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Books on the topic 'Progressive supranuclear palsy'

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Published: 4 June 2021

Last updated: 9 March 2023

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1

National Institute of Neurological Disorders and Stroke (U.S.). Office of Communications and Public Liaison, ed. Parálisis supranuclear progresiva. Bethesda, Md: U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, National Institute of Neurological Disorders and Stroke, 2000.

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2

Adolfo, Brusa, and Peloso Paolo Francesco, eds. Introduction to Progressive Supranuclear Palsy: Steele-Richardson-Olszowski Syndrome. Rome: Libbey, 1993.

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3

Irene, Litvan, and Agid Yves, eds. Progressive supranuclear palsy: Clinical and research approaches. New York: Oxford University Press, 1992.

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4

Eduardo, Tolosa, Duvoisin Roger C. 1927-, and Cruz-Sánchez F. F, eds. Progressive supranuclear palsy: Diagnosis, pathology, and therapy. Wien: Springer-Verlag, 1994.

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5

Tolosa, E., R. Duvoisin, and F. F. Cruz-Sánchez, eds. Progressive Supranuclear Palsy: Diagnosis, Pathology, and Therapy. Vienna: Springer Vienna, 1994. http://dx.doi.org/10.1007/978-3-7091-6641-3.

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6

Parker, James N., and Philip M. Parker. The official patient's sourcebook on progressive supranuclear palsy. Edited by Icon Group International Inc. San Diego, Calif: Icon Health Publications, 2002.

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7

National Institute of Neurological Disorders and Stroke (U.S.). Office of Communications and Public Liaison., ed. Parálisis supranuclear progresiva. Bethesda, Md: U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, National Institute of Neurological Disorders and Stroke, 2000.

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8

Clagett, Rita. Killing Mother: Progressive Supranuclear Palsy. Independently Published, 2011.

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9

Killing Mother: Progressive Supranuclear Palsy. Llumina Press, 2011.

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10

Progressive supranuclear palsy: Diagnosis, pathology, and therapy. Wien: Springer-Verlag, 1994.

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11

(Editor), Irene Litvan, and Yves Agid (Editor), eds. Progressive Supranuclear Palsy: Clinical and Research Approaches. Oxford University Press, USA, 1992.

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12

(Editor), Roger C. Duvoisin, Eduardo Tolosa (Editor), and F. F. Cruz-Sanchez (Editor), eds. Progressive Supranuclear Palsy: Diagnosis, Pathology, and Therapy (Journal of Neural Transmission Supplementum). Springer, 1994.

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13

Tolosa, Eduardo. Progressive Supranuclear Palsy: Diagnosis, Pathology, and Therapy (Journal of Neural Transmission). Springer, 1994.

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14

Golbe, Lawrence I. Clinician's Guide to Progressive Supranuclear Palsy. Rutgers University Press, 2018.

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15

Golbe, Lawrence I. Clinician's Guide to Progressive Supranuclear Palsy. Rutgers University Press, 2018.

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16

Golbe, Lawrence I. Clinician's Guide to Progressive Supranuclear Palsy. Rutgers University Press, 2018.

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17

(Editor), E. Tolosa, R. Duvoisin (Editor), and F. F. Cruz-Sanchez (Editor), eds. Progressive Supranuclear Palsy: Diagnosis, Pathology, and Therapy. Springer, 2003.

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18

Tolosa, E., F. F. Cruz-Sanchez, and R. Duvoisin. Progressive Supranuclear Palsy: Diagnosis, Pathology, and Therapy. Springer, 2013.

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19

Lawrence I. Golbe M.D. A Clinician's Guide to Progressive Supranuclear Palsy. Rutgers University Press, 2018.

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20

Frame, Limited. Progressive Supranuclear Palsy Journel with Teal Rainbow. Independently Published, 2021.

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21

Briggs, John, Beller Health, and Brain Research. Progressive Supranuclear Palsy: The Best Science in Everyday Language! Independently Published, 2020.

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22

Briggs, John, Jerry Beller, Beller Health, and Brain Research. Frontotemporal Related Dementias: Behavioral Variant Frontotemporal Dementia and Progressive Supranuclear Palsy. Independently Published, 2020.

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23

Tolosa, Eduardo, and Duvoisin Roger C. Progressive Supranuclear Palsy: Diagnosis, Pathology, and Therapy (Journal of Neural Transmission Supplementum). Springer-Verlag Telos, 1994.

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24

Walsh, Richard A. Falling All the Time. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190607555.003.0010.

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Progressive supranuclear palsy is a four-repeat tauopathy that is confirmed, like all neurodegenerative disease, at postmortem examination. An expanding group of clinical syndromes are now linked with this pathology in its early stages, although with disease progression there tends to be greater clinical similarity with the classical Richardson’s syndrome, an akinetic rigid form of parkinsonism with a progressive supranuclear gaze palsy and prominent frontal cognitive impairment. Currently, there are no disease-modifying therapies for progressive supranuclear palsy; however, there continues to be interest in immunotherapies targeted at tau pathology. Liaison with colleagues with an interest in palliative neurology is appropriate for patients in the advanced stages of the disease.

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25

Publications, ICON Health. Progressive Supranuclear Palsy - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References. ICON Health Publications, 2004.

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26

Scott, Kathryn Leigh. Last Dance at the Savoy: Life, Love and Caregiving for Someone with Progressive Supranuclear Palsy. Cumberland Press, 2016.

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27

Publications, ICON Health. The Official Patient's Sourcebook on Progressive Supranuclear Palsy: A Revised and Updated Directory for the Internet Age. Icon Health Publications, 2002.

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28

Watson, Max, Caroline Lucas, Andrew Hoy, and Jo Wells. Palliative care in non-malignant neurological disease. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780199234356.003.0029.

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This chapter focuses on the symptom management of multiple sclerosis, Parkinson’s disease, multiple system atrophy (MSA), progressive supranuclear palsy (PSP), motor neuron disease, neurological complications of AIDS, Creutzfeldt-Jakob disease (CJD), and useful contacts.

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29

Kaplan, Tamara, and Tracey Milligan. Movement Disorders 2: Parkinson’s Plus and Degenerative Diseases (DRAFT). Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190650261.003.0012.

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The video in this chapter explores movement disorders, and focuses on Parkinson’s Plus and degenerative diseases. It outlines the features and pathology of dementia with lewy bodies (DLB), progressive supranuclear palsy (PSP), multiple systems atrophy (MSA) and corticobasal degeneration (CBD), as well as genetic movement disorders, Wilson’s disease, and Huntington’s disease.

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30

Kotagal, Vikas, and Praveen Dayalu. Parkinson Syndromes. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0005.

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Progressive supranuclear palsy (PSP) is a neurodegenerative condition characterized by axial motor features, oculomotor abnormalities, and cognitive dysfunction. PSP is characterized by progressive tau deposition with neuronal loss in cortical and subcortical regions. The underlying etiology of PSP may reflect complex gene-environment interactions, though genetic heterogeneity in the microtubule-associated protein tau (MAPT) gene can confer increased risk. Clinical care of patients with PSP focuses on minimizing motor and non-motor morbidity using available symptomatic therapies.

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31

News, PM Medical Health. 21st Century Complete Medical Guide to Progressive Supranuclear Palsy (PSP), Steele-Richardson-Olszewski Syndrome: Authoritative Government Documents, ... for Patients and Physicians (CD-ROM). Progressive Management, 2004.

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32

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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33

Hodges, John R. Delirium and Dementia. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198749189.003.0002.

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Delirium and dementia affect one or more cognitive domains with a distributed neural basis—attention, memory, and executive function—in some instances accompanied by more focal cognitive deficits. Patients with one, or both, of these conditions constitute the commonest presentation in behavioural neurology and in geriatric psychiatry. This chapter first describes the core characteristics and causes of delirium. This is followed by a description of the major causes of dementia notably, Alzheimer’s disease, frontotemporal dementia, Huntington’s disease, dementia with Lewy bodies, and progressive supranuclear palsy. These are contrasted with pseudodementia, with mention of the causes of rapidly progressive dementia, and differential diagnosis of delirium and dementia.

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34

Roze, Emmanuel, and Frédéric Sedel. Gangliosidoses (GM1 and GM2). Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0050.

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GM1 gangliosidosis is due to beta-galactosidase deficiency. The adult-onset form is characterized by progressive generalized dystonia, often associated with akineto-rigid Parkinsonism. Mild skeletal dysplasia and short stature are good diagnostic clues. GM2 gangliosidosis is due to beta-hexosaminidase deficiency. The adult-onset form is characterized by complex neurological disorders, in which features resulting from cerebellar and motor neuron dysfunction are the most frequent. Movement disorders, psychotic symptoms, mild pyramidal signs, axonal polyneuropathy, autonomic dysfunction, and vertical supranuclear palsy can also be observed. Clinical severity and the rate of progression both vary widely from one patient to another. Diagnosis is based on measurements of enzyme activity and molecular analysis. Physiotherapy, speech therapy and management of swallowing are crucial for these patients’ quality of life and prognosis.

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35

Manni, Raffaele, and Michele Terzaghi. Sleep disorders in neurodegenerative diseases other than Parkinson disease and multiple system atrophy. Edited by Sudhansu Chokroverty, Luigi Ferini-Strambi, and Christopher Kennard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199682003.003.0026.

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This chapter examines sleep–wake disturbances occurring in the most common neurodegenerative disorders. It reviews sleep alterations in Alzheimer disease and dementia with Lewy bodies. It also discusses sleep problems in progressive supranuclear palsy, corticobasal degeneration, Huntington disease, and spinocerebellar ataxias. Status dissociatus as an extreme form of sleep alteration in advanced neurodegenerative diseases is also considered. The chapter reviews the key points for the treatment of disrupted sleep in neurodegenerative disorders, with a focus on pharmacological and nonpharmacological interventions to improve sleep continuity. It also summarizes paraphysiological age-related changes in sleep patterns and discusses indications and procedures for clinical and instrumental assessment of sleep disorders in neurodegenerative disorders.

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36

Hodges, John R. Illustrative Cases. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198749189.003.0008.

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This chapter comprises 16 case histories that illustrate methods of assessment described in the rest of this book and the use of the Addenbrooke’s Cognitive Examination (ACE)-III. Each case begins with a brief history from the patient and observations by the family followed by findings on cognitive examination focusing on the profile shown on the ACE-III, the results of imaging investigations, and a discussion of the diagnosis and its differential, with a final summary of the principal conclusions, indicating whether the services of a neuropsychologist are required or not. The cases present important common conditions (such as mild cognitive impairment, Alzheimer’s disease in the mild and moderate stages, behavioural variant frontotemporal dementia, progressive non-fluent aphasia, semantic dementia, corticobasal degeneration, progressive supranuclear palsy, and Huntington’s disease) as well as interesting neuropsychological syndromes (such as prosopagnosia, amnestic stoke, and transient epileptic amnesia).

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37

Attems, Johannes, and Kurt A. Jellinger. Neuropathology. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199644957.003.0006.

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This chapter describes the main neuropathological features of the most common age associated neurodegenerative diseases including Alzheimer's disease, Parkinson's disease and dementia with Lewy bodies as well as other less frequent ones such as multiple system atrophy, Pick's disease, corticobasal degeneration, progressive supranuclear palsy, argyrophilic grain disease, neurofibrillary tangle dominant dementia, frontotemporal lobar degeneration with TDP-43 pathology and Huntington's disease. Likewise cerebral amyloid angiopathy, hippocampal sclerosis, vascular dementia and prion diseases are described. A main aim of this chapter is to assist the reader in interpreting neuropathological reports, hence criteria for the neuropathological classifications of the major diseases are provided. One section covers general considerations on neurodegeneration and basic pathophysiological mechanisms of tau, amyloid-β, α-synuclein, TDP-43 and prions are briefly described in the sections on the respective diseases. Finally, one section is dedicated to cerebral multimorbidity and we give a view on currently emerging neuropathological methods.

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38

Sedel, Frédéric. Niemann-Pick Disease Type C. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0053.

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Niemann-Pick disease type C (NPC) is a fatal neurovisceral lipid storage disease of autosomal inheritance resulting from mutations in either the NPC1 (95% of families) or NPC2 gene. The encoded proteins appear to be involved in lysosomal/late endosomal transport of cholesterol, glycolipids, and other molecules, but their exact function is still unknown. The clinical spectrum of the disease ranges from a neonatal rapidly fatal disorder to an adult-onset chronic neurodegenerative disease characterized prominently by psychiatric disorders, cerebellar ataxia, cognitive decline, and vertical supranuclear gaze palsy. Miglustat is the only treatment approved to date which has been demonstrated to slow or halt disease progression.

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