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1 er than 1.5 hours per day (excluding morning akinesia).
2 n the most extensive network (onset of globe akinesia).
3 ical combination of disinhibition and severe akinesia.
4 ective methods of Mthal stimulation to treat akinesia.
5 nd improvements in tests of forelimb use and akinesia.
6 onstrating that pterygia resulted from fetal akinesia.
7 es and did not block MPTP-induced tremor and akinesia.
8 (MPTP) results in significant improvement of akinesia.
9 sion by thrombolysis or angioplasty leads to akinesia.
10 ocomotor deficits, such as gait freezing and akinesia.
11 nset and duration of sensory block and globe akinesia.
12 sk in either acute drug-induced parkinsonian akinesia (0.03-0.07 mg/kg haloperidol, s.c.) or control
13                           This suggests that akinesia and bradykinesia might, in fact, originate from
14                                              Akinesia and bradykinesia were strongly ameliorated by d
15  of quisqualate caused episodes of prolonged akinesia and convulsions, and major damage to pyramidal
16 glia-brainstem projections may play roles in akinesia and disturbances of gait.
17  and angular velocity data to detect tremor, akinesia and dyskinesia.
18 opa-responsive Parkinsonism, as well as pure akinesia and gait failure, there is less cortical pathol
19    Prenatal features included hypokinesia or akinesia and growth restriction.
20 nd that reduced levels of dopamine result in akinesia and lethality, developmental retardation, and d
21                Features of the SMA syndrome (akinesia and mutism) can be better understood on the bas
22 MA syndrome', characterised by contralateral akinesia and mutism.
23 pical presenting features of CBD and PSP are akinesia and rigidity that are levodopa unresponsive, al
24 h can occur even in the presence of profound akinesia and rigidity.
25 mine concentrations and a rescue of forelimb akinesia and spontaneous rotations.
26  depending on the adequacy of anesthesia and akinesia and the need for local supplementation.
27 etecting key PD motor manifestations-tremor, akinesia, and dyskinesia-on an individual movement basis
28                 Changes in tremor, rigidity, akinesia, and gait scores were also assessed using the U
29                  Time of onset of analgesia, akinesia, and intraoperative pain, if any, was noted.
30 re instability and gait disturbance, tremor, akinesia, and rigidity while not taking medication.
31 y, mouse and rat models of reserpine-induced akinesia, and the rat 6-hydroxydopamine (6-OHDA) lesion
32 irment characterized by rigidity, catalepsy, akinesia, and tremor.
33 sal ganglia output to the thalamus underlies akinesia, as seen in Parkinson's disease, and dyskinetic
34 ant clusters for suppression of rigidity and akinesia, as well as for overall motor improvement, resi
35  and the duration of sensory block and globe akinesia, as well as the duration of analgesia.
36 ose (< 10 micrograms); scar was diagnosed by akinesia at rest or dyskinesia without change and ischem
37 inson's disease (PD) include resting tremor, akinesia, bradykinesia, and rigidity, and these motor ab
38 ice expressing halorhodopsin in ChIs reduces akinesia, bradykinesia, and sensorimotor neglect.
39 insonian syndrome characterized by rigidity, akinesia, bradykinesia, decreased response to external s
40 ce of a wide range of motor deficits such as akinesia, bradykinesia, motor coordination, and sensorim
41  parkinsonian motor signs (tremor, rigidity, akinesia/bradykinesia, and gait dysfunction) and reduced
42 ndicating that apomorphine not only reversed akinesia but also induced hyper-kinesia.
43  the Mthal may be an effective site to treat akinesia, but the pattern of stimulation is critical for
44 vous system and retinal vessels; and a fetal akinesia deformation sequence (FADS) with muscular neuro
45  lissencephaly with hydrocephalus, and fetal akinesia deformation sequence (ie, arthrogryposis).
46  the presentation was consistent with foetal akinesia deformation sequence with severe intrauterine a
47 imester and characteristic features of Fetal Akinesia Deformation Sequences (FADS).
48 00%) and specificity (>= 93%) for tremor and akinesia detection, with an overall accuracy exceeding 9
49 63-0.88), D 0.71 (0.61-0.84); onset of globe akinesia: F 0.71 (0.61-0.82), C 0.70 (0.61-0.82), D 0.81
50 1.27), D 1.44 (1.34-1.55); duration of globe akinesia: F 1.38 (1.22-1.57), C 1.45 (1.26-1.67), D 1.41
51                      Adequate anesthesia and akinesia (grade 5) were achieved in 56.7% of the patient
52 aternal exercise substantially rescued fetal akinesia-impaired joint and bone development and prevent
53 striatal denervation attenuated the forelimb akinesia improvement normally induced by STN DBS.
54   The lack of an AChR subunit causes a fetal akinesia in humans, leading to death in the first trimes
55 amine depletion with 6-OHDA created complete akinesia in mice, but Pf-STN stimulation immediately and
56  thalamus (Mthal) ameliorates tremor but not akinesia in Parkinson's disease.
57 the most important determinant of upper limb akinesia in Parkinson's disease.
58  previously described measures of upper limb akinesia in Parkinson's disease.
59 idol-induced catalepsy and reserpine-induced akinesia in rats.
60 duced a marked reversal of reserpine-induced akinesia in rats.
61 and profound dopamine depletion (<0.2%) with akinesia in the same animal.
62 tor function assessment via the BRadykinesia Akinesia INcoordination (BRAIN) tap test.
63                             The BRadykinesia Akinesia INcoordination (BRAIN) test is a validated keyb
64                                              Akinesia is linked to hypoactivation of the supplementar
65 o effect in preventing the reserpine-induced akinesia, nor did it affect locomotion in control animal
66 nd had a mean total awake off-time (state of akinesia or decreased mobility) of at least 1.5 hours, n
67 otion abnormality after exercise and scar by akinesia or dyskinesia at rest.
68 sm (PD), multiple system atrophy (MSA), pure akinesia (PA), progressive supranuclear palsy (PSP), and
69 lated genes might also result in a MPS/fetal akinesia phenotype and so we analyzed 15 cases of lethal
70 oss of function can result in a lethal fetal akinesia phenotype.
71 s disease (PD) is characterized by rigidity, akinesia, postural instability and tremor.
72  catalepsy, mouse model of reserpine-induced akinesia, rat 6-hydroxydopamine (6-OHDA) lesion model of
73             The phenotype ranges from foetal akinesia resulting in in utero or neonatal mortality, to
74 e involving motor abnormalities that include akinesia, rigidity and postural instability.
75 osture instability and gait disturbance; and akinesia, rigidity, and tremor scores.
76 ssfully lesioned animals (3 or less forelimb akinesia score, and 8 or more apomorphine-induced rotati
77 is structure has also been implicated in the akinesia seen in patients with Parkinson's disease.
78 tivator resulted in improvements in forelimb akinesia, sensorimotor neglect, and amphetamine-induced
79 th three children affected with lethal fetal akinesia sequence.
80 al skeletal dysplasia characterized by fetal akinesia, shortening of all long bones, multiple contrac
81 inst alpha-syn-mediated deficits in forelimb akinesia, striatal denervation or loss of SNpc neuron, n
82 concentration more typically associated with akinesia, suggesting that (mal)adaptive postsynaptic res
83                                              Akinesia suggests a primary neuronal defect and electrop
84 nto the pathogenesis and management of fetal akinesia syndromes.
85 ns up new possibilities in the management of akinesia, the most intractable symptom of advanced Parki
86 on between dopamine-related hyperkinesia and akinesia, the overall cortical firing rate remained unch
87 and degrees of severity (ranging from foetal akinesia, through lethality in the newborn period to mil
88 de kinesia score (KS20, key taps over 20 s), akinesia time (AT20, mean dwell-time on each key) and in
89                                        Fetal akinesia was documented by ultrasonographic examination.
90  In animals treated with reserpine, profound akinesia was induced that was reversed with apomorphine.
91               Various measures of upper limb akinesia were assessed in 6 patients with bilateral DBS
92 of at least 1.5 hours, not including morning akinesia, were enrolled.
93 ether, iSPNs and TANs (i.e., D2 cells) drove akinesia, whereas movement execution deficits reflected
94 Splotch-delayed (Sp(d)) mouse model of fetal akinesia, which features intact maternofetal communicati
95 rats executed <20 reaches, displaying marked akinesia, which was significantly improved by stimulatin
96  classic Richardson's syndrome (RS) and pure akinesia with gait freezing (PAGF).
97  so we analyzed 15 cases of lethal MPS/fetal akinesia without CHRNG mutations for mutations in the CH
98  agonist RU 24213 reversed reserpine-induced akinesia, yet paradoxically increased glutamate (not asp