ライフサイエンスコーパス: cranial nerve palsy

1 and 1 (0.2%) with orbital involvement and a cranial nerve palsy.

2 nts with acute SAH and 2 patients with acute cranial nerve palsy.

3 tral nervous system disorders and peripheral cranial nerve palsies.

4 f current neuro-imaging guidelines for third cranial nerve palsies.

5 opathy (21%), papilledema (18%), diplopia or cranial nerve palsies (16%), and unspecified vision loss

6 .3%), conjunctival microvasculopathy (2.3%), cranial nerve palsies (2%), herpes zoster ophthalmicus (

7 There were more cranial nerve palsies (22 vs 0) in the endarterectomy gr

8 l symptoms were painful radiculitis (65.9%), cranial nerve palsy (43.4%), and headache (28.3%).

9 mours; abnormal gait and coordination (78%), cranial nerve palsies (52%), pyramidal signs (33%), head

10 days and up to 3 years; clinical outcome of cranial nerve palsy after PED placement; angiographic ev

11 elayed neurological complications, including cranial nerve palsies and a unique delayed-onset parkins

12 as focal motor deficit (n = 16), followed by cranial nerve palsies and cerebellar dysfunction.

13 Botulism manifests with cranial nerve palsies and flaccid paralysis in children

14 s, and focal neurological deficits including cranial nerve palsies and paresis.

15 By excluding patients with third cranial nerve palsies and those with GCA, the incidence

16 ially avoiding the surgical complications of cranial nerve palsy and hematoma.

17 but a higher risk of myocardial infarction, cranial nerve palsy, and access site haematoma with enda

18 NS3 disease (CSF WBC >= 5/muL with blasts or cranial nerve palsies, brain/eye involvement, or hypotha

19 e composite outcome of death, stroke, MI, or cranial nerve palsy during the periprocedural period (OR

20 ly benign causes of third, fourth, and sixth cranial nerve palsies in children, but a study from a te

21 ) had local side effects that included third cranial nerve palsy in 6 (40%), orbital edema in 3 (20%)

22 lower incidence of myocardial infarction and cranial nerve palsy in patients undergoing stenting.

23 There was one event of cranial nerve palsy in the stenting group compared with

24 l manifestations vary widely and can include cranial nerve palsies, meningeal involvement, parenchyma

25 = 2), small cerebral infarction (n = 2), and cranial nerve palsy (n = 1).

26 lvement (lymphoma cells in the CSF [n = 23], cranial nerve palsy [n = 9], both features [n = 4]), rep

27 cedural MI (OR: 0.45; 95% CI: 0.27 to 0.75); cranial nerve palsy (OR: 0.07; 95% CI: 0.04 to 0.14); an

28 s in an atraumatic sample or the presence of cranial nerve palsy) status.

29 ed with lower rates of periprocedural MI and cranial nerve palsy than CEA.

30 ddress movement and neurocognitive toxicity, cranial nerve palsies, tumour inflammation-associated ne

31 f other causes for isolated fourth and sixth cranial nerve palsies was 4.7% (3/64).

32 in a nontraumatic sample or the presence of cranial nerve palsy) was present.

33 all SF-36 domains, but periprocedural MI or cranial nerve palsy were not.

34 is, etiology, work-up and treatment of third cranial nerve palsies, while incorporating information f

35 93.8%) completely recovered from symptoms of cranial nerve palsy within a median of 3.5 months.