Serotonin (5-hydroxytryptamine [5-HT]) is a neurotransmitter found in the gut and central nervous system (CNS). It is thought to influence the regulation of mood, sleep, appetite and influence memory and learning. Serotonin is commonly thought of as being responsible for feelings of 'happiness'. In Tourette Syndrome, concentrations of serotonin (and nor-epinephrine), in the brain/CNS, appear to be lower than normal and are thought to play an important role, along with dopamine which is strongly involved in controlling motor activity, in reducing regulation and selective inhibition of neural activity responsible for some complex tic behaviours, obsessive and compulsive behaviours, anxiety and sleep disturbance. Selective serotonin re-uptake inhibitors (SSRIs) are a class of drug often prescribed in TS to help increase CNS serotonin concentration. SSRIs may be beneficial in ameliorating some symptoms common in TS, including obsessive thoughts, attention deficit, sensory hypersensitivity, sleep disturbance and emotional hyper-responsiveness and rage. Both fluoxetine (Prozac) and sertraline (Zoloft) are commonly used. Paroxetine (Seroxat) has some effectiveness in improving 'rage' problems in adults with TS (but is unsuitable for children). All SSRIs have some side-effects. Venlafaxine (Efexor), is a serotonin-norepinephrine re-uptake inhibitor (SNRI) and is a drug sometimes used when symptoms, such as obsessive and compulsive behaviours and anxiety are unresponsive to SSRIs. Although conventional OCD tends to respond to SSRI therapy, evidence suggests that 'Tourettic' obsessive compulsive behaviours (OCB) are not very responsive to SSRIs/SNRIs. OCB in TS appears to be more 'wired-in' (neurological) and differs, markedly, to OCD without Tourette symptoms [<R>] [<R>].
Low concentrations of serotonin or serotonergic activity (and nor-adrenaline) are thought to be a cause of depression. Low mood is frequently a problem in TS and evidence suggests that SSRIs can be of benefit, however the role of serotonin deficiency as a primary cause in 'classic' clinical depression is, increasingly, being questioned [<R>]. Patients with TS sometimes report a rapid response to SSRI administration which contrasts with the long delay (up to 6 weeks) that is usual for MMD (major depressive disorder) patients without TS. Clearly, the pathopysiological mechanisms involved and the clinical responses to serotonin-increasing drugs, are complex and a full understanding of the serotonin system and it's role in TS will require considerably more research.
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