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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
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
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
26 mans shows that deficiency in ALS2 causes an upper motor neuron disease that in humans closely resemb
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-
34 ssociated with bulbar onset and dysfunction, upper motor neuron dysfunction, cognitive impairment, de
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
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.
51 traumatic laceration, and contracture due to upper motor neuron lesion as seen in spinal cord injury,
53 It is often difficult to identify signs of upper motor neuron lesion in the limbs of patients with
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
59 This relative lack of knowledge regarding upper motor neuron pathology in these ALS model mice has
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
71 ion carriers, diffuse lower motor neuron and upper motor neuron signs evolved insidiously during a pr
84 se that I(NaR) modulates the excitability of upper motor neurons that are required for the execution
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
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