hearty. It is important to do this exercise loudly and unhesitatingly so make sure that you are not worried that others will hear you. Try it in a closet, or in the car.
It will be uncomfortable at first. Your entire thorax will feel sore. Your chest should ache during and after the exercise. The muscles you engage may be so weak that they may feel susceptible to damage. If so take it easy the first few days and build up to doing it vigorously. Consider it a much needed workout. I believe that this exercise is a powerful complement to diaphragmatic breathing exercises and will allow you to reach muscles that you otherwise couldn’t.
It will make you feel weary. This is why I recommend doing it a few minutes before bedtime. After only one week the ache will disappear, and you will be able to push harder, and will be more adept at coordinating the pulses of laughter. After a few weeks you will be good at it, and you will find yourself laughing more often.
This exercise transformed my laugh from a perfunctory courtesy laugh to something enjoyable. Now I laugh spontaneously, heartily and much more frequently. I find laughing tremendously gratifying, and things that were barely amusing to me before are now hilarious.
I believe that laughing evolved to help humans let off steam. We brace our breathing musculature during stress and a real laugh probably helped us attain a full-range, hard contraction of the diaphragm. This contraction relieves the diaphragm of the tension caused by shallow breathing. It may be an evolved exercise that rewarded instances of camaraderie and social bonding by creating a naturally rehabilitating contraction of muscles throughout the thorax. The more you rehab it, the more you increase its potential for providing you with endorphins.

Wednesday, May 22, 2019

Solving the AI Control Problem: Transmit Its Mental Imagery and Inner Speech to a Television

The "AI control problem" is the issue of how to build a superintelligent artificial intelligence, while still being able to control it. It is important to be able to control it, because we want to be able to intervene before if it starts to plan a hostile takeover. I have written articles that explain how to do this, and I will lay out the general premise here. I call it the "Mental Imagery Visualization Model."

Most professionals in the field of artificial intelligence believe that the most promising form of AI is found in neural networks. The artificial neural network is a computer architecture for building learning machines. A neural network is composed of many nodes, or neurons, that communicate with each other to process inputs and create outputs. Neural networks are generally the most intelligent and best performing versions of AI today. However, the problem with neural networks is that they are a "black box." They are so complicated that, even in a very simple network, a human could never decipher the complex mathematics to determine what was on the network's mind. This is one reason why AI researchers are afraid that the AI systems of the future will be completely inscrutable, and that we will never know about its plans for world domination until it starts to act on them. However, I believe that I have a powerful precautionary safeguard to address this problem.

There are many technologies in use today that make it possible to take the outputs of a neural network and use them to formulate a picture or a video. These technologies include inverse networks, generative networks, Hopfield networks, self-organizing maps, and Kohonen networks. In this article and on this webpage I explain how to build a superintelligent AI system that implements my model of working memory. These sources also explain how to use the above technologies to create a audio/video output of the AI's consciousness... a clear view into its mind's eye.

If the contents of the AI's consciousness (its mental imagery and inner speech) are transmitted to a television, then people can watch exactly what is going on in its mind. In the article I explain that human reasoning is propelled by a constant back and forth interaction between association areas (prefrontal cortex, posterior parietal cortex) that hold working memory, and sensory brain areas (early visual and auditory cortex) that build maps of what is going on in working memory. These interactions are key to the progression of thought.

Think of something right now. Don't you see mental images? If I ask you to imagine a green hippopotamus on a unicycle, your early visual cortex will build a topographic map of exactly that. In fact, there is brain imaging technology today that can create pictures of people's mental imagery. It doesn't work so well yet, but it uses neural networks to do what it does. The technology for creating pictures of a neural network's activity is much more advanced, and neural networks are routinely used today for building topographic maps. Slap this tech on to your superintelligent AI, and it won't be able to hide anything from you.

In my architecture for AI, the generation of imagery maps is necessary for a cognitive cycle. In order to keep thinking and reasoning, the system must be building mental imagery. It is inherently obligated to create pictures and text to initiate and inform the next state of processing. It would be a simple addition to the network to capture its internally generated imagery and display it for humans to observe. In an advanced AI, this video stream may proceed very rapidly, but it could be recorded to an external memory drive and monitored by a team of people. You could have many people observing and interpreting various parts of this video feed, or you could also have another AI scanning it for contentious elements.  As they watch its inner eye and listen to its inner voice, they can determine if its intentions become malevolent and determine if its "kill switch" should be activated. With full insight into its mind's eye, it should be possible to discover and address a hidden agenda before the AI initiates a hostile takeover.

It would be important to ensure that all of the cognitive representations held coactive in the machine's working memory were included in the composite depiction built into its maps. This would make it an open book. This way the machine could not attempt to formulate thoughts that were not transduced into mental images. The sequence of maps that are made must be consistent with the aims, hopes, and motives. This is the case with the human brain. Imagine that you are in a room with someone and the only thing in the room is a knife. Complete access to the pictures they form in their brain, along with their subvocal speech would give you near certainty about everything from their plans to their impulses.

This kind of information could also help us to develop "friendly AI." Instead of rewarding and punishing an AI's behavior, we could use this video feed to reward and punish its intentions and impulses to bring its motivations in line with our own. It could also be used to alter the machine's motivations, intentions, and utility functions to bring them in line with human objectives. Just as in a human child, compassionate, prosocial, and positive behaviors and cognitions could be programmed and engineered into it after it has already been designed and implemented.

Without using this method it would be practically impossible to predict the intentions of a recursively self-improving artificial agent that was undergoing a rapid explosion in intelligence. Many researchers have come up with good reasons why sufficiently intelligent AI might veer off the friendly course. Steve Omohundro has advanced that an AI system will exhibit basic drives that will cause AI to exhibit undesired behavior, these include resource acquisition, self-preservation, and continuous self-improvement. Similarly, Alexander Wissner-Gross has said that AIs will be highly motivated to maximize future freedom of action, despite our wants and needs. Eliezer Yudkowsky has been quoted as saying, "The AI does not hate you, nor does it love you, but you are made out of atoms which it can use for something else." Alexa Ryszard Michalski, a pioneer of machine learning, has emphasized that a machine mind is fundamentally unknowable and is therefore dangerous to humans. If the technology described above is properly implemented, the machine mind would not be unknowable, and would not necessarily be dangerous at all.

A LINK TO: My Article on AI and Working Memory

A LINK TO: My Webpage on My Architecture for AI

A diagram illustrating the reciprocal interactions between items held in working memory and sensory cortex in the brain. This would be recreated in an AI system.

A diagram illustrating how working memory interacting with sensory cortex that build mental imagery in the form of topographic maps creates a continuous narrative, a stream of thought, and progressive imagery modification. 

Tuesday, May 29, 2018

A Neural Model of Working Memory and Mental Continuity: The Iterative Updating Model

The Role of Iteration in Working Memory Updating

The following describes a new theoretical article that I am developing on the brain basis of thought and consciousness. It is an outgrowth of a previously published article that can be found here.

How The Concept of Iteration Ties Consciousness to Working Memory

As the stream of thought progresses through time some elements stay the same. Of course, elements are always being added to and subtracted from the stream of thought but working memory ensures that some of these concepts are held online temporarily. This maintenance function keeps your train of thought from being derailed and makes it so that what you are thinking at this moment is highly related to what you will be thinking one second from now. This interrelatedness of consecutive thoughts provides the fabric of consciousness and allows thought to progress.

The maintenance of working memory is made possible by a cellular phenomenon called sustained firing. Sustained firing happens when a neuron is signaled by dopamine to fire repeatedly over the course of several seconds. This type of neural activity happens in neurons in the higher brain areas (i.e. the prefrontal and parietal cortices). Sustained firing is what allows us to keep important concepts in mind so that we can manipulate them, reason with them, and think about them. Without sustained firing we would continuously forget what we were just thinking. We wouldn’t be able to think or reason. This continuity of neural activity allows us to build chains of logical thoughts that progress toward a solution or plan.

Now let’s consider the concept of iteration. 


I organized this article around the term “iteration.” I think that iteration is easy for people to understand because everyone is aware of the concept of product development. Personally, I think of the iPhone iterations. The customer feedback and R&D on the iphone 7 is combined with some of the original features of the iphone 7 to create the newest iteration: the iphone 8. In a similar way the computational products of the previous thought are combined with some of the original elements of that previous thought to create the next thought. I think the word "iterative" captures the meaning of “incremental change” and is a good word to describe the model.

The article addresses the role of iteration in the processing stream of working memory. This is a concept that has not been addressed by contemporary cognitive science. As the article documents, it was considered by William James over 100 years ago. The article describes how, when working memory is updated, elements from the previous state remain active due to sustained firing. This ensures that each state of working memory is a revised iteration of the state before it. This pattern of iterative updating is discussed in detail and it is related to a large number of cognitive and neuroscientific phenomena.

The model views working memory as activated long-term memory. It features a brief sensory store, and an FOA (focus of attention) embedded within a STM store, which in turn is embedded within LTM. Instead of focusing on stimulus reception and the controlled and automatic responses to incoming stimuli, it focuses on ongoing activity within working memory, the repeating iterative pattern inherent in it, and the search and selection of new items to be added to working memory.

The model views each instantaneous state of working memory as two things: 1) a set of solutions to the last state’s search, and 2) a set of parameters for the next search. The active items in working memory spread their activation energy throughout the brain to select the next ensembles to be added to working memory. This is how “search” is performed.

I suggest that iteration is fundamental to working memory in that it allows context to be carried from one brain state to the next. This recursive property is instrumental in implementing learned algorithms, in allowing mental continuity (interrelatedness of consecutive mental states), and creating progressive changes to the contents of working memory.
Please take a look at the figures below. These original figures are helpful in conveying the model.


Fig. 1. Atkinson and Shiffrin’s (1968) Multi-store Model

This model depicts environmental stimuli being received by the senses and held in sensory memory. If attended, this stimulus information will enter short-term memory (working memory). If it is not rehearsed, it will be forgotten; if it is rehearsed, it will remain in short-term memory; and if elaborated upon sufficiently, it will be stored in long-term memory from which it can be retrieved later.

Fig. 2. Baddeley and Hitch’s (1974) Multicomponent Model
In this model the short-term store from the Atkinson and Shiffrin model is split into four interacting components that control working memory activity: the visuospatial sketchpad; the phonological buffer; the central executive; and, added later (Baddeley, 2000), the episodic buffer. These components interact with long-term memory, represented by the bottom rectangle.

Fig. 3. Cowan’s (1988) Embedded Processes Model
Short-term storage is an activated subset of long-term storage, and the FoA is an attended subset of short-term storage. Habituated stimuli enter the short-term store but do not enter the FoA.

Fig. 4.  Hypothetical Depiction of Iteration in Neurons Exhibiting Sustained Firing
Each arc, designated by a lower-case letter, represents the active time span of a neuron exhibiting sustained firing. The x-axis represents time. Dashed arcs represent neurons that have stopped firing, whereas full arcs denote neurons that have not yet stopped firing.

Fig. 5. Schematic of Iterative Updating in the FoA Where Items are Displaced, Sustained, and Newly Activated
Items are designated by uppercase letters. White spheres indicate active items and black spheres indicate inactive ones. In time 1, item A has already been deactivated, and B, C, D, and E are coactivated, echoing the pattern of activity shown in Figure 4. When coactivated, these items spread their activation energy, resulting in the convergence of activity onto a new item, F. At time 2, B has deactivated; C, D and E have remained active; and F became active. At time 3, D exits the FoA before C indicating that the order of entry does not determine the order of exit. As with other figures in this article, this figure is an emblematic abstraction.

Repetition of a computational procedure applied to the product of a previous state, used to obtain successively closer approximations to the solution of a problem.
Working Memory
A mechanism dedicated to maintaining selected representations available for use in further cognitive processing.
Working Memory Updating
Changes in the contents of working memory occurring as processing proceeds through time.
Iterative Updating
A partial shift in the contents of working memory that occurs during updating as some contents are added, others are removed, and others are repeated.

Table 1. Definition of key terms

Fig. 6. Illustration of Four Possible State Transitions in the Iterative Function of the FoA

In the first transition at time 1, there are four active items (white spheres). In time 2, one of these four items has been replaced (1/4); that is, one white sphere becomes black (inactive) and a different black sphere becomes white (active). Thus, 25% of items have been updated between time 1 and 2 without any change in the total number of active items. Other figures in this article feature this 25% updating; however, in a store with four items, updating can occur in three other ways. The other transitions in this figure depict 50%, 75%, and 100% updating.

Fig. 7. Two Successive Instants of Coactive Assemblies in the FoA

The engrams for attended items of information B, C, D, E and F are each composed of many assemblies of neurons (represented by lowercase letters) active in association areas. In time 1, the assemblies for B, C, D, and E are active, whereas in time 2 the assemblies for C, D, E and F are active. Time 2 is an iterative update of time 1.

Fig. 8. A Schematic for Polyassociationism
Spreading activity from each of the assemblies (lowercase letters) of the four items (uppercase letters) in the FoA (B, C, D, and E) propagates throughout the cortex (represented by the field of assemblies above the items). This activates new assemblies that will comprise the newest item (F) to be added to the FoA in the next state. The assemblies that comprise items B, C, D, and E are each individually associated with a very large number of potential items, but, as a group, they are most closely associated with item F.

Fig. 9. The Iterative Updating Model
The FoA, the short-term store, and the hippocampus, as well as sensory and motor cortices, all contribute to the spreading activation that will select the next item(s) from long-term memory to be added to working memory. At time 1, two (K and L) of a potential five items are converged upon and will update the FoA in time 2. Five items are shown in gray within the short-term store but in actuality this store can hold many more.

Fig. 10. Depiction of Progressive Imagery Modification
In time 1, items B, C, D, and E, held active in association areas, all spread their activation energy to early visual cortex where a composite topographic map (sketch) is built that is based on prior experience with these items. In time 2, salient features introduced by the map from time 1 spread activation energy up the cortical hierarchy converging on the assemblies for item F. B drops out of activation, and C, D, E, and F diverge back onto visual cortex. The process repeats creating a progressive series of related images.

Fig. 11. Merging Subproblems in Working Memory

Each horizontal row is a snapshot of items coactive in the FoA at a specific time period. An original problem is activated, and iterative updating is used to reach a subsolution. This subsolution is saved in the short-term store, and a related subproblem is introduced into the FoA. This subproblem iterates until a second subsolution is generated. Relevant items from the first subsolution are combined with those from the second subsolution and iterated to generate a final solution.

Fig. 12. The Iterative Updating Model for Imagery and Behavior

Iteratively updated items in working memory interact with sensory cortices to construct progressive mental imagery and interact with motor cortices to construct progressive behavior. In the next state, the items in the FoA will undergo partial replacement. The parameters used in sensory and motor cortices will reflect this change making their output an advancement on their previous output.

Fig. 13. Schematic representation of ongoing iteration in the FoA, depicting it as a gradually shifting distribution

Fig. 14. Schematic representation of ongoing iteration in the FoA and short-term memory store
This graphic expands on Figure 13, incorporating a larger number of the present model’s theoretical features: 1) the number of items coactive in the FoA (white spheres) at any one point in time varies between three and five; 2) the percentage of updating in the FoA varies between 25% and 100%; 3) items that have exited the FoA are capable of reentering the FoA; 4) the order of entry into the FoA does not determine the order of exit; and 5) items that exit the FoA briefly enter the short-term store (gray spheres) before deactivating completely (black spheres).

1.       Items of working memory correspond to temporarily activated groups of neural assemblies that encode long-term memory information.
2.       These items enter the FoA from which they move toward unattended short-term memory and then into inert long-term memory.
3.       Items remain active in working memory as long as their neural components demonstrate persistent activity in the form of sustained firing (FoA) or synaptic potentiation (non-FoA short-term memory).
4.       The active items in the FoA and the short-term store serve as search parameters for the next additions to working memory by spreading their activation energy throughout the cortex.
5.       The newly activated items of working memory are added to the remaining active items from the previous state to form an updated set of search parameters.
6.       This iterative updating process ensures that the next search is not an entirely new search but rather a modified version (updated iteration) of the previous search.
7.       Iteration may allow progressive modification, implementation of learned algorithms, and mental continuity.
Table 2.
Information processing features of the iterative updating model

Thursday, October 12, 2017

Does Tourette's Syndrome Have Adaptive or Evolutionary Benefits?

A number of different mental "disorders" are hypothesized to have been adaptive under certain conditions during prehistoric times. What about Tourette's? An article that I wrote recently on the topic came to the following conclusions:

Possible Benefits Associated with Tourette's:

  • Reduced inhibitory pressure on reflexes and motor pathways
  • Heightened efficiency in the use of force
  • Reduced reaction time and refined rhythmic activity
  • Increased innate and instinctual behaviors
  • Advanced ability for improvisation or extemporization
  • Increased defensiveness, withdrawal, avoidance, vigilance, and opportunism
  • Stimulus hunger, adaptive restlessness and unhesitating reactivity

Click here to read the entire article for free:

Tourette Syndrome in the Context of Evolution and Behavioral Ecology


Tourette syndrome, and the closely related spectrum of tic disorders, are inherited neuropsychiatric conditions characterized by the presence of repetitive and stereotyped movements. Tics are elicited by either environmental experiences or internal signals that instruct the basal ganglia to initiate automatic or procedural movements. In most vertebrates the basal ganglia encode instructions for habitually used sequences of motor movements that are essential to survival. Tic disorders may represent evolved phenotypes with a lower threshold for basal ganglia-directed actions. This may have produced a susceptibility to extraneous tics, but also produced fast-acting tactical solutions to immediate physical problems. During periods of nonstop movement, continual foraging, and sustained vigilance, it may have been advantageous to allow subcortical motor commands to intrude into ongoing motor activities. It is clear that the engrams for individual motor responses held in the basal ganglia are selected by converging cortical and subcortical inputs. This form of convergent action selection results in the selection of the most contextually reinforced actions. Today people with Tourette’s have tics that seem arbitrary and inappropriate; however, this may be due to the vast discrepancies in reinforcement between the ancestral environment and the modern one. In prehistoric environments, the motor behaviors of individuals with tic disorders may have been appropriate in environmental context, and had ecological relevance in survival and self-promotion.

Keywords: basal ganglia, evolution, executive control, neuroecology, procedural memory, tics, Tourette’s disorder


Tourette syndrome (TS) is an inherited neuropsychiatric disorder characterized by multiple sudden, repetitive, nonrhythmic motor movements called tics. Motor tics include unplanned, stereotyped movements such as eye blinking, facial twitching, and head, arm, hand or shoulder movements. Phonic tics include noises, syllables, words and phrases. Some tics are highly conspicuous, whereas other can be very subtle and masked. Tourette’s is defined as part of a spectrum of tic disorders, which includes both transient and chronic tics, most with prepubertal onset. Although individuals with TS have been described since antiquity, the systematic study of individuals with tic disorders began in the nineteenth century [1]. Only a few decades ago Tourette syndrome was considered a rare and bizarre syndrome, most often associated with the exclamation of obscene words (coprolalia), socially inappropriate remarks, mimicking, and derogatory gestures [2]. However, none of these behaviors are universal. In fact, the most well-known symptom, coprolalia, only occurs in about 10% of cases [3].

The DSM-5 recognizes three types of tic disorders: Tourette’s disorder, persistent motor or vocal tic disorder and provisional tic disorder. The diagnostic criteria for Tourette’s in the DSM-5 are: A. Both multiple motor and one or more vocal tics have been present at some time during the illness, although not necessarily concurrently. B. The tics may wax and wane in frequency but have persisted for more than 1 year since first tic onset. C. Onset is before age 18 years. D. The disturbance is not attributable to the physiological effects of a substance or another medical condition.

Merely a few decades ago, TS symptoms were thought to be caused by pent up, or “repressed” anger, and psychoanalysis was thought to be a productive form of treatment. Today many Tourette’s researchers instead think that Tourette’s represents some kind of malfunction in the neurological systems that ensure that necessary urges are properly attended to [4]. It is now known that the disorder is neurological in etiology, rather than psychological, and symptom reduction can be achieved by modifying dopaminergic transmission. Medications and behavioral therapy are the most common forms of treatment [5]. Although Tourette’s is the most severe of the tic spectrum disorders [1], most cases are relatively mild [5], and many cases probably go undiagnosed [6]. The severity of tics decreases during adolescence and pronounced Tourette’s is relatively rare in adulthood [7]. Furthermore, Tourette’s is thought by some to be continuous with normal human variation and all people are thought to be capable of movements that qualify for the “tic” label [6].

Between 1 and 10 children per 1,000 have TS and additionally, as many as 10 per 1,000 have a tic disorder [4]. This incidence exceeds a mere chance effect due to high mutation rates (1 in 1,000) and thus may be suggestive of past positive selection [8]. Because TS has high prevalence and a very strong genetic component [4], the persistence of the polymorphisms involved suggests an origin in natural history. It presents with similar prevalence rates, worldwide [9] indicating that it was an established nosological entity before the first humans left Africa. Because it presents during the period of fertility we can assume that natural selection had the opportunity to select against these alleles. Yet, TS exists today as a relatively prevalent disorder. This amounts to an evolutionary enigma commensurate to the one identified for schizophrenia [10]. The present opinion article will explore the possibility that the clinical manifestations of tic disorders may be associated, perhaps in low levels, with certain adaptive advantages in specific environments. It is certainly possible that natural selection may have only favored subclinical traits or been advantageous in low genetic penetrance in clinically unaffected relatives.

Seizure activity, chorea, dystonia and myoclonus are other movement disorders that probably were not adaptive nor selected by evolution on the basis of their ability to adaptively alter behavior. Unlike tic disorders these movement disorders can be medical signs or symptoms, and are often precipitated by injury, drugs, or relatively rare medical disease states. Tic behavior is more complex, and may fit the adaptationist program as it has aspects of contextual responsivity and intentionality.

Tourette Syndrome and Evolutionary Medicine

The costs of TS are well known and include constrained mobility, occupational disability and psychological stress and suffering [11]. The defensive value; however, may be hidden due to discrepancies between our modern and ancestral environments. Many traits that are known to have been adaptive in our ancestral environment are now seen as maladaptive in our present society, and this has been termed an “environmental mismatch” [12]. The growing field of evolutionary medicine attempts to identify and explicate such mismatches. Researchers have shown that a large number of “pathological” conditions have compensating benefits and over time the literature has come to accept many of these as adaptive responses [13]. Clinical states associated with adaptive properties include diabetes mellitus, diarrhea, fever, inflammation, obesity, sneezing, sickle cell anemia and vomiting [14]. The literature emphasizes that disorders with evolutionary components work within physical constraints, and often involve functional compromises and tradeoffs.

Following the pioneering work of Panksepp [15] there has been a movement to understand psychiatric disturbances in terms of the underlying evolutionary mechanisms. Many articles have analyzed various forms of psychopathology in terms of evolutionary medicine [16], and this area of research has been referred to as “evolutionary psychopathology.” Researchers in this field have concluded that there were probably multiple, alternative, cognitive strategies to deal with the problems and obstacles that recurred in our evolutionary past. Furthermore, they emphasize that individual differences in developmental patterns may not always represent disease, but in fact represent biological, naturally selected responses to pressing environmental concerns [17, 18]. Many articles in the last two decades have espoused this view and reconceptualized various forms of psychopathology as adaptive, cognitive syndromes that have ecological utility [19]. These articles have given thoughtful treatments to disorders such as: anxiety, hypothesized to represent a careful, cautious strategy [20]; depression, a socially submissive strategy [21]; schizophrenia, a defensive, vigilant and impulsive strategy [22]; psychopathy, a socially selfish and opportunistic strategy [23]; and PTSD, a threat-avoidant strategy [24]. Similarly, many “behavioral syndromes” have been discovered in mammalian species and are thought to represent adaptive responses to particular scenarios, despite the fact that they appear maladaptive when taken out of their ecological context [25].

Williams and Nesse [25] suggest that in order to determine that a disorder or disease has adaptive qualities which were positively selected in the past, it is important to be able to show that the trait is relatively prevalent, heritable, and that susceptibility varies within a population. These are all true of TS. However, it is also necessary to show how the trait’s purported benefits may have outweighed the costs [13]. It does not appear that individuals with TS would have suffered great hardships or had barriers to reproduction in the ancestral environment. Furthermore, Tourette’s does not adversely affect intelligence or life expectancy [26]. Both children and adults with TS have been shown to be very psychologically hardy, and despite the frustrations associated with their symptoms, are surprisingly well-functioning in social, emotional and behavioral measures [3]. In fact, they are remarkably similar to control children without TS on most psychosocial measures. This suggests that despite the accompanying physical limitations, TS may not necessarily have unduly hampered reproductive success due to psychological or motivational factors.

Possible Compensatory Benefits of Tourette Syndrome

Compensating benefits associated with Tourette syndrome have been reported in studies comparing individuals with TS to controls [6]. Georgiou and researchers [27] found that patients with TS when tested in terms of kinematics were in certain respects more force efficient, compared to controls, and made fewer inefficient cycles of motoric acceleration and deceleration on complicated motor tasks. On average, individuals with TS perform behavioral tests of cognitive motor control more quickly and accurately than their typical developing peers do [28]. Children with TS have exhibited a significant processing advantage in judging time intervals [29]. Individuals with TS also exhibit enhanced levels of cognitive control over their oculomotor responses and increased performance is associated with tic severity [30]. The study authors speculate [31] that the enhanced cognitive control of motor activity seen in TS patients may stem from the constant requirement to suppress tics; however, the enhancements may actually be inherent to TS.

Individuals with TS have been reported to excel in certain types of competitive sports [5; 32]. Furthermore, it has been claimed that tics can allow improvisation and extemporization with musical instruments. Patients report that they are physically slower, less coordinated and have a diminished knack for repartee when they are on medicines that reduce ticcing [33] (although people without Tourette’s taking neuroleptics report this as well). There have not yet been any systematic research efforts aimed at delineating the motor advantages and deficits in individuals with TS, but further research may be illuminative.

When an individual with TS stops making a conscious effort to suppress their symptoms, or if they become emotionally aroused, tics are more likely to emerge [36]. Tics have been shown to decrease in frequency during concentration on an absorbing activity [6]. Another aspect of tics is that even though they are often described as irresistible, they are typically consciously suppressible or at least able to be delayed. Touretters describe these “premonitory urges” as having properties akin to an itching sensation. Like the impulse to scratch an itch, tics can be inhibited but only with the expenditure of some degree of mental effort and restraint [3]. Given the fact that they can be deliberately suppressed it seems clear that tics would not have compromised reproductive success and survival by bursting forth during extremely inopportune times.

Neurologist and author Oliver Sacks has written about the compensatory advantages of TS. He states that clinical observers of Tourette’s routinely note a peculiar quickness of movement. Sacks [33] also wrote a story about a pilot and surgeon with severe Tourette syndrome whose tics have been documented to go into almost complete abeyance during his operations. In fact, a dozen or so M.D.s with Tourette syndrome work quite safely as surgeons [34]. Sacks describes the musician [35], “Witty Ticcy Ray,” in the following way:

“…a weekend jazz drummer of real virtuosity, famous for his sudden and wild extemporizations, which would instantly arise from a tic or a compulsive hitting of a drum, and would instantly be made the nucleus of a wild and wonderful improvisation, so that the ‘sudden intruder’ would be turned into a brilliant advantage (p. 94).”

Many probands lose all noticeable manifestations of their Tourette’s when singing, dancing or acting and can remain tic free when moving rhythmically or continuously [33; 32]. Leckman and Cohen [6] ask, from the Darwinian viewpoint, whether there might be an advantage in having vulnerability to develop TS. They claim to have made clinical observations that TS patients have a “thinner barrier to stimulation,” and may have been more “aware of dangers” in the ancestral past. The present article will take another perspective and argue that a propensity for tics may have amounted to a form of restlessness that ensured that the individual remained physically and motorically integrated with their immediate environment. During periods of nonstop movement, and repetitive foraging motions it may have been advantageous to allow subcortical motor commands to intrude into ongoing motor activities.

TS symptomatology may therefore exist on a continuum with two ends: one extreme involving simple, isolated motor tics and vocalizations which are largely irrelevant, seemingly arbitrary and a have the potential to be a nuisance. The other extreme perhaps involves rapid inventiveness, disinhibition of basal impulses, and unhesitating reactivity. Perhaps the isolated and inappropriate tics are a natural tradeoff that occurs when the threshold for activity of the basal ganglia is adaptively lowered. Ticcing disorders may descend from an environment when social propriety mattered far less than speedy reactions. Furthermore, in the ancestral past there may have been less social stigma on wild, loose behavior. Tics often appear as risqué, irreverent or even antisocial, but this may simply be because they are not filtered by the frontal lobe. Thus tics may merely be the striatum’s most appropriate associations untempered by forethought, tolerance, empathy or compassion.

The Neuroscience of Tourette Syndrome

The mental instructions for discrete movements usually pass through a complex network of cognitive filters in the frontal cortex. The PFC normally either potentiates or inhibits the impulses originating from the dorsal striatum, permitting some and curtailing others. The putamen (which controls automatic movements previously learned by repetition) sends its instructions on to the premotor cortex which passes its activity on to the adjoining motor cortex. Normally inputs from prefrontal and premotor areas are combined and integrated with inputs from the dorsal striatum in this way, and are then sent to the motor cortex. The motor cortex delivers these motor programs to the muscles by way of the spine or cranial nerves. During tics, the frontal cortex fails to inhibit the caudate nucleus and putamen, structures which lie directly beneath it. In Tourette’s the putamen has been shown to be overactive. Furthermore, TS has been associated with lack of activity in three areas: 1) the dorsolateral prefrontal cortex (concerned with generating appropriate actions); 2) the left basal ganglia (concerned with the control of automatic movements; and 3) the anterior cingulated cortex (an area concerned with focusing attention on actions [37].

The determinants of the selection of a motor plan come from either: 1) external environmental stimuli, or 2) internal stimuli. Engrams for specific motor plans are triggered in the striatum when they are converged upon by a set of inputs from cortical and subcortical areas, and activated above a certain threshold. The cooccurrence of a specific set of stimuli in the environment, or in internally generated thinking, will initiate a complex search function, characterized by spreading activation, to select the corresponding motor outputs [38]. Thus, despite the fact that they may seem arbitrary, tics are actually chosen with high specificity.

Today individuals with Tourette’s report feeling a sense of reward accompanying their ticcing actions. Reward is associated with high levels of dopamine release which is known to promote habit formation in the basal ganglia, increasing the frequency of the action. Thus dopamine serves to capture and reinforce striatal behaviors engraining these patterns as habitual tics [39]. This process may leave individuals, especially those that are genetically predisposed to Tourette’s, to be vulnerable to maladaptive motor tics when contextually unnecessary responses are captured. In the prehistoric past humans were responsible for activities such as finding or making physical shelter, protecting their bodies from predators, and foraging for food. These activities determined their reinforcement schedule. Today we rarely do any of these things. What the basal ganglia found motivating in ancestral times, was probably very different from what it finds motivating today. In the ancestral past the motor plans that were converged upon may have been more likely to be advantageous movements rather than extraneous, idiosyncratic ones.

In his book, The Triune Brain in Evolution [40], the late Paul MacLean describes the basal ganglia as the reptilian brain (also referred to as the archipallium or R complex). He describes how it can be taken to represent the dominant mediator of adaptive behavior in reptiles, amphibians and fish. He describes the basal ganglia, limbic system and neocortex as three different biological computers linked together, different in structure and chemistry, tens of millions of years apart in provenance, and each with its own representations of time, space, motor repertoire and subjectivity. He describes their functionality as intermeshing; independent but not autonomous. Much of his life’s work was dedicated to explicating how the basal ganglia is responsible for the largest proportion of behavior in nonmammalian vertebrates, their learned behaviors, tropistic behaviors, repetitive behaviors, social displays, species-specific master routines and individual-specific, idiosyncratic subroutines. The large size and vast integration of the basal ganglia in humans is clear evidence of its importance in human behavior. Perhaps it should not be surprising that the human gene pool produces phenotypes where this system is granted increased autonomy.   

Tourette Syndrome, Stress and Phenotypic Plasticity

The phenotypic characteristics of organisms ranging from plants to mammals have been shown to make various plastic responses to environmental stressors [41]. Phenotypic plasticity is accomplished when environmental cues signal dormant genes to be expressed, or expressed genes to become silent in a process known as epigenetics. Stress has been shown to demand variant body types, behaviors, reproductive tactics, and life-history strategies. Epigenetic responses to chronic stress cause the mammalian brain to respond with a number of adaptive adjustments that increase vigilance, threat awareness, and physical responsivity [22,42]. Stressful environments probably put more pressure on animals to react quickly and efficiently [43]. Most vertebrates, under times of severe or chronic stress, must use their muscles vigorously, and for sustained periods [44]. It is known that after extended exposure to stress, higher-order cognitive brain areas are toned down relative to the areas responsible for reflexes, and the execution of coordinated, sequenced, or procedural movements [44]. The documented association between stress and TS may suggest that stress causes the expression of genes that lead to increased ticcing behaviors, because tic-like behaviors may have been particularly adaptive in a stressful, or adverse environment.

Psychogenic stress is known to exacerbate TS symptoms on the order of days, weeks and months. Psychological stress has been tied closely to early onset, and has been shown to precede flare-ups. Stress reliably accelerates TS disease progression and worsens symptoms [3]. Tics have been known to increase in frequency as a result of stress, fatigue, and anxiety [39]. Also ticcing disorders can be triggered during childhood by a traumatic event. Tic severity [45] and TS diagnosis [46] has been associated with maternal psychosocial stress during pregnancy. This strong association between TS and stress may suggest that an adverse or hostile environment may have favored tics. If TS constitutes a “predictive adaptive response” to stress then it should be informative for researchers to focus heavily on the molecular pathways that tie stress to TS exacerbation.

Stress is strongly associated with basal ganglia upregulation in mammals from rats to humans. Memory is multifaceted and different facets are mediated by different brain areas. Explicit memory for movement supports consciously accessible knowledge, such as memory of what one just did or what one did yesterday, and this is mediated by the medial temporal lobe, in particular, by the hippocampus [47]. Procedural or habit memory for movement, on the other hand, is responsible for simple stimulus-response associations such as the memory to stop a car when the light is red, and this is mediated by the caudate nucleus [48]. Hippocampus and caudate-based memory systems work in parallel and have been described as cooperative by some and competitive by others [49]. Studies have found that chronic stress significantly increases activity in the caudate nucleus [50] and improves performance on simpler, habitual and/or well-rehearsed tasks [51; 52]. In both humans and rodents, chronic stress has been associated with a substantial decrease in the use of hippocampal dependent learning strategies and a dramatic increase in the use of caudate-based learning strategies [53]. Combat veterans with PTSD, especially those that were using the caudate heavily in life-threatening situations (such as riflemen), exhibit hypertrophic caudate nuclei and atrophic hippocampi [54].  It seems that a consequence of chronic stress is to shift away from explicit processing (PFC and hippocampus dependent) and toward rigid, stimulus-response, implicit processing (caudate and amygdala dependent) [55; 56].

Humans under intense chronic stress have been shown to exhibit improved simple reaction time [57], potentiated reflexes and increased speed for habitual movements [58]. In fact, Vasterling and collaborators [57] suggest that this heightened behavioral reactivity may represent an evolutionarily-mediated neurobiological response to stress “in preparation for life-preserving action.” A similar type of behavioral disinhibition may have permitted TS individuals to react without deliberately reflecting on their decisions, helping them to escape harm and attain resources quickly and without hesitation. It seems possible that TS is an evolved phenotype, intended to adopt a different life-history strategy that allowed affected individuals to react quickly without the normal inhibitory pressures on their reflexes and natural instincts.


The present article concludes that it is plausible that the genes that predispose people to Tourette syndrome, and the spectrum of tic disorders, may have been naturally selected for their role in rapid physical responding. Tics have been conceptualized here as automatic selections from lower brain centers about appropriate tactical movements. This may be associated with the compensating benefits enumerated in Figure 1.

Figure 1

Hypothesized Benefits of Tic Disorders

  • Reduced inhibitory pressure on reflexes and motor pathways
  • Heightened efficiency in the use of force
  • Reduced reaction time and refined rhythmic activity
  • Increased innate and instinctual behaviors
  • Advanced ability for improvisation or extemporization
  • Increased defensiveness, withdrawal, avoidance, vigilance, and opportunism
  • Stimulus hunger, adaptive restlessness and unhesitating reactivity

Tic and tic-like behaviors were probably only adaptive in certain contexts. The intrusion of tics may have been most adaptive when they were incorporated into an ongoing series of movements. Tics that emerged as isolated and discrete movements, when no other behaviors were being performed, or that were not applied to physical objects in the environment may have been less likely to be adaptive. In other words, tics may have been useful, during more active times, as integrated adjustments to ongoing motor behavior.

The statistical age of highest tic severity is typically between eight and twelve, with most individuals experiencing declining tic severity as they reach adolescence. [59]. In many cases, a complete remission of tic symptoms occurs after adolescence [60, 61]. Why would this epidemiological pattern be so widespread? Is it possible that tic-like behavior is part of a learning arc, benefiting children by helping them to refine movement, coordination, and motor praxis?

It will be difficult to determine irrefutably if what we know as TS was in fact an adaptive condition in the ancestral past. The hypothesis presented here is largely exploratory, and underspecified, in part due to the paucity of related research. The present article has made untested assumptions about stress-ecology and the nature of striatal cognition in the wild. It can perhaps be argued that TS and other tic disorders in general have no adaptive qualities. Most common tics observed in modern populations would probably amount to handicaps in an ancestral environment. They might make an individual unattractive to potential mates, betray one’s location to a predator. and waste valuable energy. Common tics like toe crunching, throat clearing, and abdominal tensing would probably have been useless for prehistoric foragers that exhibited them. Moreover, the present hypothesis offers no explanation for chronic tics. However, this type of exploratory writing is generally thought to be progressive as it is well known that analyzing disease states from an evolutionary perspective can integrate seemingly unrelated findings, elucidate pathophysiology, and ultimately refocus clinical research and treatment strategy.

Comparative behavior and neurophysiology could provide insight. Perhaps other species have an equally low but consistent prevalence of ticcing phenotypes as well. It would be interesting to see if there are analogues, or possibly homologues of TS in other species. If there were homologues of TS in species closely related to humans, it would be relatively easy to use molecular techniques to show this given that the genes responsible could be identified. Looking at the evolutionary signatures in the behavioral genetics of TS, might tell us more about its possible role as an adaptation. Further kinematic and biomechanic studies comparing individuals with TS to controls on measures of fluidity, efficiency and speed could help to determine what kinesiological advantages TS individuals have if any. 

It is possible that today tics are often not contextually relevant because of the artificial nature of the modern environment. Caudate hyperactivity in the ancestral past may have led to the potentiation of important procedural and habitual movements, increasing reliance on action patterns that had proven effective. In modern society it may simply lead to the intrusion of eccentric responses. The existence of TS may represent natural human variation and may demonstrate that sometimes it was adaptive to allow the basal ganglia and its procedural memories to dominate behavior uninhibited.


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