Jump to content


From Wikipedia, the free encyclopedia

A person with medication-induced dystonia
Complicationsphysical disabilities (contractures, torticollis),[1] pain and fatigue[2]
Causeshereditary (DYT1); birth injury; head trauma; medication; infection; toxins
Diagnostic methodgenetic testing, electromyography, blood tests, MRI or CT scan
Treatmentmedication, physical therapy, botulinum toxin injection, deep brain stimulation
Medicationanticholinergics, dopamine agonists

Dystonia is a neurological hyperkinetic movement disorder in which sustained or repetitive muscle contractions occur involuntarily, resulting in twisting and repetitive movements or abnormal fixed postures.[3] The movements may resemble a tremor. Dystonia is often intensified or exacerbated by physical activity, and symptoms may progress into adjacent muscles.[4]

The disorder may be hereditary or caused by other factors such as birth-related or other physical trauma, infection, poisoning (e.g., lead poisoning) or reaction to pharmaceutical drugs, particularly neuroleptics,[3] or stress. Treatment must be highly customized to the needs of the individual and may include oral medications, chemodenervation botulinum neurotoxin injections, physical therapy, or other supportive therapies, and surgical procedures such as deep brain stimulation.



There are multiple types of dystonia, and many diseases and conditions may cause dystonia.

Dystonia is classified by:

  1. Clinical characteristics such as age of onset, body distribution, nature of the symptoms, and associated features such as additional movement disorders or neurological symptoms, and
  2. Cause (which includes changes or damage to the nervous system and inheritance).[4]

Physicians use these classifications to guide diagnosis and treatment.



Generalized dystonias


For example, dystonia musculorum deformans (Oppenheim, Flatau-Sterling syndrome): [6]

  • Normal birth history and milestones
  • Autosomal dominant
  • Childhood onset
  • Starts in lower limbs and spreads upwards

Also known as torsion dystonia or idiopathic torsion dystonia (old terminology "dystonia musculorum deformans").

Focal dystonias


These most common dystonias are typically classified as follows:

Name Location Description
Anismus muscles of the rectum Causes painful defecation, constipation; may be complicated by encopresis or fecal incontinence.
Cervical dystonia (spasmodic torticollis) muscles of the neck Causes the head to rotate to one side, to pull down towards the chest, or back, or a combination of these postures.
Blepharospasm muscles around the eyes The patient experiences rapid blinking of the eyes or even their forced closure causing functional blindness.
Oculogyric crisis muscles of eyes and head An extreme and sustained (usually) upward deviation of the eyes often with convergence causing diplopia (double vision). It is frequently associated with backward and lateral flexion of the neck and either widely opened mouth or jaw clenching. Frequently a result of antiemetics such as the neuroleptics (e.g., prochlorperazine) or metoclopramide. Can be caused by Chlorpromazine.
Oromandibular dystonia muscles of the jaw and muscles of tongue Causes distortions of the mouth and tongue.
Spasmodic dysphonia/Laryngeal dystonia muscles of larynx Causes the voice to sound broken, become hoarse, sometimes reducing it to a whisper.
Focal hand dystonia (also known as musician's or writer's cramp). single muscle or small group of muscles in the hand It interferes with activities such as writing or playing a musical instrument by causing involuntary muscular contractions. The condition is sometimes "task-specific", meaning that it is generally apparent during only certain activities. Focal hand dystonia is neurological in origin and is not due to normal fatigue. The loss of precise muscle control and continuous unintentional movement results in painful cramping and abnormal positioning that makes continued use of the affected body parts impossible.

The combination of blepharospasmodic contractions and oromandibular dystonia is called cranial dystonia or Meige's syndrome.



Symbol OMIM Gene Locus Alt Name
DYT1 128100 TOR1A 9q34 Early-onset torsion dystonia
DYT2 224500 HPCA 1p35-p34.2 Autosomal recessive primary isolated dystonia
DYT3 314250 TAF1 Xq13 X-linked dystonia parkinsonism
DYT4 128101 TUBB4[7] 19p13.12-13 Autosomal dominant whispering dysphonia
DYT5a 128230 GCH1 14q22.1-q22.2 Autosomal dominant dopamine-responsive dystonia
DYT5b 191290 TH 11p15.5 Autosomal recessive dopamine-responsive dystonia
DYT6 602629 THAP1 8p11.21 Autosomal dominant dystonia with cranio-cervical predilection
DYT7 602124 unknown 18p (questionable) Autosomal dominant primary focal cervical dystonia
DYT8 118800 MR1 2q35 Paroxysmal nonkinesigenic dyskinesia
DYT9 601042 SLC2A1 1p35-p31.3 Episodic choreoathetosis/spasticity (now known to be synonymous with DYT18)
DYT10 128200 PRRT2 16p11.2-q12.1 Paroxysmal kinesigenic dyskinesia
DYT11 159900 SGCE 7q21 Myoclonic dystonia
DYT12 128235 ATP1A3 19q12-q13.2 Rapid-onset dystonia parkinsonism and alternating hemiplegia of childhood
DYT13 607671 unknown, near D1S2667[8] 1p36.32-p36.13 Autosomal dominant cranio-cervical/upper limb dystonia in one Italian family
DYT14 See DYT5
DYT15 607488 unknown 18p11[9] Myoclonic dystonia not linked to SGCE mutations
DYT16 612067 PRKRA 2q31.3 Autosomal recessive young onset dystonia parkinsonism
DYT17 612406 unknown, near D20S107[10] 20p11.2-q13.12 Autosomal recessive dystonia in one family
DYT18 612126 SLC2A1 1p35-p31.3 Paroxysmal exercise-induced dyskinesia
DYT19 611031 probably PRRT2 16q13-q22.1 Episodic kinesigenic dyskinesia 2, probably synonymous with DYT10
DYT20 611147 unknown 2q31 Paroxysmal nonkinesigenic dyskinesia 2
DYT21 614588 unknown 2q14.3-q21.3 Late-onset torsion dystonia
DYT24 610110 ANO3[11] 11p14.2 Autosomal dominant cranio-cervical dystonia with prominent tremor

There is a group called myoclonic dystonia where some cases are hereditary and have been associated with a missense mutation in the dopamine-D2 receptor. Some of these cases have responded well to alcohol.[12][13]

Other genes that have been associated with dystonia include CIZ1, GNAL, ATP1A3, and PRRT2.[14] Another report has linked THAP1 and SLC20A2 to dystonia.[15]

Signs and symptoms

Hyperglycemia-induced involuntary movements, which, in this case, did not consist of typical hemiballismus but rather of hemichorea (dance-like movements of one side of the body; initial movements of the right arm in the video) and bilateral dystonia (slow muscle contraction in legs, chest, and right arm) in a 62-year-old Japanese woman with type 1 diabetes

Symptoms vary according to the kind of dystonia involved. In most cases, dystonia tends to lead to abnormal posturing, in particular on movement. Many individuals with the condition have continuous pain, cramping, and relentless muscle spasms due to involuntary muscle movements. Other motor symptoms are possible including lip smacking.[16]

An accurate diagnosis may be difficult because of the way the disorder manifests itself. Affected individuals may be diagnosed as having similar and perhaps related disorders including Parkinson's disease, essential tremor, carpal tunnel syndrome, temporomandibular joint disorder, Tourette's syndrome, conversion disorder or other neuromuscular movement disorders. It has been found that the prevalence of dystonia is high in individuals with Huntington's disease, where the most common clinical presentations are internal shoulder rotation, sustained fist clenching, knee flexion, and foot inversion.[17] Risk factors for increased dystonia in patients with Huntington's disease include long disease duration and use of antidopaminergic medication.[17]



Primary dystonia is suspected when the dystonia is the only sign and there is no identifiable cause or structural abnormality in the central nervous system. Researchers suspect it is caused by a pathology of the central nervous system, likely originating in those parts of the brain concerned with motor function—such as the basal ganglia and the GABA (gamma-aminobutyric acid) producing Purkinje neurons. The precise cause of primary dystonia is unknown. In many cases it may involve some genetic predisposition towards the disorder combined with environmental conditions.[18]

Meningitis and encephalitis caused by viral, bacterial, and fungal infections of the brain have been associated with dystonia. The main mechanism is inflammation of the blood vessels, causing restriction of blood flow to the basal ganglia. Other mechanisms include direct nerve injury by the organism or a toxin, or autoimmune mechanisms.[19]

Malfunction of the sodium-potassium pump may be a factor in some dystonias. The Na+
pump has been shown to control and set the intrinsic activity mode of cerebellar Purkinje neurons.[20] This suggests that the pump might not simply be a homeostatic, "housekeeping" molecule for ionic gradients; but could be a computational element in the cerebellum and the brain.[21] Indeed, an ouabain block of Na+
pumps in the cerebellum of a live mouse results in it displaying ataxia and dystonia.[22] Ataxia is observed for lower ouabain concentrations, dystonia is observed at higher ouabain concentrations. A mutation in the Na+
pump (ATP1A3 gene) can cause rapid onset dystonia parkinsonism.[23] The parkinsonism aspect of this disease may be attributable to malfunctioning Na+
pumps in the basal ganglia; the dystonia aspect may be attributable to malfunctioning Na+
pumps in the cerebellum (that act to corrupt its input to the basal ganglia) possibly in Purkinje neurons.[20]

Cerebellum issues causing dystonia is described by Filip et al. 2013: "Although dystonia has traditionally been regarded as a basal ganglia dysfunction, recent provocative evidence has emerged of cerebellar involvement in the pathophysiology of this enigmatic disease. It has been suggested that the cerebellum plays an important role in dystonia etiology, from neuroanatomical research of complex networks showing that the cerebellum is connected to a wide range of other central nervous system structures involved in movement control to animal models indicating that signs of dystonia are due to cerebellum dysfunction and completely disappear after cerebellectomy, and finally to clinical observations in secondary dystonia patients with various types of cerebellar lesions. It is proposed that dystonia is a large-scale dysfunction, involving not only cortico-basal ganglia-thalamo-cortical pathways, but the cortico-ponto-cerebello-thalamo-cortical loop as well. Even in the absence of traditional "cerebellar signs" in most dystonia patients, there are more subtle indications of cerebellar dysfunction. It is clear that as long as the cerebellum's role in dystonia genesis remains unexamined, it will be difficult to significantly improve the current standards of dystonia treatment or to provide curative treatment."[24]



Various treatments focus on sedating brain functions or blocking nerve communications with the muscles via drugs, neuro-suppression, or selective denervation surgery.[25] Almost all treatments have negative side-effects and risks. A geste antagoniste is a physical gesture or position (such as touching one's chin) that temporarily interrupts dystonia, it is also known as a sensory trick.[26] Patients may be aware of the presence of a geste antagoniste that provides some relief.[27] Therapy for dystonia can involve prosthetics that passively simulate the stimulation.[28]

Physical intervention


While research in the area of effectiveness of physical therapy intervention for dystonia remains weak,[29] there is reason to believe that rehabilitation can benefit dystonia patients.[30] Physical therapy can be utilized to manage changes in balance, mobility and overall function that occur as a result of the disorder.[31] A variety of treatment strategies can be employed to address the unique needs of each individual. Potential treatment interventions include splinting,[32] therapeutic exercise, manual stretching, soft tissue and joint mobilization, postural training and bracing,[30] neuromuscular electrical stimulation, constraint-induced movement therapy, activity and environmental modification, and gait training.[31]

Recent research has investigated further into the role of physiotherapy in the treatment of dystonia. A recent study showed that reducing psychological stress, in conjunction with exercise, is beneficial for reducing truncal dystonia in patients with Parkinson's disease.[33] Another study emphasized progressive relaxation, isometric muscle endurance, dynamic strength, coordination, balance, and body perception, seeing significant improvements to patients' quality of life after 4 weeks.[34]

Since the root of the problem is neurological, doctors have explored sensorimotor retraining activities to enable the brain to "rewire" itself and eliminate dystonic movements. The work of several doctors such as Nancy Byl and Joaquin Farias has shown that sensorimotor retraining activities and proprioceptive stimulation can induce neuroplasticity, making it possible for patients to recover substantial function that was lost due to Cervical Dystonia, hand dystonia, blepharospasm, oromandibular dystonia, dysphonia and musicians' dystonia.[35][36][37][38][39]

Due to the rare and variable nature of dystonia, research investigating the effectiveness of these treatments is limited. There is no gold standard for physiotherapy rehabilitation.[33] To date, focal cervical dystonia has received the most research attention;[31] however, study designs are poorly controlled and limited to small sample sizes.[29]



A baclofen pump has been used to treat patients of all ages exhibiting muscle spasticity along with dystonia. The pump delivers baclofen via a catheter to the thecal space surrounding the spinal cord. The pump itself is placed in the abdomen. It can be refilled periodically by access through the skin. Baclofen can also be taken in tablet form[40]

Botulinum toxin injection


Botulinum toxin injections into affected muscles have proved quite successful in providing some relief for around 3–6 months, depending on the kind of dystonia. Botox or Dysport injections have the advantage of ready availability (the same form is used for cosmetic surgery) and the effects are not permanent. There is a risk of temporary paralysis of the muscles being injected or the leaking of the toxin into adjacent muscle groups, causing weakness or paralysis in them. The injections must be repeated, as the effects wear off and around 15% of recipients develop immunity to the toxin. There is a Type A and a Type B toxin approved for treatment of dystonia; often, those that develop resistance to Type A may be able to use Type B.[41]

Muscle relaxants


Clonazepam, a benzodiazepine, is also sometimes prescribed. However, for most, their effects are limited and side-effects like mental confusion, sedation, mood swings, and short-term memory loss occur.

Ketogenic diet


One complex case study found that a ketogenic type diet may have been helpful in reducing symptoms associated with alternating hemiplegia of childhood (AHC) of a young child. However, as the researchers noted, their results could have been corollary in nature and not due to the diet itself, though future research is warranted.[42]


Schematic representation of a patient with cervical dystonia, with deep brain stimulation (DBS) electrodes implanted in the internal globus pallidus (GPi)

Surgery, such as the denervation of selected muscles, may also provide some relief; however, the destruction of nerves in the limbs or brain is not reversible and should be considered only in the most extreme cases. Recently, the procedure of deep brain stimulation (DBS) has proven successful in a number of cases of severe generalised dystonia.[43] DBS as treatment for medication-refractory dystonia, on the other hand, may increase the risk of suicide in patients. However, reference data of patients without DBS therapy are lacking.[44]



The Italian Bernardino Ramazzini provided one of the first descriptions of task-specific dystonia in 1713 in a book of occupational diseases, The Morbis Artificum.[45] In chapter II of this book's Supplementum, Ramazzini noted that "Scribes and Notaries" may develop "incessant movement of the hand, always in the same direction … the continuous and almost tonic strain on the muscles... that results in failure of power in the right hand". A report from the British Civil Service also contained an early description of writer's cramp. In 1864, Solly coined the term "scrivener's palsy" for this condition. These historical reports usually attributed the etiology of the motor abnormalities to overuse. Then, dystonia were reported in detail in 1911, when Hermann Oppenheim,[46] Edward Flatau and Wladyslaw Sterling described some Jewish children affected by a syndrome that was retrospectively considered to represent familial cases of DYT1 dystonia. Some decades later, in 1975, the first international conference on dystonia was held in New York. It was then recognized that, in addition to severe generalized forms, the dystonia phenotype also encompasses poorly-progressive focal and segmental cases with onset in adulthood, such as blepharospasm, torticollis and writer's cramp. These forms were previously considered independent disorders and were mainly classified among neuroses. A modern definition of dystonia was worded some years later, in 1984. During the following years it became evident that dystonia syndromes are numerous and diversified, new terminological descriptors (e.g., dystonia plus, heredodegenerative dystonias, etc.) and additional classification schemes were introduced. The clinical complexity of dystonia was then fully recognized.[47]

See also



  1. ^ "Dystonia". BMJ Best Practice. Retrieved 21 May 2020.
  2. ^ "Dystonia". NCH Healthcare System. Mayo Foundation for Medical Education and Research. 8 March 2006. Retrieved 21 May 2020.
  3. ^ a b "Dystonias Fact Sheet". National Institute of Neurological Disorders and Stroke. Archived from the original on 23 April 2018. Retrieved 2 May 2018.
  4. ^ a b Balint B, Bhatia KP (August 2014). "Dystonia: an update on phenomenology, classification, pathogenesis and treatment". Current Opinion in Neurology. 27 (4): 468–476. doi:10.1097/WCO.0000000000000114. PMID 24978640.
  5. ^ Hayes CM. "Down on the Pharm': All About Acute Dystonic Reaction". EMSvillage.com. Archived from the original on 15 November 2006.
  6. ^ Kamm C (November 2006). "Early onset torsion dystonia (Oppenheim's dystonia)". Orphanet Journal of Rare Diseases. 1 (1): 48. doi:10.1186/1750-1172-1-48. PMC 1693547. PMID 17129379.
  7. ^ Hersheson J, Mencacci NE, Davis M, MacDonald N, Trabzuni D, Ryten M, et al. (April 2013). "Mutations in the autoregulatory domain of β-tubulin 4a cause hereditary dystonia". Annals of Neurology. 73 (4): 546–553. doi:10.1002/ana.23832. PMC 3698699. PMID 23424103.
  8. ^ Valente EM, Bentivoglio AR, Cassetta E, Dixon PH, Davis MB, Ferraris A, et al. (March 2001). "DYT13, a novel primary torsion dystonia locus, maps to chromosome 1p36.13--36.32 in an Italian family with cranial-cervical or upper limb onset". Annals of Neurology. 49 (3): 362–366. doi:10.1002/ana.73. PMID 11261511. S2CID 20850908.
  9. ^ Grimes DA, Han F, Lang AE, St George-Hyssop P, Racacho L, Bulman DE (October 2002). "A novel locus for inherited myoclonus-dystonia on 18p11". Neurology. 59 (8): 1183–1186. doi:10.1212/WNL.59.8.1183. PMID 12391345. S2CID 22416848.
  10. ^ Chouery E, Kfoury J, Delague V, Jalkh N, Bejjani P, Serre JL, Mégarbané A (October 2008). "A novel locus for autosomal recessive primary torsion dystonia (DYT17) maps to 20p11.22-q13.12". Neurogenetics. 9 (4): 287–293. doi:10.1007/s10048-008-0142-4. PMID 18688663. S2CID 20343435.
  11. ^ Charlesworth G, Plagnol V, Holmström KM, Bras J, Sheerin UM, Preza E, et al. (December 2012). "Mutations in ANO3 cause dominant craniocervical dystonia: ion channel implicated in pathogenesis". American Journal of Human Genetics. 91 (6): 1041–1050. doi:10.1016/j.ajhg.2012.10.024. PMC 3516598. PMID 23200863.
  12. ^ Cassim F (October 2003). "[Myoclonic dystonia]" [Myoclonic dystonia]. Revue Neurologique (in French). 159 (10 Pt 1): 892–899. PMID 14615678. Archived from the original on 11 May 2020. Retrieved 22 November 2008.
  13. ^ Vidailhet M, Tassin J, Durif F, Nivelon-Chevallier A, Agid Y, Brice A, Dürr A (May 2001). "A major locus for several phenotypes of myoclonus--dystonia on chromosome 7q". Neurology. 56 (9): 1213–1216. doi:10.1212/WNL.56.9.1213. PMID 11342690. S2CID 10492653.
  14. ^ Fuchs T, Ozelius LJ (December 2013). "Genetics in dystonia: an update". Current Neurology and Neuroscience Reports. 13 (12): 410. doi:10.1007/s11910-013-0410-z. PMC 3877920. PMID 24136457.
  15. ^ Baker M, Strongosky AJ, Sanchez-Contreras MY, Yang S, Ferguson W, Calne DB, et al. (March 2014). "SLC20A2 and THAP1 deletion in familial basal ganglia calcification with dystonia". Neurogenetics. 15 (1): 23–30. doi:10.1007/s10048-013-0378-5. PMC 3969760. PMID 24135862.
  16. ^ Burda A, Webster K, Leikin JB, Chan SB, Stokes KA (October 1999). "Nefazadone-induced acute dystonic reaction". Veterinary and Human Toxicology. 41 (5): 321–322. PMID 10509438.
  17. ^ a b Louis ED, Lee P, Quinn L, Marder K (January 1999). "Dystonia in Huntington's disease: prevalence and clinical characteristics". Movement Disorders. 14 (1): 95–101. doi:10.1002/1531-8257(199901)14:1<95::AID-MDS1016>3.0.CO;2-8. PMID 9918350. S2CID 7356997.
  18. ^ Charlesworth G, Bhatia KP, Wood NW (July 2013). "The genetics of dystonia: new twists in an old tale". Brain. 136 (Pt 7): 2017–2037. doi:10.1093/brain/awt138. PMC 3692036. PMID 23775978.
  19. ^ Janavs JL, Aminoff MJ (October 1998). "Dystonia and chorea in acquired systemic disorders". Journal of Neurology, Neurosurgery, and Psychiatry. 65 (4): 436–445. doi:10.1136/jnnp.65.4.436. PMC 2170280. PMID 9771763.
  20. ^ a b Forrest MD, Wall MJ, Press DA, Feng J (2012). "The sodium-potassium pump controls the intrinsic firing of the cerebellar Purkinje neuron". PLOS ONE. 7 (12): e51169. Bibcode:2012PLoSO...751169F. doi:10.1371/journal.pone.0051169. PMC 3527461. PMID 23284664.
  21. ^ Forrest MD (2014). "The sodium-potassium pump is an information processing element in brain computation". Frontiers in Physiology. 5: 472. doi:10.3389/fphys.2014.00472. PMC 4274886. PMID 25566080.
  22. ^ Calderon DP, Fremont R, Kraenzlin F, Khodakhah K (March 2011). "The neural substrates of rapid-onset Dystonia-Parkinsonism". Nature Neuroscience. 14 (3): 357–365. doi:10.1038/nn.2753. PMC 3430603. PMID 21297628.
  23. ^ Cannon SC (July 2004). "Paying the price at the pump: dystonia from mutations in a Na+/K+ -ATPase". Neuron. 43 (2): 153–154. doi:10.1016/j.neuron.2004.07.002. PMID 15260948.
  24. ^ Filip P, Lungu OV, Bareš M (July 2013). "Dystonia and the cerebellum: a new field of interest in movement disorders?". Clinical Neurophysiology. 124 (7): 1269–1276. doi:10.1016/j.clinph.2013.01.003. PMID 23422326. S2CID 22185709.
  25. ^ Mayo Clinic Staff (18 June 2022). "Dystonia". Mayo Clinic. Retrieved 12 March 2023.
  26. ^ Watts RL, Koller WC (2004). Movement disorders: neurologic principles & practice. McGraw-Hill Professional. pp. 502–. ISBN 978-0-07-137496-5. Retrieved 30 May 2011.
  27. ^ Jahanshahi M (February 2000). "Factors that ameliorate or aggravate spasmodic torticollis". Journal of Neurology, Neurosurgery, and Psychiatry. 68 (2): 227–229. doi:10.1136/jnnp.68.2.227. PMC 1736788. PMID 10644795.
  28. ^ "Dystonia: Treatment - MayoClinic.com". Archived from the original on 2 June 2007. Retrieved 7 June 2007.
  29. ^ a b Crowner BE (November 2007). "Cervical dystonia: disease profile and clinical management". Physical Therapy. 87 (11): 1511–1526. doi:10.2522/ptj.20060272. PMID 17878433.
  30. ^ a b Lubarr N, Bressman S (June 2011). "Treatment of generalized dystonia". Current Treatment Options in Neurology. 13 (3): 274–289. doi:10.1007/s11940-011-0122-0. PMID 21455718. S2CID 21253455.
  31. ^ a b c Myers KJ, Bour B (2009). "The Role of Physical Therapy in the Management of Dystonia". In Okun, M.S. (ed.). The Dystonia Patient: A Guide to Practical Management. New York: Demos Medical. pp. 117–48. ISBN 978-1-933864-62-4. OCLC 429666586.
  32. ^ Priori A, Pesenti A, Cappellari A, Scarlato G, Barbieri S (August 2001). "Limb immobilization for the treatment of focal occupational dystonia". Neurology. 57 (3): 405–409. doi:10.1212/WNL.57.3.405. PMID 11502904. S2CID 36440551.
  33. ^ a b Kawamichi K, Taichi H, Orie I, Mineta T, Sawada Y, Shimamura M, Matsumoto K, Kawamura K (2011). "Effect of Rehabilitation on Parkinson's Disease with Truncal Dystonia" (PDF). Journal of Tokushima. 2: 47–50. Retrieved 6 May 2012.[permanent dead link]
  34. ^ Zetterberg L, Halvorsen K, Färnstrand C, Aquilonius SM, Lindmark B (2009). "Physiotherapy in cervical dystonia: six experimental single-case studies". Physiotherapy Theory and Practice. 24 (4): 275–290. doi:10.1080/09593980701884816. PMID 18574753. S2CID 20722262.
  35. ^ Bitti F. "Cervical Dystonia. Rewiring the brain through dance". TEDx Talk. Archived from the original on 25 January 2016. Retrieved 24 January 2016 – via YouTube.
  36. ^ Farias J. "Dystonia. Your movement can heal your brain". TEDx Talk. Archived from the original on 26 January 2016. Retrieved 24 January 2016 – via YouTube.
  37. ^ "Choosing music over meds, one man's quest to retrain his brain to overcome dystonia". YouTube. Archived from the original on 26 January 2016. Retrieved 24 January 2016.
  38. ^ Farias J, Sarti-Martínez MA. Elite musicians treated by specific fingers motion program to stimulate proprioceptive sense. Congreso Nacional De La Sociedad Anatómica Española. Alicante (España). p. 110 – via European Journal of Anatomy.
  39. ^ "Open Your Eyes Part 1 . Freedom from Blepharospasm. Documentary". Out of the Box Productions. Archived from the original on 11 April 2016. Retrieved 2 December 2016 – via YouTube.
  40. ^ Jankovic J, Tolosa E (2007). Parkinson's Disease & Movement Disorders (5th ed.). Philadelphia: Lippincott Williams & Wilkins. pp. 349–50. ISBN 978-0-7817-7881-7.
  41. ^ Brin MF, Lew MF, Adler CH, Comella CL, Factor SA, Jankovic J, et al. (October 1999). "Safety and efficacy of NeuroBloc (botulinum toxin type B) in type A-resistant cervical dystonia". Neurology. 53 (7): 1431–1438. doi:10.1212/WNL.53.7.1431. PMID 10534247.
  42. ^ Roubergue A, Philibert B, Gautier A, Kuster A, Markowicz K, Billette de Villemeur T, et al. (16 February 2014). "Excellent response to a ketogenic diet in a patient with alternating hemiplegia of childhood". JIMD Reports. 15: 7–12. doi:10.1007/8904_2013_292. PMC 4270868. PMID 24532324.
  43. ^ Bittar RG, Yianni J, Wang S, Liu X, Nandi D, Joint C, et al. (January 2005). "Deep brain stimulation for generalised dystonia and spasmodic torticollis". Journal of Clinical Neuroscience. 12 (1): 12–16. doi:10.1016/j.jocn.2004.03.025. PMID 15639404. S2CID 12036156.
  44. ^ Foncke EM, Schuurman PR, Speelman JD (January 2006). "Suicide after deep brain stimulation of the internal globus pallidus for dystonia". Neurology. 66 (1): 142–143. doi:10.1212/01.wnl.0000191328.05752.e2. PMID 16401868. S2CID 9070411.
  45. ^ Ramazzini B. Diseases of Workers. Translated from De Morbis Artificum of 1713 by Wilmer Cave Wright. New York: Haffner, 1964[full citation needed]
  46. ^ Tarsy D, Simon DK (August 2006). "Dystonia". The New England Journal of Medicine. 355 (8): 818–829. doi:10.1056/NEJMra055549. PMID 16928997.
  47. ^ Albanese A (August 2013). "A History of Dystonia". The International Parkinson and Movement Disorder Society. Archived from the original on 4 March 2016. Retrieved 6 January 2016.