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group_1_presentation_2_-_schizophrenia [2016/03/12 01:04] dheriaj |
group_1_presentation_2_-_schizophrenia [2018/01/25 15:18] (current) |
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| //In some cases, severe cases of just delusions or hallucinations can warrant diagnosis.// | //In some cases, severe cases of just delusions or hallucinations can warrant diagnosis.// | ||
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| ===== Etiology ===== | ===== Etiology ===== | ||
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| - | {{:messages_image_2819283020_.png?520x472}} | + | {{:messages_image_2819283020_.png?520x540}} |
| ''Figure 2: The Interaction Model'' | ''Figure 2: The Interaction Model'' | ||
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| Certain situations trigger or increase the risk of developing schizophrenia, especially in those individuals that are already at risk of developing schizophrenia due to genetic predisposition <sup>[19]</sup>. Stressful events ranging from physical stress to emotional stress can trigger symptoms relating to schizophrenia. These stressful events are the most common trigger for schizophrenia. The nature of stresses induced on an individual can range from prenatal stress in the womb to drug and alcohol abuse. | Certain situations trigger or increase the risk of developing schizophrenia, especially in those individuals that are already at risk of developing schizophrenia due to genetic predisposition <sup>[19]</sup>. Stressful events ranging from physical stress to emotional stress can trigger symptoms relating to schizophrenia. These stressful events are the most common trigger for schizophrenia. The nature of stresses induced on an individual can range from prenatal stress in the womb to drug and alcohol abuse. | ||
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| Some common stressors include: | Some common stressors include: | ||
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| * ++Adolescence| Puberty, social changes, etc.++ <sup>[19]</sup> | * ++Adolescence| Puberty, social changes, etc.++ <sup>[19]</sup> | ||
| * Winter Birth <sup>[18]</sup> | * Winter Birth <sup>[18]</sup> | ||
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| It is important to note that __environmental triggers alone are not sufficient__ to cause schizophrenia (for the most part) <sup>[14]</sup>. Thousands of individuals experience stressful situations throughout their lives without developing schizophrenia and the predetermined susceptibility is, therefore, significant. In other words, the interaction between genetics, brain activity, and other factors along with environmental triggers are generally required for the development of schizophrenia <sup>[19]</sup>. For example,++predisposing genetic factors| //such as single nucleotide polymorphisms or copy number variations,//++ may interact with a wide range of environmental factors. The combined effects may trigger a cascade of pathophysiological processes in the brain. These changes may eventually lead to maladaptive behaviors, thoughts and emotions related to schizophrenia <sup>[14]</sup>. | It is important to note that __environmental triggers alone are not sufficient__ to cause schizophrenia (for the most part) <sup>[14]</sup>. Thousands of individuals experience stressful situations throughout their lives without developing schizophrenia and the predetermined susceptibility is, therefore, significant. In other words, the interaction between genetics, brain activity, and other factors along with environmental triggers are generally required for the development of schizophrenia <sup>[19]</sup>. For example,++predisposing genetic factors| //such as single nucleotide polymorphisms or copy number variations,//++ may interact with a wide range of environmental factors. The combined effects may trigger a cascade of pathophysiological processes in the brain. These changes may eventually lead to maladaptive behaviors, thoughts and emotions related to schizophrenia <sup>[14]</sup>. | ||
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| <style float-left> | <style float-left> | ||
| - | {{:schizo_with_citationawer.png?400x400}} | + | {{:schizo_with_citationawer.png?400x415}} |
| ''Figure 3: Enlarged Cerebral Ventricles in Schizophrenia'' | ''Figure 3: Enlarged Cerebral Ventricles in Schizophrenia'' | ||
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| [[wp>Hypofrontality]] of the brain regions with increasing brain activity towards the back of the brain has been noted in individuals with schizophrenia. Pruning is known as the elimination of excess neural connections and a normal part of maturation from birth is the pruning of unneeded connections from birth <sup>[1]</sup>. However it has been noted that excessive pruning takes place during the adolescent periods in individuals developing schizophrenia – excessive neural connections in the frontal regions of the brain are eliminated <sup>[4]</sup>. | [[wp>Hypofrontality]] of the brain regions with increasing brain activity towards the back of the brain has been noted in individuals with schizophrenia. Pruning is known as the elimination of excess neural connections and a normal part of maturation from birth is the pruning of unneeded connections from birth <sup>[1]</sup>. However it has been noted that excessive pruning takes place during the adolescent periods in individuals developing schizophrenia – excessive neural connections in the frontal regions of the brain are eliminated <sup>[4]</sup>. | ||
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| In addition, [[wp>EEG]] analysis have revealed beta waves in the temporal regions of the brain and delta waves in the frontal lobes. Beta waves are associated with alertness and as there are more beta waves in the temporal regions, this reflects the symptomatology of auditory hallucinations. The temporal area is where the auditory cortex resides and the beta activity in the temporal lobes supports the presentation of these auditory symptoms <sup>[11]</sup>. Delta waves are present in the slow waves during our sleep state. Lower levels of activity are associated with delta waves and hypofrontality is reflected through the presence of delta waves in the frontal lobes. Frontal lobes are responsible for executive functions such as planning. Thus, the decreased level of activity in the frontal lobes reflects the reduced ability to perform executive functions <sup>[11]</sup>. | In addition, [[wp>EEG]] analysis have revealed beta waves in the temporal regions of the brain and delta waves in the frontal lobes. Beta waves are associated with alertness and as there are more beta waves in the temporal regions, this reflects the symptomatology of auditory hallucinations. The temporal area is where the auditory cortex resides and the beta activity in the temporal lobes supports the presentation of these auditory symptoms <sup>[11]</sup>. Delta waves are present in the slow waves during our sleep state. Lower levels of activity are associated with delta waves and hypofrontality is reflected through the presence of delta waves in the frontal lobes. Frontal lobes are responsible for executive functions such as planning. Thus, the decreased level of activity in the frontal lobes reflects the reduced ability to perform executive functions <sup>[11]</sup>. | ||
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| <style float-right> | <style float-right> | ||
| - | {{:playground:xxx.jpg?450x515}} | + | {{:playground:xxx.jpg?450x525}} |
| ''Figure 4: (Above) There is balanced excitation and inhibition between the pyramidal\\ neuron and inhibitory interneuron. | ''Figure 4: (Above) There is balanced excitation and inhibition between the pyramidal\\ neuron and inhibitory interneuron. | ||
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| Glutamate is a key excitatory neurotransmitter involved in neuronal migration, growth, synaptogenesis, and neuron pruning via apoptosis <sup>[19]</sup>. Additionally, glutamate in the hippocampus is involved in long-term potentiation, a pivotal process in learning and long-term memory <sup>[19]</sup>. The receptors involved in this process are the ionotropic glutamate receptors, amino-3-hydroxy-5-methyl-isoxazoloe-4-proprionic acid (AMPA) and N-methyl-D-aspartate (NMDA) <sup>[19]</sup>. Upon glutamate binding, the AMPA receptors are activated and allow mainly Na+ ions to flow down their gradients (inwards) <sup>[19]</sup>. When the pre-synaptic neuron receives high-frequency stimulation via action potentials, an increased amount of glutamate is released into the synaptic cleft <sup>[19]</sup>. This increased amount of glutamate allows for a large influx of positive ions, which then interacts with an Mg<sup>2+</sup> ion that normally blocks the NMDA channel pore at rest <sup>[19]</sup>. This interaction between positive ions results in the repulsion of the Mg<sup>2+</sup> block, allowing Na<sup>+</sup> and Ca<sup>2+</sup> ions to flow freely through the NMDA receptor as well <sup>[19]</sup>. | Glutamate is a key excitatory neurotransmitter involved in neuronal migration, growth, synaptogenesis, and neuron pruning via apoptosis <sup>[19]</sup>. Additionally, glutamate in the hippocampus is involved in long-term potentiation, a pivotal process in learning and long-term memory <sup>[19]</sup>. The receptors involved in this process are the ionotropic glutamate receptors, amino-3-hydroxy-5-methyl-isoxazoloe-4-proprionic acid (AMPA) and N-methyl-D-aspartate (NMDA) <sup>[19]</sup>. Upon glutamate binding, the AMPA receptors are activated and allow mainly Na+ ions to flow down their gradients (inwards) <sup>[19]</sup>. When the pre-synaptic neuron receives high-frequency stimulation via action potentials, an increased amount of glutamate is released into the synaptic cleft <sup>[19]</sup>. This increased amount of glutamate allows for a large influx of positive ions, which then interacts with an Mg<sup>2+</sup> ion that normally blocks the NMDA channel pore at rest <sup>[19]</sup>. This interaction between positive ions results in the repulsion of the Mg<sup>2+</sup> block, allowing Na<sup>+</sup> and Ca<sup>2+</sup> ions to flow freely through the NMDA receptor as well <sup>[19]</sup>. | ||
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| Under these normal conditions, there is sufficient excitation of the post-synaptic cell (inhibitory interneurons) resulting in the release of the inhibitory neurotransmitter gamma-Aminobutyric acid (GABA) <sup>[19]</sup>. This GABA allows the inhibitory interneuron to modulate the activity of the pre-synaptic cell (the excitatory neuron, or pyramidal neuron) <sup>[19]</sup>. This pyramidal neuron is also involved in releasing dopamine, the “//pleasure neurotransmitter//”, to other cells in the hippocampus <sup>[19]</sup>. This modulation allows the pyramidal cell to release balanced amounts of dopamine and glutamate to interacting neurons <sup>[19]</sup>. | Under these normal conditions, there is sufficient excitation of the post-synaptic cell (inhibitory interneurons) resulting in the release of the inhibitory neurotransmitter gamma-Aminobutyric acid (GABA) <sup>[19]</sup>. This GABA allows the inhibitory interneuron to modulate the activity of the pre-synaptic cell (the excitatory neuron, or pyramidal neuron) <sup>[19]</sup>. This pyramidal neuron is also involved in releasing dopamine, the “//pleasure neurotransmitter//”, to other cells in the hippocampus <sup>[19]</sup>. This modulation allows the pyramidal cell to release balanced amounts of dopamine and glutamate to interacting neurons <sup>[19]</sup>. | ||
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| ===== Conclusion ===== | ===== Conclusion ===== | ||
| - | Schizophrenia is a severe mental illness that can be extremely debilitating. There is a false notion that schizophrenia is a 'rare' disorder; however, it affects 1 in 100 individuals across the globe. The actual cause of this illness is unknown, however, there are numerous theories which have been tested and studied in great detail. The most promising theory is based on the assumption of brain activity imbalances and chemical changes due to the interacting roles of numerous factors such as genetics and the environment. | + | Schizophrenia is a severe mental illness that can be extremely debilitating. There is a false notion that schizophrenia is a '**__rare__**' disorder; however, it affects 1 in 100 individuals across the globe. The actual cause of this illness is unknown, however, there are numerous theories which have been tested and studied in great detail. The most promising theory is based on the assumption of brain activity imbalances and chemical changes due to the interacting roles of numerous factors such as genetics and the environment. |
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