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1 ent experienced exacerbation of pre-existing gait ataxia.
2 racterized by failure to thrive, tremor, and gait ataxia.
3 nding that is consistent with their profound gait ataxia.
4 r the presentation of daytime somnolence and gait ataxia.
5 lay impaired coordination, poor balance, and gait ataxia.
6 fantile hypotonia (74%), microcephaly (62%), gait ataxia (63%), dystonia (61%), variably combined wit
7 les are lost, mutant mice exhibit increasing gait ataxia accompanied by spike broadening and decelera
8 TAS include progressive intention tremor and gait ataxia, accompanied by characteristic white matter
15 cheinker syndrome, typically presenting with gait ataxia and painful dysaesthesiae in the legs evolvi
16 pture both shared and specific signatures of gait ataxia and provide a quantitative foundation for ma
18 absence-like spike-wave seizures, cerebellar gait ataxia and vestibular dysfunction, which limit trad
19 ing presented 4 weeks prior with dysarthria, gait ataxia, and bilateral upper extremity weakness.
21 ut also more broadly for adults with tremor, gait ataxia, and parkinsonism who are seen in movement-d
22 arkably, PTC258 treatment improves survival, gait ataxia, and retinal degeneration in the phenotypic
23 xhibit significant motor impairments such as gait ataxia, associated with multiple neuropathological
24 an FGF14 GAA>=250 expansion exhibited severe gait ataxia, autonomic dysfunction and parkinsonism, in
25 motor problems such as intention tremor and gait ataxia, cognitive decline and psychiatric problems
27 taxia that leads to moderate disability with gait ataxia, dysarthria, dysmetria, mild oculomotor abno
29 ice lacking just Kcnc3 is hypermetria, while gait ataxia emerges when additionally Kcnc1 alleles are
34 combination of reported intention tremor and gait ataxia in male carriers (17%, 38%, 47%, and 75% [lo
35 gr3 were generated by gene targeting and had gait ataxia, increased frequency of perinatal mortality,
37 Friedreich's ataxia and FXTAS carriers (e.g. gait ataxia, loss of coordination) are consistent with a
38 g epilepsy, hearing loss, visual impairment, gait ataxia, microcephaly, and hypoplastic corpus callos
40 s, we asked whether patients with cerebellar gait ataxia showed abnormal responses of otolithic vesti
41 of proprioception; this loss leads to severe gait ataxia, spinal deformities, and respiratory insuffi
43 ative disorders characterized by progressive gait ataxia, upper limb incoordination, and dysarthria.
48 by neurogenic muscular atrophy, progressive gait ataxia with tremor, cerebellar vermis atrophy, and