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Compliance with medications is one of the most significant factors that can decrease the rate and severity of relapse and have a positive impact on overall prognosis. Of the various types of the disorder, rapid cycling four or more episodes in one year is associated with the worst prognosis due to higher rates of self-harm and suicide. Early recognition and intervention also improve prognosis as the symptoms in earlier stages are less severe and more responsive to treatment.

For women, better social functioning prior to developing bipolar disorder and being a parent are protective towards suicide attempts. People with bipolar disorder often experience a decline in cognitive functioning during or possibly before their first episode, after which a certain degree of cognitive dysfunction typically becomes permanent, with more severe impairment during acute phases and moderate impairment during periods of remission. As a result, two-thirds of people with BD continue to experience impaired psychosocial functioning in between episodes even when their mood symptoms are in full remission.

Higher degrees of impairment correlate with the number of previous manic episodes and hospitalizations, and with the presence of psychotic symptoms. Despite the overly ambitious goals that are frequently part of manic episodes, symptoms of mania undermine the ability to achieve these goals and often interfere with an individual's social and occupational functioning.

One third of people with BD remain unemployed for one year following a hospitalization for mania. A naturalistic study from first admission for mania or mixed episode representing the hospitalized and therefore most severe cases found that 50 percent achieved syndromal recovery no longer meeting criteria for the diagnosis within six weeks and 98 percent within two years.

Within two years, 72 percent achieved symptomatic recovery no symptoms at all and 43 percent achieved functional recovery regaining of prior occupational and residential status. However, 40 percent went on to experience a new episode of mania or depression within 2 years of syndromal recovery, and 19 percent switched phases without recovery.

Symptoms preceding a relapse prodromal , specially those related to mania, can be reliably identified by people with bipolar disorder.

Bipolar disorder - Wikipedia

Bipolar disorder can cause suicidal ideation that leads to suicidal attempts. Individuals whose bipolar disorder begins with a depressive or mixed affective episode seem to have a poorer prognosis and an increased risk of suicide. Bipolar disorder is the sixth leading cause of disability worldwide and has a lifetime prevalence of about 1 to 3 percent in the general population. Including sub-threshold diagnostic criteria, such as one or two symptoms over a short time-period, an additional 5. There are conceptual and methodological limitations and variations in the findings.

In addition, diagnoses and therefore estimates of prevalence vary depending on whether a categorical or spectrum approach is used. This consideration has led to concerns about the potential for both underdiagnosis and overdiagnosis. The incidence of bipolar disorder is similar in men and women [] as well as across different cultures and ethnic groups. Age-standardized prevalence per , ranged from However, severity may differ widely across the globe. Disability-adjusted life year rates, for example, appear to be higher in developing countries, where medical coverage may be poorer and medication less available.

Late adolescence and early adulthood are peak years for the onset of bipolar disorder. Variations in moods and energy levels have been observed as part of the human experience throughout history. The words " melancholia ", an old word for depression, and "mania" originated in Ancient Greece. Within the humoral theories, mania was viewed as arising from an excess of yellow bile, or a mixture of black and yellow bile.

The linguistic origins of mania, however, are not so clear-cut. Several etymologies were proposed by the Ancient Roman physician Caelius Aurelianus , including the Greek word ania , meaning "to produce great mental anguish", and manos , meaning "relaxed" or "loose", which would contextually approximate to an excessive relaxing of the mind or soul. These concepts were developed by the German psychiatrist Emil Kraepelin — , who, using Kahlbaum 's concept of cyclothymia, [] categorized and studied the natural course of untreated bipolar patients.

He coined the term manic depressive psychosis , after noting that periods of acute illness, manic or depressive, were generally punctuated by relatively symptom-free intervals where the patient was able to function normally.

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The term "manic—depressive reaction " appeared in the first version of the DSM in , influenced by the legacy of Adolf Meyer. There are widespread problems with social stigma , stereotypes, and prejudice against individuals with a diagnosis of bipolar disorder. Kay Redfield Jamison , a clinical psychologist and professor of psychiatry at the Johns Hopkins University School of Medicine , profiled her own bipolar disorder in her memoir An Unquiet Mind Several dramatic works have portrayed characters with traits suggestive of the diagnosis that has been the subject of discussion by psychiatrists and film experts alike.

A notable example is Mr. Jones , in which Mr. Jones Richard Gere swings from a manic episode into a depressive phase and back again, spending time in a psychiatric hospital and displaying many of the features of the syndrome. TV specials , for example the BBC 's Stephen Fry: The Secret Life of the Manic Depressive , [] MTV 's True Life : I'm Bipolar , talk shows, and public radio shows, and the greater willingness of public figures to discuss their own bipolar disorder, have focused on psychiatric conditions, thereby, raising public awareness.

On April 7, , the nighttime drama on the CW network, aired a special episode where the character Silver was diagnosed with bipolar disorder. The storyline was developed as part of the BBC's Headroom campaign. A link between mental illness and professional success or creativity has been suggested, including in accounts by Socrates , Seneca the Younger , and Cesare Lombroso. Despite prominence in popular culture, the link between creativity and bipolar has not been rigorously studied.

This area of study also is likely affected by confirmation bias. Some evidence suggests that some heritable component of bipolar disorder overlaps with heritable components of creativity. Probands of people with bipolar disorder are more likely to be professionally successful, as well as to demonstrate temperamental traits similar to bipolar disorder.

Furthermore, while studies of the frequency of bipolar disorder in creative population samples have been conflicting, studies that have a positive finding report that full blown bipolar disorder is rare. In the s, Emil Kraepelin noted that manic episodes are rare before puberty. This issue diminished with an increased following of the DSM criteria in the last part of the twentieth century. While in adults the course of bipolar disorder is characterized by discrete episodes of depression and mania with no clear symptomatology between them, in children and adolescents very fast mood changes or even chronic symptoms are the norm.

The diagnosis of childhood bipolar disorder is controversial, [] although it is not under discussion that the typical symptoms of bipolar disorder have negative consequences for minors suffering them. Treatment involves medication and psychotherapy. Current research directions for bipolar disorder in children include optimizing treatments, increasing the knowledge of the genetic and neurobiological basis of the pediatric disorder and improving diagnostic criteria. There is a relative lack of knowledge about bipolar disorder in late life.

There is evidence that it becomes less prevalent with age but nevertheless accounts for a similar percentage of psychiatric admissions; that older bipolar patients had first experienced symptoms at a later age; that later onset of mania is associated with more neurologic impairment; that substance abuse is considerably less common in older groups; and that there is probably a greater degree of variation in presentation and course, for instance individuals may develop new-onset mania associated with vascular changes, or become manic only after recurrent depressive episodes, or may have been diagnosed with bipolar disorder at an early age and still meet criteria.

There is also some weak and not conclusive evidence that mania is less intense and there is a higher prevalence of mixed episodes, although there may be a reduced response to treatment.


Overall, there are likely more similarities than differences from younger adults. From Wikipedia, the free encyclopedia. For the medical journal, see Bipolar Disorders journal. For other uses, see Manic depression disambiguation. Main article: Major depressive disorder. Main article: Mixed affective state.

Main article: Associated features of bipolar disorder. Further information: Biology of bipolar disorder. Main article: Treatment of bipolar disorder. Main article: History of bipolar disorder. See also: List of people with bipolar disorder , Category:Books about bipolar disorder , and Category:Films about bipolar disorder.

Main article: Bipolar disorder in children. A Historical Dictionary of Psychiatry. New York: Oxford University Press. Oxford Textbook of Palliative Nursing. Oxford University Press, Incorporated. Diagnostic and Statistical Manual of Mental Disorders 5th ed. Arlington: American Psychiatric Publishing. Front Neurosci. Archived from the original on July 31, National Institutes of Health.

Archived from the original on July 27, Retrieved August 13, Journal of Psychopharmacology. Currently, medication remains the key to successful practice for most patients in the long term. At present the preferred strategy is for continuous rather than intermittent treatment with oral medicines to prevent new mood episodes. The Journal of ECT.

Lancet Review. Gender differences in bipolar disorder". International Review of Psychiatry. The American Journal of Managed Care. Kaplan and Sadock's Comprehensive Textbook of Psychiatry 10th ed. New York: Wolters Kluwer. The Journal of Clinical Psychiatry. J Affect Disord. Perspect Psychiatr Care. Progress in Neurology and Psychiatry. Br J Psychiatry. Clin Psychol Rev. Journal of Psychosomatic Research. Clinical Psychology Review. Am J Psychother. Current Psychiatry Reports. September Archived from the original on April 29, Web M.

Archived from the original on December 9, Retrieved December 6, J Pak Med Assoc. Psychiatr Serv. Ann Clin Psychiatry. Am J Psychiatry. Psychiatry and Clinical Neurosciences Review. Jornal de Pediatria. Appl Clin Genet. Rev Bras Psiquiatr. Psychiatric Times. Archived from the original on April 28, Aust N Z J Psychiatry. Unity or heterogeneity? Journal of Affective Disorders. American Journal of Psychiatry. Archives of General Psychiatry.

Nordic Journal of Psychiatry. The genetics of mania". The American Journal of Psychiatry. American Journal of Medical Genetics. Part B, Neuropsychiatric Genetics. Biological Psychiatry. JAMA Psychiatry. The American Journal of Human Genetics. Neurotox Res. Molecular Psychiatry. Development and Psychopathology. Her youngest sister, Chase, asked her to join them, but Laura said she was going outside to write. There was nothing there, really. There were two trails to the ocean, one leading to a sandy cove and the other to the rocky coast, where Laura and her sisters used to fish for striped bass.

Laura took the path to the rocks, passing a large boulder that her sister Nina, a geology major in college, had written her thesis about. The tide was low, and it was cold and windy. Laura leaned against a rock, took out her laptop, and began typing. She swallowed a handful of pills at a time, washing them down with red wine. She found it increasingly hard to sit upright, and her vision began to narrow.

She felt grateful to be ending her life in such a beautiful place. She fell over and hit her head on a rock. She heard the sound but felt no pain. She was hypothermic, her body temperature having fallen to nearly ninety-four degrees. After two days in a medically induced coma, she woke up in the intensive-care unit. Her sisters and parents watched as she opened her eyes. Now she was weak, dizzy, sweating profusely, and anemic. Her body ached from a condition called rhabdomyolysis, which results from the release of skeletal-muscle fibres into the bloodstream.

She had a black eye from hitting the rock. Nevertheless, within a few days she returned to the mode she adopted among doctors. Another doctor noted that she did not seem to meet the criteria for major depression, despite her attempted suicide. The doctor proposed that she had borderline personality disorder, a condition marked by unstable relationships and self-image and a chronic sense of emptiness. According to her medical records, Laura agreed.

She was started on a new combination of medications: lithium, to stabilize her moods, and Ativan, a benzodiazepine, in addition to the antipsychotic Seroquel, which she had already been taking. Later, a second antipsychotic, Abilify, was added—common practice, though there was limited research justifying the use of antipsychotics in combination. Shortly before Laura was discharged, she drafted a letter to the staff on her unit.

Laura moved back home to live with her parents in Greenwich and spent her nights drinking with old friends. I am floating. When it was clear that positivity was out of reach, Laura began seeing a new psychiatrist at McLean, who embraced the theory that her underlying problem was borderline personality disorder.

In , Laura moved in with her aunt Sara, who lived outside Boston, and attended a day-treatment program for borderline patients. At her intake interview, she wore stretchy black yoga pants from the Gap, one of the few garments that allowed her to feel invisible.

Laura had been content to be bipolar. Laura sometimes drank heavily, and, at the suggestion of a friend, she had begun attending Alcoholics Anonymous meetings. Laura was heartened by the stories of broken people who had somehow survived. The meetings lacked the self-absorption, the constant turning inward, that she felt at the clinic, where she attended therapy every day. If she were to quit drinking, she wanted to feel that she had done it on her own.

She was already taking Effexor an antidepressant , Lamictal, Seroquel, Abilify, Ativan, lithium, and Synthroid, a medication to treat hypothyroidism, a side effect of lithium. The medications made her so sedated that she sometimes slept fourteen hours a night. In May, , a few months after entering the borderline clinic, she wandered into a bookstore, though she rarely read anymore. The book tries to make sense of the fact that, as psychopharmacology has become more sophisticated and accessible, the number of Americans disabled by mental illness has risen. Whitaker argues that psychiatric medications, taken in heavy doses over the course of a lifetime, may be turning some episodic disorders into chronic disabilities.

The book has been praised for presenting a hypothesis of potential importance, and criticized for overstating evidence and adopting a crusading tone. Whitaker lived in Boston, and they met for coffee. Whitaker told me that Laura reminded him of many young people who had contacted him after reading the book. At her appointments with her pharmacologist, Laura began to raise the idea of coming off her drugs. The doctors at the borderline clinic initially resisted her requests, but they also seemed to recognize that her struggles transcended brain chemistry. A few weeks later, she went off Abilify, the antipsychotic.

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She began sweating so much that she could wear only black. If she turned her head quickly, she felt woozy. Her body ached, and occasionally she was overwhelmed by waves of nausea. Cystic acne broke out on her face and her neck. Her skin pulsed with a strange kind of energy. A month later, she went off Effexor, the antidepressant.

Her fear of people judging her circled her head in permutations that became increasingly invasive. She began to experience emotion that was out of context—it felt simultaneously all-consuming and artificial. Later, she found a community of people online who were struggling to withdraw from psychiatric medications. The Web forum Surviving Antidepressants, which is visited by thousands of people every week, lists the many varieties of neuro-emotion: neuro-fear, neuro-anger, neuro-guilt, neuro-shame, neuro-regret.

For many people on the forum, it was impossible to put the experience into words. It took Laura five months to withdraw from five drugs, a process that coincided with a burgeoning doubt about a diagnosis that had become a kind of career. When her aunt Sara updated the rest of the family about Laura, the news was the same: they joked that she had become part of the couch.

Her family, Laura said, learned to vacuum around her. Others in her situation might have lost their job and, without income, ended up homeless.

  • Bruno Taut, Die neue Wohnung. Die Frau als Schöpferin, Leipzig 1928 (German Edition).
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  • It took six months before she felt capable of working part time. Laura had always assumed that depression was caused by a precisely defined chemical imbalance, which her medications were designed to recalibrate. She began reading about the history of psychiatry and realized that this theory, promoted heavily by pharmaceutical companies, is not clearly supported by evidence.

    Genetics plays a role in mental disorder, as do environmental influences, but the drugs do not have the specificity to target the causes of an illness. Wayne Goodman, a former chair of the F. Few studies follow patients who take the medications for more than a year. A decade after the invention of antidepressants, randomized clinical studies emerged as the most trusted form of medical knowledge, supplanting the authority of individual case studies. For adolescents who go on medications when they are still trying to define themselves, they may never know if they have a baseline, or what it is.

    Antidepressants are now taken by roughly one in eight adults and adolescents in the U. Industry money often determines the questions posed by pharmacological studies, and research about stopping drugs has never been a priority. Barbiturates, a class of sedatives that helped hundreds of thousands of people to feel calmer, were among the first popular psychiatric drugs. Although leading medical journals asserted that barbiturate addiction was rare, within a few years it was evident that people withdrawing from barbiturates could become more anxious than they were before they began taking the drugs.

    They could also hallucinate, have convulsions, and even die. Valium and other benzodiazepines were introduced in the early sixties, as a safer option. By the seventies, one in ten Americans was taking Valium.

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    Selective serotonin reuptake inhibitors, or S. There had been other drugs used as antidepressants, but they had often been prescribed cautiously, because of concerns about their side effects. Concerns about withdrawal symptoms emerged shortly after S. A third of the patients said they felt suicidal, and four were admitted to a hospital. This optimal range is determined by patient-specific changes in D 2 receptor density, and it might prevent further compensatory up- or downregulation of these receptors [ 4 ].

    We will review 3 studies [ 34 , 35 , 36 ], 2 specifically focusing on TR schizophrenia online suppl. Table 2. We will then review 2 studies [ 37 , 38 ] investigating SP as a potential cause of relapse in schizophrenia. All studies used criteria derived from Chouinard [ 14 ] work published in Suzuki et al. The characteristics of these patients are given in online supplementary Table 2. Patients were identified as having SP if they met at least one of Chouinard's [ 14 ] criteria: rebound psychosis, tolerance to antipsychotic therapeutic effects, or TD.

    It should be noted that there were no patients taking clozapine given that it was not approved yet in Japan when the study was initiated. There were significantly more patients with Carpenter deficit schizophrenia [ 77 ] without SP than with SP. This finding is consistent with prior studies showing that SP is more prevalent in good prognosis schizophrenia [ 72 ]. TR patients with SP had significantly more drug-induced movement disorders including parkinsonism [ 79 ] than patients without SP.

    In the second study of SP by Kimura et al. Patient characteristics are given in online supplementary Table 2. Both SP and non-SP groups improved with adjunctive LA injectable risperidone, but the SP group showed significantly greater improvement in the BPRS total score and had a greater number of drug responders [ 34 ] online suppl. Kimura et al. Similar results were found in both cohorts. Patients with SP showed greater improvement in BPRS total scores, positive and negative symptom subscores, and significantly less relapses during the first- and second-year follow-up than TR patients without SP.

    The studies by Kimura et al. A better drug response in patients with SP was also previously reported in patients treated with FGAs [ 69 , 72 ]. The significant improvement in BPRS negative symptoms probably includes negative symptoms secondary to positive symptoms [ 1 ]. The studies of Kimura et al. Takase et al. All in- and outpatient medical charts of the Chiba University Hospital Japan were reviewed for a diagnosis of schizophrenia from September to December The prevalence rate of SP was found to be Drug-induced movement disorders and minor life events were not considered in this study.

    At initiation of aripiprazole, SP patients were taking significantly higher doses of SGAs equivalent to Nearly all patients in both groups were on SGAs, and only 7. It should be noted that non-SP patients treated with high antipsychotic doses mean dose equivalent to In 2 clinical studies of psychotic relapse, Fallon and Dursun [ 37 ] and Fallon et al. Patients taking clozapine or quetiapine were excluded because of the particular D 2 pharmacology of these drugs compared to other antipsychotics see Rebound Psychosis section and the different types of relapses associated with them [ 1 , 33 ].

    Seven Patients who were relapsing and who also had TD were on higher antipsychotic doses, had more positive psychotic symptoms, a longer duration of illness, more minor life events, and were older. In the second study, Fallon et al. The majority of patients on mood stabilizers This is noteworthy since antiseizure drugs have been found to have beneficial effects on SP patients [ 69 ]. Fallon et al. They replicated the results of their first study.

    In addition, Fallon et al. Based on ongoing research into SP characteristics, along with evidence for withdrawal symptoms found with other CNS drug classes, we present a conceptual framework [ 1 , 41 ] for identifying SP and other antipsychotic withdrawal syndromes Tables 1 , 2. Chouinard and colleagues [ 1 , 31 , 89 , 90 ] reported 3 types of withdrawal syndromes associated with CNS drugs, including opiates, barbiturates, and alcohol: 1 new or classical withdrawal symptoms; 2 rebound; and 3 postwithdrawal disorders Table 1.

    These 3 types of withdrawal syndromes need to be differentiated from relapse and recurrence of the original illness. Relapse is defined as the gradual return to symptoms seen before treatment and entails a return of the ongoing episode, while recurrence is defined as a new episode of the illness Table 1. New and rebound withdrawal symptoms are usually of short duration, persisting for a few hours to 2 weeks with complete recovery. However, if symptoms persist for more than 6 weeks, they become part of postwithdrawal disorders [ 41 ].

    Fava et al. The term discontinuation refers to the medical act of drug discontinuation or patient self-discontinuation. Furthermore, the term discontinuation is misleading since withdrawal symptoms may also occur with dose reduction or in-between doses for rapid-onset short-acting drugs.

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    Examples include alprazolam and lorazepam, which can induce clock watching in-between doses, and clozapine which can induce late afternoon psychosis when given as a single dose at bedtime [ 41 ]. We will give criteria for each of the 3 types of withdrawal associated with antipsychotics [ 1 , 41 , 94 ]. New symptoms are the classic symptoms of withdrawal. They are not part of the patient's illness. New symptoms can be minor anxiety, insomnia, and tremor or major seizures, psychosis, and death [ 95 ]. Some are common to all CNS drugs, including narcotics, barbiturates, and alcohol, but each class of CNS drugs has its own specific new symptoms [ 1 , 41 , 90 ].

    New symptoms common to CNS drugs include: nausea, headache, tremor, sleep disturbances, decreased concentration, anxiety, irritability, agitation, aggression, depression, or dysphoria [ 41 ], as listed in Tables 3 and 4. On the other hand, new drug-specific symptoms are linked to receptor binding affinities, and result from receptor supersensitivity which leads to increased neurotransmission due to removal of receptor blockade by antipsychotic treatment when medication is discontinued or switched, or dose is reduced [ 1 , 41 , 90 ].

    New and rebound symptoms occurring during withdrawal and switch from and to SGAs aripiprazole, asenapine, iloperidone, lurasidone, olanzapine, paliperidone, quetiapine, risperidone, sertindole, ziprasidone, and amisulpride were reviewed recently by Cerovecki et al.

    The second type of CNS drug withdrawal consists of rebound symptoms Tables 1 , 2 [ 41 ]. It refers to a sudden return of patient symptoms above pretreatment levels and is usually short lasting. Rebound symptoms should be distinguished from pharmacological rebound, which produces both new and rebound symptoms. This includes adrenergic rebound [ 99 ], cholinergic rebound [ , ], serotonin rebound [ 97 ], and histamine rebound [ 98 ].

    We make a distinction between new and rebound symptoms, though they may have the same pharmacological mechanism [ 1 , 41 , 94 ]. The difference between new and rebound symptoms is whether present before treatment and known to the patient rebound or not present before treatment new and known to the patient. Rebound anxiety and insomnia, seen with short-acting benzodiazepines [ 1 ], are also associated with new symptoms [ ].

    Withdrawal insomnia [ ] and rebound insomnia [ ] were identified as separate entities in all-night EEG recording studies. Recently, we reviewed CNS drug rebound syndromes [ 41 ]. In 2 double-blind placebo studies, patients with major depression had their maintenance paroxetine, sertraline, or fluoxetine treatment interrupted with placebo substitution and treatment reinstitution [ , ]. In one of the studies [ ], patients taking paroxetine and sertraline had a sudden worsening of depressive symptoms upon drug discontinuation with a return to baseline depression measurements after reinstitution of the treatment.

    In contrast, patients treated with paroxetine had rebound depression in both studies [ 41 , , ]. Rebound syndromes respond rapidly to reinstitution of the offending drug, which often leads patients to false beliefs about efficacy and need for the drug [ 90 ]. Rebound symptoms can be persistent in some patients, for example long-lasting insomnia after withdrawal from sustained alcohol abstinence [ 95 ] and rebound psychosis after long-term antipsychotic treatment [ 1 , 14 ].

    The proposed diagnostic criteria for rebound psychosis are given in Table 3. Rebound psychosis is defined by a rapid return above pretreatment levels of at least one positive symptom listed in the Rating Scale for Psychotic Symptoms RSPS [ 73 , 74 ]. Rebound psychosis lasts up to 6 weeks after peak onset Table 1 ; if it persists longer, it becomes a postwithdrawal disorder, as for new symptoms persisting more than 6 weeks. Rebound psychosis is generally short lasting and considered as a reversible form of SP, equivalent to reversible withdrawal TD [ 1 ].

    Any rebound symptom, such as an increase in blood pressure, myocardial infarction, insomnia, or psychosis, has the potential to become a persistent postwithdrawal disorder when lasting more than 6 weeks, often lasting several months and even years [ 1 , 41 , 95 , 96 ]. Patients on clozapine monotherapy taken as a single dose at bedtime report late afternoon return of symptoms [ 1 ].

    For both the immediate-release formulation IR and the extended-release formulation XR of quetiapine, it is common in clinical practice to have difficulty in decreasing the drug dose, as it causes rebound anxiety and rebound insomnia the drug possessing anxiolytic and hypnotic effects [ ] , and later causes an in-between dose clock watching for return of symptoms, e. The pharmacokinetics [ ] and the central D 2 receptor occupancy pharmacodynamics [ ] of IR quetiapine given twice daily and XR quetiapine given once daily are similar [ , ].

    Quetiapine and clozapine have a particular D 2 pharmacological profile compared to other SGAs: loose binding displaced rapidly from the D 2 receptor [ ], fast dissociation from the D 2 receptor [ ], brief and weak action of clozapine on brain dopamine systems [ , ], and high transient initial D 2 occupancy by quetiapine with minimal occupancy at the end of the dose interval [ ]. This D 2 profile of clozapine and quetiapine leads to differences in SP manifestations [ 1 ]: elevated incidence of rebound psychosis with clozapine [ 1 , 33 , 39 , ], which is a reversible withdrawal subtype of SP [ 1 ], and severe drug tolerance with IR quetiapine given as antipsychotic monotherapy [ 39 ].

    This might be explained by initially high D 2 occupancy followed rapidly by low occupancy at the end of the dosing interval [ ]. Postwithdrawal disorders have been described with all classes of CNS drugs [ 1 , 41 ]. Interestingly, in this first report of adrenergic rebound, major complications such as death were seen in patients who responded better to propranolol [ ], which is also a characteristic of SP, most often seen in good antipsychotic drug responders [ 14 , 72 ]. Rebound anxiety and insomnia were also first demonstrated with short-acting and potent benzodiazepines [ 90 , , ], and later as postwithdrawal disorders for alcohol [ 95 ] and benzodiazepines [ , ].

    Other known postwithdrawal disorders are major depression and dysphoria in cocaine [ , ] and amphetamine withdrawal [ ]. Within a drug class, specific drugs such as fluphenazine, perphenazine, quetiapine, clozapine, triazolam, and paroxetine permitted identification of new postwithdrawal disorders [ 1 , 33 , 39 , 41 , , ]. For SSRIs and SNRIs, several postwithdrawal disorders after long-term use have been described; interestingly, these postwithdrawal disorders consist of disorders that can be treated successfully by SSRIs and SNRIs, such as obsessive-compulsive, panic, generalized anxiety, and gambling disorders [ 1 , 41 , , , , ].

    All these postwithdrawal disorders have been shown to occur more frequently with paroxetine [ 41 , , , ]. This suggests that paroxetine should not be used anymore. For antipsychotics, two persistent postwithdrawal disorders, TD and SP, have been described [ 14 , 28 , 30 , 31 , ]. When the symptoms last less than 6 weeks, they are considered as withdrawal dyskinesia and rebound, or withdrawal psychosis, respectively. When the symptoms last longer, they become postwithdrawal disorders, TD, or SP [ 1 ].

    Similarly, it has been known since the s that long- and short-term dopamine receptor blockade by antipsychotics can both produce receptor supersensitivity [ ]. The persistence of the dopamine supersensitivity syndrome depends on the duration of the preceding blockade [ ] and on the specific antipsychotics used fluphenazine, perphenazine, clozapine, and quetiapine [ 1 , 41 ]. In addition, we took into account the results from the 2 studies by Fallon and Dursun [ 37 ]and Fallon et al. Exacerbation of psychosis by dopamine partial agonists was added as a risk factor minor criterion following the study by Takase et al.

    Vulnerability to minor life events was explicitly added to the minor criterion of exacerbation of psychosis by stress, following the results of Fallon and Dursun [ 37 ]and Fallon et al.

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    In addition, compared to criteria, major criteria define positive symptoms specifically [ 73 , 74 ]. Table 2 [ 34 , 35 , 36 ], and in the 2 relapse studies [ 37 , 38 ]. Minor criteria are risk factors for SP Table 4 ; they help to identify patients at risk for SP relapse. One minor criterion is needed if only one of the major criteria present is C1, C2, or C6 Table 4. All antipsychotics, including the most recent SGAs [ 26 ], have the potential to produce D 2 upregulation. For instance, using laboratory animals, Tarazi et al. Kusumi et al. While some antipsychotics may not elevate the density of D 2 receptors, they can still raise the number of dopamine D 2 High receptors [ 25 ].

    This may lead to more severe psychosis than seen in previous episodes during SP relapse or exacerbations, with new schizophrenic symptoms of greater severity such as disorganized behavior [ 14 ]. Patients with SP are more vulnerable to stress [ 14 , 69 ], minor life events, and daily hassles [ 14 , 37 , 38 , 69 ].

    Stress increases dopamine levels in the brain [ ]. As dopamine binds to D 2 receptors in competition with antipsychotic drugs, antipsychotics with less D 2 receptor affinity allow more dopamine to bind to the receptors, and psychotic relapses due to SP will appear more rapidly. Another feature of SP is the gradual tolerance to the therapeutic effect of antipsychotic medications, where previously efficacious doses can no longer adequately control psychotic symptoms.

    Continuous D 2 occupancy by antipsychotics, within or above the threshold for prolactin and movement disorders i. In order to improve psychotic symptoms, at least temporarily, higher doses are required [ 20 ], and therapeutic drug tolerance further develops. This has also been shown in animal models of antipsychotic-like efficacy, where continuous blockade of D 2 receptors by antipsychotics, at clinically representative levels, produces tolerance to ongoing treatment, and higher doses can temporarily restore efficacy [ 9 , 10 ].

    Following antipsychotic discontinuation or sudden dose reduction, psychotic relapse develops more rapidly in patients with SP than in those without [ 69 ]. As optimal therapeutic D 2 occupancy increases [ 4 ], increasing the antipsychotic dose would further mask TD [ ] and SP [ 1 ], produce parkinsonism and negative symptoms, but also temporarily improve positive symptoms [ 4 , 34 ]. Some patients with severe SP who are also taking high doses of antipsychotics may exhibit all of these symptoms at the same time [ 1 , 34 , ].

    This mixed syndrome of drug-induced movement disorders and psychosis is temporally improved by giving the antipsychotic in divided doses [ 69 ]. Thus, SP may be masked, overt, or mixed [ 1 ], like TD [ 19 ]. The fact that SP can be overt during dose reduction, and masked by the causing drug during treatment [ 14 , 28 , 30 ], explains the therapeutic tolerance observed when antipsychotics can no longer mask psychotic symptoms at previously efficacious doses, and further increases in doses are necessary to obtain similar therapeutic effects [ 14 , 28 , 30 ].

    Tolerance needs to be identified early to avoid increasing doses. Once therapeutic tolerance is identified, instead of dose increases to cover SP, strategies that we propose here should be considered, primarily the use of low doses of antiseizure drugs [ 1 ], the use of the minimal therapeutic dose of antipsychotic, and regular but intermittent dosing.

    Switching from one antipsychotic to another can potentially induce or uncover SP [ 14 , 37 , 69 , 94 ]. Switching antipsychotics will allow SP to emerge in patients either with or without a past history of SP [ 36 ]. SP often occurs in the presence or history of drug-induced movement disorders, most often parkinsonism or TD [ 14 , 28 , 30 , 37 ]. This is expected since parkinsonism and other drug-induced movements are the best predictors for TD [ 1 , 71 , 81 ] and SP [ 1 , 37 , 38 ].

    Iyo et al. As already mentioned, Kapur et al. The first step Table 5 is the early detection of mild drug-induced movement disorders of the parkinsonian type [ 1 , 71 ], regardless of whether dopamine blockade is continuous [ 43 ], intermittent, or repetitive [ 42 ], or produced by SGAs or FGAs. This suggests that overblockade of D 2 receptors can be detected clinically with a movement disorder examination. It will permit early recognition of iatrogenic psychiatric symptoms confounded with movement disorders [ 1 ], akinesia confounded with psychomotor retardation, akathisia with agitation, and TD with mannerisms and schizophrenic abnormal movements [ 1 , 81 ], symptoms which will often trigger dose increases and a consequent overblockade of D 2 receptors.

    In the same PET study of first-episode schizophrenia, Kapur et al. Thus, when prolactin is increased by an antipsychotic, it can be used for early detection of D 2 overblockade, which is consistent with our earlier findings with prolactin [ 28 , 30 ] and antipsychotic plasma levels [ 19 ]. Furthermore, antipsychotic plasma levels in patients were measured by the same radioreceptor technique [ 19 ], using calf caudate membranes technique from Bruce Cohen, Harvard University, MA, USA.

    Since prolactin, when elevated by antipsychotics, provided overall similar findings as antipsychotic plasma levels [ 19 ], patients with prolactin measurements appeared more practical for long-term follow-up [Chouinard and Jones: Clinical application of the neuroleptic radioreceptor assay in the management of schizophrenia Health and Welfare Canada, unpubl. Finally, the findings confirm the relevance to use of prolactin level measurements for early detection of D 2 overblockade whenever appropriate, even for antipsychotics that raise prolactin levels inconsistently. The second step Table 5 is the administration of minimal therapeutic doses during maintenance treatment following the acute phase.

    The dose given in the acute phase is reduced gradually when initiating the maintenance treatment [ ]. During the acute phase of psychosis, excessive dopamine release competes with antipsychotics for D 2 receptor binding and depletes dopamine in the synaptic cleft [ ], which creates a delay in reaching a new equilibrium. The third step Table 5 is to keep D 2 occupancy within the optimal therapeutic range while maintaining the minimal therapeutic dose. In clinical practice, one should take into account that peak-to-trough plasma concentrations vary greatly and will depend on a number of variables.

    These include dosing interval and drug formulation [ ], D 2 receptor affinities, lipophilicity, active metabolites, patient characteristics ethnicity and gender , concomitant medications, comorbid diseases, and general physical health [ , ]. For LA injectable antipsychotics, pharmacokinetic data in product monographs are of limited value for clinicians to choose the interval of administration [ ]. In their recent review, Lee et al.

    Continuous blockade of D 2 receptors could contribute to the emergence of SP according to research conducted in animals. There are reports that intermittent antipsychotic administration via daily subcutaneous injection can produce dopamine supersensitivity [ , , , ]. However, the antipsychotic doses used are quite large and would produce excessively high and clinically unrepresentative levels of striatal D 2 receptor blockade [ ].