PT  - JOURNAL ARTICLE
AU  - Zesiewicz, Theresa A.
AU  - Wilmot, George
AU  - Kuo, Sheng-Han
AU  - Perlman, Susan
AU  - Greenstein, Patricia E.
AU  - Ying, Sarah H.
AU  - Ashizawa, Tetsuo
AU  - Subramony, S.H.
AU  - Schmahmann, Jeremy D.
AU  - Figueroa, K.P.
AU  - Mizusawa, Hidehiro
AU  - Schöls, Ludger
AU  - Shaw, Jessica D.
AU  - Dubinsky, Richard M.
AU  - Armstrong, Melissa J.
AU  - Gronseth, Gary S.
AU  - Sullivan, Kelly L.
TI  - Comprehensive systematic review summary: Treatment of cerebellar motor dysfunction and ataxia
AID  - 10.1212/WNL.0000000000005055
DP  - 2018 Mar 06
TA  - Neurology
PG  - 464--471
VI  - 90
IP  - 10
4099  - http://n.neurology.org/content/90/10/464.short
4100  - http://n.neurology.org/content/90/10/464.full
SO  - Neurology2018 Mar 06; 90
AB  - Objective To systematically review evidence regarding ataxia treatment.Methods A comprehensive systematic review was performed according to American Academy of Neurology methodology.Conclusions For patients with episodic ataxia type 2, 4-aminopyridine 15 mg/d probably reduces ataxia attack frequency over 3 months (1 Class I study). For patients with ataxia of mixed etiology, riluzole probably improves ataxia signs at 8 weeks (1 Class I study). For patients with Friedreich ataxia or spinocerebellar ataxia (SCA), riluzole probably improves ataxia signs at 12 months (1 Class I study). For patients with SCA type 3, valproic acid 1,200 mg/d possibly improves ataxia at 12 weeks. For patients with spinocerebellar degeneration, thyrotropin-releasing hormone possibly improves some ataxia signs over 10 to 14 days (1 Class II study). For patients with SCA type 3 who are ambulatory, lithium probably does not improve signs of ataxia over 48 weeks (1 Class I study). For patients with Friedreich ataxia, deferiprone possibly worsens ataxia signs over 6 months (1 Class II study). Data are insufficient to support or refute the use of numerous agents. For nonpharmacologic options, in patients with degenerative ataxias, 4-week inpatient rehabilitation probably improves ataxia and function (1 Class I study); transcranial magnetic stimulation possibly improves cerebellar motor signs at 21 days (1 Class II study). For patients with multiple sclerosis–associated ataxia, the addition of pressure splints possibly has no additional benefit compared with neuromuscular rehabilitation alone (1 Class II study). Data are insufficient to support or refute use of stochastic whole-body vibration therapy (1 Class III study).AAN=American Academy of Neurology; CI=confidence interval; EA2=episodic ataxia type 2; FA=Friedreich ataxia; FARS=Friedreich Ataxia Rating Scale; ICARS=International Cooperative Ataxia Rating Scale; MS=multiple sclerosis; NESSCA=Neurological Examination Score for Spinocerebellar Ataxia; OR=odds ratio; SARA=Scale for the Assessment and Rating of Ataxia; SCA=spinocerebellar ataxia; SCA3=spinocerebellar ataxia type 3; SCD=spinocerebellar degeneration; tDCS=transcranial direct current stimulation; TMS=transcranial magnetic stimulation; TRH=thyrotropin-releasing hormone; VPA=valproic acid