Skip to main content

Advertisement

Log in

Spinocerebellar Ataxia Types 1, 2, 3 and 6: the Clinical Spectrum of Ataxia and Morphometric Brainstem and Cerebellar Findings

  • Published:
The Cerebellum Aims and scope Submit manuscript

Abstract

To assess the clinical spectrum of ataxia and cerebellar oculomotor deficits in the most common spinocerebellar ataxias (SCAs), we analysed the baseline data of the EUROSCA natural history study, a multicentric cohort study of 526 patients with either spinocerebellar ataxia type 1, 2, 3 or 6. To quantify ataxia symptoms, we used the Scale for the Assessment and Rating of Ataxia (SARA). The presence of cerebellar oculomotor signs was assessed using the Inventory of Non-Ataxia Symptoms (INAS). In a subgroup of patients, in which magnetic resonance images (MRIs) were available, we correlated MRI morphometric measures with clinical signs on an exploratory basis. The SARA subscores posture and gait (items 1–3), speech (item 4) and the limb kinetic subscore (items 5–8) did not differ between the genotypes. The scores of SARA item 3 (sitting), 5 (finger chase) and 6 (nose–finger test) differed between the subtypes whereas the scores of the remaining items were not different. In SCA1, ataxia symptoms were correlated with brainstem atrophy and in SCA3 with both brainstem and cerebellar atrophy. Cerebellar oculomotor deficits were most frequent in SCA6 followed by SCA3, whereas these abnormalities were less frequent in SCA1 and SCA2. Our data suggest that vestibulocerebellar, spinocerebellar and pontocerebellar circuits in SCA1, SCA2, SCA3 and SCA6 are functionally impaired to almost the same degree, but at different anatomical levels. The seemingly low prevalence of cerebellar oculomotor deficits in SCA1 and SCA2 is most probably related to the defective saccadic system in these disorders.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Subscribe and save

Springer+ Basic
EUR 32.99 /Month
  • Get 10 units per month
  • Download Article/Chapter or Ebook
  • 1 Unit = 1 Article or 1 Chapter
  • Cancel anytime
Subscribe now

Buy Now

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Fig. 1

Similar content being viewed by others

References

  1. Durr A. Autosomal dominant cerebellar ataxias: polyglutamine expansions and beyond. Lancet Neurol. 2010;9(9):885–94.

    Article  PubMed  CAS  Google Scholar 

  2. Paulson HL. The spinocerebellar ataxias. J Neuroophthalmol. 2009;29(3):227–37.

    Article  PubMed  Google Scholar 

  3. Orr HT, Chung MY, Banfi S, Kwiatkowski Jr TJ, Servadio A, Beaudet AL, et al. Expansion of an unstable trinucleotide CAG repeat in spinocerebellar ataxia type 1. Nat Genet. 1993;4(3):221–6.

    Article  PubMed  CAS  Google Scholar 

  4. Pulst SM, Nechiporuk A, Nechiporuk T, Gispert S, Chen XN, Lopes-Cendes I, et al. Moderate expansion of a normally biallelic trinucleotide repeat in spinocerebellar ataxia type 2. Nat Genet. 1996;14(3):269–76.

    Article  PubMed  CAS  Google Scholar 

  5. Imbert G, Saudou F, Yvert G, Devys D, Trottier Y, Garnier JM, et al. Cloning of the gene for spinocerebellar ataxia 2 reveals a locus with high sensitivity to expanded CAG/glutamine repeats. Nat Genet. 1996;14(3):285–91.

    Article  PubMed  CAS  Google Scholar 

  6. Kawaguchi Y, Okamoto T, Taniwaki M, Aizawa M, Inoue M, Katayama S, et al. CAG expansions in a novel gene for Machado–Joseph disease at chromosome 14q32.1. Nat Genet. 1994;8(3):221–8.

    Article  PubMed  CAS  Google Scholar 

  7. Zhuchenko O, Bailey J, Bonnen P, Ashizawa T, Stockton DW, Amos C, et al. Autosomal dominant cerebellar ataxia (SCA6) associated with small polyglutamine expansions in the a1A-voltage-dependent calcium channel. Nat Genet. 1997;15(1):62–9.

    Article  PubMed  CAS  Google Scholar 

  8. Orr HT, Zoghbi HY. Trinucleotide repeat disorders. Annu Rev Neurosci. 2007;30:575–621.

    Article  PubMed  CAS  Google Scholar 

  9. Dubourg O, Dürr A, Cancel G, Stevanin G, Chneiweiss H, Penet C, et al. Analysis of the SCA1 CAG repeat in a large number of families with dominant ataxia: clinical and molecular correlations. Ann Neurol. 1995;37:176–80.

    Article  PubMed  CAS  Google Scholar 

  10. Orozco-Diaz G, Nodarse-Fleites A, Cordoves-Sagaz R, Auburger G. Autosomal dominant cerebellar ataxia: clinical analysis of 263 patients from a homogeneous population in Holguin, Cuba. Neurology. 1990;40:1369–75.

    PubMed  CAS  Google Scholar 

  11. Schöls L, Gispert S, Vorgerd M, Menezes Vieira-Saecker AM, Blanke P, Auburger G, et al. Spinocerebellar ataxia type 2—genotype and phenotype in German kindreds. Arch Neurol. 1997;54(9):1073–80.

    Article  PubMed  Google Scholar 

  12. Dürr A, Stevanin G, Cancel G, Duyckaerts C, Abbas N, Didierjean O, et al. Spinocerebellar ataxia 3 and Machado–Joseph disease: clinical, molecular, and neuropathological features. Ann Neurol. 1996;39:490–9.

    Article  PubMed  Google Scholar 

  13. Bürk K, Abele M, Fetter M, Dichgans J, Skalej M, Laccone F, et al. Autosomal dominant cerebellar ataxia type I—clinical features and MRI in families with SCA1, SCA2 and SCA3. Brain. 1996;119(5):1497–505.

    Article  PubMed  Google Scholar 

  14. Filla A, De Michele G, Campanella G, Perretti A, Santoro L, Serlenga L, et al. Autosomal dominant cerebellar ataxia type I. Clinical and molecular study in 36 Italian families including a comparison between SCA1 and SCA2 phenotypes. J Neurol Sci. 1996;142(1–2):140–7.

    Article  PubMed  CAS  Google Scholar 

  15. Schöls L, Amoiridis G, Büttner T, Przuntek H, Epplen JT, Riess O. Autosomal dominant cerebellar ataxia: phenotypic differences in genetically defined subtypes? Ann Neurol. 1997;42(6):924–32.

    Article  PubMed  Google Scholar 

  16. Schöls L, Krüger R, Amoiridis G, Przuntek H, Epplen JT, Riess O. Spinocerebellar ataxia type 6: genotype and phenotype in German kindreds. J Neurol Neurosurg Psychiatry. 1998;64(1):67–73.

    Article  PubMed  Google Scholar 

  17. Matsumura R, Futamura N, Fujimoto Y, Yanagimoto S, Horikawa H, Suzumura A, et al. Spinocerebellar ataxia type 6—molecular and clinical features of 35 Japanese patients including one homozygous for the CAG repeat expansion. Neurology. 1997;49(5):1238–43.

    PubMed  CAS  Google Scholar 

  18. Schmitz-Hubsch T, du Montcel ST, Baliko L, Berciano J, Boesch S, Depondt C, et al. Scale for the assessment and rating of ataxia: development of a new clinical scale. Neurology. 2006;66(11):1717–20.

    Article  PubMed  CAS  Google Scholar 

  19. Weyer A, Abele M, Schmitz-Hubsch T, Schoch B, Frings M, Timmann D, et al. Reliability and validity of the scale for the assessment and rating of ataxia: a study in 64 ataxia patients. Mov Disord. 2007;22:1633–7.

    Article  PubMed  Google Scholar 

  20. Schmitz-Hübsch T, Coudert M, Bauer P, Giunti P, Globas C, Baliko L, et al. Spinocerebellar ataxia type 1, 2, 3, and 6. Disease severity and nonataxia symptoms. Neurology. 2008;71:982–9.

    Article  PubMed  Google Scholar 

  21. Schulz JB, Borkert J, Wolf S, Schmitz-Hübsch T, Rakowicz M, Mariotti C, et al. Visualization, quantification and correlation of brain atrophy with clinical symptoms in spinocerebellar ataxia types 1, 3 and 6. Neuroimage. 2010;49(1):158–68.

    Article  PubMed  Google Scholar 

  22. Brandauer B, Hermsdorfer J, Beck A, Aurich V, Gizewski ER, Marquardt C, et al. Impairments of prehension kinematics and grasping forces in patients with cerebellar degeneration and the relationship to cerebellar atrophy. Clin Neurophysiol. 2008;119(11):2528–37.

    Article  PubMed  CAS  Google Scholar 

  23. Luft AR, Skalej M, Welte D, Kolb R, Bürk K, Schulz JB, et al. A new semiautomated, three-dimensional technique allowing precise quantification of total and regional cerebellar volume using MRI. Magn Reson Med. 1998;40(1):143–51.

    Article  PubMed  CAS  Google Scholar 

  24. Eritaia J, Wood SJ, Stuart GW, Bridle N, Dudgeon P, Maruff P, et al. An optimized method for estimating intracranial volume from magnetic resonance images. Magn Reson Med. 2000;44(6):973–7.

    Article  PubMed  CAS  Google Scholar 

  25. Gomez CM, Thompson RM, Gammack JT, Perlman SL, Dobyns WB, Truwit CL, et al. Spinocerebellar ataxia type 6: gaze-evoked and vertical nystagmus, Purkinje cell degeneration, and variable age of onset. Ann Neurol. 1997;42(6):933–50.

    Article  PubMed  CAS  Google Scholar 

  26. Buttner N, Geschwind D, Jen JC, Perlman S, Pulst SM, Baloh RW. Oculomotor phenotypes in autosomal dominant ataxias. Arch Neurol. 1998;55(10):1353–7.

    Article  PubMed  CAS  Google Scholar 

  27. Burk K, Fetter M, Abele M, Laccone F, Brice A, Dichgans J, et al. Autosomal dominant cerebellar ataxia type I: oculomotor abnormalities in families with SCA1, SCA2, and SCA3. J Neurol. 1999;246(9):789–97.

    Article  PubMed  CAS  Google Scholar 

  28. Yabe I, Sasaki H, Takeichi N, Takei A, Hamada T, Fukushima K, et al. Positional vertigo and macroscopic downbeat positioning nystagmus in spinocerebellar ataxia type 6 (SCA6). J Neurol. 2003;250(4):440–3.

    Article  PubMed  Google Scholar 

  29. Ying SH, Choi SI, Lee M, Perlman SL, Baloh RW, Toga AW, et al. Relative atrophy of the flocculus and ocular motor dysfunction in SCA2 and SCA6. Ann N Y Acad Sci. 2005;1039:430–5.

    Article  PubMed  CAS  Google Scholar 

  30. Dichgans J, Fetter M. Compartmentalized cerebellar functions upon the stabilization of body posture. Rev Neurol (Paris). 1993;149(11):654–64.

    CAS  Google Scholar 

  31. Timmann D, Diener HC. Coordination and ataxia. In: Goetz CG, Pappert EJ, editors. Textbook of clinical neurology. 3rd ed. Philadelphia: Saunders Elsevier; 2007. p. 307–25.

    Chapter  Google Scholar 

  32. Dietrichs E. Clinical manifestation of focal cerebellar disease as related to the organization of neural pathways. Acta Neurol Scand Suppl. 2008;188:6–11.

    Article  PubMed  CAS  Google Scholar 

  33. Solomon DH, Barohn RJ, Bazan C, Grissom J. The thalamic ataxia syndrome. Neurology. 1994;44(5):810–4.

    PubMed  CAS  Google Scholar 

  34. Mitoma H, Hayashi R, Yanagisawa N, Tsukagoshi H. Gait disturbances in patients with pontine medial tegmental lesions: clinical characteristics and gait analysis. Arch Neurol. 2000;57(7):1048–57.

    Article  PubMed  CAS  Google Scholar 

  35. Marx JJ, Iannetti GD, Thömke F, Fitzek S, Galeotti F, Truini A, et al. Topodiagnostic implications of hemiataxia: an MRI-based brainstem mapping analysis. Neuroimage. 2008;39(4):1625–32.

    Article  PubMed  Google Scholar 

  36. Voogd J, Schraa-Tam CK, van der Geest JN, de Zeeuw CI. Visuomotor cerebellum in human and nonhuman primates. Cerebellum 2010. doi:10.1007/s12311-010-0204-7.

  37. Wang X, Wang H, Xia Y, Jiang H, Shen L, Wang S et al. Spinocerebellar ataxia type 6: systematic patho-anatomical study reveals different phylogenetically defined regions of the cerebellum and neural pathways undergo different evolutions of the degenerative process. Neuropathology 2010. doi:10.1111/j.1440-1789.2009.01094.x.

  38. Genis D, Matilla T, Volpini V, Rosell J, Dávalos A, Ferrer I, et al. Clinical, neuropathologic, and genetic studies of a large spinocerebellar ataxia type 1 (SCA1) kindred: (CAG)n expansion and early premonitory signs and symptoms. Neurology. 1995;45:24–30.

    PubMed  CAS  Google Scholar 

  39. Orozco G, Estrada R, Perry TL, Araña J, Fernandez R, Gonzalez-Quevedo A, et al. Dominantly inherited olivopontocerebellar atrophy from eastern Cuba. Clinical, neuropathological, and biochemical findings. J Neurol Sci. 1989;93:37–50.

    Article  PubMed  CAS  Google Scholar 

  40. Klockgether T, Skalej M, Wedekind D, Luft AR, Welte D, Schulz JB, et al. Autosomal dominant cerebellar ataxia type I. MRI-based volumetry of posterior fossa structures and basal ganglia in spinocerebellar ataxia types 1, 2 and 3. Brain. 1998;121(Pt 9):1687–93.

    Article  PubMed  Google Scholar 

Download references

Acknowledgments

We are grateful to Drs. Klopstock and Petersen (Department of Neurology, University of Munich, Munich, Germany), Dr. Abdo (Department of Neurology, Radboud University Nijmegen Medical Center, Nijmegen, the Netherlands) and Dr. Verstappen (Canisius Wilhelina Hospital, Nijmegen, the Netherlands) for contribution of patients and help in patient assessment. We thank all the patients for participating in the study. This study was supported by grant EUROSCA/LSHM-CT-2004-503304 from the European Union, GeneMove/01 GM 0503 from the German Ministry of Education and Research and grant 3 PO5B 019 24 from the Polish Ministry of Scientific Research and Information Technology.

Conflicts of Interest

The authors report no conflicts of interest.

Full Financial Disclosures

H. Jacobi, T.-K. Hauser, P. Giunti, C. Globas, T. Schmitz-Hübsch, L. Baliko, A. Filla, C. Mariotti, P. Charles, P. Ribai, S. Szymanski, J. Infante, A. Dürr, D. Timmann, R. Fancellu, R. Rola, E. Zdzienicka, J.-S. Kang, S. Ratzka, D.A. Stephenson, S. Tezenas du Montcel and J. Borkert have declared no financial disclosure in stock ownership in medically related fields, consultancies, advisory boards, partnerships, honoraria, intellectual property rights, expert testimony, contracts, royalties and others. H. Jacobi, T.-K. Hauser, C. Globas, L. Baliko, P. Charles, S. Szymanski, R. Fancellu, R. Rola, J.-S. Kang, S. Ratzka, D.A. Stephenson and J. Borkert have declared no grants. P. Giunti was supported by grants from EUROSCA FP7 and Ataxia UK; T. Schmitz-Hübsch by grants from EUROSCA; A. Filla by grants from Ministry of Health: RF-SDN-2007-666932 and MIUR (Ministry of Research): E61J10000020001; C. Mariotti by grants from E-Rare; EFACTS, FP7 no: 242193; Study No.: 12631A; EudraCT No.: 2008-003662-25; Sponsor: International Clinical Research; H. Lundbeck A/S 2500 Valby (Copenhagen), Denmark; P. Ribai by grants from Société Française de Neurologie (SFN) and Association Française contre l’ataxie de Friedreich (AFAF); J. Infante by grants from Fondo de Investigación Sanitaria (PI 070014); A. Dürr by grants from PHRC National 2003 (agency: Assistance Publique-Hôpitaux de Paris (2005–2012)), Eurosca (agency: European Union (2004–2009)) and Spax (agency: French Agency for Research (2010–2012)); D. Timmann by grants from German Research Foundation (DFG TI 239/9-1), EU (Partner Marie Curie Initial Training Network) and Bernd Fink Foundation; E. Zdzienicka by grants from EUROSCA grant LSHM-CT-2004-503304 PO5E 019 29-Myotonic Dystrophy type 1 and 2 by the Polish State Committee of Scientific Research and RISCA 511-006-10001 from the Polish Ministry of Science and Higher Education and S. Tezenas du Montcel by grants from the European Union (grant EUROSCA (LSHM-CT-2004-503304)), the Assistance Publique-Hôpitaux de Paris (grant PHRC AOM 03059) and from the European Union C08A043 (funded by the French National Agency for Research). H. Jacobi is employed by the University of Bonn while T.-K. Hauser is by the University of Tübingen; P. Giunti by the UCL/UCLH; T. Schmitz-Hübsch by the University of Bonn; L. Baliko by the County Hospital, Veszprém, Hungary; A. Filla by the Federico II University, Napoli, Italy; C. Mariotti by the Fondazione IRCCS Neurological Institute Carlo Besta, Milan; P. Charles by the Hôpital de la Salpêtrière, Département de Génétique, Paris, France; P. Ribai by the Hôpital de la Salpêtrière, Département de Génétique, Paris, France; S. Szymanski by the St. Josef Hospital, University Hospital of Bochum; J. Infante by the University of Cantabria, Santander, Spain; A. Dürr by the Hôpital de la Salpêtrière, Département de Génétique, Paris, France; D. Timmann by the University of Duisburg-Essen; R. Fancellu by the Ospedale Villa Scassi, ASL3 Genovese, Genoa, Italy; R. Rola by the Institute of Psychiatry and Neurology and The Medical University of Warsaw, Poland; E. Zdzienicka by the Institute of Psychiatry and Neurology, Warsaw, Poland; J.-S. Kang by the University of Frankfurt, Frankfurt am Main, Germany; S. Ratzka by the Klinikum Augsburg, Department of Neurology, Germany; D.A. Stephenson by the UCL Medical Institute, USA; S. Tezenas du Montcel by the Department of Biostatistics and Medical Informatics and by the University Pierre et Marie Curie, Paris, France and J. Borkert by the University of Göttingen. C. Globas was employed by the Clinic of Psychiatry, University Tübingen from April 2009 to March 2010 and is currently employed by the Clinic of Neurology, University, Zürich since May 2010.

P. Bauer has declared no financial disclosure in stock ownership in medically related fields, advisory boards, partnerships, intellectual property rights, expert testimony, contracts, royalties and other; is a consultant at CENTOGENE (Rostock, Germany) and was supported by grants from Research Council (BMBF) to GeNeMove (01GM0603), EUROSPA (01GM0807) and RISCA (09GM0820) as well as from the EU for EUROSCA (LSHM-CT-2004-503304), MarkMD (FP7-People PIAP-2008-230596) and TECHGENE (FP7-Health 2007-B 223143). A further project received funding from the HSP-Selbsthilfegruppe Deutschland e.V. Honoraria was received from Roche Diagnostics (Mannheim, Germany) and Actelion Pharmaceuticals (Basel, Switzerland). He is employed by the University of Tübingen.

M. Rakowicz has declared no financial disclosure in stock ownership in medically related fields, advisory boards, honoraria, intellectual property rights, expert testimony, contracts, royalties and other; is a consultant at the Private Neurological Office, Warsaw, Poland; is partner of Ma-Je-R Ltd, Warsaw, Poland; was supported by grants from EUROSCA grant LSHM-CT-2004-503304, PO5E 019 29 by the Polish State Committee of Scientific Research and RISCA 511-006-10001 from the Polish Ministry of Science and Higher Education and is employed by the Institute of Psychiatry and Neurology, Warsaw.

B.P.C. van de Warrenburg has declared no financial disclosure in stock ownership in medically related fields, consultancies, partnerships, intellectual property rights, expert testimony, contracts, royalties and other; is a medical advisor for the Dutch patient organizations for ADCA, dystonia and hereditary spastic paraplegia; was supported by grants from Prinses Beatrix Fonds, the Brain Foundation, Department of Neurology of the Radboud University Nijmegen Medical Centre, Ipsen Pharmaceuticals (all in the Netherlands) and from the European Union (EUROSCA/LSHM-CT-2004-503304); has received honoraria from editorial work for the Dutch Health Direct Neurology journal (Reed Elsevier) and is employed by the Radboud University Nijmegen Medical Centre, Nijmegen, the Netherlands.

S. Boesch has declared no financial disclosure in stock ownership in medically related fields, partnerships, grants, intellectual property rights, expert testimony, contracts, royalties and other; is a consultant at Lundbeck; has been a member of the advisory board of Takeda, Novartis and Glaxo; has received honoraria from Takeda, Glaxo and Novartis and is employed by the University of Innsbruck, Austria.

C. Depondt has declared no financial disclosure in stock ownership in medically related fields, consultancies, advisory boards, partnerships, honoraria, grants, intellectual property rights, expert testimony, contracts and royalties but with financial disclosure in payment of congress expenses by UCB Pharma and is employed by the Université Libre de Bruxelles, Belgium.

L. Schöls has declared no financial disclosure in stock ownership in medically related fields, consultancies, advisory boards, partnerships, intellectual property rights, expert testimony, contracts and royalties; has received support from the HSP-Selbsthilfegruppe Deutschland e.V. for research in spastic paraplegia; has received study fees for the MICONOS trial from Santhera Pharmaceuticals; was supported by grants of the German Research Council (BMBF) to Leukonet (01GM0644) and mitoNET (01GM0864) and E-RARE grants of the EU to EUROSPA (01GM0807) and RISCA (01GM0820) and is employed by the University of Tübingen.

B. Kremer has declared no financial disclosure in stock ownership in medically related fields, consultancies, partnerships, intellectual property rights, contracts, royalties and other; has been a member of the advisory board of Hersenstichting Nederland, Prinses Beatrix Foundation and Nederlandse Transplantatiestichting; has received honoraria from the Netherlands and Actelion, the Netherlands; was supported by grants from UMC Nijmegen, UMC Groningen and MS Anders; has various testimonies in legal cases and medical insurance cases and is employed by the University Medical Centre Groningen, Groningen, the Netherlands.

B. Melegh has declared no financial disclosure in stock ownership in medically related fields, honoraria, intellectual property rights, expert testimony, contracts, royalties and other; has been a consultant for national grant funding opportunities; has been a member of the advisory board of Biobanking and Biomolecular Resources (BBMRI); is partner of the WestTeam Biotech Ltd; was supported by grants from ETT (Grant from Ministry of Health) and OTKA (Hungarian Science Foundation) E-Rare-2, EU7 supported project and is employed by the University of Pécs.

M. Pandolfo has declared no financial disclosure in stock ownership in medically related fields, consultancies, partnerships, expert testimony, contracts and other; has been a member of the advisory board for Apopharma; has received honoraria from Santhera AG; was supported by grants from Repligen Corporation; has intellectual property rights: “Direct molecular diagnosis of Friedreich ataxia” M. Pandolfo, L. Montermini, M.D. Molto’, M. Koenig, V. Campuzano, M. Cossee’. US patent (2000) 6,150,091, WO patent (1997) 9705234; is employed by the University of Brussles and receives royalties from Athena Diagnostics.

J. Schulz has declared no financial disclosure in stock ownership in medically related fields, partnerships, intellectual property rights, expert testimony, contracts, royalties and other; acted as a consultant of Santhera; has been a member of the advisory board of Santhera; has received honoraria from Merz, Pfizer and GSK; was supported by grants from BMBF, EU and is employed by the University of Aachen.

T. Klockgether has declared no financial disclosure in stock ownership in medically related fields, consultancies, partnerships, intellectual property rights, expert testimony, contracts, royalties and other; has been a member of the advisory board of the The Cerebellum, Parkinsonism & Related Disorder, ataxia lay organizations; has received lecture honorarium from Lundbeck; was supported by grants from Deutsche Forschungsgemeinschaft (DFG), KFO177 Clinical Research Group (Innate Immunity in Chronic Neurodegeneration) and from the German Ministry of Education and Research (BMBF), E-Rare 01GM0819 RISCA and is employed by the University of Bonn.

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to Heike Jacobi.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Jacobi, H., Hauser, TK., Giunti, P. et al. Spinocerebellar Ataxia Types 1, 2, 3 and 6: the Clinical Spectrum of Ataxia and Morphometric Brainstem and Cerebellar Findings. Cerebellum 11, 155–166 (2012). https://doi.org/10.1007/s12311-011-0292-z

Download citation

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1007/s12311-011-0292-z

Keywords

Navigation