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1 nts with neurosyphilis who develop transient neurologic signs.
2 eight loss, fever, anorexia, depression, and neurologic signs.
3 of arrhythmia, age > 70 years) or with acute neurologic signs.
4 t EAE animals therapeutically after onset of neurologic signs.
5              Among the 20 subjects with soft neurologic signs, 10 (50%) had abnormal MRI, 13 (65%) ha
6 ative PCR presented with more frequent focal neurologic signs (4/11 [36.4%] vs 35/256 [13.7%]; p = 0.
7 fter cardiac surgery in the absence of focal neurologic signs, a poorly understood but potentially de
8 ent medical problem such as an abrupt onset, neurologic signs, age 50 years and older, presence of ca
9 t the overall burden of neuropsychiatric and neurologic signs and symptoms among survivors of COVID-1
10 ighlighting the importance of evaluating for neurologic signs and symptoms in all persons with syphil
11 g anti-TNFalpha therapy immediately when new neurologic signs and symptoms occur, pending an appropri
12 urrent headaches, with or without additional neurologic signs and symptoms, and prolonged but reversi
13 use of a wide variety of other, more subtle, neurologic signs and symptoms.
14 cation (n=4), cardiac arrest (n=2), or other neurologic signs and symptoms.
15              Presence of clinically captured neurologic signs and/or syndromes was associated with in
16 ad life-threatening hypoxic episodes or soft neurologic signs, and 10 were normal based on neurologic
17 e is manifested as vascular necrosis, edema, neurologic signs, and death.
18 ic fixation, and 6 children had cognitive or neurologic signs at the time of diagnosis (75%).
19 y 4 or 5 after infection due to anorexia and neurologic signs, but the SA EEEV-infected animals remai
20                                              Neurologic signs decreased with age in the healthy compa
21 of the infected macaques showed any fever or neurologic signs during the experimental period.
22 0-1.04), p = 0.003; and any acute pathologic neurologic sign/event, 5.04 (2.15-12.01), p < 0.001 were
23                           The persistence of neurologic signs in the adolescents with schizophrenia,
24 %; age 43 [30-52]; 73% women) presented with neurologic signs, including headaches (51%), limb weakne
25                      Without IL-12Rbeta2, no neurologic sign of ECM developed upon PbA infection.
26 sulted in the development of severe clinical neurologic signs of EAE with 100% mortality by day 17 po
27 ith a JHR, which possibly contributed to the neurologic signs of JHR.
28  testing is rarely helpful unless additional neurologic signs or symptoms are present (diagnostic yie
29  transient ischemic attack, stroke, or other neurologic signs or symptoms referable to the carotid ar
30 fants with billing codes suggestive of overt neurologic signs or symptoms were excluded.
31 ew lesions, escalating steroids, progressive neurologic signs or symptoms, or non-CNS progression.
32  transient ischemic attack, stroke, or other neurologic signs or symptoms.
33 e selected from 220 samples from horses with neurologic signs resembling EPM and examined for inhibit
34              Only one pig developed clinical neurologic signs suggestive of prion disease.
35 tients with neurologic involvement had acute neurologic signs, symptoms, or diseases on presentation
36                                Resolution of neurologic signs/symptoms occurred a median of 4 days an
37 ons, escalating corticosteroids, progressive neurologic signs/symptoms, or non-CNS progression--the t
38                          Despite progressive neurologic signs, the proviral load in tissues, includin
39  samples, including samples from horses with neurologic signs typical of EPM or with histologically o
40  resuscitation, and appearance of pathologic neurologic signs were associated with adverse outcomes i
41                                              Neurologic signs were noted clinically, and subsequent i