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Books on the topic 'Dystonic movements'

Author: Grafiati

Published: 3 June 2025

Last updated: 31 July 2025

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1

National Institute of Neurological Disorders and Stroke (U.S.). Office of Scientific and Health Reports. The dystonias. U.S. Department of Health and Human Services, Public Health Service, National Institutes of Health, 1996.

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2

Masaya, Segawa, ed. Hereditary progressive dystonia with marked diurnal fluctuation. Parthenon Pub. Group, 1993.

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3

Susan, Grube, and Patil Parag G, eds. Deep brain stimulation: A new life for people with Parkinson's, dystonia and essential tremor. Demos Health, 2012.

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4

Fletcher, Nicholas. Movement disorders. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0926.

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Almost any neurological disorder can produce a disorder of movement but the ‘movement disorders’ include the akinetic rigid syndromes, hyperkinesias, and some tremors. It can sometimes seem, especially with the use of videotape recordings, that diagnosis of movement disorders is mainly a matter of correct visual recognition. Such an approach is not recommended and can lead to mistakes unless, as in other areas of medicine, the history is considered first and the physical signs second. Obvious examples include the family history in Huntington’s disease, developmental history in dystonic cerebra

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5

de Bie, Robertus M. A., and Susanne E. M. Ten Holter. A Tremor with an Abnormal Posture. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190607555.003.0018.

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Dystonic tremors are a commonly misdiagnosed group of primary tremor disorders, typically mistaken for Parkinson’s disease or essential tremor. Like most movement disorders, this is a clinical diagnosis, so the overlap in some features between all of these disorders can be confusing to less experienced and even more experienced physicians. A tremor in the presence of a dystonia is a dystonic tremor syndrome, regardless of the clinical features. Treatment of dystonic tremor can be challenging without the same gratifying response seen to levodopa in tremor associated with Parkinson’s disease or

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6

de Bie, Robertus M. A., and Susanne E. M. Ten Holter. Advanced Treatment for Dystonia. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190607555.003.0019.

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Deep-brain stimulation is a last resort for the management of dystonia or dystonic movement disorders when oral or injectable therapies do not provide adequate relief to allow an acceptable quality of life. The underlying pathogenesis of dystonia is less well understood than in Parkinson’s disease, in which deep-brain stimulation is generally expected to provide effective and long-lasting benefit. Furthermore, it is likely that dystonia represents a number of different basal ganglia pathologies. The response of dystonia to deep-brain stimulation is typically delayed for up to weeks or months f

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7

Williams, Jeri Yvonne, and David G. Standaert. Dystonia. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0011.

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Dystonia is a movement disorder characterized by sustained or intermittent muscle contractions. Classification of dystonia is based on age of onset, distribution of body parts affected, and underlying etiology. A large number of different genetic forms of dystonia have been discovered in recent years. Although these syndromes are important to recognize, the majority of dystonias encountered in clinical practice are of unknown cause. Therapy of dystonia includes medications, particularly anticholinergic drugs, use of botulinum toxins, and deep brain stimulation.

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8

Jinnah, H. A., Bettina Balint, and Victor S. C. Fung, eds. The Dystonias. Oxford University PressNew York, 2025. https://doi.org/10.1093/med/9780197631966.001.0001.

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Abstract The dystonias are a heterogeneous group of disorders characterized by excessive muscle contractions leading to abnormal postures and movements. The clinical manifestations of this broad group of disorders are quite varied. The dystonias may emerge at any age from infancy through late adulthood, they may affect muscles in nearly any region of the body, they may occur without other clinical problems, or they may be combined with other neurological or systemic disorders. There are many etiologies for dystonia, both acquired and inherited, although many are idiopathic. The clinical manife

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9

Jinnah, H. A., Cecilia N. Prudente, Samuel J. Rose, and Ellen J. Hess. The Neurobiology of Dystonia. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0010.

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The dystonias are a large group of disorders characterized by excessive muscle activity leading to abnormal movements. They are clinically diverse, affecting different parts of the body at all ages in both humans and other animals. They also are etiologically diverse, with causes that are either inherited due to specific dystonia-causing genes, or acquired because of nervous system injury or exposure to certain drugs or chemicals. Despite the clinical and etiological heterogeneity, there is an increasing appreciation that certain subgroups of dystonias share some biological abnormalities at th

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10

Nageshwaran, Sathiji, Heather C. Wilson, Anthony Dickenson, and David Ledingham. Hyperkinetic movement disorders. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199664368.003.0010.

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This chapter discusses the clinical features and evidence-based pharmacological management of tremor, dystonia (focal, generalized, and dopa-responsive dystonia), tics and Tourette’s syndrome, chorea (Huntington’s disease (HD) and Sydenham’s chorea), ballism and athetosis, myoclonus, and restless legs syndrome (RLS).

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11

Walsh, Richard A., Robertus M. A. de Bie, and Susan H. Fox, eds. Movement Disorders. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190607555.001.0001.

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Part of the “What Do I Do Now?” series, Movement Disorders uses a case-based approach to cover common and important topics in the examination, investigation, and management of Parkinson’s disease, gait disorders, dystonia, and other movement disorders. Each chapter provides a discussion of the diagnosis, key points to remember, and selected references for further reading. For this edition, all cases and references have been updated and 15 new cases have been added, including the following: genetic testing in Parkinson’s disease, dementia with Lewy bodies, fragile X tremor ataxia syndrome, use

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12

Berardelli, Alfredo, and Mark Hallett. TMS in movement disorders. Edited by Charles M. Epstein, Eric M. Wassermann, and Ulf Ziemann. Oxford University Press, 2012. http://dx.doi.org/10.1093/oxfordhb/9780198568926.013.0021.

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Transcranial magnetic stimulation (TMS) is applied to study patients with movement disorders. This article reviews the findings of such applications in patients with Parkinson's disease, dystonia, Huntington's disease, Tourette's syndrome, and essential tremor. The findings related to Parkinson's disease are characterized by a shortening of the cortical silence period (cSP), a reduction of short intracortical inhibition, an increase in the long-lasting intracortical inhibition, and a reduction of the normal motor evoked potential facilitation after single and repetitive TMS stimuli. Studies wi

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13

Hallett, Mark, and Alfredo Berardelli. Movement Disorders. Edited by Charles M. Epstein, Eric M. Wassermann, and Ulf Ziemann. Oxford University Press, 2012. http://dx.doi.org/10.1093/oxfordhb/9780198568926.013.0044.

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This article focuses on the potential therapeutic uses of transcranial magnetic stimulation (TMS) in movement disorders. The brain can be stimulated with low levels of direct electrical current, called direct current polarization (tDCS). High-frequency repetitive TMS might increase brain excitability and be used for therapy in Parkinson's disease. Single sessions with TMS, however, have not proven to be very effective. Treatment with tDCS has been performed in some open studies with some success, but these results need confirmation. Physiological findings in dystonia reveal a decrease in intra

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14

Waln, Olga, and Joseph Jankovic. Paroxysmal Dyskinesias and Other Paroxysmal Movement Disorders. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0012.

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Paroxysmal dyskinesias are episodic, recurrent movement disorders characterized by attacks of dystonia, chorea, athetosis, ballism, or any combination of these hyperkinetic movements, with variable duration and frequency of the episodes and normal interictal neurological examination. Four main types of paroxysmal dyskinesias have been described: paroxysmal kinesigenic dyskinesia, paroxysmal nonkinesigenic dyskinesia, paroxysmal exercise-induced dyskinesia, and paroxysmal hypnogenic dyskinesia. The disorders are usually inherited in autosomal dominant fashion and have their onset in the first t

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15

Fox, Susan H. Delayed and Often Persistent. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190607555.003.0021.

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Tardive syndromes are drug-induced hyperkinetic movement disorders that occur as a consequence of dopamine D2 receptor antagonism/blockade. There are several types, including classical tardive dyskinesia, tardive dystonia, tardive tics, tardive myoclonus, and tardive tremor, and it is important to the management of these disorders that the type of movement disorder induced is identified. Tardive syndromes can occur with all antipsychotic drugs, including so-called atypical drugs. Patients taking these drugs should be evaluated frequently for side effects. Evaluating the nature of the movement

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16

Curl, James Stevens. Making Dystopia: The Strange Rise and Survival of Architectural Barbarism. Oxford University Press, 2019.

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17

Making Dystopia: The Strange Rise and Survival of Architectural Barbarism. Oxford University Press, 2018.

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18

Patil, Parag G. Deep Brain Stimulation : : A New Life for People with Parkinson's, Dystonia, and Essential Tremor. ReadHowYouWant.com, Limited, 2013.

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19

Grube, Susan, Parag Patil, and Kelvin L. Chou. Deep Brain Stimulation: A New Life for People with Parkinson's, Dystonia, and Essential Tremor. Springer Publishing Company, Incorporated, 2011.

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20

Patil, Parag G. Deep Brain Stimulation: A New Life for People with Parkinson's, Dystonia, and Essential Tremor. ReadHowYouWant.com, Limited, 2013.

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21

Tics and related disorders. Churchill Livingstone, 1985.

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22

Orwell, George. Nineteen Eighty-Four (Vintage Dystopia). Vintage Classics, 2018.

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23

Quarrell, Oliver. Huntington's Disease. 3rd ed. Oxford University Press, 2020. http://dx.doi.org/10.1093/oso/9780198844389.001.0001.

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Huntington’s disease (HD)―the facts provides an overview of the condition aimed at families and carers understanding the condition. It describes the key features of: a movement disorder, disturbance of mood (affect), and problems with thinking (cognition) and behaviour. The movement problems of chorea, dystonia, and bradykinesia are explained but there is equal emphasis on depression impulsive behaviour and temper outbursts. Understanding the cause of these may help families cope better when they arise. The genetic change is discussed as is its effect on the protein huntingtin. Options for gen

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24

Shaibani, Aziz. Weakness of the Neck Muscles. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199898152.003.0010.

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The neck is furnished by dozens ofmuscles for flexion, extension, lateral bending, and rotation. It carries a 10-pound head at least two-thirds of every day. These muscles are under delicate central control, and they are subject to different central and peripheral malfunctions. Differential involvement of the neck flexors versus extensors helps in diagnosing different neuromuscular disorders. Weakness of the cervical extensors leads to head drop, a troubling condition that is caused by many neuromuscular disorders. Movement disorders such as cervical dystonia and Parkinson disease may also lea

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25

Klepper, Joerg, and Baerbel Leiendecker. Glut1 Deficiency. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0005.

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Glut1 Deficiency (Glut1D, OMIM #606777) is caused by impaired glucose transport into the brain. The resulting cerebral “energy crisis” causes intractable seizures, developmental delay, and a complex movement disorder. The diagnosis is based on clinical features, low CSF glucose and/or mutations in the SLC2A1 gene. Paroxysmal exertion-induced dystonia (PED) and hereditary cryohydrocytosis have been described as allelic variants. Adults are increasingly being recognized through family pedigrees. The condition is effectively treatable by mimicking the metabolic state of fasting. High-fat carbohyd

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26

Shaibani, Aziz. Weakness of the Neck Muscles. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190661304.003.0010.

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The neck is furnished by tens of muscles for flexion, extension, lateral bending, and rotation. It carries a 10-pound head for at least two-thirds of every day. These muscles are under delicate central control, and they are subject to different central and peripheral malfunctions. Differential involvement of the neck flexors’ Vs extensors helps with the diagnosis of various neuromuscular disorders. Weakness of the cervical extensors leads to head drop, a troubling condition that is caused by many neuromuscular disorders. Movement disorders such as cervical dystonia and Parkinson disease lead t

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27

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 vert

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28

Roze, Emmanuel, and Nenad Blau. Biogenic Monoamine Disorders. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0031.

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Biogenic monoamine disorders are a group of inherited diseases characterized by a defect in the synthesis, transport, or degradation of catecholamines and serotonin. The phenotype mostly reflects the pattern and severity of the monoamine deficiency. Movement disorders due to cerebral dopamine deficiency are almost always prominent, mostly in the form of dystonia and/or parkinsonism. These disorders are potentially devastating yet treatable. Early diagnosis and treatment are crucial to prevent ongoing brain dysfunction. Detection of hyperphenylalaninemia in a neonate could be a good clue to the

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29

Klepper, Joerg. Glut1 Deficiency and the Ketogenic Diets. Edited by Eric H. Kossoff. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0005.

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Glucose is the essential fuel for the brain. Transport into brain is exclusively mediated by the facilitative glucose transporter Glut1. Glut1 deficiency results in a “brain energy crisis,” causing global developmental delay, epilepsy, and complex movement disorders including paroxysmal nonepileptic events. Early-onset absence epilepsy, paroxysmal exertion-induced dystonia, and stomatin-deficient cryohydrocytosis have been recognized as variants. Diagnosis is based on phenotype, isolated low CSF glucose, and mutations in the SLC2A1 gene. The condition is treated effectively by classical ketoge

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30

Callison, William, and Zachary Manfredi, eds. Mutant Neoliberalism. Fordham University Press, 2019. http://dx.doi.org/10.5422/fordham/9780823285716.001.0001.

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Tales of neoliberalism’s death are serially overstated. Seemingly repudiated by historical events and yet staggering on like an undead cadaver, neoliberalism was proclaimed a “zombie” ideology following the 2008 financial crisis. After the major political shocks of 2016, the global rise of the far right, and the rebirth of democratic socialist politics, commentators declared “the end of neoliberalism” once again. Yet even as new political forces emerge from decades of neoliberal hegemony, it remains far from certain whether they will sound neoliberalism’s death knell or rather propel new movem

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31

Staffell, Simon, and Akil Awan, eds. Jihadism Transformed. Oxford University Press, 2017. http://dx.doi.org/10.1093/acprof:oso/9780190650292.001.0001.

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Jihadist narratives have evolved dramatically over the past five years, driven by momentous events in the Middle East and beyond; the death of bin Laden; the rise and ultimate failure of the Arab Spring; and most notably, the rise of the so-called Islamic State. For many years, Al-Qaeda pointed to an aspirational future Caliphate as their utopian end goal - one which allowed them to justify their violent excesses in the here and now. Islamic State turned that aspiration into a dystopic reality, and in the process hijacked the jihadist narrative, breathing new life into the global Salafi-Jihadi

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32

Nishime, Leilani. Aliens. University of Illinois Press, 2017. http://dx.doi.org/10.5406/illinois/9780252038075.003.0004.

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This chapter examines the visual exclusion of multiracial Asians. It also looks at television and film's overt use of multiracial tropes to signal utopic/dystopic futures. The science-fiction television series Battlestar Galactica follows the logic of post-race, wherein racial differences are acknowledged but then ignored. The show's narrative hinges upon the survival of a child, Hera, the bi-species and multiracial child of the cyborg Athena (Korean American actress Grace Park) and the human Helo (Euro-American actor Tahmoh Penikett). Hera's representation resonates with images of the multira

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33

Adin, Mariah. The Brooklyn Thrill-Kill Gang and the Great Comic Book Scare of the 1950s. ABC-CLIO, LLC, 2014. http://dx.doi.org/10.5040/9798400621819.

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What caused four recently bar mitzvahed middle-class youths to go on a crime spree of assault and murder in 1954? This book provides a compelling narrative retelling of the boys, their crimes, and a U.S. culture obsessed with juvenile delinquency. After ongoing months of daily headlines about gang shootouts, stomp-killings, and millions of dollars worth of vandalism, by the summer of 1954, America had had enough of juvenile delinquency. It was in this environment that 18-year-old Jack Koslow and the other three teenage members of the Brooklyn Thrill Killers committed their heinous crimes and a

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