Schizophrenia diagnosis depends on the presence of a pattern of symptoms, both positive and negative.
- disorganized speech,
- grossly disorganized behaviour, and
- catatonic behaviour (1).
Negative symptoms are:
- affective flattening (limited range of emotional experiences, reduction of affective expressiveness, monotone speech and blunting),
- alogia (poverty of speech, reduced productivity and fluency of speech), and
- avolition-apathy (reduction, difficulty, or inability to initiate and persist in goal-directed behaviour, little interest in events or hobbies, may not take care of basic grooming and hygiene, limited desire for social interactions) (2).
Diagnosis of schizophrenia requires at least six months of continuous signs of the disturbance with at least one-month duration of two or more characteristic symptoms. At least one of these symptoms should include delusions, hallucinations or disorganized speech (1).
These symptoms should not be caused by substance use (e.g., drug of abuse, medication) or another medical condition. In addition to the above, DSM-V diagnosis of schizophrenia requires presence of impaired social and/or occupational functioning.
Schizophrenia and other psychological psychiatric disorders
Schizophrenia can often present itself along with other mental disorders such as:
- Depression with an estimated prevalence of 50%,
- Substance abuse (47%),
- Obsessive-Compulsive Disorder (23%),
- Panic Disorder (15%),
- Post-Ttraumatic Stress Disorder (29%) (3).
History of schizophrenia
The history of schizophrenia starts in 1898 when Emil Kraepelin presented a concept of dementia praecox, which united several disorders (catatonia, dementia paranoides, and hebephrenia). The term dementia praecox described two main features of the disorder: progressive cognitive deterioration (dementia) and early inception (praecox) (4).
Bleuler considered the term dementia praecox as inappropriate as he believed that the disorder did not have an inevitable progression toward dementia, and in 1908 suggested a new term, schizophrenia, to emphasize what he considered the main feature of the disorder – the splitting of psychic functioning (5).
More than a century has passed since then and the understanding of the symptomatology, as well as definitions and prognosis of schizophrenia, have changed significantly over this period while its aetiology and pathophysiology remain vague.
Aetiology of Schizophrenia
Scientific society is split in terms of aetiology of schizophrenia, some experts talk about schizophrenia as of distinct biological disease (brain abnormality, neurotransmitter disturbances, genetic predisposition) while others see it as an impaired theory of mind, and then there is a third group that honestly admits that we don’t know enough about schizophrenia (6).
Genetic predisposition to Schizophrenia?
While it is believed that genetic factors can predispose someone to development of schizophrenia, while at the same time most schizophrenia patients have no family history of psychosis (12). Genetic research has failed to detect specifically associated with schizophrenia gene variance (7), while a recent a genome-wide analysis showed that similar molecular genetic risk factors are shared between schizophrenia and four other distinct psychiatric disorders: autism, attention deficit hyperactivity disorder (ADHD), bipolar disorder, and major depression (8).
Dopamine Hypothesis of Schizophrenia
Probably the most established hypothesis of the schizophrenia aetiology is the “dopamine hypothesis” which states that schizophrenia is caused by supersensitivity to dopamine or overactivity of dopamine neurotransmission (9). The main support for this hypothesis comes from the fact that antipsychotic drugs used to treat schizophrenia symptoms (i.e. hallucinations, delusions) are acting by blocking dopamine receptors. Another support for this hypothesis comes from the fact that stimulant drugs like cocaine and methamphetamine, which increase the amount of dopamine in the synapse, can cause hallucinations and delusions in non-schizophrenic people (10).
While antipsychotic medication is effective at eliminating or reducing the positive symptoms of schizophrenia in many cases, negative symptoms are more challenging to treat, and often can be caused by antipsychotic medication (i.e. akinesia and blunted affect). Velligan and Alphs (2) noted that negative symptoms of schizophrenia contribute more to the poor quality of life of schizophrenia patients than do positive symptoms.
Zipursky, Reilly, & Murray (11) discredited the myth that schizophrenia is a deteriorating brain disease. They explain that progressive decreases in brain tissue volumes revealed by MRI findings of the patients with schizophrenia can be explained by the effects of antipsychotic medication, substance abuse, and other secondary factors. For example, according to studies, alcohol, cannabis and cigarette smoking are linked to MRI findings of reduced brain tissue volumes in both psychotic and nonpsychotic populations (11). Since proportions of alcohol, cannabis use and smoking are high in people with schizophrenia, this could be a contributing factor to brain tissue loss over time.
There is a high degree of variability in the combination and the severity of the symptoms between persons diagnosed with the disease (12). Practically no two patients display the same constellation of symptoms (3). The course and outcome of the condition vary greatly (7) and it is not possible to predict the prognosis reliably (12).
Different schizophrenia patients are helped by different medications, such as neuroleptics, lithium and benzodiazepines, some of the individuals do not respond to any of these medications (6).
About 30% to 50% of people with schizophrenia lack awareness of their condition and symptoms (i.e., anosognosia) (13), while others may have an insight of their disorder and with the help of Cognitive Behavioral Therapy (CBT) can learn to recognize when they are having disruptive thoughts and learn techniques for managing them. A two-arm, assessor-blinded, randomised controlled trial conducted by Freeman et al. (14) showed that CBT reduced both worry and persecutory delusions in patients with schizophrenia.
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Velligan, D. I., & Alphs, L. D. (2014, November 24). Negative Symptoms in Schizophrenia: An Update on Identification and Treatment. Retrieved April 27, 2016, from http://www.psychiatrictimes.com/schizophrenia/negative-symptoms-schizophrenia-update-identification-and-treatment
Seeman, M. V., & Seeman, P. (2014, January 03). Is schizophrenia a dopamine supersensitivity psychotic reaction? Progress in Neuro-Psychopharmacology and Biological Psychiatry, 48, 155-160. doi:10.1016/j.pnpbp.2013.10.003Center for Substance Abuse Treatment. (1999). How Stimulants Affect the Brain and Behavior. In Treatment for stimulant use disorders (Vol. 33, Treatment Improvement Protocol (TIP)). Rockville, MD: Substance Abuse and Mental Health Services Administration (US).
Freeman, D., Dunn, G., Startup, H., Pugh, K., Cordwell, J., Mander, H., Černis, E., Wingham, G., Shirvell, K., Kingdon, D. (2005). Effects of cognitive behaviour therapy for worry on persecutory delusions in patients with psychosis (WIT): A parallel, single-blind, randomised controlled trial with a mediation analysis. The Lancet, 2, 305-313. http://dx.doi.org/10.1016/S2215-0366(15)00039-5