戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (１語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
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 ction (GTR) or experiencing long-term facial paresis.
19 wn clinically as spasticity, hypertonia, and paresis.
20 line led to motor impairment due to hindlimb paresis.
21 deficits including cranial nerve palsies and paresis.
22 acquired at baseline, such as age or side of paresis.
23 (13), tinnitus (12), vertigo (8), and facial paresis (1).
24 resentation were cognitive impairment (41%), paresis (21%), altered consciousness (20%), sensory impa
25 s, P <.0001) and a higher rate of paraplegia/paresis (30% vs. 2%, P =.01) as compared to those withou
26 sion loss (3 malignancies), and facial nerve paresis (5 malignancies).
27 d hearing loss (12/32; 37.5%), diaphragmatic paresis (5/35; 14.3%), CNS involvement (7/40; 17.5%) and
28 hours after receiving penicillin for general paresis, a 55-year-old man developed a severe JHR charac
29          Its core elements are a suprabulbar paresis, a mild spastic tetraplegia and a significant ex
30 in both families exhibited severe vocal fold paresis, a rare feature of peripheral nerve disease that
31 children, who had mild symptoms comprised of paresis alone, fully recovered.
32 ults with chronic stroke and left hemiplegia/paresis and 22 healthy adults.
33 tients with moderate deficits, consisting of paresis and bowel/bladder dysfunction, completely recove
34 humb patented for helping patients with hand paresis and inherent loss of thumb opposition abilities.
35 apeutic target in patients with ICU acquired paresis and other forms of acute muscle wasting.
36 cal arboviral encephalitis, characterized by paresis and paralysis before death, and viral infection
37  progression profiles based on limb-specific paresis and paralysis, tremors and seizures, and other c
38                                              Paresis and sensory denervation then resolved.
39 .8%) transient neurologic events, which were paresis and visual disturbances.
40  innate immune responses to microbes (immune paresis) and are susceptible to sepsis.
41 -hemisphere subcortical ischemic stroke with paresis, and 13 age-matched healthy controls.
42 lmonary hypertension, chylothorax, diaphragm paresis, and arrhythmia.
43      The influence of delirium, ICU-acquired paresis, and cardiac performance on extubation outcome h
44 ary bladder infections, prostatitis, gastric paresis, and impaired spermatogenesis.
45             SPG5 is characterized by spastic paresis, and similar symptoms may occur in CTX.
46 three days post challenge and torticollis or paresis at later time points.
47 f life in patients with bilateral vocal fold paresis (BVFP).
48 ulted in severe disease, including hind limb paresis, conjunctivitis, weight loss, and death in 89% o
49 her ocular motility disturbances (divergence paresis, convergence insufficiency, and skew deviation)
50 s indicated that a characteristic pattern of paresis exists.
51 hat the cumulative risk of developing facial paresis following primary SRS/FSRT by the end of the pat
52 velopmental abnormalities, including spastic paresis, fore limb tremors, hind limb rigidity, and a re
53 kers have also been described for functional paresis, gait and balance disorders.
54      Eighty-five adults with upper extremity paresis &gt;/=6 months poststroke were randomized to one of
55 e repair of BAI, the incidence of paraplegia/paresis has fallen.
56 litation therapies for poststroke upper limb paresis have limited efficacy at the level of impairment
57                 No patient had isolated gaze paresis, hemianopia, or neglect.
58  physiotherapy alone in patients with severe paresis in a double-blind sham-controlled design proof o
59 ings are clinically relevant, the pattern of paresis in ALS should primarily involve those muscle gro
60  an extreme calcium perturbation, parturient paresis in dairy cows.
61 alysed retrospectively the pattern of muscle paresis in patients with ALS using the UK Medical Resear
62 dden pain attacks, followed by patchy muscle paresis in the upper extremity.
63 adverse event related to surgery (vocal cord paresis) in the control group.
64 al neurological morbidity is associated with paresis linked to involvement of gray matter in the brai
65 han GTR or experienced some degree of facial paresis long term.
66 ith multiple myeloma whose associated immune paresis may impair immune responses to these proteins.
67 adder emptying is impaired with "gallbladder paresis" occurring in approximately 20%.
68 eloped a disease characterized clinically by paresis of 1 or more limbs, ataxia, or ocular motor pare
69 d by the increasing understanding of general paresis of the insane.
70 opriate only for mild attacks (mild pain, no paresis or hyponatremia) or until hemin is available.
71 troke versus mimics such as migraine, Todd's paresis, or functional disorders.
72 whether the function of the VFs is intact or paresis/paralysis has occurred.
73           In addition, reports of vocal fold paresis/paralysis potentially suggest that patients may
74  and were associated with myositis, atrophy, paresis/paralysis, and death.
75 eports of voice alteration and 57 reports of paresis/paralysis.
76 rtery infarction, leading to upper extremity paresis, paresthesia, and sensory loss.
77 city in people with long-standing upper-limb paresis poststroke.
78  lower Barthel Index (BI) score; immobility; paresis; previous history of VTE; thrombophilia; maligna
79 ike the adults, likely had a subtle abducens paresis rather than divergence insufficiency.
80 or cataract extraction is extraocular muscle paresis/restriction and is unique to this type of proced
81 hypoventilation resulting from diaphragmatic paresis secondary to sarcoid.
82 scribed as masked bilateral superior oblique paresis simply may be a reflection of inherent poor sens
83 of a patient presenting with unilateral mild paresis, slowing of the upper limb, and parkinsonism, wh
84 toms of neuropathy, including limb weakness, paresis, sluggishness, and/or respiratory distress.
85        We show that the classic seizures and paresis that occur following i.c. infection of adult, im
86 ted; 60% of these patients had vertical gaze paresis that sometimes evolved to total external ophthal
87 ies approximately 30 days: first as hindlimb paresis, then progressive tremor and ataxia.
88                     In patients with organic paresis, there was not a significant detectable force of
89 hich correlated with lesser degrees of canal paresis to preoperative caloric testing on the operated
90                 Hereditary congenital facial paresis type 1 (HCFP1) is an autosomal dominant disorder
91 nt neurological diseases, hereditary spastic paresis type 5 (SPG5) and cerebrotendinous xanthomatosis
92                   Bilateral superior oblique paresis was defined and diagnosed by the above history,
93                                        Focal paresis was evident in 23 of 57 (40%) at presentation an
94               No gross signs of paralysis or paresis were also observed.
95 IV cancer; cancer stage progression; and leg paresis were associated with an increased hazard, and wa
96 the 19th century, when patients with general paresis were thought to have "insanity" similar to demen
97 ronment-related factors contribute to immune paresis, which facilitates the dissemination of clonal p
98 s manifested by transient muscle weakness or paresis, which in some cases progressed to respiratory f
99 uture research into the treatment of spastic paresis with botulinum toxin should use active movement
100       Affected mice showed limb weakness and paresis with motor deficits.