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1 zes the cerebral level of motor control, the upper motor neuron.
2 disease involving dying-back degeneration of upper motor neurons.
3 ease that is thought to predominantly affect upper motor neurons.
4  disease characterized by death of lower and upper motor neurons.
5 he number of inhibitory synaptic contacts on upper motor neurons.
6 ly held view of the motor cortex as just an "upper motor neuron."
7 eterogeneous group of neuropathies affecting upper motor neurons and causing progressive gait disorde
8 cally heterogeneous diseases that affect the upper motor neurons and their axonal projections.
9 d ATP production in demyelinated segments of upper motor neuron axons impacts ion homeostasis, induce
10  (ALSFRS-R total, upper limb and bulbar) and upper motor neuron burden assessments in a longitudinal
11 llosal body, and linked strongly to clinical upper motor neuron burden, but also to limb disability s
12 r sensory abnormalities and/or a significant upper-motor-neuron component, and there is often an over
13                          Whereas measures of upper motor neuron connectivity have been readily establ
14  Kv3.1 to ensure precise, rapid AP firing in upper motor neurons controlling fast and complex motor s
15 g mechanisms that promote precise spiking in upper motor neurons controlling fine motor skills are no
16 cted a thorough study of the excitability of upper motor neurons controlling somatic motor function i
17 ese include loss of lower (ventral horn) and upper motor neurons (corticospinal motor neurons in laye
18 magnetic stimulation has been used to detect upper motor neuron damage and to explore cortical excita
19 ipheral neurodegeneration, including ataxia, upper-motor-neuron damage, peripheral neuropathy, hearin
20  from families affected by diabetes, ataxia, upper-motor-neuron damage, peripheral neuropathy, or hea
21  weakness in ALS2(-/-) mice, consistent with upper motor neuron defects that lead to spasticity in hu
22 RA MRI may be a promising tool for assessing upper motor neuron degeneration in the lateral CST in pa
23 ically and clinically heterogeneous group of upper-motor-neuron degenerative diseases characterized b
24 n developmental principles of both lower and upper motor neuron development that have led to specific
25                            Konzo, a distinct upper motor neuron disease associated with a cyanogenic
26 mans shows that deficiency in ALS2 causes an upper motor neuron disease that in humans closely resemb
27 tin, which is dysfunctional in some forms of upper motor neuron disease.
28 e possible by including tests of subclinical upper motor neuron disease.
29 d findings at MR imaging in the detection of upper motor neuron disease.
30 nt, especially for drug discovery efforts in upper motor neuron diseases.
31                     Konzo is an irreversible upper-motor neuron disorder affecting children dependent
32  (HR, 1.48; 95% CI, 0.58-3.75; P = .41), and upper motor neuron dominant ALS (HR, 0.12; 95% CI, 0.02-
33                         Clinical measures of upper motor neuron dysfunction correlated with reduction
34 ssociated with bulbar onset and dysfunction, upper motor neuron dysfunction, cognitive impairment, de
35 orsal column dysfuction, and spasticity with upper motor neuron dysfunction.
36  of the MRCP may serve as a useful marker of upper motor neuron dysfunction.
37 ding one family with exclusively adult-onset upper motor neuron features, consistent with a diagnosis
38 ysfunction and thus an important role of the upper motor neuron in this animal model of ALS and perha
39 cospinal/corticobulbar motor neurons (CSMN; "upper motor neurons") in cerebral cortex, and spinal/bul
40 d progressive consequence of a wide range of upper motor neuron injuries that affect skeletal muscle
41 be used as an electrophysiological marker of upper motor neuron integrity in such patients.
42 mirror properties of Betz cells, specialized upper motor neurons involved in fine digit control in hu
43 n age, 57.3 years) with clinical evidence of upper motor neuron involvement and 10 healthy control su
44     Elevation in NFL levels in patients with upper motor neuron involvement and FTD might reflect the
45 imaging spectroscopy can be used to identify upper motor neuron involvement and predict disease durat
46 ential as a quantitative test of subclinical upper motor neuron involvement in motor neuron disease.
47 on disease phenotypes, with clinically overt upper motor neuron involvement.
48 mary lateral sclerosis, suggesting prominent upper motor neuron involvement.
49 er motor neurons, with or without additional upper motor neuron involvement.
50 tor neuron disorder that exclusively affects upper motor neurons leading to their degeneration.
51 traumatic laceration, and contracture due to upper motor neuron lesion as seen in spinal cord injury,
52                It is also suggested that the upper motor neuron lesion in amyotrophic lateral scleros
53   It is often difficult to identify signs of upper motor neuron lesion in the limbs of patients with
54 aging also provide useful information on the upper motor neuron lesion.
55 en associated with spasticity in humans with upper motor neuron lesions.
56  progressive degeneration of lower (LMN) and upper motor neurons, likely due to the same unknown toxi
57 endpoint, we wanted to establish whether the upper motor neuron might still play a critical role in d
58            Thus, the overall excitability of upper motor neurons only displays negligible changes des
59    This relative lack of knowledge regarding upper motor neuron pathology in these ALS model mice has
60                  Differentiation of PLS from upper motor neuron-predominant forms of amyotrophic late
61  a more benign form of MND that only affects upper motor neurons, results in life-long progressive mo
62 ional rating scale, slow vital capacity, and upper motor neuron score) and between muscle data and cl
63 o also correlated with both the ALSFRS-R and upper motor neuron scores (r=0.50 and 0.54, respectively
64 gnized limited change in individual clinical upper motor neuron scores, despite advancing disability.
65 der marked by progressive death of lower and upper motor neurons, several cell types in the CNS expre
66 e layer 5 pyramidal neurons, which represent upper motor neurons, show a decrease in intrinsic excita
67 ontotemporal dementia (20 patients [22.7%]), upper motor neuron signs (11 patients [12.5%]), memory i
68  abnormalities, including a constellation of upper motor neuron signs (n = 19), ataxia (n = 22), and
69 res, including regional disability, clinical upper motor neuron signs and cognitive impairment.
70                                              Upper motor neuron signs are a prominent feature in a su
71 ion carriers, diffuse lower motor neuron and upper motor neuron signs evolved insidiously during a pr
72 at lead to difficulty in detecting classical upper motor neuron signs, are discussed.
73             Hyporeflexia, hypopallesthaesia, upper motor neuron signs, chorea, dystonia, oculomotor s
74 , and generalized symmetric weakness without upper motor neuron signs.
75 h prominent cognitive, neuropsychiatric, and upper motor neuron signs.
76 e impairment, movement disorders, ataxia and upper motor neuron signs.
77  psychiatric changes, movement disorders and upper motor neuron signs.
78           Typically, the initial progressive upper motor neuron spastic and general proprioceptive at
79            Typical features are disorders of upper motor neurons, spastic quadriparesis and pseudobul
80        To examine how diverse populations of upper motor neurons subserve distinct functions and the
81                It forms one component of the upper motor neuron syndrome and often leads to muscle st
82        Characterised by a slowly progressive upper motor neuron syndrome, the diagnosis is clinical,
83 on may be thought to be the Babinski sign of upper-motor-neuron syndromes.
84 se that I(NaR) modulates the excitability of upper motor neurons that are required for the execution
85       Group 2: Five women developed signs of upper motor neuron (UMN) disease, initially resembling p
86            There was no clinical evidence of upper motor neuron (UMN) involvement in 10 FALS A4V subj
87 was to localize the anatomic distribution of upper motor neuron (UMN) loss through examining cortical
88 l rating scale (ALSFRS-R score), whereas the upper motor neuron (UMN) score correlated with widesprea
89  and energy homeostasis that are detected in upper motor neurons (UMNs) with TDP-43 pathology, a path
90  tested for improving the health of diseased upper motor neurons (UMNs).
91 or skills in vertebrates require specialized upper motor neurons with precise action potential (AP) f
92 , neurodegenerative disease of the lower and upper motor neurons with sporadic or hereditary occurren