It can also inhibit the clearance of CYP2D6 substrates such as dextromethorphan, potentiating their effects. Other drugs like codeine and tamoxifen, which require CYP2D6-mediated activation into their respective active metabolites, may have their therapeutic effects attenuated. Likewise, CYP2D6 inhibitors such as paroxetine or fluoxetine can reduce chlorpromazine clearance, increasing serum levels of chlorpromazine and potentially its adverse effects. Chlorpromazine also reduces phenytoin levels and increases valproic acid levels. It also reduces propranolol clearance and antagonizes the therapeutic effects of antidiabetic agents, levodopa (a Parkinsons medication. This is likely due to the fact that chlorpromazine antagonizes the D2 receptor which is one of the receptors dopamine, a levodopa metabolite, activates), amphetamines and anticoagulants. It may also interact with anticholinergic drugs such as orphenadrine to produce hypoglycaemia (low blood sugar).Chlorpromazine may also interact with epinephrine (adrenaline) to produce a paradoxical fall in blood pressure. Monoamine oxidase inhibitors (MAOIs) and thiazide diuretics may also accentuate the orthostatic hypotension experienced by those receiving chlorpromazine treatment. Quinidine may interact with chlorpromazine to increase myocardial depression. Likewise, it may also antagonize the effects of clonidine and guanethidine. It also may reduce the seizure threshold and hence a corresponding titration of anticonvulsant treatments should be considered. Prochlorperazine and desferrioxamine may also interact with chlorpromazine to produce transient metabolic encephalopathy.Other drugs that prolong the QT interval, such as quinidine, verapamil, amiodarone, sotalol and methadone, may also interact with chlorpromazine to produce additive QT interval prolongation. Discontinuation
The British National Formulary recommends a gradual withdrawal when discontinuing antipsychotics to avoid acute withdrawal syndrome or rapid relapse.
Complex motor tics include copropraxia (obscene or forbidden gestures, or inappropriate touching), echopraxia (repetition or imitation of another persons actions) and palipraxia (repeating ones own movements). Onset and progression
There is no typical case of Tourette syndrome, but the age of onset and the severity of symptoms follow a fairly reliable course. Although onset may occur anytime before eighteen years, the typical age of onset of tics is from five to seven, and is usually before adolescence. A 1998 study from the Yale Child Study Center showed that tic severity increased with age until it reached its highest point between ages eight and twelve. Severity declines steadily for most children as they pass through adolescence, when half to two-thirds of children see a dramatic decrease in tics.In people with TS, the first tics to appear usually affect the head, face, and shoulders, and include blinking, facial movements, sniffing and throat clearing. Vocal tics often appear months or years after motor tics but can appear first. Among people who experience more severe tics, complex tics may develop, including "arm straightening, touching, tapping, jumping, hopping and twirling". There are different movements in contrasting disorders (for example, the autism spectrum disorders), such as self-stimulation and stereotypies.The severity of symptoms varies widely among people with Tourettes, and many cases may be undetected. Most cases are mild and almost unnoticeable; many people with TS may not realize they have tics. Because tics are more commonly expressed in private, Tourette syndrome may go unrecognized, and casual observers might not notice tics.