Abstract

     The diagnosis of TS (Tourette syndrome) according to the DSM IV (Diagnostic and Statistical Manual, American Psychiatric Association) criteria is based upon the presentation of movement and vocal "tics" over the course of at least one year. Affecting one in a hundred persons with its classic motor and vocal symptoms, TS is an often misdiagnosed and misunderstood but prevalent, hereditary disorder with perhaps up to twenty five percent of the general population being carriers of the TS gene.

     This paper will submit evidence that the genetic etiology of TS maintains connections to that of other "common" neurological disorders, including ADHD (Attention Deficit Hyperactivity Disorder), learning disorders such as dyslexia, conduct disorders, addictive behaviors such as compulsive eating, shopping, gambling and alcohol consumption, obsessive-compulsive behaviors, depression and mood swings, anxiety including panic attacks, phobias and paranoia.

     Because the symptoms are often misdiagnosed as psychological aberrations, and because these behaviors are so rampant in our society, it is important for the mental health community to know when they are genetically and neurochemically caused and not environmentally induced, although the impact of environmental triggers must be recognized and assessed. Given an increased professional and lay understanding of TS and associated disorders, this author predicts and encourages a dramatic shift in treatment paradigms and how clinicians respond to troublesome behaviors in our communities.

     The reader should note that this author has been afflicted with TS since age three and can personally validate the sometimes very painful and disabling but wonderfully complex and intriguing experience of this disorder.

TS Symptomology

TS literature presents a diverse number of representative cases:

A woman who compulsively vacuums her carpets eight times daily,

A man with severe conduct disorder who has been in psychotherapy for two years with no improvement,

A boy who is punished by school officials for acting out by noise making and slapping desk tops and walls,

A seven year old who, after biting his nails completely away, could not stop chewing the skin from the sides of his fingers,

An intelligent nine year old who is failing school because he cannot read or focus on a task,

A young woman who began to have panic attacks and cannot go to work,

A high school student who must remain in air conditioned rooms because heat causes severe convulsions of the neck and legs,

A newly married woman whose husband left her because of her violent temper,

A respected doctor who must continue blurting out-of-context profanity during staff conferences,

A five year old who cannot use glass cups due to his compulsion to chew on them...

     Some of these individuals I have read about and have personally met many of them. All of them are possibly TS gene carriers. Neurologist Oliver Sacks wrote, "In 1885 George de la Tourette described the astonishing ailment that now bears his name, a syndrome of strange motions and notions.... tics, jerks, mannerisms, grimaces, noises, curses, and compulsions of all sorts... TS is a disorder of animation, quite the strangest and most complex there is... It involves every aspect of the emotional, the instinctual and the imaginative life." (1.) TS was once considered to be a very rare disorder, and still so in many circles, with comparatively little attention in even the contemporary psychological literature. Yet much evidence points decisively to TS being one of the most common genetic diseases affecting people now and throughout history, perhaps as high as twenty five percent of the population carrying the trait. Medical and mental health practitioners are beginning to abandon the notion that a person must present a scene of violent twitching, swearing, spitting and grunting to make a positive assessment of instead are more carefully examining family history and behaviors previously explained by psychological/pathological models.

     This researcher and author asserts a widespread and more accurate understanding of TS will mean the crumbling of a psychological Berlin Wall, allowing great unification in territories of understanding and modifying all human behavior.

Motor Tics

The following is a partial listing of repetitive movements associated with TS:

Face: eye blinking and rolling, grimacing, licking lips, blowing or whistling, biting the inside cheek, grinding teeth

Head, neck, shoulders: hair stroking, neck flexing, moving head back and forth or side to side rapidly, touching shoulders with chin or shrugging shoulders.

Arms and hands: flailing arm, reaching for impossible-to-reach places (such as way behind the back), biting nails or picking at skin or scabs, poking or finger strumming, hand waving.

Diaphragm: inhaling and/or exhaling forcefully, gasping for breath, diaphragmatic convulsions.

Legs and feet: kicking, hopping, skipping, jumping, flexing or extending ankles, turning foot in, dragging or shaking foot, stomping or tapping, toe curling or walking on toes.

Others: chewing on clothing, hitting, scratching or cutting self, smelling objects, twirling hair, sticking finger in throat, touching hot surfaces, whole body jerking, hunching over while walking.

Vocal Tics

     Animal noises (barking), coughing, deep breathing, grunting, hissing, humming, screaming, sniffing, snorting, stuttering, sucking, throat clearing, whistling, yelling, swearing (coprolalia), teeth tapping.

Tic Characteristics and Onset

     Of those persons in whom the TS gene is penetrant, 20 percent start between the ages of 1 and 4, 65 percent between 5 and 8, 15 percent between 9 and 16. The penetrance for chronic motor or vocal tics was 70 percent in males and 30 percent in females over several studies by Pauls and Leckman (2), estimating the percent of females manifesting the gene only as obsessive-compulsiveness at 15. Other disorders with a strong genetic basis, such as autism, antisocial behavior, attention deficit, conduct disorder and alcoholism, also demonstrate a predominance of males. Females who are having trouble with these same genes may be expressing them as different disorders and researching these will provide valuable insight into human behavior.

     Two characteristics of motor and vocal tics which detract from accurate diagnosis are their suppressibility and "waxing and waning". Like other normally involuntary functions such as breathing, tics can be controlled by having them blend into more purposeful behavior and thus hiding them, or stopping them altogether for certain time periods. Throughout the course of a month, year or life time, the severity and frequency of the tics may vary greatly or actually go into permanent remission. Although a cause-effect relationship may appear between the onset or exacerbation of tics and events or circumstance in the person's environment, it is important to understand that genes cause TS and not events.

Etiology of TS: Genetics

     Oliver Sacks wrote, "The day after seeing Ray, it seemed to me that I noticed three Touretters in the street in downtown New York. I was confounded, for Tourette syndrome was said to be excessively rare. It has an incidence, I had read, of one in a million, yet I had apparently seen three examples in an hour... Was it possible that I have been overlooking this all the time, either not seeing such patients or vaguely dismissing them as 'nervous', 'cracked', or 'twitchy'? Was it possible that Tourette's was not a rarity, but rather common -- a thousand times more common, say, than previously supposed? The next day, without looking, I saw another two in the street. At this point I conceived a whimsical fantasy or private joke: Suppose (I said to myself) that Tourette's is very common but fails to be recognized, but once recognized is easily and constantly seen." (3)

     A school psychologist familiar with TS watched for symptoms in 3000 children over two years and reported a definite TS diagnosis in one out of one hundred male students. (4) Family studies have provided evidence of TS inherited as a dominant trait in which some who have the gene show no symptoms. (5)

     Reports from the National Institutes of Health based on family history and genogram studies established that motor tics and verbal tics alone were genetically related to TS along with other apparently "psychological" disorders. (6)

     Identical twins carry the same sets of genes being formed by the splitting of one embryo, while fraternal twins do not possess the same genes any more than brothers or sisters born years apart. Comparing identical and fraternal twins can therefore be a substantial tool for exploring genetic versus environmental causes. Concordance, the rate at which a disorder will be present in two people, will be 100 percent for identical twins and between 25 to 50 percent for fraternal twins. If a disorder is purely environmentally caused, then the rate of its appearance will be about the same in fraternal and identical twins. If the disorder is purely genetic, yet somewhat influenced by the environment (as most everything is), then its rate of concordance will be far greater in identical twins than in fraternal twins or siblings. Several studies demonstrate the genetics of TS, one reporting 83 percent concordance of TS in identical twins against a 0 percent in fraternal twins; and a 100 percent concordance in identical twins for tics and ADHD against 50 percent in the fraternal twins. (7)

Neurochemical Etiology

     From its discovery and well into the 1960's, TS has been an exciting playground for psychoanalysts who saw its varies symptoms as a release of deep mental damage inflicted by parents or the discharging and redirecting of deep seated repressions or the convoluted expressions of a monstrous libido. The entire psychotherapeutic world had to sit up and take notice, however, when Seignot (8) immediately reduced TS symptoms with haloperidol (Haldol) in 1961. This drug is a dopamine receptor blocker and thus indicates that TS is based upon over-productive dopamine neurons or oversensitive dopamine receptors. Furthermore, it was demonstrated that drugs which stimulate these neurons or receptors aggravate TS, including amphetamines, Ritalin, cocaine and morphine. (In small doses morphine was observed to reduce TS, yet is a dopamine stimulator, providing seeming contradiction. However, this effect actually supports the evidence since small doses binds first to the receptors, stimulating them and comparatively inhibiting the neuron discharge. In higher doses it binds to and stimulates the neurons, making the symptoms worse.)

     Dopamine breaks down into HVA (Homovanillic acid) and the amount of HVA in the spinal fluid will indicate the dopamine turnover in the brain. The HVA level of TS persons is significantly lower compared to a control group.

   Dopamine is converted to norepinephrine. There is evidence that too little of the latter results in depression while too much causes mania. Clonidine, one of the medications of choice for treatment of TS, decreases norepinephrine in the brain and increases se  rotonin.

     Serotonin is another major neurotransmitter essential to governing impulse disorders such as TS and thus deserves the label of "the Great Inhibitor". Low brain serotonin gives way to an explosion of emotion and impulses. All of the various and diverse behaviors of TS and other disorders caused by the TS gene can be explained by a genetic defect in brain serotonin. The film, "The Exorcist", was inspired by a TS case treated at Georgetown University in Washington, D.C. A "devil made me do it" etiology is on par with a psychoanalytic one and both are admirably surpassed by the more useful neurochemical model.

     5-HIAA (5-hydroxyindole acetic acid) is a break down product of serotonin. As measured in the spinal fluid, a study reported an increase in the severity of tics in persons with the lowest levels of 5-HIAA. (9) Furthermore, when a TS patient was given a drug that inhibits serotonin (cyproheptadine), the result was an "explosion of motor and verbal tics." (10)

     A defect in the metabolism of serotonin is strongly connected to the following disorders: Aggression, hyperactivity, conduct problems, drug and alcohol abuse, heat intolerance, EEG abnormalities, mood swings, obsessive-compulsiveness, schizoid symptoms, temper outbursts and sleep interruption.

ADHD (Attention Deficit Hyperactivity Disorder)

     Attention Deficit Disorder is the most prevalent symptom of TS second to motor and vocal tics, and is far more disruptive. In any cases the TS gene may present itself only as ADHD, which, in most cases, is a genetic disorder.

     Stefl and Rubin questioned over 400 members of the Ohio Tourette Syndrome Association and reported that 26 percent of TS afflicted individuals were also diagnosed as ADHD, 31 percent as learning disabled and 25 percent as conduct disordered, or a total of 48 percent with one of these diagnoses.

     Amphetamines, such as Ritalin, are known to be effective in reducing ADHD. This class of medication increases rain tryptophan which in turn increases serotonin levels. Children with phenylketonuria (PKU) suffering from varying degrees of retardation show low levels of serotonin and behaviors similar to those with ADHD.

     People who were placed on low tryptophan diets to decrease their serotonin levels manifested depression and difficulties in concentration. A 25 percent decrease in the the ability to focus on as task such as reading resulted from only a moderate reduction in brain serotonin. (11)

     A drug that has been widely used recreationally on college campuses, known as Ecstasy or MDM has characteristics of both mescaline and amphetamine. Aside from the euphoric effects, others include jaw clenching and teeth grinding. Students, however, also reported they would avoid using the drug on school nights because the next day's effects included difficulty in concentrating. Studies on monkeys have shown the drug to selectively destroy serotonin nerve endings and deplete serotonin levels in the brain. (12)

In one study, 38 percent of all TS children failed a grade compared to 8.5 percent of a control group. An interesting converse of this was a report of 6 percent of TS children skipping a grade against 4 percent of the general population, indicating that TS children can be very intelligent and do well when lacking ADHD or a learning disorder as one of their symptoms. (13)

     Like many TS symptoms, stuttering has been assumed to be a psychological disorder due to stress and other reasons when, in fact, it has been identified as a genetic condition. Just as in TS, three times as many males stutter as females with positive family history for stuttering, against 5 percent of the population. The literature includes a study documenting 32 percent of TS patients having a stuttering problem compared to 6 percent of the control group and evidence pointing to the TS gene as one of the genes causing stuttering. (14)

Obsessive-Compulsive Disorder (OCD)

     Next to motor and vocal tics, the TS gene presents itself most frequently in illogical repetitive and ritualistic behaviors affecting 30 to 90 percent of TS patients. According to studies in 5 major cities, 1 to 3 percent of the general population manifest this disorder, being present without tics most commonly in TS gene-carrying women. (15)

     Compulsive behavior include: eating, touching objects over and over until it feels right or for an exact number of times, placing things in the right places, fiddling with objects or clothes, symmetrical touching (evening up), pulling hair out, pulling up socks or folding them around the foot in a particular fashion, walking in a certain way with measured steps, self-destructive impulses, nail biting, thumb sucking, vomiting, mimicking, stealing.

     Obsessive thinking and behaviors include: violence, spelling things forward and backward, counting things, cleanliness, mind racing, textures needing to be just right, repetitive thinking of a thought or question, dwelling on silly or unreasonable thoughts, thought intrusions regarding death.

     Connections between TS and OCD include: Onset early in life, lifelong development, waxing and waning, intrusive and ego-attacking behaviors, bizarre violent and aggressive themes, family history, aggravated by anxiety and depression, responds to medication, can be caused by other neurological disruptions such as postencephalic states and amphetamine overdose. In a study of OCD in 93 twins, concordance was recorded in 70 percent of identical twins and only 15 percent in fraternal twins. All these twins lived separately and were not aware of each others' symptoms, yet the OCD started at their same ages and developed a very similar course. (16) Another study reported 25 percent of OCD patients had a parent or sibling with the disorder. (17)

     In a study of 50 TS patients, 68 percent demonstrated OCD, 48 percent with self-destructive behaviors, 40 percent with learning disabilities and 26 percent with antisocial behavior. (18)

Autism and TS

     Kanner first described autism in 1943 and wrote that he was impressed with the "extreme aloneness from the beginning of life and an anxiously obsessive desire for the preservation of sameness." (19) His fostering of the prevailing view that autism was a result of psychological damage caused by rejecting parents who unconsciously wished the child was never born, must have triggered great pain in many.

     Davison and Neale wrote of the obsessional character of autistic behavior: "In their play they may continually line up toys or construct intricate patterns out of household objects. They may become preoccupied with train schedules, subway routes, and number sequences. By adolescence, full-blown obsessions sometimes appear." They go onto describe autistic children's stereotypical behavior, "peculiar ritualistic hand movements," explaining "Often toys are used in a compulsive and ritualistic manner rather than for their intended purpose." (20)

     As evident in the literature, milder cases of autism are very similar to that of TS and, interestingly, 2 percent of TS children begin their lives with autistic behavior. Autism involves the same brain locations and neurotransmitters as in TS.

     Panksepp, in 1979, pointed out remarkable similarities between autism and narcotic addiction, including insensitivity to pain, ignoring the mother, lack of socialization, seizures and walking on toes. (21) During pregnancy, endorphin levels (the brain's "natural sedative") are high, keeping the fetus quiet and content. During the first years of life the longer acting endorphins shift over to shorter acting enkephalins. While normal brains are able to rapidly turn on and off their own "opiate systems", the autistic child's dramatic changes from dissociated and dreamy states to extreme panic, turmoil and crying may indicate a defect in the switching process. The high levels of endorphic opiates in autistic children keep them "high" and eliminates the need for a mother contact. Affectionate hugs and other touching provides a surge of euphria-producing endorphin in the brains of normal children, thus addicting them to their mothers, a useful survival reaction. Autistic children do not need this surge, providing a more simple and perhaps useful rationale for socially apathetic behavior (as seen in narcotic addiction) than that of repressed libido or unexpressed rage.

     While endorphin levels produce high serotonin levels and play a part in preventing autistic children from getting high on motherly love, TS children represent the other end of the opiate level range. Their low level of serotonin, causing a low endorphin level, would be expected to increase their vulnerability to addictive behaviors in an attempt to raise their levels by external means. These may include activity (such as running, sports, gambling, risk-taking) as well as through ingestion (as with food, drugs, alcohol).

     The two disorders of TS and autism share similar symptoms and yet each exhibits some opposing ones. This suggests other genetic mutations responsible for autism other than the TS gene. The children whose autism is due to the TS gene would likely consist of the reported TS cases which were diagnosed as autism due to the severe delay in speech and cognitive development, preventing the full picture of TS from being realized until as late as 9 years old. Nonetheless, the essential defect in both autism and TS appears to be a regulation problem with metabolizing serotonin.

Depression and TS

     Endogenous depression, and its flip side of mania, is more severe, longer lasting (2 weeks or more) and not triggered by an event or circumstance necessarily. It is signaled by a combination of some of these symptoms: increase or decrease in sleep time, apathy (even for pleasure), fatigue or restlessness, weight loss or gain, low self esteem, continuing thoughts of suicide or death in general.

     Research looking at the prevalence of depression in TS reported 21 percent of the control group (non-TS afflicted persons) experienced 2 or more weeks of depression against 60 percent of TS patients. (22) In the end of the 1950 decade antidepressant medications were increasingly used and soon recognized to increase the brain levels of neurotransmitters. A drug, reserpine, used in treating high blood pressure, often caused severe depression. Reserpine robs the synapses of serotonin, whose level is already low in TS patients. In fact, all treatments of depression elevate the serotonin brain levels, including tricyclics, monamine oxidase inhibitors and lithium, as well as electroshock therapy, sleep deprivation and physical activity.

     A study of 203 patients who were hospitalized for depression revealed that patients who had low levels of 5-HIAA (a breakdown product of serotonin) attempted suicide twice as often as other patients and of those, violent suicides were 4 times more prevalent than non-violent ones. (23) Another study reported that of those persons with low 5-HIAA in their spinal fluid, 20 percent had killed themselves within a year. (24) It seems that low serotonin levels can be a marker for suicidal risk in both depressed and non-depressed persons. It is not surprising that, given the TS gene's implication in other disorders, drugs that affect brain serotonin are used in both the treatment of TS and depression. Popular ones include chlorimipramine (Anafranil), fluoxetine (Prozac), and clonidine.

Addictions and TS

     At a rate many times the general population, close to 20 percent of alcoholics commit suicide. Patients with depression and a family history of alcoholism have lover levels of 5-HIAA than persons without a family history but who suffered from depression.

     A valid hypothesis of the cause of alcoholism involves the attempt of the alcoholic to raise serotonin levels (which alcohol does.) Alcoholism, quite often resistant to treatment, may be efficiently addressed with drugs which increase serotonin and inhibits its turnover. Several studies support this. (25) Others provide evidence that alcoholism and/or drug abuse and obesity are more common in TS relatives. (26) Addictive agents such as alcohol, morphine, nicotine, even food, and addictive activities such as running, gambling and sexual engagement, results in the elevation of serotonin. Once these agents and activities are removed from a person's life who has abnormally low brain serotonin to begin with, the rebound drop in its level can truly be uncomfortable and even painful.

     Anorexia nervosa and bulimia are eating disorders, with bulimics tending to be more impulsive and sexually active, and have more problems with stealing, alcohol and drugs, suicide and self-mutilation. Bulimia is both a mood and an impulse disorder, characterized also by abnormally low serotonin levels in the spinal fluid.

Miscellaneous TS Connections

     Miscellaneous does not mean trivial. This is evident by a consideration of the frequency of the following examples in TS: Colic in infants, explosive personality, false paralysis, heat intolerance, stress sensitivity, migraine headaches, poor memory, self-mutilation, somatization, speech problems, sweating.

     Although colic is a catch-all term implying intestinal spasms causing pain, sleeping poorly and colic are very common early signs of TS and an early onset of ADHD. It is likely that colicky babies are at a high risk of ADHD and the irritation and crying are due to a brain dysfunction rather than an intestinal one.

     Self-abusive behaviors common in TS include bead banging and hair pulling, hitting one's self, licking lips to the point of infection, washing hands until raw, picking at sores and scabs, grinding and even pulling one's own teeth out and biting hands, lips, cheeks. Such activities occur in 12 to 50 percent of TS patients, depending on the study. Comings writes, "I have a rule that any skin lesion in a TS patient is self-induced until proven otherwise." (27)

     Enuresis or bedwetting is quite common in both TS and ADHD. Sleep problems as well as sleep-walking, nightmares, enuresis and encopresis, are fairly common in both TS and ADHD. It may be more useful to see these disorders as a result of genetic loading rather than learned behavior.

     Conduct, having a genetic basis as well, demonstrates a broad range of socially unacceptable behaviors. Conduct disorders often respond well to medications which elevate serotonin brain levels, such as clonidine (Catapres), imipramine (Trofranil), fluoxetine (Prozac), and pimozide (Orap).

     Sleep problems, particularly arousal disorders such as sleep walking, night terrors and enuresis, are more frequent with TS persons than in general. Sleep apnea, a tendency for breathing to stop for short periods, was found in 23 percent of TS persons and sleep walking in almost half. Night terrors, as opposed to nightmares, are not dreams and do not happen during REM sleep. Children with the arousal disorder sit up in bed and scream hysterically with great fear, breathing heavily and sweating. Only 2 percent of the general population report night terrors against 32 percent with TS. (28)

     Simple and social phobias which disrupt daily living are also common in TS. One fourth of TS patients exhibit panic attacks (including agoraphobia) and family history studies indicate that panic can sometimes be the only symptom of the TS gene. (29) Anxiety disorder, phobic and panic reactions respond well to the same antidepressants that are used in treating OCD and have their predominant effect on serotonin metabolism. An interesting tidbit of research includes the finding of even lower levels of spinal fluid 5-HIAA in arsonists compared to violent offenders, with both groups significantly lower than controls. (30)

Treatment Implications

     In their discussion of treatment modalities, Davison and Neale suggest a paradigm: Diathesis-stress. (31) Diathesis refers to the predisposition toward a disease, be it a result of genetics or birth trauma, etc., while acknowledging the impact of the environment (the stressor) on the progression of the disease. This is easy to perceive in an example of a person born with a genetic tendency toward alcoholism but would never manifest the disorder unless alcohol is available. However, if one accepts the evidence that the TS gene presents in a great variety of symptoms and disorders, the question remains of what determines the course of that presentation.

     In addition to predisposition and environment, a third factor needs to be considered, that of randomness. This factor has been well established (and even mathematically expressed) in the hard sciences such as physics. The movement of the planets is a linear and periodic event, and therefore can be predicted with almost 100 percent accuracy (really limited only by our instruments.) The weather, on the other hand, reflects a nonlinear and nonperiodic process, and therefore would remain essentially unpredictable even if 100 percent of the variables were known and assessed. For this reason, while common in weather forecasting, one would never hear an astronomer report "There is a 70 percent chance of a solar eclipse today."

     When a DNA based genetic test for the TS gene is available, after the genome is mapped, it could be used to test persons with various disorders and could with some accuracy connect the disorder with the presence of the gene. But if a baby was tested and found to be a TS gene carrier, we will could not determine what disorder would be manifested and to what degree... and that factor of randomness would still be there even if 100 percent of the person's environment and stressors were controlled.

     A refinement of the diathesis-stress model includes the component of randomness. In a person who carries no TS or other behavior shaping genes, the environment will clearly play the major role in behavioral development. In persons carrying a single TS gene, more equal portions of their behavior would be determined by genetics, environment and randomness. In those carrying a double TS gene the great majority of the behavior would be postulated as being determined by the genotype.

     Treatment of these three groups of people would need to be different. Appropriate methods for the first, non-gene carrying group would include psychotherapy and community based programs and a combination of this and medical intervention for the second group with a single gene. For those with a dominant genotype or a double gene, medication would play a crucial role with therapy devoted to increasing personal strength and management skills.

     Many treatment programs proudly announce their clients are not permitted the use of medications and boast of a 12 to 20 percent success rate. If would be sadly laughable if medical doctors or teachers would boast of such low success rates (although many schools, unfortunately, are approaching that). Indeed, low rates of success and high recidivism are reflections of the skills of knowledge of mental health practitioners in many cases. This researcher would hypothesize, however, that it is more a reflection of "paradigm paralysis", a rampant stubbornness to rationalize and integrate one's perception of the reasons behind human behavior into one's own model or understanding. Some models are far more useful and congruent with outcome performance than others, and an accurate diagnosis along with a selection of the therapeutic model most productively useful will enhance success rates. This paper suggests a medical model for the respectful consideration of all mental health practitioners.

     Personal postscript from the author: I do not wish to render the impression that the genetic evidence for TS and related disorders calls for across-the-board medication treatment. As a TS afflicted person myself, while believing in the physiological basis for symptomology, I also contend that medication is only one of the many ways to positively impact physiology and neurology, others being nutrition, hypnotherapeutic interventions, physical conditioning, logotherapy, meditative practices, and most of all, spiritual devotions. It is no coincidence that one of the most effective, successful and widely applied therapy for a diversity of disorders is the 12-step program, which is essentially spiritual, calling for personal reflection and surrendering to the Higher Power.

© John S. Hilkevich, Ph.D.

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Footnote References

1. Sacks, O. (1985). The Man Who Mistook His Wife for a Hat. New York: Summit Books

2. Comings, D.E. and Commings, B.G. (1988). Tourette syndrome and attention deficit disorder. John Wiley & Sons, New York, pp. 119-135.

3. Sacks, O. (1985). The Man Who Mistook His Wife for a Hat. New York: Summit Books, p. 89

4. Comings, D. E., Himes, J. and Comings, B.G. (1989). An Epidemiological Study of Tourette Syndrome in a School District. J. Clinical Psychiatry (in press).

5. Pauls, D.L. , Leckman, J.F.

4. Comings, D. E., Himes, J. and Comings, B.G. (1989). An Epidemiological Study of Tourette Syndrome in a School District. J. Clinical Psychiatry (in press).

5. Pauls, D.L. , Leckman, J.F., Raymond, C.L.R., Hurst, C.R. and Stevenson, J.M. (1988). A Family Study of Tourette Syndrome: Evidence against the hypothesis of association with a wide range of psychiatric phenotypes. Am. J. Hum. Genetics 43:A64

6. Pauls, D.L., Lechman, J.F., Kidd, K.K. and Cohen, D.J. (1988). Tourette Syndrome and Neuropsychiatric Disorders: Is there a genetic relationship? Am. J. Genet 43:206-209.

7. Price, R.A., Kidd, K.K., Cohen, D.J., Pauls, D.I. and Lechman, J.F. (1986). A Twin Study of Tourette Syndrome. Arch. Gen. Psychiatry 42:815-820.

8. Seignot, M.J.N. (1961). A Tourette's Case Cured with R-1163. Am. Med. Psychol. 119:578-579.

9. Butler, L.J., Koslow, S.H., Seifert, W.E. Jr., Caprioli, R.M. and Singer, H.S. (1979) Biogenic Amine Metabolism in Tourette Syndrome. Am. Neurology 6:37-39.

10. Crosley, C.J. (1979). Neurotransmitter-related pathways. Biochemical Correlates of Brain Structure and Function, Academic Press, New York.

11. Young, S.N., Smith, S.E., Pihl, R.O. and Ervin, F.R. (1985). Tryptophan Depletion Causes a Rapid Lowering of Mood in Normal Males. Psychopharmacol. 87:173-177.

12. Barnes, D.M. (1988). New Data Intensify the Agony over Ecstasy. Science 239:864-866.

13. Comings, D.E. (1990). Tourette Syndrome and Human Behavior. Hope Press, CA p. 107

14. Kidd, K.K. and Records, M.A. (1982). Genetic Methodologies for the Study of Speech. Elsevier, New York, pp. 311-343.

15. Karno, M. Golding, J.M., Sorenson, S.B. and Burnam, M.A. (1988). The Epidemiology of Obsessive-compulsive Disorder in Five US Communities. Arch. General Psychiatry 45:1094-1099.

16. McGuffin, P. and Mawson, D. (1980). Obsessive-compulsive Neurosis: Two Identical Twin Pairs. Br.J. Psychiatry 137:285-287.

17. Swedo, S.E., Rapoport, J.L. Leonard, H., Lenane, M. and Cheslow, D. (1989). Obsessive-compulsive Disorder in Children and Adolescents. Arch. General Psychiatry 46:335-341.

18. Comings, D. E. (1990). Tourette Syndrome and Human Behavior, Hope Press, CA p. 171

19. Kanner, L. (1949). Problems with Nosology and Psychodynamics in Early Childhood Autism. Am. J. Orthopsychiatry 19:416

20. Davison, G.C., Neale, J.N. (1990). Abnormal Psychology, Wiley & Sons, New York, p. 467.

21. Panksepp, J. (1979). A Neurochemical Theory of Autism. Trends Neurosci. 2:174-177.

22. Comings, D.E., (1990) Tourette Syndrome and Human Behavior, Hope Press, CA. p. 184.

23. VanPraag, H.M. (1981). Neurotransmitters and CNS Disease. Lancet 2:1259-1264.

24. Traskman, L., Asberg, M., Bertilsson, L. and Sjostrand, L. (1981). Monamine Metabolites in CSF and Suicidal Behavior. Arch. Gen. Psychiatry 38:631-636

25. Naranjo, C.A., Sellers, E.M., Sullivan, J.I., Woodley, D.V., Kadlec, K. and Sykora (1987). The Serotonin Uptake Inhibitor Citalopram Attentuates Ethanol Intake. Clinical Pharmocal. Ther. 41:266.

26. Comings, D.E., (1990). Tourette Syndrome and Human Behavior, Hope Press, CA p. 437

27. Ibid, p. 291.

28. Ibid, p. 251.

29. Ibid, p. 182.

30. Brown, G.A., Ebert, M.F., Goyer, P.H., Jimerson, D.C., Klein, W. J., Bunney, W.E. and Goodwin, F.K. (1982). Aggression, Suicide, and Serotonin Relationships to CSF Amine Metabolism. Am. J. of Psychiatry 139: 741-746

31. Davison, G.C., Neale, J.N. (1990). Abnormal Psychology, Wiley and Sons, New York, p. 55.