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1 and sympathetic nervous system dysfunction (dysautonomia).
2 ptors cause acute postganglionic cholinergic dysautonomia.
3 ysfunction, urinary tract malformations, and dysautonomia.
4 cal features such as vibratory urticaria and dysautonomia.
5 ized by parkinsonism, cerebellar ataxia, and dysautonomia.
6 structural plasticity and the development of dysautonomia.
7 m a therapeutic opportunity to treat cardiac dysautonomia.
8 , breathlessness, neurocognitive effects and dysautonomia.
9 between subjective and objective measures of dysautonomia.
10 uanylate cyclase coupling to cGMP in cardiac dysautonomia.
11 r Ca(2+) impairment underpinning sympathetic dysautonomia.
12 laints, connective tissue abnormalities, and dysautonomia.
13 mpathetic dysfunction similar to humans with dysautonomia.
14 esponsible for the milder course in familial dysautonomia.
15 nt disorders, reduction in consciousness and dysautonomia.
16 ion abnormalities and profound physiological dysautonomia.
17 and this syndrome and others with associated dysautonomia.
18 (AAN) is an acquired, often severe, form of dysautonomia.
19 tically and pathophysiologically in acquired dysautonomia.
20 ic dysfunction and more frequent cholinergic dysautonomia.
21 ic function, both can be considered forms of dysautonomia.
22 nguishes these disorders from other types of dysautonomia.
23 from 157 patients with a variety of types of dysautonomia.
24 , we assess CG-2 as a candidate for familial dysautonomia.
25 of 6-[18F]fluorodopamine in 26 patients with dysautonomia.
26 questionnaires are frequently used to assess dysautonomia.
27 pathetic neurons leading to diabetes-induced dysautonomias.
28 ent clinical manifestation (64%) followed by dysautonomia (16 patients [8%]) and encephalopathy (15 p
36 ntial for neuromodulation to block or reduce dysautonomia after severe high-level SCI.SIGNIFICANCE ST
37 Migraine, post-concussional syndrome, and dysautonomias also cause persistent dizziness and may be
38 and highlight their contribution to cardiac dysautonomia and deterioration of cardiac function durin
41 otype resembles that of the adults, although dysautonomia and hypoventilation are less frequent or se
42 midodrine supports the hypothesis of partial dysautonomia and indicates that the use of alpha1-agonis
43 vere group, AAPI patients had increased POTS/dysautonomia and respiratory symptoms, and NHB patients
45 its strong link with chronic pain, fatigue, dysautonomia and the adverse impact on quality of life.
48 enriched phenotype, including parkinsonism, dysautonomia, and cognitive decline, showed posterior co
49 metry, levodopa-induced motor complications, dysautonomia, and dementia than those without mutations.
51 her syndromes such as Klippel-Feil, familial dysautonomia, and Marfan syndrome demonstrate high rates
52 ion of SCI-induced structural plasticity and dysautonomia, and reveal the potential for neuromodulati
53 hesias, cranial nerve abnormalities, ataxia, dysautonomia, and skeletal muscle injury with normal ori
56 y with clinical features similar to familial dysautonomia as well as contractures, we identified a de
57 evolve, along with cognitive impairment and dysautonomia, as the disease progresses, often dominatin
58 clinical pathophysiologic classification of dysautonomias, based on the occurrence of sympathetic ne
60 G-2 (C9ORF5), was isolated from the familial dysautonomia candidate region on 9q31 using a combinatio
62 tis or encephalitis, sympathetic storming or dysautonomia, cardiac arrest, coma, delirium, and stroke
63 also known as Riley-Day syndrome or familial dysautonomia, do not have functional muscle spindle affe
65 gene DYS, which is responsible for familial dysautonomia (FD) and has been mapped to a 0.5-cM region
67 nalyze the mechanism whereby IKBKAP-familial dysautonomia (FD) exon 20 inclusion is specifically prom
69 The autosomal recessive disorder familial dysautonomia (FD) has recently been demonstrated to be c
90 e defects occur in fibroblasts from Familial Dysautonomia (FD) patients bearing an autosomal recessiv
91 neuropathy in the genetic disorder familial dysautonomia (FD), (3) to show parasymN dysfunction duri
94 ere generated from individuals with familial dysautonomia (FD), a rare, fatal genetic disorder affect
95 (IKBKAP) gene as the major cause of familial dysautonomia (FD), a recessive sensory and autonomic neu
101 d autonomic neuropathy type III, or familial dysautonomia [FD; Online Mendelian Inheritance in Man (O
102 cluding gastric reflux, joint hypermobility, dysautonomia, flushing and pruritus, and hymenoptera all
103 s including cutaneous flushing and pruritus, dysautonomia, functional gastrointestinal symptoms, chro
106 sing fibroblasts from patients with familial dysautonomia (hereditary sensory and autonomic neuropath
107 65.5%, amnesia 55.6%, hallucinations 51.9%), dysautonomia (hyperhidrosis 86.2%, cardiovascular 48.3%)
110 are common manifestations of cardiovascular dysautonomia in Parkinson's disease and related synuclei
114 this apparently disease specific peripheral dysautonomia is unknown and would be the subject of much
115 sis, patent ductus arteriosus with ligation, dysautonomia, low blood pressure, hypotonic bladder requ
117 mic questionnaires correlates with objective dysautonomia measured by quantitative autonomic testing.
122 sfunctional brainstem/vagus nerve signaling, dysautonomia or autonomic dysfunction, ongoing activity
126 well defined although exercise intolerance, dysautonomia, pain, as well as neurocognitive and psychi
127 s had accompanying dream enactment behavior, dysautonomia, parkinsonism, sleep transition-related hal
128 sleep behaviour disorder, pain, anxiety and dysautonomia (particularly orthostatic hypotension and u
129 ificantly more abundant in cells of familial dysautonomia patients with IKBKAP (I-kappa-B kinase comp
131 tural and functional indices of pathological dysautonomia, providing further evidence that microglia
133 tion of ASIC2 recapitulates the pathological dysautonomia seen in heart failure and hypertension and
134 Here, we describe a novel syndrome of pain, dysautonomia, small hands and small feet in a kindred ca
135 out detectable cardiac pathology, as well as dysautonomia, some specific features, and the principles
136 inical manifestation of primary degenerative dysautonomias such as multiple system atrophy (MSA) and
137 es like spinal muscular atrophy and familial dysautonomia that allowed partial modeling of the diseas
138 heart in patients with acquired, idiopathic dysautonomias using thoracic positron-emission tomograph
140 m supraspinal control, causing systems-wide "dysautonomia." We recently showed that remarkable struct
142 igrostriatal system of the brain, but also a dysautonomia, with norepinephrine loss in the sympatheti
143 vascular disease associated with sympathetic dysautonomia would have significant therapeutic utility.