*7.3.1. Detection of TBEV*

results in patients with encephalomyelitic manifestation of TBE; 11 (19%) out of 57 included patients fully recovered, 29 (51%) patients had long‐lasting sequelae (paresis or other impairments), and 17 (30%) died 1–10 years after the acute disease. The most substantial improvements were seen in the first year after acute disease [75]. Recently published case‐control study on the long-term sequelae after TBE from Sweden has showed that the neurocognitive and motor symptoms in patients significantly differ from those in the age‐ and gender‐

 leukocytes/L), and (c) microbiologic evidence of TBEV infection (i.e., the presence of specific IgM and IgG an-

In the initial (viremic) phase of TBE leukopenia and/or thrombocytopenia are ascertained in around 70% of patients, and abnormal liver test results are seen in about 20% [78]. In the second (meningoencphalitic) phase, platelet count is normal, whereas peripheral blood leukocyte

and erythrocyte sedimentation rate is usually in normal range throughout the entire course of TBE. In the initial phase of TBE, CSF findings are in the normal range, whereas in the second

glucose concentration are present. A typical finding is lymphocytic pleocytosis; however, in the first few days of the meningoencephalitic phase of TBE, neutrophils may predominate in CSF. Elevated lymphocyte counts may persist for several weeks after clinical recovery [32, 79].

MRI abnormalities of brain and spinal cord are present only in about 20% of patients with TBE. According to a study performed by Kaiser [46], they are found more often in patients with meningoencephalomyelitis (7/25, 29%) than in patients with meningoencephalitis (11/64, 17%), and are not seen in those with meningitis (0/13). Increased signal intensity is most often seen in the thalamus, but can (also) be present in basal ganglia, internal capsule, splenium, cerebellum, peduncles and brain stem [46, 80–92]; in patients with myelitis, the abnormalities are seen predominantly in the anterior horns of the spinal cord [84, 85, 89, 93–97]. Studies of

/L), a normal to moderately elevated protein concentration, and a normal

(meningoencephalitic) phase, elevated CSF leukocyte counts (usually <500 × 10<sup>6</sup>

/L). Concentration of C‐reactive protein

/L, extremely

matched control group [76].

(b) elevated CSF cell count (>5 × 10<sup>6</sup>

**7.1. Blood and cerebrospinal fluid analysis**

count is normal or mildly elevated (rarely >15 × 109

**7.2. Magnetic resonance imaging (MRI) abnormalities**

specificity are lacking but the specificity is probably low [89].

For a diagnosis of TBE, three criteria should be fulfilled:

(a) symptoms/signs indicating meningitis or meningoencephalitis,

30 Meningoencephalitis - Disease Which Requires Optimal Approach in Emergency Manner

**7. Diagnosis**

tibodies) [77].

rarely ≥1000 × 10<sup>6</sup>

Due to limited diagnostic yield, direct approaches to demonstrate TBEV, such as detection of viral RNA by reverse transcriptase PCR and isolation of the virus, are as a rule not used in clinical practice. TBEV is present in blood in the initial (viremic) phase of TBE but not in the meningoencephalitic phase of the disease and is only very exceptionally present in CSF [98].
