1 re than did antibiotic-treated patients with facial palsy.

2 gnosis of Lyme borreliosis in cases of acute facial palsy.

3 educed the burden of long-term disability in facial palsy.

4 e (GST)-Arp, as did 59% of the patients with facial palsy and 68% of those with Lyme arthritis.

5 burgdorferi infection in patients with acute facial palsy and a positive enzyme immunoassay result.

6 underlie changes in blinking associated with facial palsy and may play a role in the development of d

7 c criteria (MDC) (congenital, nonprogressive facial palsy, and abduction deficit) and genetic testing

8 ommands, gaze palsy, abnormal visual fields, facial palsy, arm drift, leg drift, and abnormal languag

9 e neuropsychiatric disorders, e.g. stroke or facial palsy, had a physical basis requiring the attenti

10   The resulting phenotype includes bilateral facial palsy, hearing loss, and strabismus and correlate

11  because they had abduction deficits without facial palsy or facial palsy with full ocular motility.

12 onnecticut, region who had erythema migrans, facial palsy, or Lyme arthritis 10-20 years ago and 30 u

13 aise (39%), paresthesias (32.5%), peripheral facial palsy (PFP) (36.4%), meningeal signs (19.5%), and

14 he rates of granulation tissue, otalgia, and facial palsy were 90.9%, 31.8%, and 9.1%, respectively.

15                      Moreover, patients with facial palsy who did not receive antibiotics for acute n

16  were apparent primarily among patients with facial palsy who did not receive antibiotics for acute n

17                       However, patients with facial palsy, who frequently had more widespread nervous

18 us syndrome, especially in patients who have facial palsy with full ductions.

19 d abduction deficits without facial palsy or facial palsy with full ocular motility.