Page 120 - TBE_Book_V2_2019

Chapter 5: TBE in adults

Figure 7: Additional visualization of modulate endothelial cell permeability,
TBE-related abnormalities disrupt the blood–brain barrier, and lead to
A B the passage of the TBEV into CNS; II. Trojan
horse hypothesis, in which immune cells
migrate into CNS and establish an infection of
the neural cells, endothelial cells, or chorioid
plexus epithelial cells, with budding of TBEV
into the parenchymal compartment; 22,23,50,51
III. Digestive tract infections from epithelial
cells to DCs; and IV. Infection via olfactory
epithelium and olfactory neurons.

The second stage of TBE begins with an
Axial fluid-attenuated inversion recovery (FLAIR) increasing body temperature. This second
image (A) and T2-weighted MR image (B) show febrile phase is characterized by temperatures
bilateral hyperintensity of the caudate nuclei, 1–2°C higher than peak body temperatures in
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putamina and thalamus. The right side is slightly the first phase, frequently exceeding 40°C.
more involved than the left side. Patient with The further course of acute TBE can be
immunosuppression.
classified as mild, moderate, or severe
Photo 4.
A

B

C Muscle atrophy after remote TBE:
• Atrophy of the muscles with limitation of
elevation both limbs (both sides R>L)-A,
• one side-B,
• lower limb-C.

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