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Chapter 5: TBE in adults

these, 60 patients (48%) had no symptoms of There is only a limited chance for improve-
PES; 15 patients (12%) had symptoms that ment of muscle paresis, because neurons have
were mild and of short duration; and the restricted regenerative capabilities. TBEV has a
remaining 49 patients (40%) developed PES high affinity for cranial nerve nuclei, the cells
lasting for 3–18 months. In 15/49 patients of the anterior horn of the spinal cord, the
(12%) PES was severe. The main characteris- Purkinje cells in the cerebellum, and cellular
tics of PES were psychiatric symptoms, components of the thalamus. Clinical
balance and movement disorders, headache, improvements achieved in patients with
general malaise, and reduced working paresis are linked to physical exercise
41
ability. Kaiser et al. followed patients with increasing the muscular strength of
meningoencephalomyelitis for 10 years. 41,43,73 neighboring muscle groups and, to a lesser
There were 57 patients with complete follow- extent, to learning effects in the context of
up data, of whom 19% recovered, 51% had neuronal plasticity. However, if cellular
moderate/severe sequelae, and 30% died. The damage is multisegmental, the resulting
most substantial improvements were seen in neuronal muscle atrophy has little or no
the first 12 months after acute TBE. These chance for regeneration (Photo 4).
follow-up results indicate that the chance for

clinical improvement reaches a maximum in
the first 12 months after acute TBE and Treatment
decreases substantially after the first 3 years.
The severity of acute TBE correlates with long- Treatment is mainly supportive and
term prognosis. Patients who died during the symptomatic. No specific antiviral therapy is
10-year follow-up had a significantly higher
currently available and approved for TBEV
deficit sum than those who survived. By
infections. Some antiviral agents, specific
contrast, patients with complete recovery immunoglobulins, and other potentially
within 5 years had the lowest initial deficit protective substances are under investigation
measured in a standardized scoring system. for their anti-TBEV efficacy in vitro and
Mechanical ventilation was required in 30 77–80
clinically ; however, a detailed review of
patients with TBE in the acute phase of the
these ‘pipeline’ agents is beyond the scope of
disease–14 patients died during the follow-up this chapter. If there are clinical signs and
period (7 within the first year). Respiratory symptoms such as status epilepticus, severe
symptoms resolved completely in 14 patients meningoencephalitis, encephalitis, and
with TBE. Overall, there is a correlation of
myelitis, the patient should be admitted to an
disease severity and prognosis. Patients with
NICU (neurological intensive care unit) for
ataxia, impaired consciousness, double vision, further monitoring and treatment. In a large
urinary retention, or mild paresis of only 1 study of 709 patients with TBE in Germany,
extremity had the best prognosis. However,
12% of patients required intensive care and
TBE patients with tetraparesis and concurrent 43
5% required assisted ventilation. Mainte-
respiratory paralysis, dysphagia, or dysarthria nance of an adequate cerebral perfusion and
were among those with the highest risk for a prevention of secondary complications are the
fatal outcome. main objectives of treatment. Correct position
-ing, deep analgosedation, and osmotherapy
Post-mortem examinations of deceased TBE
(mannitol, hypertonic saline) can be consider-
patients and animal studies provided some ed, but only for 1–2 days and provided
explanations and insights into the neuro- exclusively as boluses. However, the use of
pathological mechanisms of the disease. 75,76
mannitol did not affect the outcome in terms
Viral infection of neurons causes cell lysis.
of survival. In the case of an increasing

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