THE ESSENCE OF SCHIZOPHRENIA
Schizophrenia: Memory, Hallucinations, and Neurotransmissions Possible Correlations and Implications; Observational Analysis
Christopher J. Mitchell
Abstract
Behaviors in schizophrenic patients have been observed extensively. Many defects are distinguishable. Among them is memory, and recall insufficiencies. In addition, individuals who suffer from schizophrenia generally demonstrate disorganized thinking patterns, and may also experience delusions or hallucinations. The correlation between dopamine inadequacies and memory as well as recall deficiencies is comprehensible and widely supported. It is unclear, however, whether it is the only absolute determinant, or if it is just one factor among many. Studies have expressed that a potential factor may be a failure to organize the information to be encoded. Inferential data shows that the use of various stimulants is prevalent in people with schizophrenia. Further, people with schizophrenia seem to lack the ability to organize thoughts or strategize. Perception and motivation seem to be absent in their life. In addition, a number of studies have shown that these individuals are moody, aggressive or homicidal in nature. Correlations have been discovered between cognition, recall, and memory. Further, false recognitions and other types of memory errors were positively associated with hallucinations. Experiments showed that antipsychotic medications used to treat Schizophrenia increased the number of dopamine receptors in schizophrenic patients. Further, analysis indicated that increased blood flow is a major contributor to the effects of schizophrenia. The cause of this disorder is unknown. However, if schizophrenia is a chemical imbalance, then identifying and attending to the surplus instead of the deficit of dopamine may actually bring the system to a balance.
Schizophrenia: Memory, Hallucinations, and Neurotransmissions Possible Correlations and Implications; Observational Analysis
Observation
This paper discusses the nature, severity, and possible causes, and effects of Schizophrenia. According to the National Institute of Mental Health, “Schizophrenia affects 2.2 million adults or about 1.1 percent of adults ages 18 and older throughout the United States.” Further they reported, “The numbers country to country are roughly the same.” Suggesting that, “The percentage of the worlds’ population; over 18 years of age suffering from this disorder is about 1 percent.” (2004, October 14).
Schizophrenia is a severe mental illness. It’s characterized by “defects in perception.” Individuals who suffer from schizophrenia typically demonstrate disorganized thinking patterns and may also experience delusions or hallucinations. Delusions are defined as “false beliefs or distorted truths.” Whereas, a hallucination is “a perception of an experience when there is no external stimuli present to cause that experience.” Hallucinations can involve visual, auditory, tactile, olfactory, or gustatory experiences. “The most common type of hallucinatory experience in people who suffer from this disorder is auditory, however.” (Oxford Dictionary of Psychology)
The cause of this disorder is currently unknown. Schizophrenia could be caused by situations or happenings during prenatal care. It could be a genetic disorder or its causation could have something to do with chemical imbalances. More specifically, the question is: Is it possible that abnormal deficits of the chemicals that excite neurons involved in memory cause abnormal surpluses that could have an adverse affect on other areas of the brain that are involved in processing auditory stimuli, and may alter perception? Moreover, can one deduce from previous studies that the cause of auditory hallucinations experienced in people with schizophrenia may be a product of an over stimulation of auditory processes; thus, disabling these parts of the brain from perceiving selective stimuli, causing the stimuli to be intertwined, and in turn cause the person to hear abnormal sounds?
The difficultly in determining the causal components of this disorder, is partly because of the complexity of the composition of the human body, and of the brain. However, based on the definition of the disorder, there seems to be an interrelationship between its symptoms, memory inefficiencies, and sensory perception. Further, there is a significant amount of evidence that suggests that people with schizophrenia experience deficits in memory.
According to Koh (1978); “a factor that may contribute to impaired memory in schizophrenic patients is failure to organize the information to be encoded.” In fact, one study showed, “in patients with schizophrenia, coding deficits have been observed with verbal and non-verbal material.” Brébion, Jones, Pilowsky (2004), however, these findings were originally attributed to (Jones, Harrison, Mirsky, Seidman, & Stonen, 1998; Tracy et al., 2001).
In addition to the shortcoming of memory, there are many authors that have obtained sufficient evidence to suggest that the usage of various stimulants is prevalent in people with schizophrenia. For example, one study found “tobacco use is significantly associated with schizophrenia” Roll, Higgins, Steingard,& McGinley (1998). Another study revealed, "nicotine may alleviate cognitive deficits in schizophrenia by increasing dopamine neurotransmission in the prefrontal cortex” (Davis, Kahn, Ko, & Davidson, 1991; Sandyk, 1993; Taiminen et al., 1998). Furthermore, studies have shown, "smoking also improves cognitive performance in normal smokers” Wesnes, & Warburton, (1983). Observations have also found that “nicotine withdrawals lead to an exacerbation of schizophrenic symptoms” Dalack, & Woodruff (1996). In addition people who are schizophrenic tend to abuse drugs like cocaine. One observation has suggested, “the use of the drug itself is a form of operant behavior that is maintained by the reinforcement of the effects of the drug itself”, Stephen, Higgens, Steingard, & McGinley (1998). Cocaine is a stimulant of the central nervous system, and a suppressant of appetite. Moreover, it has been suggested that smoking is correlated with a loss of appetite, in addition to a benefit for memory, and recall processes.
Many studies have been performed to explore the memory and recall deficits experienced by people with schizophrenia. One study was carried out by four scholars from Kings College London, Brébion, David, Jones, Pilowsky, (2004). The participants
in this study consisted of thirty-nine individuals who were diagnosed with chronic schizophrenia. Thirty-six of the patients were taking atypical antipsychotic medication, and the other three were not taking any antipsychotic medication. In addition, thirty-nine healthy controls were gathered by geographical broadcast. The healthy controls were screened for any current or recent psychiatric history. Both groups were equivalent in respect to age, gender, education, and verbal IQ. The material used in this study comprised of eight lists containing 16 words. Four of the lists were composed of asymmetrically related words. The four lists were not organized in any way; however, were equivalent in length and word frequency. The four other lists were symmetrically organized containing, two lists that were atypically organized, and two were typically organized. The unsymmetrical list was given to the participants and they were told that they had 45 seconds to learn the words and had to read them out loud at least once. Immediately after the words were learned they were supplied with a piece of paper and told to write down all of the words they could recall. The four other lists were given following the same procedure.
The results showed that the “patients with schizophrenia would obtain lower scores if they had a tendency to use serial clustering strategies.” For example, by using serial learning by rote rehearsal the patients were impaired in the number of words that could remember in sequence. In addition, this study showed that the patients were limited in the recall of the list also the typical arrangement led to a greater recall than the atypical arrangement. This observation suggested that the people with schizophrenia demonstrate a lack semantic organization, and a dysfunction in recall.
This study emphasized the impairment of certain functionalities of the brain involved in memory and recall. In addition, it discussed the differences of the ability of unimpaired persons to use semantic clustering vs. the inability of its use in schizophrenic patients. Furthermore, it provides a dissertation about the links between a normal brain functions and anomalous brain functioning as it relates to memory and recall. Another research published by Brébion, et al. (1999), established a strong correlation between hallucinations and recognitions. More specifically, “false recognitions and other types of memory errors were positively associated with hallucinations and inversely analogous with certain negative symptoms.” In addition, researches have established a relationship between the antipsychotics used to treat Schizophrenia and dopamine receptor deficits in schizophrenic patients.
Bio-Chemical Components of Memory Deficits
A research project done by Seeman (1984) implied that “long-term treatment of neuroleptics could result in an increase in dopamine receptors.” This observation involved postmortem brains. The study examined 71 controls for the caudate nucleus, 56 for the putamen nucleus, and 47 for the nucleus accoumbens. Some subjects had used nuroleptics. Three of the subjects who had Alzheimer’s disease had used trifluperanzine for two years. Another had taken an undetermined amount of neuroleptics. In this research the only patients that were considered to be drug free were those schizophrenic patients that had not used neuroleptics for six months. The results indicated that the two caudate modes were significantly higher in the control mode. In addition, it showed that the putamens from schizophrenics had modes hat were greater than those of the controls. Further, the schizophrenic accumbens tissues showed that the modes exceeded the control mode.”
The caudate nucleus is said to be involved in voluntary movement, the putamen is said to play a role in reinforcement learning, and the nucleus accumbens is said to be involved in reward, pleasure, and addiction (Oxford Dictionary of Psychology). Does an increase of dopamine receptors that may be caused by a long-term use of neuroleptic drugs such as: typical anti-psychotics and atypical anti-psychotics explain the memory deficits in schizophrenic patents? More specifically, does it mean that the memory deficiencies are caused by the lack of dopamine produced in the synaptic vesicles of the pre-synaptic neuron or is the causation due to an insufficient number of dopamine receiving receptor cites in the pre-synaptic neuron? If so, what explains the hallucinations?
One explanation was presented by GD Johnston (2000) in a study that observed the effects of drugs. It suggests “an overdose of Antimuscarinic agents antagonize the effects of sympathetic acetylcholine at the receptor producing wide variety of phenomena, including: hallucinations and muscle paralysis.” Thus, a decrease in the normal amount of acetylcholine may cause hallucinations. Another study that was done reported an increase of blood flow in several brain regions such as: “the thalamus, basal ganglia, anterior cingulated, the right and left parahippocampal, gyri, and cerebellum in patents with schizophrenia.” In addition, it showed that certain “regions had a decrease of flow such as the prefrontal cortex, including: the lateral, orbital, and medial regions” (Andreasen et all,. 1997).
Observational Analysis
Behaviors in schizophrenic patients have been observed extensively. Many defects are distinguishable. Among them is memory, and recall insufficiencies. In addition, individuals who suffer from schizophrenia generally demonstrate disorganized thinking patterns, and may also experience delusions or hallucinations. The correlation between dopamine inadequacies and memory, as well as recall deficiencies is comprehensible and widely supported. It is unclear, however, whether it is the only absolute determinant, or if it is just one factor among many. Although, there is supporting evidence to denote that dopamine deficits produce memory problems, there is also an abundance of compelling empirical data that implies that a surplus can have similar noticeable reactions as well. These findings suggest that chemical changes may occur, and a dependency can arise over many years or generations of constant exposure to these particular elements. Therefore, the tendency to use stimulants, such as cigarettes, coffee, and other drugs, and other biochemicals may serve as a kind of balancing mechanism, and also the actual cause. Likewise, the unpredictable moods in people with schizophrenia may be a product of an interdependence of chemo-electrical energy, between the amygdala, the prefrontal cortex, and the hippocampus. By understanding these energy balances we may get closer to solving many of the problems that we see in younger and older people today.
Many theorists including: Darwin, “Theory of Natural Selection”, Einstein, E=MC² and Newton: “every action has an equivalent opposite reaction” has provided the foundation for the universal laws of all matter, including the composition of the human brain. If these notions are true then it seems logical to claim that the brain works at a normal pace only when all components are at equilibrium. Thus, if one part of the brain under-stimulated, then another part of the brain is over-stimulated which may contribute to mood, fluctuations, hallucinations, and delusions. If this is true then treating the deficit may actually make the disorder worse in the long run; however, attending to the surplus may actually bring the system to a balance. It will take many more years of research in order to understand the complications, correlations, and possible causes of this disorder. However, by using behavioral as well as cognitive tactics we may final succeed,
References
Andreasen, N., O'Leary D., Flaum, M., Nopoulos, P., Watkins, L., Boles, L., Hichwa, R (1997) Hypofrontality in Schizophrenia: Distributed Dysfunctional Circuits in Neuroleptic-Naive Patients
Colman, A (2003) Oxford Dictionary of Psychology
Dalack, G. W., & Meador-Woodruff J. H., (1996). Smoking, Smoking
Withdrawal and Schizophrenia: Case Reports and a Review of the Literature 133-144.
Davis, K. L., Kahn, R. S., Ko, G., & Davidson, M. (1991). Dopamine in
Schizophrenia: A review and Reconceptualization. American Journal of
Psychiatry, 148, 1474–1486.
Johnston, GD (2000) Effects of Poisons on the Autonomic Nervous System Journal of
Toxicology: Clinical Toxicology
Koh, S. D. (1978) Remembering of Verbal Materials by Schizophrenic Young Adults. Language and cognition in schizophrenia (pp. 59-69).
Maner, M. (1999, 14 April). Women and eighteenth-century literature. Retrieved August 9, 1999 from the World Wide Web: http://www.wright.edu/~martin.maner/18cwom99.html
National Institute of Mental Health, (2004, October 14). World Wide Web
Retrieved November 1, 2005 from http://www.nimh.nih.gov/publicat/schizsoms.cfm
Pickar, D., Labarca, R., Linnoila, M., Roy, A., Hommer, D., Everett, D., Paul, S. (1984) Neuroleptic-Induced Decrease in Plasma Homovanillic Acid and Antipsychotic Activity in Schizophrenic Patients. American Association for the Advancement of Science.
Roll, M. J., Higgins, T. S., Steingard, S., & McGinley, M (1998) Use of Monetary Reinforcement to Reduce the Cigarette Smoking of Persons With Schizophrenia: A Feasibility Study. Experimental and Clinical Psychopharmacology, 2, 157-161.
Seeman, P., Ulpian, C., Begeron, C., Riederer, P., Jellinger, K., Gabriel, E., Reynalds, G.P. Tourtellotte, W.W. (1984) Bimodal Distribution of Dopamine Receptor Densities in Brains of Schizophrenics. American Association for the Advancement of Science.
Seidman, L. J., Stone, W.S., Jones, R., Harrison, R. H., & Mirsky, A. F. (1998). Comparative Effects of Schizophrenia and Temporal Lobe Epilepsy on Memory. Journal of the international neuropsychological Society, 4, 342-352
Wesnes, K., & Warburton, D. M. (1983). Smoking, Nicotine and Human
Performance. Pharmacological Therapy, 21, 189–208.
Schizophrenia: Memory, Hallucinations, and Neurotransmissions Possible Correlations and Implications; Observational Analysis
Christopher J. Mitchell
Abstract
Behaviors in schizophrenic patients have been observed extensively. Many defects are distinguishable. Among them is memory, and recall insufficiencies. In addition, individuals who suffer from schizophrenia generally demonstrate disorganized thinking patterns, and may also experience delusions or hallucinations. The correlation between dopamine inadequacies and memory as well as recall deficiencies is comprehensible and widely supported. It is unclear, however, whether it is the only absolute determinant, or if it is just one factor among many. Studies have expressed that a potential factor may be a failure to organize the information to be encoded. Inferential data shows that the use of various stimulants is prevalent in people with schizophrenia. Further, people with schizophrenia seem to lack the ability to organize thoughts or strategize. Perception and motivation seem to be absent in their life. In addition, a number of studies have shown that these individuals are moody, aggressive or homicidal in nature. Correlations have been discovered between cognition, recall, and memory. Further, false recognitions and other types of memory errors were positively associated with hallucinations. Experiments showed that antipsychotic medications used to treat Schizophrenia increased the number of dopamine receptors in schizophrenic patients. Further, analysis indicated that increased blood flow is a major contributor to the effects of schizophrenia. The cause of this disorder is unknown. However, if schizophrenia is a chemical imbalance, then identifying and attending to the surplus instead of the deficit of dopamine may actually bring the system to a balance.
Schizophrenia: Memory, Hallucinations, and Neurotransmissions Possible Correlations and Implications; Observational Analysis
Observation
This paper discusses the nature, severity, and possible causes, and effects of Schizophrenia. According to the National Institute of Mental Health, “Schizophrenia affects 2.2 million adults or about 1.1 percent of adults ages 18 and older throughout the United States.” Further they reported, “The numbers country to country are roughly the same.” Suggesting that, “The percentage of the worlds’ population; over 18 years of age suffering from this disorder is about 1 percent.” (2004, October 14).
Schizophrenia is a severe mental illness. It’s characterized by “defects in perception.” Individuals who suffer from schizophrenia typically demonstrate disorganized thinking patterns and may also experience delusions or hallucinations. Delusions are defined as “false beliefs or distorted truths.” Whereas, a hallucination is “a perception of an experience when there is no external stimuli present to cause that experience.” Hallucinations can involve visual, auditory, tactile, olfactory, or gustatory experiences. “The most common type of hallucinatory experience in people who suffer from this disorder is auditory, however.” (Oxford Dictionary of Psychology)
The cause of this disorder is currently unknown. Schizophrenia could be caused by situations or happenings during prenatal care. It could be a genetic disorder or its causation could have something to do with chemical imbalances. More specifically, the question is: Is it possible that abnormal deficits of the chemicals that excite neurons involved in memory cause abnormal surpluses that could have an adverse affect on other areas of the brain that are involved in processing auditory stimuli, and may alter perception? Moreover, can one deduce from previous studies that the cause of auditory hallucinations experienced in people with schizophrenia may be a product of an over stimulation of auditory processes; thus, disabling these parts of the brain from perceiving selective stimuli, causing the stimuli to be intertwined, and in turn cause the person to hear abnormal sounds?
The difficultly in determining the causal components of this disorder, is partly because of the complexity of the composition of the human body, and of the brain. However, based on the definition of the disorder, there seems to be an interrelationship between its symptoms, memory inefficiencies, and sensory perception. Further, there is a significant amount of evidence that suggests that people with schizophrenia experience deficits in memory.
According to Koh (1978); “a factor that may contribute to impaired memory in schizophrenic patients is failure to organize the information to be encoded.” In fact, one study showed, “in patients with schizophrenia, coding deficits have been observed with verbal and non-verbal material.” Brébion, Jones, Pilowsky (2004), however, these findings were originally attributed to (Jones, Harrison, Mirsky, Seidman, & Stonen, 1998; Tracy et al., 2001).
In addition to the shortcoming of memory, there are many authors that have obtained sufficient evidence to suggest that the usage of various stimulants is prevalent in people with schizophrenia. For example, one study found “tobacco use is significantly associated with schizophrenia” Roll, Higgins, Steingard,& McGinley (1998). Another study revealed, "nicotine may alleviate cognitive deficits in schizophrenia by increasing dopamine neurotransmission in the prefrontal cortex” (Davis, Kahn, Ko, & Davidson, 1991; Sandyk, 1993; Taiminen et al., 1998). Furthermore, studies have shown, "smoking also improves cognitive performance in normal smokers” Wesnes, & Warburton, (1983). Observations have also found that “nicotine withdrawals lead to an exacerbation of schizophrenic symptoms” Dalack, & Woodruff (1996). In addition people who are schizophrenic tend to abuse drugs like cocaine. One observation has suggested, “the use of the drug itself is a form of operant behavior that is maintained by the reinforcement of the effects of the drug itself”, Stephen, Higgens, Steingard, & McGinley (1998). Cocaine is a stimulant of the central nervous system, and a suppressant of appetite. Moreover, it has been suggested that smoking is correlated with a loss of appetite, in addition to a benefit for memory, and recall processes.
Many studies have been performed to explore the memory and recall deficits experienced by people with schizophrenia. One study was carried out by four scholars from Kings College London, Brébion, David, Jones, Pilowsky, (2004). The participants
in this study consisted of thirty-nine individuals who were diagnosed with chronic schizophrenia. Thirty-six of the patients were taking atypical antipsychotic medication, and the other three were not taking any antipsychotic medication. In addition, thirty-nine healthy controls were gathered by geographical broadcast. The healthy controls were screened for any current or recent psychiatric history. Both groups were equivalent in respect to age, gender, education, and verbal IQ. The material used in this study comprised of eight lists containing 16 words. Four of the lists were composed of asymmetrically related words. The four lists were not organized in any way; however, were equivalent in length and word frequency. The four other lists were symmetrically organized containing, two lists that were atypically organized, and two were typically organized. The unsymmetrical list was given to the participants and they were told that they had 45 seconds to learn the words and had to read them out loud at least once. Immediately after the words were learned they were supplied with a piece of paper and told to write down all of the words they could recall. The four other lists were given following the same procedure.
The results showed that the “patients with schizophrenia would obtain lower scores if they had a tendency to use serial clustering strategies.” For example, by using serial learning by rote rehearsal the patients were impaired in the number of words that could remember in sequence. In addition, this study showed that the patients were limited in the recall of the list also the typical arrangement led to a greater recall than the atypical arrangement. This observation suggested that the people with schizophrenia demonstrate a lack semantic organization, and a dysfunction in recall.
This study emphasized the impairment of certain functionalities of the brain involved in memory and recall. In addition, it discussed the differences of the ability of unimpaired persons to use semantic clustering vs. the inability of its use in schizophrenic patients. Furthermore, it provides a dissertation about the links between a normal brain functions and anomalous brain functioning as it relates to memory and recall. Another research published by Brébion, et al. (1999), established a strong correlation between hallucinations and recognitions. More specifically, “false recognitions and other types of memory errors were positively associated with hallucinations and inversely analogous with certain negative symptoms.” In addition, researches have established a relationship between the antipsychotics used to treat Schizophrenia and dopamine receptor deficits in schizophrenic patients.
Bio-Chemical Components of Memory Deficits
A research project done by Seeman (1984) implied that “long-term treatment of neuroleptics could result in an increase in dopamine receptors.” This observation involved postmortem brains. The study examined 71 controls for the caudate nucleus, 56 for the putamen nucleus, and 47 for the nucleus accoumbens. Some subjects had used nuroleptics. Three of the subjects who had Alzheimer’s disease had used trifluperanzine for two years. Another had taken an undetermined amount of neuroleptics. In this research the only patients that were considered to be drug free were those schizophrenic patients that had not used neuroleptics for six months. The results indicated that the two caudate modes were significantly higher in the control mode. In addition, it showed that the putamens from schizophrenics had modes hat were greater than those of the controls. Further, the schizophrenic accumbens tissues showed that the modes exceeded the control mode.”
The caudate nucleus is said to be involved in voluntary movement, the putamen is said to play a role in reinforcement learning, and the nucleus accumbens is said to be involved in reward, pleasure, and addiction (Oxford Dictionary of Psychology). Does an increase of dopamine receptors that may be caused by a long-term use of neuroleptic drugs such as: typical anti-psychotics and atypical anti-psychotics explain the memory deficits in schizophrenic patents? More specifically, does it mean that the memory deficiencies are caused by the lack of dopamine produced in the synaptic vesicles of the pre-synaptic neuron or is the causation due to an insufficient number of dopamine receiving receptor cites in the pre-synaptic neuron? If so, what explains the hallucinations?
One explanation was presented by GD Johnston (2000) in a study that observed the effects of drugs. It suggests “an overdose of Antimuscarinic agents antagonize the effects of sympathetic acetylcholine at the receptor producing wide variety of phenomena, including: hallucinations and muscle paralysis.” Thus, a decrease in the normal amount of acetylcholine may cause hallucinations. Another study that was done reported an increase of blood flow in several brain regions such as: “the thalamus, basal ganglia, anterior cingulated, the right and left parahippocampal, gyri, and cerebellum in patents with schizophrenia.” In addition, it showed that certain “regions had a decrease of flow such as the prefrontal cortex, including: the lateral, orbital, and medial regions” (Andreasen et all,. 1997).
Observational Analysis
Behaviors in schizophrenic patients have been observed extensively. Many defects are distinguishable. Among them is memory, and recall insufficiencies. In addition, individuals who suffer from schizophrenia generally demonstrate disorganized thinking patterns, and may also experience delusions or hallucinations. The correlation between dopamine inadequacies and memory, as well as recall deficiencies is comprehensible and widely supported. It is unclear, however, whether it is the only absolute determinant, or if it is just one factor among many. Although, there is supporting evidence to denote that dopamine deficits produce memory problems, there is also an abundance of compelling empirical data that implies that a surplus can have similar noticeable reactions as well. These findings suggest that chemical changes may occur, and a dependency can arise over many years or generations of constant exposure to these particular elements. Therefore, the tendency to use stimulants, such as cigarettes, coffee, and other drugs, and other biochemicals may serve as a kind of balancing mechanism, and also the actual cause. Likewise, the unpredictable moods in people with schizophrenia may be a product of an interdependence of chemo-electrical energy, between the amygdala, the prefrontal cortex, and the hippocampus. By understanding these energy balances we may get closer to solving many of the problems that we see in younger and older people today.
Many theorists including: Darwin, “Theory of Natural Selection”, Einstein, E=MC² and Newton: “every action has an equivalent opposite reaction” has provided the foundation for the universal laws of all matter, including the composition of the human brain. If these notions are true then it seems logical to claim that the brain works at a normal pace only when all components are at equilibrium. Thus, if one part of the brain under-stimulated, then another part of the brain is over-stimulated which may contribute to mood, fluctuations, hallucinations, and delusions. If this is true then treating the deficit may actually make the disorder worse in the long run; however, attending to the surplus may actually bring the system to a balance. It will take many more years of research in order to understand the complications, correlations, and possible causes of this disorder. However, by using behavioral as well as cognitive tactics we may final succeed,
References
Andreasen, N., O'Leary D., Flaum, M., Nopoulos, P., Watkins, L., Boles, L., Hichwa, R (1997) Hypofrontality in Schizophrenia: Distributed Dysfunctional Circuits in Neuroleptic-Naive Patients
Colman, A (2003) Oxford Dictionary of Psychology
Dalack, G. W., & Meador-Woodruff J. H., (1996). Smoking, Smoking
Withdrawal and Schizophrenia: Case Reports and a Review of the Literature 133-144.
Davis, K. L., Kahn, R. S., Ko, G., & Davidson, M. (1991). Dopamine in
Schizophrenia: A review and Reconceptualization. American Journal of
Psychiatry, 148, 1474–1486.
Johnston, GD (2000) Effects of Poisons on the Autonomic Nervous System Journal of
Toxicology: Clinical Toxicology
Koh, S. D. (1978) Remembering of Verbal Materials by Schizophrenic Young Adults. Language and cognition in schizophrenia (pp. 59-69).
Maner, M. (1999, 14 April). Women and eighteenth-century literature. Retrieved August 9, 1999 from the World Wide Web: http://www.wright.edu/~martin.maner/18cwom99.html
National Institute of Mental Health, (2004, October 14). World Wide Web
Retrieved November 1, 2005 from http://www.nimh.nih.gov/publicat/schizsoms.cfm
Pickar, D., Labarca, R., Linnoila, M., Roy, A., Hommer, D., Everett, D., Paul, S. (1984) Neuroleptic-Induced Decrease in Plasma Homovanillic Acid and Antipsychotic Activity in Schizophrenic Patients. American Association for the Advancement of Science.
Roll, M. J., Higgins, T. S., Steingard, S., & McGinley, M (1998) Use of Monetary Reinforcement to Reduce the Cigarette Smoking of Persons With Schizophrenia: A Feasibility Study. Experimental and Clinical Psychopharmacology, 2, 157-161.
Seeman, P., Ulpian, C., Begeron, C., Riederer, P., Jellinger, K., Gabriel, E., Reynalds, G.P. Tourtellotte, W.W. (1984) Bimodal Distribution of Dopamine Receptor Densities in Brains of Schizophrenics. American Association for the Advancement of Science.
Seidman, L. J., Stone, W.S., Jones, R., Harrison, R. H., & Mirsky, A. F. (1998). Comparative Effects of Schizophrenia and Temporal Lobe Epilepsy on Memory. Journal of the international neuropsychological Society, 4, 342-352
Wesnes, K., & Warburton, D. M. (1983). Smoking, Nicotine and Human
Performance. Pharmacological Therapy, 21, 189–208.
