Schizophrenia refers to a mental condition characterized by failure to recognize what is real as well as abnormal social behavior. Its common signs include confused or unclear thinking, false beliefs, reduced social engagement, and emotional expression, lack of motivation, and hearing false voices that others do not understand. The condition has both psychological and biological aspects. This essay, however, will focus on the natural element of the state.
The condition is linked to subtle brain structure differences, observed in 40 to 50 percent of the cases. It has also been found in the brain chemistry while in acute psychotic states. Research applying brain imaging and neuropsychological test technology like PET and fMRI in the examination of functional distinctions in brain performance has indicated that differences appear to be prominent in the hippocampus, frontal lobes, and temporary lobes. The decline in brain volume are pronounced in grey matter formations and are correlated with the illness duration. However, white matter abnormalities have been observed as well. A consistent incline in ventricular volume and the gradual decline in grey matter in the temporal and parietal lobes are also notable. These distinctions are linked to the neurocognitive deficits attributed to schizophrenia. Due to alterations of the neural circuits, it has been suggested that schizophrenia could be a neurodevelopmental disorder with psychosis happening as a possibly preventable late stage. Debates have been there as to whether diagnosis with antipsychotics can lead to reduced brain volume (Cannon 737-738).
Particular focus has been on the activities of dopamine in the brain’s mesolimbic pathway. This attention significantly resulted from the unexpected observation that phenothiazine medicines which tend to block dopamine roles could decrease psychotic signs. The fact that amphetamines which trigger the production of dopamine may increase the schizophrenic, psychotic symptoms supports the observation above. According to the dopamine schizophrenia hypothesis, activation of D2 receptors in excess leads to positive symptoms of schizophrenia. The PET and SPET imaging studies introduced in the mid-1990s provided supporting evidence after 20 years of speculations regarding D2 blockage effects prominent in all antipsychotics (Galderisi and Maj 493-500). Effect size in schizophrenia is small despite elevations of dopamine D2/D3 receptors and is only observable in medication-naïve schizophrenics. Consequently, released and presynaptic dopamine metabolism is inclined despite no contrast in dopamine transporter. The altered dopamine synthesis in the nigrostriatal structure has been observed in several human types of research. There have also been observations of dopamine D1 receptor hypoactivity activation in the frontal cortex. It is suggested that D2 receptor hyperactivity stimulation and D1 receptor relative hyperactivity trigger contribute to cognitive dysfunction through signal disruptions to noise ratio in cortical microcircuits. Currently, the dopamine hypothesis is perceived to be simplistic, partly because modern antipsychotic or atypical antipsychotic medication is just as effective and efficient as the typical antipsychotic or older medication but also impacts functions of serotonin and is likely to experience slightly fewer effects of dopamine-blocking (Gur 45-51).
Attention has also been paid to the neurotransmitter glutamate and the decreased NMDA glutamate receptor function in schizophrenia, mostly because of the abnormally reduced levels of glutamate receptors present in the postmortem brains of individuals diagnosed with schizophrenia and the observation that glutamate-blocking medicines such as ketamine and phencyclidine can take the form of the schizophrenic symptoms and cognitive problems. Low glutamate activity correlates with poor performance on practical in need of hippocampal and frontal lobe function, and glutamate can alter dopamine performance, of which both have been noted in schizophrenia; this has proposed a significant mediating and likely causal glutamate pathways role in the condition. However, positive symptoms are irresponsive to glutamate medication. There are observations of changes in the GABAergic transmission which closely relate to proof of glutamate dysfunction in schizophrenia. Post-Mortem studies indicate a decline in GADA67, GABAA, and GAT-1 receptor subunits expression in the prefrontal cortex, although this seems to be limited to various parvalbumin subsets containing GABAergic neurons. Treatment and the disease stage may influence vivo imaging of GABAergic signaling which may appear to be reduced moderately (“GENETIC, EPIGENETIC, AND MOLECULAR ASPECTS OF GABA FUNCTION IN THE PATHOPHYSIOLOGY OF SCHIZOPHRENIA” 157).
Biological aspects attempt to account for the condition. However, psychological issues can be considered and used to explain schizophrenia in a situation where organic explanations are not clear.
Work Cited
Cannon, Tyrone D. “Neurodevelopment And The Transition From Schizophrenia Prodrome To Schizophrenia: Research Imperatives.” Biological Psychiatry 64.9 (2008): 737-738. Web.
Galderisi, S., and M. Maj. “Deficit Schizophrenia: An Overview Of Clinical, Biological And Treatment Aspects.” European Psychiatry 24.8 (2009): 493-500. Web.
“GENETIC, EPIGENETIC, AND MOLECULAR ASPECTS OF GABA FUNCTION IN THE PATHOPHYSIOLOGY OF SCHIZOPHRENIA.” Schizophrenia Research 117.2-3 (2010): 157. Web.
Gur, Raquel E. “Neuropsychiatric Aspects Of Schizophrenia.” CNS Neuroscience & Therapeutics 17.1 (2011): 45-51. Web.
