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Books on the topic 'Psychotic disease'

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Author: Grafiati
Published: 4 June 2021
Last updated: 20 February 2023

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1

Mania and depression: A classification of syndrome and disease. Baltimore: Johns Hopkins University Press, 1991.

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2

Vulnerability to psychosis: From neurosciences to psychopathology. Hove, East Sussex: Psychology Press, 2012.

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3

Impasse and interpretation: Therapeutic and anti-therapeutic factors in the psychoanalytic treatment of psychotic, borderline and neurotic patients. London: Routledge, 1990.

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4

Rosenfeld, Herbert A. Impasse and interpretation: Therapeutic and anti-therapeutic factors in the psychoanalytic treatment of psychotic, borderline and neurotic patients. London: Tavistock, 1987.

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5

Metzl, Jonathan. The protest psychosis: How schizophrenia became a black disease. Boston: Beacon Press, 2010.

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6

1961-, Fujii Daryl, and Ahmed Iqbal 1951-, eds. The spectrum of psychotic disorders: Neurobiology, etiology, and pathogenesis. Cambridge, UK: Cambridge University Press, 2007.

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7

Tesla, Paul Gabriel. Crime and mental disease in the hand: A proven guide for the identification and pre-identification of criminality, psychosis, and mental defectiveness. Lakeland, FL: Osiris Press, 1991.

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8

Thomas, Jobe, Gaviria Moises, and Kovilparambil Antony, eds. Clinical neuropsychiatry. Malden, Mass., USA: Blackwell Science, 1997.

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9

B, Joseph Anthony, and Young Robert R. 1934-, eds. Movement disorders in neurology and neuropsychiatry. 2nd ed. Malden, MA: Blackwell Science, 1999.

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10

B, Joseph Anthony, and Young Robert R. 1934-, eds. Movement disorders in neurology and neuropsychiatry. Boston: Blackwell Scientific Publications, 1992.

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11

Aging and neuropsychological assessment. New York: Plenum Press, 1992.

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12

Organic psychiatry: The psychological consequences of cerebral disorder. 3rd ed. Oxford: Blackwell Science, 1998.

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13

Organic psychiatry: The psychological consequences of cerebral disorder. 2nd ed. Oxford: Blackwell Scientific ; Chicago, Ill. : Distributors, USA, Year Book Medical Publishers, 1987.

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14

Lishman, William Alwyn. Organic psychiatry: The psychological consequences of cerebral disorder. 3rd ed. Oxford: Blackwell Scientific, 1987.

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15

Rosenfeld, David. Psychotic: Aspects of the Personality. Taylor & Francis Group, 2018.

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16

Rosenfeld, David. Psychotic: Aspects of the Personality. Taylor & Francis Group, 2018.

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17

Psychotic: Aspects of the Personality. Karnac Books, 1992.

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18

Rosenfeld, David. The Psychotic: Aspects of the Personality. Karnac Books, 1992.

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19

Bjørk, Marte Helene, and Malin Eberhard-Gran. Perinatal Depression in Neurological Disease and Disability. Edited by Emma Ciafaloni, Cheryl Bushnell, and Loralei L. Thornburg. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190667351.003.0034.

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Women and men with neurological disease more often suffer from depression in relation to pregnancy and delivery than other parents. Perinatal depression may harm the parent-child relationship as well as the health of the child. Postnatal psychosis, suicide, and infanticide are rare but severe consequences of the disorder. Symptoms of perinatal depression may overlap with symptoms of neurological disease. Both disorders may aggravate each other. Side effects from neurological treatment could mimic symptoms of depression, and antidepressive drugs could worsen neurological symptoms and interact with other treatment. Neurological patients should be evaluated for risk factors for perinatal depression before delivery. These include previous psychiatric disease, sexual or psychical abuse, sleep problems, high neurological disease activity, and low social support. Pregnant women with previous psychotic episodes or bipolar disease should be referred for psychiatric evaluation before delivery. All patients should be screened for depressive symptoms during follow-up using a 3-step method.
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20

Pletnikov, Mikhail V., Guo-Li Ming, and Christopher A. Ross. Animal and Cellular Models of Psychotic Disorders. Edited by Dennis S. Charney, Eric J. Nestler, Pamela Sklar, and Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0015.

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Animal and cell models are experimental systems developed to study particular aspects of a disease, as no model can accurately reflect all features of the disease. In this critical review we mention some of the nongenetic models but focus on genetic mouse models, evaluate their advantages and limitations, and comment on potential new prospects for the field. The ability to reprogram somatic cells from patients and unaffected donors to induced pluripotent stem cells (iPSCs) has the potential to substantially enhance our knowledge of normal cellular development and disease pathogenesis. The use of cell and animal models will help elucidate basic cellular and molecular mechanisms of pathogenesis, which will enable the development of targeted therapeutic approaches.
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21

Nichols, Mary, Suzanne Button, Katherine Hoople, and Laura Lappan. Early Identification, Palliative Care, and Prevention of Psychotic Disorders in Children and Youth. Lantern Books, 2016.

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22

DeRenzo, Evan G., and Philip J. Candilis. Ethics and the Paradigm Shift in Schizophrenia. Edited by John Z. Sadler, K. W. M. Fulford, and Werdie (C W. ). van Staden. Oxford University Press, 2015. http://dx.doi.org/10.1093/oxfordhb/9780198732372.013.38.

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Early intervention strategies for treating psychosis before the manifestation of frank disease have blossomed as research shows the positive impact of treatment earlier in the development of psychotic illness. Because of the uncertainty of individual patients’ conversion to an easily diagnosable condition however, ethical concerns have arisen in establishing the appropriate balance of risks and harms, in obtaining informed consent, and in conducting general research and treatment of minors. This chapter examines the ethics of early intervention from a historical perspective, tracing advances in research ethics that allowed the conduct of research with children who may develop psychotic illness to the clinical ethics required in offering early interventions themselves. The authors explore the implications of early intervention’s introduction into the psychiatric diagnostic manual and recommend avenues for further discourse.
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23

Perminder, Sachdev, and Keshavan Matcheri S. 1953-, eds. Secondary schizophrenia. Cambridge: Cambridge University Press, 2010.

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24

Acute and Transient Psychoses. Cambridge University Press, 2006.

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25

Fusar-Poli, Paolo, Philip McGuire, and Stefan J. Borgwardt. Vulnerability to Psychosis: From Neurosciences to Psychopathology. Taylor & Francis Group, 2013.

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26

Fusar-Poli, Paolo, Philip McGuire, and Stefan J. Borgwardt. Vulnerability to Psychosis: From Neurosciences to Psychopathology. Taylor & Francis Group, 2013.

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27

Fusar-Poli, Paolo, Philip McGuire, and Stefan J. Borgwardt. Vulnerability to Psychosis: From Neurosciences to Psychopathology. Taylor & Francis Group, 2013.

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28

Fusar-Poli, Paolo, Philip McGuire, and Stefan J. Borgwardt. Vulnerability to Psychosis: From Neurosciences to Psychopathology. Taylor & Francis Group, 2013.

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29

Fusar-Poli, Paolo, Philip McGuire, and Stefan J. Borgwardt. Vulnerability to Psychosis: From Neurosciences to Psychopathology. Taylor & Francis Group, 2013.

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30

D, Simon Pierre M., Soubrié P, and Widlöcher Daniel, eds. Selected models of anxiety, depression, and psychosis. Basel: Karger, 1988.

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31

McDonald, Colm. Maudsley Family Study of Psychosis: A Quest for Intermediate Phenotypes. Taylor & Francis Group, 2008.

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32

McDonald, Colm. Maudsley Family Study of Psychosis: A Quest for Intermediate Phenotypes. Taylor & Francis Group, 2008.

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33

McDonald, Colm. Maudsley Family Study of Psychosis: A Quest for Intermediate Phenotypes. Taylor & Francis Group, 2008.

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34

McDonald, Colm. Maudsley Family Study of Psychosis: A Quest for Intermediate Phenotypes. Taylor & Francis Group, 2008.

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35

McDonald, Colm. Maudsley Family Study of Psychosis: A Quest for Intermediate Phenotypes. Taylor & Francis Group, 2008.

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36

Colm, McDonald, ed. The Maudsley family study of psychosis: A quest for intermediate phenotypes. Hove, East Sussex: Psychology Press, 2008.

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37

The Spectrum of Psychotic Disorders. Cambridge University Press, 2007.

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38

Killingsworth, Jerry. Teknosis Psychosis Disease: Artificial-Virtual-Un-Reality. Independently Published, 2018.

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39

Grant, Seth G. N. Synaptic Mechanisms of Psychotic Disorders. Edited by Dennis S. Charney, Eric J. Nestler, Pamela Sklar, and Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0017.

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Synapses are the hallmark of the neuroanatomy of the brain. The million billion synapses of the human brain connect the nerve cells into the networks that underpin all behavior. The molecular anatomy of synapses is also remarkably complicated with ~2000 proteins in the synapse proteome. The proteins are physically organized into a hierarchy of molecular machines that control synapse biology. These proteins integrate and compute the information in patterns of nerve cell activity. Mutations in hundreds of genes that encode synaptic proteins contribute to over one hundred brain diseases, including common mental disorders. The synapse proteome is of fundamental importance to mental illness.
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40

Mogul, Joey L., Andrea J. Ritchie, and Kay Whitlock. Protest Psychosis: How Schizophrenia Became a Black Disease. Beacon Press, 2011.

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41

Metzl, Jonathan. The Protest Psychosis: How Schizophrenia Became a Black Disease. Beacon Press, 2011.

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42

Nageshwaran, Sathiji, Heather C. Wilson, Anthony Dickenson, and David Ledingham. Parkinson’s disease and parkinsonism. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199664368.003.0009.

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This chapter discusses the evidence-based pharmacological management of motor and non-motor (autonomic disease, dementia, psychosis, depression, and sleep disorder) Parkinson’s disease (PD) and Parkinson’s plus syndromes (progressive supranuclear palsy (PSP), multiple system atrophy (MSA), and corticobasal degeneration (CBD)). Drugs to use with caution in parkinsonism are highlighted. Clinical features and evidence-based management of impulse control disorders (ICDs), serotonin syndrome, dopamine agonist withdrawal syndrome (DAWS), and neuroleptic malignant syndrome (NMS)/Parkinson’s hyperpyrexia syndrome (PHS) are also reviewed.
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43

James, Anthony. Depressive Disorders in Childhood and Adolescence. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780198801900.003.0008.

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This chapter focuses on depressive disorders in childhood and adolescence. Depression in children and adolescents is a complex and debilitating disease, and typically has a lifelong, chronic, and recurrent course. The peak age of onset of depression is between 13 and 15 years. After providing a clinical picture of depression, this chapter discusses early childhood depression and differential diagnosis, including paediatric bipolar disorder, psychotic depression and seasonal affective disorder, oppositional and conduct disorder, and substance misuse and medical conditions. It then examines comorbidity, paying attention to bipolar disorder and suicidal behaviour, along with the assessment and prevention of depression. It also considers some of the determinants of depression, such as stress, trauma, life events, and biological factors such as genetics, brain mechanisms, hormones, and resilience. Finally, it describes treatment options for childhood and adolescent depression.
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44

Ahmed, Iqbal, and Daryl Fujii. Spectrum of Psychotic Disorders: Neurobiology, Etiology and Pathogenesis. Cambridge University Press, 2007.

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45

Ahmed, Iqbal, and Daryl Fujii. Spectrum of Psychotic Disorders: Neurobiology, Etiology and Pathogenesis. Cambridge University Press, 2007.

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46

Ahmed, Iqbal, and Daryl Fujii. Spectrum of Psychotic Disorders: Neurobiology, Etiology and Pathogenesis. Cambridge University Press, 2010.

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47

Depression, psychosis, and dementia in Parkinson's disease: Diagnosis and treatment. Hagerstown, Md: Lippincott Williams & Wilkins, 1999.

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48

Burdick, Katherine E., Luz H. Ospina, Stephen J. Haggarty, and Roy H. Perlis. The Neurobiology and Treatment of Bipolar Disorder. Edited by Dennis S. Charney, Eric J. Nestler, Pamela Sklar, and Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0020.

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Bipolar disorder (BPD) is a severe mood disorder that often has psychotic features. Its most severe forms are more common and significantly more likely to cause disability than originally thought. Studies of high-risk children have found them to be at increased risk for a variety of symptoms and neurobiological abnormalities. In contrast to schizophrenia, there is no formal prodromal syndrome that has been identified, and cognitive abnormalities do not precede the onset of the disorder. Abnormal sleep and circadian rhythms are prominent and have led to intriguing biological models. Neurobiological experiments have primarily focused on candidate pathways and include circadian abnormalities, epigenetic processes including histone modification, WNT/GSK3 signaling, other modulators of neuroplasticity, and mitochondrial dysfunction. Recent data suggest that BPD is a highly polygenic disease and that integration of prior modeling and data with the wide variety of new genetic risk loci will be productive in the future.
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49

Rucci, Jennifer M., and Robert E. Feinstein. Neurocognitive Disorders and Mental Disorders Due to Another Medical Condition. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199326075.003.0005.

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The defining feature of neurocognitive disorders is a decline in cognitive functioning. Patients suffering from delirium experience an acute change in mental status, fluctuating levels of consciousness, and an inability to acquire new information. Patients with major neurocognitive disorder experience significant cognitive decline in complex attention, executive function, learning and memory, language, perceptual-motor, and social cognition. The chapter also discusses mental disorders due to another medical condition. These patients can experience psychotic, mood, or anxious symptoms or a personality change; their intellectual functioning usually remains intact. A patient presenting with a first episode of psychiatric symptoms and no prior psychiatric history should be evaluated for an acute medical etiology causing the psychiatric symptoms, particularly if he or she is over 40 years of age. Anticholinesterase inhibitors (donepezil, galantamine, and rivastigmine) may slow the rate of cognitive decline in Alzheimer’s disease, and the combination of an anticholinesterase inhibitor and memantine may be more effective than either medication alone.
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50

(Editor), Daryl Fujii, and Iqbal Ahmed (Editor), eds. The Spectrum of Psychotic Disorders: Neurobiology, Etiology & Pathogenesis. Cambridge University Press, 2007.

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