Phenomenological Psychology

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What Are Some Areas of Continued Debate in the Understanding of the Origin and Maintenance of Schizophrenia?

June 15th, 2009 by David Kronemyer · No Comments

The modern history of schizophrenia began with Kraepelin in 1887 who developed the concept of dementia praecox or mental weakness. He identified its most important distinguishing features as disconnection from reality, disordered thought and inability to develop relationships with others. Lacking even basic coping skills schizophrenics live in their own private world. They are inclined to adopt postures (catatonic stupor) or engage in behaviors (paranoid rages) that discourage others from helping them (Mitchell & Black, 1995, p. 61).

For some time thereafter schizophrenia was hijacked by psychoanalysis, which presumptively attempted to diagnose and treat it. Illustrative is the work of Melanie Klein who invented the term “paranoid-schizoid position” to describe the fragmentation of an infant’s world as it attempted to relate to the ambiguous presence or absence of objects. Another example is the work of R. D. Laing (1970) who viewed schizophrenia as misattribution of reference – a conviction that events or occurrences in the world really are about oneself. The interpersonal theorist Carl Rogers thought he could talk people out of the symptoms of schizophrenia by being friendly and empathetic with them (Rogers, 1967).

While some psychological mechanisms may be at work in the development and maintenance of schizophrenia these pale in significance to the influence of neurochemical dysregulation. Although not harmful it is not likely that psychotherapy is of much use to treat schizophrenia. Studies claiming that CBT is useful for treatment of schizophrenia (e.g. Turkington et al., 2006) are not persuasive. At best any cognitive approach only will enhance the patient’s coping skills prospectively and facilitate her/his interactions with the real world.

These and other approaches essentially were made irrelevant beginning in the 1950s with the advent of psychopharmacology and the invention/discovery of substances with various psychoactive properties. For schizophrenia these include thiothixene, chlorpromazine, haloperidol and thioridazine. Their molecular action blocks dopamine receptors in the brain. Both the dopamine D2 receptor (D2R) and dopamine transporter (DAT) influence dopaminergic neurotransmission and activation of presynaptic D2R affects dopamine (DA) synthesis, while DA released into the synapse largely is removed by rapid reuptake by the DAT (Lee et al., 2009). The DA action of information processing in turn is essential to the proper functioning of the prefrontal cortex in mediating executive functions and goal-directed behavior.

Because of synaptic plasticity the PFC undergoes neuronal adaptation processes such as long-term potentiation and short-term potentiation. DA is the essential modulatory molecule in this activity (Goto & Otani, 2007). Neuroimaging studies also report deficits in functional integration between the PFC and the hippocampus (Benetti et al., 2009) and identify the thalamus as the primary nodal link for the multiple functional circuits that are impaired in schizophrenia (Byne et al., 2008).

The main issues in schizophrenia research at present are the precise nature of these molecular mechanisms; the possible influence of other neurochemicals such as serotonin; and their impact on physical brain anatomy (Mailman et al., 2009). Clinical, genetic and epidemiological data derived from longitudinal studies must be integrated with neurochemical and neuroanatomical research. As with other DSM-IV critiques a bio-psychosocial dimensional approach might be more useful than adherence to strict diagnostic categories. Relevant axes might include reality distortion, mood abnormalities and cognitive impairment (Heckers, 2008). In this respect DSM inadequacies with regards to schizophrenia are a subset of criticism directed to the DSM generally.

References

Benetti, S., Mechelli, A., Picchioni, M., Broome, M., Williams, S. & McGuire, P. (2009). “Functional integration between the posterior hippocampus and prefrontal cortex is impaired in both first episode schizophrenia and the at risk mental state.” Brain, advance access 6 May 2009.

Byne, W., Hazlett, E., Buchsbaum, M. & Kemether, E. (2008). “The thalamus and schizophrenia: current status of research.” Acta Neuropathol., 117, 347 – 368.

Goto, Y. & Otani, S. (2007). “Prefrontal Cortical Synaptic Plasticity: The Roles of Dopamine and Implication for Schizophrenia.” In Teseng, K. & Atzori, M. (eds.). Monoaminergic Modulation of Cortical Excitability. New York, NY: Springer.

Heckers, S. (2008). “Making Progress in Schizophrenia Research.” Schizophrenia Bulletin, 34(4), 591 – 594.

Laing, R. & Esterson, A. (1970). Sanity, madness and the family. Harmondsworth, Middlesex, England: Penguin.

Lee, F., Pei, L. & Liu, F. (2009). “Disruption of the Dopamine Transporter-Dopamine D2 Receptor Interaction in Schizophrenia.” Synapse, 63(8), 710 – 712.

Mailman, R., Wang, Y., Kant, A. & Brown, J. (2009). “Functional Selectivity at Dopamine Receptors.” In Functional Selectivity of G Protein-Coupled Receptor Ligands, pp. 1 – 33. New York, NY: Humana Press.

Mitchell, S. & Black, M. (1995). Freud and Beyond – A History of Modern Psychoanalytic Thought. New York, NY: Basic Books.

Rogers, C. (ed.) (1967). The Therapeutic Relationship and Its Impact – a Study of Psychotherapy with Schizophrenics. Madison, WI: University of Wisconsin Press.

Turkington, D., Kingdon, D. & Weiden, P. (2006). “Cognitive Behavior Therapy for Schizophrenia.” Am. J. Psychiatry, 163, 365 – 373.