Schizophrenia

Sign/Symptoms
Drugs
Treatments
Attributes
Incidence is approximately 1 in 100 people
Further Tests
Our Records are Incomplete for Further Tests

Efficacy of Alternative and Other Treatments According to GRADE* Ranking:

Vitamin D [1, 8, 9, 10, 11, 12, 13, 14, 15, 16]:

Please note, this management does NOT treat the condition itself. It may mildly help in preventing some of the symptoms, and even then has insufficient evidence to back up this claim at present. Please note, this acts as a PREVENTATIVE treatment, and not necessarily symptomatic relief.

Recommendation: No recommendation (There is insufficient evidence to support claims that Vitamin D can help prevent schizophrenia)

Grade of Evidence: very low quality of evidence

Megavitamin Therapy (Multivitamin, Vitamin Supplements) [1, 2, 3, 4, 5, 6, 7]:

Please Note that while supplements are effective in correcting deficiencies in the body, their long-term usage is not helpful in preventing diseases like cancer and heart disease. To prevent these illnesses one should eat the natural foods which these vitamins and minerals come from. Replacing natural sources with artificial supplements actually increases the risk of heart disease, cancer, and other diseases. Supplements should be taken only as a balanced multivitamin supplement that contains no more than 100% of the recommended daily allowance. It would be most helpful in people with restricted food intakes, pregnant women and women of childbearing age.

Recommendation: Weakly against. (There is no evidence that Megavitamin therapy can prevent or treat schizophrenia. In fact, long term therapy can lead to increased risk for other diseases)

Grade of Evidence: moderate quality of evidence

* www.gradeworkinggroup.org

Schizophrenia

Schizophrenia (pronounced /ˌskɪtsəˈfrɛniə/ or /ˌskɪtsəˈfriːniə/), from the Greek roots schizein (σχίζειν, "to split") and phrēn, phren- (φρήν, φρεν-, "mind") is a severe and disabling brain disorder[1][2][3] characterized by abnormalities in the perception or expression of reality. It most commonly manifests as auditory hallucinations, paranoid or bizarre delusions, or disorganized speech and thinking with significant social or occupational dysfunction. Onset of symptoms typically occurs in young adulthood,[4] with approximately 0.4–0.6%[5][6] of the population affected. Diagnosis is based on the patient's self-reported experiences and observed behavior. No laboratory test for schizophrenia currently exists.[7]

Studies suggest that genetics, early environment, neurobiology, psychological and social processes are important contributory factors; some recreational and prescription drugs appear to cause or worsen symptoms. Current psychiatric research is focused on the role of neurobiology, but no single organic cause has been found. Due to the many possible combinations of symptoms, there is debate about whether the diagnosis represents a single disorder or a number of discrete syndromes. For this reason, Eugen Bleuler termed the disease the schizophrenias (plural) when he coined the name. Despite its etymology, schizophrenia is not the same as dissociative identity disorder, previously known as multiple personality disorder or split personality; in popular culture the two are often confused.

Increased dopamine activity in the mesolimbic pathway of the brain is consistently found in schizophrenic individuals. The mainstay of treatment is antipsychotic medication; this type of drug primarily works by suppressing dopamine activity. Dosages of antipsychotics are generally lower than in the early decades of their use. Psychotherapy, vocational and social rehabilitation are also important. In more serious cases—where there is risk to self and others—involuntary hospitalization may be necessary, although hospital stays are less frequent and for shorter periods than they were in previous years.[8]

The disorder is thought to mainly affect cognition, but it also usually contributes to chronic problems with behavior and emotion. People with schizophrenia are likely to have additional (comorbid) conditions, including major depression and anxiety disorders;[9] the lifetime occurrence of substance abuse is around 40%. Social problems, such as long-term unemployment, poverty and homelessness, are common. Furthermore, the average life expectancy of people with the disorder is 10 to 12 years less than those without, due to increased physical health problems and a higher suicide rate.[10]

 

Signs and symptoms

A person diagnosed with schizophrenia may demonstrate auditory hallucinations, delusions, and disorganized and unusual thinking and speech; this may range from loss of train of thought and subject flow, with sentences only loosely connected in meaning, to incoherence, known as word salad, in severe cases. Social isolation commonly occurs for a variety of reasons. Impairment in social cognition is associated with schizophrenia, as are symptoms of paranoia from delusions and hallucinations, and the negative symptoms of avolition (apathy or lack of motivation). In one uncommon subtype, the person may be largely mute, remain motionless in bizarre postures, or exhibit purposeless agitation; these are signs of catatonia. No one sign is diagnostic of schizophrenia, and all can occur in other medical and psychiatric conditions.[7] The current classification of psychoses holds that symptoms need to have been present for at least one month in a period of at least six months of disturbed functioning. A schizophrenia-like psychosis of shorter duration is termed a schizophreniform disorder.[7]

Late adolescence and early adulthood are peak years for the onset of schizophrenia. These are critical periods in a young adult's social and vocational development, and they can be severely disrupted. To minimize the effect of schizophrenia, much work has recently been done to identify and treat the prodromal (pre-onset) phase of the illness, which has been detected up to 30 months before the onset of symptoms, but may be present longer.[11] Those who go on to develop schizophrenia may experience the non-specific symptoms of social withdrawal, irritability and dysphoria in the prodromal period,[12] and transient or self-limiting psychotic symptoms in the prodromal phase before psychosis becomes apparent.[13]

 

Schneiderian classification

The psychiatrist Kurt Schneider (1887–1967) listed the forms of psychotic symptoms that he thought distinguished schizophrenia from other psychotic disorders. These are called first-rank symptoms or Schneider's first-rank symptoms, and they include delusions of being controlled by an external force; the belief that thoughts are being inserted into or withdrawn from one's conscious mind; the belief that one's thoughts are being broadcast to other people; and hearing hallucinatory voices that comment on one's thoughts or actions or that have a conversation with other hallucinated voices.[14] The reliability of first-rank symptoms has been questioned,[15] although they have contributed to the current diagnostic criteria.

 

Positive and negative symptoms

Schizophrenia is often described in terms of positive and negative (or deficit) symptoms.[16] Positive symptoms include delusions, auditory hallucinations, and thought disorder, and are typically regarded as manifestations of psychosis. Negative symptoms are so-named because they are considered to be the loss or absence of normal traits or abilities, and include features such as flat or blunted affect and emotion, poverty of speech (alogia), inability to experience pleasure (anhedonia), and lack of motivation (avolition). Despite the appearance of blunted affect, recent studies indicate that there is often a normal or even heightened level of emotionality in schizophrenia, especially in response to stressful or negative events.[17] A third symptom grouping, the disorganization syndrome, is commonly described, and includes chaotic speech, thought, and behavior. There is evidence for a number of other symptom classifications.[18]

 

Diagnosis

Diagnosis is based on the self-reported experiences of the person, and abnormalities in behavior reported by family members, friends or co-workers, followed by a clinical assessment by a psychiatrist, social worker, clinical psychologist or other mental health professional. Psychiatric assessment includes a psychiatric history and some form of mental status examination.

 Symptoms

  1. Characteristic symptoms: Two or more of the following, each present for much of the time during a one-month period (or less, if symptoms remitted with treatment).
    If the delusions are judged to be bizarre, or hallucinations consist of hearing one voice participating in a running commentary of the patient's actions or of hearing two or more voices conversing with each other, only that symptom is required above. The speech disorganization criterion is only met if it is severe enough to substantially impair communication.
  2. Social/occupational dysfunction: For a significant portion of the time since the onset of the disturbance, one or more major areas of functioning such as work, interpersonal relations, or self-care, are markedly below the level achieved prior to the onset.
  3. Duration: Continuous signs of the disturbance persist for at least six months. This six-month period must include at least one month of symptoms (or less, if symptoms remitted with treatment).

Schizophrenia cannot be diagnosed if symptoms of mood disorder or pervasive developmental disorder are present, or the symptoms are the direct result of a general medical condition or a substance, such as abuse of a drug or medication.

 

Subtypes

The DSM-IV-TR contains five sub-classifications of schizophrenia.

  • Paranoid type: Where delusions and hallucinations are present but thought disorder, disorganized behavior, and affective flattening are absent. (DSM code 295.3/ICD code F20.0)
  • Disorganized type: Named hebephrenic schizophrenia in the ICD. Where thought disorder and flat affect are present together. (DSM code 295.1/ICD code F20.1)
  • Catatonic type: The subject may be almost immobile or exhibit agitated, purposeless movement. Symptoms can include catatonic stupor and waxy flexibility. (DSM code 295.2/ICD code F20.2)
  • Undifferentiated type: Psychotic symptoms are present but the criteria for paranoid, disorganized, or catatonic types have not been met. (DSM code 295.9/ICD code F20.3)
  • Residual type: Where positive symptoms are present at a low intensity only. (DSM code 295.6/ICD code F20.5)

The ICD-10 defines two additional subtypes.

  • Post-schizophrenic depression: A depressive episode arising in the aftermath of a schizophrenic illness where some low-level schizophrenic symptoms may still be present. (ICD code F20.4)
  • Simple schizophrenia: Insidious and progressive development of prominent negative symptoms with no history of psychotic episodes. (ICD code F20.6)

Epidemiology

Schizophrenia occurs equally in males and females, although typically appears earlier in men—the peak ages of onset are 20–28 years for males and 26–32 years for females.[4] Onset in childhood is much rarer,[37] as is onset in middle- or old age.[38] The lifetime prevalence of schizophrenia—the proportion of individuals expected to experience the disease at any time in their lives—is commonly given at 1%. However, a 2002 systematic review of many studies found a lifetime prevalence of 0.55%.[6] Despite the received wisdom that schizophrenia occurs at similar rates worldwide, its prevalence varies across the world,[39] within countries,[40] and at the local and neighbourhood level.[41] One particularly stable and replicable finding has been the association between living in an urban environment and schizophrenia diagnosis, even after factors such as drug use, ethnic group and size of social group have been controlled for.[42] Schizophrenia is known to be a major cause of disability. In a 1999 study of 14 countries, active psychosis was ranked the third-most-disabling condition after quadriplegia and dementia and ahead of paraplegia and blindness.[43]

 

Causes

While the reliability of the diagnosis introduces difficulties in measuring the relative effect of genes and environment (for example, symptoms overlap to some extent with severe bipolar disorder or major depression), evidence suggests that genetic and environmental factors can act in combination to result in schizophrenia.[45] Evidence suggests that the diagnosis of schizophrenia has a significant heritable component but that onset is significantly influenced by environmental factors or stressors.[46] The idea of an inherent vulnerability (or diathesis) in some people, which can be unmasked by biological, psychological or environmental stressors, is known as the stress-diathesis model.[47] The idea that biological, psychological and social factors are all important is known as the "biopsychosocial" model.

 

Genetic

Estimates of the heritability of schizophrenia tend to vary owing to the difficulty of separating the effects of genetics and the environment although twin studies have suggested a high level of heritability.[48] It is likely that schizophrenia is a condition of complex inheritance, with several genes possibly interacting to generate risk for schizophrenia or the separate components that can co-occur leading to a diagnosis.[49] These genes appear to be non-specific, in that they may raise the risk of developing other psychotic disorders such as bipolar disorder.[50][51] Rare deletions or duplications of tiny DNA sequences within genes (known as copy number variants) may be linked to increased risk for schizophrenia.[52]

 

Prenatal

Causal factors are thought to initially come together in early neurodevelopment to increase the risk of later developing schizophrenia. One curious finding is that people diagnosed with schizophrenia are more likely to have been born in winter or spring, (at least in the northern hemisphere).[53] There is now evidence that prenatal exposure to infections increases the risk for developing schizophrenia later in life, providing additional evidence for a link between in utero developmental pathology and risk of developing the condition.[54]

 

Social

Living in an urban environment has been consistently found to be a risk factor for schizophrenia.[55][42] Social disadvantage has been found to be a risk factor, including poverty[56] and migration related to social adversity, racial discrimination, family dysfunction, unemployment or poor housing conditions.[57] Childhood experiences of abuse or trauma have also been implicated as risk factors for a diagnosis of schizophrenia later in life.[58][59] Parenting is not held responsible for schizophrenia but unsupportive dysfunctional relationships may contribute to an increased risk.[60][61]

 

Drugs

Although about half of all patients with schizophrenia abuse drugs or alcohol, a clear causal connection between drug use and schizophrenia has been difficult to prove. The two most often used explanations for this are "substance use causes schizophrenia" and "substance use is a consequence of schizophrenia", and they both may be correct. A relatively strong evidence based on multiple studies suggests that cannabis may play a role in the development of schizophrenia. However, there is no sufficient evidence for the role alcohol or other drugs. On the other hand, that people with schizophrenia are known to use drugs to alleviate the depression, anxiety and loneliness resulting from their disorder. [62]

 

Psychological

A number of psychological mechanisms have been implicated in the development and maintenance of schizophrenia. Cognitive biases that have been identified in those with a diagnosis or those at risk, especially when under stress or in confusing situations, include excessive attention to potential threats, jumping to conclusions, making external attributions, impaired reasoning about social situations and mental states, difficulty distinguishing inner speech from speech from an external source, and difficulties with early visual processing and maintaining concentration.[63][64][65][66] Some cognitive features may reflect global neurocognitive deficits in memory, attention, problem-solving, executive function or social cognition, while others may be related to particular issues and experiences.[67][60] Despite a common appearance of "blunted affect", recent findings indicate that many individuals diagnosed with schizophrenia are highly emotionally responsive, particularly to stressful or negative stimuli, and that such sensitivity may cause vulnerability to symptoms or to the disorder.[17][68][69] Some evidence suggests that the content of delusional beliefs and psychotic experiences can reflect emotional causes of the disorder, and that how a person interprets such experiences can influence symptomatology.[70][71][72][73] The use of "safety behaviors" to avoid imagined threats may contribute to the chronicity of delusions.[74] Further evidence for the role of psychological mechanisms comes from the effects of therapies on symptoms of schizophrenia.[75]

 

Neural

Studies using neuropsychological tests and brain imaging technologies such as fMRI and PET to examine functional differences in brain activity have shown that differences seem to most commonly occur in the frontal lobes, hippocampus, and temporal lobes.[76] These differences have been linked to the neurocognitive deficits often associated with schizophrenia.[77] The role of antipsychotic medication, which nearly all those studied had taken, in causing such abnormalities is unclear.[78]

Particular focus has been placed upon the function of dopamine in the mesolimbic pathway of the brain. This focus largely resulted from the accidental finding that a drug group which blocks dopamine function, known as the phenothiazines, could reduce psychotic symptoms. It is also supported by the fact that amphetamines, which triggers the release of dopamine may exacerbate the psychotic symptoms in schizophrenia.[79] An influential theory, known as the Dopamine hypothesis of schizophrenia, proposed that a malfunction involving dopamine pathways was the cause of (the positive symptoms of) schizophrenia. This theory is now thought to be overly simplistic as a complete explanation, partly because newer antipsychotic medication (called atypical antipsychotic medication) can be equally effective as older medication (called typical antipsychotic medication), but also affects serotonin function and may have slightly less of a dopamine blocking effect.[80]

Interest has also focused on the neurotransmitter glutamate and the reduced function of the NMDA glutamate receptor in schizophrenia. This has largely been suggested by abnormally low levels of glutamate receptors found in postmortem brains of people previously diagnosed with schizophrenia[81] and the discovery that the glutamate blocking drugs such as phencyclidine and ketamine can mimic the symptoms and cognitive problems associated with the condition.[82] The fact that reduced glutamate function is linked to poor performance on tests requiring frontal lobe and hippocampal function and that glutamate can affect dopamine function, all of which have been implicated in schizophrenia, have suggested an important mediating (and possibly causal) role of glutamate pathways in schizophrenia.[83] Further support of this theory has come from preliminary trials suggesting the efficacy of coagonists at the NMDA receptor complex in reducing some of the positive symptoms of schizophrenia.[84]

There have also been findings of differences in the size and structure of certain brain areas in schizophrenia, starting with the discovery of ventricular enlargement in those for whom negative symptoms were most prominent.[85] However, this has not proven particularly reliable on the level of the individual person, with considerable variation between patients. More recent studies have shown various differences in brain structure between people with and without diagnoses of schizophrenia.[86] While brain structure changes have been found in people diagnosed with schizophrenia who have never been treated with antipsychotic drugs[87] there is evidence that the medication itself might cause additional changes in the brain's structure.[88] However, as with earlier studies, many of these differences are only reliably detected when comparing groups of people, and are unlikely to predict any differences in brain structure of an individual person with schizophrenia.

 

Treatment and services

The concept of a cure as such remains controversial, as there is no consensus on the definition, although some criteria for the remission of symptoms have recently been suggested.[89] The effectiveness of schizophrenia treatment is often assessed using standardized methods, one of the most common being the Positive and Negative Syndrome Scale (PANSS).[90] Management of symptoms and improving function is thought to be more achievable than a cure. Treatment was revolutionized in the mid-1950s with the development and introduction of chlorpromazine.[91] A recovery model is increasingly adopted, emphasizing hope, empowerment and social inclusion.[92]

Hospitalization may occur with severe episodes of schizophrenia. This can be voluntary or (if mental health legislation allows it) involuntary (called civil or involuntary commitment). Long-term inpatient stays are now less common due to deinstitutionalization, although can still occur.[8] Following (or in lieu of) a hospital admission, support services available can include drop-in centers, visits from members of a community mental health team or Assertive Community Treatment team, supported employment[93] and patient-led support groups.

In many non-Western societies, schizophrenia may only be treated with more informal, community-led methods. Multiple international surveys by the World Health Organization over several decades have indicated that the outcome for people diagnosed with schizophrenia in non-Western countries is on average better there than for people in the West.[94] Many clinicians and researchers suspect the relative levels of social connectedness and acceptance are the difference,[95] although further cross-cultural studies are seeking to clarify the findings.

 

Medication

The first line psychiatric treatment for schizophrenia is antipsychotic medication.[96] These can reduce the positive symptoms of psychosis. Most antipsychotics take around 7–14 days to have their main effect.

Although expensive, the newer

atypical antipsychotic

drugs are usually preferred for

initial treatment

over the older

typical antipsychotics

; they are often better tolerated and associated with lower rates of

tardive dyskinesia

, although they are more likely to induce weight gain and

obesity

-related diseases.

[97]

Prolactin elevations have been reported in women with schizophrenia taking atypical antipsychotics.

[98]

It remains unclear whether the newer antipsychotics reduce the chances of developing

neuroleptic malignant syndrome

, a rare but serious and potentially fatal neurological disorder most often caused by an adverse reaction to

neuroleptic

or antipsychotic drugs.

 

References

American Psychiatric Association. APA Practice Guidelines for the Treatment of Psychiatric Disorders: Quick Reference Guidelines. 1st ed. Arlington, VA: American Psychiatric Association; 2006.

Thomas P[, Alptekin K, ksal [2], et al. Management of Patients Presenting with Acute Psychotic Episodes of Schizophrenia. CNS Drugs. 2009;23:193-212.

Gaebel W, Weinmann S, Sartorius N, Rutz W, McIntyre JS. Schizophrenia practice guidelines: international survey and comparison. The British Journal of Psychiatry. 2005;187(3):248-255.

 

 

Summary References

Treatments:

1. Ades T, Alteri R, Gansler T, Yeargin P, "Complete Guide to Complimentary & Alternative Cancer Therapies", American Cancer Society, Atlanta USA, 2009

2. http://www.cancer.org/Treatment/TreatmentsandSideEffects/ComplementaryandAlternativeMedicine/HerbsVitaminsandMinerals/orthomolecular-medicine

3. http://archpedi.ama-assn.org/cgi/reprint/163/2/192.pdf

4. http://www.quackwatch.org/01QuackeryRelatedTopics/ortho.html

5. http://pediatrics.aappublications.org/cgi/content/abstract/72/5/707

6. http://www.ama-assn.org/ama/no-index/about-ama/13638.shtml

7. http://www.ncbi.nlm.nih.gov/pubmed/17327526

8. http://onlinelibrary.wiley.com/o/cochrane/clsysrev/articles/CD006164/frame.html

9. http://www.ncbi.nlm.nih.gov/pubmed/10824056

10. http://onlinelibrary.wiley.com/doi/10.1002/jcb.10338/abstract

11. http://pain-topics.org/pdf/vitamind-report.pdf

12. http://informahealthcare.com/doi/abs/10.1185/030079908X253519

13. http://www.theglobeandmail.com/life/article756975.ece

14. http://www.ncbi.nlm.nih.gov/pubmed/17556697

15. http://www.ncbi.nlm.nih.gov/pubmed/18065602

16. http://www.nlm.nih.gov/medlineplus/vitamind.html


 

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