Fluvoxamine Case Study

At first it was the cure all people were looking for. Then it became the drug they were afraid to take. Somewhere between these two extremes lies the truth about the drug Flouxetine, better known as Prozac, the most widely prescribed drug on the globe. It is mainly prescribed to patients suffering from clinical depression. It was first brought to the market in 1988 by the pharmaceutical giant Eli Lilly co. Even though it was originally prescribed for depression, it has been prescribed for everything from eating disorders to insomnia. It was first considered the wonder drug of the new decade because of the way it helped depression patients when no other anti-depressant could

Serotonin, (or 5-hydroxytryptamine) is a neurotransmitter released by neurones in the brain. It is a chemical responsible for good mood and well-being. Therefore one of the possible causes of depression is a chemical imbalance of Serotonin levels in the brain and consequently, ineffective neuronal transmission at the synaptic cleft. (Lovatt, 2010) This has negative implications on mood, sleep and appetite.

According to the Handbook of Clinical Psychopharmacology for Therapists, “bipolar disorders are mood disorders characterized by the essential diagnostic feature of mania or hypomania – these disorders follow cyclic patterns of moods, behavior, and thought alterations, alternating between mania or hypomania and depression” (p. 100). In the experiment of The efficacy of flupenthixol decanoate in bipolar disorder patients who have no sufficient remission with existing treatments, experimenters are making an attempt to evaluate the effect of flupenthixol decanoate in remitted bipolar disorder patients. Flupenthixol decanoate (also known as Fluanxol Depot) is a neuroleptic agent that is administered as an injection of 20 mg/mL into the gluteal

Other clinical studies have implicated fluoxetine’s effects on serotonin neurotransmitters, based on the fact that serotonin is synthesized from the essential amino acid tryptophan. Patients taking fluoxetine who were in remission from major depression were given a special diet which was tryptophan-free. This rapidly decreased plasma serotonin levels, and after a short period of time (as little as 30 minutes) many of the patients began to have signs of specific depressive symptoms. Later, the reappearance of more general depressive symptoms were observed in a majority of the patients. Thus it was shown that fluoxetine has a profound effect on the neurotransmitter serotonin, and decreased

that this drug's antipsychotic activity is mediated through a combination of dopamine type 2 (D2) and serotonin type 2 (5-HT2) antagonism. It is an antagonist at multiple neurotransmitter receptors in the brain: Serotonin 5-HT1A and 5-HT2, dopamine D1 and D2, histamine H1, and adrenergic alpha1- and alpha2-receptors; but appears to have no appreciable affinity at cholinergic muscarinic and benzodiazepine receptors. Norquetiapine, an active metabolite, differs from its parent molecule by exhibiting high affinity for muscarinic M1 receptors. Antagonism at receptors other than dopamine and 5-HT2 with similar receptor affinities may explain some of the other effects of quetiapine. The drug's antagonism of histamine H1-receptors may explain the

There are more than a few types of antidepressants as well as selective serotonin reuptake inhibitors (SSRIs). SSRIs are a set of antidepressants that consist of drugs such as escitalopran (brand name: Celexa), fluoxetine (brand name: Prozac). Selective serotonin reuptake inhibitors act only the neurotransmitters serotonin. The tricyclics have been used to treat depression for a long time. They act on serotonin and another neurotransmitter, norepinephrine, and might work together with other substances all over the body. They include cimitriptyhne (brand name: Elavil), despiramine (brand name: Norpromin)

Similarly as with different neuroleptics, the mechanism of action of haloperidol has not been totally clarified, but has been attributed to the inhibition of the transport mechanism of cerebral monoamines, particularly

three groups.Monoamine oxidase inhibitor (MAOI) medicines block the monoamine oxidase enzyme (MAO) from destroying monoamine neurotransmitters, which allows them to accumulate, alleviating depression. Serotonin selective reuptake inhibitor (SSRI) medications block the serotonin reuptake pump, allowing the serotonin neurotransmitter to remain and accumulate in the receptor for longer. Speaking of serotonin specifically, depression has been related to a deficiency of the 5-hydroxytryptamine (serotonin) neurotransmitter as evidenced by the concentrations of the

Fluoxetine is also known as Prozac, common antidepressant drug (1). It works as selective, competitive reversible antagonist of serotonin receptor that prevent reuptake of serotonin from synapse (2). Due to selectivity, little effect on other neurotransmitters, such as dopamine and noradrenaline. It increase the concentration of serotonin at the synapse and serotonergic neuronal transmission strength, and it triggers negative feedback loop of serotonin, which reduce the conversion of tryptophan to serotonin (3). Fluoxetine does not display species difference, but effect as antidepressant is depend on the dose thought out number of studies. Fluoxetine is administrated as tablets with usual starting dose of fluoxetine is 20mg per day, and it

Depression is the fourth leading cause of disease burden worldwide and is expected to show a rising trend over the next 20 years. Depression is associated with a marked personal, social and economic morbidity, loss of functioning and productivity, and creates significant demands on service providers in terms of workload. Although pharmacological and psychological interventions are both effective for major depression, antidepressant drugs remain the mainstay of treatment. During the last 20 years, selective serotonin reuptake inhibitors (SSRIs) have progressively become the most commonly prescribed antidepressants. Sertraline, one of the first SSRIs introduced in the market, is a potent and specific inhibitor of serotonin uptake into the presynaptic

Prozac (fluoxetine) is a selective serotonin reuptake inhibitors (SSRI) antidepressant .Prozac is used to treat major depressive disorder. In 1970 the company Eli Lilly came up with the compound for Prozac. It was first tested as a treatment for high blood pressure, which worked in some animals but not human’s .It was also tested on psychotic patients and people in hospitals with depression by now given the generic name fluoxetine had no obvious benefit, with a number of patients getting worse. Finally it was tested on people with mild depressives. It was tested on five recruits all five started to show signs of cheering up by 1999. Depression was rarely discussed and antidepressants largely restricted people went to their GPs with anxiety

VPA, carbamazepine and phenobarbitone were the most commonly used traditional AEDs in our study. Previous studies showed a significant decrease in the serum level of fT4 and increase in the serum level of TSH in patients treated with VPA; and these changes persisted throughout study period[8,11,26,27,28]. In a study conducted on adolescent girls with epilepsy, the group received VPA showed higher serum levels of TSH and lower serum levels of fT4 than did the untreated group, although still within the normal range[9]. Other studies found that TSH levels increased in patients using VPA while fT4 levels were found to be unchanged[12,26,29,30].3,4,9,11 On the other side, some studies found that both fT4 and TSH concentrations were unaffected in patients treated with VPA[10,30]

The linkage of serotonin to depression has been known for the past five years. From numerous studies, the most concrete evidence of this connection is the decreased concentration of serotonin metabolites like 5-HIAA (5-hydroxyindole acetic acid) in the cerebrospinal fluid and brain tissues of depressed people. If depression, as suggested, is a result of decreased levels of serotonin in the brain, pharmaceutical agents that can reverse this effect should be helpful in treating depressed patients. Therefore, the primary targets of various antidepressant medications are serotonin transports of the brain. Since serotonin is activated when released by neurons into the synapse, antidepressants function at the synapse to enhance serotonin activity. Normally, serotonin's actions in the synapse are terminated by its being taken back into the neuron then releases it at which point "it is either recycled for reuse as a transmitter or broken down into its metabolic by products and transported out of the brain." As a result, antidepressants work to increase serotonin levels at the synapse by blocking serotonin reuptake (2).

Carbamazepine, an anticonvulsant structurally similar to tricyclic antidepressants, is used to treat partial seizures, tonic-clonic seizures, pain of neurologic origin such as trigeminal neuralgia, and psychiatric disorders including manic-depressive illness and aggression due to dementia. The response to carbamazepine is variable and may be due to its variable transport, especially across the blood-brain-barrier. The transporter that may confer drug resistance is

2008; Sheline et al. 2010), we hypothesized that atypical anti-psychotics (e.g., quetiapine) may augment the anti-depressant effects by altering white matter impairments.