ライフサイエンスコーパス: paresis

1 , dysarthria-dysmetria and dysarthria-facial paresis).

2 diagnosis of true bilateral superior oblique paresis.

3 identifying true bilateral superior oblique paresis.

4 entiating between functional and organic arm paresis.

5 liver resulting from right hemidiaphragmatic paresis.

6 pia in diagnosing bilateral superior oblique paresis.

7 diagnosis of true bilateral superior oblique paresis.

8 sed with acquired bilateral superior oblique paresis.

9 disease phenotype characterized by forelimb paresis.

10 e., spared, PMd and SMA in patients with arm paresis.

11 renic nerve may result in hemi-diaphragmatic paresis.

12 of 1 or more limbs, ataxia, or ocular motor paresis.

13 s often causes contralateral upper extremity paresis.

14 recombinant human EPO (rhEPO) upon onset of paresis.

15 xhibit tremor, ataxia, and significant motor paresis.

16 rbidity, including weight loss and hind limb paresis.

17 uction and assessed for presence of forelimb paresis.

18 (13), tinnitus (12), vertigo (8), and facial paresis (1).

19 s, P <.0001) and a higher rate of paraplegia/paresis (30% vs. 2%, P =.01) as compared to those withou

20 sion loss (3 malignancies), and facial nerve paresis (5 malignancies).

21 hours after receiving penicillin for general paresis, a 55-year-old man developed a severe JHR charac

22 Its core elements are a suprabulbar paresis, a mild spastic tetraplegia and a significant ex

23 children, who had mild symptoms comprised of paresis alone, fully recovered.

24 tients with moderate deficits, consisting of paresis and bowel/bladder dysfunction, completely recove

25 apeutic target in patients with ICU acquired paresis and other forms of acute muscle wasting.

26 cal arboviral encephalitis, characterized by paresis and paralysis before death, and viral infection

27 Paresis and sensory denervation then resolved.

28 .8%) transient neurologic events, which were paresis and visual disturbances.

29 innate immune responses to microbes (immune paresis) and are susceptible to sepsis.

30 -hemisphere subcortical ischemic stroke with paresis, and 13 age-matched healthy controls.

31 lmonary hypertension, chylothorax, diaphragm paresis, and arrhythmia.

32 The influence of delirium, ICU-acquired paresis, and cardiac performance on extubation outcome h

33 ary bladder infections, prostatitis, gastric paresis, and impaired spermatogenesis.

34 SPG5 is characterized by spastic paresis, and similar symptoms may occur in CTX.

35 three days post challenge and torticollis or paresis at later time points.

36 ulted in severe disease, including hind limb paresis, conjunctivitis, weight loss, and death in 89% o

37 her ocular motility disturbances (divergence paresis, convergence insufficiency, and skew deviation)

38 velopmental abnormalities, including spastic paresis, fore limb tremors, hind limb rigidity, and a re

39 Eighty-five adults with upper extremity paresis >/=6 months poststroke were randomized to one of

40 e repair of BAI, the incidence of paraplegia/paresis has fallen.

41 No patient had isolated gaze paresis, hemianopia, or neglect.

42 physiotherapy alone in patients with severe paresis in a double-blind sham-controlled design proof o

43 an extreme calcium perturbation, parturient paresis in dairy cows.

44 al neurological morbidity is associated with paresis linked to involvement of gray matter in the brai

45 ith multiple myeloma whose associated immune paresis may impair immune responses to these proteins.

46 adder emptying is impaired with "gallbladder paresis" occurring in approximately 20%.

47 eloped a disease characterized clinically by paresis of 1 or more limbs, ataxia, or ocular motor pare

48 d by the increasing understanding of general paresis of the insane.

49 opriate only for mild attacks (mild pain, no paresis or hyponatremia) or until hemin is available.

50 and were associated with myositis, atrophy, paresis/paralysis, and death.

51 rtery infarction, leading to upper extremity paresis, paresthesia, and sensory loss.

52 city in people with long-standing upper-limb paresis poststroke.

53 ike the adults, likely had a subtle abducens paresis rather than divergence insufficiency.

54 or cataract extraction is extraocular muscle paresis/restriction and is unique to this type of proced

55 hypoventilation resulting from diaphragmatic paresis secondary to sarcoid.

56 scribed as masked bilateral superior oblique paresis simply may be a reflection of inherent poor sens

57 toms of neuropathy, including limb weakness, paresis, sluggishness, and/or respiratory distress.

58 We show that the classic seizures and paresis that occur following i.c. infection of adult, im

59 ted; 60% of these patients had vertical gaze paresis that sometimes evolved to total external ophthal

60 ies approximately 30 days: first as hindlimb paresis, then progressive tremor and ataxia.

61 In patients with organic paresis, there was not a significant detectable force of

62 hich correlated with lesser degrees of canal paresis to preoperative caloric testing on the operated

63 nt neurological diseases, hereditary spastic paresis type 5 (SPG5) and cerebrotendinous xanthomatosis

64 Bilateral superior oblique paresis was defined and diagnosed by the above history,

65 Focal paresis was evident in 23 of 57 (40%) at presentation an

66 No gross signs of paralysis or paresis were also observed.

67 IV cancer; cancer stage progression; and leg paresis were associated with an increased hazard, and wa

68 the 19th century, when patients with general paresis were thought to have "insanity" similar to demen

69 s manifested by transient muscle weakness or paresis, which in some cases progressed to respiratory f

70 uture research into the treatment of spastic paresis with botulinum toxin should use active movement

71 Affected mice showed limb weakness and paresis with motor deficits.