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1 disease involving dying-back degeneration of upper motor neurons.
2 ease that is thought to predominantly affect upper motor neurons.
3 ly held view of the motor cortex as just an "upper motor neuron."
4 cally heterogeneous diseases that affect the upper motor neurons and their axonal projections.
5 d ATP production in demyelinated segments of upper motor neuron axons impacts ion homeostasis, induce
6 llosal body, and linked strongly to clinical upper motor neuron burden, but also to limb disability s
7 r sensory abnormalities and/or a significant upper-motor-neuron component, and there is often an over
8 ese include loss of lower (ventral horn) and upper motor neurons (corticospinal motor neurons in laye
9 magnetic stimulation has been used to detect upper motor neuron damage and to explore cortical excita
10 ipheral neurodegeneration, including ataxia, upper-motor-neuron damage, peripheral neuropathy, hearin
11  from families affected by diabetes, ataxia, upper-motor-neuron damage, peripheral neuropathy, or hea
12  weakness in ALS2(-/-) mice, consistent with upper motor neuron defects that lead to spasticity in hu
13 ically and clinically heterogeneous group of upper-motor-neuron degenerative diseases characterized b
14 n developmental principles of both lower and upper motor neuron development that have led to specific
15 mans shows that deficiency in ALS2 causes an upper motor neuron disease that in humans closely resemb
16 tin, which is dysfunctional in some forms of upper motor neuron disease.
17 e possible by including tests of subclinical upper motor neuron disease.
18 d findings at MR imaging in the detection of upper motor neuron disease.
19                     Konzo is an irreversible upper-motor neuron disorder affecting children dependent
20  (HR, 1.48; 95% CI, 0.58-3.75; P = .41), and upper motor neuron dominant ALS (HR, 0.12; 95% CI, 0.02-
21                         Clinical measures of upper motor neuron dysfunction correlated with reduction
22 ssociated with bulbar onset and dysfunction, upper motor neuron dysfunction, cognitive impairment, de
23 orsal column dysfuction, and spasticity with upper motor neuron dysfunction.
24  of the MRCP may serve as a useful marker of upper motor neuron dysfunction.
25 ding one family with exclusively adult-onset upper motor neuron features, consistent with a diagnosis
26 ysfunction and thus an important role of the upper motor neuron in this animal model of ALS and perha
27 cospinal/corticobulbar motor neurons (CSMN; "upper motor neurons") in cerebral cortex, and spinal/bul
28 be used as an electrophysiological marker of upper motor neuron integrity in such patients.
29 n age, 57.3 years) with clinical evidence of upper motor neuron involvement and 10 healthy control su
30     Elevation in NFL levels in patients with upper motor neuron involvement and FTD might reflect the
31 imaging spectroscopy can be used to identify upper motor neuron involvement and predict disease durat
32 ential as a quantitative test of subclinical upper motor neuron involvement in motor neuron disease.
33 er motor neurons, with or without additional upper motor neuron involvement.
34 on disease phenotypes, with clinically overt upper motor neuron involvement.
35 mary lateral sclerosis, suggesting prominent upper motor neuron involvement.
36 tor neuron disorder that exclusively affects upper motor neurons leading to their degeneration.
37                It is also suggested that the upper motor neuron lesion in amyotrophic lateral scleros
38   It is often difficult to identify signs of upper motor neuron lesion in the limbs of patients with
39 aging also provide useful information on the upper motor neuron lesion.
40  progressive degeneration of lower (LMN) and upper motor neurons, likely due to the same unknown toxi
41 endpoint, we wanted to establish whether the upper motor neuron might still play a critical role in d
42    This relative lack of knowledge regarding upper motor neuron pathology in these ALS model mice has
43 o also correlated with both the ALSFRS-R and upper motor neuron scores (r=0.50 and 0.54, respectively
44 gnized limited change in individual clinical upper motor neuron scores, despite advancing disability.
45  abnormalities, including a constellation of upper motor neuron signs (n = 19), ataxia (n = 22), and
46 res, including regional disability, clinical upper motor neuron signs and cognitive impairment.
47                                              Upper motor neuron signs are a prominent feature in a su
48 at lead to difficulty in detecting classical upper motor neuron signs, are discussed.
49  psychiatric changes, movement disorders and upper motor neuron signs.
50 h prominent cognitive, neuropsychiatric, and upper motor neuron signs.
51           Typically, the initial progressive upper motor neuron spastic and general proprioceptive at
52            Typical features are disorders of upper motor neurons, spastic quadriparesis and pseudobul
53                It forms one component of the upper motor neuron syndrome and often leads to muscle st
54 on may be thought to be the Babinski sign of upper-motor-neuron syndromes.
55       Group 2: Five women developed signs of upper motor neuron (UMN) disease, initially resembling p
56            There was no clinical evidence of upper motor neuron (UMN) involvement in 10 FALS A4V subj
57 l rating scale (ALSFRS-R score), whereas the upper motor neuron (UMN) score correlated with widesprea

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