Books on the topic 'Parkinson’s tremor'
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1
Susan, Grube, and Patil Parag G, eds. Deep brain stimulation: A new life for people with Parkinson's, dystonia and essential tremor. New York, NY: Demos Health, 2012.
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2
Molnar, Gregory F. Neuronal firing rates in motor thalamus of Parkinson's disease (PD) and Essential tremor (ET) patients. Ottawa: National Library of Canada, 2000.
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3
Walsh, Richard A. Parkinson’s Disease or Essential Tremor? Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190607555.003.0016.
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Fragile X-associated tremor ataxia syndrome is a heredodegenerative syndrome that presents in older men as a tremor syndrome with less prominent ataxia and cognitive impairment initially. The underlying genetic cause, a premutation in the FMR1 gene, results in a toxic accumulation of mRNA. The full mutation, a triple-repeat expansion of more than 200 CGG repeats, gives rise to a reduction in FMR1 protein expression and fragile X, a neurodevelopmental disorder that may be identified in successive male generations. The prevalence of carrier status is high in the general population, and it is likely that most movement disorders clinics will have one or more patients with this syndrome, potentially carrying a label of essential tremor.
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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 to beta-blockers and primidone in essential tremor. Deep-brain stimulation remains an option in the most disabling cases.
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Walsh, Richard A. Parkinson’s Disease with an Unusual Tremor. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190607555.003.0009.
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Multiple system atrophy represents a form of atypical parkinsonism that is challenging to manage and results in rapidly progressive disability and dependence in the absence of effective disease-modifying or symptomatic therapies. Two syndromes are recognized, both associated with autonomic dysfunction—MSA-C and MSA-P, with a predominance of parkinsonian and cerebellar features, respectively. Magnetic resonance imaging can assist with an early diagnosis, demonstrating certain features that can be considered diagnostic in the right clinical context. The typical changes described may not be apparent on an initial scan, so it is worth repeating imaging 1 or 2 years later if the clinical features and course are typical of multiple system atrophy.
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de Bie, Robertus M. A. The Stand-Alone Tremor. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190607555.003.0022.
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Essential tremor is defined as long-standing bilateral hand/arm tremor that is visible and may occur persistently during posture-holding, simple movements, and action. The tremor may be slightly asymmetrical. Other areas of the body that may be affected are head and neck (most frequently), the voice, and legs. Head tremor without limb tremor is accepted as essential tremor, although this definition remains controversial. Essential tremor is a progressive disease and manifests at any age. Tremor in Parkinson’s disease mostly starts unilaterally. A no–no or yes–yes tremor of the head indicates essential tremor, whereas a tremor of the jaw or tongue fits with Parkinson’s disease. The cogwheel phenomenon may also occur in patients with essential tremor. Toxins and medications as the cause for postural/kinetic tremor must be ruled out. Pharmacological options for essential tremor can be unsatisfactory.
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Kaplan, Tamara, and Tracey Milligan. Movement Disorders 1: Tourette’s Syndrome, Essential Tremor, and Parkinson’s Disease (DRAFT). Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190650261.003.0011.
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The video in this chapter explores movement disorders, and focuses on Tourette’s Syndrome, Essential tremor, and Parkinson’s Disease. It outlines the characteristics of each, such as motor and vocal tics in Tourette’s Syndrome, postural or kinetic tremor in Essential tremor, and the four hallmark features of Parkinson’s Disease (bradykinesia, resting tremor, cogwheel rigidity, and postural instability).
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de Bie, Robertus M. A. Beyond Tremor, Slowness, and Stiffness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190607555.003.0004.
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Parkinson’s disease may be accompanied by a variety of nonmotor symptoms, such as autonomic, cognitive, psychiatric, sensory, and sleep disorders. These may even precede the motor symptoms, and in a considerable proportion of patients nonmotor symptoms are the major determinant of disability, especially in the more advanced stages of the disease. The patient in this chapter is experiencing two nonmotor symptoms—pain and insomnia. If present, it should be determined whether nonmotor symptoms fluctuate, because many are worse in the “off” period. The most common cause for insomnia is untreated or undertreated nocturnal parkinsonism, which is very responsive to levodopa therapy. If a medical condition requiring further evaluation is excluded and a temporal relationship between pain and the medication schedule is recognized, the emphasis should be on adjusting dopaminergic medication accordingly.
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Fletcher, Nicholas. Tremor, ataxia, and cerebellar disorders. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0898.
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Tremors are characterized by rhythmic oscillations of one or more body parts. Although typically seen in the upper limbs, almost any area may be involved, including the trunk, head, facial muscles, and legs. Sometimes, tremor is not visible at all but may be heard or palpated, for example, in vocal or orthostatic tremor, respectively. In neurological practice, the diagnosis and treatment of tremor is an everyday problem. A common scenario is the distinction between essential tremor and Parkinson’s disease. In this chapter, the wide range of tremors are discussed, with their aetiolology, pathophysiology, diagnosis and management described.Ataxia is a term used to describe a wide range of neurological disorders affecting muscle coordination, speech and balance that reflect dysfunction of a part of the central nervous system involved in motor function. Many of ataxias have a cerebellar pathology as root cause, although it must be remembered that ataxia, clumsiness, disordered ocular motility, dysarthria, and even kinetic or intention tremor are not always caused by cerebellar disease. This chapter describes the wide range of cerebellar disorders and ataxias, as are non-cerebellar ataxias such as Friedreich’s ataxia.
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Bowker, Lesley K., James D. Price, Ku Shah, and Sarah C. Smith. Neurology. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198738381.003.0007.
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This chapter provides information on the ageing brain and nervous system, tremor, neuropathic pain/neuralgia, presentation of Parkinson’s disease, management of Parkinson’s disease, diseases masquerading as Parkinson’s disease, epilepsy and its drug treatment, neuroleptic malignant syndrome, motor neuron disease, peripheral neuropathies, subdural haematoma, sleep and insomnia, and other sleep disorders.
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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 of botulinum toxin in dystonia, catatonia, and serotonin syndrome. Movement Disorders is an engaging collection of thought-provoking cases that clinicians can utilize when they encounter difficult patients. The volume is also a self-assessment tool that tests the reader’s ability to answer the question, “What do I do now?”
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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 cerebral palsy, and neuroleptic drug treatment in patients with tardive dyskinesia. In addition, a single disorder may give rise to several different types of involuntary movement. For example, Huntington’s disease may give rise to an akinetic rigid state, chorea, myoclonus, tics, or dystonia. Patients with Parkinson’s disease taking levodopa may show different types of movement disorder at different times of the day.In akinetic rigid states the diagnostic issue will be whether the patient has idiopathic Parkinson’s disease or one of the other Parkinsonian syndromes. With involuntary movements, the first step in diagnosis is to classify these as dystonia, tics, tremor, chorea, or myoclonus. It must be remembered that involuntary movements are merely physical signs, not diagnostic entities, and that they do not always occur in a pure form; for example, patients with dystonia may have additional choreiform movements or tremor. If more than one form of abnormal movement seems to be present, the diagnosis should be based on the most obvious one. The next step is to decide on the cause of the movements and at this stage the diagnosis must be based upon an accurate and complete history as noted above.The movement disorders are often associated with abnormalities of the basal ganglia and, to some extent, vice versa. This is not entirely correct. Disturbances of basal ganglia function certainly have profound effects on movement with the development of bradykinesia, rigidity, tremor, or the various forms of dyskinesia. However, it is not correct when considering the pathophysiology of movement disorders to regard the basal ganglia as an isolated movement control centre. In fact, they are an important but poorly understood component of a much wider motor system. It is also important to remember that the basal ganglia are involved in the processing of limbic and other cognitive processes which may also be disturbed by basal ganglia dysfunction.
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Soileau, Michael J., and Kelvin L. Chou. Parkinson Disease. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0002.
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Parkinson disease is a neurodegenerative disorder characterized clinically by tremor, rigidity, bradykinesia, and postural instability and pathologically by loss of nigrostriatal neurons and deposition of alpha-synuclein in neuronal cell bodies and neuritis. Non-motor symptoms such as psychiatric disorders, cognitive abnormalities, sleep dysfunction, autonomic dysfunction, and sensory manifestations are also common. This chapter gives a broad overview of this disorder. Sections cover pathophysiology, genetics, clinical manifestations, and disease course. The chapter also briefly discusses how to make the diagnosis, and alternative conditions that should be considered.
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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 with paired-pulse TMS have provided controversial information on cortical motor excitability in Huntington's disease. The findings in dystonia include: a reduction of the short intracortical inhibition and a shortening of the cSP. In Tourette's syndrome patients, the cSP is short and intracortical inhibition is decreased. Patients with essential tremor have normal corticospinal conduction, normal duration of the cSP, and normal intracortical inhibition. Such application of TMS has produced enormous data and continues to do so.
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Walsh, Richard A. “I Am Not Sure If I Should Do DaT”. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190607555.003.0008.
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Nuclear medicine-based imaging techniques can provide an estimation of nigrostriatal tract denervation based on radionucleotide uptake in the distal presynaptic terminals of dopaminergic neurons. Although unhelpful in differentiating between differing etiologies of denervation in varied neurodegenerative disorders associated with parkinsonism, this imaging is justified in situations in which parkinsonism is believed to be drug-induced or functional or in cases in which subclinical parkinsonism is suspected. The most common clinical situation in which dopamine transporter imaging is helpful is in the patient on neuroleptic therapy that cannot be stopped who has developed parkinsonism. Dopamine transporter imaging should be normal in drug-induced tremor.
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Machado, Sandra. Deep Brain Stimulation/Stereotaxic Surgery. Edited by David E. Traul and Irene P. Osborn. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190850036.003.0019.
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Deep brain stimulation (DBS) is now a widely accepted treatment option for patients with movement disorders such as parkinsonism and essential tremor. DBS surgery presents challenges to the anesthesiologist as often these patients are required to be awake for accurate placement of the stimulators. Additionally, patients with movement disorders often have comorbidities that increase their risk of perioperative and postoperative complications. DBS surgery is often divided into two stages (1) stereotactic implantation of the DBS leads and (2) internalization of the pulse generator, with each of these stages stage having distinct anesthesia demands. Ongoing studies are exploring other indications for the effective use of DBS surgery.
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Fox, Susan H. Could It Possibly Be … ? Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190607555.003.0027.
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There is increasing recognition of adult presentations of metabolic diseases typically associated with children. These phenotypes are often milder and potentially mistaken for more common adult-onset disorders, therefore requiring a high index of suspicion. The most common adult-onset clinical features involve focal dystonias and parkinsonism. Making a diagnosis of dopa-responsive dystonia in an adult typically involves a therapeutic trial of low-dose levodopa. Genetic testing may be useful to confirm dopa-responsive dystonia and rule out other causes of dystonia and tremor. The neurological examination should be performed carefully to ensure that subtle dystonia is not missed. A trial of levodopa may be warranted to ensure that late-onset dopa-responsive dystonia is not missed.
18
Shannon, Joyce Brennfleck. Movement Disorders Sourcebook: Basic Consumer Health Information About Neurological Movement Disorders, Including Essential Tremor, Parkinson's Disease, ... Reference Series) (Health Reference Series). Omnigraphics, Inc., 2002.
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19
G, Bain Peter, ed. Deep brain stimulation. Oxford: Oxford University Press, 2009.
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20
Chitnis, Shilpa, Pravin Khemani, and Michael S. Okun, eds. Deep Brain Stimulation. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780190647209.001.0001.
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The fundamental principles of deep brain stimulation treatment are derived from decades of empirical and experiential observations. Through a case-based approach, this book is an effort to distill the expertise of clinical teams who are at the frontlines of managing patients with deep brain stimulation. The vast majority of patients with tremors, Parkinson disease, dystonia and other hyperkinetic disorders treated with DBS obtain significant relief of their neurological symptoms with conventional programming techniques that are outlined at the beginning of each section in this book. However, perioperative complications, stimulation induced side-effects and unexpected clinical symptoms such as freezing of gait after globus pallidus implantation for dystonia (Case 20), persistent dyskinesia after subthalamic stimulation (Case 17), and erosion of device hardware (Case 24) warrant unconventional and creative troubleshooting techniques to improve surgical outcomes while being constantly cognizant of their impact on the patient. Each case in the book is illustrative of the iterative process of managing deep brain stimulation patients who have entrusted their health to specialists who are not only determined to improve their quality of life regardless of the complexity of the clinical scenario but also share their invaluable observations with readers who may someday face a similar challenge when treating their patients.