5 Myths About Schizophrenia

1. It is the severest mental illness.
It is really mysterious, we don't know everything there is to know about it yet, it is accompanied by many productive symptoms (delusions, hallucinations), but this does not give the right to call it the worst mental illness.
Since the mid-1950s, pharmacotherapy has been actively used in the treatment of mental illness. Thanks to the introduction of drugs, many institutions have almost completely abandoned the physical methods of restraining patients. In many clinics, there are labor workshops for the rehabilitation of patients and the possibility of acquiring new knowledge due to the loss of previous ones as a result of the disease.
Qualified assistance that was given in time allows for long-term remission. A person will be able to return to the usual life, they can do the same things as they did. A small percentage of patients will experience mild disorders, but they will not lead to acquiring a disability a further deterioration in their quality of life. According to some authors, 20-25% of patients had a complete recovery after the first attack of the illness (It was conducted by M. Tsuang. M. Winokur, L. Chiompi, C. Muller, M. Bleuler, G. Huber, J. Westermeyer, M. Harrow)

2. Its main syndrome is split personality disorder.
Split personality does not mean that within a person there are several different personalities. Schizophrenic split personality means the split processes of the psyche. For example, the splitting of emotions: the manifestation of positive and good feelings towards a person or an animal are subsequently replaced by unmotivated anger and aggression. A person can be very upset at a minor event but experience absolutely no emotions when a loved one dies.

3. It ends with dementia
Yes, in fact, there were some cases in which dementia is the last stage of this illness. However, excellent results can be observed with properly selected and applied therapy throughout life. Among patients you can meet famous cultural figures, scientists and ordinary people who have lived a full-fledged high-quality life, without missing a step.

4. It is dangerous to others.
Considering all of the things that are known about this sickness, one would think that it is dangerous to people that surround a person who is ill.
It is not contagious, which means that it cannot be transmitted. Even the hereditary form of transmission of schizophrenia has not yet been proven. And when it comes to human interactions, the violence rate among schizophrenics is not higher than that of normal people.

5. It is incurable
According to some statistics, approximately 25% of those who survive a psychotic attack do not develop recurrent relapses, or they do develop them but only after many decades after an attack. Only a small percentage of patients with schizophrenia experience further progression of their illness. But, with the timely detection and its treatment, you can block psychotic attacks and increase the time of remission of a patient.

How to Fight Depression

Surely you have already heard a million times how any form of physical activity is beneficial to the body. Well, guess what, physical activity is useful! And not only for your heart or your hips but also for the brain. Almost all the negative manifestations of depression can be dealt with through body training.

  • It makes you sleepy and tired. Physical activity gives energy and vitality;
  • It messes up with your sleep. Physical exercise improves it, it restores your brain;
  • It worsens your appetite. As a result, you don't want to eat and when you do - you consume small portions of food. Physical activity increases appetite, normalizes nutrition and improves your health.

Set goals, make decisions

There was a study during which scientists grouped rats in pairs and injected them with cocaine. Rat A received a dose of the drug by pulling the appropriate lever, while Rat B had to wait for this moment.
Thus, they had the same portions of cocaine at the same time, but rat A was constantly pulling on the lever, and rat B did nothing. As a result, rat A received a significantly larger influx of dopamine (a hormone that increases the sense of joy and pleasure from life).
So, setting a goal and achieving it brings both humans and animals more satisfaction than something that was obtained by chance. Of course, introducing cocaine to rats is not too noble, but this mechanism applies to all of us.


Your brain constantly receives signals from the body about the things that it feels. In a state of depression, people inevitably perform numerous actions that negatively affect the connection between the body and the brain. For example, they adopt a self-deprecating or a somewhat detached attitude to life which is usually characterized by the lowered arms and head that is leaning forward. This position only makes the feeling of sadness even stronger.

Communicate with your relatives and friends

In depression, you often want to be alone with yourself. However, it is well known that time spent with friends and family members softens the depressive mood. Surprisingly, the support of family and friends can even increase the effectiveness of antidepressants.
If you do not want to talk to anyone, try to invite over a friend that does not require active communication to spend some quality time. Go out to see some movie together or play a board game. At the same time, you will not feel obliged to discuss your condition if you do not want to do it. However, if you wish to communicate, you will always have this opportunity.
The mere thoughts about the people you love will help to make it easier for you. Dutch researchers conducted an experiment, the participants of which were asked to think about someone who was really dear to them, about someone to whom they would turn during hard times.
The subjects were asked to imagine that this person was standing behind them, providing them with moral support. Then the participants were put in artificial conditions that imitated their social rejection. Thoughts about their friends significantly eased their stress.

Drug description

Citalopram is a selective inhibitor of serotonin reuptake used for treating depression. In this sense citalopram is similar to fluoxetine, sertraline and paroxetine though its chemical structure is different from the previous antidepressants, the tricyclic antidepressants and monoamine oxidase inhibitors. Citalopram is a relatively weak inhibitor of CYP2D6 liver enzyme system so it probably will interfere to a lesser extent in the metabolism of other drugs fluoxetine and other selective inhibitors of serotonin reuptake that are potent inhibitors of the hepatic enzyme. Clinically, citalopram is as effective as sertraline or fluoxetine but in some comparative clinical studies, was better tolerated than fluoxetine.

Mechanism of action

Citalopram potentiates the pharmacological effects of serotonin in the central nervous system. Other selective inhibitors of serotonin reuptake, citalopram does not affect or affects very little other neurotransmitters. Although the complete mechanism of citalopram has not been elucidated, it is believed that the drug inhibits serotonin reuptake in the neuron membrane. Selective inhibitors of serotonin reuptake are less sedating, anticholinergic and cardiovascular effects are less than tricyclic antidepressants because of its zero or very low activity on histamine receptors, cholinergic and adrenergic receptors. Nor has the citalopram no effect on monoamine oxidase.


Citalopram is administered orally rather well absorbed in the digestive tract with an absolute bioavailability of 80% after a single dose. Citalopram absorption is unaffected by the presence of food. Peak plasma concentrations are reached within 4 hours of administration and an equilibrium ("steady state") is achieved after one week, then the plasma concentrations being about 2.5 times those observed after single doses. In the therapeutic dose range, citalopram shows linear pharmacokinetics, being proportional to the dose concentrations. Citalopram and its metabolites bind to plasma proteins by approximately 80%.

Citalopram is metabolised by N-demethylation mainly by the cytochrome P450 CYP3A4 and CYP2C19, although the native citalopram is the predominant product in the plasma. Pharmacological studies have shown that citalopram is between 8 and 10 times more potent than its metabolites as an inhibitor of serotonin reuptake. Approximately 30% of citalopram is excreted by the kidneys, with the elimination half-life in normal individuals of about 35 hours.

Individual pharmacokinetic parameters may vary significantly between the elderly and patients with kidney or liver failure. In patients over 65, the AUC and elimination half-life is 23% and 30% higher than in younger patients. In patients with renal failure, drug clearance is reduced by 37% and half-life is doubled, while there is a correlation between the state of liver function according to Child-Pugh classification and reduction in the clearance. In patients with moderate renal impairment, renal clearance of citalopram is reduced by 17%. There are no data in patients with severe renal impairment (CrCl <20 ml / min). It is unlikely that citalopram is removed in dialysis.

In all these patients, due to the variability of pharmacokinetic parameters, the dose should be adjusted individually.

Indications and dosing

Treatment of depression


  • Initially, 20 mg once daily, subsequently increasing the dose to 40 mg once. Increases in doses of 20 mg each time, must be made at intervals of at least one week, up to 60 mg once daily. However, as a rule, more than 40 mg per day is not recommended.


  • Recommended for most of these patients is 20 mg once a day. In patients who do not respond doses can be increased to 40 mg after one week.

Adolescents and children aged > 9 years:

  • Not many controlled studies in this population. However, some evidence suggests that doses between 10-40 mg / day may be adequate.

Children < 9 years of age:

  • The efficacy and safety of this drug have not been established

Treatment of obsessive-compulsive disorder


  • dose of 20-30 mg once daily have proved more effective than placebo in controlling panic attacks in patients with panic disorder with or without agoraphobia. Higher doses (40-60 mg / day) appear to be more effective than lower


  • for elderly patients, the recommended dose is 20 mg daily. These doses can be increased up to 40 mg / day after one week in patients who do not respond.

Treatment of panic attacks


  • Dose of 20-30 mg once daily have proved more effective than placebo in controlling panic attacks in patients with panic disorder with or without agoraphobia. Higher doses (40-60 mg / day) appear to be more effective than lower.


  • For elderly patients, the recommended dose is 20 mg daily. These doses can be increased up to 40 mg / day after one week in patients who do not respond.

Adjunctive therapy of chronic schizophrenia


  • in a placebo-controlled clinical study, citalopram in a dose of 20 mg once a day for a week, followed by 40 mg once daily was administered to patients with stable chronic schizophrenia under treatment with neuroleptic medication. Although after 12 weeks no significant differences in psychopathological symptoms in subjects treated with citalopram and placebo, patients treated with citalopram showed a better overall clinical status and greater subjective well-being.


  • the recommended dose is 20 mg once a day can be increased to 40 mg / day at weekly intervals.

Treatment of dementia


  • initially a dose of 20 mg once daily. After two weeks of treatment, doses should be adjusted according to the responses. If this was not successful and the treatment is well tolerated the dose may be increased to 30 mg once daily. Conversely, if the patient does not tolerate 20 mg / day, these should be reduced to 10 mg / day.

treatment of PMDD

Adult women:

  • 10-30 mg dose once daily during the menstrual cycle. Alternatively, the same doses may be used during the luteal phase of the cycle (ie during the 14 days prior to menses).

Maximum recommended dose


  • 60 mg / day. But usually not recommended, doses above 40 mg / day


  • 40 mg/day


  • the data are very limited. It has been suggested a maximum dose of 40 mg / day

Children over 9 years:

  • the data are very limited. It has been suggested a maximum dose of 40 mg / day

Children <9 years of age:

  • The efficacy and safety of this drug have not been established

Patients with hepatic impairment: recommended for most patients with liver dysfunction dose is 20 mg once daily, increasing to 40 mg / day if the response is not satisfactory. The Child-Pugh classification is not a good predictor of liver failure to adjust the dose of citalopram. Doses should be adjusted individually depending on the tolerance and clinical response. Patients with renal impairment: if creatinine clearance 20-70 ml / min, no adjustments are required doses. If the CrCl <20ml. Manufacturer dose reduction but does not provide specific treatment guidelines.

Patients on intermittent hemodialysis: the manufacturer recommends caution but did not provide specific treatment guidelines. It is unlikely that citalopram is removed by dialysis due to its large volume of distribution.


Citalopram is contraindicated in patients with hypersensitivity to the drug or any component of the formulation

You should avoid abrupt discontinuation of citalopram to prevent the development of withdrawal syndrome.

The possibility of a suicide or suicide attempt is inherent in all patients with depression, whether it is a primary depression, whether depression associated with another primary disorder and obsessive-compulsive disorder. Patients with a history of attempted suicide should be carefully monitored when starting treatment with citalopram. Moreover, doses of this drug should be the smallest possible to avoid an overdose thereof.

Citalopram is absolutely contraindicated in patients who are under treatment with monoamine oxidase inhibitors (MAOIs)

There is no evaluated effects of citalopram during electroconvulsive therapy

All antidepressants can transform depression into mania or hypomania in some predisposed patients. If a patient develops symptoms suggestive of mania, citalopram should be discontinued and suitable treatment of manic symptoms.

Citalopram has demonstrated anticonvulsant effects in pharmacological studies in animals but has not been systematically evaluated in patients with a history of convulsive disorders. It is therefore recommended to use the drug with caution in patients with epilepsy or other seizure disorders. In clinical studies, administration of citalopram was associated with seizures in 0.3% of patients versus 0.5% in patients treated with placebo.

Although significant abnormalities on electrocardiogram were not observed in clinical studies with citalopram, this drug has not been systematically studied in patients with a recent history of myocardial infarction or unstable heart disease.

Citalopram is excreted unmetabolized in urine only in small amounts. However, it should be used with caution in patients with severe renal dysfunction (eg CrCl <20 ml / min) until there are more data on these patients. There is no information regarding use of citalopram in patients with chronic renal failure receiving hemodialysis.

Citalopram should be administered with caution in patients with liver disease because this drug is extensively metabolized in the liver. In these patients reduced doses is recommended.

Rarely, citalopram may precipitate a syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is presented as serum hiposmolalidad and hyponatremia. The incidence of this syndrome in the case of patients treated with other selective inhibitors of serotonin reuptake is higher in the elderly, patients treated with diuretics or patients with significant dehydration. Caution is advised in these patients if treated with citalopram

There have not been established the safety and efficacy of citalopram in children and citalopram data in adolescents are limited.

Citalopram should be used with caution during lactation. The manufacturer has observed some cases of drowsiness, poor appetite and weight loss in infants whose mothers were treated with citalopram. It has also published a case of an infant with sleep disturbances. Drug concentrations in milk were comparable to those presented in the plasma of the mother, and also came to quantify plasma levels in children. Sleep problems subsisted splitting the dose into two doses mother and replaced by two of bottle jacks infant. The American Academy of Pediatrics suggests that administration of selective inhibitors of serotonin reuptake could be dangerous during lactation. If citalopram is imperative for the mother, it will seek to breastfeed after 4 hours after administration of the drug to avoid peak plasma concentrations. Another possibility is to change the child's feeding bottle feeding passing.

Citalopram is classified in category C pregnancy risk. In animal studies, citalopram produced adverse effects on embryonic and fetal development and postnatal development when administered at the highest dose used in clinical. In general, selective reuptake inhibitors of serotonin in serotoninergic receptors reduce fetal cortex and these changes are maintained for some time after birth. Some epidemiological studies in humans in the case of fluoxetine suggests that cognitive development of children prenatally exposed to selective inhibitors of serotonin reuptake not differ from controls. In 267 women who were treated during pregnancy with selective inhibitors of serotonin reuptake number of spontaneous abortions or elected and the number of malformations in newborns were similar to controls. They were also identical birth weight and gestational age. However, none of these women was treated with citalopram and neither have been no controlled studies with this drug. Therefore, citalopram only be administered during pregnancy if the benefits to the mother outweigh the possible risks to the fetus. The effects of citalopram on the work of labor and delivery is unknown.

Citalopram has not shown impair intellectual function and psychomotor performance in volunteer studies. However, there remains a psychotropic drug and, therefore, occasionally could alter the intellectual or psychomotor functions, so that patients treated with this drug should be warned, especially when driving or handling heavy machinery.

Drug interaction

Citalopram inhibits CYP2D6 CYP450 enzyme system, affecting the metabolism of a number of drugs. Accordingly, they can increase plasma levels of these and therefore toxicity. Any other enzyme system appears to be affected, at least in vitro, by citalopram.

Citalopram powers serotonin by inhibiting their neuronal reuptake. As serotonin is deaminated by monoamine oxidase type A, administration of drugs that inhibit this enzyme concomitantly with a selective serotonin reuptake inhibitor may lead to serotonin syndrome. This syndrome characterized by confusion, convulsions and severe hypertension. Most of monoamine oxidase inhibitors (eg furazolidone, linezolid, procarbazine and tranylcypromine) are nonspecific inhibitors of this enzyme and, therefore, should not be used while selective inhibitors serotonin reuptake as citalopram. As a general rule should not be administered citalopram with MAOIs. A notable exception is selegiline, which administered with citalopram showed no significant pharmacokinetic or pharmacodynamic interactions.

Isoniazid also has some MAOI activity and its administration is not recommended together with citalopram. In addition, it is recommended to wait at least two weeks between discontinuation of treatment and the beginning of another.

Pharmacokinetic interactions between citalopram and tricyclic antidepressants may occur. The in vitro studies suggest that citalopram is a relatively weak inhibitor of the cytochrome P450 CYP2D6 and / or CYP3A4 are responsible for the metabolism of many of tricyclic antidepressants. Co-administration of citalopram and imipramine not significantly affect plasma concentrations of either drug. However, the concentration of desipramine, the major metabolite of imipramine increased by 50%. The clinical significance of this increase is unknown

There have been reported symptoms of toxicity when used in conjunction with other tricyclic antidepressants citalopram so should reduce the doses of tricyclic antidepressants or avoid concomitant administration.

An interaction between citalopram and fenfluramine or dexfenfluramine may occur. These drugs stimulate the release and inhibit serotonin reuptake and, moreover, are metabolized by CYP2D6 which is inhibited by citalopram. Thus, concomitant administration of both drugs causes an increase in serotonin may lead to serotonin syndrome.

The same effects can be produced by other drugs with serotonergic properties such as buspirone, cocaine, lithium, nefazodone and trazodone, venlafaxine, sibutramine, tryptophan and 5-HTP.

Although the manufacturer has not provided any interaction between citalopram and lithium, patients should be warned that the combination of both drugs can cause excessive increase in adverse reactions.

At therapeutic doses, citalopram affects functionalism CYP2D6, causing increases in concentrations of drugs that use the same metabolic pathway including some opioid agonists (eg. Ex. Meperidine, methadone, morphine and oxycodone). Besides converting codeine and hydrocodone their respective active forms it is reduced, reducing its analgesic efficacy.

Citalopram effect on the metabolism of benzodiazepines is unknown. However, co-administration of citalopram with benzodiazepines such as alprazolam or diazepam may result in additive effects on the central nervous system.

Inhibition of CYP2D6 may lead to increased concentrations of some beta-blockers (eg bisoprolol metoprolol, pindolol or propranolol). For example, concomitant administration of citalopram and metoprolol, increasing at twice the plasma concentrations of the latter, although in this case has not been found clinically significant effect on blood pressure or heart rate. However, increased plasma levels of beta-blockers may alter its cardioselectivity and other clinical effects.

For the same reason, citalopram may increase plasma concentrations of some antiarrhythmic agents (encainide, flecainide, propafenone and mexiletine). Other drugs that increase plasma concentrations in the presence of citalopram are some antipsychotics such as clozapine, haloperidol, phenothiazines, risperidone and thiothixene

Citalopram is metabolized by CYP2C19 and CYP3A4. Several drugs are capable of inducing these isoenzymes, increasing metabolism of citalopram. It is theoretically possible that is necessary to increase doses of the latter in patients chronically treated with enzyme-inducing drugs such as barbiturates, carbamazepine, dexamethasone, phenytoin, primidone, rifabutin, rifampin, and troglitazone. However there is no clinical evidence to support these theoretical interactions.

In one study, the combination of citalopram and carbamazepine administration did not significantly affect the pharmacokinetics of either drug

In contrast drugs that inhibit CYP3A4 and CYP2C19 isozyme may theoretically increase plasma levels of citalopram and consequently the side effects and toxicity associated with high plasma concentrations of the drug. The following drugs can affect the metabolism of citalopram if administered concomitantly inhibitors, anti-retroviral protease, calcium antagonists, cannabinoids, cimetidine, clarithromycin, clotrimazole, erythromycin, ethinyl estradiol, fluconazole, fluvastatin, isoniazid, itraconazole, ketoconazole, methyl prednisolone, metronidazole, modafinil, nefazodone, norfloxacin omeprazole, prednisone, quinine, topiramate and zafirlukast. Thus, the combination of citalopram and cimetidine administration for eight days caused an increase in AUC and Cmax of citalopram by 43% and 39%, respectively. The clinical relevance of these findings is unknown because the combination of both drugs showed no significant side effects.

Cyproheptadine a serotonin antagonist in the central nervous system being the opposite pharmacological action of the selective inhibitors of serotonin reuptake. Furthermore cyproheptadine it is metabolized by CYP2D6 enzyme weakly inhibited by citalopram. You should probably avoid combining cyproheptadine and citalopram. Similarly granisetron, ondansetron and methysergide antagonize serotonin receptors although no reported interactions between these drugs and citalopram.

The combination of warfarin and citalopram was a small increase in prothrombin time without clinical significance.

The combination of tramadol with selective inhibitors of serotonin reuptake has been associated with the development of a serotonin syndrome. Some publications have reported cases of seizures during concomitant use of tramadol and selective inhibitors of serotonin reuptake. There have also been reports of serotonin syndrome when tramadol was administered with paroxetine and sertraline.

Selective inhibitors of serotonin reuptake inhibit the formation of the active metabolite of tramadol M1 to inhibit the cytochrome P450 A2D6. Although citalopram is a weak inhibitor of this enzyme system administration may decrease the analgesic efficacy of tramadol and increase plasma levels of native drug is more serotonin to its active metabolite.

Dexamphetamine and amphetamine stimulate the secretion of serotonin in the central nervous system and can interact with other serotonergic agents as selective inhibitors of serotonin reuptake, venlafaxine and nefazodone. These interactions may result in an excess of serotonin and potentially serotonin syndrome. If serotonin syndrome is suspected suspected drugs should be removed immediately. In addition, the monoamine oxidase inhibitory activity of amphetamines can be dangerous when they are administered with citalopram.

Cevimeline is metabolized by CYP3A4 and CYP2D6 at which co-administration with citalopram may increase plasma concentrations. But so far no documented clinical interactions.

Concomitant administration of inhibitors of serotonin reuptake and agonists of the 5-HT1 receptors such as sumaptriptán, naratriptan and rizatriptan results in increased plasma concentrations of the first associated with weakness, hyperreflexia and incoordination. If necessary simultaneous treatment with citalopram and agonists 5HT1 receptors, patients should be warned that interaction may occur and if this happens it will take appropriate action.

All centrally acting drugs should be administered with caution if added to inhibitors of serotonin reuptake. In some patients treated with citalopram, administration of zolpidem has been associated with episodes of disorientation and hallucinations, most often of short duration, but occasionally they lasted up to 7 hours. The mechanism of this interaction is unknown, although it should be pharmacodynamic nature. In one study, zolpidem metabolism was inhibited when chronically administered sertraline, indicating that selective inhibitors of serotonin reuptake may also interfere with zolpidem from the standpoint of pharmacokinetics.

Pentazocine administration increases the risk of serotonin syndrome in patients treated with citalopram, its joint administration must be avoided or, in any case, with caution.

It is recommended to avoid drinking alcohol during treatment with citalopram.

Psychotropic drugs, including selective reuptake inhibitors of serotonin can interact with medicinal herbs Kava kava (Piper methysticum) and valerian (Valeriana officinalis).

They have documented interactions between citalopram and grapefruit juice. Grapefruit juice contains a number of bioflavonoids which are potent inhibitors of CYP3A4 and may interfere with the metabolism of citalopram. Consumption of this juice is not recommended during treatment with citalopram.

Side effects

There is observed a dose-dependent relationship between citalopram doses of 10, 20, 40 and 60 mg in the following side effects: sweating, drowsiness, fatigue, impotence and insomnia. A total of 1063 patients with depression who were treated with citalopram in doses of 10-80 mg / day in a series of controlled clinical trials placebo for 6 weeks, 16% had to be withdrawn from treatment due to side effects compared with 8% of those receiving placebo.

The following adverse reactions led to discontinuation of treatment with citalopram in a double proportion of treatment with placebo, affecting 1-4% of patients: agitation, fatigue, dizziness, somnolence, insomnia, nausea / vomiting and xerostomia

The following adverse reactions occurred in >2% of patients treated with citalopram with a greater incidence than patients treated with placebo: abdominal pain (3% vs. 1%), agitation (3% vs. 1%), anorexia (4% vs. 2%), anxiety (4% vs. 3%), arthralgia (2% vs. 1%), sweating (11% vs. 9%), diarrhea (8% vs. 5%), somnolence (18% vs. 10%), dysmenorrhoea (3% vs. 2%), dyspepsia (5% vs. 4%), ejaculatory dysfunction (6% vs. 1%), fatigue (5% vs. 3%) , fever (2% vs. <1%), impotence (3% vs. <1%), insomnia (15% vs. 14%), decreased libido (2% vs. <1%), myalgia (2 % vs. 1%), nausea / vomiting (21% vs. 14% and 4% vs. 3%), rhinitis (5% vs. 3%), sinusitis (3% vs. <1%), tremor (8 % vs. 6%), upper respiratory tract infections (5% vs. 4%) and xerostomia (20% vs. 14%).

Other adverse reactions detected in 4422 patients who were treated in clinical studies with this drug with an incidence of > 1% were amenorrhea, amnesia, apathy, increased appetite, blurred vision, cognitive impairment, confusion, cough, depression, flatulence , hypotension, migraine headaches, paresthesias, polyuria, pruritus, maculopapular rash, salivation, thoughts of suicide, sinus tachycardia, dysgeusia, and weight gain or loss.

Although sexual dysfunction often part of depression and other psychiatric disorders, there is growing evidence that selective inhibitors of serotonin reuptake induce sexual side effects. According to the manufacturer, citalopram marketed once the incidence of adverse effects of a sexual nature is greater than was observed in clinical studies and in fact, many clinicians suggest that may be affected by these symptoms up to 90% of patients . It is recommended to be discussed and investigated these effects with patients.

Although citalopram is a long-term drug withdrawal syndrome can occur if the medication is discontinued abruptly, symptoms such as fatigue, abdominal pain, nausea, tremors and chills, sweating and incoordination can occur. Withdrawal symptoms appear citalopram and 1-3 days to subside after 1 to 2 weeks. Although this syndrome is quite rare (only 3 have been reported cases of more than 8 million patients treated with citalopram) is recommended that the dose is progressively reduced until complete discontinuation of the drug.