How does tick‑borne encephalitis present? - briefly
Initially patients develop a nonspecific febrile illness with headache, malaise and muscle aches lasting 3–7 days. In a subset, a second stage appears with meningitic or encephalitic signs—neck rigidity, altered consciousness, seizures, and focal neurological deficits.
How does tick‑borne encephalitis present? - in detail
Tick‑borne encephalitis (TBE) typically follows a biphasic course. After an incubation period of 7–14 days, the first phase presents with nonspecific, flu‑like symptoms: fever, headache, malaise, myalgia, and occasionally gastrointestinal upset. This stage lasts 2–7 days and may resolve spontaneously, leading some patients to believe the illness has ended.
A short asymptomatic interval (often 1–5 days) precedes the second phase, during which central nervous system involvement becomes evident. Clinical manifestations vary according to the predominant neuro‑anatomical region affected:
- Meningitis: Neck stiffness, photophobia, severe headache, and positive meningeal signs. Cerebrospinal fluid shows lymphocytic pleocytosis, elevated protein, and normal or slightly reduced glucose.
- Encephalitis: Altered mental status, confusion, lethargy, agitation, or coma. Focal neurological deficits may appear, such as aphasia, hemiparesis, or ataxia.
- Cerebellar involvement: Truncal instability, dysmetria, intention tremor, and gait disturbance. Patients may experience dysarthria and nystagmus.
- Myelitis or poliomyelitis‑like syndrome: Acute flaccid paralysis, often asymmetric, with reduced reflexes and muscle weakness. Sensory loss is uncommon.
- Seizures: Generalized or focal seizures may occur, particularly in severe encephalitic forms.
Severity correlates with age; individuals over 50 years frequently develop more pronounced encephalitic or cerebellar signs and have higher rates of long‑term sequelae, such as persistent cognitive deficits, motor impairment, or chronic fatigue.
Diagnostic clues include a recent tick bite or exposure in endemic regions, a biphasic pattern, and positive serology for TBE virus IgM/IgG. Magnetic resonance imaging may reveal hyperintense lesions in the thalamus, basal ganglia, brainstem, or cerebellum, supporting the clinical picture.
Prognosis depends on the neurological subtype and patient age. Meningitic presentations often resolve without residual deficits, whereas encephalitic and cerebellar forms carry a risk of lasting impairment. Early recognition of the second phase is essential for supportive care and monitoring of complications.