Wednesday, December 21, 2011

The way memories are recorded and reused is analogous to the way tracks of water form on a window pane

New droplets fall into the paths of old droplets
On a rainy bus ride in 2004 I was staring out of the window, hoping to push myself into thinking up a novel conceptualization of the neurological basis of memory. Looking up from an article on axonal migration, my attention turned to the tracks of water that had formed on the window. You know how they look. Water droplets leave trails of water behind them as gravity pulls them down the pane. Early drops form trails that subsequent drops fall into and travel within. Of course these are trails of water on glass, whereas memories are recorded in tracts made of neurons and their projections. But the analogy felt substantial to me, and I think that it can be carried at least a short way before it fails.
The qualities of the surface of the glass and the placement of the water droplets on the glass determine how the drops will travel. This is similar to how the current physical state of the brain and the locations of the activations therein determine how neural pathways are selected. During every perception, cognition and experience old neural pathways are being retraced (memories, familiar perceptions) and new pathways are being created.

Some water droplet's trails extend long distances and subsequent drops fall directly within their borders. Depending on dirt and smudges on the glass other trails dry up before they extend very far and when a subsequent drop reaches this point, it is free to delimit its own path. Similarly our memories and experiences involve the activation of neural trails some of which are only small snippets of the original encodings.
Altering synaptic weights among groups of neurons creates patterns in the nervous system that are stable and that serve as preexisting pathways that constrain the future propagation of nervous energy. In this way, previous experiences imprint stable conduits that act as barriers for subsequent stimulation, thus the activation patterns elicited by new stimuli will not be random, they will be constrained by past activity. This accounts for how humans respond to disparate situations in the same inflexible ways, it accounts for how stubborn and resilient our personalities are, and accounts for how most of our actions are simply pastiches of previously used techniques. Consciousness and higher-order thought really are composed of multiple stable states organized in different configurations. In this way, consciousness is akin to the entire window and its current streaming activity.
This perspective feels limiting and deterministic, but it is important to point out that our window is huge and that we should stimulate and push ourselves to increase the number and complexity of stable states in our repertoire ensuring that our pane of glass has many possible tracks. Also, the pane of glass on the bus sits passively as water streams down its side and creates the pathways. Humans, on the other hand do not have to have sit passively and be written upon. With the right environmental provocations we can intentionally seek out activities that will influence the creation of new pathways.
I had always wondered how memories, thoughts and behaviors were made possible by something physical. I wondered how alterations in the connections between brain cells allowed mental representations that could remain stable over days or years. Like the water droplets, neural energy finds the path of least resistance, and information in the form of action potentials is pushed down those avenues that are best facilitated by the synaptic weights in the network. The analogy here is very simple. Today it seems so obvious as to be trivial, but I remember it being powerful and instructive for me at first consideration.

How The PFC Leads to Behavioral Inhibition

After hitting snooze this morning I had a dream that I was reading a Wolverine comic written by Chris Claremont and drawn by John Byrne. In the comic, Wolverine was confronted with a villain he was in an argument with and he was being provoked. The dream’s narrator said something along the lines of: “Wolverine had an inclination to unsheathe his claws and cleave his foe in two that moment but another impulse, to remain composed and noncombative outlasted it. This second impulse subdued the first. It won out merely because it remained firing in his brain for just a moment longer than the first.”
The PFC has cells with higher-order receptive fields that can help the brain to conceptualize abstract things like long-term goals, cost-benefit analyses and the repercussions of risky acts. Often its instructions are the opposite of what our lower-order brain systems try to impel us to do. The PFC also has cells that fire for longer. Could it be that simple? In Wolverine’s case above, could that instinctive impulse to attack have been impelling and strong but temporally more fleeting than the one that stayed his hand? If that hypothetical inhibitory ensemble in his PFC would have stopped firing earlier would he have engaged?  In humanity’s case could our culture and history be due to the fact that the brain areas that hold the more complex representations fire for just a few milliseconds longer, enabling the more complex behavioral instructions to narrowly outlast the more base ones?

How Are PFC Neurons Tuned to High Complexity?

Why are the receptive fields for neurons in the PFC so “complex?” Is it simply because they normally fire for longer and thus have been able to become more broadly tuned to temporally discontinuous occurrences? If this is so, PFC neurons then would be like listeners who were able to overhear an entire lecture, instead of just snippets from it. Surely the longer a neuron fires the more time it has to “fire together and wire together” with other neurons. The high tonicity found in PFC neurons, combined with their high connectivity throughout the brain, must lead them to become maximally excited by events that do not always occur together immediately in time. In other words, their prolonged activation allows them to capture time-delayed pairings unlike other more transiently active neurons that can only capture simultaneous pairings.

Yet, how does an organism with a PFC know which nonsimultaneous, temporally discontinuous associations are valid? Where do humans get the rationale from to make these kinds of links between topics? Well, it is very clear that the PFC comes online very slowly during early childhood development. Perhaps we spend a good deal of early time without the PFC making associations between nearly simultaneous occurrences. This early knowledge base allows us the environmental logic to be able to infer higher order associations in late childhood, adolescence and adulthood. 

Read the full article that I wrote on this topic here:

Identifying the Link Between Creativity and Madness

I feel like recently I have started to put my finger on that elusive ‘link’ between creativity and madness. I think that madness may boost some forms of creativity by freeing up associations that a sane person’s subconscious would not allow them to entertain. The main point is that hyperfrontality, saneness, or the opposite of madness, is restrictive and actually inhibits some forms of creativity and the dark horse associations that can underlie it.
For a long time I have been reading about the associations between creativity and madness. I agree with the notion that madness, schizophrenia, some forms of psychosis and some drug induced states may be conducive to a certain brand of creative energy, but I have not been quite able to understand exactly why. Coming home on the bus today, I related the concept of lateral inhibition to the problem, and in doing so, contrived a plausible solution that has begun to satisfy my curiosity about the subject.
The mind of someone with schizophrenia is altered in a way that makes them process things differently. For them there is less continuity over time. When we think, we hold a number of different concepts in our association areas at any one time. Neurons in association areas and especially in the PFC remain active for a few seconds at a time, allowing their content to persist. This makes it so that some concepts are sustained for extended periods allowing them to affect subsequent thoughts. This process keeps human thought on a tight and narrow track. What it really does is it allows people to have precise thoughts, where each thought is very closely related to the preceding thought. Clearly this is the only way that planning can happen, if you continue juggling the same concepts without dropping the ones that have just come into play. Just think, if more nodes of activation are conserved during the transition between the present thought and the next thought, the two will be very closely related conceptually. If a sequence of thoughts are very closely related, there is little room for wild additions. This keeps sane people from injecting new conceptualizations and non sequiturs.  In schizophrenia these PFC and association area neurons cannot persist for as long (cannot maintain tonic firing) and thus the thought process is continually derailed by tangential (or more emotional and less cerebral) associations. Importantly, the driving element(s) may fall out of the equation and leave room for unexpected, unpredictable substitutions.
When you have a group of concepts that coactivate together and that keep each other mutually active, they inhibit “lateral” concepts and this puts specific limits on where the train of thought can go next. When you think about walking down the street and ducking to grab a dollar bill certain neurons responsible for representing the verb ducking laterally inhibit the noun duck corresponding to the bird. This makes it so that conceptualizing the word dollar bill in this context does not automatically evoke a picture of a duck bill. Lateral inhibition puts constraints on the associations that the unconscious can draw from. The brain does a fantastic job of inhibiting lateral concepts, which is good because it keeps us from making faulty associations. The drawback; however, is it limits the capacity to creatively insert a new concept in to that mix.
When you are constantly dropping association assemblies, when you continually cannot remember what you were just thinking, a new association may have the “relative momentum” to carry the train of thought off on a novel tangent. Because you may, now all at once, be missing the main theme, peripherally associated concepts can end up entering the mix - specifically because they may cohere well with what is left after the earlier ones have dropped out. So what you end up with, if you are very lucky, is something novel. They are based on true associations that are good, but are usually kept from entering the mix. Going from a dollar bill to a duck bill is absurd in some contexts but potentially innovatory in a poetic, artistic or comedic context.
Of course, creativity does not only come from madness, it can also come from its opposite. Higher-order thinking patterns can memorize creative algorithms and apply them when they deem appropriate. In these instances creativity is less spontaneous, more contrived, but also more “volitional.” Sometimes I catch myself consciously applying certain rules to my thought, attempting to infuse creativity into my thinking or attempting to think outside the box. As I see it there are two paths to creativity, more conscious ones and  less conscious ones.

Both 1 and 2 represent a train of thoughts. In example 1 a normal person thinks about A, then B, then C. Even though A was the first thought, some of the neurons responsible for it are still firing and so it influences what comes after C. In other words, the thought that comes after C is influenced by the coactivation of A,B and C. Coactivity is indicated by the box encompassing A,B and C. Example 2 is supposed to represent someone who, because of schizophrenia, dementia or PFC damage cannot keep the third-to-last thought (A) active. Here the fourth thought, E, is not the same as D because it was not influenced by thought A at all, it is only influenced by B and C. Thus, if previous thoughts drop out of the equation early, attention is not as narrowly focused, possibly leading to the creation of new, novel thoughts.

An Analogy for Top-Down to Bottom-Up Communication: Cake Baking and Tasting

The creation of mental imagery by bottom-up sensory areas, and the subsequent analysis of this by top-down association areas are like a cycle of interactions between a cake baker and a cake taster. The cake baker is the sensory area, the mental imagery that is built is analogous to the finished cake. We have more than one sensory area in the brain so we have multiple cake bakers but for now, let’s just take vision for example. The visual area takes the specifications (ingredients) handed down to it from higher-order, top-down, association areas such as the PFC (the cake taster).
The visual sensory area has tons of baking experience, it is a genius of a baker, but it can only use a certain proportion of the specifications handed down to it to bake the cake. The visual area baker says: “ok, I see the ingredients that the PFC has given me, I know how to combine some of them to make a suitable cake that obeys the laws held in my networks, but some of the ingredients are just not going to work with the others.” The baker might be able to bake a cake with ¾ of the requested ingredients, combining them in certain ways that are consistent with its past baking experiences. 25% of the ingredients the top-down areas are recommending, have to be left aside though. Another caveat, the baker cannot bake the cake using only the ingredients handed down to it by the top-down areas. It has to use other ingredients as it sees fit. This is almost like a baker that says, “ok I can use these ingredients, but to make it work, I have to throw in a few of my own.” So the finished recipe for the cake (the visual imagery that is created) might be made up by 75% of the ingredients recommended to the baker but perhaps 25% of the ingredients used were improvised, not mentioned by the top-down taster (PFC).
So the top-down cake taster takes the cake once the bottom-up areas finish it and takes a bite. In the brain, this happens when higher order brain areas begin to perceive the mental imagery that has been mapped topologically across the early sensory area. The cake taster can appreciate the mix of different elements together and is able to integrate all of these different ingredients into one overall, wholistic taste. To the baker, they are just ingredients. To the taster, the ingredients come together to be more than the sum of their parts. Then the cake baker decides, from the taste of the cake, what ingredients need to be changed. It will say: “I like this aroma, I liked this taste, these ingredients go well together, do it all over baker, but this time use the following ingredients…” The baker takes these ingredients and makes a new cake. The fact that they each pay attention to what the other is doing, but selectively ignore certain aspects keeps their reciprocating conversation going.
 If the visual area is a cake maker, perhaps the auditory area is a soup maker. Importantly soup ingredients can affect cake ingredients, just like processes in the visual areas can affect those in the auditory areas. The taster eats the two, the cake and the soup together, and considers it as an overall meal, and then lets its assessment of the meal affect the ingredients that it hands back down to both the baker and the soup maker. The more intelligent the animal is, the more similar each set of ingredients handed down is to the last. The more scattered and impulsive the animal, the less similarity there is between subsequent cakes.

Read the full article that I wrote on this topic here:

How Thought Propagates

At I have been writing a theory about how I think thought works - how it "propagates" or moves through space and time. I write about how thought is made up of the comingling of several concepts at once. In the brain, this involves the simultaneous firing of all of the neurons that represent each of these comingling concepts. The various neurons involved coactivate together and spread their activation energy leading to the activation of new neurons corresponding to the concept that is the most closely linked (associatively or causally) to this particular set of concepts. Every second, as thoughts change, old concepts are removed, new ones are added, but yet a large number persist. Here is a diagram attempting to show how concepts are displaced, newly activated, and coactivated in working memory to form the “stream” or “train” of thought.

Each concept is represented by a letter and the order in which they are pulled into consciousness follows alphabetical order. 1) Shows that concept A has already been displaced from working memory and that now B, C and D are coactivated. When coactivated, these concepts combine (or spread) their activation energy to activate a new concept, E. Once E is active it immediately becomes a coactivate, restarting the cycle. 2) Shows that concept B has been displaced from working memory, C, D and E are coactivated, and F is newly activated. 3) Shows that concept E, but not C has been displaced from working memory. In other words, what is displaced is not necessarily what came first, but what has proven, within the network, to be the most valuable to the given set of coactivates. C, D and F coactivate to make G active.
Importantly, it would be almost impossible to break down the activation dynamics in the brain into discrete time frames as is shown here. Also, this model makes it seem that only three concepts are coactivated at a time, whereas this number would be larger (perhaps Cowan's 4 chunks or maybe Miller's “7 plus or minus 2”). Further, the concepts that are displaced from working memory may not be in immediate cortical memory, but may still be held in another form of working memory that involves cortical priming or hippocampal memory. This scheme makes it seem that it is only the concepts that we consciously experience that activate subsequent concepts, but the concepts (or nodes) that are unconsciously primed also contribute to the activation of subsequent concepts.

To read part 2, click here on How Thought Propagates Part 2.

Read the full article that I wrote on this topic here:

Wednesday, November 16, 2011

Solitary Mammals Provide An Animal Model for Autism Spectrum Disorders

What follows is the text for the poster that I created and presented at the Cell Symposium on autism, November 2011.

Solitary mammalian species are known to have specialized, neurological adaptations that prepare them to focus working memory on food procurement and survival rather than on social interaction. Both individuals on the autism spectrum and certain solitary mammals have been shown to be low on measures of affiliative need, bodily expressiveness, bonding and attachment, direct and shared gazing, emotional engagement, empathy, facial recognition, gregariousness, joint attention, partner preference, pretend play, separation distress and social approach behavior. Individuals on the autism spectrum also exhibit certain biological markers that are characteristic of solitarily mammals including: altered oxytocin and vasopressin signaling, dysregulation of the endogenous opioid system, early cortical myelination, enhanced amygdalar activation to social events, decreased activation of brain regions associated with conspecific recognition, anomalies in vagal tone and parasympathetic response, and reduced activity in social brain regions. The extent of these similarities suggests that solitary mammals may offer a useful model of endophenotypes associated with autism spectrum disorders and an opportunity for investigating genetic and epigenetic, etiological factors. If the brain in autism can be shown to exhibit distinct homologous or homoplastic similarities to the brains of solitary animals, it will reveal that these changes are central to the phenotype and should be targeted for investigation. Research into the neurological, cellular and molecular basis of these specializations may provide insight for behavioral analysis, communication intervention, gene-environment interactions and psychopharmacology for autism.

Most animals, many mammals and several species of primates are solitary. Adjustments to neural social circuits and associated neurotransmitters, neuromodulators and their receptors, fine-tune solitary mammals to live solitarily. Many of these changes are highly conserved throughout different species of nongroup-living and nonmonogomous mammals. Biologists are beginning to elucidate the neurological pathways that underlie physiological specializations involved in attachment, affiliative intent, bonding and their absence. Also being identified are the neurological traits that correlate with group size and social proclivities. Even though the pathways involved are currently not well-resolved, continued experimental research may have important implications for autism spectrum disorders (ASD) because individuals on the autism spectrum share a variety of traits with solitary species. Individuals with ASD exhibit both behaviors and biological markers that are common in solitary mammals (listed in the abstract). It is the author’s view that modeling inherited autism using these comparative approaches may offer insight into the nature of underlying factors.
Species that are obligately social form groups even under very low population densities (Bothman & Walker, 1999), whereas some species like whistling rats (Paratomys brantsii) maintain solitarily living even under very high population densities (Jackson, 1999). In primates, savanna baboons are always found in groups, orangutans show no consistent grouping and chimpanzees show intermediate tendencies. There are many mammals that have been categorized as solitary including well-known animals such as armadillos, opossums, orangutans, red pandas, red squirrels, Tasmanian devils as well as most bears, cougars, tigers and skunks. The reclusive predilections of these species are thought to be largely innate. The neurochemicals oxytocin, vasopressin and endogenous morphine control many aspects of grouping, affiliation and sociality in mammals and are also play a significant role in autism.

Oxytocin Signaling
Monogamous prairie voles and promiscuous montane voles, two closely related species of rodent, differ widely in bonding behavior. The montane vole, relative to the prairie vole, has a much smaller number of receptors in the caudate nucleus and nucleus accumbens for oxytocin and unlike the amorous prairie voles they do not form pair bonds (Marler, 1968). The montane voles have fewer receptors and thus are less responsive to oxytocin making them more wary, suspicious and more easily frightened of other members of their species (Marler, 1968). Pups of the monogamous prairie vole, but not the promiscuous montane vole, show a robust stress response to maternal separation along with increased vocalization and increased serum corticosterone levels (Shapiro and Insel, 1990). It is thought that the wide discrepancy in social behavior between these two species is genetic, was naturally selected and reflects adaptation to two very different physical and social environments (Adolfs, 2001). Other promiscuous/asocial species such as the rhesus monkey and the white-footed mouse, Peromyscus leucopus, have oxytocin and vasopressin receptor profiles that are highly similar to that of the montane vole and monogamous/social rodents and primates are similar to the prairie vole (Bales et al., 2007; Wang et al., 1997). This may indicate that caudate and nucleus accumbens and their quality of oxytocin reception should be attended to by researchers and targeted by autism therapeutics. Oxytocin is known to be reduced in the brains of autism patients and symptoms are known to be reduced after oxytocin infusion (Hollander et al., 2003). There is only one receptor for oxytocin in humans, but there are several alleles which differ in their binding effectiveness. Individuals homozygous for the “G” allele, when compared to carriers of the “A” allele, show higher empathy, lower stress response, as well as lower prevalence of autism (Rodrigues et al., 2009). It would be interesting to compare the details of oxytocin action - such as receptor number and distribution - in solitary animals with that of people with autism. The comparable data about receptor density in humans has not been determined because injection methods to tag receptors cannot be done in living humans, and do not yield results when performed on dead brains.

Vasopressin Signaling

Experimental studies in several species have indicated that the precise distribution of vasopressin receptors in the brain is associated with species-typical patterns of social behavior (Young, 2009). Infusions of vasopressin directly in the brain facilitate partner preference formation and receptor antagonists block it in male prairie voles (Winslow et al., 1993). Experimentally increasing the AVPR1A levels in the ventral pallidum of promiscuous meadow voles using the injection of a viral vector directly in the ventral pallidum resulted in the formation of strong partner preferences (Hammock and Young, 2006).

There is also evidence for a role of the gene that codes for vasopressin receptor, AVPR1A, in autism that comes from genetic studies of the polymorphic microsattelite repeats in the 5’ flanking region of the gene. Of these repeats overtransmission of RS3 and undertransmission of RS1 has been associated with ASD (Yirmiya et al., 2006; Wassink et al., 2004). Interestingly, microsatellite repeats have also been found in AVPR1A in prairie voles and have been viewed as instrumental in regulating social behavior. The repetitive microsatellite locus in humans and bonobos is 3,625 base pairs upstream of the transcription start site of AVPR1A. Chimpanzees, which are thought to exhibit slightly lower levels of social reciprocity, empathy and sociosexual bonding, do not have this microsatellite locus and Hammock and Young (2005) have suggested that this is reminiscent of the genetic differences between highly social and asocial voles at this same locus. Instability of microsatellite sequences may serve as a kind of evolutionary “tuning knob” (King, 1994) and Hammock and Young have done extensive research suggesting that the AVPR1A locus may be such a tuning knob.

Endogenous Opioids
Endogenous opioids are thought to be associated with the consummatory phase of affiliation. Blockade of endogenous opioid receptors by an opioid antagonist in primates increases the need for social attachment and therefore the solicitation of affiliative behavior from social partners (Martel et al., 2004).

Acute treatment with nonseditive doses of morphine significantly decreases grooming solicitations in primates as well as decreases grooming performed. Morphine also reduces huddling duration and social activity in prairie voles (Shapiro et al., 1989). Because individuals on the autism spectrum have higher opioid levels and higher opioid receptor activation, it is thought that they may be missing the consumatory phase of affiliation also seen in solitary mammals (Gilberg, 1995; Machin & Dunbar, 2011). Clearly autistic children lack the normal motivation to engage others socially, as indicated by their lower social initiative and lack of spontaneous communication (Sahley & Panksepp, 1986). Oxytocin and vasopressin also facilitate the effects of endogenous opiates. In rodents, oxytocin neurons in the paraventricular nucleus of the hypothalamus project to the neurons in the arcuate nucleus and increase their release of opioids (Csiffary et al., 1992). These might be among the first areas that call for further examination in autism.

This review helps to illustrate that analyzing the neurobiological bases of social behaviors in divergent species may, with appropriate caution, constitute a valuable method for investigating autism. Basic research looking at the neurological foundation of behavior in solitary mammals may allow substantial insights into the neuropathophysiology of ASDs. Not only may the study of solitary mammals affect the study of autism, but research in autism may also help to elucidate phenomena in social neuroscience and social cognition. An important question is: are the neurobiological mechanisms found in solitary mammals sufficient to capture the nuanced social impairments featured in the autism diagnosis? Because of the various etiological contributions to autism it is clear that not all of autism can be attributable to natural cognitive specializations for solitary living.

Other species have found myriad ways to reduce social contact for adaptive purposes, and understanding how this is accomplished may provide insight into prosocial pharmacotherapeutics or even gene therapy for autism. It will be interesting to see if receptor distribution patterns of oxytocin, vasopressin, endogenous opiates, serotonin and dopamine in the brains of solitary mammals match that seen in autism. If so, it will be important for scientists to compare the relative distributions of these receptors in different animals to determine which areas in the autism brain are not affected enough by social neurochemicals so that these areas can be targeted. The model may also allow a privileged vantage point into the autistic brain, which can only be studied in limited ways because of technical limitations and ethical concerns. It may be possible to test drugs and even behavioral interventions in solitary or nonmonogamous animals to determine if these have the capacity to reverse social interaction deficits.

To see the entire manuscript click here.

Thursday, November 3, 2011

Evolution, Alzheimer's and Neuroecology

Click on the images below to see the posters that I created for the Alzheimer's Association's Research Update. The posters are based on a manuscript about the natural history of Alzheimer's disease that can be found at the following URL:

The paper attempts to reconceptualize the pathological changes that accompany aging. It points out that many vital areas are spared by the senile plaques and tangles and that it is predominately the brain areas associated with learning new, higher-order concepts that are burdened with neuropathological load. These changes uncanilly follow another transition, seen in early adolescence, where rapid learning is slowed down because a large proportion of what a child needs to learn has already been learned. The demands on working memory seem to diminish throughout life and alzheimers may represent a pathological extension of an adaptive age-related decline in working memory function.

The original paper is entitled: "Alzheimer's Disease and Natural Cognitive Aging May Represent Metabolism Reduction Programs"

 ...Oh, added 12/12/11... The work was mentioned by an excellent article in Alzheimer's and Dementia entitled: "Some evolutionary perspectives on Alzheimer's disease pathogenesis and pathology." It was a very interesting article that should be read because of its insightful take on the history and function of neuritic plaques and neurofibrillary tangles. Here is some of what they had to say about the theory:

"Reser [1] discusses the intriguing possibility that preclinical or prodromal AD itself is an adaptation, a kind of “rescue program” that allows the body to conserve resources in food-scarce environments. Many other body systems downregulate in response to low caloric intake, shunting precious calories from the least crucial areas to the most vital ones, and because the brain is a bioenergetically high-cost organ, it might be expected to do the same. Reser suggests that the parts of the brain involved in attending to and encoding new information are expendable in a natural environment once an animal reaches the age where it has learned all the skills it needs to survive. In such an environment, the loss of the least crucial brain areas in exchange for precious calories is a utilitarian trade. In modern human society, however, those brain regions (the hippocampus and higher-order association cortices) are involved in domains that we now highly value, such as higher-level executive functions, personality, working memory, and episodic memory. Also, contemporary civilization, public health initiatives, and medical advances, especially in infectious disease, cardiovascular disease, and cancer, have extended the life span far beyond what we would assume to be that of Homo in the wild, who generally would have died of predation, starvation, injury, or infectious disease. Therefore, clinical AD, in Reser’s view, is “the unnatural progression of natural brain aging changes.” Circumstances notwithstanding, apoE influences the deposition, aggregation, activity, and neurotoxicity of Abeta, and APOE e4 correlates with increased Abeta load in AD patients relative to the other alleles [16]. Next, we examine how Abeta and neurofibrillary tangles, the two signature pathologies of AD, fit into this integrated evolutionary picture and how evolutionarily informed research should approach them."

Wednesday, October 26, 2011

Subliminal Frowning Can Create A Powerfully Negative Somatic Marker

I woke up this morning an hour before my alarm clock sounded. I realized that I would not be able to get back to sleep so I held a few yoga stretches and lay back down to meditate. I was doing so concertedly, concentrating on abating the chaotic negative thinking that is constantly going on in my mind. I tried to notice the recurring waves of negative thought crash on the forefront of my consciousness and I was trying to break them up slowly but methodically by examining the sensations involved. I found myself actually making some headway. I felt some of the storm clouds in my mind begin to dissipate and then I realized what was really happening… I was slowly relaxing a low-grade, perpetual frown or grimace from my face that I must have learned to ignore long ago. This is a subtle wincing, barely perceptible in a mirror, that I believe may afflict many of us and contribute to psychological distress and even psychiatric disorder.

I stayed in bed for a full hour keeping the contorting expression from coming back. As soon as my mind wandered, the tension around my eyes would resurface and I realized that my motor systems had become accustomed to sustaining it. Similarly, I have found that, ever since a series of "traumatic" incidents 8 months ago, I wake up every morning clinching my teeth. There are many examples of our muscles retaining tension that is completely unnecessary. This happens because the brain systems responsible have compensated for the constant demand and moved on without continuing to apprise us of their relentless activity. By habituating to such burdens we force ourselves to carry them unknowingly. I think that this subliminal frown has contributed a good deal to my anxious and depressive thinking.

After contemplating this and attempting to bring awareness to the feeling of frowning (and its absence) for an hour, I got dressed and went on with my day. But something was very different. It was as if a huge weight was lifted. I felt like I had taken a powerful antidepressant - the feeling was unmistakable. Throughout the day today I noticed that the frown would return all on its own. Each time I noticed it, I allowed my face to turn placid again and the calm, tranquil feeling would reinstate. Now, at the end of the day, just thinking about frowning makes me feel nauseous. Holding a frown now feels like I am reinflicting a wound. I hope I never go back to inadvertently and subconsciously maintaining a discomfort-inducing countenance.

Now you might be a little skeptical. You might not believe that people have the capacity to unwittingly carry mental hardship with them in the form of a frown. But imagine a small monkey. Imagine this monkey was traumatized as a baby and ever since has trod around with a wince on his little face. He will derive pain from it. Just imagine how this would affect his inner world, his encounters with others and their impressions of him. He inevitably will perceive things as more negative than they really are because of the powerful interrelationships between bodily expression and emotional condition. The biological underpinnings of this have been explored by the "facial feedback hypothesis." I think a frown actually has the capacity to create a “somatic marker,” anchoring you to an aversive state. Please, spend a few moments of your own looking for this in yourself and taking measures to counteract it.

Addendum 2/15

I recently had a cup of coffee and bedded down in my garage for three hours in a search for the source of tension in my mind. I continued my search as I did before (in the anecdote above) when I realized that I was continually wincing. I had previously traced the source of a good proportion of unease and anxiety to the tension that I unconsciously held in my eyes and cheeks. Even though it seemed that my entire face was now fully relaxed I still figured that there must be another tense cramp somewhere in my psyche that I had to discover and unravel. I was in total dark, there were no noises and I tried to get as comfortable as possible so that I was not distracted by the urges to reposition myself. I imagined myself searching in the dark for a large knot somewhere in the recesses in my brain. The imagery was unrealistic but it helped to drive me toward what I was searching for. I expected to notice that my anxiety was maintained by a certain thought pattern. I half expected that this would generally consist of a string of normal thoughts followed by a brief, subtle state of panic repeated over and over again. I was searching for this pattern so that I could understand and interrupt it. But the pattern wasn’t psychological as I expected, it was still facial.
I must have been ignoring the sensation for 15 years, but when it finally reemerged into my consciousness it was clear and unmistakable. Lying in the dark, I felt a tingling sensation on a small strip on the bridge of my nose. I realized that the muscles that led up to this strip were highly flexed or tonic. The muscles fibers in this area constitute the superior portion of the nasalis muscle and especially the procerus muscle which crosses the bridge of the nose and anchors near the cheeks. For the first time, I could tell that even when I thought I was relaxing my face, these muscles were still in overdrive. It took an hour of meditative thought and exploration to even notice; however, once I became aware of the sensation it was impossible to ignore – it was all I could feel for several minutes. I felt that the muscles were very tense and stiff, but I could not relax them. I could feel that they were flexed but I couldn’t intervene, as in the hypertonia or spasticity that is seen in some cases of partial paralysis (or paresis).
Immediately after first feeling the sensation on the bridge of my nose I remembered that I had been struck over the head with a weapon in a fight in high school in this exact same location. The blow had shattered my nasal bone in several places and must have affected the nearby musculature and nerves. I realized that somehow this damage is still affecting me and that I couldn’t do anything to curtail it. I wondered how long I had been frustrated or burdened by this constant tension without realizing where it was coming from. I knew that I had an ongoing personal problem with psychological stress but I never guessed that it had such a simplistic physical anchor. Now that I had finally brought conscious awareness to the sensation of the tension I was determined to arrest it.
At this point I had been lying supine for over an hour and it took another full hour to develop some voluntary control over this muscle. For the first few several minutes I could not control it at all. I eventually “found” the muscle by trial and error. Actually, I first had to learn to clench the muscle before I could learn to relax it. Slowly, after several minutes of clenching I began to develop a sense for what it feels like to relax it. Interestingly, every time I actively tightened or relaxed the muscle, the patch of scar tissue on the bridge of my nose would tingle and feel numb. This was the exact same tingle and numbness that I have felt accompanying other examples of nerve damage. If you have ever had a deep tissue cut or wound where a nerve has been damaged then you know this feeling. It often indicates that the cortex is relearning how to control or receive feedback from an area of the body whose nerves have been damaged . My control over the flexion and relaxation of the muscles in my nose was feeble and imprecise at first. It got better, but every time I relaxed it I felt the numb and tingling sensation. I believe that nerve damage to this area was wholly responsible for over a decade and a half of unremitting wincing which in turn led to persistent anxiety.
Another issue that I think may have been involved is the following: The impact damaged my nasal muscles and nerves and gave my face a general dull, inattentive look that I tried to make up for by keeping my nose and eyes muscles tight. Especially in social situations I attempted to compensate for the hypotonia, in an effort to bring some life and energy back to damaged facial expressions. I think this made my social interactions neurotic and frenzied. Coincidentally, this kind of damage also happened to my cat, Niko. The little guy was tracking a bird’s nest and was pecked in the forehead by a protective mother bird. For at least a month Niko’s face looked dull and inattentive because his brow muscles were lax. The muscles or nerves must have been damaged because his eyes looked dull and tired even when I was trying to play with him. After a few months his eyes returned to their former state. Luckily, unlike me, Niko didn’t try to compensate for the damage, but he sure did look funny (and less attractive overall) for several weeks.
After a few weeks of working with the muscle every day I have gained enough control of it so that whenever I am alone it remains in a resting state. Interestingly though, every time I find myself in a social situation I have a tendency to flex this muscle and it causes social anxiety. It seems that having this muscle flexed became an integral component to the way I used my face socially. In fact, at this point, many of my social facial expressions cannot be expressed authentically or completely if I do not flex this nasal muscle. It seems that my entire facial repertoire has been built around this nasal flexion and when I relax it during a conversation, looks of concern, knowing glances and social smiles just do not come out properly.  I am now relearning how to make social expressions without the muscle and it is a slow but steady process. I used to flex this nasal muscle when I modeled or reenacted social interactions in my imagination. I would do this on a daily basis in the past and it was usually very stressful. Now I am able to relax, at least whenever I am alone, and this has brought renewed calm to my life as a whole. I am very grateful because I feel confident that I have been able to pinpoint the source of a good deal of my anxiety and neuroticism. I feel a little bit like I have a new lease on life because I have overridden a previously unconscious burden. Now I find that if I inhibit facial tension, it is actually difficult to become stressed. I think that this must be true of everyone and I wish to encourage people to master their emotions by becoming aware of and learning to subdue their negative expressions.