EDITOR’S NOTE: This multipart series first appeared in the March 2010 edition of the Journal of Clinical Psychology Practice and also can be found on Life’s A Twitch, a website run by Canadian psychologist Dr. B. Duncan McKinlay.
“Insider” observations, passed through the more current lens of my discipline and training, hint to me that aspects of this disorder are likely learned. I do not suggest an alternative understanding of the etiology or pathology of TS, nor are my observations in contradiction to exemplary work many giants in this field have contributed to uncovering the underlying physiology of this complex neurodevelopmental disorder.
Rather, what I suggest serves as an expansion of the same. Neurological explanations are necessary for understanding TS but, to date, findings have not been sufficient to account for much of the phenomenology of the disorder. The dysregulatory stage may be set, but the play performing upon it remains a mystery warranting scrutiny as well. Individual and contextridden learning experiences likely mould the shape of any neurodevelopmental skill deficits, just as home computers are influenced by each owner’s tastes.
Once indistinguishable from all others, customized machines are created based upon programs and content loaded, internet sites visited, and choices each owner makes within constrained options — regardless of the uniformity of each machine’s various innards.
Of course learning components have neurological substrates as well, and perhaps one day neuroimaging technology will be such that these can be readily identified. Until that time (and perhaps even to expedite its arrival), the use of existing learning theory can serve to provide direction in broader strokes – akin to surveying a beach to determine which particular grains of sand then bear further analysis.
Each day, beneath our awareness and beneath our cortex, our brains are busy memorizing patterns of movement. Routine and simple things – like my eye-blink – would be ripe to be incidentally associated with countless other goal-directed behaviours, actions and sounds preceding them (e.g. walking through a doorway and blinking, picking up a pen and blinking, seeing a good friend and blinking).
Over the course of years these incidental associations no doubt occur here and there; in the absence of a “normal” ability to prune and/or inhibit such associations they might strengthen as per Hebbian principles.
What if eventually these associations became so strong that various goaldirected behaviours, actions or sounds actually served to elicit any stereotyped movements or noises “accidentally” associated with them?
This would indeed “hijack” something like an eye-blink from context, and this “hijacking” would occur both frequently and at seemingly random intervals given the countless daily goal-directed behaviours, actions and sounds that eye-blinking would be networked with. Not blinking might very well create a nagging, free-floating Zeigamik-like sense of incompletion which remains until the pairing is complete. What we call a premonitory urge.
This model is not so far-fetched: it weds well with the concept of neuronal plasticity. Nor is it so far-flung from good neuroscience. We know a function of the basal ganglia is to learn motor patterns and that frontal lobes play a role in inhibition of said patterns; two areas implicated in the pathophysiology of TS.
And in my 2001 doctoral dissertation I demonstrated that while associations do form between various motor movements serendipitously occurring together, only those individuals with demonstrated difficulties in motoric inhibition and exposure to the incidental learning trial subsequently demonstrated the expected behaviour; a weak, context-dependent “tic.”
Youth with TS unexposed to learning trials, and all controls, did not acquire the behaviour. This “tic” exhibited the same signature burst-like pattern typically seen in TS; moreover, those exposed to the incidental learning trial reported significantly higher urges to engage in the “tic” than did unexposed groups.
When I apply this model (which I’ve termed the Incidental Associations Model of Tic Formation) to my personal experiences the logic of it is persuasive. To begin with, I have a wide repertoire of tics — but with parameters. Not everything and anything is disinhibited; only those things in me that tend to occur often enough, and similarly enough each time, to be vulnerable to a great many incidental associations are affected. And the more universal a human experience this thing is that I do, the more it seems to be shared among the TS population as a tic.
Even my more complex symptoms have their lineage traced back to these simple behaviours – multiple simple tics which over time chained together (a kind of higher-order conditioning) and/or over time gelled into something new and not immediately recognizable from its component parts. Perhaps this is why complex tics tend to appear some time after simple tics.
My tics first appeared somewhere around the age of 7; this “sudden” appearance of symptoms might only have been an illusion, analogous to a submarine cresting the water’s surface. The rising strength of my own incidental associations would be masked only until the urges for completion were of sufficient strength to elicit those simple movements and noises lashed to my goal-directed behaviours. The tics themselves may have “broken the surface” abruptly; however, their origins (and the increasing salience of the premonitory urge sensations) were perhaps more insidious.
Tic suggestibility may not have been the work of malevolent inner demons after all: a spreading activation of associations (from “I see my mother” to “things I know about my mother” to “my mother hates it when I make certain noises” to “don’t make those noises” to the noises themselves) would naturally prime the exact wrong thing at the exact wrong time. This rebound to what we don’t want to think is called an ironic process and is a universal human experience; the only difference with me is that my ironic process is on display — I wear it on my sleeve as a result of my poor self-regulation.
Drawing my attention to a particular body part, object, or behaviour would also trigger the arousal of any associations to it, including incidental motoric ones. Premonitory urges are then induced, seemingly “following” my attention wherever it may roam. Like a bored and aggravating younger sibling.
The calmness of my tics each morning – each “reset” in anticipation of my first movement – would occur because each of my tics are joined to voluntary behaviours. Until I arise, engage in one, and unwittingly activate the chain no impetus (or “priming”) for their expression yet exists.
Purposeful components of goal-directed behaviour occur together much more reliably and in a much more consistent order than would any accompanying incidental behaviours. Hence, any incidental associations would likely not be as strong as the purposeful ones. It’s conceivable then that in the case of highly complex tasks with a variety of simultaneous demands (like presenting, assessing, juggling and drumming) all cognitive resources are devoted to the orchestration of the required purposeful movements.
In this scenario, with no reserves to “bleed off,” there is no room for incidental associations (and therefore any urges or tics) to establish. Even more convincingly, I’ve noted that only when a complex task becomes more routine (i.e. I am utilizing fewer resources to execute it) do tics gradually begin to encroach upon it.
“Older” tics would be ones more deeply “entrenched” in their associations; they’ve had opportunity to attach themselves to many more goaldirected behaviours in an ever-growing web of complexity and have generalized and accommodated in their learning. Premonitory urge sensations operate as “markers” for tic age and strength in this model, likely why I found premonitory urges more salient and identifiable over time.