Schizophrenia Clinical Presentation

  • Author: Frances R Frankenburg, MD; Chief Editor: Eduardo Dunayevich, MD   more...
 
Updated: Feb 17, 2012
 

History

Information about the medical and psychiatric history of the family, details about pregnancy and early childhood, history of travel, and history of medications and substance abuse are all important. This information is helpful in ruling out other causes of psychotic symptoms.

The patient usually had an unexceptional childhood. In retrospect, family members may describe the person with schizophrenia as a physically clumsy and emotionally aloof child. The child may have been anxious and preferred to play by himself or herself. The child may have been late to learn to walk and may have been a bedwetter.[9, 10] The person often begins to experience a noticeable change in personality and a decrease in academic, social, and interpersonal functioning during mid-to-late adolescence.

Usually, 1-2 years pass between the onset of these vague symptoms and the first visit to a psychiatrist.[11]

The first psychotic episode usually occurs between the late teenage years and mid 30s.

The symptoms of schizophrenia may be divided into the following 4 domains:

  1. Positive symptoms: These include psychotic symptoms, such as hallucinations, which are usually auditory; delusions; and disorganized speech and behavior.
  2. Negative symptoms: These include a decrease in emotional range, poverty of speech, loss of interests, and loss of drive. The person with schizophrenia has tremendous inertia.
  3. Cognitive symptoms: These include neurocognitive deficits, such as deficits in working memory and attention and executive functions such as the ability to organize and abstract. Patients also have difficulty understanding nuances and subtleties of interpersonal cues and relationships. A new initiative from the National Institutes of Mental Health, known as Measurement and Treatment Research to Improve Cognition in Schizophrenia (MATRICS), is a collaboration between various programs to develop tools for measuring cognition in clinical trials and aiding drug development that is targeted at these symptoms.
  4. Mood symptoms: Schizophrenia patients often seem cheerful or sad in a way that does not make sense to others. They often are depressed.
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Physical

Findings on a general physical examination are usually not contributory. This examination is necessary to rule out other illnesses.

A neurologic examination is sometimes helpful before the initiation of antipsychotic medications as a baseline, because these drugs can change the findings. Some patients with schizophrenia have motor disturbances before exposure to antipsychotic agents. Schizophrenia has been associated with left and mixed handedness, minor physical anomalies, and soft neurological signs.

Mental Status Examination

On a detailed Mental Status Examination in the office, the following observations are often made when talking with a person with schizophrenia:

  • The person may be dressed oddly, such as wearing heavy jackets in the summer. The person may pay insufficient attention to personal hygiene.
  • The person may be unduly suspicious of the examiner or be socially awkward.
  • The person may admit to a variety of odd beliefs or delusions.
  • He or she often has a flat affect, meaning that they have little range of expressed emotion.
  • The person may admit to hallucinations or respond to auditory or visual stimuli not apparent to the examiner.
  • The person may show thought blocking in which long pauses occur before he or she answers a question.
  • The person's speech may be difficult to follow, because of the looseness of his or her associations. This means that the sequence of thoughts follows a logic that is clear to the patient but not to the interviewer.
  • Conversation and initiation of speech may be limited.
  • Schizophrenia patients may demonstrate their difficulty in abstract thinking by not being able to understand common proverbs or by giving idiosyncratic interpretation.
  • The speech of a person with schizophrenia can be circumstantial, meaning that the person takes a long time and uses a lot of words in answering a question, or tangential, meaning the person speaks at length but never actually answers the question.
  • The patient often shows poor attention, disorganized thinking, and stereotyped or perseverative thinking.
  • The patient may make odd movements (which may or may not be related to neuroleptic medication).
  • The person has little insight into his or her problems (the term for this is anosognosia).
  • The person may have thoughts about hurting or harming themselves or others or may hear voices telling them to commit some kind of violence. (Note that suicide in schizophrenia is not uncommon; violence towards others is. Both of these issues are discussed in greater detail below.)
  • Attention is intact. (This is important in distinguishing psychosis from delirium.)
  • Orientation (knowing their own identity, where he or she is, and what the time is) is usually intact.

Patients with schizophrenia may show a repertoire of strange and poorly understood behaviors that are rarely observed in others. These include water drinking to the point of intoxication, staring at oneself in the mirror, stereotyped behaviors, hoarding useless objects, self-mutilation, and a disturbed wake-sleep cycle. They often experience difficulty dealing with change.

According to the American Psychiatric Association'sDiagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR), the patient must have experienced at least 2 of the following symptoms: delusions, hallucinations, disorganized speech, disorganized or catatonic behavior, or negative symptoms. Only 1 symptom is required if the delusions are bizarre or if auditory hallucinations occur in which the voices comment in an ongoing manner on the person's behavior, or if 2 or more voices are talking with each other. The patient must experience at least 1 month of symptoms (or less if successfully treated) during a 6-month period, and social or occupational deterioration problems occur over a significant amount of time. These problems must not be attributable to another condition for the diagnosis of schizophrenia to be made.[12]

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Causes

The causes of schizophrenia are not known. Most likely, at least 2 groups of risk factors exist: genetic and perinatal.

Genetic

The risk of schizophrenia is elevated in biological relatives of patients but not in adopted relatives.[13]

The risk of schizophrenia in first-degree relatives of people with schizophrenia is 10%.

If both parents have schizophrenia, the risk of schizophrenia in their child is 40%.

Concordance for schizophrenia is about 10% for dizygotic twins and 40-50% for monozygotic twins.

The gene variants that have been implicated so far are responsible for only a small fraction of schizophrenia, and these findings have not always been replicated in different studies. The genes that have been found mostly change a gene’s expression or a protein’s function in a small way. Interactions with the rest of the genome and with environment will doubtless prove to be important.

Some loci of particular interest are the following:

  • The catechol-O-methyltransferase (COMT) gene codes for the postsynaptic intracellular enzyme, COMT, which is involved in the methylation and degradation of the catecholamine neurotransmitters dopamine, epinephrine, and norepinephrine. The several allelic variants of COMT affect its activity. The valine-valine variant degrades dopamine faster than does the valine-methionine variant; subjects with 2 copies of the methionine allele were less likely to develop psychotic symptoms if they used cannabis than other cannabis-using subjects without that variant.[14]
  • The RELN gene codes for the protein reelin, which plays a role in brain development and GABAergic activity. In an international study using a genome-wide association scan, a common variant in this gene increased the risk of schizophrenia, but only in women.[15]
  • A Canadian group has looked at the gene for nitric oxide synthase 1 adaptor, known as NOS1AP. This gene codes for the enzyme nitric oxide synthetase, which is found in high concentration in inhibitory neurons in the brain. Nitric oxide acts as an intracellular messenger. Using a newly developed statistical technique, the posterior probability of linkage disequilibrium, the authors identified a single nucleotide polymorphism associated with higher levels of expression of this gene in postmortem brain samples.[16]

Other genetic changes involve the structure of the gene. For example, copy number variants are deletions and duplications of segments of DNA. Copy number variants can involve genes or regulatory regions. These variants are usually inherited, but can spontaneously arise. Copy number variants, such as deletions found at 1q21.1, 15q13.3, and 22q11.2 increase the risk of patients developing schizophrenia.[17] These findings account for only a small part of the heritability of schizophrenia.

Also, the effects of some of these copy number variants are not restricted to schizophrenia. Some copy number variant disorders include autism, intellectual disability, attention-deficit hyperactivity disorder, and epilepsy.[18] In a study of 39,000 people referred to a diagnostic laboratory, about 1000 had a copy number variant at one of the following loci: 1q21.1, 15q11.2, 15q13.3, 16p11.2, 16p13.11, and 22q11.2. Clinically, these people had various neurological/psychiatric disorders, including developmental delay, intellectual disability and autism-related disorders. Subjects also had congenital anomalies.[19] Many people with schizophrenia have no family history of the disorder. This may be due to the occurrence of new mutations in the patient. De novo mutations in the exome, which is the part of the chromosome that codes for proteins, seem to be more common in patients with schizophrenia than is otherwise expected.[20, 21]

Perinatal

Women who are malnourished or who have certain viral illnesses during their pregnancy may be at greater risk of giving birth to children who later develop schizophrenia.

Children born to Dutch mothers who were malnourished during World War II have a high incidence of schizophrenia.

The 1957 influenza A2 epidemics in Japan, England, and Scandinavia resulted in an increase in schizophrenia in the offspring of women who developed this flu during their second trimester.

Women in California who were pregnant between 1959 and 1966 were more likely to have children who developed schizophrenia if they had flu in the first trimester of their pregnancy.[22]

Obstetric complications may be associated with a higher incidence of schizophrenia.

Children born in the winter months may be at greater risk for developing schizophrenia.[23]

A study in Finnish women by Clarke et al supports an interaction between genetic and environmental influences on causation of schizophrenia. A review of the 9,596 women in Helsinki who received hospital treatment during pregnancy for an upper urinary tract infection between 1947 and 1990 found no overall significant increase in the risk of schizophrenia among their offspring but a 5-fold higher risk among the offspring of women who also had a family history of psychosis. Clarke et al estimated that, among offspring of women with both prenatal pyelonephritis and a positive family history of psychotic disorders, 38-46% of schizophrenia cases resulted from the synergistic action of both risk factors.[24]

Other

Finally, undefined socio-environmental factors may increase the risk of schizophrenia in international migrants or urban populations of ethnic minorities.[25, 26, 27]

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Contributor Information and Disclosures
Author

Frances R Frankenburg, MD  Professor, Department of Psychiatry, Boston University School of Medicine; Chief of Inpatient Psychiatry and Consulting Psychiatrist, Edith Nourse Rogers Memorial Veterans Administration Medical Center; Associate Psychiatrist, McLean Hospital

Frances R Frankenburg, MD is a member of the following medical societies: Alpha Omega Alpha and American Psychiatric Association

Disclosure: Nothing to disclose.

Specialty Editor Board

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  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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 None None; Pfizer Grant/research funds Speaking and teaching; Northstar None None; Novartis Grant/research funds research; Pfizer Honoraria Speaking and teaching; Sunovion Speaking and teaching; Otsuke Grant/research funds reseach; GlaxoSmithKline Grant/research funds research; Merck Honoraria Speaking and teaching

Chief Editor

Eduardo Dunayevich, MD  Adjunct Assistant Professor, Department of Psychiatry, University of Cincinnati; Clinical Research Physician, Neuroscience, Lilly Research Laboratories

Eduardo Dunayevich, MD is a member of the following medical societies: American Psychiatric Association

Disclosure: Nothing to disclose.

Additional Contributors

I am grateful to Drs Lawrence Herz and Jennifer Kymalainen and also to Stephen Proper for their careful reading of this article; all mistakes are my own.

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