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Chapter 5: TBE in adults

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adults. Neurological sequelae occur in 30–80% mg/dL; range 1–60 mg/dL). TBE-specific IgM
of survivors, especially residual flaccid paral- and IgG antibodies are already present in CSF
yses of the shoulder girdle and arms. Overall, samples at the time when patients are
there is little information available on the admitted to hospitals because of CNS
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virulence of the recently described TBEV-Sib symptoms. Meningeal signs can be absent in
with respect to the course of disease in TBE patients with CSF pleocytosis. For
humans. The few systematic and unsystematic microbiological confirmation of TBE please see
data accumulated over the past 20 years show Chapter 12.
that TBE is a chronic disease in 1–1.7% of
cases. Chronic TBE affects mainly working-age
people and children, often leading to their Neuroimaging
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debilitation. The frequency of the chronic Magnetic resonance imaging (MRI) is the
form is described as approximately 1–1.8% of standard for the evaluation of patients with
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patients.
any type of encephalitis, including TBE.
Hyperkinetic syndrome is the main However, only about 18% of patients with TBE
manifestation of chronic TBE (86%), which have abnormalities on cranial MRI (cMRI)
presents as myoclonic hyperkinesia in examination. These abnormalities are mainly
paralyzed muscles, myoclonus of oral muscles, located in the thalamus, the cerebellum, the
myoclonus of the oral, shoulder girdle, and brainstem, and the nucleus caudatus (Figure 5
57,60,61
abdominal wall muscles with Parkinson –7). MRI findings are bilateral or
tremor, and spontaneous progressive form of unilateral. The most characteristic MRI finding
chronic TBE (from myoclonic hyperkinesia in is the bilaterally-increased signal intensity in
the arm to typical Kozevnikoff epilepsy). T2-weighted images and in fluid-attenuated
inversion recovery (FLAIR) images within the
basal ganglia or thalamus. The localization of
the MRI lesions corresponds with neuro-
Laboratory findings pathological findings. The cerebellum, brain-
stem, cerebral cortex, and spinal cord are
Compared with other forms of viral further brain structures that may be clinically
meningitis, white blood cell counts in the CSF
affected; however, pathological MRI enhance-
are low in TBE (median 60/µL, range 5–1200/ ments are rarely seen in these locations. There
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µL). The CSF albumin is moderately is usually no restricted diffusion on diffusion-
increased; indeed, in some TBE cases, an weighted imaging (DWI) in patients with TBE.
increased albumin concentration may be the Sometimes single-voxel 1H-MRI spectroscopy
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only pathological finding in the CSF.
may show pathological patterns, indicating
Increased CSF-to-serum-albumin ratio lactate or lipid peaks or other metabolic
indicates an impaired blood–brain barrier, alterations in the otherwise unremarkably
significant disruption of which can be appearing basal ganglia or thalami. TBE
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observed in up to 60% of patients with TBE. patients with meningoencephalitis and un-
Initially there is a predominance of poly-
favorable prognosis are more likely to present
nuclear cells (granulocytes) in the CSF cell with MRI lesions; however, anecdotal reports
count; however, the immune response show that even some patients with normal
switches within a few days towards an cMRI scans may die from TBE. It is difficult to
increased lymphocytic cell count (Figures 2–4).
correlate MRI results with clinical findings or
In serum samples, patients with TBE display
even outcomes in TBE patients. However,
only moderate markers of inflammation. For there is one prospective cohort study from
example, CRP is marginally altered (median 3
Germany that enrolled 111 TBE patients from

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