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