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Tourette’s Syndrome: Cause, Onset, Symptoms, and Treatment Options

June 15th, 2010 Comments off

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Tourette’s syndrome, once believed to be an extremely rare neurological spectrum disorder, is now demanding increased attention in the field of medicine as more is learned about the condition, specifically focusing on its biological and environmental causes, developing affective treatments, and the associated astoundingly high comorbidity with other neurological disorders. An inherited, neurological disorder characterized by repeated and involuntary body movements and uncontrollable vocal sounds often manifested in situations that inappropriate in both time and location, Tourette’s syndrome was first assessed by Georges Gilles de la Tourette, a French neuropsychiatrist, in the late 1800s. According to the Tourette Syndrome Association, vocal outbursts that are a defining characteristic of the disorder, including coprolalia, a vocal tic containing socially unsuitable words, are neither intentional nor purposeful and often cause great anxiety in the patient with this disorder. Broadly resulting from a chemical imbalance in the brain, Tourette’s syndrome is one of the most misunderstood and perhaps misdiagnosed neurological disorders that significantly impacts a child’s educational performance and social and emotional well-being (Tourette Syndrome Association). Children with Tourette’s syndrome often develop poor peer relationships and are comparatively more withdrawn and aggressive particularly during adolescence when symptoms, specifically motor and phonic tics, peak. Although many people with this syndrome have not been diagnosed, one hundred thousand Americans are estimated by the National Institutes of Health to have full-blown Tourette’s.

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The first symptoms of Tourette’s syndrome often manifest themselves during a child’s third year of life and will increase in severity and frequency throughout childhood, reaching greatest severity during puberty and up until twenty years of age when at this time, a small percentage of the affected population will begin to see a significant reduction in symptoms. To be diagnosed with Tourette’s syndrome according to the DSM-IV, an individual must fit within the following criteria: (1) age onset between two and fifteen years of age; (2) multiple involuntary muscular and verbal tics; (3) tic severity and frequency wax and wane (increase and decrease) but are present for more than one year. The first symptom to be recognized in small children with this disorder is the presence of phonic tics which can begin as early as the age of three. A phonic or vocal tic can be defined as the repeated uttering of a sound, word, or phrase and can be divided into two categories: simple vocal tics and complex vocal tics. Examples of simple vocal tics which frequently begin in toddlers include throat clearing, yelping and other noises, sniffing and tongue clicking (Tourette Syndrome Association). The complex variety of vocal tics include cases where an individual will utter words or phrases out of context or when one exhibits coprolalia, verbalizing socially unacceptable words, and are later present in middle childhood. Motor tics or rapid, repetitive movements of any voluntary muscle group in the body will begin to occur between the ages of three and eight years old and these again are classified into simple and complex variations. Simple motor tics are distinguished by eye blinking, head jerking, shoulder shrugging, arm flailing and/or finger tapping, and facial grimacing and can often be exhibited in bouts that sometimes seem quite purposeful. On the other hand, many individuals will develop complex motor tic symptoms later in childhood such as jumping, touching other people or things, smelling, twirling erratically and only rarely, self-injurious actions including hitting and biting oneself. Just before a tic occurs, sufferers may experience sensory symptoms, or the “premonitory urge that incessantly prompt tics. ” (Tourette Syndrome Association), or auditory and visual cues can lead to tics as well. Finally, tics often present themselves in a pattern known as waxing and waning, implying that tics change persistently over time, especially more frequently in children than in adults, and in severity depending on environmental circumstances such as stress and anxiety, excitement and fatigue.

Many neurological disorders occur in conjunction with Tourette’s syndrome suggesting a high degree of comorbidity. Attention Deficit Hyperactivity Disorder is often a precursor to Tourette’s syndrome in very young children and can result in increased irritability, impulsivity leading to rage attacks, depression and anti-social behavior, and increased tendencies towards drug use, leading to poor performance in school and personal low self-esteem. Obsessive Compulsive Disorder often occurs in combination with Tourette’s syndrome when symptoms begin to become apparent during the first two and a half years in a child’s life.

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Tourette’s Syndrome: Cause, Onset, Symptoms, and Treatment Options (Part 2)

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OCD is characterized by an obsession or a thought that one’s mind tends to get stuck on, causing great anxiety. To alleviate the anxiety created by this obsession, one must perform a compulsion, such as a tic. Learning disabilities are commonly diagnosed among individuals with Tourette’s syndrome as well, primarily problematic in nonverbal tasks usually in the areas of auditory processing, fine motor and visual-motor impairment. In a classroom setting, those with visual-motor impairment may have difficulty copying information from a chalkboard to paper, while fine motor impairments translate into messy and time-consuming handwriting (Tourette Syndrome Association). Finally sleep disorders are common ailment among individuals with Tourette’s syndrome as brought on by frequent awakenings or walking or talking in one’s sleep.

Onset during childhood, the symptoms of Tourette’s syndrome must be displayed between the ages of two and eighteen years of age to be classified as true Tourette’s based on DSM-IV criteria. However, the most common age of onset is between a child’s sixth and seventh birthday (Handler 33). The disorder occurs in all ethnic groups with males affected three to four times as often as females. Although individuals may experience varying levels of severity, the great majority of patients fall into the mild category of symptoms, which decrease significantly in many during adulthood. In fact, one third of patients with Tourette’s syndrome experience remission of the tic symptoms in adulthood.

Although a concrete explanation has yet to be established, current research presents convincing evidence that Tourette’s syndrome results from the abnormal metabolism of at least one brain chemical, perhaps the interaction of many more. Although numerous central neurochemical systems are thought to be involved in the manifestations of tic disorders, including cholinergic, serotonergic, noradrenergic, GABAergic, endogenous oppioid, and gender-specific neuroendocrine systems, according to Cohen, “the strongest evidence supports the role of midbrain dopaminergic systems acting in concert with compensatory and modulating neurotransmitter systems. ” (11). According to the Tourette Syndrome Association, “Tourette syndrome appears to arise from defects in neural circuits passing from the cerebral cortex through the structures constituting the basal ganglia and back to the cerebrum. ” To help integrate brain functioning, neural circuits run from the cerebrum through the basal ganglia and then back to the cerebral cortex, providing a feedback loop in which volitional acts are transmitted to the nerves and muscles that carry out their instruction. The primary function of the basal ganglia is to regulate the expression of discrete mechanisms of behavior, including particular movements and thoughts connected with tic symptoms. Further evidence in the significance of the basal ganglia in this disorder is based on the notion that eye blinking that occurs in tics is similar to the abnormalities of blink reflex recovery cycle diseases which begin in the basal ganglia (Raffaele). Because most symptoms resulting from Tourette’s syndrome appear to stem from abnormal functioning in the basal ganglia, it is believed that such symptoms are caused by altered dopamine functioning, a neurotransmitter produced in midbrain structures. A defect in norepinephrine can lead to an overactivity of dopamine throughout the midbrain, specifically in the basal ganglia. However, measurements of the breakdown products of dopamine in the spinal fluid of Tourette’s patients have been inconsistent, suggesting that dopamine may only be part of the problem (Bruun 56). Furthermore the observation that stress will cause an increase in tic symptoms suggests that norepinephrine, specifically known for its association with stress, may contribute to the disorder. (Bruun 56) Acetylcholine is also present in the basal ganglia along side of dopamine and is released by neurons outside the brain that send signals to muscle cells, causing them to contract and facilitating physical movement such as tics. Subjects actively attempting to suppress these tics have been shown to have marked activation in the frontal superior temporal and anterior cingulated cortices in testing by blood oxygen level-depending functional MRI, suggesting that “Tourette’s syndrome stems from an underactive prefrontal governing system. ” (Chae et al. Finally, the differing rates in which Tourette’s syndrome are exhibited in men versus women could imply a hormonal induce abnormality in the neurotransmitter systems. Estrogen, androgens, progestins, and steroids may all be a significant factor in the display of symptoms, and it has been shown in experiments with animals that androgens present early in life are capable of changing dopamine receptors (Chae et al.

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Tourette’s Syndrome: Cause, Onset, Symptoms, and Treatment Options (Part 3)

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In addition to disagreement among researchers concerning the biological brain mechanisms responsible for the symptoms of Tourette’s syndrome, a debate has developed pertaining to the origin of this disorder: Is Tourette’s syndrome inherited genetically or through environmental interactions? The Tourette Syndrome Association proposes that Tourette’s may result from an autosomal dominant gene with high sex-specific penetrance, while other researchers feel that a combination of genes working together may be responsible. Genome scans of family history pedigrees of those affected suggest that three regions may be to blame for Tourette’s syndrome on chromosome five, ten, and thirteen (Curtis), although there is no conclusive evidence. Additionally, the dominant gene is expressed differently in each affected family member along a specific history pedigree, and only ten percent of the offspring of an individual affected by Tourette’s syndrome will develop severe enough symptoms to warrant medical attention (Tourette Syndrome Association). In a scientific study conducted by Klug et al, researchers have concluded that in terms of parental, prenatal, and perinatal risk markers, manifestations of interacting environmental and genetic variables, “Tourette’s syndrome is influenced by genetic factors, and is less influenced by environmental factors. ” Approximately seventy percent of Tourette’s syndrome cases are reflections of either an autosomal dominant or polygenetic disorder. In the instances of Tourette’s syndrome that do not have obvious lines of inheritance, environmental roots are suspected in a variation known as sporadic Tourette’s syndrome. Environmental influences on the expression of this condition appear to occur primarily during childhood, and may result from low birth weight (Klug et al. Another discovery recently made in biological research involves the role of immune related disease in the acquisition of Tourette’s syndrome in the form of Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcus (PANDAS) (Snider et al. In this theoretic diagnosis, doctors suggest that streptococcal infections, the cause of rheumatic fever, might be behind some cases of Tourette’s because many children first shown signs of the disorder after a strep infection and later infections seem to increase tics in this group of children (Packer). In this conjecture, antibodies generated to combat strep misidentify and damage neurons in the basal ganglia. Further research has shown that the average sizes of the caudate, putamen, and globus pallidus, structures of the basal ganglia, but not the thalamus or total cerebrum are significantly larger in a sample of children with streptococcus-associated OCD and/or tics than in healthy children (Leckman). Although there is no way to determine if streptococcal antibodies are actually “cross-reacting” (Tourette Syndrome Association) with proteins in the basal ganglia, specialized blood tests can be used to indirectly determine ASO and AntiDNA-se-B titers (Leckman). Despite strong evidence from both an environmental and genetic standpoint, an interaction of the two is most likely to blame for the origin of Tourette’s syndrome. This prominent and unresolved question continues to obtain funding to develop a solid understanding. I personally would follow-up the research conducted on PANDAS with the creation of a vaccine that will prevent streptococcal or a development of early diagnosis for this bacterial infection so that it may be treated immediately with the proper antibiotics. Taking a large sample size of vaccinated children or those who had been treated immediately after exposure to the bacteria and comparing these children to a control group, which for ethical reasons would have to voluntarily refuse these early treatments of streptococcal first before joining the study, I would conduct a longitudinal study to determine if there is a high degree of correlation between the illness and the development of Tourette’s. Although I would be unable to infer causation from correlation data, this specific information could provide another avenue for research. In another follow-up experiment, I would also advise a more in-depth study of the human genome now that its initial mapping is completed.

In terms of treatment, various forms of therapy including cognitive behavioral psychotherapy have proven to be helpful in assisting the affected patient and his or her family cope with the implications of diagnosis, and behavioral therapies including behavioral modification, habit reversal, awareness training, competing response, group therapy, hypnosis, exposure-response prevention, relaxation, and a variety of vitamin diets, herbs and trace elements are found to be affective on varying levels of treating symptoms (Tourette Syndrome Association).

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Tourette’s Syndrome: Cause, Onset, Symptoms, and Treatment Options (Part 4)

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Because tics change in severity often weekly and are exhibited in differing bouts throughout a single day, it is important initially for the doctor to observe the patterns so that he or she may decide upon the most effective treatment regime. Additionally, it is extremely important to treat Tourette’s syndrome as early as possible to reduce ridicule and rejection by peers, exclusion from activities and prevention from enjoying normal interpersonal relationships due to the perception of those in the child’s immediate environment who may observe the bizarre behavior and become frightened. To avoid such psychological harm, early diagnosis and treatment is key (Tourette Syndrome Association). While many children with Tourette’s syndrome of school age have similar IQs to the majority of the school population, many will have special educational needs which must be addressed to optimize learning. Tape recorders, typewriters, or computers for reading and writing problems, un-timed exams to reduce stress and anxiety which aggravate tics, and permission to leave the classroom when tics become noticeable and embarrassing to the child are affective methods of gaining control of symptoms in the school environment (Tourette Syndrome Association). In terms of professional assistance, habit reversal therapy, or making a patient aware of tics or the urge to tic building up and training and then training him or her to “engage in a response that would be muscularly competing or incompatible with tic” (Packer) as well as the similar exposure response-prevention therapy in which patients are instructed to suppress their tics have mixed results. Relaxation techniques may also be utilized, instructing patients in a simple breathing-based approach to train themselves to relax as a way of decreasing the incidence of tics in stressful situations. Moreover, neurofeedback can be performed using the biofeedback of an EEG machine where “individual receives immediate feedback about a physiological or biological process, with hopes that the immediate feedback and reinforcement will enable the individual to modulate a physiological process that is usually not easily modifiable. ” (Packer). One megahertz of transcranial magnetic stimulation over the prefrontal cortex or motor cortex delivered to the primary motor area have reduced the frequency of tics during stimulation as well (Chae et al. The most dramatic treatments those found in surgical operations when all other treatments have failed. Lesioning of the brain known as stereotactic zona incerta and ventrolatral/lamella medialis thalamotomy may provide a significant long term decrease in motor tics if further developed. A less risky surgery with fewer side effects was recently attempted by a neurosurgical team at University Hospitals of Cleveland where the use of deep brain stimulation, similar to the device used to treat Parkinson’s disease and tremor, was attempted. Electrodes placed around cells inside the thalamus portion of the brain, a structure which forms part of the circuit connecting the basal ganglia to the cerebral cortex, deliver continuous high frequency electrical stimulation, thus producing messages that are rebalanced through movement centers in the brain (News Medical). Within hours of surgery and activation, the patient noticed a disappearance of jerking motions, muscle tics, and grunting symptoms associated with Tourette’s. With the discovery of the streptococcal factor involved in Tourette’s syndrome, clinical researchers have explored experimental methods such as plasmapheresis (plasma exchange, PEX) and intravenous injection of immunoglobin (IVIG) to treat PANDAS related symptoms themselves. However, neither of these treatments have been proven to be effective. Also significant improvement has been documented in the symptoms of Tourette’s patients supposedly affected by PANDAS after undergoing tonsillectomies or adenotonsillectomy for recurrent streptococcal pharyngitis (Packer).

The great majority of people diagnosed with Tourette’s syndrome are not significantly impaired by their symptoms and thus do not re quire medication, but when medication becomes necessary, many options are available. To achieve maximum control of symptoms, dosages of specific drugs vary significantly from patient to patient and must be carefully monitored. In most circumstances, doctors prescribe medications in small doses and gradually increase these doses until a maximum alleviation of symptoms with minimal side effects are achieved. Some undesired side effects incurred during treatment include weight gain, muscle rigidity, fatigue, motor restlessness and social withdrawal. Most drugs administered to treat this disorder are dopamine agonists and antagonists which can often reduce abnormal movements and vocal tics in Tourette’s syndrome (Hershey et al.

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Tourette’s Syndrome: Cause, Onset, Symptoms, and Treatment Options (Part 5)

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Neuroleptics is a specific class of drugs primarily used to treat motor and phonic tics and include Primozide, Fluphenazine, Thiothixene, Chlorpromazine, Triflueoperazine, Thioridazine which alter the effects of dopamine in the central nervous system while possessing anticholinergic and alpha-adrenergic blocking activity. Risperidone, another neuroleptic drug, acts as a dopamine and serotonin receptor antagonist to decrease motor and phonic tics. Clonazepam, an anticonvulsant, produces sedative effects in central nervous system with a high affinity for the y-gamma aminoburic acid (GABA) receptor, increasing synaptic serotonin. This medication decreases aggressive behavior, emotionally labile behavior, and tics. Clonidine, an antihypertensive alpha blocker, stimulates the alpha adrenergic receptors in the central nervous system to inhibit cardioacceleration and vasoconstriction. This medication is an adrenergic agonist that decrease tics while increasing attention levels. Finally, the drug Nifedipine, an antihypertensive calcium channel blocker, acts upon slow calcium channels invascular smooth muscle and myocardium to produce vasodilation in decreasing tic symptoms (Tourette Syndrome Online). Overall, many pharmacological advances have been effective in decreasing symptoms; however, more research is needed on a medication that could cure Tourette’s syndrome.

Tourette’s syndrome is a very complex disorder resulting in vocal and motor tics, aggressive behavior and is often associated with Attention Deficit Hyperactivity Disorder and Obsessive Compulsive Disorder. Although behavioral therapeutic, surgical, pharmacological, and other treatments are available, continued research will be needed to determine the exact cause of this syndrome and improve treatments.

Works Cited

Brunn, Ruth Dowling and Bertel Brunn. A Mind of Its Own: Tourette’s Syndrome: A

Story and a Guide. New York: Oxford University Press, 1994

Chae, Jeong Ho, Ziad Nahas, Xingbao Li, Gopalan Sethuraman, Donald Gilbert, Floyd R.

Sallee, and Mark S. George. “A Pilot Safety Study of Repetitive Transcranial

Magnetic Stimulation in Tourette’s Syndrome. ” Cognitive and Behavioral Neurology.

Jun. 2004. Academic Universe. Lexis-Nexis. University of North Carolina Lib.

Chapel Hill. 18 Nov. 2004 <http://www. lexis-nexis. com>

Chang, Hsueh Ling, Ming Je Tu, and Huei Shyong Wang. “Tourette’s Syndrome:

Psychopathology in Adolescents. ” Psychiatry and Clinical Neurosciences. Aug. 2004.

Academic Universe. Lexis-Nexis. University of North Carolina Lib. Chapel Hill. 18

Nov. 2004 <http://www. lexis-nexis. com>

Cohen, Donald J. Ruth D. Brunn, and James F. Leckman. Tourette’s Syndrome and Tic

Disorders: Clinical Understanding and Treatment. New York: John Wiley and Sons,

1988

Curtis, David. “Genome Scan of Tourette Syndrome in a Single Large Pedigree Shows

Some Support for Linkage to Regions of Chromosomes 5, 10, and 13. ” Psychiatric

Genetics. Jun. 2004. Academic Universe. Lexis-Nexis. University of North Carolina

Lib. Chapel Hill. 18 Nov. 2004 <http://www. lexis-nexis. com>

“Diagnosing and Treating Tourette Syndrome. ” Tourette Syndrome Association, Inc. 19

Nov. 2004 <http://www. tsa-usa. org>

Handler, Lowell. Twitch and Shout. New York: Dutton, 1998

Hershey, Tamara, Kevin J. Black, Johanna M. Hartlein, Deanna Barch, Todd S. Braver,

Juanita L. Carl, Joel S. Pelmutter, and Kevin J. Black. “Cognitive-Pharmacologic

Functional Magnetic Resonance Imaging in Tourette Syndrome: A Pilot Study. ”

Biological Psychiatry. May 2004. Academic Universe. Lexis-Nexis. University of

North Carolina Lib. Chapel Hill. 18 Nov. 2004 <http://www. lexis-nexis. com>

Klug, Marilyn G. Larry Burd, Jacob Kerbeshian, Becky Benz, and John T. Martsolf. “A

Comparison of the Effects of Parental Risk Markers on Pre- and Perinatal Variables in

Multiple Patient Cohorts with Fetal Alcohol Syndrome, Autism, Tourette Syndrome,

and Sudden Infant Death Syndrome: An Environic Analysis. ” Neurotoxicology and

Teratology. Dec. 2003. Academic Universe. Lexis-Nexis. University of North

Carolina Lib. Chapel Hill. 18 Nov. 2004 <http://www. lexis-nexis. com>

Leckman, James F. “Tourette’s Syndrome. ” Lancet. 16 Nov. 2002. Academic Universe.

Lexis-Nexis. University of North Carolina Lib. Chapel Hill. 18 Nov. 2004

<http://www. lexis-nexis. com>

“New Treatment for Tourette Syndrome, Patients Experience Significant Resolution of

Symptoms Following Brain Surgery. ” News Medical. 17 Nov. 2004

<http://www. news-medical. net/? id=256>

Packer, Leslie E. “Treatment of Tics and Tourette’s Syndrome? ” Tourette Syndrome

Plus. 22 Nov. 2004 <http://tourettesyndrome. net/pandas_treatment. htm>

Raffaele, Rocco, Iganzio Vecchio, Alessandro Alvano, Giuliana Proto, Giovanni

Nicoletti, and Liborio Rampello. “Blink Reflex Abnormalities in Tourette Syndrome. ”

Clinical Neurophysiology. Feb. 2004. Academic Universe. Lexis-Nexis. University of

North Carolina Lib. Chapel Hill. 18 Nov. 2004 <http://www. lexis-nexis. com>

Snider, Lisa A. and Susan E. Swedo. “Childhood-Onset Obsessive-Compulsive Disorder

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of North Carolina Lib. Chapel Hill. 18 Nov. 2004 <http://www.

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Tourette’s Syndrome: Cause, Onset, Symptoms, and Treatment Options (Part 6)

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lexis-nexis. com>

“Tourette Syndrome, ADD and ADHD Information Center. ” Tourette Syndrome Online.

19 Nov. 2004 http://www. tourette-syndrome. com

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