ライフサイエンスコーパス: akinesia

1 er than 1.5 hours per day (excluding morning akinesia).

2 ective methods of Mthal stimulation to treat akinesia.

3 nd improvements in tests of forelimb use and akinesia.

4 onstrating that pterygia resulted from fetal akinesia.

5 es and did not block MPTP-induced tremor and akinesia.

6 (MPTP) results in significant improvement of akinesia.

7 sion by thrombolysis or angioplasty leads to akinesia.

8 ical combination of disinhibition and severe akinesia.

9 sk in either acute drug-induced parkinsonian akinesia (0.03-0.07 mg/kg haloperidol, s.c.) or control

10 This suggests that akinesia and bradykinesia might, in fact, originate from

11 Akinesia and bradykinesia were strongly ameliorated by d

12 of quisqualate caused episodes of prolonged akinesia and convulsions, and major damage to pyramidal

13 glia-brainstem projections may play roles in akinesia and disturbances of gait.

14 opa-responsive Parkinsonism, as well as pure akinesia and gait failure, there is less cortical pathol

15 nd that reduced levels of dopamine result in akinesia and lethality, developmental retardation, and d

16 Features of the SMA syndrome (akinesia and mutism) can be better understood on the bas

17 MA syndrome', characterised by contralateral akinesia and mutism.

18 pical presenting features of CBD and PSP are akinesia and rigidity that are levodopa unresponsive, al

19 h can occur even in the presence of profound akinesia and rigidity.

20 depending on the adequacy of anesthesia and akinesia and the need for local supplementation.

21 Changes in tremor, rigidity, akinesia, and gait scores were also assessed using the U

22 Time of onset of analgesia, akinesia, and intraoperative pain, if any, was noted.

23 re instability and gait disturbance, tremor, akinesia, and rigidity while not taking medication.

24 y, mouse and rat models of reserpine-induced akinesia, and the rat 6-hydroxydopamine (6-OHDA) lesion

25 irment characterized by rigidity, catalepsy, akinesia, and tremor.

26 sal ganglia output to the thalamus underlies akinesia, as seen in Parkinson's disease, and dyskinetic

27 ose (< 10 micrograms); scar was diagnosed by akinesia at rest or dyskinesia without change and ischem

28 inson's disease (PD) include resting tremor, akinesia, bradykinesia, and rigidity, and these motor ab

29 ice expressing halorhodopsin in ChIs reduces akinesia, bradykinesia, and sensorimotor neglect.

30 insonian syndrome characterized by rigidity, akinesia, bradykinesia, decreased response to external s

31 ce of a wide range of motor deficits such as akinesia, bradykinesia, motor coordination, and sensorim

32 parkinsonian motor signs (tremor, rigidity, akinesia/bradykinesia, and gait dysfunction) and reduced

33 ndicating that apomorphine not only reversed akinesia but also induced hyper-kinesia.

34 the Mthal may be an effective site to treat akinesia, but the pattern of stimulation is critical for

35 vous system and retinal vessels; and a fetal akinesia deformation sequence (FADS) with muscular neuro

36 lissencephaly with hydrocephalus, and fetal akinesia deformation sequence (ie, arthrogryposis).

37 imester and characteristic features of Fetal Akinesia Deformation Sequences (FADS).

38 Adequate anesthesia and akinesia (grade 5) were achieved in 56.7% of the patient

39 striatal denervation attenuated the forelimb akinesia improvement normally induced by STN DBS.

40 The lack of an AChR subunit causes a fetal akinesia in humans, leading to death in the first trimes

41 thalamus (Mthal) ameliorates tremor but not akinesia in Parkinson's disease.

42 the most important determinant of upper limb akinesia in Parkinson's disease.

43 previously described measures of upper limb akinesia in Parkinson's disease.

44 idol-induced catalepsy and reserpine-induced akinesia in rats.

45 duced a marked reversal of reserpine-induced akinesia in rats.

46 and profound dopamine depletion (<0.2%) with akinesia in the same animal.

47 Akinesia is linked to hypoactivation of the supplementar

48 o effect in preventing the reserpine-induced akinesia, nor did it affect locomotion in control animal

49 nd had a mean total awake off-time (state of akinesia or decreased mobility) of at least 1.5 hours, n

50 otion abnormality after exercise and scar by akinesia or dyskinesia at rest.

51 sm (PD), multiple system atrophy (MSA), pure akinesia (PA), progressive supranuclear palsy (PSP), and

52 lated genes might also result in a MPS/fetal akinesia phenotype and so we analyzed 15 cases of lethal

53 oss of function can result in a lethal fetal akinesia phenotype.

54 catalepsy, mouse model of reserpine-induced akinesia, rat 6-hydroxydopamine (6-OHDA) lesion model of

55 The phenotype ranges from foetal akinesia resulting in in utero or neonatal mortality, to

56 e involving motor abnormalities that include akinesia, rigidity and postural instability.

57 osture instability and gait disturbance; and akinesia, rigidity, and tremor scores.

58 ssfully lesioned animals (3 or less forelimb akinesia score, and 8 or more apomorphine-induced rotati

59 is structure has also been implicated in the akinesia seen in patients with Parkinson's disease.

60 tivator resulted in improvements in forelimb akinesia, sensorimotor neglect, and amphetamine-induced

61 th three children affected with lethal fetal akinesia sequence.

62 al skeletal dysplasia characterized by fetal akinesia, shortening of all long bones, multiple contrac

63 inst alpha-syn-mediated deficits in forelimb akinesia, striatal denervation or loss of SNpc neuron, n

64 concentration more typically associated with akinesia, suggesting that (mal)adaptive postsynaptic res

65 Akinesia suggests a primary neuronal defect and electrop

66 nto the pathogenesis and management of fetal akinesia syndromes.

67 ns up new possibilities in the management of akinesia, the most intractable symptom of advanced Parki

68 on between dopamine-related hyperkinesia and akinesia, the overall cortical firing rate remained unch

69 and degrees of severity (ranging from foetal akinesia, through lethality in the newborn period to mil

70 Fetal akinesia was documented by ultrasonographic examination.

71 In animals treated with reserpine, profound akinesia was induced that was reversed with apomorphine.

72 Various measures of upper limb akinesia were assessed in 6 patients with bilateral DBS

73 of at least 1.5 hours, not including morning akinesia, were enrolled.

74 ether, iSPNs and TANs (i.e., D2 cells) drove akinesia, whereas movement execution deficits reflected

75 rats executed <20 reaches, displaying marked akinesia, which was significantly improved by stimulatin

76 classic Richardson's syndrome (RS) and pure akinesia with gait freezing (PAGF).

77 so we analyzed 15 cases of lethal MPS/fetal akinesia without CHRNG mutations for mutations in the CH

78 agonist RU 24213 reversed reserpine-induced akinesia, yet paradoxically increased glutamate (not asp