Purpose: Schizophrenia is a severe and persistent disease that damages the lives of not only those it afflicts but their families and friends. This course prepares the nurse to play a role in identifying, educating, monitoring, and referring patients to appropriate health services to get them on the road to managing this chronic, disabling disease.
Schizophrenia affects one percent of the population with men and women being equally affected. Men, on average, present earlier (late teens or early twenties) with the disease than women (late twenties or early thirties) (National Institute of Medicine, 2014). Women tend to present with less severe symptoms possibly because of the effect estrogen has on dopamine.
Schizophrenia adversely affects the lives of schizophrenic patients in many ways. About five percent of people with schizophrenia will commit suicide over their lifetime (Hor & Taylor, 2010). Patients with schizophrenia marry less frequently and have higher divorce rates. Fifteen percent are in jail and another 15% live in mental health facilities. Approximately 60% live in poverty while 20% are homeless (Javitt & Coyle, 2007). Individuals with schizophrenia have higher rates of other psychiatric conditions including: anxiety, depression and alcohol/substance abuse.
Schizophrenia is associated with many costs to the health care system as it often presents early in life, has no cure, requires repeated interaction with the health care system, lifelong medications and frequent hospitalizations. Medications that currently treat the disease, do not cure it, they just manage the symptoms. Unfortunately, most individuals do not respond fully to the current treatments available. An analysis showed that a patient with chronic schizophrenia has more than 15,000 dollars of health care related expenses every year (Nichols, 2010).
Many factors put one at risk for schizophrenia with family history being the greatest risk factor. Scientists found nine genetic markers that can increase a person's risk for schizophrenia (Lencz, Lambert, DeRosse, Burdick, Morgan, Kane, Kucherlapati & Malhotra, 2008). If a first degree relative has schizophrenia then the life-time risk is about 10 percent; if both parents are affected then life-time risk is 40% (Frankenburg, 2014).
Socioeconomic status is associated with schizophrenia. Factors that are linked include: living in a poorer residential area, lower occupational status of the father and years of education of the father and mother (Werner, Malaspina & Rabinowitz, 2007).
Pregnancy and birth complications may be linked to schizophrenia. Poor nutritional status of the mother during pregnancy has been connected to schizophrenia. Certain viral illness, such as influenza (during certain years), contracted by the mother during pregnancy has also been coupled to schizophrenia. Obstetric complications are linked to schizophrenia (Frankenburg, 2014).
Location and season of birth are correlated to schizophrenia. Being born in an urban center (compared to a rural or suburban center) confers a greater risk. Being born in February or March is also a risk factor but that risk is not as great as being born in an urban setting. Being born in August and September is associated with the lowest risk (Mortensen, Pedersen, Westergaard, Wohlfahrt, Ewald, Mors, Anderson & Melbye, 1999).
Other factors associated with schizophrenia include:
It is hypothesized that schizophrenia stems from an imbalance in the neurotransmitters in the brain because medications that effectively manage the symptoms of schizophrenia affect these neurotransmitters. Abnormalities in dopamine are a main contributor to the pathophysiology of schizophrenia. High dopamine activity in the mesolimbic system leads to positive symptoms while low dopamine levels in the mesocortical system leads to negative symptoms. There are multiple dopamine receptors in the brain, with varying concentrations in different sections of the brain.
In the lab settings, researchers were able to stimulate the release of dopamine and showed that psychotic symptoms worsened. Those with acute schizophrenia release higher levels of dopamine than in normal subjects and this is likely a large contributor to the acute psychosis (Vukadinovic, 2014).
Dopamine is not the only neurotransmitter responsible for the symptoms of schizophrenia. Other neurotransmitters are likely involved in the schizophrenic brain and they may include norepinephrine, serotonin, glutamine and gama-aminobutyric acid (GABA). The NMDA receptor, which is a key target for glutamine on the neuron, is another abnormality in schizophrenia.
The key to finding adequate treatments in schizophrenia may be finding a treatment to target the diverse chemical pathology of the disease. A medication that can target elevated dopamine levels in one section of the brain, target low levels in another section, and address all of the other chemical abnormalities is a challenge for the scientific community.
When compared to the healthy brain neuroimaging has shown bilateral ventriculomegaly and decreased brain volume in the medial temporal lobes, particularly in the superior temporal gyrus in the schizophrenic brain (Frankenburg, 2014). While this is an interesting finding it provides little in the way of diagnostic clues or treatment options.
Chronicling the development of signs and symptoms is a useful tactic to make the diagnosis. Getting input from family members or loved ones is helpful as schizophrenic patients often have altered perceptions.
An accurate history will help make an accurate diagnosis and rule out other diagnoses. Key information about risk factors is the first step and includes getting a family history of schizophrenia and other mental diseases, history of medication and drug use, early childhood problems and maternal health during pregnancy. It is also helpful to determine if there were problems during the teenager years with social or academic problems.
The history should look for positive and negative symptoms. Positive symptoms refer to obvious symptoms, typically psychotic symptoms, and include: hallucinations and delusions. Auditory hallucinations (e.g., voices, music, and machinery) are the most common type of hallucinations. Positive symptoms are most responsive to medications. Delusions may be bizarre or non-bizarre and the content may be paranoid, grandiose, nihilistic or erotomanic (falsely thinks that they have a special relationship with another person).
egative symptoms refer to a loss or decrease of normal functioning and include symptoms such as flat affect, social withdrawal, loss of pleasure, poor grooming, poor social skills, catatonia, poverty of speech and lack of motivation or energy. These symptoms often present earlier than the positive symptoms. The presence of negative symptoms is highly correlated to occupational function and quality of life. Those with high levels of negative symptoms often have poor work performance, inadequate self-care or problems with interpersonal relationships.
Disorganized symptoms show the patients inability to think clearly and are common in schizophrenia. Thought and speech are often disorganized and may manifest in multiple ways. Speech may make use of nonsense words or thoughts shifting quickly from one thought to the next. The patient may have forgetfulness or frequently lose items. Movement may be slow. Speech is often repetitive and confusing. The patients may demonstrate repeated movements or gestures such as pacing, strange hand movements or odd facial expressions. The patients may act like a child or have unpredictable agitation.
Many schizophrenic patients have vague or odd symptoms such as odd dressing habits, poor personal hygiene, odd believes, thought blocking (having long pauses before answering questions), limited conversation, social withdrawal and poor insight. Orientation is typically intact.
Those with schizophrenia may also have problems with attention, working memory, processing speed, reasoning, social cognition, verbal comprehension, executive functioning, and visual learning/memory. An individual with schizophrenia typically performs about 1-2 standard deviations below healthy individuals on neuropsychological testing (Gold, Hahn, Strauss & Waltz, 2009). Cognitive impairments typically occur prior to the presentation of positive symptoms (Bora & Murry, 2014).
While multiple symptoms may define schizophrenia, when the symptoms are taken together they must be present for a significant portion of one month to make the diagnosis. This interval may be less if successfully treated. Some symptoms must be present for at least six months (American Psychiatric Association, 2013).
Signs and symptoms typically come on gradually as evidence by loss of interest in activities, work or school. Hygiene and grooming gets worse and there are often increasing number of anger outbursts. Part of making the diagnosis is to rule out schizoaffective, other mood disorders and other syndromes that present similarly (Table 1). The symptoms are not related to substance abuse, a medication effect, or a general medical condition.
hysical exam is typically not helpful, but any underlying neurological conditions should be evaluated. Any movement disorder is important to document so a baseline level is known. This way when antipsychotic medications are started the baseline is known and any change can be attributed to the medication and not to their baseline function.
Schizophrenics may present with subtle neurological signs such as impaired sensation or impaired motor coordination. Many of the neurological problems seen in schizophrenics may be related to antipsychotic medications as they often block dopamine and may cause tremor, rigidity, dystonias and bradykinesis. Catatonia may also be seen. Metabolic abnormalities (hypertension, diabetes and abnormal lipids) may be seen in schizophrenia.
|Differential diagnosis||Differentiating characteristics|
|Substance abuse||There is current use of or withdrawal from drugs or other substances.|
|Delirium||Similar features but a shorter course of illness; delirium symptoms typically come on faster.|
|Brain lesions||Brain tumors, intracranial bleeds or idiopathic calcification of the basal ganglia can potentially present with similar symptoms.|
|Brief psychotic disorder||Similar symptoms but duration of symptoms is less than 1 month.|
|Depression||Depression especially if severe can present with psychotic symptoms.|
|Bipolar disorder||May be difficult to differentiate as psychotic symptoms may be present during a manic or depressive state. When the patients mood is stable there are no psychotic symptoms.|
|Delusional disorder||Other symptoms of schizophrenia are not present. Typically no impairment in functioning and overall behavior is not bizarre.|
|Schizophreniform disorder||Similar symptoms; it lasts one to six months.|
|Schizoaffective disorder||A combination of thought disorder and mood disorder.|
|Schizotypal personality disorder||These individuals do not form close relationships and they have odd behaviors and thoughts typically behaviors and thoughts are not as severe as in schizophrenia.|
|Seizure disorder||Temporal lobe epilepsy occasionally present with odd behavior including memory/cognitive changes or hallucinations - before, during, or after a seizure.|
|Systemic lupus erythematosus||May present with fever, joint pain, cognitive changes or psychosis.|
|Hypoglycemia||Similar symptoms at times, but accompanied by low blood sugar and symptoms correct when sugar is treated.|
|Wilson disease||Disorder of copper metabolism; initial symptoms are vague; changes in behavior during the teenage years.|
|Endocrine disorders||Hyper/hypothyroidism may present with psychosis; parathyroid disease can lead to mental status change.|
|Medication induced||Drugs that can induce schizophrenic type symptoms include: anticholinergics, phenytoin, steroids, cimetidine and some Parkinsons medications.|
|Infections||Infections that may present with similar symptoms include: neurosyphilis, human immunodeficiency virus, sepsis, cerebral abscess and Creutzfeldt-Jakob disease.|
|Vitamin deficiency||Thiamine, vitamin B12 or folate deficiencies can cause similar signs and symptoms.|
|Electrolyte disorder||Hyponatremia, hypo/hypercalcemia can present with similar symptoms.|
Schizophrenics must have at least two of the following symptoms: delusions, hallucinations, disorganized speech, catatonic or disorganized behavior or negative symptoms. For full criteria see table 2.
Subtypes of schizophrenia (paranoid, disorganized, catatonic, undifferentiated and residual) are no longer required due to poor reliability, no proven validity and this classification not helping the treatment of the disease. These subtypes were used prior to the last update of the Diagnostic and Statistical Manual of Mental Disorders.
No lab test is able to diagnose schizophrenia but a battery of tests should be run to rule out conditions that may be causing the presenting symptoms. A comprehensive drug screen should be done on anyone who presents with psychosis. Other important tests to obtain include: a complete blood count, electrolytes, liver and renal function, thyroid studies, glucose level, vitamin B-12, folate and a calcium level.
Other tests to be considered on an individual basis include human immunodeficiency virus serology, serology for hepatitis C, syphilis serology, ceruloplasmin, urinalysis and culture, an anti-nuclear antibody (ANA), and 24-hour urine for porphyrins, copper or heavy metals (Frankenburg, 2014). A pregnancy test should be done on females. An EKG should be done for those on antipsychotics that prolong the QT interval (e.g., clozapine, iloperidone, thioridazine, and ziprasidone).
Imaging exams computed tomography scan or magnetic resonance imaging - will rule out other conditions (subdural hematoma, tumors, vasculitis and cerebral abscess) that may mimic the disease. Chest x-ray may be preformed if there is suspicion of a malignancy. Electroencephalography (EEG) may be indicated as it may assist in the diagnosis and may help with treatment options (Brauser, 2014).
Schizophrenia is a chronic illness that affects every aspect of life. Treatment goals include:
Treatment of schizophrenia is a process and with each health care encounter treatment plans and diagnosis needs to be reevaluated and adjusted if needed. Acute phase treatment should prevent harm, reduce psychosis, determine causes of the acute episode, control disturbing behaviors, reduce symptoms, and develop a plan with the patient and family for treatment. Any other medical conditions need to be evaluated and stabilized.
Evaluating for suicide and any aggressive behaviors is a critical part of the initial evaluation. Any risk for suicide or aggressive behaviors that would put others or the patient at risk should lead to hospitalization of the patient.
Antipsychotic medications are the mainstay of treatment in schizophrenia. During the acute phase these medications need to be titrated to target quickly and then the patient should be monitored.
During stabilization the main goal is to prevent relapse. In addition, the patient should be adapted back into the community, symptoms need to be controlled and stress reduced. Medication is typically continued for at least 6 months, but many are left on therapy for longer periods of time.
Antipsychotics treat positive symptoms, but not negative symptoms. They are effective at preventing relapse when taken, but those who stop mediations relapse about 80% of the time within one year (Frankenburg, 2014).
Antipsychotics can be classified as typical (first-generation) or atypical (second-generation). Typical antipsychotics have been available since the 1950s. They include the drugs: Thioridazine (Mellaril), Molindone (Moban), Fluphenazine (Prolixin), Haloperidol (Haldol), and Perphenazine (Trilafon). Typical antipsychotics are associated with more neurological side effects. Prescribers often dose these medications at the EPS threshold, which is the dose that will induce minimal rigidity on exam. This is a dose that is found most effective and higher doses are no more effective and are typically associated with poor compliance due to side effects.
Atypical antipsychotics have been around since the late 1980s. These medications are less likely to cause neurological side effects, which results in better compliance. This class of medication is associated other side effects such as weight gain, diabetes and elevated cholesterol.
While first and second-generation medications are effective at treating positive symptoms they are less effective at treating negative symptoms. Negative symptoms can be challenging to treat. No effective treatment exists for primary negative symptoms but negative symptoms caused by something else can be treated. For example, if depression is causing flat affect then antidepressants may be effective. Treatment of the cause of the negative symptoms is the goal and if negative symptoms continue, they are probably primary negative symptoms and will likely not be amenable to treatment.
|First-generation antipsychotics||Second-generation antipsychotics|
|High Potency||Ziprsidone (Geodon)|
|Thiothixene (Navane)||Aripiprazole (Abilify)|
|Fluphenazine (Prolixin)||Risperidone (Risperdal)|
|Perphenazine (Trilafon)||Quetiapine (Seroquel)|
|Haloperidol (Haldol)||Olanzapine (Zyprexa)|
|Low potency||Clozapine (Clozaril)|
|Thioridazine (Mellaril)||Lurasidone (Latuda)|
|Chlorpromazine (Thorazine)||Paliperidone (Invega)|
When medications are started the psychosis typically resolves over several days, but may take up to six weeks. When the dose is at the therapeutic range (see table 4), it should be used for a few days with no improvement before the dose is increased as higher doses are associated with increased risk of side effects. If the patient only has a minimal response to the antipsychotic agent in the first two weeks it is not likely that they will have a strong response (Kinon, Chen, Ascher, Stauffer, Kollack-Walker, Kapur & Kane 2010). Patients should be trailed on antipsychotics for 2-6 weeks before concluding that the medication is ineffective. Iloperidone and quetiapine require longer titration and may require longer trials.
Being able to recognize and treat side effects is a key component to pharmacotherapy in schizophrenia. Those who are afflicted with too many side effects will discontinue therapy and likely relapse.
The first-generation antipsychotic medications, known as typical antipsychotics, are associated with a higher degree of neurological side effects than second-generation antipsychotics. The degree of side effects is related to the potency of the medication. High potency first-generation antipsychotics (Table 3) have a high risk of extrapyramidal side effects (EPS) and medium risk of sedation. Low potency first-generation medications are associated with a lower risk of EPS side effects and a high risk of sedation and anticholinergic effects (Muench, 2010). As a class these medications are associated with weight gain and sexual side effects (breast tenderness, lack of sexual interest, or erectile dysfunction). The selection of antipsychotics may be based on side effect profile.
The next few paragraphs will discuss the neurological side effects associated with anti-psychotics. Extrapyramidal neurological effects include: tardive dyskinesia, dystonia, Parkinsonism and akathisia. The most severe neurological side effect is neuroleptic malignant syndrome.
The most permanent of these side effects is tardive dyskinesia (TD) and is associated with repetitive and involuntary movements of the face and mouth. It may look like the patient is grimacing, chewing or sucking. The risk of TD is higher in the elderly and females. It often occurs after months or years of treatment and has no reliable remedy. This is a permanent side effect and is much more common in first-generation agents. Treatment includes reducing the medication dose or switching to a second-generation medication. Symptoms may persist despite stopping medications. Regularly performing the Abnormal Involuntary Movement Scale (AIMS) is a reliable method to evaluate side effects. The test takes about ten minutes and looks at seven body areas using a 5-point scale which looks for abnormal movements.
Dystonic reactions entail muscle spasms of the back, face and neck with neck twisting and an upward gaze. They come on within one to five days and can be treated with antiparkinsonian medications, diphenhydramine (Benadryl), or benztropine (Cogentin).
A set of symptoms that mimics Parkinsons disease typically occurs within one month of starting the medication and includes the symptoms of bradykinesis, tremor and rigidity. This is the most common side effect of first-generation anti-psychotics. Discontinuing or reducing the medication is the best treatment but anti-Parkinsons medications can be used to treat the symptoms. Second-generation medications can also be used in the management of schizophrenic symptoms in those who are unable tolerate the first-generation medications.
Akathisia, a sense of restlessness, mental unease, irritability, and inability to sit still, is another side effect that may occur up to 2 months after stating the medication. It is treated with antiparkinsonian medications, benzodiazepines, propranolol or by decreasing or changing the antipsychotic medication.
Neuroleptic malignant syndrome is a life-threatening syndrome associated with antipsychotic use. It is characterized by fever, rigidity, labile blood pressure, catatonia, stupor and myoglobinemia. The risk peaks from four days to two weeks after starting the medication. Treatment involves stopping the mediation, supportive treatment and using dantrolene (Dantrium), amantadine (Symmetrel) or bromocriptine (Parlodel). Patients with this condition are hospitalized.
Sedation commonly occurs with most first-generation medications and some second generation medications. The body tends to develop some tolerance to this side effect so the symptoms lessen the longer the patient is on the medication.
Some antipsychotic medications are associated with anticholinergic symptoms such as dry mouth, urinary retention, constipation, confusion and blurred vision. Risperidone, aripiprazole and ziprasidone are the least likely medications to cause these symptoms.
Cardiovascular side effects are a risk with antipsychotic medications. Orthostatic hypotension can occur especially in risperidone, clozapine and quetiapine. Abnormal heart rhythms, including the often fatal torsades de pointes, may be caused by a prolonged QT interval in patients on antipsychotic medications. Some antipsychotics clozapine being the most significant increase the risk of venous thromboembolism.
The atypical antipsychotic medications have less risk of neurological side effects but they are not without risk. These agents are associated with an increased risk of weight gain, diabetes and abnormal cholesterol levels. Antipsychotics may cause weight gain and diabetes, but they are independent of one another and diabetes may be reversed when the medication is stopped.
The most common cause of natural death in schizophrenia is cardiovascular disease (Riodan & Antonni, 2011). Metabolic syndrome is a contributing factor to cardiovascular disease and the use of atypical antipsychotics contribute to metabolic syndrome. Metabolic syndrome involves increased blood pressure, elevated body weight, insulin resistance and dyslipidemia. Metabolic syndrome needs to be assessed and monitored for in those taking atypical antipsychotics.
It is unclear how to monitor for these side effects but most clinicians recommend regularly monitoring blood pressure, weight, blood sugar and cholesterol.
Clozapine (Clozaril), the first second generation antipsychotic medication developed, is considered the most efficacious second generation antipsychotic at treating positive symptoms but it is associated with the most severe side effects of the class. Agranulocytosis, seizures, and rarely cardiomyopathy may occur with this drug. It requires intensive monitoring by checking the white blood cell and absolute neutrophil count every week for 6 months, then every 2 weeks, and then every 4 weeks. It is also associated with sedation, anticholinergic effects, deep vein thrombosis, weight gain, drooling and orthostatic hypotension.
Risperidone (Risperdal) has a higher risk of EPS compared with other second generation antipsychotics especially with higher doses (greater than 6 mg). It is also associated with a risk of orthostatic hypotension, sexual side effects, weight gain and elevated prolactin level.
Olanzapine (Zyprexa) is effective and is dosed once a day. It is more effective than haloperidol at the treatment of negative symptoms (Eisendrath & Lichtmacher, 2006). It is associated with a low risk of EPS, sedation and orthostatic hypotension. It is linked to sexual side effects, weight gain and diabetes.
Quetiapine (Seroquel) is sedating and associated with risk of orthostatic hypotension, weight gain and the development of diabetes is possible. The risks of sexual side effects are low. Eye exams need to be done every 6 months on those on this medication as it was associated with cataracts in animals.
Ziprasidone (Geodon) is associated with a low risk of EPS, orthostatic hypotension, anticholinergic effects, weight gain and sexual side effects. This drug may lead to sedation and prolong the QT interval and theoretically may increase the risk of cardiac arrhythmia.
Aripiprazole (Abilify) is pharmacologically different then other second-generation antipsychotics. It is associated with a risk of cardiac conduction abnormalities and sedation but it is at low risk of any other side effects.
Lurasidone (Latuda) has a larger affinity for receptors other than dopamine and serotonin and may be better able to manage the symptoms of mood, memory and cognition (Lemieux, Sopko & Ehret, 2011). Major drug-to-drug interactions include ketoconazole (contraindication), rifampin (contraindication) and diltiazem (reduce dose of lurasidone). It should be taken with food (at least 350 calories).
Paliperidone (Invega, Invega Sustenna) was approved in 2006 and is approved for schizophrenia and schizoaffective disorder. It is a major active metabolite of risperidone, but is thought to lead to less EPS symptoms (Scarff & Casey, 2011). For schizophrenia it is dosed 6 mg in the morning and it may be increased by 3 mg, no sooner than every five days, to a maximum of 12 mg a day. It is also available as an intramuscular injection, with tolerability being established with oral paliperidone or oral risperidone prior to initiation.
Asenapine (Saphris) is indicated for schizophrenia and is formulated as a sublingual tablet. It is initially dosed 5 mg two times a day with a maximum dose of 20 mg a day. Patients should not eat or drink for 10 minutes after taking the sublingual form of this medication as it reduces absorption.
Iloperidone (Fanapt) is initially dosed 1 mg two times a day. A dose reduction of iloperidone should occur in those on paroxetine, fluoxetine, ketoconazole or clarithromycin.
(per day) in mg
(per day) in mg
|Typical max dose|
(per day) in mg
|Quetiapine||50||150-750 (IR); 400-800 (ER)||750 (IR); 800 (ER)|
Antipsychotics treat aggression, hallucinations, delusions, irritability and sleep disturbances. They work well for those who have good function prior to taking these medications. Improper escalation of the dosage and non-compliance are common causes of drug failure.
Medication will not work if they are not taken. As with many mental diseases, compliance with mediation regimes is a real challenge for schizophrenic patients. As many as 74 percent of patients stop taking their medication after 16 months (Lieberman, Stroup, McEvoy, Swartz, Rosenheck, Perkins Keef, Davis, Lebowitz, Severe & Hsiao, 2005). Non-compliance with medication regimes are made worse by paranoia that results in a lack of trust of health care professionals. Not taking medications leads to reoccurrence of symptoms. Managing the medications so side effects are minimized and providing education to the family and patient are the two important strategies in improving compliance.
Determining how to manage medications is a challenging task for the treating physician. It is necessary to determine which medication, at which dose is most likely to provide a benefit without excessive side effects.
Depot injections are a specialized formulation that allows an injection of the medication that lasts for two to four weeks. In the United States, haloperidol, fluphenazine, risperidone, olanzapine, paliperidone and aripiprazole are all available in depot form. This form of medication is theoretically helpful for those who do not comply with medications. It provides a reliable method to deliver medication and is often used in those who have a long history of medication non-adherence. It is not clear if long-acting injectable medications are more effective than oral medications in regards to compliance (Frankenburg, 2014). One study showed that long-acting injectable risperidone was no better than oral antipsychotics in the treatment of schizophrenia and the injectable form was associated with more side effects (Rosenheck, Krystal, Lew, Barnett, Fiore, Valley, Thwin, Vertress, Liang & CCP555 Research Group, 2011).
Adjunct medications are often needed to properly manage the disease. Antidepressants for co-morbid depression, anti-anxiety medications for anxiety or agitation can be helpful. Adding lithium, valproic acid, or carbamazepine may be necessary in resistant cases.
Medications should be started right away during the acute phase of schizophrenia. If they are delayed it may have negative effects on symptoms and social adjustment (Frankenburg, 2014).
A 19 year-old male patient presents to the clinic with his mother and it is reported that he frequently hears his brother (who lives 500 miles away) and father (who does not live in the same home as his mother) talking in the other room of the house where he and his mother live. He reports that they are plotting against him and he collects pop cans and places them in front of his door to prevent his father and brother from going into the closet to spy on him. He also recently dropped out of school as he has no interest in pursuing a college degree any more. His mom reports that he just sits around the house all day and only bathes about two times a week.
Upon further evaluation the patients mother reports that the patient has always enjoyed playing by himself and was an anxious child. About 18 months prior the presentation to the doctor the patient had some vague symptoms including social withdrawal and a flattened affect. In the early part of his senior year of high school he was noted to have a significant reduction in the quality of his school work. He went from being an A and B student to a C student. The physical exam is generally unremarkable except the mental status exam suggests that the patient is suspicious of the doctor, has a flat affect, some looseness of associations and he is noted to speak tangential (speaks at length but never answers the question). The neurological exam is unremarkable. The laboratory work up including a serum/urine toxicology; complete blood count; electrolytes; glucose; liver, renal, and thyroid function tests; HIV test, hepatitis screen and a syphilis test is unremarkable.
The patient was assessed to be at low risk for suicide or aggressive behaviors and it was determined that he could be managed as an outpatient.
He is started on risperidone one mg two times a day. He is brought back to the clinic two days later and he is noted to be free of significant sedation, akathisia or hypotension. On the third day the dose is increased to 1 mg in the morning and 2 mg in the evening than the next day 2 mg twice a day. Four mg a day is considered a therapeutic dose and is therefore maintained for two weeks.
After two weeks the patient shows significant improvement as he reports he no longer hears his brother and father talking in the other room. His mother reports his thinking appears much less delusional and his grooming is much improved. He still is showing no motivation to go back to college or to get a job.
It was decided to continue with intensive therapy and not increase the medication dose. If no improvement is seen in a few weeks increasing the dose to 4 mg twice a day with careful assessment of side effects will be considered. If no improvement is seen with this dose the dose is not increased as doses above 8 mg a day are associated with significant risk of EPS and the risk is more than the slight benefit that may be noticed with the increase in the dose.
The patient was provided information regarding his disease and medications. He was also educated about the effect stress and over stimulation may have on the disease. Patients need to understand the importance of recognizing the signs and symptoms of early decompensation, which may lead to relapse, such as irritability or insomnia. His family was referred to the National Alliance for the Mentally Ill.
The stable schizophrenic patient needs multiple interventions above medications to maximize quality of life and minimize the effects of the disease. Interventions include: cognitive and behavioral therapy, family intervention, skill and vocational training and community support groups.
Psychotherapy, individual, group or family, is helpful for the schizophrenic patient. These sessions offer education, improve coping skills and provide support. Goals are to improve quality of life and reduce symptoms and hospitalizations.
Family therapy educates the family and provides training in how to communicate, solve problems, and provides coping methods. A recent study that looked at the effects of education and regular follow up on the phone after an inpatient stay over a six month period showed that caregivers in a group of individuals who received education had less depression and family burden when compared to those who did not have the education (Ozkan, 2013). Involved and engaged families improve the treatment of the patient (Pharoah, Mari, Rathbone & Wong, 2010).
Skills training help the schizophrenic patient enter the work force. Supportive employment can help patients find jobs and maintain steady employment.
The use of other health care professionals can significantly aide the schizophrenic patient and their families manage this disease. Social workers can help work with the family and set up services such as vocational training, support groups, and living arrangements if necessary. Many schizophrenic patients live in specialized housing as many are unable to live alone. Dietitians can help the patient manage dietary issues. Schizophrenic patients often have poor diets. The use of antipsychotic medications increases the risk of weight gain, diabetes and hypercholesterolemia. Dietitians can help improve diets to minimize the risk of these conditions.
Referring patients to the National Alliance for the Mentally Ill is helpful. They can provide information and support to schizophrenic patients and their families.
Schizophrenic patients smoke cigarettes more than the general population. This may be one reason that their rates of heart disease are two to three times higher. Helping to get the patients to cease smoking is an important job of the health care system.
Schizophrenics have a 5 percent lifetime prevalence of suicide. Those at greatest risk are male, young, those with a previous attempts, family history of suicide, active hallucinations and delusions, drug use, co-morbid depression, poor adherence to treatment or recent loss (Hor & Taylor, 2010). Health care professionals and families need to recognize these risk factors and monitor patients appropriately. Adequate treatment and adherence to treatment is critical in the prevention of suicide.
Health care follow up is poor in the schizophrenic population. Patients often neglect to take medications, attend follow up appointments or attain necessary medical care. The health care system has to work with these patients to help assure that they have good medical follow up.
KL is a 22 year-old male who is studying accounting at a community college. His roommate and family have been concerned because over the last month he has been acting bizarre. He has been talking to himself in an agitated voice. He has recently got rid of his computer because he is concerned that the government is tracking all of his activity and reading his emails. He will not go to the psychiatrist as he believes this is a plot by his father, a postal worker, who is a government employee. He has no medical, surgical or psychiatric history.
One evening he presents to the emergency department because he punched his father at a local restaurant when he suspected his father was going to "take him in". When the police came, he was yelling at the police and accusing them of being part of the government plot to control him. The police eventually transported him to the local ER. At the ER he continues to make comments about a government plot to destroy him, he is noted to be talking to the wall. Even though it is summer and over 80 degrees he is wearing long pants, a sweater and a jacket.
Upon exam, he is noted to be confused and unable to provide information about his medical or surgical history. His knows his name, but is unable to recite the date or place. While he is in the ER he is seen by psychiatry. When the psychiatrist sees him, he becomes very defensive and begins to raise his voice and thrash around. When the nursing staff comes into assist the physician, the patient attempts to choke the nurse. The patient is placed in 4 point restraints and given haloperidol10 mg intramuscularly. He calms down over the next thirty minutes.
He is admitted to the mental health unit and is stabilized on olanzapine over a period of a week. The social worker gets involved with his case to help him connect with a community psychiatrist and develop short and long-term treatment plans. The patient was provided information regarding his disease and medications.
Nurses have key roles in the management of the schizophrenic patient. Teaching the patient about the disease and the importance of compliance with the treatment plan is important. They need to be taught to take medications as prescribed. Patients should be encouraged to participate in social skills training including vocational training. Nurses need to perform regular screening for abnormal movements utilizing tests such as the AIMS test. Nurses should encourage a healthy lifestyle such as smoking cessation, regular exercise, good nutrition, and maintenance of regular health care appointments, not just for their mental disease but also for medical conditions as schizophrenic patients have higher rates of disease. Nurses have key roles in the management of the schizophrenia.
American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders. 5th ed. Washington, D.C.: American Psychiatric Association.
Bora E & Murray RM. (2014). Meta-analysis of cognitive deficits in ultra-high risk to psychosis and first-episode psychosis: do the cognitive deficits progress over, or after, the onset of psychosis? Schizophrenia Bulletin, 40(4), 744-755.
Brauser D. (2014). EEG May Help Diagnose Schizophrenia, Improve Treatment. Retrieved December 13, 2014 from (Visit Source).
Brown AS & Derkits EJ. (2010). Prenatal infection and schizophrenia: a review of epidemiologic and translational studies. American Journal of Psychiatry, 167(3), 261-280.
Frankenburg FR. (2014). Schizophrenia. Retrieved November 20, 2014 from: URL (Visit Source).
Gold JM, Hahn B, Strauss GP & Waltz JA. (2009). Turning it upside down: areas of preserved cognitive function in schizophrenia. Neuropsychology Review, 19(3), 294-311.
Hor K & Taylor M. (2010). Suicide and schizophrenia: a systematic review of rates and risk factors. Journal of Psychopharmacology, 24(4 Suppl):81-90.
Javitt DC & Coyle JT. (2007). Decoding Schizophrenia. In Bloom FE, Editor. Best of the Brain from Scientific American: Mind, Matter, and Tomorrows Brain. New York: Dana Press, p. 1158-1168.
Kinon BJ, Chen L, Ascher- H, Stauffer VL, Kollack-Walker S, Kapur S & Kane JM. (2010). Early response to antipsychotic drug therapy as a clinical marker of subsequent response in the treatment of schizophrenia. Neuropsychopharmacology, 35(2), 581-90.
Lemieux T, Sopko MA & Ehret MJ. (2010). Focus on Lurasidone: A new atypical antipsychotic for the treatment of schizophrenia. Formulary Journal, 45, 313-317.
Lencz T, Lambert C, DeRosse P, Burdick KE, Morgan TV, Kane JM, Kucherlapati R & Malhotra AK. (2007). Runs of homozygosity reveal highly penetrant recessive loci in schizophrenia. PNAS, 104(50), 19942-19947.
Lieberman JA, Stroup TS, McEvoy JP, Swartz MS, Rosenheck RA, Perkins DO, Keefe RSE, Davis SM, Davis CE, Lebowitz BD, Severe J, Hsiao JK, for the Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE) Investigators. (2005). Effectiveness of antipsychotic drugs in patients with chronic schizophrenia. New England Journal of Medicine, 353, 1209-23.
McGrath JJ, Eyles DW, Pedersen CB, Anderson C, Ko P, Burne TH, Norgaard-Pedersen B, Hougaard DM & Morthensen PB. (2010). Neonatal vitamin D status and risk of schizophrenia: a population-based case-control study. Archives of General Psychiatry, 67(9), 889-94.
Miller B, Messias E, Miettunen J, Alarisnen A, Jrvelin MR, Koponen, H., Rsnen P, Isohanni M & Kirkpatrick B. (2011). Meta-analysis of paternal age and schizophrenia risk in male versus female offspring. Schizophrenia Bulletin, 37(5), 1039-47.
Mortensen PB, Pedersen CB, Westergaard T, Wohlfahrt J, Ewald H, Mors O, Andersen PK & Melbye M. (1999). Effects of Family History and Place and Season of Birth on the Risk of Schizophrenia. New England Journal of Medicine, 240, 603-608.
Meuench, J. (2010). Low potency first-generation medications are associated with a lower risk of EPS side effects and a high risk of sedation and anticholinergic effects. American Family Physician, 81(5), 617-622.
Nicholl D, Akhras KS, Diels J & Schadrack J. (2010). Burden of schizophrenia in recently diagnosed patients: healthcare utilisation and cost perspective. Current Medical Research and Opinion, 26(4), 943-55.
National Institute of Mental Health. Schizophrenia. Retrieved November 20, 2014 from (Visit Source).
Ozkan B, Erdem E, Ozsoy SD & Zararsiz G. (2013). Effect of psychoeducation and telepsychiatric follow up given to the caregiver of the schizophrenic patient on family burden, depression and expression of emotion. Pakistan Journal of Medical Sciences, 29(5), 1122-1127.
Pharoah F, Mari J, Rathbone J & Wong W. (2010). Family Intervention for Schizophrenia. Cochrane Database Syst Rev. Dec 8; 2010, (12):CD000088. doi: 10.1002/14651858.CD000088.pub2.
Riordan HJ, Antonini P, & Murphy MF. (2011). Atypical Antipsychotics and Metabolic Syndrome in Patients with Schizophrenia: Risk Factors, Monitoring, and Healthcare Implications. American Health and Drug Benefits, 4(5), 292-302.
Rosenheck RA, Krystal JH, Lew R, Barnett PG, Fiore L, Valley D, Thwin SS, Vertress JE, Liang MH & CCP555 Research Group. (2011). Long-acting risperidone and oral antipsychotics in unstable schizophrenia. New England Journal of Medicine, 364(9), 842-51.
Samaroo D, Dickerson F, Kasarda DD, Green PH, Briani C, Yolken RH & Alaedini A. (2010). Novel immune response to gluten in individuals with schizophrenia. Schizophrenia Research, 118(1-3), 248-55.
Scarff JR & Casey DA. (2011). Newer Oral Atypical Antipsychotic Agents: A Review. Pharmacy and Therapeutics, 36(12), 832-838.
Schizophrenia Working Group of the Psychiatric Genomics Consortium. (2014). Biological insights from 108 schizophrenia-associated genetic loci. Nature, 511(7510), 421-7.
Vukadinovic Z. (2014). Elevated striatal dopamine attenuates nigrothalamic inputs and impairs transthalamic cortico-cortical communication in schizophrenia: A hypothesis. Medical Hypotheses, S0306-9877(14), 00410-1.
Werner S, Malaspina D & Rabinowitz J. (2007). Socioeconomic Status at Birth Is Associated with Risk of Schizophrenia: Population-Based Multilevel Study. Schizophrenia Bulletin, 33(6),1373-1378.
This course is applicable for the following professions:
Advanced Registered Nurse Practitioner (ARNP), Clinical Nurse Specialist (CNS), Licensed Practical Nurse (LPN), Licensed Vocational Nurses (LVN), Registered Nurse (RN)
CPD: Practice Effectively, Psychiatric