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Women's Primary Health Grand Rounds at the University of Michigan; Timothy R.B. Johnson, MD, and Barbara Apgar, MD, Series Editors

Postpartum Depression


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Despite the recent growth in publicity, postpartum depression is still all too often unrecognized or cavalierly dismissed. However, this common disorder is readily diagnosed and treated by the primary care physician who is willing to take the most basic measures.
Kathryn A. Leopold, MD, Lauren B. Zoschnick, MD
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Historically, the connection between childbirth and psychiatric illness has been well-recognized. In 460 BC, Hippocrates described "puerperal fever," theorizing that suppressed lochial discharge was transported to the brain, where it produced "agitation, delirium and attacks of mania."1 The 11th century writings of the gynecologist Trotula of Salerno speculated: "if the womb is too moist, the brain is filled with water, and the moisture running over to the eyes, compels them to involuntarily shed tears."2 Attempts to describe and classify postpartum mental illness became more systematic in the mid-19th century, when Esquirol wrote of the "mental alienation of those recently confined and of nursing women."2 Additionally, accounts of puerperal psychosis and depression are specifically delineated by Marce in his 18th century Treatise on Insanity in Pregnant and Lactating Women.2

Nonetheless, while more common than gestational diabetes, preeclampsia, and preterm delivery, postpartum depression has received much less attention in contemporary medical literature, training, and clinical practice. Although both the academic and lay press have recently increased the focus on postpartum depression, this condition remains a frequently overlooked illness despite its potentially devastating consequences. Debate continues about its cause, definition, diagnostic criteria, and even its existence as a distinct entity.

INCIDENCE

Depression is an exceedingly common disorder, affecting 15% to 25% of the population2,3 and representing a yearly economic burden of $44 billion.4 Overall, depression is frequently undetected; indeed, fewer than 25% of patients suffering from mental illness are actually under the care of a mental health specialist.2,4 Depression is twice as common in women as it is in men, with its peak incidence during the primary reproductive years (25 to 45). The link between reproductive status and depressive illness is further evidenced by the high frequency of depression during the premenstrual phase, the perimenopausal period, and the immediate postpartum period.4

As one of the major physical, psychological, and social stresses of a woman's life, childbirth is gaining growing recognition as a major risk factor in the development of mental illness. Early descriptive studies have been bolstered by a series of reports that document the temporal relationship between psychiatric admissions and childbirth.1,5,6 Using data from more than 35,000 deliveries with sequential 90-day intervals over a 2-year period preceding and following the delivery, Kendell and colleagues clearly demonstrate a sevenfold increase in the risk of psychiatric hospitalization in the first 3 months after delivery.5 In this study, the risk of psychosis was 22 times higher than the prepregnancy rate, and the calculated relative risk (RR) of childbirth for the development of psychosis was 16. However, 87% of the admissions were for affective disorders, with the majority of diagnoses being major depression.5,6

This significant incidence of depression--and the remarkable peak in the number of new cases diagnosed shortly after delivery--makes it clear that the puerperal period is unique in the development of mental illness. It is estimated that of the approximately 4 million births occurring annually in this country, 40% are complicated by some form of a postpartum mood disorder.7

PRESENTATION

Although the current literature divides the spectrum of postpartum mood disorders into three distinct categories, these classifications frequently blend at the margins. At the mildest end of the spectrum is the "maternity blues" or "baby blues." Because this condition arises after 40% to 85% of deliveries, practitioners and patients often view it as a "normal" phenomenon. Nonetheless, patients and their families are distressed by the patients' depressed mood, irritability, anxiety, confusion, crying spells, mood lability, and disturbances in sleep and appetite. These symptoms peak between postpartum days 3 and 5, and typically resolve spontaneously within 24 to 72 hours. The primary treatment is supportive care and reassurance about the transient nature of the condition.8

At the other end of the spectrum is the truly devastating puerperal psychosis. A comparatively rare disease, it complicates only 0.1% to 0.2% of deliveries--but this is 12 to 14.5 times the prenatal incidence of psychosis.6,9 Symptoms generally present within the first 4 weeks postpartum, when the risk of hospitalization is 22 times greater, but can manifest up to 90 days after delivery. A second, smaller, peak in incidence is evident at 18 to 24 months. Patients suffering from puerperal psychosis are severely impaired, suffering from hallucinations and delusions that frequently focus on the infant dying or being divine or demonic. These hallucinations often command the patient to hurt herself or others, placing these mothers at the highest risk for committing infanticide and/or suicide. Most of these patients suffer from affective disorders (primarily bipolar illness), but schizophrenia and even organic brain syndromes are also diagnosed.7

Between these two extremes is postpartum depression, which is increasingly recognized as a unique and serious complication of childbirth (Table 1). Its insidious onset and chronic course complicates 10% to 15% of all deliveries7,10,11 and a staggering 26% to 32% of all adolescent deliveries.12 The majority of patients suffer from this illness for more than 6 months and, if untreated, 25% of patients are still depressed a year later.13 Postpartum onset is the index depression episode in more than 50% of cases, again underscoring the unique triggering effect of childbirth. More than 60% of patients have an onset of symptoms within the first 6 weeks postpartum,14 providing the primary care physician with the perfect opportunity for diagnosis.

Table 1. Symptoms of Postpartum Depression

Dysphoric mood

Loss of interest in usually pleasurable activities

Difficulty concentrating or making decisions

Psychomotor agitation or retardation

Fatigue

Changes in appetite or sleep

Recurrent thoughts of death/suicide

Feelings of worthlessness or guilt, especially failure at motherhood

Excessive anxiety over child's health

As these patients often suffer from delusions and suicidal tendencies, the consequences of this disease to both mother and child are significant. Furthermore, depressed mothers have an increased risk of relapsing and/or continued psychiatric illness. Both Kumar and Robson10 and Philips and O'Hara15 found that during a 4-year follow-up period, approximately 80% of patients sought help again for psychiatric complaints. In addition, depressed mothers often show a more negative attitude toward their children, and a debilitated new mother puts significant emotional and perhaps economic burdens on family relationships. The patients themselves are often the most sensitive to these consequences. A recent study reports that 32% of women who suffered an episode of postpartum depression dramatically changed their future childbearing plans, re-sorting to adoption, abortion, or in some cases even sterilization.16

The children of these women also suffer because of this illness. Hospitalization of a mother in the early postpartum period increases the incidence of emotional disturbance in children. Conflicting results have been published regarding the effects on the social and emotional development of the children of patients who are not hospitalized, but long-term follow-up studies of up to 4 years suggest that depressive episodes in a mother during the postpartum period were linked to poorer cognitive test scores in their children.11

One of the primary risks of postpartum depression is continued or relapsing illness. Practitioners must recognize that the highest risk of relapse is in subsequent deliveries, where the recurrence risk is 1:3 to 1:4.8 The risk of recurrence may also be correlated to the severity of the initial symptoms; in a subset of women with onset of psychotic symptoms within the first 24 months postpartum, the recurrence risk approaches 100%.17

DIAGNOSIS

Given this incidence and impact, identification of patients suffering from postpartum depression should be a priority for all physicians who treat women. The diagnostic criteria for a major depressive disorder are no different in the postpartum period, with the exception that symptoms must be present for more than 2 weeks postpartum to distinguish them from the "baby blues." Diagnosis requires that the patient experiences either dysphoric mood or anhedonia most of the day, nearly every day, for at least 2 weeks. Additionally, at least four of the following symptoms must be present: difficulty concentrating or making decisions; psychomotor agitation or retardation; fatigue; changes in appetite and/or sleep; recurrent thoughts of death or suicide; feelings of worthlessness or guilt, especially focusing on failure at motherhood; excessive anxiety, frequently focusing on the child's health.2,18

The predominance of anxiety and delusions among these patients often leads authors to describe postpartum depression as "atypical."8 Weight and appetite changes in recently delivered (and often breast-feeding) women are expected, and sleep deprivation is universal in early motherhood. Therefore, the detection of pathologic changes requires specifically directed questions. For example, the physician might ask the mother if she is tired and able to sleep when the infant sleeps, or if food appeals and tastes good to her.

As with other common complications of pregnancy, physicians must remember that all women are at risk. However, certain factors have been identified that may place a patient at particular risk. There is a clear association between postpartum depression and a family history of depression--especially a prior personal episode of depression--that may raise the patient's risk as high as 30%. One episode of postpartum depression may result in a recurrence risk of up to 70%.4 Women experiencing a poor marital relationship (particularly an abusive relationship), a lack of other social supports, and/or child care stressors are also at increased risk. The comorbidities of substance abuse and anxiety or somatization disorders substantially increase the risk of postpartum depression. Primiparous women have been reported to suffer from postpartum depression more frequently, but other studies refute this; the documented finding that patients frequently change their reproductive plans after suffering from postpartum depression confounds the research. Other controversial risks reported in the literature include breast-feeding and obstetric factors such as the length and difficulty of labor, multiple gestation, and advanced maternal age.14,19,20 Postpartum depression is a cross-cultural phenomenon, and likewise has not been associated with socioeconomic class or education level.7,14

EMOTIONAL/HORMONAL CONSIDERATIONS

Multiple investigations into the etiology of postpartum depression have not reached a consensus. The aforementioned risk factors increase stress, and have been postulated as psychological factors leading to depression. Some psychologists have also ascribed the etiology of postpartum depression as inherent to the patient's psychological construct. The cognitive model postulates that a patient's negative view of the world and herself leads to depression through low self-esteem and disturbed relationships, and that patients with abnormal attitudes of self-control may develop a learned helplessness leading to depression.7 Nonetheless, all patients with a negative outlook on the world do not become pathologically depressed, and there is no well-defined etiology for depression in general. Moreover, there is no clear evidence that the mechanisms that produce nonpuerperal depression operate in the postpartum period.

The two leading biologic theories for the cause of nonpuerperal major depression lie in the deregulation of the neurotransmitters serotonin and the other biogenic amines such as norepinephrine, epinephrine, and dopamine. The role of these factors has also been investigated in postpartum depression. Tryptophan is the main precursor for serotonin, and it has been postulated that low circulating tryptophan levels lead to low serotonin levels, which may lead to depression. Despite three separate studies demonstrating decreased tryptophan levels in women suffering from postpartum depression, a double-blind, placebo-controlled trial replacing tryptophan showed no effect.7 Catecholamines have not been studied as thoroughly, but low norepinephrine levels and the severity of postpartum depression have been correlated.7

Other biologic factors examined in the etiology of postpartum depression have included hormonal factors known to change in the puerperium. Postpartum thyroiditis and hypothyroidism are not uncommon phenomena. Patients with documented hypothyroidism do have a mild increase in depressive symptoms, but studies of patients with postpartum depression have demonstrated conflicting findings regarding thyroid function.7 The hypothalamic pituitary axis is also implicated, and has been widely investigated in depression. Cortisol levels rise in pregnancy, peak in labor, then fall dramatically following delivery, after which they decline more slowly to normal levels.21 A strong correlation between cortisol levels and the incidence of depression is not apparent; both high and low levels of cortisol have been documented during the postpartum period in women suffering from postpartum depression.7,14 Prolactin levels, which also rise throughout pregnancy and fall more slowly after delivery, have also been considered as a potential factor in postpartum depression. Once again, conflicting results have been obtained; higher levels of prolactin have been found in women with depressed mood on postpartum days 2, 4, and 6, while lower levels have been correlated with a depressed mood in postpartum week 6.7

Unique to the puerperium are the rapid changes in the levels of ovarian steroids. These hormones fall from very high levels at term to near follicular levels within 48 hours. The rapid withdrawal of progesterone--whose metabolite hydroxy-5a-dihydropro- gesterone is a potent, barbiturate-like ligand of g-aminobutyric acid (GABA) receptors22--occurs with the delivery of the placenta, and has been postulated as a causative factor. The magnitude of decline of progesterone from 38 weeks' gestation to 1 day postpartum was associated with depressed mood in the first week, while a later study showed no association between progesterone levels and postpartum depressive symptoms. An interesting finding was lower levels of progesterone in breast-feeding, depressed women versus nondepressed women, while a reverse association was found in nondepressed women.7 These findings suggest some interplay between progesterone and prolactin, and a need for further research into this connection.

Estrogen levels, like progesterone, fall by 90% to 95% in the first 48 hours following delivery. There is recent accumulating evidence of estrogen's important role in memory and cognition, as well as mood. Moreover, there is a well-established body of literature regarding estrogen's profound effects on brain function. These effects are as basic as causing new neuronal spine and dendrite formation, to very specific interactions on all of the relevant neurochemical systems.23 The specific effects are best characterized in the dopamine system, where estrogen increases dopamine turnover through the regulation of tyrosine hydroxylase (the rate limiting synthetic enzyme), degradative enzymes such as monoamine oxidase, and turnover of dopaminergic receptors. Estrogen has similar effects on the serotonergic and gabaminergic systems, increasing the sensitivity of neurons to norepinephrine and inducing the messenger ribonucleic acid for endogenous opiates such as proenkephalin.23 Despite this circumstantial evidence, however, no link between estrogen levels and postpartum depression has been established. Indeed, both low predelivery levels and high postpartum levels of estrogen have been reported in depressed women.7

Taken together, the data suggest that the etiology of postpartum depression is multifactorial. Causative components include both organic and conditional changes arising from both parturition as well as the mother's surrounding situation, which likely combine to influence the patient's psychological function.

Table 2. Dose Ranges and Side-Effect Profiles of Antidepressants Commonly Used to Treat Postpartum Depression

Side Effects1



Drug

Therapeutic range (mg/d)

Anticholinergic2

Orthostatic hypotension

Arrhythmia

Weight gain ( >6 kg)


Tricyclics
Amitriptyline 75–300 4+ 4+ 3+ 4+
Desipramine 75–300 1+ 2+ 2+ 1+
Imipramine 75–300 3+ 4+ 3+ 3+
Nortriptyline 40–200 1+ 2+ 2+ 1+


SSRIs
Fluoxetine 10–40 0 0 0 0
Paroxetine 20– 50 0 0 0 0
Sertraline 50–150 0 0 0 0



10 = absent or rare; 4+ = relatively common.


2Dry mouth, blurred vision, urinary hesitancy, constipation, drowsiness.


TREATMENT

Despite the possibility of a unique etiology for postpartum depression and the lack of controlled comparative therapeutic trials, there is no reason to believe it responds differently to treatment than other types of depression. As in other episodes of depression, early identification and treatment are the keys to successful therapy. Treatment of depression involves three phases--acute treatment (6 to 12 weeks) aimed at remission of symptoms, continuation treatment (4 to 9 months) aimed at stabilization and recovery, and maintenance treatment aimed at preventing recurrence in patients with prior episodes.18

Postpartum depression is successfully treated with medications, psychotherapy, or a combination of both.7,14 Pharmacologic treatment is preferred to psychotherapeutic intervention in patients with more severe or chronic symptoms, prior episodes or family histories, or a prior response to treatment. Medications have the advantage of being less costly and time-consuming. Psychotherapy should be added in patients with more severe depression, chronic psychosocial problems, incomplete response to medication, or evidence of a concurrent personality disorder.18

Criteria for consultation or referral include clinician preference, suicidal or homicidal ideation, presence of psychotic symptoms, severely impaired functioning (including obsessing about or avoiding the infant), failure to respond to an antidepressant treatment trial, and comorbid substance abuse.18 Primary care physicians who initiate treatment of patients' postpartum depression should be familiar with the dosages and side effects of one or two drugs from the major categories listed in Table 2. In general, the tricyclic antidepressants--which block norepinephrine and to a lesser degree serotonin reuptake--are effective, but treatment is burdened with side effects such as weight gain, sedation, dry mouth, and cardiovascular effects. These may be particularly unacceptable in the postpartum period. Moreover, these are very toxic medications, making them particularly dangerous in patients with high overdose potential. The selective serotonin reuptake inhibitors (SSRIs) have fewer and less prominent side effects and provide a wider margin of safety. Monoamine oxidase inhibitors are rarely used now owing to the obligatory dietary restrictions, while newer drugs such as bupropion and venlafaxine have not been tested in the postpartum period but only under psychiatric care.

Patients need frequent monitoring of side effects and treatment response, with a formal 6-week evaluation of partial or nonresponders; this should involve a reevaluation of the diagnosis, compliance with medication, and the need to increase dosing or to change treatment. Electroconvulsive therapy is an important, effective therapeutic intervention that can be useful in treating recalcitrant cases of postpartum depression.

As with all postpartum treatment decisions, special consideration must be given to breast-feeding women. The tricyclic antidepressants have been extensively studied, and no negative effects or detectable serum levels have been demonstrated in the infants of treated mothers. The newer SSRIs have not yet been fully evaluated. Their long-half life is of special concern, as neonates have only 33% to 50% of the adult hepatic metabolic capacity. In fact, treatment of a mother with fluoxetine has been associated with both colic and high serum levels in the infant.24 Therefore, the current recommendations are to treat breast-feeding depressed patients with tricyclics at the minimum effective dose, and to evaluate the infant's level if it is less than 10 weeks old or if symptoms develop.24

To date, prophylactic treatment for women with perceived risks of postpartum depression has not been widely examined. Several uncontrolled studies have attempted to prevent recurrent severe postpartum depression with antidepressants,25 progesterone,26 and estrogen17 with promising results. However, the only prospective treatment trial aimed at a potential etiologic factor in postpartum depression was a double-blind, placebo-controlled trial by Gregoire and colleagues,13 who randomly treated 61 patients affected by postpartum depression with either transdermal estrogen or placebo for 6 months. They showed a significant, rapid, and stable fall in the patient- and clinician-rated depression scores of the estrogen-treated group, with only 50% and 20% of treated patients depressed at 1 and 4 months, respectively. By contrast, 74% and 69% remained depressed in the placebo group. This study represents an important development in the understanding and treatment of postpartum depression. While it needs replication prior to widespread clinical use, this study raises important issues about the general antidepressant nature of estrogen.

Practitioners have the ability to decrease the impact and devastation of postpartum depression by following some simple guidelines for its prevention and treatment. Information about the incidence and the warning signs of postpartum depression should be an intrinsic part of prenatal education. This ideally should include information about mothering classes that may help patients' expectations and suggest ways to make use of existing support systems. Even more importantly, clinicians need to identify patients who have suffered prior episodes of depression, have poor support, or who have other comorbidities putting them at highest risk for postpartum depression. These patients need careful postpartum follow-up, and consideration should be given to prophylactic treatment of those at highest risk.

During the postpartum phase of care, clinicians need to recognize the symptoms of depression and to realize that patients are embarrassed about feeling unhappy during a time when society expects them to be elated. Therefore, it is important to ask patients specifically about their mood and adjustment. The Edinburgh Postnatal Depression Scale is an excellent tool for use in patient evaluation.

CONCLUSION

Postpartum depression is a common, frequently unrecognized, yet devastating disorder. The keys to successful treatment are early identification and intervention, both supportive and pharmacologic. These treatments are effective, and the ability to lessen the impact of this disease is congruent with the primary care provider's role.

REFERENCES

Thurtle V. Post-natal depression: the relevance of sociological approaches. J Adv Nurs. 1995;22(3):416-424.
Steiner M. Postpartum psychiatric disorders. Can J Psychiatry. 1990;35:89-95.
Yonkers KA, Gullion C, Williams A, et al. Paroxetine as a treatment for premenstrual dysphoric disorder. J Clin Psychopharmacol. 1996;16(1):3-8.
Yonkers KA, Chantilis SJ. Recognition of depression in obstetric/gynecology practices. Am J Obstet Gynecol. 1995;173(2):632-638.
Kendell RE, Wainwright S, Hailey A, Shannon B. The influence of childbirth on psychiatric morbidity. Psychol Med. 1976;6(2):297-302.
Kendell RE, Rennie D, Clarke JA, Dean C. The social and obstetric correlates of psychiatric admission in the puerperium. Psychol Med. 1981;11(2):341-350.
O'Hara MW. Postpartum Depression. In: Alloy LB, ed. Series in Psychopathology. New York: Springer-Verlag; 1995:1-27.
Hamilton JA. Postpartum psychiatric syndromes. Psychiatr Clin North Am. 1989;12(1):89-103.
Nott PN. Psychiatric illness following childbirth in Southhampton: a case register study. Psychol Med. 1982;12:557-561.
Kumar R, Robson KM. A prospective study of emotional disorders in childbearing women. Br J Psychiatry. 1984;144:35-47.
O'Hara MW, Neunaber DJ, Zekoski EM. A prospective study of postpartum depression: prevalence, course, and predictive factors. J Abnormal Psychology. 1984;91:158-171.
Troutman BR, Cutrona CE. Nonpsychotic postpartum depression among adolescent mothers. J Abnorm Psychol. 1990;99(1):69-78.
Gregoire AJ, Kumar R, Everitt B, et al. Transdermal oestrogen for treatment of severe postnatal depression [see comments]. Lancet. 1996;347(9006):930-933.
Stowe ZN, Nemeroff CB. Women at risk for postpartum-onset major depression. Am J Obstet Gynecol. 1995;173(2):639-645.
Philipps LH, O'Hara MW. Prospective study of postpartum depression: 4 1/2-year follow-up of women and children. J Abnorm Psychol. 1991;100(2):151-155.
Peindl KS, Zolnik EJ, Wisner KL, Hanusa BH. Effects of postpartum psychiatric illnesses on family planning. Int J Psychiatry Med. 1995;25(3):291-300.
Sichel DA, Cohen LS, Robertson LM, et al. Prophylactic estrogen in recurrent postpartum affective disorder. Biol Psychiatry. 1995;38(12):814-818.
Research, A.f.H.C.P.a. Depression in Primary Care: Detection, Diagnosis, and Treatment. Rockville, MD: US Department of Health and Human Services; 1993.
Warner R, Appleby L, Whitton A, Faragher B. Demographic and obstetric risk factors for postnatal psychiatric morbidity. Br J Psychiatry. 1996;168(5):607-611.
Cox JL, Connor Y, Kendell RE. Prospective study of the psychiatric disorders of childbirth. Br J Psychiatry. 1982;140:111-117.
Harris B, Lovett L, Smith J, et al. Cardiff puerperal mood and hormone study. III. Postnatal depression at 5 to 6 weeks postpartum, and its hormonal correlates across the peripartum period. Br J Psychiatry. 1996;168(6):739-744.
Majewska MD, Harrison NL, Schwartz RD, et al. Steroid hormone metabolites are barbiturate-like modulators of the GABA receptor. Science. 1986;232(4753):1004-1007.
McEwen BS. Ovarian steroids have diverse effects on brain structure and function. In: Hammar GBaM, ed. The Modern Management of Menopause. New York: Parthenon Publishing; 1993:269-278.
Wisner KL, Perel JM, Findling RL. Antidepressant treatment during breast-feeding. Am J Psychiatry. 1996;153(9):1132-1137.
Wisner KL, Wheeler SB. Prevention of recurrent postpartum major depression. Hosp Community Psychiatry. 1994;45(12):1191-1196.
Dalton K. Progesterone prophylaxis used successfully in postnatal depression. The Practitioner. 1985;229:507-508.
Kathryn A. Leopold, MD, is an Assistant Professor of Obstetrics and Gynecology at Albany Medical College, New York. Lauren B. Zoschnick, MD, is a Clinical Instructor in the Department of Obstetrics and Gynecology at the University of Michigan Medical Center in Ann Arbor.

For more information, visit The Female Patient on the web at www.femalepatient.com

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Agoraphobia

The most common phobic disorder, agoraphobia is the fear of being alone in public places from which the person thinks escape would be difficult or help unavailable if he were incapacitated.

These people avoid being on busy streets or in crowded stores, theatres and churches.
Normal activities become restricted as the person avoids these situations. Many agoraphobia victims became so disabled they literally will not leave their homes. If agoraphobic's do venture into public places, they do so only when accompanied by a friend or family member.

Two-thirds of those suffering from agoraphobia are women, The disorder tends to be more common among families where other members also suffer from an anxiety disorder and/or possibly abuse alcohol. Most agoraphobia’s develop symptoms between the ages of 18 and 35. The onset may be sudden or gradual.

Many agoraphobia victims develop the disorder after first suffering a series of panic attacks in public places. The attacks seem to occur randomly and without warning, making it impossible for a person to predict what situation will trigger such a reaction.

The unpredictability of the panic attacks "trains" the victims to anticipate future panic attacks and, therefore, to fear any situation in which an attack may occur. As a result, they avoid going out in public. Agoraphobia victims also are likely to develop depression, fatigue, tension, spontaneous panic and obsessive disorders.
Compiled in association with the "Mental Health Association of Ireland"

[Stagger_Lee]

Agoraphobia

The most common phobic disorder, agoraphobia is the fear of being alone in public places from which the person thinks escape would be difficult or help unavailable if he were incapacitated.

These people avoid being on busy streets or in crowded stores, theatres and churches.
Normal activities become restricted as the person avoids these situations. Many agoraphobia victims became so disabled they literally will not leave their homes. If agoraphobic's do venture into public places, they do so only when accompanied by a friend or family member.

Two-thirds of those suffering from agoraphobia are women, The disorder tends to be more common among families where other members also suffer from an anxiety disorder and/or possibly abuse alcohol. Most agoraphobia’s develop symptoms between the ages of 18 and 35. The onset may be sudden or gradual.

Many agoraphobia victims develop the disorder after first suffering a series of panic attacks in public places. The attacks seem to occur randomly and without warning, making it impossible for a person to predict what situation will trigger such a reaction.

The unpredictability of the panic attacks "trains" the victims to anticipate future panic attacks and, therefore, to fear any situation in which an attack may occur. As a result, they avoid going out in public. Agoraphobia victims also are likely to develop depression, fatigue, tension, spontaneous panic and obsessive disorders.

Compiled in association with the "Mental Health Association of Ireland"

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Schizophrenia is a psychiatric diagnosis that describes a mental disorder characterized by impairments in the perception or expression of reality and by significant social or occupational dysfunction. A person experiencing untreated schizophrenia is typically characterized as demonstrating disorganized thinking, and as experiencing delusions or auditory hallucinations. Although the disorder is primarily thought to affect cognition, it can also contribute to chronic problems with behavior and emotion. Due to the many possible combinations of symptoms, there is ongoing and heated debate about whether the diagnosis necessarily or adequately describes a disorder, or alternatively whether it might represent a number of disorders. For this reason, Eugen Bleuler deliberately called the disease "the schizophrenias" plural, when he coined the present name.

Diagnosis is based on the self-reported experiences of the patient, in combination with secondary signs observed by a psychiatrist, clinical psychologist or other competent clinician. There is no objective biological test for schizophrenia, though studies suggest that genetics, neurobiology and social environment are important contributing factors. Current research into the development of the disorder often focuses on the role of neurobiology, although a reliable and identifiable organic cause has not been found. In the absence of objective laboratory tests to confirm the diagnosis, some question the legitimacy of schizophrenia's status as a disease. Furthermore, some question the status of schizophrenia as a disease on the basis that they do not consider their condition to be an impairment.

The term schizophrenia translates roughly as "shattered mind," and comes from the Greek σχίζω (schizo, "to split" or "to divide") and φρήν (phrēn, "mind"). Despite its etymology, schizophrenia is not synonymous with dissociative identity disorder, also known as multiple personality disorder or "split personality"; in popular culture the two are often confused. Although schizophrenia often leads to social or occupational dysfunction, there is little association of the illness with a predisposition toward aggressive behavior.

Patients diagnosed with schizophrenia are highly likely to be diagnosed with other disorders. The lifetime prevalence of substance abuse is typically around 40%. Comorbidity is also high with clinical depression, anxiety disorders, social problems, and a generally decreased life expectancy is also present. Patients diagnosed with schizophrenia typically live 10-12 years less than their healthy counterparts, owing to increased physical health problems and a high suicide rate.

Contents
1 Overview
2 History
3 Diagnosis
3.1 Criteria (signs and symptoms)
3.2 Subtypes
3.3 Presentation
3.4 Diagnostic issues and controversies
4 Causes
4.1 Genetic and environmental influences
4.1.1 Genetic
4.1.2 Environmental
4.2 Neurobiological influences
4.2.1 Early neurodevelopment
4.2.2 Role of dopamine
4.2.3 Role of glutamate and the NMDA receptor
4.2.4 Anatomy and physiology of the brain
5 Incidence and prevalence
6 Treatment
6.1 Medication and hospitalization
6.2 Therapy and community support
6.3 Dietary supplements
7 Prognosis
8 Recovery and Rehabilitation
9 Schizophrenia and drug use
9.1 Hallucinogens
9.2 Cannabis
9.3 Tobacco
10 Schizophrenia and violence
10.1 Violence perpetrated by people with schizophrenia
10.2 Violence against people with schizophrenia
11 Alternative approaches to schizophrenia
12 See also
13 Notable people thought to have been affected by schizophrenia
14 Portrayals of schizophrenia in the arts
15 General reading
16 External links
16.1 News, information and further description
16.2 Charities and support groups
16.3 Critical approaches to schizophrenia
17 References



Overview
Schizophrenia is often described in terms of "positive" and "negative" symptoms. Positive symptoms include delusions, auditory hallucinations and thought disorder and are typically regarded as manifestations of psychosis. Negative symptoms are so named because they are considered to be the loss or absence of normal traits or abilities, and include features such as flat, blunted or constricted affect and emotion, poverty of speech and lack of motivation. Some models of schizophrenia include formal thought disorder and planning difficulties in a third group, a "disorganization syndrome."

Additionally, neurocognitive deficits may be present. These may take the form of reduced or impaired psychological functions such as memory, attention, problem-solving, executive function or social cognition.

Onset of schizophrenia typically occurs in late adolescence or early adulthood, with males tending to show symptoms earlier than females.

In 1893 Psychiatrist Emil Kraepelin was the first to draw a distinction between what he termed dementia praecox ("premature dementia") and other psychotic illnesses. In 1908, "dementia praecox" was renamed "schizophrenia" by psychiatrist Eugen Bleuler, who found Kraepelin's term to be misleading, as the disorder is not a form of dementia, premature or otherwise.

The diagnostic category of schizophrenia has been widely criticised as lacking in scientific validity or reliability, consistent with evidence of poor levels of consistency in diagnostic practices and the use of criteria. One alternative suggests that the problems and issues making up the diagnosis of schizophrenia would be better addressed as individual dimensions along which everyone varies, such that there is a spectrum or continuum rather than a cut-off between normal and ill. This approach appears consistent with research on schizotypy and of a relatively high prevalence of psychotic experiences and delusional beliefs amongst the general public.

The wider anti-psychiatry movement also often argues against the diagnosis, for example arguing that classifying unusual thoughts, feelings and behaviors as a medical illness in this way is unscientific, stigmatizing, and legitimises the social control of people whom society finds undesirable but who have committed no crime.

Although no common cause of schizophrenia has been identified in all individuals diagnosed with the condition, currently most researchers and clinicians believe it results from a combination of both brain vulnerabilities (either inherited or acquired) and stressful life-events. This widely-adopted approach is known as the 'stress-vulnerability' model, and much scientific debate now focuses on how much each of these factors contributes to the development and maintenance of schizophrenia.

It is also thought that processes in early neurodevelopment are important, particularly prenatal processes. In adult life, particular importance has been placed upon the function (or malfunction) of dopamine in the mesolimbic pathway in the brain. This theory, known as the dopamine hypothesis of schizophrenia largely resulted from the accidental finding that a drug group which blocks dopamine function, known as the phenothiazines, reduced psychotic symptoms. However, this theory is now thought to be overly simplistic as a complete explanation. These drugs have now been developed further and antipsychotic medication is commonly used as a first-line treatment. Although effective in many cases, these medications are not well tolerated by many patients due to significant side-effects, and have little effect on some individuals.

Differences in brain structure have been found between people with schizophrenia and those without. However, these tend only to be reliable on the group level and, due to the significant variability between individuals, may not be reliably present in any particular individual.

History
Accounts that may relate to symptoms of schizophrenia date back as far as 2000 BC in the Book of Hearts, part of the ancient Ebers papyrus. However, a recent study1 into the ancient Greek and Roman literature showed that, while the general population probably had an awareness of psychotic disorders, there was no recorded condition that would meet the modern diagnostic criteria for schizophrenia in these societies.

This nonspecific concept of "madness" has been around for many thousands of years, but schizophrenia was only classified as a distinct mental disorder by Kraepelin in 1887. He was the first to make a distinction in the psychotic disorders between what he called dementia praecox (a term first used by psychiatrist Benedict A. Morel) and manic depression. Kraepelin believed that dementia praecox was primarily a disease of the brain2, and particularly a form of dementia. Kraepelin named the disorder 'dementia praecox' (early dementia) to distinguish it from other forms of dementia (such as Alzheimer's disease) which typically occur late in life. He used this term because his studies focused on young adults with dementia.49

The term schizophrenia is derived from the Greek words 'schizo' (split) and 'phren' (mind) and was coined by Eugene Bleuler in 1908 to refer to the lack of interaction between thought processes and perception. He was also the first to describe the symptoms as "positive" or "negative."2 Blueler described the main symptoms as 4 "A"'s: flattened Affect, Autism, impaired Association of ideas and Ambivalence. 78 Bleuler suggested the name schizophrenia, as it was obvious that Kraepelin's name was misleading. The word "praecox" implied precocious or early onset, hence premature dementia, as opposed to senile dementia from old age. Bleuler realized the illness was not a dementia, as it did not lead to mental deterioration and could occur early or late in life. Rather, schizophrenia led to a sharpening of the senses and a greater awareness of memories and experiences.

With the name 'schizophrenia' Bleuler intended to capture the separation of function between personality, thinking, memory, and perception, however it is commonly misunderstood to mean that affected persons have a 'split personality' (something akin to the character in Robert Louis Stevenson's The Strange Case of Dr Jekyll and Mr Hyde). Although some people diagnosed with schizophrenia may hear voices and may experience the voices as distinct personalities, schizophrenia does not involve a person changing among distinct multiple personalities. The confusion perhaps arises in part due to the meaning of Bleuler's term 'schizophrenia' (literally 'split mind'). Interestingly, the first known misuse of this word schizophrenia to mean 'split personality' (in the Jekyll and Hyde sense) was in an article by the poet T. S. Eliot in 1933.3

In the first half of the twentieth century schizophrenia was considered by many to be a "hereditary defect", and individuals affected by schizophrenia became subject to eugenics in many countries. Hundreds of thousands were sterilized, with or without consent, the majority in Nazi Germany, the United States, and Scandinavian countries.76,77 Many people diagnosed with schizophrenia, together with other people labeled "mentally unfit", were murdered in the Nazi "Operation T-4" program.


Diagnosis
Criteria (signs and symptoms)
Like many mental illnesses, the diagnosis of schizophrenia is based upon the behavior of the person being assessed. There is a list of criteria that must be met for someone to be so diagnosed. These depend on both the presence and duration of certain signs and symptoms.

The most commonly used criteria for diagnosing schizophrenia are from the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders (DSM) and the World Health Organization's International Statistical Classification of Diseases and Related Health Problems (ICD). The most recent versions are ICD-10 and DSM-IV-TR.

Below is an abbreviated version of the diagnostic criteria from the DSM-IV-TR; the full version is available here.

To be diagnosed as having schizophrenia, a person must display:

A) Characteristic symptoms: Two or more of the following, each present for a significant portion of time during a one-month period (or less, if successfully treated)
delusions
hallucinations
disorganized speech (e.g., frequent derailment or incoherence; speaking in abstracts). See thought disorder.
grossly disorganized behavior (e.g. dressing inappropriately, crying frequently) or catatonic behavior
negative symptoms, i.e., affective flattening (lack or decline in emotional response), alogia (lack or decline in speech), or avolition (lack or decline in motivation).
Note: Only one Criterion A symptom is required if delusions are bizarre or hallucinations consist of hearing one voice participating in a running commentary of the patient's actions or of hearing two or more voices conversing with each other.
B) Social/occupational dysfunction: For a significant portion of the time since the onset of the disturbance, one or more major areas of functioning such as work, interpersonal relations, or self-care, are markedly below the level achieved prior to the onset.
C) Duration: Continuous signs of the disturbance persist for at least six months. This six-month period must include at least one month of symptoms (or less, if successfully treated) that meet Criterion A.
Additional criteria (D, E and F) are also given that exclude a diagnosis of schizophrenia if symptoms of mood disorder or pervasive developmental disorder are present. Additionally a diagnosis of schizophrenia is excluded if the symptoms are the direct result of a substance (e.g., abuse of a drug, medication) or a general medical condition.


Subtypes
Historically, schizophrenia in the West was classified into simple, catatonic, hebephrenic, and paranoid. The DSM now contains five sub-classifications of schizophrenia, the ICD-10 identifies 7:

(295.2/F20.2) catatonic type (where marked absences or peculiarities of movement are present),
(295.1/F20.1) disorganized type (where thought disorder and flat affect are present together),
(295.3/F20.0) paranoid type (where delusions and hallucinations are present but thought disorder, disorganized behavior, and affective flattening is absent),
(295.6/F20.5) residual type (where positive symptoms are present at a low intensity only) and
(295.9/F20.3) undifferentiated type (psychotic symptoms are present but the criteria for paranoid, disorganized, or catatonic types has not been met).
NB: Brackets indicate codes for DSM and ICD-10 diagnostic manuals, respectively. Some older classifications still use "Hebephrenic schizophrenia" instead of "Disorganized schizophrenia".

Presentation
Symptoms may also be described as 'positive symptoms' (those additional to normal experience and behavior) and 'negative symptoms' (the lack or decline in normal experience or behavior). 'Positive symptoms' describe psychosis and typically include delusions, hallucinations and thought disorder. 'Negative symptoms' describe inappropriate or nonpresent emotion, poverty of speech, and lack of motivation. In three-factor models of schizophrenia, a third symptom grouping, the so-called 'disorganization syndrome', is also given. This considers thought disorder and related disorganized behavior to be in a separate symptom cluster from delusions and hallucinations.

Some symptoms, such as social isolation, may be caused by a number of factors. One possible factor is impairment in social cognition, which is associated with schizophrenia, but isolation may also result from an individual reacting to psychotic symptoms (such as paranoia) or avoiding potentially stressful social situations which may exacerbate mental distress in some people.

It is worth noting that many of the positive or psychotic symptoms may occur in a variety of disorders and not only in schizophrenia. The psychiatrist Kurt Schneider tried to list the particular forms of psychotic symptoms that he thought were particularly useful in distinguishing between schizophrenia and other disorders that could produce psychosis. These are called first rank symptoms or Schneiderian first rank symptoms and include delusions of being controlled by an external force, the belief that thoughts are being inserted or withdrawn from your conscious mind, the belief that your thoughts are being broadcast to other people and hearing hallucinated voices which comment on your thoughts or actions, or may have a conversation with other hallucinated voices. As with other diagnostic methods, the reliability of 'first rank symptoms' has been questioned4, although they remain in use as diagnostic criteria in many countries.

Diagnostic issues and controversies
It has been argued that the diagnostic approach to schizophrenia is flawed, as it relies on an assumption of a clear dividing line between what is considered to be mental illness (fulfilling the diagnostic criteria) and mental health (not fulfilling the criteria). Recently it has been argued, notably by psychiatrist Jim van Os and psychologist Richard Bentall, that this makes little sense, as studies have shown that many people have psychotic experiences5 65 and have delusion-like ideas67 without becoming distressed, disabled or diagnosable by the categorical system (potentially because they interpret their experiences in more positive ways, or hold more pragmatic and commonly accepted beliefs).

Of particular concern is that the decision as to whether a symptom is present is a subjective decision by the person making the diagnosis or relies on an incoherent definition (for example, see the entries on delusions and thought disorder for a discussion of this issue). More recently, it has been argued that psychotic symptoms are not a good basis for making a diagnosis of schizophrenia as "psychosis is the 'fever' of mental illness — a serious but nonspecific indicator".6

Perhaps because of these factors, studies examining the diagnosis of schizophrenia have typically shown relatively low or inconsistent levels of diagnostic reliability. Most famously, David Rosenhan's 1972 study, published as On being sane in insane places, demonstrated that the diagnosis of schizophrenia was (at least at the time) often subjective and unreliable. More recent studies have found agreement between any two psychiatrists when diagnosing schizophrenia tends to reach about 65% at best7. This, and the results of earlier studies of diagnostic reliability (which typically reported even lower levels of agreement) have led some critics to argue that the diagnosis of schizophrenia should be abandoned.8

Proponents have argued for a new approach that would use the presence of specific neurocognitive deficits to make a diagnosis. These often accompany schizophrenia and take the form of a reduction or impairment in basic psychological functions such as memory, attention, executive function and problem solving. It is these sorts of difficulties, rather than the psychotic symptoms (which can in many cases be controlled by antipsychotic medication), which seem to be the cause of most disability in schizophrenia. However, this argument is relatively new and it is unlikely that the method of diagnosing schizophrenia will change radically in the near future.

The diagnostic approach to schizophrenia has also been opposed by the proponents of the anti-psychiatry movement, who argue that classifying specific thoughts and behaviors as an illness allows social control of people that society finds undesirable but who have committed no crime. They argue that this is a way of unjustly classifying a social problem as a medical one to allow the forcible detention and treatment of people displaying these behaviors, which is something which can be done under mental health legislation in most western countries.

An example of this can be seen in the Soviet Union, where an additional sub-classification of sluggishly progressing schizophrenia was created. Particularly in the RSFSR (Russian Soviet Federated Socialist Republic), this diagnosis was used for the purpose of silencing political dissidents or forcing them to recant their ideas by the use of forcible confinement and treatment. In 2000 similar concerns about the abuse of psychiatry to unjustly silence and detain practitioners of the Falun Gong movement by the Chinese government led the American Psychiatric Association's Committee on the Abuse of Psychiatry and Psychiatrists to pass a resolution to urge the World Psychiatric Association to investigate the situation in China.

Western psychiatric medicine tends to favor a definition of symptoms that depends on form rather than content (an innovation first argued for by psychiatrists Karl Jaspers and Kurt Schneider). Therefore, you should be able to believe anything, however unusual or socially unacceptable, without being diagnosed delusional, unless your belief is held in a particular way. In principle, this would stop people being forcibly detained or treated simply for what they believe. However, the distinction between form and content is not easy, or always possible, to make in practice (see delusion). This had led to accusations by anti-psychiatry, surrealist and mental health system survivor groups that psychiatric abuses exist to some extent in the West as well.


Causes

Genetic and environmental influences
While the reliability of the schizophrenia diagnosis introduces difficulties in measuring the relative effect of genes and environment (for example, symptoms overlap to some extent with severe bipolar disorder or major depression), there is evidence to suggest that genetic vulnerability and environmental stressors can act in combination to result in diagnosis of schizophrenia12.

The extent to which these factors influence the likelihood of being diagnosed with schizophrenia is debated widely, and currently, controversial. Schizophrenia is likely to be a diagnosis of complex inheritance (analogous to diabetes or high blood pressure). Thus, it is likely that several genes interact to generate risk for it75. This, combined with disagreements over which research methods are best, or how data from genetic research should be interpreted, has led to differing estimates over genetic contribution.


Genetic
There is substantial evidence that the diagnosis of schizophrenia has a heritable component (some estimates are as high as 80%). Current research suggests that environmental factors play a significant role in the expression of any genetic disposition towards schizophrenia (i.e. if someone has the genes that increase risk, this will not automatically result in a diagnosis of schizophrenia later in life). A recent review of the genetic evidence has suggested a 28% chance of one identical twin obtaining the diagnosis if the other already has it9 (see twin studies), but such studies are not noted for pondering the likelihood of similarities of social class and/or other socio-psychological factors between the twins. The estimates of heritability of schizophrenia from twin studies varies a great deal, with some notable studies10 11 showing rates as low as 11.0%–13.8% among monozygotic twins, and 1.8%–4.1% among dizygotic twins.

A recent review of linkage studies listed seven genes as likely to be involved in the diagnosis of schizophrenia or the risk of developing diagnosis of the disease.12 Evidence comes from research suggesting multiple chromosomal regions are transmitted to people who are later diagnosed as having schizophrenia. Genetic association studies have suggested some strong candidate genes which may contribute to risk of getting the diagnosis.75 The strongest evidence points towards genes called COMT (involved in encoding the dopamine catabolic enzyme catechol-O-methyl transferase,13) dysbindin (DTNBP1) and neuregulin-1 (NRG1).


Environmental
There is considerable evidence indicating that stressful life events cause or trigger schizophrenia.15 Childhood experiences of abuse or trauma have also been implicated as risk factors for a diagnosis of schizophrenia later in life.16 17 18But overt diagnosis of trauma/PTSD tends to be restricted to highly specific situations and groups, perhaps inappropriately.

There is also consistent evidence that negative attitudes towards individuals with (or with a risk of developing) schizophrenia can have a significant adverse impact. In particular, critical comments, hostility, authoritarian and intrusive or controlling attitudes (termed 'high expressed emotion' by researchers) from family members have been found to correlate with a higher risk of relapse in schizophrenia across cultures.70 It is not clear whether such attitudes play a causal role in the onset of schizophrenia, altho those diagnosed in this way may claim it to be the primary causal factor. The research has focused on family members but also appears to relate to professional staff in regular contact with clients.71 While initial work addressed those diagnosed as schizophrenic, these attitudes have also been found to play a significant role in other mental health problems.66 This approach does not blame 'bad parenting' or staffing, but addresses the attitudes, behaviors and interactions of all parties. Some go as far as to criticise the whole approach of seeking to localise 'mental illness' within one individual - the patient - rather than his/her group and its functionality, citing a scapegoat effect.

Factors such as poverty and discrimination also appear to be involved in increasing the risk of schizophrenia or schizophrenia relapse, perhaps due to the high levels of stress they engender, or faults in diagnostic procedure/assumptions. Racism in society, including in diagnostic practices, and/or the stress of living in a different culture, may explain why minority communities have shown higher rates of schizophrenia than members of the same ethnic groups resident in their home country. The "social drift hypothesis" suggests that the functional problems related to schizophrenia, or the stigma and prejudice attached to them, can result in more limited employment and financial opportunities, so that the causal pathway goes from mental health problems to poverty, rather than, or in addition to, the other direction. Some argue that unemployment and the long-term unemployed and homeless are simply being stigmatised.

One particularly stable and replicable finding has been the association between living in an urban environment and schizophrenia diagnosis, even after factors such as drug use, ethnic group and size of social group have been controlled for.19 A recent study of 4.4 million men and women in Sweden found an alleged 68%–77% increased risk of diagnosed psychosis for people living in the most urbanized environments, a significant proportion of which is likely to be described as schizophrenia.20

One curious finding is that people diagnosed with schizophrenia are more likely to have been born in winter or spring21 (at least in the northern hemisphere). However, the effect is not large and it is still not clear to scientists why this may occur.


Neurobiological influences

Early neurodevelopment
It is also thought that processes in early neurodevelopment are important, particularly during pregnancy. For example, women who were pregnant during the Dutch famine of 1944, where many people were close to starvation, had a higher chance of having a child who would later develop schizophrenia22. Similarly, studies of Finnish mothers who were pregnant when they found out that their husbands had been killed during the Winter War of 1939–1940 have shown that their children were much more likely to develop schizophrenia when compared with mothers who found out about their husbands' death after pregnancy23, suggesting that even psychological trauma in the mother may have an effect. Furthermore, there is now significant evidence that prenatal exposure to infections increases the risk for developing schizophrenia later in life, providing additional evidence for a link between developmental pathology and risk of developing the condition.73

Some researchers have proposed that environmental influences during childhood also interact with neurobiological risk factors to influence the likelihood of developing schizophrenia later in life. The neurological development of children is considered sensitive to features of dysfunctional social settings, such as trauma, violence, lack of warmth in personal relationships and hostility. These have all been found to be risk factors for the later development of schizophrenia. Research has suggested that effects of the childhood environment, favorable or unfavorable, interact with genetics and the processes of neurodevelopment, with long-term consequences for brain function. Consequently, this is thought to influence the underlying vulnerability for psychosis later in life, particularly during the adult years.24


Data from a PET study25 suggests the less the frontal lobes activated (red) during a working memory task, the greater the increase in abnormal dopamine activity in the striatum (green), thought to be related to the neurocognitive deficits in schizophrenia.[edit]
Role of dopamine
In adult life, particular importance has been placed upon the function (or malfunction) of dopamine in the mesolimbic pathway in the brain. This theory, known as the dopamine hypothesis of schizophrenia, largely resulted from the accidental finding that a drug group which blocks dopamine function, known as the phenothiazines, reduced psychotic symptoms. These drugs have now been developed further and antipsychotic medication is commonly used as a first line treatment.

However, this theory is now thought to be overly simplistic as a complete explanation, partly because newer antipsychotic medication (called atypical antipsychotic medication) is equally effective as older medication (called typical antipsychotic medication), but also affects serotonin function and may have slightly less of a dopamine blocking effect. Psychiatrist David Healy has also argued that pharmaceutical companies have promoted certain oversimplified biological theories of mental illness to promote their own sales of biological treatments.26


Role of glutamate and the NMDA receptor
Interest has also focused on the neurotransmitter glutamate and the reduced function of the NMDA glutamate receptor in the development of schizophrenia. This theory has largely been suggested by abnormally low levels of glutamate receptors found in postmortem brains of people previously diagnosed with schizophrenia27 and the discovery that the glutamate blocking drugs such as phencyclidine and ketamine can mimic the symptoms and cognitive problems associated with the condition.59 The fact that reduced glutamate function is linked to poor performance on tests requiring frontal lobe and hippocampal function and that glutamate can affect dopamine function, all of which have been implicated in schizophrenia, have suggested the glutamate hypothesis of schizophrenia as an increasingly popular explanation.28 Further support of this theory has come from trials showing the efficacy of molecules, which are coagonists at the NMDA receptor complex, in reducing schizophrenic symptoms. The precursors D-serine, glycine, and D-cycloserine all enhance NMDA function through the glycine co-agonist site. Several placebo controlled trials have shown a reduction mainly in negative symptoms with high dose therapy.60 Currently type 1 glycine transporter inhibitors are in late-state preclinical for the treatment of schizophrenia. They increase glycine concentrations in the brain thus causing increased NMDA receptor activation and a reduction in symptoms.61

Anatomy and physiology of the brain
Much recent research has focused on differences in structure or function in certain brain areas in people diagnosed with schizophrenia.

Early evidence for differences in the neural structure came from the discovery of ventricular enlargement in people diagnosed with schizophrenia, for whom negative symptoms were most prominent29. However, this finding has not proved particularly reliable on the level of the individual person, with considerable variation between patients. A letter to the editor of the American Journal of Psychiatry links ventricular enlargement with exposure to antipsychotic drugs [1].

More recent studies have shown a large number of differences in brain structure between people with and without diagnoses of schizophrenia.30 However, as with earlier studies, many of these differences are only reliably detected when comparing groups of people, and are unlikely to predict any differences in brain structure of an individual person with schizophrenia.

Studies using neuropsychological tests and brain imaging technologies such as fMRI and PET to examine functional differences in brain activity have shown that differences seem to most commonly occur in the frontal lobes, hippocampus, and temporal lobes31. These differences are heavily linked to the neurocognitive deficits which often occur with schizophrenia, particularly in areas of memory, attention, problem solving, executive function and social cognition.

Electroencephalograph (EEG) recordings of persons with schizophrenia performing perception oriented tasks showed an absence of gamma band activity in the brain, indicating weak integration of critical neural networks in the brain.32 Those who experienced intense hallucinations, delusions and disorganized thinking showed the lowest frequency synchronization. None of the drugs taken by the persons scanned had moved neural synchrony back into the gamma frequency range. Gamma band and working memory alterations may be related to alterations in interneurons that produced the neurotransmitter GABA. Alterations in a subclass of GABAergic interneurons which produce the calcium binding protein parvalbumin have been shown to exist in the DLPFC in schizophrenia. 33

Incidence and prevalence
Schizophrenia is typically diagnosed in late adolescence or early adulthood. It is found approximately equally in men and women, though the onset tends to be later in women, who also tend to have a better course and outcome. Although rare, there are also instances of childhood onset schizophrenia and late-onset schizophrenia that occurs in the elderly.

The lifetime prevalence of schizophrenia is commonly given at 1%; however, a recent review of studies from around the world estimated it to be 0.55%34. The same study also found that prevalence may vary greatly from country to country, despite the received wisdom that schizophrenia occurs at the same rate throughout the world. It is worth noting however, that this may be in part due to differences in the way schizophrenia is diagnosed. The incidence of schizophrenia was given as a range of between 7.5 and 16.3 cases per year per 100,000 population.

Schizophrenia is also a major cause of disability. In a recent 14-country study35, active psychosis was ranked the third most disabling condition after quadriplegia and dementia and before paraplegia and blindness.


Treatment

Medication and hospitalization
The first line pharmacological therapy for schizophrenia is usually the use of antipsychotic medication 72. The concept of 'curing' schizophrenia is controversial as there are no clear criteria for what might constitute a cure, although some criteria for the remission of symptoms have recently been suggested63. Therefore, antipsychotic drugs are only thought to provide symptomatic relief from the positive symptoms of psychosis. The newer atypical antipsychotic medications (such as clozapine, risperidone, olanzapine, quetiapine, ziprasidone, aripiprazole, and amisulpride) are usually preferred over older typical antipsychotic medications (such as chlorpromazine and haloperidol) due to their favorable side-effect profile. Compared to the typical antipsychotics, the atypicals are associated with a lower incident rate of extrapyramidal side effects (EPS) and tardive dyskinesia (TD) although they are more likely to induce weight gain and so increase risk for obesity-related diseases62. It is still unclear whether newer drugs reduce the chances of developing the rare but potentially life-threatening neuroleptic malignant syndrome (NMS). While the atypical antipsychotics are associated with less EPS and TD than the conventional antipsychotics, some of the agents in this class (especially olanzapine and clozapine) appear to be associated with metabolic side effects such as weight gain, hyperglycemia and hypertriglyceridemia that must be considered when choosing appropriate pharmacotherapy.

Atypical and typical antipsychotics are generally thought to be equivalent for the treatment of the positive symptoms of schizophrenia. It has been suggested by some researchers that the atypicals have some beneficial effects on negative symptoms and cognitive deficits associated with schizophrenia, although the clinical significance of these effects has yet to be established. However, recent reviews have suggested that typical antipsychotics, when dosed conservatively, may have similar effects to atypicals.36 The atypical antipsychotics are much more costly as they are still within patent, whereas the older drugs are available in inexpensive generic forms. Aripiprazole is a drug from a new class of antipsychotic drugs (variously named 'dopamine system stabilizers' or 'partial dopamine agonists'37) that have recently been developed and is now widely licensed to treat schizophrenia.

The efficacy of schizophrenia treatment is often assessed by using standardized assessment methods, one of the most common being the positive and negative syndrome scale (PANSS).68

Hospitalization may occur with severe episodes. This can be voluntary or (if mental health legislation allows it) involuntary (called civil or involuntary commitment). Mental health legislation may also allow people to be treated against their will. However, in many countries such legislation does not exist, or does not have the power to enforce involuntary hospitalization or treatment.


Therapy and community support
Psychotherapy or other forms of talk therapy may be offered, with cognitive behavioral therapy being the most frequently used. This may focus on the direct reduction of the symptoms, or on related aspects, such as issues of self-esteem, social functioning, and insight. Although the results of early trials with cognitive behavioral therapy (CBT) were inconclusive38, more recent reviews suggest that CBT can be an effective treatment for the psychotic symptoms of schizophrenia39.

A relatively new approach has been the use of cognitive remediation therapy, a technique aimed at remediating the neurocognitive deficits sometimes present in schizophrenia. Based on techniques of neuropsychological rehabilitation, early evidence has shown it to be cognitively effective, with some improvements related to measurable changes in brain activation as measured by fMRI.40

Electroconvulsive therapy (also known as ECT or 'electroshock therapy') may be used in countries where it is legal. It is not considered a first line treatment but may be prescribed in cases where other treatments have failed. Psychosurgery has now become a rare procedure and is not a recommended treatment for schizophrenia.

Other support services may also be available, such as drop-in centers, visits from members of a 'community mental health team' or assertive community treatment team, and patient-led support groups. In recent years the importance of service-user led recovery based movements has grown substantially throughout Europe and America. Groups such as the Hearing Voices Network and more recently, the Paranoia Network, have developed a self-help approach that aims to provide support and assistance outside of the traditional medical model adopted by mainstream psychiatry. By avoiding framing personal experience in terms of criteria for mental illness or mental health, they aim to destigmatize the experience and encourage individual responsibility and a positive self-image.

In many non-Western societies, schizophrenia may be treated with more informal, community-led methods. A particularly sobering thought for Western psychiatry is that the outcome for people diagnosed with schizophrenia in non-Western countries may actually be much better41 than for people in the West. The reasons for this recently discovered fact are still far from clear, although cross-cultural studies are being conducted to find out why.


Dietary supplements
Omega-3 fatty acids (found naturally in foods such as oily fish, flax seeds, hemp seeds, walnuts and canola oil) have recently been studied as a treatment for schizophrenia. Although the number of research trials has been limited, the majority of randomized controlled trials have found omega-3 supplements to be effective when used as a dietary supplement.64


Prognosis
Prognosis for any particular individual affected by schizophrenia is particularly hard to judge as treatment and access to treatment is continually changing, as new methods become available and medical recommendations change.

One retrospective study has shown that about a third of people make a full recovery, about a third show improvement but not a full recovery, and a third remain ill.42 A more recent study using stricter recovery criteria (i.e. concurrent remission of positive and negative symptoms and specific instances of adequate social / vocational functioning) reported a recovery rate of 13.7%.43

The exact definition of what constitutes a recovery has not been widely defined, however, although criteria have recently been suggested to define a remission in symptoms.63 Therefore, this makes it difficult to give an exact estimate as recovery and remission rates are not always comparable across studies.

The World Health Organization conducted two long-term follow-up studies involving more than 2,000 people suffering from schizophrenia in different countries, and discovered these patients have much better long-term outcomes in poor countries (India, Colombia and Nigeria) than in rich countries (USA, UK, Ireland, Denmark, Czechoslovakia, Japan, and Russia),44 despite the fact antipsychotic medication is typically not widely available in poorer countries.

Prognosis also depends on some other factors. Females tend to show recovery rates higher than males, and acute and sudden onset of schizophrenia is associated with higher rates of recovery, while gradual onset is associated with lower rates. Most studies done on this subject, however, are correlational in nature, and a clear cause-and- relationship is difficult to establish. Pre-morbid functioning and positive prognosis also seem to be correlated.

In a study of over 168,000 Swedish citizens undergoing psychiatric treatment, schizophrenia was associated with an average life expectancy of approximately 80-85% of that of the general population. Women with a diagnosis of schizophrenia were found to have a slightly better life expectancy than that of men, and as a whole, a diagnosis of schizophrenia was associated with a better life expectancy than substance abuse, personality disorder, heart attack and stroke.45

There is an extremely high suicide rate associated with schizophrenia. A recent study showed that 30% of patients diagnosed with this condition had attempted suicide at least once during their lifetime.46 Another study suggested that 10% of persons with schizophrenia die by suicide.47


Recovery and Rehabilitation
Just as the diagnosis itself is mired in controversy and counter-accusation, it is difficult to establish a clear picture of recovery and rehabilitation. Both long ago and in the recent past, patients in developed countries were told that chances of recovery were limited, with statistics being quoted to support this negative prognosis. Today, with the advent of a vocal Recovery Movement in mental health, statistics are quoted in a conflicting fashion, and attention is drawn to cultural and local factors in impeding or accelerating recovery. Rehabilitation provision is uneven and strongly dependent on local political culture and/or resources.

The developed world, in spite of a greater set of resources, tends to hamper rehabilitation with difficult welfare regulations, competitive recruitment and political correctness. This often leads to a failure to give due consideration to groups not always equally able to deal with the diagnostic stigma, such as male breadwinners and displaced ethnic minorities. Instead of assisting in recognising group problems, there may be an imposed sense of equality that does not accurately reflect the true situation.

Social stigma is also a factor in undermining the image of recovery from schizophrenia. Given the prevalence of the diagnosis and the role of chance in personal success, it is likely that that the number of famous, successful people who received the diagnosis is far greater than indicated on this page. Stigma is the likely factor for non-disclosure of many people.

Given the implications of work-incompetence of the schizophrenia diagnosis, patients inevitably become the scapegoat for all these cultural and local shortcomings.

Schizophrenia and drug use
The relationship between schizophrenia and drug use is complex, meaning that a clear causal connection between drug use and schizophrenia has been difficult to tease apart. There is strong evidence that using certain drugs can trigger either the onset or relapse of schizophrenia in some people. It may also be the case, however, that people with schizophrenia use drugs to overcome negative feelings associated with both the commonly prescribed antipsychotic medication and the condition itself, where negative emotion, paranoia and anhedonia are all considered to be core features.

The rate of substance use is known to be particularly high in this group. In a recent study, 60% of people with schizophrenia were found to use substances and 37% would be diagnosable with a substance use disorder.74


Hallucinogens
Schizophrenia can sometimes be triggered by heavy use of stimulant or hallucinogenic drugs, although some claim that a predisposition towards developing schizophrenia is needed for this to occur. There is also some evidence suggesting that people suffering schizophrenia but responding to treatment can have relapse because of subsequent drug use. Some widely known cases where hallucinogens have been suspected of precipitating schizophrenia are Pink Floyd founder-member Syd Barrett and Beach Boys songwriter Brian Wilson.

Drugs such as methamphetamine, ketamine, PCP, and LSD have been used to mimic schizophrenia for research purposes, although this has now fallen out of favor with the scientific research community, as the differences between the drug induced states and the typical presentation of schizophrenia have become clear.

Hallucinogenic drugs were also briefly tested as possible treatments for schizophrenia by psychiatrists such as Humphry Osmond and Abram Hoffer in the 1950s. It was mainly for this experimental treatment of schizophrenia that LSD administration was legal, briefly before its use as a recreational drug led to its criminalization.


Cannabis
There is increasing evidence that cannabis use can contribute to the onset of schizophrenia. Some studies suggest that cannabis is neither a sufficient nor necessary factor in developing schizophrenia, but that cannabis may significantly increase the risk of developing schizophrenia and may be, among other things, a significant causal factor. Nevertheless, some previous research in this area has been criticised as it has often not been clear whether cannabis use is a cause or effect of schizophrenia. To address this issue, a recent review of studies from which a causal contribution to schizophrenia can be assessed has suggested that cannabis statistically doubles the risk of developing schizophrenia on the individual level, and may be responsible for up to 8% of cases in the population.48

Tobacco
It has been noted that the majority of people with schizophrenia (estimated between 75% and 90%) smoke tobacco. However, people diagnosed with schizophrenia have a much lower than average chance of developing and dying from lung cancer. While the reason for this is unknown, it may be because of a genetic resistance to the cancer, a side-effect of drugs being taken, or a statistical effect of increased likelihood of dying from causes other than lung cancer49.

It is argued that the increased level of smoking in schizophrenia may be due to a desire to self-medicate with nicotine. A recent study of over 50,000 Swedish conscripts found that there was a small but significant protective effect of smoking cigarettes on the risk of developing schizophrenia later in life.50 While the authors of the study stressed that the risks of smoking far outweigh these minor benefits, this study provides further evidence for the 'self-medication' theory of smoking in schizophrenia and may give clues as to how schizophrenia might develop at the molecular level. Furthermore, many people with schizophrenia have smoked tobacco products long before they are diagnosed with the illness, and some groups advocate that the chemicals in tobacco have actually contributed to the onset of the illness and have no benefit of any kind.

It is of interest that cigarette smoking affects liver function such that the antipsychotic drugs used to treat schizophrenia are broken down in the blood stream more quickly. This means that smokers with schizophrenia need slightly higher doses of antipsychotic drugs in order for them to be effective than do their non-smoking counterparts.


Schizophrenia and violence

Violence perpetrated by people with schizophrenia
Although schizophrenia is sometimes associated with violence in the media, only a small minority of people with schizophrenia become violent51, and only a minority of people who commit criminal violence have been diagnosed with schizophrenia52 53.

Research has suggested that schizophrenia is associated with a slight increase in risk of violence, although this risk is largely due to a small sub-group of individuals for whom violence is associated with concurrent substance abuse and ceasing psychiatric drugs51. For the most serious acts of violence, long-term independent studies of convicted murderers in both New Zealand52 and Sweden53 found that 3.7%–8.9% had been given a previous diagnosis of schizophrenia.

There is some evidence to suggest that in some people, the drugs used to treat schizophrenia may produce an increased risk for violence, largely due to agitation induced by akathisia, a side effect sometimes associated with antipsychotic medication.54 Similarly, abuse experienced in childhood may contribute both to a slight increase in risk for violence in adulthood, as well as the development of schizophrenia.16


Violence against people with schizophrenia
Research has shown that a person diagnosed with schizophrenia is more likely to be a victim of violence (4.3% in a one month period) than the perpetrator55.


Alternative approaches to schizophrenia
An approach broadly known as the anti-psychiatry movement, notably most active in the 1960s, has opposed the orthodox medical view of schizophrenia as an illness.

Psychiatrist Thomas Szasz argues that psychiatric patients are not ill but are just individuals with unconventional thoughts and behavior that make society uncomfortable. He argues that society unjustly seeks to control such individuals by classifying their behavior as an illness and forcibly treating them as a method of social control. It is worth noting that Szasz has never considered himself to be "anti-psychiatry" in the sense of being against psychiatric treatment, but simply believes that it should be conducted between consenting adults, rather than imposed upon anyone against their will. Szasz co-founded the anti-psychiatry group Citizens' Commission on Human Rights with the Church of Scientology, who are well-noted for their anti-psychiatric stance.

Similarly, psychiatrists R. D. Laing, Silvano Arieti, Theodore Lidz and to a certain degree Colin Ross have argued that the symptoms of what is normally called mental illness are comprehensible reactions to impossible demands that society and particularly family life places on some sensitive individuals. Laing, Arieti and Lidz were revolutionary in valuing the content of psychotic experience as worthy of interpretation, rather than considering it simply as a secondary but essentially meaningless marker of underlying psychological or neurological distress. Laing's work, co-authored with Aaron Esterson, Sanity, Madness and the Family (1964) described eleven case studies of people diagnosed with schizophrenia and argued that the content of their actions and statements was meaningful and logical in the context of their family and life situations. Arieti's Interpretation of Schizophrenia won the 1975 scientific National Book Award in the United States.

In the 1976 book The Origin of Consciousness in the Breakdown of the Bicameral Mind, psychologist Julian Jaynes proposed that until the beginning of historic times, schizophrenia or a similar condition was the normal state of human consciousness. This would take the form of a "bicameral mind" where a normal state of low affect, suitable for routine activities, would be interrupted in moments of crisis by "mysterious voices" giving instructions, which early people characterized as interventions from the gods. This theory was briefly controversial. Continuing research has failed to either further confirm or refute the thesis.

Psychiatrist Tim Crow has argued that schizophrenia may be the evolutionary price we pay for a left brain hemisphere specialization for language.56 Since psychosis is associated with greater levels of right brain hemisphere activation and a reduction in the usual left brain hemisphere dominance, our language abilities may have evolved at the cost of causing schizophrenia when this system breaks down.

Researchers into shamanism have speculated that in some cultures schizophrenia or related conditions may predispose an individual to becoming a shaman57. Certainly, the experience of having access to multiple realities is not uncommon in schizophrenia, and is a core experience in many shamanic traditions. Equally, the shaman may have the skill to bring on and direct some of the altered states of consciousness psychiatrists label as illness. (See anti-psychiatry.) Speculations regarding primary and important religious figures as having schizophrenia abound. Some commentators have endorsed the idea that major religious figures experienced psychosis, heard voices and displayed delusions of grandeur.

Alternative medicine tends to hold the view that schizophrenia is primarily caused by imbalances in the body's reserves and absorption of dietary minerals, vitamins, fats, and/or the presence of excessive levels of toxic heavy metals. The body's adverse reactions to gluten are also strongly implicated in some alternative theories (see gluten-free, casein-free diet).

One theory put forward by psychiatrists E. Fuller Torrey and R.H. Yolken is that the parasite Toxoplasma gondii leads to some, if not many, cases of schizophrenia.58

An additional approach is suggested by the work of Richard Bandler who argues that "The usual difference between someone who hallucinates and someone who visualizes normally, is that the person who hallucinates doesn't know he's doing it or doesn't have any choice about it." (Time for a Change, p107). He suggests that because visualization is a sophisticated mental capability, schizophrenia is a skill, albeit an involuntary and dysfunctional one that is being used but not controlled. He therefore suggests that a significant route to treating schizophrenia might be to teach the missing skill - how to distinguish created reality from consensus external reality, to reduce its maladaptive impact, and ultimately how to exercise appropriate control over the vizualization or auditory process. Hypnotic approaches have been explored by the physician Milton H. Erickson as a means of facilitating this.

Regarding schizophrenia as a waking dreamer syndrome, Jie Zhang hypothesizes that the hallucinations of schizophrenia are caused by the activation of the continual-activation mechanism during waking, a mechanism that induces dreaming while asleep, due to the malfunction of the continual-activation thresholds in the conscious part of brain.69


See also
Antipsychotic
Disorganized schizophrenia
Dopamine hypothesis of schizophrenia
Delusion
Formal thought disorder
Hallucination
On the Origin of the ‘Influencing Machine’ in Schizophrenia. (Victor Tausk)
Psychoanalysis
Psychosis
Schizoaffective disorder
Schizotypy
Tardive dysphrenia
Soteria
Further information about schizophrenia and approaches to it, suggested by authors such as R.D. Laing, Emil Kraepelin, Eugene Bleuler, Karl Jaspers, Victor Tausk, and Kurt Schneider, as well as books, can be found within the articles for those authors.


Notable people thought to have been affected by schizophrenia
This article or section does not cite its references or sources.
Actress Clara Bow was diagnosed with schizophrenia in 1949.6025 (former rhythm guitarist of the Dead Kennedys)
Talal ibn Abdullah (King of Jordan from 1951 to 1952)
Lionel Aldridge (American football player, Green Bay Packers)
Antonin Artaud (artist, poet, actor, theater philosopher)
John Balance (vocalist and percussionist of Coil)
Syd Barrett (founder of Pink Floyd)
Maria Bernoulli (wife of German novelist Hermann Hesse)
Nick Blinko (founder, singer, songwriter, guitarist and artist for Rudimentary Peni)
Buddy Bolden (jazz pioneer)
Clara Bow (actress)
Eduard Einstein (son of Albert Einstein)
Don Elkins, (engineer, metaphysician, writer, ufologist)
Roky Erickson (founder of 13th Floor Elevators)
Zelda Fitzgerald (painter and wife of F. Scott Fitzgerald)
Frederick Frese (psychologist in Ohio and current Vice President of the National Alliance on Mental Illness)
The Genain quadruplets (a set of four girls who each developed schizophrenia)
Kurt Gödel (mathematician)
Andy Goram (former footballer)
Jim Gordon (drummer for the rock group Derek and the Dominos)
Peter Green (founder of rock group Fleetwood Mac)
Josef Hassid (violinist)
Houston (R&B artist)
H.R. Hudson (affected lightly by schizophrenia, leader of hardcore punk band Bad Brains)
Lucia Joyce (dancer, daughter of James Joyce)
Theodore Kaczynski (the Unabomber)
Veronica Lake (actress)
James Tilly Matthews (subject of first book-length psychiatric case study)
William Chester Minor (army surgeon and major contributor to the Oxford English Dictionary)
John Forbes Nash Jr (mathematician)
Vaslav Nijinsky (ballet dancer and choreographer)
Per Yngve Ohlin A.K.A. Dead (vocalist of black metal band Mayhem)
Gene Ray (self-proclaimed doctor of cubicism)
Daniel Paul Schreber (German judge)
Ingo Schwichtenberg (original drummer for rock group Helloween)
Dr Vashishtha Narayan Singh (mathematician and scientist)
Phil Spector (music producer credited with creating the "Wall of Sound"
Skip Spence (band member of Moby Grape and Jefferson Airplane)
Nancy Spungen (girlfriend of Sid Vicious of the punk rock band The Sex Pistols)
Vincent van Gogh (artist)
Mark Vonnegut (son of the writer Kurt Vonnegut)
Louis Wain (artist)
Wesley Willis (musician)
Adolf Wolfli (artist)
Brian Wilson (member of The Beach Boys)

Portrayals of schizophrenia in the arts
The book and film A Beautiful Mind chronicled the life of John Nash, a Nobel-Prize-winning mathematician who was afflicted with schizophrenia.

General reading
Bentall, R. (2003) Madness explained: Psychosis and Human Nature. London: Penguin Books Ltd. ISBN 0713992492
Boyle, Mary, (1993), Schizophrenia: A Scientific Delusion, Routledge, ISBN 0415097002 (Amazon Review).
Fallon, J.H. et. al. (2003) The Neuroanatomy of Schizophrenia: Circuitry and Neurotransmitter Systems. Clinical Neuroscience Research 3:77-107. [2]
Green, M.F. (2001) Schizophrenia Revealed: From Neurons to Social Interactions. New York: W.W. Norton. ISBN 0393703347
Jones, S. and Hayward, P. (2004) Coping with Schizophrenia: A Guide for Patients, Families and Caregivers. ISBN 1851683445
Keen, T. M. (1999) Schizophrenia: orthodoxy and heresies. A review of alternative possibilities. Journal of Psychiatric and Mental Health Nursing, 1999, 6, 415-424. PDF. An article reviewing the dominant (orthodox) and alternative (heretical) theories, hypotheses and beliefs about schizophrenia.
Read, J., Mosher, L.R., Bentall, R. (2004) Models of Madness: Psychological, Social and Biological Approaches to Schizophrenia. ISBN 1583919066. A critical approach to biological and genetic theories, and a review of social influences on schizophrenia.
Szasz, T. (1976) Schizophrenia: The Sacred Symbol of Psychiatry. New York: Basic Books. ISBN 0465072224
Viktor Tausk : "Sexuality, War, and Schizophrenia: Collected Psychoanalytic Papers", Publisher: Transaction Publishers 1991, ISBN 0887383653 (On the Origin of the ‘Influencing Machine’ in Schizophrenia.)
Harold F Searles : "Collected Papers on Schizophrenia and Related Subjects" , Publisher: International Universities Press, 1966, ISBN 0823609804
P.-C. Racamier : "Les Schizophrènes", Publisher: Payot, 2001, French, ISBN 2228894273
Torrey, E.F., M.D. (2006) Surviving Schizophrenia: A Manual for Families, Consumers, and Providers (5th Edition). Quill (HarperCollins Publishers) ISBN 0060842598
Vonnegut, M. The Eden Express. ISBN 0553027557. A personal account of schizophrenia.

External links

News, information and further description
Understanding Schizophrenia - A factsheet from the mental health charity Mind.
DSM-IV-TR Full diagnostic criteria for schizophrenia
World Health Organisation data on schizophrenia from 'The World Health Report 2001. Mental Health: New Understanding, New Hope'
Schizophrenia in history
National Institute of Mental Health (USA) Schizophrenia information
Childhood Schizophrenia Summary
UCLA Laboratory of Neuro Imaging definition
The current World Health Organisation definition of Schizophrenia
A directory of free full-text articles on diagnosis and management of schizophrenia
Symptoms in Schizophrenia Film made in 1940 showing some of the symptoms of Schizophrenia.
http://www.sciencedaily.com/news/mind_b ... zophrenia/
Schizophrenia by WebMD (pharmaceutical company sponsored).
Open The Doors - information on global programme to fight stigma and discrimination because of Schizophrenia. The World Psychiatric Association (WPA)
Scientific American Magazine (January 2004 Issue) Decoding Schizophrenia

Charities and support groups
SANE UK mental health charity focused on schizophrenia that supports sufferers, runs a helpline and carries out research into mental illness
The Schizophrenia Association of Great Britain

Critical approaches to schizophrenia
Successfulschizophrenia.org A website critical of Schizophrenia as a disorder, with many links and resources, by Al Siebert, psychologist Ph.D.
Schizophrenia: A Nonexsistent Disease by Lawrence Stevens, J.D
Loren Mosher, M.D. (Chief of the Center for Studies of Schizophrenia at the U.S. National Institute of Mental Health 1969-1980) Still Crazy After All These Years
Bola, John R., Ph.D.; & Mosher, Loren R., M.D. (2003). Treatment of Acute Psychosis Without Neuroleptics: Two-Year Outcomes From the Soteria Project. The Journal of Nervous and Mental Disease, (191: 219-229). Available as PDF.
Jonathan Leo, Ph.D. Schizophrenia: Medical students are taught it's all in the genes, but are they hearing the whole story?

References
Note 1: Evans, K., McGrath, J., & Milns, R. (2003) Searching for schizophrenia in ancient Greek and Roman literature: a systematic review. Acta Psychiatrica Scandanavica, 107(5), 323–330.
Note 2: Kraepelin, E. (1907) Text book of psychiatry (7th ed) (trans. A.R. Diefendorf). London: Macmillan.
Note 3: Turner, T. (1999) 'Schizophrenia'. In G.E. Berrios and R. Porter (eds) A History of Clinical Psychiatry. London: Athlone Press. ISBN 0485242117
Note 4: Bertelsen, A. (2002) Schizophrenia and Related Disorders: Experience with Current Diagnostic Systems. Psychopathology, 35, 89–93.
Note 5: Verdoux, H., & van Os, J. (2002) Psychotic symptoms in non-clinical populations and the continuum of psychosis. Schizophrenia Research, 54(1–2), 59–65.
Note 6: Tsuang, M. T., Stone, W. S., & Faraone, S. V. (2000) Toward reformulating the di

[Stagger_Lee]

What is ADHD?

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Attention-Deficit/Hyperactivity Disorder (ADHD) is a neurological condition related, in part, to the brain's chemistry and anatomy. ADHD manifests itself as a persistent pattern of inattention and/or hyperactivity/impulsivity that occurs more frequently and more severely than is typically observed in people at comparable levels of development. These symptoms must occur for at least six months and have been present since before age 7.

ADHD begins in childhood and can persist into adulthood as well. While some children outgrow ADHD, about 60% continue to have symptoms into adulthood.

According to the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR), the symptoms of ADHD fall into three categories: Inattention, Hyperactivity/Impulsivity, and a combination of the two.

How Can ADHD Be Treated?

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The good news is that ADHD is very treatable. Current ADHD treatment practices focus on management of symptoms through a combination of treatment methods:


Medications
Behavior modification
Combination therapy

ADHD treatment is best approached as a partnership between the child, family, school personnel, and healthcare professionals. Making sure everyone involved understands his or her contribution to a child's successful treatment plan is fundamental to symptom management. Since every child's treatment should be customized to his or her needs, be sure to help your healthcare professional understand your child's particular challenges.

What Can I Do to Get Help?

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Many types of specialists help manage ADHD; these may include Pediatricians, Family Physicians, Psychiatrists, Psychologists, Neurologists, Social Workers, Nurse Practitioners, and Behavioral Therapists. Depending on their qualifications and licensing, these experts can offer different services. Patients may use different healthcare professionals for diagnosis, behavioral therapy, and prescribing medication. Whatever the specialty, it is important for people to find ADHD experts with whom they are comfortable.

When choosing a healthcare professional to work with, some considerations may be:



The healthcare professional's experience with treating ADHD.
You may want to find someone who specializes in ADHD, or has extensive experience with the condition.
What types of treatment are preferred.
Do you understand and approve of the healthcare professional's methodology? Do they use a behavioral approach, offer medication, and provide family counseling?
Does the healthcare professional work as part of a treatment team.
In most cases, you will be working with a group of specialists. You will want to know who else is part of your "team."
Your comfort level with the healthcare professional or team.
Choose a therapist or healthcare professional that is easy to talk with. Make sure you are comfortable with their attitude toward ADHD and their approaches in treating it.

Information supplied by Eli Lilly & Co, Indianapolis, IN USA
For more information about ADHD and Adult ADD, contact your doctor or other healthcare professional.

[Stagger_Lee]

ADULT ADHD

This info is a bit nefarious, it comes from an independant sourse in Florida that seems a bit serelf serving to me, but here it is anyway..

ATTENTION DEFICIT DISORDER AND ATTENTION DEFICIT HYPERACTIVITY DISORDER

At Florida Detox, our clinical research demonstrates that over 50 percent of our opioid dependent patients suffer from undiagnosed/untreated Attention Deficit Disorder (ADD) or Attention Deficit Hyperactivity Disorder (ADHD). Most of our cocaine dependent patients and many of our alcohol patients also suffer from ADD or ADHD. Many of these patients "feel more normal" when using oxycontin, vicodin, alcohol or cocaine. These drugs produce a temporary increase of dopamine, in the prefrontal cortex (ADD area) of the brain. This effectually allows the patient to self-medicate their genetic dopamine deficiency. Relapse rates are much lower, when ADD and ADHD are accurately diagnosed and adequately treated.

With the advent of neuroimaging, there is no longer a scientific dispute over the reality of the ADD and ADHD diagnoses. Single photon emission computed tomography (SPECT) and positron emission tomography (PET) neuroimaging demonstrate altered brain blood flow distribution in ADD and ADHD. Increased dopamine transporter reuptake has also been found in ADHD subjects. (increased dopamine reuptake decreases dopamine availability to the next neuron, decreasing firing of brain dopamine circuits) Recent research reveals decreased brain volume in both un-medicated and medicated ADHD patients. Decreased essential fatty acid levels have also been measured in ADHD patients These recent scientific observations help explain the beneficial effect of psychostimulant medication, targeted amino acid therapy and essential fatty acid supplementation in patients suffering from ADHD and ADD.

Percocet, Vicodin, and Oxycontin increase dopamine release from nerve A to nerve B, in the brain. Opiate medications initially help the ADD patient feel more focused, when the overactive brain begins relaxing. ADD patients also use alcohol to relax and allow sleep. Patients describe a "freight train of thoughts" traveling through their mind, while they attempt to fall asleep. Cocaine is often used by ADD patients to normalize dopamine levels, in their prefrontal cortex.

Many corporate executives seeking treatment, at Florida Detox, were self medicating with both oxycontin and cocaine to manage their ADD. ADD patients with high IQ are seldom diagnosed in school, since they perform well academically, despite poor focus.

The prefrontal cortex is the executive center of the brain. Ordinarily, the prefrontal cortex filters extraneous stimuli protecting the rest of the cortex from distraction. Other tasks performed by the prefrontal cortex include braking racing thoughts, controlling mood swings, decreasing verbal and physical impulsivity and prioritizing tasks.

When the prefrontal cortex in understimulated, secondary to inadequate dopamine levels, it can not perform it's job. Patients fight continuous boredom, lack of focus, mood swings, and lack of task completion. They often feel they can not turn down their brain, at night. Many patients wake up, at 700 AM, but feel their brain does not wake up, till 1000 AM. They experience difficulty prioritizing the morning's tasks.

ALTERED BRAIN GLUCOSE DISTRIBUTION IN ADD and ADHD

SPECT and PET Brain neuroimaging scans reveal altered brain blood flow distribution and brain glucose utilization in ADD and ADHD patients. Normally, when the brain concentrates, faster beta brain waves increase, in frontal brain lobes. When brainwaves of ADD children and teenagers were measured, using electroencephalograms (EEG), faster beta waves did not increase. Instead, slower alpha waves increased, during concentration tasks, in children suffering from ADD.<

Dopamine activity should increase in the prefrontal cortex, during concentration.

The brain's basal ganglia produce much of the brain dopamine supply. Studies reveal smaller basal ganglia volume in ADD brains. The basal ganglia contain dopamine circuits extending through the limbic region of the brain, to the prefrontal cortex. If inadequate dopamine is produced, in the basal ganglia, the prefrontal cortex usually lacks sufficient dopamine to activate, when increased concentration is required.

The following SPECT brain scans are used with permission from Daniel Amen, MD, who has viewed over 28,000 SPECT brain scans. Many additional brain scans are viewable at his extremely informative website, amenclinics.com. Dr. Amen has authored many excellent books, including Healing ADD: The Breakthrough Program That Allows You to See and Heal the 6 Types of ADD

We highly recommend his website and books.



AD/HD, combined type with both symptoms of inattention and hyperactivity-impulsivity. Brain SPECT imaging typically shows decreased activity in the basal ganglia and prefrontal cortex during a concentration task. This subtype of ADD typically responds best to psychostimulant medication
Rest, Concentration & Concentration with Medication

<![endif]>
undersurface view, resting
mild decrease prefrontal area

>
undersurface view, concentration
marked decrease prefrontal cortex
and left temporal lobe


undersurface view, w/Adderall
overall marked improved activity


In a study of 54 medication free children, diagnosed with ADHD, 65 percent displayed prefrontal lobe deactivation, during intellectual stress, compared to 5 percent of the non-ADHD comparison group. (p=.0001) (Statistically, a difference this large, in a study population, of this size could occur, once in 10,000 times, by chance.) "Prefrontal lobe functions include attention span, concentration, judgment, activity level, critical thinking and impulse control." Thirty four percent of the ADHD children did not display decreased prefrontal lobe activity with intellectual stress, however 63 percent, of those who did not suppress prefrontal lobe function, during concentration, displayed reduced prefrontal lobe activation, at rest. When ADHD children who exhibited decreased prefrontal lobe activation, during intellectual stress (65 percent) are combined with the ADHD children, who exhibited reduced prefrontal lobe activity, at rest (22 percent), 87 percent of the medication free ADHD children exhibited decreased prefrontal lobe activity.

Amen, DG, Paldi, JH, Thisted, R Evaluating ADHD with Brain SPECT Imaging J of Child and Adol Psychiatry 32:1080-1081, 1993

2. AD/HD, primarily inattentive subtype with symptoms of inattention and also chronic boredom, decreased motivation, internal preoccupation and low energy. Brain SPECT imaging typically shows decreased activity in the basal ganglia and dorsal lateral prefrontal cortex during a concentration task. This subtype of ADD also typically responds best to psychostimulant medication.

Before & After Treatment with Ritalin & Adderall


undersurface view, NO MEDS
poor prefrontal and
temporal lobe activity

<![endif]>
undersurface view, with Adderall
marked overall improvement

<![endif]>
undersurface view, NO MEDS
overall severe decreased activity


undersurface view, w/Ritalin
overall marked improved activity


3. Overfocused ADD, with symptoms of trouble shifting attention, cognitive inflexibility, difficulty with transitions, excessive worrying, and oppositional and argumentative behavior. There are often also symptoms of inattention and hyperactivity-impulsivity. Brain SPECT imaging typically shows increased activity in the anterior cingulate gyrus and decreased prefrontal cortex activity. This subtype typically responds best to medications that enhance both serotonin and dopamine availability in the brain, such as venlafaxine or a combination of an SSRI (such as fluoxetine or sertraline) and a psychostimulant.


front on active view
increased cingulate activity

<![endif]>
active top down view
increased cingulate activity


top down active view
increased cingulate activity


active side view
increased cingulate activity


4. Temporal lobe ADD, with symptoms of inattention and/or hyperactivity-impulsivity and mood instability, aggression, mild paranoia, anxiety with little provocation, atypical headaches or abdominal pain, visual or auditory illusions, and learning problems (especially reading and auditory processing). Brain SPECT imaging typically shows decreased or increased activity in the temporal lobes with decreased prefrontal cortex activity. Aggression tends to be more common with left temporal lobe abnormalities. This subtype typically responds best to anticonvulsant medications (such as gabapentin, divalproate, or carbamazepine and a psychostimulant.


undersurface view
decreased left temporal lobe activity


underside active view
increased left temporal lobe activity

<![endif]>
undersurface view
marked decreased left
temporal lobe activity


undersurface view
marked decreased temporal
and prefrontal cortex bilaterally




INCREASED DOPAMINE TRANSPORTER REUPTAKE IN ADHD

In a study of six adult patients with ADHD, single photon emission computed tomography (SPECT) imaging revealed a 70 percent increase in dopamine transporter density, compared to 30 healthy control subjects. The dopamine transporter essentially recycles dopamine, from the neurosynapse, to the afferent (upstream) neuron, reducing the effect of dopamine. Higher dopamine levels are associated with motivation, drive, satisfaction, increased concentration and mental performance. Patients were excluded from the study, for the following: other evident psychiatric impairment, known drug or alcohol dependency, known drug allergy, or medication within past month, with dopamine altering medication. Dougherty DD, Bonab AA, Spencer TJ, Rauch SL, Madras BK, Fischman AJ.
Dopamine transporter density in patients with attention deficit hyperactivity disorder.
Lancet 1999 Dec 18-25;354(9196):2132-3

DECREASED BRAIN VOLUME IN UNMEDICATED AND MEDICATED CHILD AND ADOLESCENT ADHD PATIENTS

A study of 152 children and adolescents with ADHD and 139 age and sex matched controls, detected decreased brain volumes, in unmedicated and medicated ADHD subjects, compared to the control group. The ADHD patients exhibited total cerebral volumes 3.2 percent lower, (p = .004), and cerebellar volumes 3.5 percent lower (p = .001), compared to controls. Previously unmedicated ADHD patients exhibited 5.8 percent lower, (p = .002) cerebral volumes and 6.2 percent lower (p < .001) cerebellar volumes. Compared to controls, unmedicated ADHD children exhibited larger decreases in total white matter, 10.7 percent, (p < .001),than medicated children with ADHD, who exhibited 8.9 percent decreases (p < .001) in total white matter.

Brain volumes were determined using automated magnetic resonance imaging (MRI). ADHD neuroimaging studies have been frequently criticized, with differences between ADHD subjects and controls attributed to effects of medication, since most ADHD studies have failed to include unmedicated ADHD subjects. This study disputes these claims, since it found unmedicated AHHD subjects had significantly smaller white matter volume, compared to medicated ADHD subjects and controls. Differences detected persisted after statistical correction for height, weight and handedness.

F. Xavier Castellanos, MD; Patti P. Lee, MD; Wendy Sharp, MSW; Neal O. Jeffries, PhD; Deanna K. Greenstein, PhD; Liv S. Clasen, PhD; Jonathan D. Blumenthal, MA; Regina S. James, MD; Christen L. Ebens, BA; James M. Walter, MA; Alex Zijdenbos, PhD; Alan C. Evans, PhD; Jay N. Giedd, MD; Judith L. Rapoport, MD. Developmental Trajectories of Brain Volume Abnormalities in Children and Adolescents With Attention-Deficit/Hyperactivity Disorder JAMA. 2002;288:1740-1748

(The entire JAMA article is available on the internet, in pdf format, at intramural.nimh.nih.gov/chp/adhd/castellanos.pdf )

ATTENTION DEFICIT DISORDER AND SUBSTANCE ABUSE

Adolescent substance abusers with ADHD were 2.5 times more likely to suffer alcohol relapse, than adolescent substance abusers without ADHD. This study was conducted in a drug treatment study of 220 adolescent substance abusers. The higher risk for alcohol relapse persisted after statistical corrections for conduct disorder, pre-treatment alcohol use frequency and demographics were made. Latimer WW; Ernst J; Hennessey J; Stinchfield RD; Winters KC. Relapse among adolescent drug abusers following treatment: The role of probable ADHD status. Journal of Child & Adolescent Substance Abuse 13(3): 1-16, 2004.

In a study of 314 alcoholics of German descent, 21 percent were diagnosed with ADHD, with symptoms persisting in adulthood.Wodarz N, Lange K, Laufkotter R, Johann M. [ADHD and alcohol dependence: a common genetic predisposition?] Psychiatr Prax. 2004 Nov;31 Suppl 1:S111-3.

PSYCHOSTIMULANT MEDICATION DECREASED SUBSTANCE ABUSE DISORDERS, IN MALE ADOLESCENTS

Unmedicated adolescent males with ADHD were 6.3 times (adjusted OR: 6.3 [1.8-21.6]) more likely to report substance abuse disorders than non ADHD control subjects in a study of 56 medicated ADHD subjects, 19 nonmedicated ADHD subjects and 137 non ADHD control subjects. The prevalence of substance abuse disorders in medicated ADHD subjects was only 15 percent (adjusted OR: 0.15 [0.04-0.6]) of the rate of substance abuse, in non medicated ADHD subjects. In other words, ADHD medication was associated with an 85 percent decrease in substance abuse disorders, in the 75 ADHD adolescent males. Abused substances evaluated included alcohol, marijuana, hallucinogens, stimulants and tobacco. Decreased substance abuse occurred, in the medicated ADHD group, compared to the non ADHD group, for each of the substances studied. Joseph Biederman, MD, Timothy Wilens, MD, Eric Mick, ScDv, Thomas Spencer, MD, and Stephen V. Faraone, PhD. Pharmacotherapy of Attention-deficit/Hyperactivity Disorder Reduces Risk for Substance Use Disorder PEDIATRICS Vol. 104 No. 2 August 1999, p. e20 (This article is available in PDF format, at pediatrics.aappublications.org/cgi/reprint/104/2/e20)

Dr. Bankole Johnson, Chairman of Psychiatric Medicine, at University of Virgina, states "Dopamine is responsible for a lot of pleasureable experiences." Eating triples dopamine levels. "Sex is 10 times the normal surge and cocaine is 100 times the normal surge. If you told someone to give up sex, it would be very hard, so you can imagine how hard it is to ask someone to give up cocaine." Charlottesville Daily Progress, May 31, 2006

Newer research indicates enhancing glutamate levels decreases ADD symptoms. Provigil (modafinal) has been primarily used for narcolepsy and shift work sleep disorders, but has proven effective for attention deficit and cocaine treatment.

ADHD Psychostimulant Medications Are Safer Than Aspirin And Auto Travel

Adderall, Ritalin and other psychostimulant medications, for ADHD, are safer than Aspirin, Acetaminophen and automobile travel. The annual risk of being struck by lightning is 33 times higher than the risk of a serious cardiac event, for adults, treated with psychostimulants.


The following probabilities help place these risks in perspective

Annual risk per 100,000 persons or patients :



Adults without high blood pressure, psychostimulant fatalities, 0.05/100,000

Adult psychostimulant fatalities, 0.125/100,000



Psychostimulant fatalities per patient, (includes children),0.18/100,000

Psychostimulant adverse cardiac events, (includes children),0.56/100,000

Being struck by lightning, 4.2/100,000

Viagra fatalities per patient, 5.0/100,000

Auto travel fatality risk, 16/100,000


NSAID Deaths per arthritis patient, 38.3/100,000
(aspirin, Motrin, Advil, Feldene, Clinoril, Indocin, Daypro, Aleve, etc.)

Fatalities/acetaminophen(Tylenol) overdose, 360/100,000

Auto property damage collision, 10,000/100,000






Data and annual risk probabilities, for the preceding table and chart were derived from the following sources:

Between 1999 and 2003, 25 people had died suddenly, and 54 suffered serious cardiac events such as a stroke, heart attack, hypertension or arrhythmia, while taking psychostimulant medications. www.healthyskepticism.org/library/ref.php

About 2.5 million children and teens take ADHD medications. Most of the drugs contain methylphenidate, found in Ritalin and Concerta and many generic ADHD medications. An estimated 1 million adults also use psychostimulant medications. (The National Institutes of Mental Health estimates 68 % of adolescents with ADHD continue to experience adult ADHD) www.healthyskepticism.org/library/ref.php

Using these numbers, the probability of a cardiac fatality was 0.18 in 100,000, annually, for patients using Ritalin, Concerta or Adderall, during the 4 year reporting period. This fatality rate is much lower than the fatality rate for Viagra, aspirin or automobile travel and less than the probability of being struck by lightning.

The Association of Reproductive Health Professionals cites a mortality rate of five per 100,000 for Viagra, the erectile dysfunction drug.

A 1998 article in the New England Journal of Medicine estimated that non steroidal anti-inflammatory medications cause 16,500 deaths annually in arthritis sufferers.

www.arthritis-depot.info/articles/arthr ... s-per-year

The Arthritis Foundation estimated there were 43, 000,000 arthritis sufferers, in the United States, in 1998. www.arthritis.org/resources/gettingstarted/default.asp

These medications include aspirin, Motrin, Aleve, Naproxn, Feldene, Sulindac, Toradol and Indocin. Assuming every arthritis sufferer, in the United States, in 1998, used non steroidal anti-inflammatory medications, the annual fatality risk was 38.3 per 100,000.

Another common activity, with a higher fatality risk than psychostimulant medication is automobile travel. Although motor-vehicle accidents claimed 43,300 lives in 1996, the rate per 100,000 Americans has dropped significantly in the last two decades because of safer cars, safer roads, and efforts to curb drunk driving, says Alan Hoskin, manager of research and statistics at NSC. The 1996 rate of 16 automobile travel deaths annually per 100,000 population was down 18 percent from 1986, and down 41 percent from 1966 www.defendu.com/realrisk

The Toxic Exposure Surveillance System (TESS) for 2003 showed an increase in acetaminophen poisonings with 40,833 accidental overdoses leading to 147 fatalities. Acetaminophen produced 360 deaths/100,000 overdoses.

Our 80 year lifetime probability of being struck by lightning is 1 in 3,000. www.lightningsafety.noaa.gov/medical.htm
A 1 in 3,000 risk, in 80 years is a 4.2 per 100,000 annual risk of being struck by lightning and much higher than a 0.18 in 100,000 annual risk of a cardiac fatality, on psychostimulant medication. Our risk of being struck by lightning is much higher than the risk of a cardiac death, from psychostimulant medication!

How much sleep are you losing, worrying about being struck by lightning?


Florida Detox uses Attention Deficit Disorder (ADD) and Attention Deficit Hyperactivity Disorder (ADHD) diagnostic screens, which have been well validated by SPECT brain scans. We also confirm our Attention Deficit Disorder and Attention Deficit Hyperactivity Disorder diagnosis with neurotransmitter testing for homovanillic acid, phenylethylamine and hydoxy indole acetic acid. We carefully monitor our patients for cardiovascular complications-our Detox patients receive Electrocardiogram testing. How many physicians prescribing psychostimulants obtain electrocardiograms and neurotransmitter tests, on their patients?

Since Adderall is a Schedule II controlled substance, our Adderall patients are seen, at least every thirty days. If every physician and methadone clinic tested patients as thoroughly as Florida Detox does, medication side effects would decrease.




The FDA warning does not distinguish between Ritalin which significantly increases norepinephrine and Adderall. Norepinephrine elevates blood pressure and cardiac risk. High blood pressure, usually decreases with medication discontinuation.

Although Florida Detox believes Adderall medication is very safe when used properly, for Attention Deficit Disorders, we do recommend nutritional therapies including high dose EPA and DHA essential fatty acids, tyrosine, phenylalanine, micuna, S-Adenosyl Methionine, folate, and ferrous bisglycinate supplementation, based on test results. Thyroid hormone supplementation can reduce attention deficit disorder symptoms, when patients are hypothyroid. Deprenyl (Selegiline) medication can also enhance dopamine levels and reduce attention deficit disorder symptoms.

Food and food additive allergies and nutritional deficiencies also can cause or aggravate Attention Deficit Disorders. One of our Attention Deficit patients tested allergic to Yellow #5 food dye, in a serum immunoglobin test. Many of our patients with ADD/ADHD have low ferritin levels, especially if they suffer from restless leg syndrome. Increasing ferritin nutritionally can reduce Attention Deficit Disorders, if ferritin level is low.




GENETIC EVIDENCE

ADHD occurred twice as often in full siblings, compared to half siblings in a study of ADHD children who were placed in foster care. ). Safer DJ. A familial factor in minimal brain dysfunction. Behav Genet. 1973;3(2):175-186.

ESSENTIAL FATTY ACIDS AND ADHD

Neurotransmitter receptors are located on cell membranes. Receptor membrane permeability strongly influences neurotransmitter firing in the brain. Cell membranes contain layers of fatty acids called phospholipids. Highly unsaturated fatty acids, including Decosahexanoeic Acid (DHA), and Eicosapentaenioc Acid (EPA) build membranes which flow nutrients and wastes more easily. Considerable research indicates higher intake of the essential fatty acids Decosahexanoeic Acid (DHA) Eicosapentaenioc Acid (EPA) and Arachidonic Acid (AA ) deceases symptoms of Attention Deficit Disorders.

Purdue University researchers studied 53 boys with ADHD and found significantly lower levels of Arachidonic Acid (AA), Eicosapentaenoic Acid (EPA) and Docosahexaenoic Acid (DHA) in plasma lipids, compared to 43 boys, without ADHD. Red blood cell lipid Arachidonic Acid (AA ) and Docosatetraenoic Acid were also significantly lower, in the 53 boys with ADHD. A subgroup of 21 boys with ADHD and more numerous symptoms of essential fatty acid deficiency, possessed considerably lower Arachidonic Acid (AA) and Docosahexaenoic Acid (DHA), than 32 ADHD boys, with fewer essential fatty acid symptoms. LJ Stevens, SS Zentall, JL Deck, ML Abate, BA Watkins, SR Lipp and JR Burgess. Essential fatty acid metabolism in boys with attention-deficit hyperactivity disorder. American Journal of Clinical Nutrition, Vol 62, 761-768

The Omega 3 essential fatty acids, Eicosapentaenoic Acid (EPA) and Docosahexaenoic Acid (DHA) appear especially helpful, in ADD or ADHD. Frontal cortex dopamine levels decreased 40 to 60 percent, in rats fed an Omega 3 fatty acid deficient diet. Dopamine release was 90 percent lower in the Omega 3 deficient rats. Logan, Alan C. Neurobehavioral aspects of omega-3 fatty acids: possible mechanisms and therapeutic value in major depression Alternative Medicine Review; 11/1/2003

Many anecdotal case history reports of decreased attention deficit symptoms, after essential fatty supplementation, have been published on attention deficit bulletin boards and self help sites.

S-ADENOSYL METHIONINE

S-Adenosyl Methionine (SAMe) is the activated form of the amino acid methionine. It is available, without a prescription, at health food stores. SAMe has activity at dopamine and norepinephrine receptors. In a small 8 person open label trial, 75 percent of adult male ADHD subjects exhibited moderate to marked improvement, in ADHD symptoms. Patients who failed to improve, also failed to improve with methylphenidate (Ritalin).

Shekim, W., Antun, F., Hanna,G., McCracken, J., Hess, E. S-adenosyl-L-methionine (SAM) in adults with ADHD, RS: preliminary results from an open trial. Psychopharmacol Bull . 1990;26(2):249-53


AMINO ACID SUPPLEMENTATION

The naturally occurring amino acids l- tyrosine and l-phenylalanine are enzymatically transformed to dopamine. Tyrosine or phenylalanine supplementation can reduce attention deficit symptoms.

At Florida Detox, Dr. Sponaugle considers us to be in a race to reduce or eliminate alcohol or drug withdrawal symptoms, before they trigger a relapse. Since prescription medications usually work faster, we generally use them first. Frequently, we can replace all or part of an Adderall dose with the naturally occurring amino acid, Tyrosine. Since Tyrosine is naturally occurring, it is available at health food stores, and is relatively inexpensive. It needs to be taken on an empty stomach, or at least separated an hour from other proteins or amino acids. It is more effective taken sublingually, (under the tongue). This is done by emptying a 500 milligram powder capsule, under the tongue and holding the powder, for about 2 minutes, before swallowing. This allows the amino acid to be absorbed into the mucous membrane, directly into the bloodstream, and increases absorption of the tyrosine. The 500 milligram powder capsule is available at almost any health food store. General Nutrition Centers stock a 750 milligram tablet, which may be chewed, before holding under the tongue. We have a patient who successfully replaced 20 milligrams Adderall, taken 3 times per day (TID), using this method, while he waited for his appointment with a local doctor, willing to continue prescribing Adderall for him. Dosage used to replace Adderall or reduce or eliminate cocaine cravings is 1,500 to 6,000 milligrams per day, split into at least two doses, per day.

PLEASE DO NOT DISCONTINUE ADDERALL MEDICATION, ABRUPTLY, WITHOUT CONSULTING A PHYSICIAN. In some patients, tyrosine may decrease in effectiveness, with time. Decreased conversion of tyrosine to dopamine, occurs due to down regulation of tyrosine hydoxylase, by norepinephrine. Recently, concentrated herbal extracts of a plant, called Mucuna Pruriens, which concentrates Dopa, have become available. Since conversion of Dopa to dopamine, is not downregulated, by increased dopamine and norepinephrine levels, Micuna supplementation could be continued indefinitely, without reduction in dopamine levels. MICUNA SUPPLEMENTATION SHOULD NOT BE DONE WITHOUT SUPERVISION, OR CONSULTATION, BY A PHYSICIAN.

Excess Dopamine production can cause low blood pressure, headache, tremors, eyelid tics, paranoia and hypomania or mania. Tyrosine and Mucuna supplementation can potentially cause these symptoms. Tyrosine and Mucuna Pruriens both can alter blood pressure and should not be used without consultation with a physician. The proceeding information is not considered to be a substitute for medical diagnosis, evaluation or treatment.

We recently recommended Mucuna to a previous patient, to help raise his dopamine level. He is a 40 y/o male, with several years of opiate use for chronic pain issues. On several occasions, he related that he felt low energy, and has also said he would like to feel what he felt on the opiates without the dangerous addictive and withdrawal symptoms. He also had an issue with taking Adderall, for ADD, because he has high blood pressure. This patient reported that since he has started taking the Mucuna, he feels great. He says he feels like he has plenty of energy, and it has had no effect on his blood pressure.

Florida Detox recommends targeted amino acid and essential fatty acid supplementation to all of our patients suffering from attention deficit disorders. In view of clear and convincing scientific evidence, ignorance is no longer an excuse to deny effective treatment to attention deficit sufferers.

[Stagger_Lee]

Last Sunday, I was sent to hospital with a Transichemic Attack (also known as TIA). Although a neurological, not psychiatric disorder, I thought I'd lend a brief description of it here.

For any interested, I'm finally back up & around and starting to feel like myself again... albeit scared and shaken by the whole ordeal. So, I urge you, if you feel ANY symptoms, don't wait... get to a hospital ASAP.

transischemic attack (TIA) “Mini-strokes” that occur when a small blood clot blocks an artery leading to the brain for a short time. Symptoms are the same as for a stroke but go away in a few minutes. TIAs often warn that a full-fledged stroke is on the way

Anyone wishing to take a health-risk appraisal can do so annonymously on line, provided by the University Of San Francisco at:

http://www.usfca.edu/hr/wellness/appraisal.html

[canucker]

That's scary... there are so many biological ticking time bombs anyone could be carrying.

Some of the posts in this thread are quite interesting minus the crap. I suffer from anxiety too, especially more recently, but I am being treated for it, as well as my PTSD.

Good thread.

[canucker]

I've heard about a type of therapy for PTSD patients where you re-live the moment that traumatized you and while you do that, you move your eyes from side to side...

Know anything about that?

[Stagger_Lee]

Yeah, it's called 'Flooding Therapy', mostly used to treat agrophobics. It's usually done by Psychologists rather than Psychiatrists. It's use in treating agrophobia is well documented, but it's relatively new in PTSD.

But, combined with Clonazepam and Effoxor XR or some other Seratonin Reuptake Med, I think it might be very effective.

Only bad thing, Medicare in Canada does not cover Psychologists, and most private health plans only cover on average 5 hours a year. But if you can swing it, I'd sure ask your Dr. about it's availability in your area.

[Stagger_Lee]

Organic Brain Syndrome
This is a general term that refers to physical disorders that cause a decrease in mental function, usually not including psychiatric disorders. Also known as: chronic organic brain syndrome; OBS; organic mental disorder

Symptoms vary with the specific disease. In general, organic brain syndromes cause varying extent of confusion, delirium (severe, short term losses of brain function), agitation, and dementia (long-term, often progressive, losses of brain function).

Associated Features:

Organic brain syndrome associated with consumption of drugs.

Differential Diagnosis:

Some disorders have similar symptoms. The clinician, therefore, in his diagnostic attempt, has to differentiate against the following disorders which need to be ruled out to establish a precise diagnosis.

Organic brain syndrome (OBS) is a common "diagnosis" of the elderly. It is not an inevitable part of aging, however. OBS is not a separate disease entity, but is a general term used to categorize physical conditions that can cause mental changes.

Disorders associated with OBS include, but are not limited to:

Degenerative Disorders:
Creutzfeldt-Jacob disease
Huntington disease
Multiple Sclerosis
Normal Pressure Hydrocephalus
Pick's disease
Senile Dementia/Alzheimer's type
Cardiovascular Disorders
Hypertensive Brain Injury
Multi-infarct Dementia
Stroke
Trauma-induced brain injury
Dementia due to metabolic causes
Meningitis
Encephalitis
Drug and alcohol related conditions
Wernicke-Korsakoff syndrome
Parkinson's disease
Other conditions that may be related to organic brain syndrome include depression, neuroses, and psychoses of various types, which may occur simultaneously with the OBS.

Cause:

It is not an inevitable part of aging, however. OBS is not a separate disease entity, but is a general term used to categorize physical conditions that can cause mental changes.

Treatment:

Treatment varies with the specific disorder. Many of the disorders have nonspecific treatments, primarily supportive care to assist the person in areas where brain function is lost. Medications may be needed to reduce aggressive behaviors typical of some of the conditions in this category.

Provided By Psych-Net UK

[Stagger_Lee]

Munchausen by Proxy (Overview)

Topics addressed in the following article include: What are Factitious Disorder and Munchausen Syndrome?
What is Munchausen by Proxy/Factitious Disorder by Proxy?
Munchausen by Proxy (MBP) - The Basics
Some Differences Between MBP and Other Kinds of Maltreatment
MBP Situational Suspicion Indicators
Usual MBP Perpetrator Characteristics (Not to Be Considered a Profile)
MBP Confirmation-Disconfirmation Process

FACTITIOUS DISORDER, (of which MUNCHAUSEN SYNDROME is a sub-type), (also called "Adult Munchausen", and "Adult Factitious Disorder") is a formal, DSM-IV mental health diagnosis in which people deliberately exaggerate and/or fabricate and/or induce physical and/or psychological-behavioral-mental health problems in themselves. The primary purpose of this behavior is to gain some form of internal gratification, such as attention, for themselves.

MUNCHAUSEN BY PROXY (MBP) (also called Munchausen Syndrome by Proxy, Munchausen by Proxy Syndrome, and Factitious Disorder by Proxy) is a label for a pattern of behavior in which caretakers deliberately exaggerate and/or fabricate and/or induce physical and/or psychological-behavioral-mental health problems in others.

This pattern of behavior constitutes a separate kind of maltreatment (abuse/neglect) that manifests as physical abuse, sexual abuse, emotional abuse, neglect, or a combination. The primary purpose of this behavior is to gain some form of internal gratification, such as attention, for the perpetrator.



Munchausen by Proxy (MBP) - The Basics
MBP/FDP is NOT a formal DSM-IV mental health diagnosis. It is a recognized form of maltreatment.

Many MBP maltreatment cases happen within the outpatient setting, rather than inpatient settings.
Most MBP maltreatment cases are confirmed through solid circumstantial evidence; very few are confirmed through direct evidence such as covert video surveillance.
There is virtually no physical or psychological-behavioral-mental health problem that cannot be exaggerated and/or fabricated and/or induced.

Exaggerate: The perpetrator deliberately embellishes a genuine problem.
Fabricate: The perpetrator deliberately makes up a problem story - OR makes it look as if a problem exists.
Induce: The perpetrator deliberately causes a problem to exist.

Exaggeration/fabrication cases should be considered as potentially lethal as cases in which inducing is suspected or confirmed.
A caretaker may perpetrate MBP maltreatment through one or a combination of exaggeration, fabrication, or inducing. The perpetrator may change methods throughout the life of the case.



Some Differences Between MBP and Other Kinds of Maltreatment
The varied ways cases can present
Usual perpetrator characteristics
Usual perpetrator-victim dynamics
Suspicion indicators
Initial and subsequent methods and activities of investigation
Expertise and methodology to determine presence or absence of MBP maltreatment
Court preparation and presentation
Victim risk assessment
Out-of-home victim placement decision making
Dangers of victim placement with relatives and need for specialized relative evaluation
Selecting and working with foster parents
Case plan design and implementation
Victim visitation and supervision
Therapist selection and role
Other short and long term victim protection and case management activities and issues



MBP Situational Suspicion Indicators
Difference between reported history and what is seen, or what makes sense physically or psychologically-behaviorally.
Problem does not respond to treatment as expected.
Problem appears to originate only in association with suspected perpetrator’s presence.
Problem disappears or begins to improve when suspected victim is separated from suspected perpetrator.
Problem resumes after suspected perpetrator is told suspected victim has recovered, is improving, or is soon to be released from the facility, program, course of treatment, etc. - OR problem resumes shortly after suspected victim goes home, treatment is discontinued, etc.
Unexplained symptoms, illness, or death of other nuclear or extended family members.
A pattern of "Usual MBP Perpetrator Characteristics".
Suspected MBP perpetrator behavior that appears to be consistent with exaggeration and/or fabrication and/or induction of physical and/or psychological-behavioral problems in the suspected victim.


Usual MBP Perpetrator Characteristics (Not to Be Considered a Profile)
MBP perpetrators are usually mothers.
MBP perpetrators usually present initially as "normal", "good" caretakers.
MBP perpetrators are usually accomplished liars, deceivers, and manipulators - and extremely believable, convincing, and superb in their ability to give seemingly plausible reasons for their behavior.
MBP perpetrators know what they are doing. They are not simply overanxious, overprotective caretakers.
MBP perpetrators may have extensive health care knowledge - or they may not.
MBP perpetrators usually deny all or part of the maltreatment they have perpetrated - even when there is extensive evidence.
MBP perpetrators do not usually stop their MBP behavior when they are suspected or caught - but the behavior may change.
MBP perpetrators may add or change health care providers, or "doctor shop" - or they may not.
MBP perpetrators may have "normal" mental health evaluations - or there may be identified mental health pathology.
MBP perpetrators may have a history of symptom/illness falsification with regard to themselves.
MBP perpetrator-victim dynamics usually initially appear good - even excellent.
MBP perpetrators often have no prior child protection agency involvement.
MBP perpetrators should be considered even more dangerous once they believe they are suspected.
MBP perpetrators use their victims as objects in trying to satisfy internal needs through the attention they receive from having a child with "problems". These needs are much more important to them than the needs of their victims. External gain may also be present.
MBP perpetrators may seek attention from a variety of people - professionals and non-professionals.
MBP perpetrators may have a "dramatic flair" or be involved in exciting or dramatic events.
MBP perpetrators may change their maltreatment methods.



MBP Confirmation-Disconfirmation Process
MBP is a recognized kind of maltreatment (abuse/neglect) - it is something someone does, NOT something someone "has" or "suffers from". It is behavior that one person deliberately perpetrates on another. For MBP to be confirmed, there must be:

(1) proof, through direct or circumstantial evidence (usually strong circumstantial evidence), that the suspected perpetrator has deliberately exaggerated and/or fabricated and/or induced a problem (physical and/or psychological-behavioral-mental health) regarding another person, and
(2) rationale that the behavior is consistent with MBP maltreatment, rather than something else.
There is no mental health test or evaluation that can rule MBP maltreatment in or out. There is no "profile" or combination of personal characteristics or traits that can determine whether someone is or is not an MBP perpetrator. The MBP confirmation-disconfirmation process involves the gathering and specialized evaluation of all possible information regarded suspected perpetrator(s), suspected victim(s), other children presently or formerly in the home - even if now adults or deceased, and sometimes others - depending on the case situation.

MBP physical and emotional victim risk results from medical and mental health interventions as well as from actual symptoms/illness induced by the perpetrator.
Although labeling a case MBP maltreatment may not be necessary in criminal cases, a confirmation of MBP maltreatment by or with the assistance of a credible MBP professional, and finding of MBP maltreatment in child protection courts, is extremely important. Child protection case plans must correspond to the kind of maltreatment that is confirmed. Appropriate MBP case plans include elements unique to MBP maltreatment - activities that must be successfully completed prior to consideration of reunification between victim and perpetrator, and other activities related to where the victim will live, other children in the home, contact between perpetrator and victim and potential victims, visitation with others, and other short and long term issues related to child protection.

Provided by L.J. Lasher, MA (Psych)

[Stagger_Lee]

Sex and Love Addiction


Definition
Symptoms
Causes
Treatment
Read Psychology Today articles on "Sex and Love Addiction"
Go to Condition Center for more terms

Definition


Love addicts are characteristically familiar with desperate hopes and seemingly unending fears. Fearing rejection, pain, unfamiliar experiences, and having little faith in their ability or right to inspire love, they wait, wish, and hope for love, perhaps their least familiar experience.

Addictive sexuality is like most other compulsive behaviors: a potentially destructive twist on a normal life-enhancing activity. Defining sex addiction depends less on the behavior itself than on the person's motivation.

Sex addicts display a lack of the ability to control or postpone sexual feelings and actions. The need for arousal often replaces the need for intimacy. Eventually, thrill seeking becomes more important than family, career, even personal health and safety.

As sexual preoccupation increases in terms of energy and time, the sex addict follows a routine or ritual leading to acting out on desires which is then followed by feelings of denial then shame, despair and confusion.

It may be helpful to examine the definition of addiction more closely. Addiction is characterized by the repeated, compulsive seeking or use of a substance or activity despite adverse social, psychologic and/or physical consequences. Addiction is often (but not always) accompanied by physical dependence, a withdrawal syndrome and tolerance. Physical dependence is defined as a physiologic state of adaptation to a substance, the absence of which produces symptoms and signs of withdrawal.

Withdrawal syndrome consists of a predictable group of signs and symptoms resulting from abrupt removal of, or a rapid decrease in the regular dosage of, a psychoactive substance or activity; the syndrome is often characterized by overactivity of the physiologic functions that were suppressed by the drug and/or depression of the functions that were stimulated by the object of addiction.

Tolerance is a state in which a drug or activity produces a diminishing biologic or behavioral response; in other words, higher doses or in the case of sex addicts, riskier behavior is needed to produce the same effect that the user experienced initially.



Symptoms
For love addicts, love:

Is all consuming and obsessive
Is inhibited
Avoids risk or change
Lacks true intimacy
Is manipulative, strikes deals
Is dependent and parasitic
Demands the loved one's devotion

Sexual addictions usually are revealed in stages:

Preoccupation: continual fantasies about sexual prospects or situations. This can trigger an episode of sexual "acting-out"
Ritualization: a preferred sexual activity or situation is often stereotyped and repetitive
Compulsion: continual engagement in sexual activity despite negative consequences and desire to stop
Despair: guilt or shame over their inability to control behavior or feel remorse
Other behavioral problems, particularly chemical dependency and eating disorders



Causes
In the case of love addicts, often their own growth and development were thwarted earlier in life. Similarly, many sex addicts report some form of abuse or neglect as children and frequently see themselves as diminished or damaged in the process. Their parents are often sex addicts themselves.

Stress also plays a part in fueling compulsive sexual behavior by feeding the addict's need for withdrawal and fantasy.

Levels of phenylethylamine (PEA)—a chemical in the brain involved in the euphoria that comes with falling in love—rise with feelings of infatuation, boosting euphoria and excitement.

Love and sex addicts, may simply be dependent upon the physical and psychological arousal triggered by PEA and stress-related neurotransmitters.



Treatment
If you discover you are in an addictive relationship, you may want to seek professional assistance. Specialized counseling is available for those dealing directly or indirectly with this form of addiction.

Overcoming sexual compulsivity and addiction starts with recognizing that you are out of control sexually. Getting to that point requires taking a hard look at yourself and the problems—emotional, physical, or financial—caused by your sexual behavior.

Treatment should probably involve at least some of the following:

A commitment to abstinence
Rebuilding relationships
Managing stress
Self-help

Some treatment for sex addicts follows the format employed by alcoholics. This model views addicts as individuals chronically addicted to a behavior in spite of their attempts to change. They are in a vicious cycle of use, self-judgment, and avoidance that is repeated time and again. The model focuses on three elements of the cycle:

Use of sex
Self-judgment
Avoidance behaviors

The approach to counseling is strongly based on 12-step models.

The three elements of the addictive cycle are impacted by a process created by using:

A therapeutic environment
A thorough assessment
A group process
Education
Self/peer assessment

All five items are incorporated into a therapeutic process, which begins with the first contact.

The creation of an environment that supports the therapeutic process is essential to this approach. Clients must be provided with an opportunity to explore their self-judgments without fear of the judgment of others. They must feel they are listened to with empathy and respect. In earlier models of this approach, the counselor was the only one who possessed so-called counselor characteristics. Although this element is still critical, it now applies to the whole multidisciplinary team, a staff of professionals who are naturally therapeutic.

The counselor conducts an initial assessment, identifies the presenting problem, and, if indicated, schedules the client for treatment.

A thorough psychosocial assessment is conducted, and identified blocks to treatment or problems are noted. The counselor begins the bonding with the client during the assessment process. All counseling skills come into play. The counselor then prepares a therapeutic or treatment plan (i.e., the change model) to help the client deal with those identified problems or blocks that will prevent response to the treatment process.

The client follows a simple change model that closely aligns with the 12 steps of NA and AA.




Last Reviewed By: Psychology Today Staff
Courtesy of Psychology Today

[Stagger_Lee]

still a miscreat, huh, WDHIII... pity you weren't hugged much as a child... I pity you

[Stagger_Lee]

Dependent Personality Disorder


Definition
Symptoms
Causes
Treatment
Read Psychology Today articles on "Dependent Personality Disorder"
Go to Condition Center for more terms

Definition






Personality traits are enduring patterns of perceiving, relating to and thinking about one's environment and oneself that are exhibited in a wide range of social and personal contexts. Only when personality traits are inflexible, maladaptive and cause significant functional impairment or subjective distress are they considered personality disorders. The essential feature of a personality disorder is a continuing pattern of inner experience and behavior that deviates noticeably from the expectations of the individual's culture and is manifested in at least two of the following areas: cognition/thinking, affectivity/interpersonal functioning or impulse control.

This persistent pattern is inflexible and pervasive across a broad range of personal and social situations, and leads to clinically significant distress or impairment in social, occupational or other important areas of functioning. The pattern is stable and of long duration, which means its onset can be traced back to at least adolescence or early adulthood. This pattern is not better accounted for as a manifestation or consequence of another mental disorder and is not due to the direct physiological effects of a substance (such as drug abuse, medication, exposure to a toxin) or a general medical condition (such as head trauma).

Dependent personality disorder is described as a pervasive and excessive need to be taken care of that leads to a submissive and clinging behavior as well as fears of separation. This pattern begins by early adulthood and is present in a variety of contexts. The dependent and submissive behaviors are designed to elicit caregiving and arise from a self-perception of being unable to function adequately without the help of others.

Individuals with dependent personality disorder have great difficulty making everyday decisions (such as what shirt to wear or whether to carry an umbrella) without an excessive amount of advice and reassurance from others. These individuals tend to be passive and allow other people (often a single other person) to take the initiative and assume responsibility for most major areas of their lives. Adults with this disorder typically depend on a parent or spouse to decide where they should live, what kind of job they should have and which neighbors to befriend. Adolescents with this disorder may allow their parent(s) to decide what they should wear, with whom they should associate, how they should spend their free time and what school or college they should attend.

This need for others to assume responsibility goes beyond age-appropriate and situation-appropriate requests for assistance from others (such as the specific needs of children, elderly persons and handicapped persons). Because they fear losing support or approval, individuals with dependent personality disorder often have difficulty expressing disagreement with other people, especially those on whom they are dependent. These individuals feel so unable to function alone that they will agree with things that they feel are wrong rather than risk losing the help of those to whom they look for guidance. Individuals with this disorder have difficulty initiating projects or doing things independently.

They may go to excessive lengths to obtain nurturance and support from others, even to the point of volunteering for unpleasant tasks if such behavior will bring the care that they need. Individuals with this disorder feel uncomfortable or helpless when alone, because of their exaggerated fears of being unable to care for themselves. When a close relationship ends (such as a breakup with a lover or the death of a caregiver), individuals with dependent Personality disorder may urgently seek another relationship to provide the care and support they need. They are often preoccupied with fears of being left to care for themselves.



Symptoms
People with this disorder do not trust their own ability to make decisions and feel that others have better ideas. They may be devastated by separation and loss, and they may go to great lengths, even suffering abuse, to stay in a relationship. Other symptoms include:

Inability to make decisions
Passivity
Avoiding personal responsibility
Avoiding being alone
Devastation or helplessness when relationships end
Unable to meet ordinary demands of life
Preoccupied with fears of being abandoned
Easily hurt by criticism or disapproval
Complications to this disorder may include depression, alcohol and drug abuse, and susceptibility to physical, emotional and sexual abuse.



Causes
The cause of this disorder is not known. The disorder usually appears in early adulthood. This disorder is common but not well studied; however, more women than men have been found to have dependent personality disorder.



Treatment
There is no specific treatment for this disorder. Psychotherapy may be useful in gradually helping people to make choices that affect their own lives. Medication may also be helpful. Improvements are usually seen only with long-term therapy or treatment.

Medications

Medication may be helpful to treat any other underlying conditions. Certain types of drugs such as antidepressants, sedatives and tranquilizers are often prescribed for patients with dependent personality disorder to treat co-occurring conditions.

Psychotherapy

Psychotherapy is the preferred form of treatment for people with dependent personality disorder. Cognitive-behavioral therapy focuses on patterns of thinking that are maladaptive, the beliefs that underlie such thinking and resolving symptoms or traits that are characteristic of the disorder, such as the inability to make important life decisions or the inability to initiate relationships.

Sources:

American Psychiatric Association
National Institutes of Health
National Library of Medicine



Last Reviewed By: Laura Stephens