Updated: Jun 3, 2009
The term schizoaffective disorder was coined by Dr. Jacob Kasanin in 1933. Schizoaffective disorder is a perplexing mental illness distinguished by a combination of symptoms of a thought disorder or other psychotic symptoms such as hallucinations or delusions (schizophrenia component) and those of a mood disorder (depressive or manic component). The coupling of symptoms from these divergent spectrums makes treating patients who are schizoaffective difficult.
Schizoaffective disorder is defined using the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR) criteria or by International Classification of Diseases, Tenth Revision (ICD-10) coding. Schizoaffective disorder has features of both schizophrenia, including hallucinations, delusions, and distorted thinking, and a mood component, such as depression or mania.
The diagnosis is made when the patient has features of both illnesses but does not strictly meet diagnostic criteria for either schizophrenia or a mood disorder alone. Unfortunately, determining if a patient has 2 separate illnesses (schizophrenia or a mood disorder), a combination of illnesses (schizophrenia and a mood disorder), or perhaps even a distinct and separate illness apart from schizophrenia or a mood disorder is difficult. Making the diagnosis of schizoaffective disorder can be difficult because it encompasses 2 other diagnostic entities, namely schizophrenia and mood disorders. An accurate diagnosis is made when the patient meets criteria for major depressive disorder or mania while also meeting the criteria for schizophrenia. Moreover, the patient must have psychosis for at least 2 weeks without a mood disorder.
Men with schizoaffective disorder tend to exhibit antisocial personality traits. The age of onset is later for women than for men, and the exact etiology and epidemiology is unclear because of limited research in this area. Patients with schizoaffective disorder are thought to have a better prognosis than that of patients with schizophrenia. Treatment consists of both pharmacotherapy and psychotherapy.
Although the exact etiology of schizoaffective disorder is unknown, it may involve the balance of dopamine and serotonin in the brain.1 Others believe that it may be due to in utero exposure to viruses, malnutrition, or even birth complications.
The lifetime prevalence of schizoaffective disorder is thought to be approximately 0.32%2 , with a range of 0.5-0.8%3 . This rate is only an estimate because no studies have been performed.
The international prevalence rates are difficult to determine because the diagnostic criteria have changed over the last few years.
The prognosis for patients with schizoaffective disorder is thought to lie between that of patients with schizophrenia and that of patients with a mood disorder. That is, the prognosis is better with schizoaffective disorder than with schizophrenic disorder but worse than with a mood disorder alone.
No race-based difference in diagnosis is observed.
Schizoaffective disorder is more common in women than in men. Men with schizoaffective disorder tend to exhibit antisocial traits and behavior in contrast to other personality traits. In addition, the age of onset is later for women than for men, and the exact etiology and epidemiology is unclear because of limited research in this area.
Young people with schizoaffective disorder tend to have a diagnosis with the bipolar subtype, whereas older people tend to have the depressive subtype.
Obtain a complete medical history, and perform a complete mental status examination, physical examination, and neurologic examination to assist with the evaluation and rule out other disease processes.
Although the mental status examination varies for each patient, examples of items to assess are listed below. Because of the variability of the presentation of the disorder, any or all symptoms of schizophrenia, bipolar disorder, or major depressive disorder may manifest depending on the presenting subtype.
Although the cause of schizoaffective disorder is unknown, the cause may be similar to schizophrenia nature versus nurture. To date, no specific genetic markers have been identified. Environmental causes of malnutrition, viral infections, or complication at birth may play a role. Finally, abnormalities of the neurotransmitters serotonin, norepinephrine, and/or dopamine could all have a role in this disorder. More research is needed to fully elucidate the causes of schizoaffective disorder.
| Amphetamine-Related Psychiatric
Disorders | HIV Disease |
| Bipolar Affective Disorder | Hyperparathyroidism |
| Brief Psychotic Disorder | Phencyclidine (PCP)-Related Psychiatric
Disorders |
| Cocaine-Related Psychiatric Disorders | Schizophrenia |
| Cushing Syndrome | |
| Depression | |
| Hallucinogens |
Steroid use
Temporal lobe epilepsy
Complex partial seizure disorder
Neurosyphilis
Thyroid problems
Alcohol abuse or dependence
Metabolic syndrome
Delirium
Narcolepsy
Findings include decreased amounts of cortical gray matter and increased fluid-filled spaces.
Several medications are used to treat schizoaffective disorder. Agent selection depends on whether the depressive or manic subtype is present. Early treatment with medication along with good premorbid function often improves outcomes. In the depressive subtype, combinations of antidepressants (eg, sertraline, fluoxetine) plus an antipsychotic (eg, haloperidol, risperidone, olanzapine) are used. In refractory cases, clozapine has been used as an antipsychotic agent. In the manic subtype, combinations of mood stabilizers (eg, lithium, carbamazepine, divalproex) plus an antipsychotic are used. Of the many medications and combinations available to treat schizoaffective disorder, a few are reviewed below.
These agents ameliorate psychosis and aggressive behavior.
For management of psychosis. Also for motor and vocal tics in children and adults. Mechanism of action not clearly established, but has selective effect on CNS by competitively blocking postsynaptic dopamine (D2) receptors in mesolimbic dopaminergic system; increases in dopamine turnover responsible for tranquilizing effect. With subchronic therapy, depolarization blockade and D2 postsynaptic blockade responsible for antipsychotic action.
0.5-5 mg PO bid; 2-5 mg IM q4-8h
<3 years: Not established
3-12 years (15-40 kg): 0.05-0.15 mg/kg/d PO
>12 years: Administer as in adults
May increase serum concentration of tricyclic antidepressants and hypotensive action of antihypertensive agents; phenobarbital or carbamazepine may decrease effects; coadministration with anticholinergics may increase intraocular pressure; encephalopathic syndromes associated with concurrent lithium
Documented hypersensitivity; narrow-angle glaucoma; bone marrow suppression; severe cardiac or liver disease; severe hypotension; subcortical brain damage
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Severe neurotoxicity (eg, rigidity, inability to walk or talk) may occur in patients with thyrotoxicosis also receiving antipsychotics if IV/IM, watch for hypotension; caution in diagnosed CNS depression or cardiac disease; in history of seizures, benefits must outweigh risk; significant increase in body temperature may indicate intolerance to antipsychotics (discontinue if occurs); elevates prolactin levels
Selective monoaminergic antagonist binds to dopamine D2 receptor with 20 times lower affinity than to 5-HT2 receptors. Also binds to alpha1-adrenergic receptors with lower affinity to H1-histaminergic and alpha2-adrenergic receptors. Improves negative symptoms of psychosis and decreases occurrence of extrapyramidal effects.
Also available in long-acting IM formulation (Risperdal Consta).
0.25-6 mg/d PO qd/bid
Not established
Coadministration with carbamazepine may decrease effects; may inhibit effects of levodopa; clozapine may increase levels
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Extrapyramidal reactions, tachycardia, arrhythmias, orthostatic hypotension, seizures, dysphasia, hyperprolactinemia, cognitive and motor impairment, priapism, and rare thrombotic thrombocytopenia purpura
Atypical antipsychotic with broad pharmacologic profile across receptor systems (eg, serotonin, dopamine, cholinergic muscarinic, alpha adrenergic, histamine). Antipsychotic effect from antagonism of dopamine and serotonin type 2 receptors. Indicated for treatment of psychosis and bipolar disorder.
5-10 mg/d PO, increase to 10-15 mg/d within 5-7 d; adjust by 5 mg/d q1wk; doses >15 mg/d not evaluated
Not established
Fluvoxamine may increase effects; antihypertensives may increase risk of hypotension and orthostatic hypotension; levodopa, pergolide, bromocriptine, charcoal, carbamazepine, omeprazole, rifampin, and cigarette smoking may decrease effects
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in narrow-angle glaucoma, cardiovascular disease, cerebrovascular disease, prostatic hypertrophy, seizure disorders, hypovolemia, paralytic ileus, heat exposure, and dehydration
Weak D2-receptor and D1-receptor blocking activity, but noradrenolytic, anticholinergic, antihistaminic, and arousal reaction inhibiting effects are significant. Antiserotonergic properties. Risk of agranulocytosis limits use to patients nonresponsive to or intolerant of classic neuroleptic agents.
12.5 mg PO qd/bid, increase 25-50 mg/d as tolerated to a therapeutic target of 300-450 mg/d after 2 wk; titrate to avoid hypotension, seizure, and sedation
Not established
Enhances CNS effects of alcohol, MAOIs, and CNS depressants (ie, narcotics, antihistamines, benzodiazepines); increased risk of circulatory collapse leading to cardiac and/or respiratory arrest with benzodiazepine or other antipsychotic agent; risk of additive effects with anticholinergic, hypotensive, or respiratory depressants; increased plasma levels and toxicity with warfarin; enhanced metabolism and/or decreased plasma levels with phenytoin, carbamazepine, rifampicin, and St John's wort; increased toxicity and serum levels with fluoxetine, paroxetine, sertraline, and fluvoxamine; increased risk of neuroleptic malignant syndrome occurring with lithium; decreases effectiveness of epinephrine
Documented hypersensitivity; WBC count <3500 cells/mm3 before or during therapy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Seizures, orthostatic hyperglycemia, hepatitis, anticholinergic toxicity, and impaired cognitive and motor performance; because of risk of agranulocytosis, perform a required weekly blood test (CBC d/p); do not stop abruptly; if stopped for 2 d, do not restart at current dose, start at initial dose with titration
Newer antipsychotic for long-term management. May antagonize dopamine and serotonin effects. Improvements over earlier antipsychotics include fewer anticholinergic effects and less dystonia, parkinsonism, and tardive dyskinesia.
Initial: 25 mg PO bid/tid; increase by 25-50 mg bid/tid on day 2 or 3 to 300-400 mg divided bid/tid by day 4; adjust prn at intervals of at least q2d with adjustments of 25-50 mg bid
Maintenance: 150-750 mg/d PO; not to exceed 800 mg/d
Not established
May antagonize levodopa and dopamine agonists; phenytoin, thioridazine, and other liver enzyme inducers may reduce levels; CYP450 3A inhibitors (eg, ketoconazole, fluconazole, erythromycin) increase serum concentration
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
May induce orthostatic hypotension associated with dizziness, tachycardia, and syncope; neuroleptic malignant syndrome and tardive dyskinesia have been associated with this treatment
Antagonizes dopamine D2, D3, 5-HT2A, 5-HT2C, 5-HT1A, 5-HT1D, alpha1-adrenergic. Has moderate antagonistic effect for histamine H1. Moderately inhibits reuptake of serotonin and norepinephrine.
20 mg PO bid initially; may increase q2-3d to 80 mg PO bid; not to exceed 160 mg/d
Alternative: 10-20 mg IM for rapid tranquilization, as required, to maximum 40 mg/d; 10 mg may be administered q2h; 20 mg may be administered q4h to maximum 40 mg/d; IM administration for > 3 d not studied; if long-term therapy indicated, replace IM with PO as soon as possible
Not established
CYP450-3A4 inhibitors (eg, erythromycin, ketoconazole) may increase serum levels; CYP450-3A4 inducers (eg, carbamazepine, rifampin) may decrease serum levels; coadministration with drugs that increase QT/QTc interval (eg, amiodarone, fluoroquinolones) increases risk of life-threatening arrhythmias; amphetamines may decrease efficacy of ziprasidone; ziprasidone may decrease efficacy of levodopa
Documented hypersensitivity; history of prolonged QT
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Prolongs QT/QTc (caution in patients with known risk factors eg, hypomagnesemia, hypokalemia); caution in seizure disorders; may cause hypotension, extrapyramidal symptoms, and somnolence; hyperglycemia may occur and in some cases be extreme, resulting in ketoacidosis, hyperosmolar coma, or death
Improves positive and negative schizophrenic symptoms. Mechanism of action unknown, but hypothesized to differ from that of other antipsychotics. Aripiprazole thought to be partial dopamine (D2) and serotonin (5HT1A) agonist, and antagonizes serotonin (5HT2A). No QTc-interval prolongation noted in clinical trials.
10-15 mg PO qd; if needed, may increase dose gradually q2wk, not to exceed 30 mg/d
Not established
CYP450 3A4 and 2D6 isoenzyme substrate; therefore, inhibitors (ie, ketoconazole, quinidine, fluoxetine, paroxetine) or inducers (ie, carbamazepine) may increase or decrease serum levels, respectively
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Common adverse effects include headache, anxiety, somnolence, or insomnia; rare reports of tardive dyskinesia and neuroleptic malignant syndrome; may cause orthostatic hypotension, seizure, dysphagia, or suicidal ideation; hyperglycemia may occur and in some cases be extreme, resulting in ketoacidosis, hyperosmolar coma, or death
Atypical antipsychotic agent indicated for acute treatment of schizophrenia. Precise mechanism of action unknown. Antagonizes receptors for dopamine-2 and serotonin type 2 (5-HT2).
1 mg PO bid initially on day 1; to reach target dose of 12-24 mg/d, adjust dose daily by smallest possible increments (ie, 2 mg bid on day 2; 4 mg bid on day 3; 6 mg bid on day 4) to avoid orthostatic hypotension
<18 years: Not established
CYP3A4 and CYP2D6 substrate; CYP3A4 inhibitors (eg, ketoconazole) or CYP2D6 inhibitors (eg, fluoxetine, paroxetine) may inhibit elimination and increase blood levels; do not use with other drugs that prolong QT interval (eg, class 1A antiarrhythmics [quinidine, procainamide], class III antiarrhythmics [amiodarone, sotalol], antipsychotics [chlorpromazine, thioridazine], antibiotics [moxifloxacin, erythromycin]); additive CNS effects may occur when coadministered with other centrally acting drugs or alcohol
Documented hypersensitivity; coadministration with other drugs that prolong QT interval
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Boxed warning: Increased risk of TIAs, CVA, and death with off-label use to treat dementia-related psychosis in elderly individuals
Common dose-related adverse effects include dizziness, xerostomia, fatigue, nasal congestion, orthostatic hypotension and syncope, tachycardia, and weight gain; serious adverse effects include QT interval prolongation, neuroleptic malignant syndrome, tardive dyskinesia, hyperglycemia, seizures, leukopenia, neutropenia, agranulocytosis, hyperprolactinemia, disruption of body temperature, and dysphagia; avoid with hepatic impairment
These agents decrease aggression and treat the underlying illness.
Selective serotonin reuptake inhibitors (SSRIs) are greatly preferred over the other classes of antidepressants. Because the adverse-effect profile of SSRIs is less prominent than the profiles of other drugs, improved compliance is promoted. SSRIs do not have the cardiac arrhythmia risk associated with tricyclic antidepressants. Arrhythmia risk is especially pertinent in overdose, and suicide risk must always be considered when one treats a child or adolescent with a mood disorder.
Physicians are advised to be aware of the following information and to use appropriate caution when they consider treatment with SSRIs in the pediatric population.
In December 2003, the UK Medicines and Healthcare Products Regulatory Agency (MHRA) issued an advisory that most SSRIs are not suitable for use by persons younger than 18 years for treatment of depressive illness. After review, this agency decided that the risks to pediatric patients outweigh the benefits of treatment with SSRIs, except fluoxetine (Prozac), which appears to have a positive risk-benefit ratio in the treatment of depressive illness in patients younger than 18 years.
In October 2003, the US Food and Drug Administration (FDA) issued a public health advisory regarding reports of suicidality in pediatric patients being treated with antidepressant medications for major depressive disorder. This advisory reported suicidality (both ideation and attempts) in clinical trials of various antidepressant drugs in pediatric patients. The FDA has asked that additional studies be performed because suicidality occurred in both treated and untreated patients with major depression and thus could not be definitively linked to drug treatment.
SSRI to treat impulse-control problems or underlying illness. Selectively inhibits presynaptic serotonin reuptake with minimal or no effect in reuptake of norepinephrine or dopamine.
10-80 mg PO qd
<18 years: Not established; suggested initial dose for 6-14 y is 20 mg/d PO
Increases toxicity of diazepam and trazodone by decreasing clearance; also increases toxicity of MAOIs and highly bound protein drugs
Documented hypersensitivity; concurrently taking MAOIs or took them in the last 2 wk
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in hepatic impairment and history of seizures; discontinue MAOIs at least 14 d before initiating therapy
These drugs stabilize mood associated with bipolar disorder.
May increase brain GABA levels by inhibiting aminobutyrate aminotransferase. GABA inhibits presynaptic and postsynaptic discharges. In addition to use as mood stabilizer, also used for migraine headaches, epilepsy, and mania.
750 mg/d PO in divided doses; target plasma levels are 50-125 mcg/mL; not to exceed 60 mg/kg/d
Initial dose: 10-15 mg/kg/d PO, not to exceed 60 mg/kg/d; if total exceeds 250 mg, should be given in divided dosages
<2 years: Increased risk for fatal hepatotoxicity
>2 years: Benefits outweigh risk but risk of hepatotoxicity decreases considerably
Coadministration with cimetidine, salicylates, felbamate, and erythromycin may increase toxicity; rifampin may significantly reduce levels; in pediatric patients, protein binding and metabolism decrease with concomitant salicylates; coadministration with carbamazepine variably change carbamazepine concentrations with possible loss of seizure control; may increase diazepam and ethosuximide toxicity (monitor closely); may increase phenobarbital and phenytoin levels, while either one may decrease valproate levels; may displace warfarin from protein-binding sites (monitor coagulation tests); may increase zidovudine levels in HIV-positive patients
Documented hypersensitivity; hepatic disease; significant disfunction
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Thrombocytopenia and abnormal coagulation parameters have occurred; risk of thrombocytopenia increases significantly at total trough valproate plasma concentrations >110 mcg/mL in females and 135 mcg/mL in males; periodically and before surgery, determine platelet counts and bleeding time before start of therapy; reduce dose or discontinue therapy if hemorrhage, bruising, or a hemostasis and/or coagulation disorder occurs; hyperammonemia may occur, resulting in hepatotoxicity; closely monitor patients for appearance of malaise, weakness, facial edema, anorexia, jaundice, and vomiting; may cause drowsiness
Pharmacologic activity primarily from 10-monohydroxy metabolite (MHD) of oxcarbazepine. May block voltage-sensitive sodium channels, inhibit repetitive neuronal firing, and impair synaptic impulse propagation. Anticonvulsant effect may also occur by affecting potassium conductance and high-voltage activated calcium channels. Drug pharmacokinetics similar in children > 8 y and adults. Children <8 y have a 30-40% increased clearance compared with older children and adults. Use in children <2 y not studied in controlled trials.
Adjunctive therapy: 600 mg/d PO divided bid initially; may increase by maximum of 600 mg/d qwk; recommended dose is 1200 mg/d; monitor patients for anticonvulsant adverse effects
Conversion to monotherapy: 600 mg/d PO divided bid initially; gradually reduce dose of concomitant anticonvulsants in about 3-6 wk and gradually increase oxcarbazepine dose in 2-4 wk; may increase oxcarbazepine dose prn by a maximum of 600 mg/d qwk; closely monitor patients during transition phase for anticonvulsant adverse effects
Start of monotherapy: 600 mg/d PO divided bid initially; increase by 300 mg/d PO q3d to 1200 mg/d; monitor patients for anticonvulsant adverse effects
<4 years: Not established
4-16 years:
Adjunctive therapy: 8-10 mg/kg/d PO divided bid initially, not to exceed 600 mg/d; gradually increase to target dose over 2 wk; target adjunctive dose based on body weight, as follows<20 kg: Not established
20-29 kg: 900 mg/d
29-39 kg: 1200 mg/d
>39 kg: 1800 mg/d
Conversion to monotherapy: 8-10 mg/kg/d PO divided bid initially; gradually reduce dose of concomitant anticonvulsants over 3-6 wk; may gradually increase oxcarbazepine dose if clinically indicated by increments not to exceed 10 mg/kg/d qwk to recommended monotherapy dose; closely monitor patients during transition phase for anticonvulsant adverse effects
Monotherapy: 8-10 mg/kg/d PO divided bid; may increase by 5 mg/kg/d q3d to recommended daily dose
Maintenance monotherapy dose is based on body weight as follows:<20 kg: Not established
20-24 kg: 600-900 mg/kg/d
25-34 kg: 900-1200 mg/kg/d
35-44 kg: 900-1500 mg/kg/d
45-49 kg: 1200-1500 mg/kg/d
50-59 kg: 1200-1800 mg/kg/d
60-69 kg: 1200-2100 mg/kg/d
>70 kg: 1500-2100 mg/kg/d
May decrease levels of dihydropyridine calcium antagonists and oral contraceptives; can reduce serum concentrations of carbamazepine, phenobarbital, phenytoin and valproic acid; doses >1200 mg/d may increase phenytoin and phenobarbital serum concentrations significantly; can reduce serum concentrations of oral contraceptives and make them ineffective; can increase clearance of felodipine
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Can cause cognitive adverse effects (eg, psychomotor slowing, impaired concentration, impaired speech, impaired language); decrease initiation dose by 50% with renal impairment (CrCl <30 mL/min) and increase dose slowly; can cause hyponatremia (sodium <125 mmol/L); 25-30% of persons with hypersensitivity to carbamazepine have hypersensitivity to oxcarbazepine; rapid withdrawal can exacerbate seizures; observe for adverse effects and monitor plasma levels of concomitant anticonvulsants during titration
Indicated to treat bipolar disorder. Specific mechanism of action unknown but alters sodium transport in nerve and muscle cells and influences reuptake of serotonin and/or norepinephrine at cell membranes.
300 mg PO tid/qid
<6 years: Not established
6-12 years: 15-60 mg/kg/d PO tid/qid; not to exceed usual adult dose
>12 years: Administer as in adults
Thiazide diuretics increase toxicity of lithium, haloperidol, phenothiazines, neuromuscular blockers, carbamazepine, fluoxetine, and ACE inhibitors
Documented hypersensitivity; severe cardiovascular disease
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Lithium toxicity (ie, diarrhea, vomiting, tremor, ataxia, drowsiness, muscle weakness) closely related to serum levels and can occur at therapeutic doses; serum lithium determinations required to monitor therapy
Indicated to treat epilepsy and trigeminal neuralgia. Research and clinical experience indicate effectiveness in treating manic subtype schizoaffective disorder.
200-600 mg PO bid; 800-1200 mg/d maintenance
<6 years: 10-20 mg/kg/d PO bid; <35 mg/kg/d maintenance
6-12 years: 100 mg PO bid; 400-800 mg/d maintenance
>12 years: Administer as in adults
Serum levels may increase significantly within 30 d of danazol coadministration (avoid whenever possible); do not coadminister with MAOIs; cimetidine may increase toxicity, especially if taken in the first 4 wk of therapy; may decrease primidone and phenobarbital levels (coadministration may increase levels)
Documented hypersensitivity; history of bone marrow depression; administration of MAOIs within 14 d
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Caution with elevated intraocular pressure, mixed seizure disorders, cardiac problems, renal problems, liver problems, or hematological problems; obtain CBCs and serum iron (before treatment, at 2 mo, and every other year); can cause anemia, drowsiness, dizziness, blurred vision
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mental illness, psychosis, mental disorder, hallucinations, delusions, schizophrenia, depression, mania, manic depressive, manic subtype, major depressive disorder, viral infection, malnutrition, birth complications, mood disorder, distorted thinking, bipolar disorder, antisocial personality traits, psychotherapy
Guy E Brannon, MD, Associate Clinical Professor of Psychiatry, Louisiana State University Health Sciences Center; Director, Adult Psychiatry Unit, Chemical Dependency Unit, Clinical Research, Brentwood Behavior Health Company
Guy E Brannon, MD is a member of the following medical societies: American Medical Association, American Medical Writers Association, American Psychiatric Association, American Society of Addiction Medicine, Association of Clinical Research Professionals, Louisiana State Medical Society, and Southern Medical Association
Disclosure: AstraZeneca Honoraria Speaking and teaching; Takeda Honoraria Speaking and teaching; Wyeth Honoraria Speaking and teaching; Janssen Honoraria Speaking and teaching; Pfizer Honoraria Speaking and teaching
Ronald C Albucher, MD, Chief Medical Officer, Westside Community Services; Consulting Staff, California Pacific Medical Center
Ronald C Albucher, MD is a member of the following medical societies: American Psychiatric Association
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.
David Bienenfeld, MD, Vice-Chair, Program Director, Professor, Department of Psychiatry, Wright State University School of Medicine
David Bienenfeld, MD is a member of the following medical societies: American Medical Association, American Psychiatric Association, and Association for Academic Psychiatry
Disclosure: Nothing to disclose.
Harold H Harsch, MD, Program Director of Geropsychiatry, Department of Geriatrics/Gerontology, Associate Professor, Department of Psychiatry and Department of Medicine, Froedtert Hospital, Medical College of Wisconsin
Harold H Harsch, MD is a member of the following medical societies: American Psychiatric Association
Disclosure: lilly Honoraria Speaking and teaching; Forest Labs Honoraria Speaking and teaching; AstraZeneca Honoraria Speaking and teaching; Pfizer Grant/research funds Speaking and teaching; Northstar Grant/research funds Research; Novartis Grant/research funds research; Pfizer Speaking and teaching; Sanofi-avetis Grant/research funds research; Otsuke Grant/research funds reseach; GlaxoSmithKline Grant/research funds research
Stephen Soreff, MD, President of Education Initiatives, Nottingham, NH; Faculty, Metropolitan College of Boston University, Boston, MA
Stephen Soreff, MD is a member of the following medical societies: American College of Mental Health Administration and American Psychosomatic Society
Disclosure: Nothing to disclose.
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