Schizoaffective Disorder

What Causes Schizoaffective Disorder?

The exact cause of schizoaffective disorder is unknown. Like schizophrenia, it’s likely caused by a combination of factors, including genetics, chemical interactions in the brain, and external environmental situations or events.

People with a family history of SAD or schizophrenia are more likely to develop the disorder. In addition, the brains of people with schizophrenia and related disorders have been shown through imaging studies to function differently from healthy brains. These findings suggest that the condition has a genetic component and involves physical dysfunction in the brain. However, the precise mechanism by which these factors come together to produce schizophrenia or SAD has not yet been discovered.

Other possible risk factors for SAD may include:

• Stress or trauma. Some studies have suggested that people exposed to abuse, trauma, or consistently stressful situations may be at increased risk for SAD.
• Drug use. The use of psychoactive drugs, including marijuana and LSD, has been associated with increased risk for SAD.

Is Schizoaffective Disorder Hereditary?

There is a consensus among scientists that genetics play a significant role in the development of schizophrenia, and the same genetic factors are likely at play in schizoaffective disorder. Several studies have estimated that between 50% and 80% of the risk of developing schizophrenia comes from inherited genetic traits. A broader study in 2017 put the heritability rate at the top end of that range, suggesting that about 80% of the risk comes from an individual’s genes.

A family history of SAD or schizophrenia is a significant risk factor. For example, one study indicated that If an individual has an identical twin with SAD, they have a 40% chance of developing the disorder themselves.

Scientists have not yet determined which genes introduce a SAD risk, and the risk probably comes from a complex interaction of multiple genes.

How Is Schizoaffective Disorder Detected?

Early detection, diagnosis, and treatment of schizoaffective disorder are crucial. Identifying the condition and pursuing an effective treatment plan can help prevent potentially life-threatening complications. 

SAD is especially challenging to diagnose because its symptoms overlap with schizophrenia and mood disorders. As a result, the disorder is often mistaken for one of the two other disorders rather than a distinct disorder with a combination of symptoms.

Warning signs of SAD may include:

• Depression, apathy, or lethargy
• Withdrawal from social situations or daily activities
• Decline in performance at school
• Irritability or agitation
• Sleep disruptions

The symptoms should be addressed immediately if they interfere with normal functioning. Seek professional help immediately if there is evidence of self-harm, suicidal thoughts, or suicide attempts.

How Is Schizoaffective Disorder Diagnosed?

The symptoms of schizoaffective disorder can be similar to those of other neurological conditions or illnesses, substance abuse, other mental health-related issues, or various medical issues. Therefore, the initial diagnostic process involves ruling out these other potential causes of the symptoms.

Diagnostic steps will probably include:

• Physical exam. This exam will look for physical problems or illnesses that may explain the symptoms.
• Laboratory tests and imaging exams. These tests and exams may be ordered if the doctor suspects an underlying medical condition could account for the symptoms.
• Psychological assessment. If medical causes are ruled out, the doctor may call for a psychiatric evaluation to rule out other mental health conditions or to confirm a diagnosis of schizoaffective disorder. The mental health practitioner will use the diagnostic criteria for SAD in the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) to determine if a diagnosis is appropriate.

The diagnostic criteria for schizoaffective disorder include:

• Presence of two or more symptoms, including delusions, hallucinations, disorganized speech, disorganized or catatonic movement, or negative symptoms. A major mood episode (manic or depressive) must occur during these psychotic symptoms.
• Hallucinations or delusions occur for a period of at least two weeks when there are no affective symptoms.
• Symptoms that meet the criteria for a mood disorder are present during the majority of the illness.
• Symptoms are not caused by substance use or a medical condition.
• To diagnose the bipolar type, both manic and depressive episodes must occur. To diagnose the depressive type, only depressive episodes must occur.

PLEASE CONSULT A PHYSICIAN FOR MORE INFORMATION.

How Is Schizoaffective Disorder Treated?

Treatment of schizoaffective disorder is typically based on medications used to control symptoms. In addition, psychotherapy may be used to build coping skills and improve functioning once symptoms are brought under control by medication. People deemed a risk to themselves or others may be hospitalized during the initial treatment.

Medications

• Antipsychotic drugs can be used to manage the symptoms of schizophreniform disorder. Paliperidone is the only antipsychotic specifically authorized by the FDA for treatment of SAD, but doctors may sometimes prescribe other antipsychotics as well.
• Mood-stabilizing drugs such as lithium may be used to control manic and depressive episodes.
• Antidepressants may be used to improve depressive symptoms.

Psychotherapy

After a successful treatment plan using medications has been established, various therapies may provide further support. Individual psychotherapy, group therapy, family therapy, vocational rehabilitation, and social therapies are often used.

How Does Schizoaffective Disorder Progress?

Untreated schizoaffective disorder may lead to severe consequences. The symptoms may drive the sufferer away from loved ones and social support systems, putting them at risk of situations that can profoundly impact their health.

As the symptoms progress and prevent the sufferer from functioning in a safe, productive way, the likelihood that they will develop social, legal, and health problems becomes greater.

Left untreated, SAD can lead to complications that include:

• Suicidal thoughts, suicide attempts, or successful suicide
• Alcohol and substance abuse
• Lack of success at school or work
• Anxiety
• Financial problems
• Homelessness
• Exposure to dangerous situations and crime
• Legal problems

In rare cases, schizoaffective disorder can produce aggressive, violent behavior. Sufferers are also at risk of coming into conflict with law enforcement because their behavior is often treated as criminal rather than as a mental health issue.

How Is Schizoaffective Disorder Prevented?

Because the cause of schizoaffective disorder remains unknown, there’s no known way to prevent the disorder from occurring in the first place. However, once SAD has been diagnosed, and an effective treatment plan is in place, relapses of symptoms can often be successfully prevented.

It’s important to continue taking medications as directed by your healthcare providers, even after your symptoms have diminished. If the drug is causing side effects, it is much better to work with your provider to find a better solution than to stop taking the medication on your own.

Schizoaffective Disorder Caregiver Tips

When the symptoms of schizoaffective disorder are severe, sufferers may be incapable of safely taking care of themselves. The weight of responsibility on caregivers when their loved ones are coping with the disorder is monumental.

To keep your loved one and yourself as safe and healthy as possible, keep these tips in mind:

• Be an active advocate for your loved one’s treatment. SAD patients often don’t have an accurate perception of their disorder or how to treat it. It’s up to caregivers to ensure that treatment plans are working and they’re being followed. Don’t depend on your loved one’s judgment in seeking treatment.
• Take suicidal thoughts and attempts seriously. The risk of suicide risk for people with SAD is real. Don’t let your loved one be unsupported in risky situations, and seek professional help when you see signs of suicidal thoughts.
• Be safe in dangerous situations. There may be times when your loved one’s erratic or irrational behavior requires you to call 911 to get them the medical attention they need. Be aware that many law enforcement agencies are not effectively trained or equipped to deal with mental health situations. Provide as much information as possible to first responders to help keep your loved one safe.

People with schizoaffective disorder often suffer from different brain-related issues, a condition called co-morbidity. Here are a few of the disorders commonly associated with SAD:

• People with SAD often have a co-morbid anxiety disorder.
• Substance abuse is common in people with SAD.

Schizoaffective Disorder Brain Science

Scientists are searching for links between genetic variations and schizoaffective disorder. Studies have found associations between SAD and several different genes, some of which are unique to SAD. Other gene variations are associated with schizophrenia or bipolar disorder in addition to SAD. The studies seem to suggest that a combination of multiple genetic variations, rather than a single gene mutation, is responsible for the increased risk of SAD.

Some genes potentially associated with SAD include:

• Genes that regulate the body’s normal cycle of sleep and wakefulness
• Genes that affect the movement of nerve cells during early brain development, a process called neuronal migration
• Genes vital to the production of chemicals called neurotransmitters, which help brain cells communicate with one another. A neurotransmitter called gamma-amino butyric acid (GABA), which helps prevent brain cells from getting over-excited, may be especially relevant to schizoaffective disorder.

Schizoaffective Disorder Research

Title: Enhancing Cognitive Training Through Exercise Following a First Schizophrenia Episode (CT&E-RCT)

Stage: Recruiting 

Principal Investigator: Keith H Nuechterlein, PhD     

University of California, Los Angeles

Los Angeles, CA

This is a confirmatory randomized controlled trial of the efficacy of a novel intervention combining neuroplasticity-based cognitive training with aerobic exercise, compared to the same systematic cognitive training alone. Treatment occurs for six months after randomization, with a follow-up assessment at 12 months. The investigators hypothesize that combining neuroplasticity-based computerized cognitive training and neurotrophin-enhancing physical exercise will produce neurotrophin increases and cognitive and functional improvements, even relative to cognitive training alone. The investigators target the period shortly after a first episode of schizophrenia to maximize the generalization of cognitive improvement to the functional outcome before chronic disability is established.

The Cognitive Training and Exercise intervention consists of 24 weeks of systematic computerized cognitive training, 4 hours per week, plus aerobic exercise, 150 minutes per week. The Cognitive Training Intervention includes the same systematic cognitive training. The first 12 weeks involve neurocognitive training, using training exercises from Posit Science Brain HQ. The second 12 weeks involve social cognitive training, using the Posit Science SocialVille modules. Aerobic exercise occurs as two 45-minute sessions at the clinic and two 30-minute sessions at home weekly. The aerobic exercise intensity is tailored to maintain an individualized target heart rate zone and is monitored by a heart rate recorder. A weekly one-hour Bridging Skills Group with other members of the treatment condition is designed to aid the generalization of training to everyday life situations. The immediate target is brain-derived neurotrophic factor. The primary treatment outcomes are overall cognitive deficit level and global functioning level.

Title: Neuromodulation of Social Cognitive Circuitry in People With Schizophrenia Spectrum Disorders (ModSoCCS)

Stage: Recruiting 

Principal Investigator: Dielle Miranda, MA     

Centre for Addiction and Mental Health

Toronto, Ontario

In this study, the investigators will be examining the effects of repetitive transcranial magnetic stimulation (rTMS) and intermittent theta burst stimulation (iTBS) on social cognitive impairments in individuals with schizophrenia spectrum disorders. Participants will be chosen by chance to receive either active rTMS stimulation, active iTBS stimulation, sham rTMS, or sham iTBS. The investigators predict that active 10Hz and iTBS stimulation will improve social cognitive impairments compared to sham stimulation. We aim to identify which type of active stimulation is most effective at inducing changes in social cognition brain circuitry and, secondarily, which type of active stimulation is best tolerated and most effective at inducing changes in social cognitive performance.

This study is a randomized, double-blind, sham-controlled study that aims to use repetitive transcranial magnetic stimulation (rTMS), a form of neuromodulation, to target the neural circuitry of social cognitive (SCog) impairments in people with Schizophrenia Spectrum Disorders. We will randomize 60 people with SSDs to three groups: 20 to a conventional form of rTMS (i.e. 10 Hz rTMS); 20 to intermittent theta burst stimulation (iTBS); and 20 to either sham 10Hz rTMS stimulation or sham iTBS. We will determine whether these treatments can change the functional connectivity of key SCog brain circuits by targeting a brain region known as the dorsomedial prefrontal cortex (DMPFC). Since each person’s anatomical and functional brain profile is slightly different, we will optimize the orientation and location of coil placement in each individual. Overall, our proposal follows a target engagement framework, including specifics regarding testing brain stimulation parameters (i.e., rTMS vs. iTBS) and individualizing coil placement for optimal targeting. We anticipate that active 10 Hz rTMS or iTBS will demonstrate target engagement compared to sham and potentially ameliorate SCog deficits in people with SSDs. Our primary goal is to identify which treatment best induces a change in SCog brain circuitry and, secondarily, which treatment is best tolerated and induces changes in social cognitive performance.

Title: The Effects of Kynurenine Aminotransferase Inhibition in People With Schizophrenia (TrypNAC-II)

Stage: Recruiting 

Principal Investigator: Dielle Miranda, MA     

Centre for Addiction and Mental Health

Toronto, Ontario

Kynurenic acid (KYNA) is a naturally occurring chemical in the brain. Studies with rodents indicate that levels of KYNA can impact levels of the neurotransmitters glutamate and dopamine. One way to reliably increase KYNA levels is by ingesting the amino acid tryptophan. Tryptophan is a normal part of the human diet. Tryptophan gets metabolized/changed to other chemicals in the body- including KYNA. By giving people 6 grams of tryptophan, the investigators will be able to increase the KYNA level in a controlled way. The investigators will then be able to study the effects of KYNA on neurotransmitters by using cognitive tests and magnetic resonance imaging techniques (measuring brain activity and brain chemistry using the MRI magnet).

The study’s overall goal is to examine how the medication N-acetylcysteine (NAC), when added to tryptophan, affects various cognitive functions, such as verbal and visual memory. The investigators will also use magnetic resonance imaging (MRI) to examine how NAC affects brain activity and chemicals.

The purpose of the study is to examine whether high dose N-acetylcysteine (NAC) blocks the adverse effects of increased kynurenic acid (KYNA) on selected measures of brain chemistry, function, and behavior, through the inhibition of kynurenine aminotransferase (KAT) II, which converts kynurenine to KYNA. The study will be a double-blind, placebo-controlled, randomized cross-over challenge study, in which people with schizophrenia are pretreated with either high-dose NAC, 140 mg/kg up to a maximum of 15 g, or placebo, then receive tryptophan (TRYP), 6 g.