Schizophreniform disorder Background

Schizophreniform disorder is a serious mental disorder with symptoms similar to those of schizophrenia. Early diagnosis of this disorder is crucial, as is early intervention with medication, supportive therapy, and patient and family education.

Schizophreniform disorder is characterized by the presence of the criterion A symptoms of schizophrenia, including delusions, hallucinations, disorganized speech, disorganized or catatonic behavior, and negative symptoms. The disorder, including its prodromal, active, and residual phases, lasts longer than 1 month but less than 6 months.

Unlike schizophrenia, in which prodromal symptoms may develop over several years, schizophreniform disorder requires, among other features, a rather rapid period from the onset of prodromal symptoms to the point at which all criteria for schizophrenia (except duration and deterioration) are met (within 6 mo).

As with schizophrenia, the prevalence of schizophreniform disorder is equally distributed between the sexes, with peak onset between the ages of 18-24 years in men and ages 24-35 years in women.

Go to Schizoaffective Disorder, Emergent Treatment of Schizophrenia, and Childhood-Onset Schizophrenia for complete information on these topics. Pathophysiology

Patients with schizophreniform disorder and patients with schizophrenia share many anatomic and functional cortical deficits on neuropsychological studies, magnetic resonance imaging (MRI), singlephoton emission computed tomography (SPECT), and positron emission tomography (PET).

A study of delay-dependent memory performed by Mathes et al found that patients with schizophreniform disorder and schizophrenia demonstrated a decreased ability to form an internal representation of complex objects.[1] Such neuropsychological tests help clinicians to further understand the psychopathology of the disorder.

This study investigated 55 patients with schizophreniform psychosis, 50 patients with established schizophrenia, and a control group of 56 healthy controls, using the delayed matching-to-sample task from the Cambridge Neuropsychological Test Automated Battery (CANTAB). Performance deficits were found in both patient groups after controlling for age and premorbid intelligence quotient (IQ).

Even when simultaneous matching-to-sample ability (ie, perceptual matching) was controlled for, impaired performance in both patient groups was found as soon as the stimuli were removed. Impaired performance was not due to different types of performance errors in patients as compared with control individuals. Performance in the 2 patient groups was comparable, except for a slight decrease in overall task performance. These findings suggest that the deficit is relatively stable during the course of the illness.

Similar deficits notwithstanding, schizophreniform disorder is distinct from schizophrenia, as confirmed by a trial by Sautter et al that compared the course of illness of 36 patients who received a diagnosis of schizophreniform disorder or schizophrenia.[2] Approximately 3.5 and 4 years after their initial index hospitalization, 2 groups of patients were compared for differences in positive and negative symptoms of psychosis, interpersonal and occupational role functioning, and other aspects of the deficit state.

The patients with schizophreniform disorder showed a low level of negative symptoms at both follow-up examinations. The patients with schizophrenia initially showed a higher level of negative symptoms, but these symptoms decreased significantly over time. Data from this trial indicate that the course of schizophreniform disorder is distinct from the course of schizophrenia. Prognosis

The persistence of symptoms beyond 6 months predicts a worse prognosis for schizophrenia as compared with schizophreniform disorder. Clarke and associates demonstrated that [a] longer duration of untreated psychosis was associated with a significantly poorer functional and symptomatic outcome 4 years later.[3]

Confusion and perplexity at the height of the psychotic episode in schizophreniform disorder correlates with better outcome. A significant risk of suicide exists in patients with schizophreniform disorder, especially when they are more likely to go into a depression after the psychotic period. Psychotherapy during this phase, aimed at helping patients understand the psychotic episodes, is likely to improve the prognosis and recovery. Drake et al found that patients ending up with better insight into their illness were less likely to experience relapse.[4]

Fraguas et al examined the diagnostic stability and the functional outcome of patients with earlyonset psychosis, including schizophreniform disorder, over a 2-year follow-up period; they found a 50% predictability for future psychotic episodes for schizophreniform disorder and the presence of negative symptoms as a predictor of lower level of functioning at the end of 2 years.[5]

According to the American Psychiatric Association, approximately two thirds of patients diagnosed with schizophreniform disorder progress to a diagnosis of schizophrenia. According to Benazzi et al, patients with a good prognosis tend to be retrospectively associated with the affective spectrum of diagnoses rather than the schizophrenic.[6]

According to Troisi et al, in some patients with a schizophreniform disorder, the presence of negative symptoms and poor eye contact appear to be prognostic of a poor outcome.[7] Studies have not yet elicited a consensus about whether ventricular enlargement is predictive of poor outcome in patients with a schizophreniform disorder. Patient Education

Efforts should be made to educate both the patients and their families about the early signs of relapse and the need for continuing treatment. Those approaches advance the overall aim of helping patients regain productive roles in society while reducing the risk of relapse. Families with a high degree of emotional expression are likely to cause additional stress to the patient and to increase the likelihood of relapse.

The patients condition, the patients family, and the patients system of care are a few of the many factors that likely affect treatment engagement early in the course of schizophreniform disorder and schizophrenia. Clinicians should give special attention to these factors when caring for patients who experience their first episode. History

A detailed history (which may require the assistance of family members or others familiar with the patient) should be obtained, focusing on the following: Time of symptom onset Course Premorbid functioning

Precipitants Physical health Use of medications Use of alcohol and other substances Family history Previous episodes (if any)

Distinguishing schizophreniform disorder from other medical and psychiatric conditions that may present in a floridly psychotic state can be challenging. Such conditions include schizophrenia; brief psychotic disorder; substance-induced mood disorders, depression, and mania; bipolar affective disorder; and depression.

The symptom profile of a schizophreniform disorder is identical to that of schizophrenia; however, the total duration of illness, including prodromal or residual phases, must be less than 6 months. Also, a deterioration in social or vocational functioning, required as part of criterion B to make the diagnosis of schizophrenia (see Differentials), is not required for schizophreniform disorder.

A diagnosis of brief psychotic disorder requires that symptoms last 1 day to 1 month. A diagnosis of schizophreniform disorder, like a diagnosis of schizophrenia, requires that symptoms be present for at least 1 month.

Although substance-induced psychoses frequently resolve in less than 1 month, sustained substance-induced psychoses in abstinent persons may be indistinguishable from schizophreniform disorder. In the absence of objective diagnostic criteria, the distinction is made on the basis of the extent to which the clinician believes substances have contributed to the current symptom profile.

In bipolar disorder and major depression with mood-incongruent features, the affective symptoms are clearly more prominent. In mood disorder, the psychotic symptoms are secondary and less intense if present. Sometimes, in the absence of an accurate history, diagnosis must be deferred until longitudinal observation or a more accurate history is available. Diagnostic Considerations

To establish the diagnosis of schizophreniform disorder, according to the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR),[8] at least 2 of the following signs must be present, each for a significant length of time during a 1-month period (or less, if successfully treated): Delusions/hallucinations Disorganized speech (eg, frequent derailment, incoherence) Grossly disorganized or catatonic negative behavior symptoms (eg, affective flattening, alogia, or avolition)

Only 1 criterion A symptom is required if delusions are bizarre, if hallucinations consist of a voice that is keeping up a running commentary on the persons behavior or thoughts, or if 2 or more voices are conversing with each other.

Schizoaffective disorder and mood disorder with psychotic features must be excluded, based on determining that (1) no major depressive, manic, or mixed episodes have occurred concurrently with the active-phase symptoms or (2) if mood episodes have occurred during active-phase symptoms, their total duration has been brief relative to the duration of the active and residual periods.

The disturbance must not be the result of the direct physiologic effects of a substance (eg, a drug of abuse or a medication) or a general medical condition.

An episode of the disorder (including prodromal, active, and residual phases) must last at least 1 month but less than 6 months. If the diagnosis must be made without waiting for recovery, it should be qualified as provisional.

Specify if the patient is without good prognostic features, defined as 2 or more of the following: Onset of prominent psychotic symptoms within 4 weeks of the first noticeable change in usual behavior or functioning Perplexity and thought disorganization at the height of the psychotic episode Good premorbid social and occupational functioning Absence of blunted or flat affect Approach Considerations

The often abrupt onset of symptoms, in many cases coupled with the lack of previous episodes, underscores the need for a toxicologic and medical evaluation.

A full Mental Status Examination helps to establish the diagnosis. Mental status is likely to manifest as a neutral or blunted mood and affect. Evidence of paranoia, ideas of reference, delusions, and hallucinations are usually present. The patient is usually fully oriented with intact memory. A strong possibility of homicidal and even suicidal ideation exists.

Attempt to elicit command hallucinations because these could drive a patient to hurt themselves and others. Disorientation and difficulties with recall suggest an organic psychosis rather than a schizophreniform disorder.

Laboratory tests, including electrolytes, drug screen, and thyroid studies, also help in establishing the diagnosis. Case example

The patient is a 15-year-old girl. Two months ago, she started accusing her mother of taking her things. Gradually, she started keeping to herself more and more. She began smiling to herself and mumbling. She continued to attend school, and until recently, her teacher did not notice the patients problems. The patient subsequently became unable to respond to the teachers instructions because she was completely preoccupied by internal stimuli. The school referred the patient to me.

She sat calmly and made little eye contact. When I looked at her, she looked away, smiled blandly, and mumbled, I am not going to tell you. When I gently pressed her, she told me that she heard God talking to her and that she also heard Gods enemy sometimes. She refused to elaborate, saying it was a secret.

Her mood was neutral, and her affect was inappropriate at times. She was alert and fully oriented. She could recall 3 of 3 items in 5 minutes; memory was intact. She was very guarded, and no delusions were elicited. She denied any suicidal or homicidal ideation. She did not exhibit any abnormal movements and tics. She was attentive and followed 3-step commands. Her general fund of knowledge was average, and she appeared to have average intellect. Her insight and judgment were poor. Her sleep had been reduced, and her appetite was fair.

She did not have any physical problems and did not exhibit any signs or symptoms of depression or of elations or euphoria. She did not take any drugs or alcohol and did not have evidence of trauma. Electrolytes, thyroid profile, and drug screen findings were unremarkable. Approach Considerations

Treatment may involve psychotherapy, family and social-educational therapies, and pharmacotherapy. In general, treatment aims to protect and stabilize the patient, to minimize the psychosocial consequences, and to resolve the target symptoms with minimal adverse effects. The patient who may be at risk of harming himself or herself or others requires hospitalization. This allows for complete diagnostic evaluation and helps to ensure the safety of the patient and others. A supportive environment with minimal stimulation is most helpful.

As improvement progresses, help with coping skills, problem-solving techniques, and psychoeducational approaches may be added for patients and their families. Patients may benefit from a structured intermediate environment, such as a day hospital, during the initial phases of returning to the community.

According to Stromgren, electroconvulsive therapy has been helpful in treating brief reactive psychoses but is generally reserved for medication-resistant cases of schizophreniform disorder.[9]

Compton described barriers to treatment after the first episode of psychosis, including inadequate remission of paranoia, impaired insight, and involvement with the criminal justice system between the patients discharge from the hospital and the patients first outpatient appointment.[10] Strong family support appeared to be an important facilitator of treatment engagement during the first several months of outpatient treatment. Various other potential barriers to treatment, such as involuntary status at the time of hospital discharge, are also considered. Psychotherapy

Virtually all psychotherapeutic treatment modalities used in the treatment of patients with schizophrenia may be helpful in treating patients with schizophreniform disorder. Insight-oriented therapy is not indicated in patients with schizophreniform disorder, because they have limited ability to explore and may also be in denial.

Patients may experience a high degree of distress related to the onset of symptoms. Both supportive and educational approaches may help patients manage feelings of turmoil or distress. Group psychotherapy may be helpful; however, patients with schizophreniform disorder who are

concerned about their prognosis may become frightened in groups where they are mixed with patients who have chronic schizophrenia. Thus, care must be taken when forming therapy groups. Family and Social-Vocational Therapies

Treatment of patients with schizophreniform disorder frequently involves working with family members and significant others. The family therapy strategies used in working with the families of patients with schizophrenia are highly appropriate for patients with schizophreniform disorder and their families.

In light of the variable course of schizophreniform disorder, brief treatment strategies with clear goals may initially be helpful, though treatment strategies must remain flexible to allow for the transition to longer-term treatments for patients who progress to schizophrenia. Similarly, socialvocational function may be preserved in patients with schizophreniform disorder. However, in patients exhibiting impairments in these areas, rehabilitative strategies similar to those described for patients with schizophrenia are appropriate. Pharmacotherapy

Pharmacotherapy for schizophreniform disorder is similar to that for schizophrenia.[11] At this time, atypical antipsychotics, such as risperidone, olanzapine, quetiapine, and ziprasidone, are commonly used. Dosing strategies appear to be similar to recent approaches to treating patients with schizophrenia, which emphasize the use of minimal but effective doses.

Adequate treatment or prophylaxis of adverse extrapyramidal effects is critical to patient tolerance of neuroleptic treatment and to medication therapy compliance. Neuroleptic-resistant psychosis in patients with schizophreniform disorder may be managed through approaches similar to those used in patients with schizophrenia, including adjustment of the neuroleptic dose, addition of lithium, or addition of anticonvulsant agents and older typical antipsychotics.

Antidepressants may be helpful for mood disturbances associated with schizophreniform disorder, but care must be taken to monitor for possible exacerbations of psychotic symptoms.

In November 2003, aripiprazole (Abilify) was approved by the US Food and Drug Administration (FDA). Aripiprazole has a novel mechanism of action because it is a partial agonist at the dopamine receptors, unlike its predecessors.

Paliperidone (Invega) was FDA approved in 2006. It is a major active metabolite of risperidone and the first oral agent allowing once-daily dosing. Ziprasidone (Geodon) is available in injection form to help control acute psychosis; aripiprazole is also now available as an injection. These injections are less likely to cause acute extrapyramidal side effects.

Iloperidone (Fanapt), an atypical antipsychotic, was approved in 2009 for acute treatment of schizophrenia in adults. The initial dose is 1 mg PO bid on day 1 and is titrated upward daily to reach target dose of 12-24 mg/d by day 7 (orthostatic hypotension is the dose-limiting adverse effect).

Sajatovic et al concluded in one study that both risperidone and quetiapine improved scores on the Hamilton Depression Rating Scale (HAMD), although quetiapine demonstrated greater improvement than risperidone in all patients.[12]

Emsley, in an international, multicenter, double-blind study conducted on 183 patients who had a first psychotic episode (ie, provisional schizophreniform disorder or schizophrenia) and who were treated with flexible doses of risperidone or haloperidol for 6 weeks, found that 63% of patients treated with risperidone and 56% of those treated with haloperidol were clinically improved (350% reduction in Positive and Negative Syndrome Scale [PANSS] total scores).[13] Risperidone was tolerated better than haloperidol.

Emsley stated that a post-hoc analysis revealed that low doses of these antipsychotics were efficacious in some patients. Other findings from this research also suggest that patients with a first psychotic episode may require low doses of antipsychotic medications. Studies specifically designed to compare low and high doses of antipsychotics are warranted to help optimize treatment for these patients.

Sanger et al, in a study examining patients with first-episode psychosis to determine the efficacy and safety of olanzapine and haloperidol treatment, found that in patients who experience first-episode psychosis, olanzapine had a risk-benefit profile significantly superior to that of haloperidol and concluded that novel antipsychotic agents (eg, olanzapine) should be considered a preferred option in managing first-episode psychosis because of safety and efficacy advantages.[14]

This clinical trial involved a subpopulation of first-episode patients selected from a pool of patients who were diagnosed with schizophrenia, schizoaffective disorder, or schizophreniform disorder. The duration of the patients current psychotic episodes had to be 5 years or less, and the patients had to be aged 45 years or younger at the onset of their first psychotic symptoms.

Medication Summary

Several medications are used to treat schizophreniform 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, aripiprazole, or ziprasidone) 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 schizophreniform disorder, a few are reviewed below. Antipsychotics Class Summary

Antipsychotic agents ameliorate psychosis and aggressive behavior. View full drug information Haloperidol

Haloperidol is used for management of psychosis, as well as motor and vocal tics in children and adults. The mechanism of action not clearly established, but the drug has a selective effect on the central nervous system (CNS) by competitively blocking postsynaptic dopamine (D2) receptors in the mesolimbic dopaminergic system; increases in dopamine turnover are responsible for the tranquilizing effect. With subchronic therapy, depolarization blockade and D2 postsynaptic blockade are responsible for antipsychotic action. View full drug information Risperidone (Risperdal, Risperdal Consta)

Risperidone is a selective monoaminergic antagonist that binds to dopamine D2 receptors with a 20 times lower affinity than it binds to serotonin type 2 (5-HT2) receptors. It also binds to alpha1adrenergic receptors with lower affinity to H1-histaminergic and alpha2-adrenergic receptors. It improves negative symptoms of psychosis and decreases occurrence of extrapyramidal effects.

Risperidone is also available in a long-acting intramuscular (IM) formulation (Risperdal Consta). View full drug information Olanzapine (Zyprexa)

Olanzapine is an atypical antipsychotic with a broad pharmacologic profile across receptor systems (eg, serotonin, dopamine, cholinergic muscarinic, alpha-adrenergic, histamine). Its antipsychotic effect is from antagonism of dopamine and serotonin type 2 receptors. It is indicated for treatment of psychosis and bipolar disorder. View full drug information Clozapine (Clozaril, FazaClo)

Clozapine has a weak affinity for D1, D2, D3, and D5 receptors, and a high affinity for the D4 receptor. It also acts as an antagonist at adrenergic, cholinergic, histaminergic, and serotonergic receptors. However, it does not induce catalepsy, nor does it inhibit apomorphine-induced stereotypy. The risk of agranulocytosis limits the use of clozapine to patients who are nonresponsive to or intolerant of classic neuroleptic agents. View full drug information Quetiapine (Seroquel)

Quetiapine is a newer antipsychotic for long-term management. It may antagonize dopamine and serotonin effects. Improvements over earlier antipsychotics include fewer anticholinergic effects and less dystonia, parkinsonism, and tardive dyskinesia. View full drug information Ziprasidone (Geodon)

Ziprasidone antagonizes D2, D3, 5-HT2A, 5-HT2C, 5-HT1A, 5-HT1D, and alpha1-adrenergic receptors. It has a moderate antagonistic effect for histamine H1. It moderately inhibits reuptake of serotonin and norepinephrine. View full drug information Aripiprazole (Abilify)

Aripiprazole improves positive and negative schizophrenic symptoms. Its mechanism of action is unknown but is hypothesized to differ from that of other antipsychotics. Aripiprazole is thought to be a partial D2 and 5-HT1A) agonist and antagonizes 5-HT2A. No QTc-interval prolongation is noted in clinical trials. View full drug information Iloperidone (Fanapt)

Iloperidone is an atypical antipsychotic agent that is indicated for acute treatment of schizophrenia. Its precise mechanism of action is unknown. It antagonizes D2 and 5-HT2 receptors. View full drug information Paliperidone (Invega)

It is the active metabolite of risperidone with the therapeutic effects consisting of mixed central serotonergic and dopaminergic antagonism. View full drug information Lurasidone (Latuda)

Lurasidone is an atypical antipsychotic, and its precise mechanism action is unknown. Its suggested efficacy is thought to be due to mediation of central dopamine type-2 and serotonin type-2 (5HT-2A) receptor antagonism. View full drug information Asenapine maleate (Saphris)

The mechanism of action of asenapine maleate is unknown. Its efficacy is thought to be mediated via combined antagonist activity at dopamine-2 and serotonin (5-HT2) receptors. It is indicated for acute treatment and maintenance therapy of schizophrenia. Antidepressants Class Summary

Antidepressant 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 profiles of SSRIs are less prominent than the profiles of other drugs, improved compliance is promoted. SSRIs do not have the cardiac dysrhythmia risk associated with tricyclic antidepressants. Dysrhythmia 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 in the case of 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 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. View full drug information Fluoxetine (Prozac)

Fluoxetine is an SSRI used to treat impulse-control problems or underlying illness. It selectively inhibits presynaptic serotonin reuptake with minimal or no effect in reuptake of norepinephrine or dopamine. View full drug information Sertraline (Zoloft)

Sertraline is an SSRI used to treat impulse-control problems or underlying illness. It selectively inhibits presynaptic serotonin reuptake, with minimal or no effect in reuptake of norepinephrine or dopamine. View full drug information Paroxetine (Paxil)

Paroxetine is a potent selective inhibitor of neuronal serotonin reuptake. It also has a weak effect on norepinephrine and dopamine neuronal reuptake.

For maintenance dosing, make dosage adjustments to maintain patient on lowest effective dosage, and reassess patient periodically to determine need for continued treatment. View full drug information Fluvoxamine (Luvox)

Fluvoxamine enhances serotonin activity due to selective reuptake inhibition at the neuronal membrane. It does not significantly bind to alpha-adrenergic, histamine, or cholinergic receptors and thus has fewer adverse effects than tricyclic antidepressants.

It has been shown to reduce repetitive thoughts, maladaptive behaviors, and aggression and to increase social relatedness and language use. View full drug information Citalopram (Celexa)

Citalopram enhances serotonin activity due to selective reuptake inhibition at the neuronal membrane. No head-to-head comparisons of SSRIs exist, although, based on metabolism and adverse effects, citalopram is considered the SSRI of choice for patients with head injury.

SSRIs are the antidepressants of choice owing to their minimal anticholinergic effects. View full drug information Escitalopram (Lexapro)

Escitalopram is an SSRI and S-enantiomer of citalopram. It is used for the treatment of depression. Its mechanism of action is thought to be potentiation of serotonergic activity in the CNS, resulting from inhibition of CNS neuronal reuptake of serotonin. The onset of depression relief may be obtained after 1-2 weeks, which is sooner than other antidepressants. Mood Stabilizers Class Summary

Mood stabilizers stabilize the mood imbalance associated with bipolar disorder. View full drug information Valproic acid, divalproex sodium (Depakote, Depakene, Depacon, Stavzor)

Valproic acid may increase brain gamma-aminobutyric acid (GABA) levels by inhibiting aminobutyrate aminotransferase. GABA inhibits presynaptic and postsynaptic discharges. In addition to its use as mood stabilizer, valproic acid is also used for migraine headaches, epilepsy, and mania. View full drug information Oxcarbazepine (Trileptal)

Oxcarbazepine's pharmacologic activity is primarily from its 10-monohydroxy metabolite (MHD). It may block voltage-sensitive sodium channels, inhibit repetitive neuronal firing, and impair synaptic impulse propagation. Its anticonvulsant effect may also occur by affecting potassium conductance and high-voltage activated calcium channels.

Drug pharmacokinetics are similar in children older than 8 years and adults. Children younger than 8 years have a 30-40% increased clearance compared with older children and adults. Use of oxcarbazepine in children younger than 2 years has not been studied in controlled trials. View full drug information Lithium (Lithobid)

Lithium is indicated to treat bipolar disorder. The specific mechanism of action unknown, but the drug alters sodium transport in nerve and muscle cells and influences reuptake of serotonin, norepinephrine, or both at cell membranes. View full drug information Carbamazepine (Tegretol, Carbatrol, Epitol, Equetro)

Carbamazepine is indicated to treat epilepsy and trigeminal neuralgia. Research and clinical experience indicate that it is effective in treating manic subtype schizoaffective disorder.