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Like epilepsy, Tourette Syndrome is another interesting phenomenon that involves the random generation of outputs from the nervous system without any understandable input to the nervous system and thus would seem to fit our model of the internal generation of action potentials and through them visible behavior. Tourette syndrome involves the production of both physical (motor) and verbal (phonic) "tics" that occur intermittently and unpredictably out of a background of normal motor activity" 1 having the appearance of "normal behaviors gone wrong."2 However, the cause for Tourette syndrome is largely unknown (i.e. the exact gene that pertains to the susceptibility of the phenomenon has still yet to be identified), although it does tend to be an inheritable trait. The cause of the "tics" themselves (excessive blinking, twitching, bodily jerking, coprolalia--the utterance of social unacceptable words or comments---etc.) are believed to be related to particular cable dysfunctions (i.e. axonal operations) in the thalamus, basal ganglia and the frontal cortex of the brain, in which "models implicate failures in circuits connecting the brain's cortex and subcortex"3. Could these circuit failures possibly be related to leaky circuits i.e. leaky cables?

What's more is that the state of these circuitry failures, these potentially leaky cables, are very plastic and mercurial. The very nature of Tourette’s is that the symptoms are almost always entirely sporadic and unpredictable, often occurring in irregular bouts with great stretches of time taking place in between episodes. Also, in most cases, Tourette’s is a phenomenon that tends to decrease in both number and severity of episodic occurrence as a person ages and often almost disappears entirely by the time a patient reaches adulthood. If we are to suggest that the circuitry failures underlining the visible symptoms of Tourette’s (i.e. the tics) is related to sodium leaky axons than what accounts for the change in the relative leakiness of these cables (i.e. how can they change their state of leakiness and if relative leakiness is plastic is leakiness then not part of the overall design of the nervous system...is Tourette’s just some kind of unregulated phenomenon of inappropriate leakiness?).

Also, in relation to Nelly's questions about voluntary behavior versus involuntary neurological phenomenon (the control of our own action potentials) Tourette syndrome also deals with "premonitory sensory phenomenon", in which Tourette's tics are understood as a semi-voluntary or "unvoluntary" (v. involuntary) 3 action, i.e. the "I-function" is conscious of the onset of their implementation and can suppress them to a certain degree the same way we anticipate a sneeze or an itch and, to a limited extent, can exercise some control over these actions. I am curious to known where this idea of the "unvoluntary" action, of the tic that is at once a seemingly random neurological generation beyond our perception, as well as, a semi-cognitive action, falls into our spectrum of "conscious v. unconscious" inputs and outputs, "random action potentials v. coordinated behavior".

1. The Tourette Syndrome Classification Study Group. "Definitions and classification of tic disorders". Arch Neurol. 1993 Oct;50(10):1013–16. PMID 8215958 Archived April 26, 2006.

2. Dure LS 4th, DeWolfe J. "Treatment of tics". Adv Neurol. 2006;99:191-96. PMID 16536366

3. "Tourette Syndrome". Wikipedia the Free Online Encyclopedia. Wikipedia Foundation. <http://en.wikipedia.org/wiki/Tourette_syndrome>.