Ataxia

For other uses, see Ataxia (disambiguation).

Ataxia (from Greek - [a negative prex] + - [or-der] = lack of order) is a neurological sign consistingof lack of voluntary coordination of muscle movements.Ataxia is a non-specic clinical manifestation implyingdysfunction of the parts of the nervous system that coor-dinate movement, such as the cerebellum. Several pos-sible causes exist for these patterns of neurological dys-function. Dystaxia is a mild degree of ataxia.[1]

1 Types

1.1 CerebellarThe term cerebellar ataxia is used to indicate ataxia thatis due to dysfunction of the cerebellum. The cerebel-lum is responsible for integrating a signicant amount ofneural information that is used to coordinate smoothlyongoing movements and to participate in motor plan-ning. Although ataxia is not present with all cerebel-lar lesions, many conditions aecting the cerebellumdo produce ataxia.[2] People with cerebellar ataxia mayhave trouble regulating the force, range, direction, veloc-ity and rhythm of muscle contractions.[3] This results ina characteristic type of irregular, uncoordinated move-ment that can manifest itself in many possible ways,such as asthenia, asynergy, delayed reaction time, anddyschronometria. Individuals with cerebellar ataxia couldalso display instability of gait, diculty with eye move-ments, dysarthria, dysphagia, hypotonia, dysmetria anddysdiadochokinesia.[2] These decits can vary dependingon which cerebellar structures have been damaged, andwhether the lesion is bilateral or unilateral.People with cerebellar ataxia may initially present withpoor balance, which could be demonstrated as an in-ability to stand on one leg or perform tandem gait. Asthe condition progresses, walking is characterized by awidened base and high stepping, as well as staggeringand lurching from side to side.[2] Turning is also prob-lematic and could result in falls. As cerebellar ataxiabecomes severe, great assistance and eort are neededto stand and walk.[2] Dysarthria, an impairment with ar-ticulation, may also be present and is characterized byscanning speech that consists of slower rate, irregularrhythm and variable volume.[2] There may also be slur-ring of speech, tremor of the voice and ataxic respira-tion. Cerebellar ataxia could result with incoordination

of movement, particularly in the extremities. There isovershooting with nger to nose testing, and heel to shintesting; thus, dysmetria is evident.[2] Impairments withalternating movements (dysdiadochokinesia), as well asdysrhythmia, may also be displayed. There may also betremor of the head and trunk (titubation) in individualswith cerebellar ataxia.[2]

It is thought that dysmetria is caused by a decit in thecontrol of interaction torques in multijoint motion.[4] In-teraction torques are created at an associated joint whenthe primary joint is moved. For example, if a movementrequired reaching to touch a target in front of the body,exion at the shoulder would create a torque at the elbow,while extension of the elbow would create a torque atthe wrist. These torques increase as the speed of move-ment increases and must be compensated and adjustedfor to create coordinated movement. This may, there-fore, explain decreased coordination at higher movementvelocities and accelerations.

Dysfunction of the vestibulocerebellum(occulonodular lobe) impairs the balance andthe control of eye movements. This presents itselfwith postural instability, in which the person tendsto separate his/her feet upon standing, to gain awider base and to avoid titubation (bodily oscilla-tions tending to be forward-backward ones). Theinstability is therefore worsened when standing withthe feet together, regardless of whether the eyesare open or closed. This is a negative Rombergstest, or more accurately, it denotes the individualsinability to carry out the test, because the individualfeels unstable even with open eyes.

Dysfunction of the spinocerebellum (vermis andassociated areas near the midline) presents itselfwith a wide-based drunken sailor gait (called trun-cal ataxia),[5] characterised by uncertain starts andstops, lateral deviations, and unequal steps. As a re-sult of this gait impairment, falling is a concern inpatients with ataxia. Studies examining falls in thispopulation show that 74-93% of patients have fallenat least once in the past year and up to 60% admit tofear of falling.[6][7]

Dysfunction of the cerebrocerebellum (lateralhemispheres) presents as disturbances in carryingout voluntary, planned movements by the extrem-ities (called appendicular ataxia).[5] These include:

intention tremor (coarse trembling, accentu-

1

2 2 CAUSES

ated over the execution of voluntary move-ments, possibly involving the head and eyes aswell as the limbs and torso);

peculiar writing abnormalities (large, unequalletters, irregular underlining);

a peculiar pattern of dysarthria (slurredspeech, sometimes characterised by explosivevariations in voice intensity despite a regularrhythm).

inability to perform rapidly alternating move-ments, known as dysdiadochokinesia. Thiscould involve rapidly switching from pronationto supination of the forearm. Movementsbecome more irregular with increases ofspeed.[8]

inability to judge distances or ranges of move-ment. This is known as dysmetria and is oftenseen as undershooting, hypometria, or over-shooting, hypermetria, the required distanceor range to reach a target. This is sometimesseen when a patient is asked to reach out andtouch someones nger or touch his or her ownnose.[8]

the rebound phenomenon, also known as theloss of the check reex is also sometimes seenin patients with cerebellar ataxia. For exam-ple, when a patient is exing his or her elbowisometrically against a resistance. When theresistance is suddenly removed without warn-ing, the patients arm may swing up and evenstrike themselves. With an intact check reex,the patient will check and activate the oppos-ing triceps to slow and stop the movement.[8]

1.2 SensoryThe term sensory ataxia is employed to indicate ataxiadue to loss of proprioception, the loss of sensitivity to thepositions of joint and body parts. This is generally causedby dysfunction of the dorsal columns of the spinal cord,because they carry proprioceptive information up to thebrain. In some cases, the cause of sensory ataxia mayinstead be dysfunction of the various parts of the brainwhich receive positional information, including the cere-bellum, thalamus, and parietal lobes.Sensory ataxia presents itself with an unsteady stomp-ing gait with heavy heel strikes, as well as a postural in-stability that is usually worsened when the lack of propri-oceptive input cannot be compensated for by visual input,such as in poorly lit environments.Physicians can nd evidence of sensory ataxia duringphysical examination by having the patient stand withhis/her feet together and eyes shut. In aected patients,this will cause the instability to worsen markedly, produc-ing wide oscillations and possibly a fall. This is called a

positive Rombergs test. Worsening of the nger-pointingtest with the eyes closed is another feature of sensoryataxia. Also, when the patient is standing with armsand hands extended toward the physician, if the eyes areclosed, the patients nger will tend to fall down andthen be restored to the horizontal extended position bysudden muscular contractions (the ataxic hand).

1.3 Vestibular

The term vestibular ataxia is employed to indicate ataxiadue to dysfunction of the vestibular system, which inacute and unilateral cases is associated with prominentvertigo, nausea and vomiting. In slow-onset, chronic bi-lateral cases of vestibular dysfunction, these characteris-tic manifestationsmay be absent, and dysequilibriummaybe the sole presentation.

2 CausesThe three types of ataxia have overlapping causes, andtherefore can either coexist or occur in isolation.

2.1 Focal lesions

Any type of focal lesion of the central nervous system(such as stroke, brain tumour, multiple sclerosis) willcause the type of ataxia corresponding to the site of thelesion: cerebellar if in the cerebellum, sensory if in thedorsal spinal cord (and rarely in the thalamus or parietallobe), vestibular if in the vestibular system (including thevestibular areas of the cerebral cortex).

2.2 Exogenous substances

Exogenous substances that cause ataxia mainly do sobecause they have a depressant eect on central ner-vous system function. The most common example isethanol, which is capable of causing reversible cerebel-lar and vestibular ataxia. Other examples include var-ious prescription drugs (e.g. most antiepileptic drugshave cerebellar ataxia as a possible adverse eect),Lithium level over 1.5mEq/L, cannabis ingestion[9] andvarious other recreational drugs (e.g. ketamine, PCPor dextromethorphan, all of which are NMDA recep-tor antagonists that produce a dissociative state at highdoses). A further class of pharmaceuticals which cancause short term ataxia, especially in high doses arethe benzodiazepines.[10][11] Exposure to high levels ofmethylmercury, through consumption of sh with highmercury concentrations, is also a known cause of ataxiaand other neurological disorders.[12]

2.9 Arnold-Chiari malformation 3

2.3 Radiation poisoning

Ataxia can be induced as a result of severe acute radiationpoisoning with an absorbed dose of more than 30 Grays.

2.4 Vitamin B12 deciency

Vitamin B12 deciency may cause, among several neuro-logical abnormalities, overlapping cerebellar and sensoryataxia.

2.5 Hypothyroidism

Symptoms of neurological dysfunction may be the pre-senting feature in some patients with hypothyroidism.These include reversible cerebellar ataxia, dementia,peripheral neuropathy, psychosis and coma. Most ofthe neurological complications improve completely afterthyroid hormone replacement therapy.[13][14]

2.6 Causes of isolated sensory ataxia

Peripheral neuropathies may cause generalised or lo-calised sensory ataxia (e.g. a limb only) depending onthe extent of the neuropathic involvement. Spinal dis-orders of various types may cause sensory ataxia fromthe lesioned level below, when they involve the dorsalcolumns[15][16][17]

2.7 Non-hereditary cerebellar degenera-tion

Non-hereditary causes of cerebellar degeneration in-clude chronic ethanol abuse, head injury, paraneoplasticcerebellar degeneration, high altitude cerebral oedema,coeliac disease, normal pressure hydrocephalus andcerebellitis.

2.8 Hereditary ataxias

Ataxia may depend on hereditary disorders consistingof degeneration of the cerebellum and/or of the spine;most cases feature both to some extent, and thereforepresent with overlapping cerebellar and sensory ataxia,even though one is often more evident than the other.Hereditary disorders causing ataxia include autosomaldominant ones such as spinocerebellar ataxia, episodicataxia, and dentatorubropallidoluysian atrophy, as well asautosomal recessive disorders such as Friedreichs ataxia(sensory and cerebellar, with the former predominating)and Niemann Pick disease, ataxia-telangiectasia (sen-sory and cerebellar, with the latter predominating), andabetalipoproteinaemia. An example of X-linked ataxic

condition is the rare fragile X-associated tremor/ataxiasyndrome.

2.9 Arnold-Chiari malformation

Arnold-Chiari malformation is a malformation of thebrain. It consists of a downward displacement of thecerebellar tonsils and the medulla through the foramenmagnum, sometimes causing hydrocephalus as a result ofobstruction of cerebrospinal uid outow.

2.10 Wilsons disease

Wilsons disease is an autosomal-recessive gene disorderwhereby an alteration of the ATP7B gene results in aninability to properly excrete copper from the body.[18]Copper accumulates in the nervous system and liver andcan cause ataxia as well as other neurological and organimpairments.[19]

2.11 Gluten ataxia

Gluten ataxia is a gluten-related disorder, a wide spec-trum of disorders marked by an abnormal immunologicalresponse to gluten. Like celiac disease, it is an autoim-mune disease.[20] With gluten ataxia, damage takes placein the cerebellum, the balance center of the brain thatcontrols coordination and complex movements like walk-ing, speaking and swallowing.[21] Gluten ataxia is the sin-gle most common cause of sporadic idiopathic ataxia.[22]

Gluten ataxia is an immune-mediated disease triggeredby the ingestion of gluten in genetically susceptible indi-viduals. It should be considered in the dierential diag-nosis of all patients with idiopathic sporadic ataxia. Earlydiagnosis and treatment with a gluten free diet can im-prove ataxia and prevent its progression. Readily avail-able and sensitive markers of gluten ataxia include anti-gliadin antibodies. Immunoglobulin A (IgA) depositsagainst transglutaminase 2 (TG2) in the small bowel andat extraintestinal sites are proving to be additionally re-liable and perhaps more specic markers of the wholespectrum of gluten sensitivity. They may also hold thekey to its pathogenesis.[23]

Gluten ataxia is dened as sporadic cerebellar ataxia asso-ciated with the presence circulating antigliadin antibodiesand in the absence of an alternative etiology for ataxia.[24]

2.12 Sodium-potassium pump

Misfunction of the sodium-potassium pumpmay be a fac-tor in some ataxias. The Na+-K+pump has been shown to control and set the intrinsic ac-tivity mode of cerebellar Purkinje neurons.[25] This sug-

4 4 OTHER USES

gests that the pump might not simply be a homeostatic,housekeepingmolecule for ionic gradients; but could bea computational element in the cerebellum and the brain.Indeed, an ouabain block of Na+-K+pumps in the cerebellum of a live mouse results in itdisplaying ataxia and dystonia.[26] Ataxia is observed forlower ouabain concentrations, dystonia is observed athigher ouabain concentrations.

3 Treatment

The treatment of ataxia and its eectiveness depend onthe underlying cause. Treatment may limit or reduce theeects of ataxia, but it is unlikely to eliminate them en-tirely. Recovery tends to be better in individuals with asingle focal injury (such as stroke or a benign tumour),compared to those who have a neurological degenerativecondition.[27] A review of the management of degenera-tive ataxia was published in 2009.[28]

The movement disorders associated with ataxia can bemanaged by pharmacological treatments and throughphysical therapy and occupational therapy to reducedisability.[29] Some drug treatments that have been usedto control ataxia include: 5-hydroxytryptophan (5-HTP),idebenone, amantadine, physostigmine, L-carnitine orderivatives, trimethoprimsulfamethoxazole, vigabatrin,phosphatidylcholine, acetazolamide, 4-aminopyridine,buspirone, and a combination of coenzyme Q10 andvitamin E.[28]

Physical therapy requires a focus on adapting activity andfacilitating motor learning for retraining specic func-tional motor patterns.[30] A recent systematic review sug-gested that physical therapy is eective, but there is onlymoderate evidence to support this conclusion.[31] Themost commonly used physical therapy interventions forcerebellar ataxia are vestibular habituation, Frenkel Ex-ercises, proprioceptive neuromuscular facilitation (PNF),and balance training; however, therapy is often highly in-dividualized and gait and coordination training are largecomponents of therapy.Current research suggests that, if a person is able to walkwith or without a mobility aid, physical therapy shouldinclude an exercise program addressing ve components:static balance, dynamic balance, trunk-limb coordina-tion, stairs, and contracture prevention. Once the physicaltherapist determines that the individual is able to safelyperform parts of the program independently, it is im-portant that the individual be prescribed and regularlyengage in a supplementary home exercise program thatincorporates these components to further improve longterm outcomes. These outcomes include balance tasks,gait, and individual activities of daily living. While theimprovements are attributed primarily to changes in thebrain and not just the hip and/or ankle joints, it is still un-

known whether the improvements are due to adaptationsin the cerebellum or compensation by other areas of thebrain.[30]

Decomposition, simplication, or slowing of multi-joint movement may also be an eective strategy thattherapists may use to improve function in patientswith ataxia.[32] Training likely needs to be intense andfocusedas indicated by one study performed withstroke patients experiencing limb ataxia who underwentintensive upper limb retraining.[33] Their therapy con-sisted of constraint-induced movement therapy which re-sulted in improvements of their arm function.[33] Treat-ment should likely include strategies to manage dicul-ties with everyday activities such as walking. Gait aids(such as a cane or walker) can be provided to decreasethe risk of falls associated with impairment of balance orpoor coordination. Severe ataxia may eventually lead tothe need for a wheelchair. To obtain better results, possi-ble coexisting motor decits need to be addressed in ad-dition to those induced by ataxia. For example, muscleweakness and decreased endurance could lead to increas-ing fatigue and poorer movement patterns.There are several assessment tools available to thera-pists and health care professionals working with patientswith ataxia. The International Cooperative Ataxia RatingScale (ICARS) is one of the most widely used and hasbeen proven to have very high reliability and validity.[34]Other tools that assess motor function, balance and co-ordination are also highly valuable to help the therapisttrack the progress of their patient, as well as to quantifythe patients functionality. These tests include, but are notlimited to:

The Berg Balance Scale Tandem Walking (to test for Tandem gaitability) Scale for the Assessment and Rating of Ataxia[35]

tapping tests The person must quickly and repeat-edly tap their arm or leg while the therapist monitorsthe amount of dysdiadochokinesia.[36]

nger-nose testing[36] This test has several varia-tions including nger-to-therapists nger, nger-to-nger, and alternate nose-to-nger.[37]

4 Other usesThe term ataxia is sometimes used in a broader sense toindicate lack of coordination in some physiological pro-cess. Examples include optic ataxia (lack of coordina-tion between visual inputs and hand movements, resultingin inability to reach and grab objects) and ataxic respi-ration (lack of coordination in respiratory movements,usually due to dysfunction of the respiratory centres inthe medulla oblongata). Optic ataxia may be caused by

5lesions to the posterior parietal cortex, which is respon-sible for combining and expressing positional informa-tion and relating it to movement. Outputs of the posteriorparietal cortex include the spinal cord, brain stem motorpathways, pre-motor and pre-frontal cortex, basal gan-glia and the cerebellum. Some neurons in the posteriorparietal cortex are modulated by intention. Optic ataxiais usually part of Balints syndrome, but can be seen inisolation with injuries to the superior parietal lobule, asit represents a disconnection between visual-associationcortex and the frontal premotor and motor cortex.[38]

5 See also Ataxic cerebral palsy Spinocerebellar ataxia

6 References[1] dystaxia. (n.d.). The American Heritage Stedmans Med-

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[3] Fredericks CM (1996). Disorders of the Cerebellumand Its Connections. In Saladin LK, Fredericks CM.Pathophysiology of the motor systems: principles and clin-ical presentations. Philadelphia: F.A. Davis. ISBN 0-8036-0093-3.

[4] Bastian AJ, Zackowski KM, Thach WT (May 2000).Cerebellar ataxia: torque deciency or torque mismatchbetween joints?". J. Neurophysiol. 83 (5): 301930.PMID 10805697.

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[10] Browne TR (May 1976). Clonazepam. A review ofa new anticonvulsant drug. Arch. Neurol. 33 (5):32632. doi:10.1001/archneur.1976.00500050012003.PMID 817697.

[11] Gaudreault P, Guay J, Thivierge RL, Verdy I (1991).Benzodiazepine poisoning. Clinical and pharmacologi-cal considerations and treatment. Drug Saf 6 (4): 24765. doi:10.2165/00002018-199106040-00003. PMID1888441.

[12] Dez S (2009). Human health eects of methylmercuryexposure. Rev Environ Contam Toxicol. Reviews of En-vironmental Contamination and Toxicology 198: 11132. doi:10.1007/978-0-387-09647-6_3. ISBN 978-0-387-09646-9. PMID 19253038.

[13] Victor M, Ropper AH, Adams RD, Samuels M (2009).Adams and Victors Principles of Neurology (Ninth ed.).McGraw-Hill Medical. pp. 7888. ISBN 0-07-149992-X.

[14] PavanMR, DeepakM, Basavaprabhu A, Gupta A (2012).Doctor i am swaying An interesting case of ataxia.Journal of Clinical and Diagnostic Research. Retrieved 2May 2013.

[15] Spinazzi M, Angelini C, Patrini C (May 2010). Suba-cute sensory ataxia and optic neuropathy with thiaminedeciency. Nature Reviews Neurology 6 (5): 28893.doi:10.1038/nrneurol.2010.16. PMID 20308997.

[16] Sghirlanzoni A, Pareyson D, Lauria G (June 2005).Sensory neuron diseases. Lancet Neurol 4 (6):34961. doi:10.1016/S1474-4422(05)70096-X. PMID15907739.

[17] Moeller JJ, Macaulay RJ, Valdmanis PN, Weston LE,Rouleau GA, Dupr N (September 2008). Autosomaldominant sensory ataxia: a neuroaxonal dystrophy. ActaNeuropathol. 116 (3): 3316. doi:10.1007/s00401-008-0362-6. PMID 18347805.

[18] Walshe JM. Clarke CE, Nicholl DJ, ed. Wilsons Dis-ease. Birmingham Movement Disorders Coursebook.

[19] Haldeman-Englert, C. Wilsons disease - PubMedHealth. PubMed Health.

[20] Sapone A, Bai JC, Ciacci C, Dolinsek J, Green PH,Hadjivassiliou M et al. (2012). Spectrum ofgluten-related disorders: consensus on new nomencla-ture and classication. BMC Medicine (Review) 10: 13.doi:10.1186/1741-7015-10-13. PMC 3292448. PMID22313950.

[21] Boyd C (FebMar 2011). Gluten Attack: Ataxia A Con-troversial Call. Living Without.

[22] Hadjivassiliou M, Grnewald R, Sharrack B, Sanders D,Lobo A, Williamson C et al. (March 2003). Glutenataxia in perspective: epidemiology, genetic susceptibil-ity and clinical characteristics. Brain 126 (Pt 3): 68591.doi:10.1093/brain/awg050. PMID 12566288.

6 8 EXTERNAL LINKS

[23] Hadjivassiliou M, Sanders DS, Woodroofe N, WilliamsonC, Grnewald RA (2008). Gluten ataxia. Cerebellum7 (3): 4948. doi:10.1007/s12311-008-0052-x. PMID18787912.

[24] Hadjivassiliou M, Mki M, Sanders DS, Williamson CA,Grnewald RA, Woodroofe NM et al. (February 2006).Autoantibody targeting of brain and intestinal transg-lutaminase in gluten ataxia. Neurology 66 (3): 3737. doi:10.1212/01.wnl.0000196480.55601.3a. PMID16476935.

[25] Forrest MD, Wall MJ, Press DA, Feng J (De-cember 2012). The Sodium-Potassium PumpControls the Intrinsic Firing of the CerebellarPurkinje Neuron. PLoS ONE 7 (12): e51169.doi:10.1371/journal.pone.0051169. PMC 3527461.PMID 23284664.

[26] Calderon DP, Fremont R, Kraenzlin F, Khodakhah K(March 2011). The neural substrates of rapid-onsetDystonia-Parkinsonism. Nature Neuroscience 14 (3):35765. doi:10.1038/nn.2753. PMC 3430603. PMID21297628.

[27] Morton SM, Bastian AJ (December 2009). Can re-habilitation help ataxia?". Neurology 73 (22): 18189. doi:10.1212/WNL.0b013e3181c33b21. PMID19864635.

[28] Trujillo-MartnMM, Serrano-Aguilar P,Monton-AlvarezF, Carrillo-Fumero R (June 2009). Eectiveness andsafety of treatments for degenerative ataxias: a sys-tematic review. Mov. Disord. 24 (8): 111124.doi:10.1002/mds.22564. PMID 19412936.

[29] Perlman SL (November 2006). Ataxias.Clin. Geriatr. Med. 22 (4): 85977, vii.doi:10.1016/j.cger.2006.06.011. PMID 17000340.

[30] Ilg W, Synofzik M, Brtz D, Burkard S, Giese MA,Schls L (December 2009). Intensive coordina-tive training improves motor performance in degener-ative cerebellar disease. Neurology 73 (22): 182330. doi:10.1212/WNL.0b013e3181c33adf. PMID19864636.

[31] Martin CL, Tan D, Bragge P, Bialocerkowski A(January 2009). Eectiveness of physiotherapyfor adults with cerebellar dysfunction: a system-atic review. Clinical Rehabilitation 23 (1): 1526.doi:10.1177/0269215508097853. PMID 19114434.

[32] Bastian AJ (June 1997). Mechanisms of ataxia. Physi-cal Therapy 77 (6): 6725. PMID 9184691.

[33] Richards L, Senesac C, McGuirk T, Woodbury M, How-land D, Davis S et al. (2008). Response to inten-sive upper extremity therapy by individuals with ataxiafrom stroke. Top Stroke Rehabil 15 (3): 26271.doi:10.1310/tsr1503-262. PMID 18647730.

[34] Schmitz-Hbsch T, Tezenas du Montcel S, Baliko L,Boesch S, Bonato S, Fancellu R et al. (May 2006).Reliability and validity of the International Coopera-tive Ataxia Rating Scale: a study in 156 spinocerebel-lar ataxia patients. Mov. Disord. 21 (5): 699704.doi:10.1002/mds.20781. PMID 16450347.

[35] Schmitz-Hbsch T, du Montcel ST, Baliko L, BercianoJ, Boesch S, Depondt C et al. (June 2006). Scalefor the assessment and rating of ataxia: developmentof a new clinical scale. Neurology 66 (11): 171720. doi:10.1212/01.wnl.0000219042.60538.92. PMID16769946.

[36] Notermans NC, van Dijk GW, van der Graaf Y, vanGijn J, Wokke JH (January 1994). Measuring ataxia:quantication based on the standard neurological exam-ination. J. Neurol. Neurosurg. Psychiatr. 57 (1): 226. doi:10.1136/jnnp.57.1.22. PMC 485035. PMID8301300.

[37] OPETA: Neurologic Examination. Online physicalexam teaching assistant. The UF College of MedicineHarrell Center. Retrieved 7 May 2012.

[38] Vallar G (July 2007). Spatial neglect, Balint-Homes andGerstmanns syndrome, and other spatial disorders. CNSSpectr 12 (7): 52736. PMID 17603404.

7 Further reading Pagon RA, Bird TD, Dolan CR, Stephens K, AdamMP, Bird TD (1998). Hereditary Ataxia Overview(last revision 2012). All GeneReview. PMID20301317.

Manto M, Gruol D, Schmahmann J, Koibuchi N,Rossi F (2013). Handbook of the Cerebellum andCerebellar Disorders. Springer.

8 External links Friedreichs Ataxia Research Alliance (FARA) Ataxia Connect Social Network Ataxia UK, including guidelines Brasil, Rio Grande do Sul - Associao dos Amigos,Parentes e Portadores de Ataxias Dominantes

Canadian Association for Familial Ataxias - ClaudeSt-Jean Foundation

International Ataxia Awareness Day LivingWithAtaxia Forums & Community Overview at National Institute of Neurological Dis-orders and Stroke (NINDS)

Rochester Ataxia Foundation, Rochester, NY The latest news and research on Ataxia US National Ataxia Foundation University of Minnesota Ataxia Center Video demonstration of ataxic gait

7 Gluten Ataxia Range of Neurologic Disorders in Patients WithCeliac Disease

The Cerebellum Cerebellum and Ataxias

8 9 TEXT AND IMAGE SOURCES, CONTRIBUTORS, AND LICENSES

9 Text and image sources, contributors, and licenses9.1 Text

Ataxia Source: http://en.wikipedia.org/wiki/Ataxia?oldid=644428974 Contributors: Eloquence, ErdemTuzun, Matusz, Heron, Edward,Skysmith, Bemoeial, Robbot, RedWolf, Sbisolo, Aleron235, Dave6, Jfdwol, Eequor, Chowbok, Mike Rosoft, Chris Howard, Cacy-cle, CanisRufus, Sortior, Arcadian, Kensai, Mpulier, Ben davison, Rd232, Minority Report, Echuck215, SidP, Woohookitty, Ormy,Daniel Case, Thivierr, Eleassar777, Dolfrog, Benuski, SqueakBox, BD2412, Rjwilmsi, Vegaswikian, Aechris, DickClarkMises, Mit-sukai, Nimur, RobyWayne, Michele Bini, Gleagle, Markmichaelh, Gwernol, YurikBot, Gaius Cornelius, A314268, Gary84, Rmky87,Robotico, Theda, GrinBot, SmackBot, Federalist51, Ron E, Jprg1966, Stubblyhead, Jwy, Acdx, SashatoBot, Kashmiri, Ric, Mrj-cleaver, Phuzion, Hu12, Mig77, Shoeofdeath, VeeJay, Mauricev, Markhu, KnightLago, Linberry, Cydebot, Siberian Husky, Anthonyhcole,Skittleys, Thijs!bot, Faigl.ladislav, AgentPeppermint, Escarbot, MER-C, Epeeeche, Magioladitis, Yyyikes, Smpjrk, Xiaata, CliC, Ne-hwyn, Day4iguanas, Nono64, Mtyrone, J.delanoy, VELVET, Nbauman, Peter Chastain, Boghog, Shawn in Montreal, Squids and Chips,VolkovBot, TreasuryTag, Bendav, Sporti, Je G., PGSONIC, NPrice, Blacksnowdog, Lova Falk, Doc James, SieBot, Dawn Bard, Oxy-moron83, Rosiestep, Lazarus1907, Tattery, ClueBot, Rockfang, TonyBallioni, EhJJ, SchreiberBike, GKantaris, XLinkBot, Shunju-kun,Fletcherbrian, MrOllie, Orlandoturner, Jasper Deng, Gjfjhgfjhfg, Lorddarion, Blaylockjam10, Arquin, Tide rolls, 55, Mfhulskemper,Frehley, Legobot, Luckas-bot, Vedran12, Yobot, Treige, R500Mom, Kamal111, Flewis, Citation bot, Plumpurple, Halladay.jerey, Grou-choBot, Kikodawgzzz, Dplazagon, Benny White, Izvora, FreeEnergyFromTheSun, HJ Mitchell, HamburgerRadio, Lovemeusemeloseme,Openmouth, Triplestop, Cfcrareproject, David Hedlund, Thomasimov, Jchapple88, DARTH SIDIOUS 2, EmausBot, John of Reading,Katherine, RenamedUser01302013, Ron.demena, ZroBot, Millsysj, Madhatter198, , Scipilot, Donner60, ChuispastonBot, 2012-nurse,ClueBot NG, Joefromrandb, Desc0004, Genemedicd, Helpful Pixie Bot, Curb Chain, PersiaD, Ngojobsindia, BG19bot, SBrake7, Ecan-eld, Heloda, AvocatoBot, Palaxzorodice, Lotuswr62, Smettems, Spinningsea, Rob Hurt, ChrisGualtieri, Nike Noodle, Netsirk Meglab,Melissa.Alexander87, Krb20048, Neuororockstar, Lookitsbecky, Anrnusna, Monkbot, CarollynThomas, RoBuA and Anonymous: 219

9.2 Images

9.3 Content license Creative Commons Attribution-Share Alike 3.0

Types Cerebellar Sensory Vestibular

Causes Focal lesions Exogenous substances Radiation poisoning Vitamin B12 deficiency Hypothyroidism Causes of isolated sensory ataxia Non-hereditary cerebellar degeneration Hereditary ataxias Arnold-Chiari malformation Wilsons disease Gluten ataxia Sodium-potassium pump

Treatment Other uses See also References Further reading External links Text and image sources, contributors, and licensesTextImagesContent license