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1 eight loss, fever, anorexia, depression, and neurologic signs.
2 of arrhythmia, age > 70 years) or with acute neurologic signs.
3 t EAE animals therapeutically after onset of neurologic signs.
4 nts with neurosyphilis who develop transient neurologic signs.
6 fter cardiac surgery in the absence of focal neurologic signs, a poorly understood but potentially de
7 g anti-TNFalpha therapy immediately when new neurologic signs and symptoms occur, pending an appropri
8 urrent headaches, with or without additional neurologic signs and symptoms, and prolonged but reversi
11 ad life-threatening hypoxic episodes or soft neurologic signs, and 10 were normal based on neurologic
13 y 4 or 5 after infection due to anorexia and neurologic signs, but the SA EEEV-infected animals remai
18 sulted in the development of severe clinical neurologic signs of EAE with 100% mortality by day 17 po
20 testing is rarely helpful unless additional neurologic signs or symptoms are present (diagnostic yie
22 e selected from 220 samples from horses with neurologic signs resembling EPM and examined for inhibit
25 ons, escalating corticosteroids, progressive neurologic signs/symptoms, or non-CNS progression--the t
27 samples, including samples from horses with neurologic signs typical of EPM or with histologically o
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