Schizophrenia Flashcards
(57 cards)
What is the estimated prevalence of schizophrenia?
The estimated prevalence is 1%
What is the mean duration of schizophrenia?
The mean duration is 15 years.
How does schizophrenia affect basic human processes?
Schizophrenia affects the most basic human processes of perception, emotion, and judgment.
Why is SCZ called a heterogeneous syndrome?
It has no single defining symptom or sign. It is considered a ‘spectrum of disease states’ grouped under one umbrella term.
How is schizophrenia diagnosed?
SCZ cannot be identified with a diagnostic laboratory test. Diagnosis is based on observing psychotic phenomena (hallucinations, delusions, and thought disorder) after other causes of psychosis (such as affective disorder or delirium) have been excluded. It is also based on operational criteria defined in manuals like DSM-V or ICD-11, considering positive, negative, and cognitive symptoms. PANS scale remains the gold standard for evaluating the effect of antipsychotics on SCZ in both clinical and research setting.
What is the age of onset for schizophrenia?
Onset typically occurs in late teens to early 20s, often presenting as a first psychotic episode. Onset typically occurs in adolescence or early adulthood.
What is the life course of schizophrenia?
It is a lifelong course of illness with exacerbations, remissions, substantial residual symptoms, and functional impairment. The outcome can range from complete recovery to chronic need of care.
What are the three main categories of symptoms in schizophrenia?
Symptoms fall into three main categories: positive symptoms, negative symptoms, and cognitive symptoms.
Describe positive symptoms.
Positive symptoms are characterised by abnormal thoughts, perceptions, language, and behaviour. They represent a gain of function or mental phenomena that do not occur in healthy people. They essentially cover symptoms related to recurrent psychosis.
List examples of positive symptoms.
Examples include delusions, hallucinations (including auditory and visual hallucinations), disorganized thinking/speech, disorganised behaviour, and lack of insight (unawareness that delusions/hallucinations aren’t real). Individuals with schizophrenia are more likely to have persecutory delusions.
Describe negative symptoms.
Negative symptoms are characterised by restrictions in the range and intensity of emotional expression, communication, body language, and interest in normal activities. They represent a loss of function.
List examples of negative symptoms.
Examples include blunted (flat) affect, alogia (reduced speech, curt and detached responses, less fluid speech), avolition (lacking motivation, spontaneity, initiative, e.g., sitting for long periods, ceasing participation in activities), and anhedonia (lacking pleasure or interest in enjoyable activities).
Describe cognitive symptoms.
Subtle cognitive problems are increasingly recognised as a central feature of schizophrenia. Individuals often present with cognitive dysfunction long before diagnosis.
List examples of cognitive symptoms.
Examples include impairments in attention, working memory, learning, verbal fluency, motor speed, and executive functions. Cognitive deficits remain relatively stable and are apparent even in first-episode patients. These deficits lead to impairment of skills and diminished functional capacity.
What is poor working memory associated with?
Poor working memory is linked to dysfunction of the dorsolateral pre-frontal cortex, and even patients with good performance are inefficient in using prefrontal networks.
Are all symptoms equally treatable with pharmacological intervention?
No, positive symptoms are generally best treated by pharmacological intervention, followed by negative symptoms, and then cognitive symptoms. There is a significant unmet need for the pharmacological treatment of cognitive symptoms. Cognitive deficits seem to remain after treatment and are difficult to treat pharmacologically.
What factors contribute to the onset of schizophrenia?
Both environmental and genetic factors play a role in the onset of schizophrenia. It is suggested to be an accumulation of events rather than a single cause.
What environmental factors are linked to schizophrenia?
Environmental factors include urban populations being more affected than rural populations, obstetric complications (premature birth, low birth weight, pre-eclampsia, resuscitation at birth), prenatal nutritional deficiency, seasonal influences of birth month (small increase in winter months), and drug use.
Is there a genetic component to schizophrenia?
Yes, schizophrenia is more common in relatives of those with the disorder, suggesting a genetic component. For example, MZ twins of affected individuals have an increased risk of ~50%. Aspects of cognitive impairment may be under genetic control.
What are the two main neurotransmitter systems implicated in schizophrenia?
The two main transmitter systems implicated are Dopamine and Glutamate.
What is the “dopamine hypothesis” of schizophrenia?
The dopamine hypothesis suggests that schizophrenia arises from DA hyperfunction. It proposes that an excess of dopamine signalling, particularly in midbrain pathways projecting to the striatum, drives psychosis. The hypothesis derived in part from the discovery of antipsychotics in the 1950s.
What evidence supports the dopamine hypothesis?
Evidence includes:
▪Amphetamine or L-Dopa administration can mimic symptoms of SCZ.
▪Antipsychotic drugs alleviate some symptoms of amphetamine psychosis.
▪Excess DA release occurs in SCZ. Neurochemical imaging studies show abnormalities in DA synthesis and release, with meta-analyses concluding an increased presynaptic capacity of DA neurons to synthesise and release DA.
▪Increased DA receptor binding, specifically D2 receptors, is seen in patient brains and scans. Individuals with SCZ have more D2 receptor occupancy in the striatum.
▪Genetic evidence, such as variation in loci for the D2 receptor, supports the hypothesis.
How does the aberrant salience hypothesis explain the link between dopamine and psychotic symptoms?
This hypothesis suggests that DA dysregulation in the dorsal striatum causes irrelevant environmental stimuli to become salient (losing correct signal to noise balance), forming the basis of delusion formation. A feedback loop is suggested where environmental/genetic factors contribute to a sensitised DA system, priming psychotic episodes, and cognitive schemas are impacted by aberrant DA levels, leading to biased sensory perception and further potentiated DA release, potentially tipping individuals over a threshold into psychosis.
What is the perceptual expectations hypothesis?
An alternative mechanism suggests that DA dysfunction leads to false associations and misperceptions because too much DA alters the threshold for what is inferred to be important in internal representations.
