PHILOSOPHICAL REFLECTION ON CHRISTENSEN ET AL.'S PROPOSED EXPLANATION OF SCHIZOPHRENIA AND THE EMERGENCE OF PSYCHOTIC SYMPTOMS
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In the explanation of this facts, Christensen et al. related many scientific findings and made some explanatory hypothesis about some possible causes (see Christensen et al., 2004). I will represent only the intelligible core of their explanatory proposal.
The retroviral activation in the brain and cerebrospinal fluid of some patients with schizophrenia, during acute exacerbations (Karlsson et al., 2001), may cause, consider Christensen et al., an inflamatory process in brain's white matter.
This inflamatory process can be folowed by the activation of a glutamatergic state in brain to which oligodendrocites,
specialized glia that encircle axons with myelin, are very sensitive.
This hyper-glutamatergic state is considered as being toxical.
The ultimate consequence of this toxicity, consider Christensen et al., may be the decrease of the number of oligodendroglia (Orlovskaya et al., 2000)
and of the physiological alteration of myelination in patients with schizophrenia,
as were suggested by many studies (Buchsbaum et al., 1998; Lim et al., 1999 and Foong et al., 2000, Lim et al., 1999, Pettegrew et al., 1991 and Fukuzako et al., 1999).
The disruptions of myelin integrity alter, decreases, the velocity of transmission of information traversing some myelinated neuronal networks.
This decrease causes the dyssynchrony of the reverberating networks integrating perception, thought and action, and thereby the emergence of poorly processed perceptions, disconnected thought processes, and dys-integrated behavior.
The same dyssynchrony disrupts the elements of perception, attention, complex processing of information, and behavior in schizophrenia (Miller, 2000).
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