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1 ks relating separately to gene status and to abnormal movement.
2 , suggesting that both receptors mediate the abnormal movements.
3 y be difficult to differentiate from organic abnormal movements.
4 e orchestration of the modules, resulting in abnormal movements.
5 of the vehicle-treated animals displayed any abnormal movements.
6 he C. elegans unc-33 gene lead to worms with abnormal movements.
7 are characterized by paroxysmal onset of the abnormal movements.
8  neurological symptoms, such as seizures and abnormal movements.
9 aste, thirst, chronic cough, chest pain, and abnormal movements.
10 racterized by over-active muscles leading to abnormal movements.
11 inct neurological conditions presenting with abnormal movements.
12 , memory deficit, depressive-like behaviour, abnormal movements (14% of mice), and lower threshold fo
13 ionally, the fasting glucose level predicted abnormal movements after the authors controlled for age.
14 e magnitude of the fasting insulin level and abnormal movements after the authors controlled for fast
15 nded survival, reduced associated tremor and abnormal movements and ameliorated weight loss.
16 lity, and simultaneous occurrence of various abnormal movements and dysfunctions.
17 The authors examined the association between abnormal movements and impaired glucose metabolism, whic
18  overexpression rescues torsinA LOF-mediated abnormal movements and neurodegeneration.
19  or intermittent muscle contractions causing abnormal movements and postures, often occurring in abse
20 s involuntary muscle contractions leading to abnormal movements and postures.
21 g how dysfunction in the CNS causes specific abnormal movements and postures.
22 came completely unresponsive with no further abnormal movements and ultimately died.
23 ith catatonic features often associated with abnormal movements, and autonomic and breathing instabil
24 ehavioral and speech problems, seizures, and abnormal movements are common early symptoms.
25 t the striatal cell types that contribute to abnormal movements are poorly defined.
26 ld caution clinicians to not assume that all abnormal movements are seizures.
27 ients report that they do not experience the abnormal movement as voluntary.
28 When treatment began after the appearance of abnormal movements, cystamine extended survival, reduced
29 tients may have cardiovascular syncope, with abnormal movements due to cerebral hypoxia, which may be
30 long-term levodopa therapy, patients develop abnormal movements, dyskinesias, the pathophysiological
31            Mutant mice, which do not display abnormal movements, exhibited significant CbTC tract cha
32 re intimately related to normal movement and abnormal movement in Parkinson's disease (PD), are sculp
33 bserved during normal voluntary movement and abnormal movement in Parkinson's disease (PD).
34 ngitudinal stability of lack of awareness of abnormal movements in schizophrenia.
35 n ability to follow simple commands only and abnormal movements, including myoclonus, tongue and orof
36 ysregulated in proportion to the severity of abnormal movements induced by l-DOPA in a rat model of p
37 delayed epibolic movement of the deep cells, abnormal movement of dorsal forerunner cells, and dissoc
38 nce and extension phenotype, demonstrated by abnormal movement of dorsolateral cells during gastrulat
39 ssion levels impact the onset or severity of abnormal movements or neuropathological features in DYT1
40  symptoms or cognitive impairment, seizures, abnormal movements, or coma of unknown cause, had an aut
41  movement notation, we present evidence that abnormal movement patterns can be detected in AS in infa
42 illness beliefs, self-directed attention and abnormal movement patterns through a process of educatio
43                                        These abnormal movements resemble drug-induced dyskinesia more
44 h impaired glucose tolerance had higher mean abnormal movement scores than those without glucose into
45 secutive glutamines exhibit ataxia, tremors, abnormal movements, seizures, and premature death.
46 ellectual disability (ID), muscle hypotonia, abnormal movements, seizures, feeding difficulties, and
47 ng-term L-DOPA treatment induces involuntary abnormal movements such as dyskinesias.
48 overall locomotor activity and did not cause abnormal movement, such as stereotypy.
49  zebrafish decreased motility while inducing abnormal movements suggestive of seizures.
50 , resting biases mirrored characteristics of abnormal movement synergies, in line with a shared mecha
51 e seen in psychogenic movement disorder, and abnormal movements that would not normally be considered
52 ttention to manifest yet patients report the abnormal movement to be out of their control.
53 sorders presenting with recurrent attacks of abnormal movements, typically dystonia, chorea or a comb
54                                          The abnormal movements were not associated with kainate-indu