Critique of the Dopamine Hypothesis of Schizophrenia
Critique of the Dopamine Hypothesis of Schizophrenia
Schizophrenia is a serious and chronic mental disorder that affects 1% of the world’s population. It is characterized by a range of striking disturbances in mental functioning that can be grouped into both positive and negative symptoms, and also cognitive and psychosocial dysfunctions (Hales, Yudofsky, & Gabbard, 2008) (Abi-Dargham, 2004) (DeLeon, Patel, & Crismon, 2004). The aetiology of schizophrenia is yet to be concluded and while there are several hypotheses that are generally accepted such as genetics and environmental factors, it is the classical dopamine hypothesis that is discussed in this paper. The classical dopamine hypothesis postulates that the mental disorder is a manifestation of a hyperdopaminergic state (Davis, Kahn, Ko, & Davidson, 1991). It had emerged in the 1960s through the observation of the effects of antipsychotic drugs and stimulants that increase dopaminergic activity (Birtwistle & Baldwin, 1998) (van Rossum, 1966). It will be argued in this paper that while the dopamine hypothesis is compelling there are limitations to be considered. Using the study of first generation antipsychotics such as chlorpromazine and sympathomimetic drug amphetamine it will be asserted that the classical theory does not account for the negative symptoms of schizophrenia. Further, using the study of a second generation antipsychotic or atypical antipsychotic, aripiprazole, it would elucidate that other neurotransmitter systems may be involved in the pathophysiology of schizophrenia.
The early dopamine hypothesis had focused on excessive dopamine neurotransmission as the main aetiology of schizophrenia. This was supported when positive symptoms of the illness and other psychotic behaviors in patients were alleviated after the administration of antipsychotic drugs chlorpromazine (Carlsson & Lindqvist, 1963) (van Rossum, 1966). According to Creese, Burt, & Snyder (1976) the reason behind its effectiveness
Schizophrenia is a serious and chronic mental disorder that affects 1% of the world’s population. It is characterized by a range of striking disturbances in mental functioning that can be grouped into both positive and negative symptoms, and also cognitive and psychosocial dysfunctions (Hales, Yudofsky, & Gabbard, 2008) (Abi-Dargham, 2004) (DeLeon, Patel, & Crismon, 2004). The aetiology of schizophrenia is yet to be concluded and while there are several hypotheses that are generally accepted such as genetics and environmental factors, it is the classical dopamine hypothesis that is discussed in this paper. The classical dopamine hypothesis postulates that the mental disorder is a manifestation of a hyperdopaminergic state (Davis, Kahn, Ko, & Davidson, 1991). It had emerged in the 1960s through the observation of the effects of antipsychotic drugs and stimulants that increase dopaminergic activity (Birtwistle & Baldwin, 1998) (van Rossum, 1966). It will be argued in this paper that while the dopamine hypothesis is compelling there are limitations to be considered. Using the study of first generation antipsychotics such as chlorpromazine and sympathomimetic drug amphetamine it will be asserted that the classical theory does not account for the negative symptoms of schizophrenia. Further, using the study of a second generation antipsychotic or atypical antipsychotic, aripiprazole, it would elucidate that other neurotransmitter systems may be involved in the pathophysiology of schizophrenia.
The early dopamine hypothesis had focused on excessive dopamine neurotransmission as the main aetiology of schizophrenia. This was supported when positive symptoms of the illness and other psychotic behaviors in patients were alleviated after the administration of antipsychotic drugs chlorpromazine (Carlsson & Lindqvist, 1963) (van Rossum, 1966). According to Creese, Burt, & Snyder (1976) the reason behind its effectiveness
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