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1 resis, epilepsy and progressive cerebral and cerebellar atrophy.
2 volume loss, corpus callosum hypoplasia and cerebellar atrophy.
3 associated with intellectual disability and cerebellar atrophy.
4 addition to ataxia, one patient also showed cerebellar atrophy.
5 iation of the repeat size with the degree of cerebellar atrophy.
6 lopmental delay, cognitive disabilities, and cerebellar atrophy.
7 oclonic jerks, progressive microcephaly, and cerebellar atrophy.
8 MRI showed progressive cerebral and cerebellar atrophy.
9 xhibited moderately progressive brain and/or cerebellar atrophy.
10 nia, non-progressive ataxia, and progressive cerebellar atrophy.
11 ted in neurodegenerative processes including cerebellar atrophy.
12 sal cerebellar sulci widening, supportive of cerebellar atrophy.
13 seases involving progressive gait ataxia and cerebellar atrophy.
14 f the brains of our patients revealed marked cerebellar atrophy.
15 ive children showed generalised cerebral and cerebellar atrophy.
16 Neuroimaging showed isolated cerebellar atrophy.
17 drome, hallmarks of which include ataxia and cerebellar atrophy.
18 p1 resulted in age-dependent and progressive cerebellar atrophy.
19 pands the genetic differential diagnosis for cerebellar atrophy.
20 terior forceps and non-specific cortical and cerebellar atrophy.
21 , hypotonia, seizures, visual impairment and cerebellar atrophy.
22 ion tensor MRI metrics, suggesting secondary cerebellar atrophy.
23 in OXR1 were reported to be associated with cerebellar atrophy.
24 g pair demonstrated progressive cerebral and cerebellar atrophy.
25 ght be considered in the etiopathogenesis of cerebellar atrophy: (1) transneuronal degeneration and n
28 ng features included cerebral atrophy (75%), cerebellar atrophy (60%), callosal anomalies (57%) and s
29 cerebellar Purkinje neurons with consecutive cerebellar atrophy, although Purkinje neurons are only m
30 son, who died at age 3 years) had pronounced cerebellar atrophy and a renal biopsy specimen that show
31 P firing frequency that correlates with both cerebellar atrophy and ataxia over the animal's first ye
32 atter fraction, T2 lesion volume, metrics of cerebellar atrophy and cerebellar lesion volume) and mot
33 impairment was predicted by a combination of cerebellar atrophy and decreased cerebellar-sensorimotor
34 nically by ataxia and neuropathologically by cerebellar atrophy and granule cell loss, gliosis, and P
35 an absent or disappearing putamen, variable cerebellar atrophy and highly variable cerebral atrophy.
37 ble for ARCA that is mainly characterized by cerebellar atrophy and lack of peripheral neuropathy.
39 ataxias (SCAs) are diseases characterized by cerebellar atrophy and loss of Purkinje neurons caused b
41 tage-gated calcium channel, Cacna1a, develop cerebellar atrophy and mutations in the homologous human
43 heterogeneous group of disorders exhibiting cerebellar atrophy and Purkinje cell degeneration whose
44 pes arising from Purkinje cell degeneration, cerebellar atrophy and varying degrees of degeneration o
47 a significant correlation with MRI scores of cerebellar atrophy, and a significant correlation with c
48 ities, ipsilateral thalamic or contralateral cerebellar atrophy, and compensatory calvarial changes.
49 velopmental syndrome with sleep disturbance, cerebellar atrophy, and facial dysmorphisms, and suggest
52 h as perisylvian polymicrogyria, cerebral or cerebellar atrophy, and hypoplasia of the corpus callosu
53 netic movement disorders, severe early-onset cerebellar atrophy, and in part olivary and brainstem de
58 ng cerebral atrophy (aOR = 2.69, p = 0.027), cerebellar atrophy (aOR = 3.34, p = 0.013), cerebellar w
59 and intellectual disability, with prominent cerebellar atrophy as a key neuroradiographic finding.
60 gly efficient in preventing motor neuron and cerebellar atrophy, as demonstrated in mouse models, fli
62 been shown to display mid-onset progressive cerebellar atrophy, but genetic modeling of SCA13 by exp
63 als with ataxia-telangiectasia have reported cerebellar atrophy; but abnormalities of motor control c
64 lizumab treatment, especially in cases where cerebellar atrophy can be visualized by magnetic resonan
65 ture epilepsy, tremor, nystagmus, hypotonia, cerebellar atrophy, cognitive deficits, and global devel
67 ed with volumetric measures of T2 lesions or cerebellar atrophy, diffusivity measures of middle or su
68 sive encephalopathy characterized by extreme cerebellar atrophy due to almost total granule neuron lo
69 brain magnetic resonance imaging feature was cerebellar atrophy, even in patients without cerebellar
71 disorder consisting of cognitive impairment, cerebellar atrophy/hypoplasia, motor dysfunction with at
72 erebral volume loss in 87.5% and progressive cerebellar atrophy in 70.8%, indicating a neurodegenerat
73 c quadriparesis and progressive cortical and cerebellar atrophy in an effort to determine the genetic
75 h ataxia or severe hypotonia, nystagmus, and cerebellar atrophy in more than half of the patients.
81 ze in SCI compared with control subjects and cerebellar atrophy increased with increasing time post i
84 tural abnormalities (eg, rapidly progressive cerebellar atrophy), myopathies (including congenital mu
85 gies, including motor coordination disorder, cerebellar atrophy, neuronal loss in the cerebellum and
90 itive/psychiatric features, and cerebral and cerebellar atrophy on magnetic resonance imaging but abs
93 e ataxia with Purkinje cell degeneration and cerebellar atrophy, partially resembling the consequence
95 with infantile spinal motor neuron disease, cerebellar atrophy, progressive microcephaly and profoun
97 these mice exhibited neuronal preservation, cerebellar atrophy reduction, smaller mutant ataxin-3 in
100 hat coexpress cyPrP and PrP(C) exhibit focal cerebellar atrophy, scratching behavior, and gait abnorm
101 l disability, cerebellar ataxia, early-onset cerebellar atrophy, sensorineural hearing loss, and the
104 hable recessive syndrome in 12 families with cerebellar atrophy together with ataxia, coarsened facia
105 y, delayed myelination, callosal hypoplasia, cerebellar atrophy, walking and speech impairments, dysm
109 lido-pyramidal syndrome, iron deposition and cerebellar atrophy, we identified a homozygous p.G53R mu
111 netic resonance imaging revealed symmetrical cerebellar atrophy, which appeared progressive, and a pr
114 Magnetic resonance imaging demonstrated cerebellar atrophy without white matter lesions and ster