Dystonia:
Gespeichert in:
Weitere Verfasser: | , , |
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Format: | Buch |
Sprache: | English |
Veröffentlicht: |
Cambridge, MA ; San Diego, CA
Academic Press, an imprint of Elsevier
2023
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Ausgabe: | First edition |
Schriftenreihe: | International review of neurobiology
volume 169 |
Schlagworte: | |
Online-Zugang: | Inhaltsverzeichnis |
Beschreibung: | xvi, 491 Seiten Illustrationen, Diagramme |
ISBN: | 9780323990264 |
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245 | 1 | 0 | |a Dystonia |c edited by Alberto Albanese (Department of Neurology, IRCCS Humanitas Research Hospital; Department of Neuroscience, Catholic University, Milano, Italy), Kailash Bhatia (UCL Queen Square Institute of Neurology, United Kingdom), H.A. Jinnah (Departments of Neurology, Human Genetics, and Pediatrics, Atlanta, GA, United States) |
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adam_text | Contents Contributors xiii 1. Clinical features of dystonia and the science of classification 1 Alberto Albanese 1. Early observations 1 2. Phenomenology 2 2.1 Tremor in dystonia 4 2.2 The spectrum of dystonia 9 3. Motor features 10 3.1 Core features 10 3.2 Additional features 11 4. Diagnosis 12 5. Classification 13 6. Current status and beyond References 2. What can epidemiological studies teach on the pathophysiology of adult-onset isolated dystonia? 16 17 21 Davide Martino 1. Introduction 22 2. Studies of birth sex in AOID: Suggestions for pathophysiology 23 3. How does age affect phenotype and natural history of AOID? 26 4. Extra-genetic risk factors and mechanisms of AOID 30 5. 4.1 Physical trauma 30 4.2 Repetitive activities 35 4.3 Geographic variations 36 4.4 Lifestyle and medical comorbidities 40 Clinical and epidemiological studies of non-motor symptoms in AOID: 43 Implications for pathophysiology 6. Brain-wide mechanisms and network dysfunction: Supporting 46 evidence from epidemiologic data 6.1 Defective inhibitory mechanisms 6.2 Altered synaptic plasticity and imbalance in the cortico-basal 46 47 ganglia circuitry v
Contents vi 6.3 Dysfunctional connectivity beyond the cortico-basal ganglia 48 circuitry 7. 8. Form-specific mechanisms: Supporting evidence fromepidemiologic data 49 7.1 Cervical dystonia 49 7.2 Blepharospasm 50 7.3 Upper limb dystonia 51 Where to go next investigating risk- andcourse-modifying factors of 52 dystonia? Conclusive remarks 8.1 Non-modifiable factors 8.2 “Modifiable factors 52 53 54 References •’v 3. Dystonia genes and their biological pathways 61 Alessio Di Fonzo, H. A. Jinnah, and Michael Zech 1. Introduction 1.1 Dopamine signaling abnormalities 62 64 1.2 Heavy metal accumulation and brain calcifications 70 1.3 Defects of the nuclear envelope and stress response 73 1.4 Perturbation of gene-expression control in the nucleus 76 1.5 Mitochondrial and energy homeostasis dysfunction 79 1.6 Cellular trafficking alterations with lysosomal-autophagosomal 82 pathology 1.7 Calcium abnormalities and mutant ion channels 84 1.8 Other established and newly emerging mechanisms 87 2. Concluding remarks and future perspectives 90 2.1 Dystonia molecular pathways—Lumping or splitting? 90 2.2 Unmet needs and strategies to address them 91 References 4. The functional anatomy of dystonia: Recent developments 92 105 Daniel T. Corp, Jordan Morrison-Ham, H. A. Jinnah, and Juho Joutsa 1. Introduction 106 2. Neuroimaging in idiopathic dystonia 106 2.1 Structural magnetic resonance imaging 107 3. 2.2 Functional magnetic resonance imaging 109 2.3 Molecular neuroimaging 110 2.4 Summary of neuroimaging in idiopathic dystonia 112 Lesion studies 113
vii Contents 3.1 Traditional lesion Studies in dystonia 113 3.2 Lesion network mapping in dystonia 118 4. Animal studies in dystonia 120 5. Pathways of dystonia 122 6. Future directions 124 7. Conclusions 126 Acknowledgements 127 References 127 5. Physiology of dystonia: Human studies 137 Peter Fischer, Dan Piña-Fuentes, Panagiotis Kassavetis, and Anna Sadnicka 1. Introduction 138 2. Inhibition 138 3. Plasticity 142 4. Limitations of inhibition and plasticity hypothesis 144 5. Peripheral contributions and disrupted sensorimotor integration 146 6. Oscillations in dystonia 149 6.1 Low-frequency oscillations in dystonia 149 6.2 The effect of DBS on LF-oscillations 150 6.3 Significance of prominent LF oscillations 151 6.4 Clinical implications of LF-oscillations in dystonia 152 6.5 Other sources of osillations in dystonia and oscillations in other 153 frequency bands 7. Conclusions 153 References 154 6. Physiology of Dystonia: Animal Studies 163 Alejandro G. Rey Hipolito, Meike E. van der Heijden, and Roy V. Sillitoe 1. Introduction 164 2. Genetic mouse models with mutations in dystonia-associated genes 166 that are affected in human patients 2.1 DYT1 (TOR IA) 2.2 DYT5a (GCH1) 2.3 DYT5b (TH) 2.4 DYT6 (THAP1) 166 172 172 173 2.5 DYT11 (SGCE) 174 2.6 DYT12 (ATP (A3) 175
viii Contents 3. 4, 5. 2.7 DYT25 (GNAL) 176 2.8 FGF14 177 2.9 Manganese transporter genes (SLC30A10 and SLC39A14) 178 2.10 TSPOAP1 179 2.11 SECISBP2 179 Spontaneous genetic models with dystonic movements 180 3.1 180 BTBR Г Itpr3 /J (BTBR) 3.2 Cacnala mutations (including tottering and leanermice) 181 3.3 dt Rat (Atcay) 185 3.4 Dťz hamster 187 3.5 Dystonia musculorum (Bpagl) 188 3.6 Lamb! 190 * 3.7 Scn8a 190 3.8 Waddles mouse (Car8) 191 Neural circuit manipulations causing dystonia 4.1 Agranular mice (EnlCre; Atohl^) 192 192 4.2 Cerebellar serotonergic hyperactivity (virus induced) 193 4.3 GyZ 4.4 Olivocerebellar silencing (PtflaCre; Vglut^ 193 194 Pharmacologically-induced dystonia models 194 5.1 Kainie acid injection (AMPA receptor activation) 195 5.2 Ouabain injection (ATP1A3 sodium/potassiumpump inhibition) 196 6. Other models of induced dystonia 198 7. Conclusions 198 References 201 7. Advances in targeting neurotransmitter systems indystonia 217 Dora Steel, Kimberley Μ. Reid, Antonio Pisani, Ellen J. Hess, Susan Fox, and Manju A. Kurian 1, Introduction 218 1.1 A brief overview 1.2 The spectrum ofbrain neurotransmitters of dystonia 2. Physiology of the principal brain neurotransmitters 219 221 223 2.1 Dopamine 223 2.2 Noradrenaline 225 2.3 Serotonin (5-hydroxytryptamine) 226 2.4 Acetylcholine 226 2.5 GABA 228 2.6 Glutamate 229
ix Contents 2.7 Adenosine 230 2.8 Cannabinoids 231 3. Neurotransmitter-targeting pharmacological therapies 231 3.1 Dopamine 231 3.2 Noradrenaline 234 3.3 Serotonin (5-hydroxytryptamine) 234 3.4 Acetylcholine 235 3.5 GABA 236 3.6 Glutamate 237 3.7 Adenosine 238 3.8 Cannabinoids 240 4. New evolving genetictherapies targeting neurotransmitter systems 241 4.1 Gene replacement strategies 4.2 Gene editing 244 4.3 RNA therapies 244 241 5. Discussion 246 Acknowledgements 248 References 248 8. Experimental pharmacology: Targetingmetabolic pathways 259 Vincenzo Leuzzi and Serena Gaiosi 1. Introduction 260 2. Genetic-metabolic conditions causing dystonia with available 270 disease-specific treatment 3. Trace element metabolism disorders and NBIA disorders 271 3.1 271 Wilson disease 4. Manganese transport disorders 5. Aceruloplasminemia 275 6. PKAN 277 7. Energetic metabolism alterations 280 8. Lysosomal disorders 287 9. Neurotransmitter defects 293 273 10. Channelopathies and synaptopathies 300 11. Conclusive remarks 301 References 302
x Contents 9. Adult-onset focal dystonias: To lump or split 317 H, A. Jinnah and Giovanni DeFazio 1. Introduction 318 2. Lumping 2.1 318 318 Shared evolution 2.2 Shared genetics 319 ՜ 2.3 Shared physiology 319 2.4 Shared neuroanatomical basis 320 2.5 Shared treatments 320 3. Splitting 321 3.1 Clinical heterôgeneity 321 3.2 Genetic heterogeneity 321 322 3.3 Anatomical heterogeneity 3.4 Physiological heterogeneity 322 3.5 Therapeutic heterogeneity 322 4. Resolving the paradox 5, Conclusions and future 323 prospects References 324 . 10. Early-onset inherited dystonias versus late-onset idiopathic dystonias: Same or different biological mechanisms? 325 329 Roberto Erro, Edoardo Monfrini, and Alessio Di Fonzo 1. Introduction 2, Epidemiology, genetics and age at onset of dystonias 3, Age-related modifiers of genetic dystonias 330 331 332 4. Converging biochemical and physiologic abnormalities 334 5, Critical periods of vulnerability for the sensorimotor system: Does it 337 apply to dystonia? 6. A possiblecommonframework: Thedouble-hit hypothesis 339 Disclosures 341 References 341 11. Dystonia andParkinson s disease: Do they have a shared biology? 347 Eli© Matar and Kailash Bhatia 1, Introduction 348 2, Pathophysiological considerations—Convergence and divergence 348
Contents xi 2.1 Anatomy of the basal ganglia 349 2.2 The direct, indirect, and hyper-direct pathways 352 2.3 Matrix and striosome compartments 354 2.4 Cholinergic signaling in the striatum 355 2.5 Motor networks and cerebellum 356 2.6 Oscillatory activity in motor control 3. Dystonia and Parkinson s disease 359 360 3.1 Pathology underlying motor symptoms of Parkinson sdisease 360 3.2 Dystonia in pre-clinical and early PD 362 3.3 Treatment-associated dystonia/dyskinesia 364 3.4 Dystonia in monogenic PD 368 4. Dystonia and parkinsonism—Beyond PD 372 5. 4.1 Drug-induced dystonia-parkinsonism 377 4.2 Dopamine synthesis and transport disorders 378 4.3 Disorders of brain iron accumulation and metal metabolism 382 4.4 Neurodegenerative atypical parkinsonian disorders 386 . Conclusion and future directions—One pathway or many? 390 References 12. Dystonia and tremor: Do they have a shared biology? 392 413 Abhishek Lenka and Sanjay Pandey 1. Introduction 414 2. Evidence in favor of shared biology 415 2.1 Evidence from the clinical and epidemiological studies 415 2.2 Evidence from the genetic studies 424 2.3 Evidence from the neuroimaging studies 426 2.4 Evidence from postmortem histopathology studies 428 2.5 Evidence from neurophysiology studies 428 3. Evidence against a shared biology 429 3.1 The pathophysiology of subtypes of tremor is likely different 429 3.2 Genetic and anatomical overlaps are unclear 430 3.3 Therapeutic responses are inconsistent 431 Conclusion and future perspectives 431 Funding source 432 Conflicts of interest 432 References 432
Contents xii 13. How does botulinum toxin really work? 441 Daniele Belvisi, Giorgio Leodori, Matteo Costanzo, Antonella Conte, and Alfredo Berardelli 1. Background 1.1 What is the evidence that the primary mechanism is inhibition of 442 443 neuromuscular junction transmission? 1.2 What is the evidence for alteration of peripheral sensory 453 feedback from muscle spindles? 2. What is the evidence for a central effect? 2.1 Evidence of retrograde and anterograde BoNT transportation in 458 458 animal models 3. Neurophysiological evidence of BoNT effects on brainstem excitability 459 in humans 3.1 Neurophysiological evidence of BoNT effects on motor cortex 464 excitability in humans 4. Neurophysiological evidence of BoNT effects on the sensory system 466 In humans 5. Neuroimaging evidence of central effects of BoNT in humans 468 6. Conclusions 470 References 471 14. What have we learned about the biology of dystonia from deep brain stimulation? 481 Vidailhet Marie References 488
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adam_txt |
Contents Contributors xiii 1. Clinical features of dystonia and the science of classification 1 Alberto Albanese 1. Early observations 1 2. Phenomenology 2 2.1 Tremor in dystonia 4 2.2 The spectrum of dystonia 9 3. Motor features 10 3.1 Core features 10 3.2 Additional features 11 4. Diagnosis 12 5. Classification 13 6. Current status and beyond ' References 2. What can epidemiological studies teach on the pathophysiology of adult-onset isolated dystonia? 16 17 21 Davide Martino 1. Introduction 22 2. Studies of birth sex in AOID: Suggestions for pathophysiology 23 3. How does age affect phenotype and natural history of AOID? 26 4. Extra-genetic risk factors and mechanisms of AOID 30 5. 4.1 Physical trauma 30 4.2 Repetitive activities 35 4.3 Geographic variations 36 4.4 Lifestyle and medical comorbidities 40 Clinical and epidemiological studies of non-motor symptoms in AOID: 43 Implications for pathophysiology 6. Brain-wide mechanisms and network dysfunction: Supporting 46 evidence from epidemiologic data 6.1 Defective inhibitory mechanisms 6.2 Altered synaptic plasticity and imbalance in the cortico-basal 46 47 ganglia circuitry v
Contents vi 6.3 Dysfunctional connectivity beyond the cortico-basal ganglia 48 circuitry 7. 8. Form-specific mechanisms: Supporting evidence fromepidemiologic data 49 7.1 Cervical dystonia 49 7.2 Blepharospasm 50 7.3 Upper limb dystonia 51 Where to go next investigating risk- andcourse-modifying factors of 52 dystonia? Conclusive remarks 8.1 "Non-modifiable" factors 8.2 “Modifiable" factors 52 53 54 References •’v 3. Dystonia genes and their biological pathways 61 Alessio Di Fonzo, H. A. Jinnah, and Michael Zech 1. Introduction 1.1 Dopamine signaling abnormalities 62 64 1.2 Heavy metal accumulation and brain calcifications 70 1.3 Defects of the nuclear envelope and stress response 73 1.4 Perturbation of gene-expression control in the nucleus 76 1.5 Mitochondrial and energy homeostasis dysfunction 79 1.6 Cellular trafficking alterations with lysosomal-autophagosomal 82 pathology 1.7 Calcium abnormalities and mutant ion channels 84 1.8 Other established and newly emerging mechanisms 87 2. Concluding remarks and future perspectives 90 2.1 Dystonia molecular pathways—Lumping or splitting? 90 2.2 Unmet needs and strategies to address them 91 References 4. The functional anatomy of dystonia: Recent developments 92 105 Daniel T. Corp, Jordan Morrison-Ham, H. A. Jinnah, and Juho Joutsa 1. Introduction 106 2. Neuroimaging in idiopathic dystonia 106 2.1 Structural magnetic resonance imaging 107 3. 2.2 Functional magnetic resonance imaging 109 2.3 Molecular neuroimaging 110 2.4 Summary of neuroimaging in idiopathic dystonia 112 Lesion studies 113
vii Contents 3.1 Traditional lesion Studies in dystonia 113 3.2 Lesion network mapping in dystonia 118 4. Animal studies in dystonia 120 5. Pathways of dystonia 122 6. Future directions 124 7. Conclusions 126 Acknowledgements 127 References 127 5. Physiology of dystonia: Human studies 137 Peter Fischer, Dan Piña-Fuentes, Panagiotis Kassavetis, and Anna Sadnicka 1. Introduction 138 2. Inhibition 138 3. Plasticity 142 4. Limitations of inhibition and plasticity hypothesis 144 5. Peripheral contributions and disrupted sensorimotor integration 146 6. Oscillations in dystonia 149 6.1 Low-frequency oscillations in dystonia 149 6.2 The effect of DBS on LF-oscillations 150 6.3 Significance of prominent LF oscillations 151 6.4 Clinical implications of LF-oscillations in dystonia 152 6.5 Other sources of osillations in dystonia and oscillations in other 153 frequency bands 7. Conclusions 153 References 154 6. Physiology of Dystonia: Animal Studies 163 Alejandro G. Rey Hipolito, Meike E. van der Heijden, and Roy V. Sillitoe 1. Introduction 164 2. Genetic mouse models with mutations in dystonia-associated genes 166 that are affected in human patients 2.1 DYT1 (TOR IA) 2.2 DYT5a (GCH1) 2.3 DYT5b (TH) 2.4 DYT6 (THAP1) 166 172 172 173 2.5 DYT11 (SGCE) 174 2.6 DYT12 (ATP (A3) 175
viii Contents 3. 4, 5. 2.7 DYT25 (GNAL) 176 2.8 FGF14 177 2.9 Manganese transporter genes (SLC30A10 and SLC39A14) 178 2.10 TSPOAP1 179 2.11 SECISBP2 179 Spontaneous genetic models with dystonic movements 180 3.1 180 BTBR Г Itpr3"/J (BTBR) 3.2 Cacnala mutations (including tottering and leanermice) 181 3.3 dt Rat (Atcay) 185 3.4 Dťz hamster 187 3.5 Dystonia musculorum (Bpagl) 188 3.6 Lamb! 190 '* 3.7 Scn8a 190 3.8 Waddles mouse (Car8) 191 Neural circuit manipulations causing dystonia 4.1 Agranular mice (EnlCre; Atohl^) 192 192 4.2 Cerebellar serotonergic hyperactivity (virus induced) 193 4.3 GyZ 4.4 Olivocerebellar silencing (PtflaCre; Vglut^ 193 194 Pharmacologically-induced dystonia models 194 5.1 Kainie acid injection (AMPA receptor activation) 195 5.2 Ouabain injection (ATP1A3 sodium/potassiumpump inhibition) 196 6. Other models of induced dystonia 198 7. Conclusions 198 References 201 7. Advances in targeting neurotransmitter systems indystonia 217 Dora Steel, Kimberley Μ. Reid, Antonio Pisani, Ellen J. Hess, Susan Fox, and Manju A. Kurian 1, Introduction 218 1.1 A brief overview 1.2 The spectrum ofbrain neurotransmitters of dystonia 2. Physiology of the principal brain neurotransmitters 219 221 223 2.1 Dopamine 223 2.2 Noradrenaline 225 2.3 Serotonin (5-hydroxytryptamine) 226 2.4 Acetylcholine 226 2.5 GABA 228 2.6 Glutamate 229
ix Contents 2.7 Adenosine 230 2.8 Cannabinoids 231 3. Neurotransmitter-targeting pharmacological therapies 231 3.1 Dopamine 231 3.2 Noradrenaline 234 3.3 Serotonin (5-hydroxytryptamine) 234 3.4 Acetylcholine 235 3.5 GABA 236 3.6 Glutamate 237 3.7 Adenosine 238 3.8 Cannabinoids 240 4. New evolving genetictherapies targeting neurotransmitter systems 241 4.1 Gene replacement strategies 4.2 Gene editing 244 4.3 RNA therapies 244 241 5. Discussion 246 Acknowledgements 248 References 248 8. Experimental pharmacology: Targetingmetabolic pathways 259 Vincenzo Leuzzi and Serena Gaiosi 1. Introduction 260 2. Genetic-metabolic conditions causing dystonia with available 270 disease-specific treatment 3. Trace element metabolism disorders and NBIA disorders 271 3.1 271 Wilson disease 4. Manganese transport disorders 5. Aceruloplasminemia 275 6. PKAN 277 7. Energetic metabolism alterations 280 8. Lysosomal disorders 287 9. Neurotransmitter defects 293 273 10. Channelopathies and synaptopathies 300 11. Conclusive remarks 301 References 302
x Contents 9. Adult-onset focal dystonias: To lump or split 317 H, A. Jinnah and Giovanni DeFazio 1. Introduction 318 2. Lumping 2.1 318 318 Shared evolution 2.2 Shared genetics 319 ՜ 2.3 Shared physiology 319 2.4 Shared neuroanatomical basis 320 2.5 Shared treatments 320 3. Splitting 321 3.1 Clinical heterôgeneity 321 3.2 Genetic heterogeneity 321 322 3.3 Anatomical heterogeneity 3.4 Physiological heterogeneity 322 3.5 Therapeutic heterogeneity 322 4. Resolving the paradox 5, Conclusions and future 323 prospects References 324 . 10. Early-onset inherited dystonias versus late-onset idiopathic dystonias: Same or different biological mechanisms? 325 329 Roberto Erro, Edoardo Monfrini, and Alessio Di Fonzo 1. Introduction 2, Epidemiology, genetics and age at onset of dystonias 3, Age-related modifiers of genetic dystonias 330 331 332 4. Converging biochemical and physiologic abnormalities 334 5, Critical periods of vulnerability for the sensorimotor system: Does it 337 apply to dystonia? 6. A possiblecommonframework: Thedouble-hit hypothesis 339 Disclosures 341 References 341 11. Dystonia andParkinson's disease: Do they have a shared biology? 347 Eli© Matar and Kailash Bhatia 1, Introduction 348 2, Pathophysiological considerations—Convergence and divergence 348
Contents xi 2.1 Anatomy of the basal ganglia 349 2.2 The direct, indirect, and hyper-direct pathways 352 2.3 Matrix and striosome compartments 354 2.4 Cholinergic signaling in the striatum 355 2.5 Motor networks and cerebellum 356 2.6 Oscillatory activity in motor control 3. Dystonia and Parkinson's disease 359 360 3.1 Pathology underlying motor symptoms of Parkinson'sdisease 360 3.2 Dystonia in pre-clinical and early PD 362 3.3 Treatment-associated dystonia/dyskinesia 364 3.4 Dystonia in monogenic PD 368 4. Dystonia and parkinsonism—Beyond PD 372 5. 4.1 Drug-induced dystonia-parkinsonism 377 4.2 Dopamine synthesis and transport disorders 378 4.3 Disorders of brain iron accumulation and metal metabolism 382 4.4 Neurodegenerative atypical parkinsonian disorders 386 . Conclusion and future directions—One pathway or many? 390 References 12. Dystonia and tremor: Do they have a shared biology? 392 413 Abhishek Lenka and Sanjay Pandey 1. Introduction 414 2. Evidence in favor of shared biology 415 2.1 Evidence from the clinical and epidemiological studies 415 2.2 Evidence from the genetic studies 424 2.3 Evidence from the neuroimaging studies 426 2.4 Evidence from postmortem histopathology studies 428 2.5 Evidence from neurophysiology studies 428 3. Evidence against a shared biology 429 3.1 The pathophysiology of subtypes of tremor is likely different 429 3.2 Genetic and anatomical overlaps are unclear 430 3.3 Therapeutic responses are inconsistent 431 Conclusion and future perspectives 431 Funding source 432 Conflicts of interest 432 References 432
Contents xii 13. How does botulinum toxin really work? 441 Daniele Belvisi, Giorgio Leodori, Matteo Costanzo, Antonella Conte, and Alfredo Berardelli 1. Background 1.1 What is the evidence that the primary mechanism is inhibition of 442 443 neuromuscular junction transmission? 1.2 What is the evidence for alteration of peripheral sensory 453 feedback from muscle spindles? 2. What is the evidence for a central effect? 2.1 Evidence of retrograde and anterograde BoNT transportation in 458 458 animal models 3. Neurophysiological evidence of BoNT effects on brainstem excitability 459 in humans 3.1 Neurophysiological evidence of BoNT effects on motor cortex 464 excitability in humans 4. Neurophysiological evidence of BoNT effects on the sensory system 466 In humans 5. Neuroimaging evidence of central effects of BoNT in humans 468 6. Conclusions 470 References 471 14. What have we learned about the biology of dystonia from deep brain stimulation? 481 Vidailhet Marie References 488 |
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illustrated | Illustrated |
index_date | 2024-07-03T22:39:04Z |
indexdate | 2024-07-10T10:00:55Z |
institution | BVB |
isbn | 9780323990264 |
language | English |
oai_aleph_id | oai:aleph.bib-bvb.de:BVB01-034561766 |
oclc_num | 1401198493 |
open_access_boolean | |
owner | DE-355 DE-BY-UBR |
owner_facet | DE-355 DE-BY-UBR |
physical | xvi, 491 Seiten Illustrationen, Diagramme |
publishDate | 2023 |
publishDateSearch | 2023 |
publishDateSort | 2023 |
publisher | Academic Press, an imprint of Elsevier |
record_format | marc |
series | International review of neurobiology |
series2 | International review of neurobiology |
spelling | Dystonia edited by Alberto Albanese (Department of Neurology, IRCCS Humanitas Research Hospital; Department of Neuroscience, Catholic University, Milano, Italy), Kailash Bhatia (UCL Queen Square Institute of Neurology, United Kingdom), H.A. Jinnah (Departments of Neurology, Human Genetics, and Pediatrics, Atlanta, GA, United States) First edition Cambridge, MA ; San Diego, CA Academic Press, an imprint of Elsevier 2023 xvi, 491 Seiten Illustrationen, Diagramme txt rdacontent n rdamedia nc rdacarrier International review of neurobiology volume 169 Dystonie (DE-588)4131690-3 gnd rswk-swf (DE-588)4143413-4 Aufsatzsammlung gnd-content Dystonie (DE-588)4131690-3 s DE-604 Albanese, Alberto edt Bhatia, Kailash P. (DE-588)1084602253 edt Jinnah, H. A. edt International review of neurobiology volume 169 (DE-604)BV002534817 169 Digitalisierung UB Regensburg - ADAM Catalogue Enrichment application/pdf http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=034561766&sequence=000001&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA Inhaltsverzeichnis |
spellingShingle | Dystonia International review of neurobiology Dystonie (DE-588)4131690-3 gnd |
subject_GND | (DE-588)4131690-3 (DE-588)4143413-4 |
title | Dystonia |
title_auth | Dystonia |
title_exact_search | Dystonia |
title_exact_search_txtP | Dystonia |
title_full | Dystonia edited by Alberto Albanese (Department of Neurology, IRCCS Humanitas Research Hospital; Department of Neuroscience, Catholic University, Milano, Italy), Kailash Bhatia (UCL Queen Square Institute of Neurology, United Kingdom), H.A. Jinnah (Departments of Neurology, Human Genetics, and Pediatrics, Atlanta, GA, United States) |
title_fullStr | Dystonia edited by Alberto Albanese (Department of Neurology, IRCCS Humanitas Research Hospital; Department of Neuroscience, Catholic University, Milano, Italy), Kailash Bhatia (UCL Queen Square Institute of Neurology, United Kingdom), H.A. Jinnah (Departments of Neurology, Human Genetics, and Pediatrics, Atlanta, GA, United States) |
title_full_unstemmed | Dystonia edited by Alberto Albanese (Department of Neurology, IRCCS Humanitas Research Hospital; Department of Neuroscience, Catholic University, Milano, Italy), Kailash Bhatia (UCL Queen Square Institute of Neurology, United Kingdom), H.A. Jinnah (Departments of Neurology, Human Genetics, and Pediatrics, Atlanta, GA, United States) |
title_short | Dystonia |
title_sort | dystonia |
topic | Dystonie (DE-588)4131690-3 gnd |
topic_facet | Dystonie Aufsatzsammlung |
url | http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=034561766&sequence=000001&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA |
volume_link | (DE-604)BV002534817 |
work_keys_str_mv | AT albanesealberto dystonia AT bhatiakailashp dystonia AT jinnahha dystonia |