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Chapter 39 - Treatment of Focal Hand Dystonia
- Edited by Daniel Truong, University of California, Riverside, Dirk Dressler, Hannover Medical School, Mark Hallett, National Institutes of Health (NIH), Christopher Zachary, University of California, Irvine, Mayank Pathak, Truong Neuroscience Institute
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- Book:
- Manual of Botulinum Toxin Therapy
- Published online:
- 02 November 2023
- Print publication:
- 23 November 2023, pp 332-347
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Summary
Focal hand dystonia (FHD) is characterized by dystonic hand contractions that are often aggravated by purposeful actions and may be specific to a particular task. The term “occupational dystonia” is used when dystonia affecting performance of the job arises in individuals with a particular occupation, usually an occupation requiring repetitive and excessive fine motor activity.
One task-specific FHD, writer’s cramp, causes disabling spasms of the hands when attempting to write, and is particularly likely in people whose profession involves excessive writing. Musician’s dystonia (cramp) is applied to a focal dystonia localized to hand muscles controlling fine movements of the digits or the embouchure muscles involved in playing instruments.
Injection of botulinum neurotoxin (BoNT) is effective in writer’s cramp and other occupational dystonias. This chapter discusses the different common patterns of dystonic movement of the hand and arm, identifies the particular muscles active in each dystonia pattern to aid in target selectio, and illustrates the muscular anatomy and injection approach using anatomical diagrams. Guidance of injections with EMG is discussed. Dosing recommendations for three different BoNT formulations are tabulated.
36 - Botulinum Toxin Therapy for Writer’s Cramp and Other Focal Hand Dystonias
- from Section II - Botulinum Toxin Therapy
- Edited by Dirk Dressler, Eckart Altenmüller, Joachim K. Krauss
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- Book:
- Treatment of Dystonia
- Published online:
- 31 May 2018
- Print publication:
- 07 June 2018, pp 178-181
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Chapter 10 - Treatment of focal hand dystonia
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- By Barbara Illowsky Karp, Combined NeuroScience IRB, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA, Chandi Das, Neurology Department, Canberra Hospital, Garren Act Health, ACT, Australia, Daniel Truong, The Parkinson’s and Movement Disorders Institute, Fountain Valley, California, Mark Hallett, George Washington University School of Medicine and Health Sciences, Washington, DC
- Edited by Daniel Truong, Dirk Dressler, Mark Hallett, Christopher Zachary
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- Book:
- Manual of Botulinum Toxin Therapy
- Published online:
- 05 February 2014
- Print publication:
- 23 January 2014, pp 71-84
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Summary
Introduction
Focal hand dystonia (FHD) is characterized by dystonic hand contractions that are often aggravated by purposeful actions and may be specific to a particular task. For example, a patient may have dystonia when using the hand for writing but not for other tasks such as eating or typing. The term “occupational dystonia” is used when dystonia affecting performance of the job arises in individuals with a particular occupation, usually an occupation requiring repetitive and excessive fine motor activity. The occupations particularly prone to have focal task-specific dystonia are listed in Table 10.1. Most of these hand dystonias fall under the rubric of primary focal dystonias.
This chapter discusses writer’s cramp and musician’s dystonia (cramp) in detail, the two most common occupational dystonias, followed by a discussion of other focal occupational dystonias.
Pathogenesis
The exact cause of FHD is not yet elucidated. A consistent physiological finding is excessive activation of antagonists and overflow and prolongation of muscle activation. Both of these are thought to reflect deficiency of inhibition at multiple levels of the motor system circuitry (Hallett, 2000, 2006a,b). Dopamine dysfunction has also been implicated. Although FHD is a movement disorder, somatosensory dysfunction is also present, including distorted sensory maps of the affected hand (Bara-Jimenez et al., 1998) and impaired sensory discrimination (Sanger et al., 2001). Structural MRI analyses have shown increased gray matter volume in the basal ganglia of musicians (Granert et al., 2011) and writers (Garraux et al., 2004) with FHD. Functional MRI has shown impaired activation of the primary sensorimotor and supplementary motor cortex during voluntary muscle relaxation and contraction (Oga et al., 2002). A genetic factor in the development of hand dystonia is possible, as up to 20% of patients with writer’s cramp have family members with dystonia.
37 - Dystonia
- from PART III - DISORDERS OF MOTOR CONTROL
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- By Barbara Illowsky Karp, Office of the Clinical Director and Human Motor Control Section NINDS, NIH, Bethesda, Maryland, USA, Susanne Goldstein, Office of the Clinical Director and Human Motor Control Section NINDS, NIH, Bethesda, Maryland, USA, Mark Hallett, Office of the Clinical Director and Human Motor Control Section NINDS, NIH, Bethesda, Maryland, USA
- Edited by Arthur K. Asbury, University of Pennsylvania School of Medicine, Guy M. McKhann, The Johns Hopkins University School of Medicine, W. Ian McDonald, University College London, Peter J. Goadsby, University College London, Justin C. McArthur, The Johns Hopkins University School of Medicine
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- Book:
- Diseases of the Nervous System
- Published online:
- 05 August 2016
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- 11 November 2002, pp 532-550
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Summary
Dystonia is a movement disorder characterized by sustained involuntary muscle contraction causing abnormal twisting, repetitive movements or posturing that tend to have a directional predominance.Descriptions of dystonic patients, who were often believed to be hysterical, first appeared at the beginning of the twentieth century (Zeman & Dyken, 1968). In 1908, Schwalbe ascertained the hereditary nature of the illness and its variable expression (Schwalbe, 1908). The term‘dystonia musculorum deformans’ was first used by Oppenheim (1911), while Mendel and Flateau, emphasizing the twisted posture, called the disease ‘torsion dystonia’ or ‘torsion spasm’ (Flateau & Sterling, 1911; Zeman & Dyken, 1968).
After a period of relative inattention, interest in dystonia revived in the 1970s with a fuller delineation of the symptomatology allowing the recognition of focal forms. More recent technological developments have culminated in the identification of genetic mutations underlying generalized torsion dystonia, dopa-responsive dystonia, and some focal dystonias. New therapies have been developed including botulinum toxin injections, stereotactic surgery, and deep brain stimulation.
Classification
Dystonia can be classified by etiology, by the body area involved, and by the age of onset. The division by etiology into primary (idiopathic) and secondary (symptomatic) dystonia provides a schema for evaluating the patient. The classification by affected region is especially useful for the primary dystonias, where the epidemiology, prognosis, treatment and genetics differ by dystonia type. Classifying dystonia by age of onset is also most applicable to primary dystonia, where it serves to separate idiopathic generalized torsion dystonia of childhood onset from the focal dystonias which typically present in adulthood.
A classification suggested by Fahn et al., divides dystonias into primary dystonia, ‘dystonia-plus’ syndromes in which dystonia combines with other neurological symptomatology, secondary dystonia where an underlying pathological process causing dystonia can be identified, and heredofamilial dystonia in which there is an underlying neurodegenerative disorder (Fahn et al., 1998).
Signs and symptoms
Idiopathic dystonia often first manifests as a feeling of discomfort or stiffness in the affected body part. Abnormal movement ensues and initially may only be apparent when performing specific acts, interfering with smooth and accurate performance. As it progresses, dystonia occurs with other voluntary movements and may eventually be present even at rest. Dystonic muscles may hypertrophy; fixed contractures and deformity occur in severe cases. Dystonia disappears during sleep.