A 38-year-old man was admitted to the hospital in Bialystok, Poland, because of fever (40 C), headache, vomiting, and drowsiness that had lasted for 1 week. The patient was a forest worker who reported frequent tick bites; for religious reasons, he had not been vaccinated against TBE. Physical examination revealed palsy in the seventh facial nerve, tremor in the facial muscles on the left side, muscle weakness in the left upper and lower limbs, and positive meningeal signs. Testing of cerebrospinal fluid (CSF) revealed inflammatory features (cytosis, 63 cells/microL, and protein concentration 68 mg/dL). Immunologic test results showed CSF IgM of 9.04 IU/mL and IgG of 55.1 IU/mL against TBE virus (cutoff 1.4 for IgM, 7.0 for IgG). Computed tomography scan and magnetic resonance imaging (MRI) of the brain revealed widening of ventricles. The patient was treated with mannitol, dexamethasone, third-generation cephalosporin, and diazepam; after signs and symptoms improved, the patient was discharged home on his request.
Eleven days after discharge, the patient was readmitted to the hospital because of deteriorating clinical signs (progressive muscle weakness and excessive tremor of the left-side limbs). Intensive propulsion, involuntary muscle movements (limbs and face), muscle weakness of left upper and lower limbs, and "walk dance" were observed (Video). Results of CSF analysis showed continued inflammatory features (pleocytosis, 64 cells/microL, and protein concentration 119.4 mg/dL). Results of testing for antibodies against TBE virus in CSF and serum were strongly positive (CSF IgM >14 U/mL, IgG 107 U/mL; serum IgM 7.92 U/mL, IgG 87.6 U/mL). Test results for Borrelia burgdorferi were negative 3 times. MRI of the brain showed lesions in the lenticular nucleus, caudate nucleus on the right side, and internal capsules of both sides (Figure). 
After neurologic and psychiatric consultations, chorea in the course of TBE was diagnosed. The patient was treated with haloperidol, dexamethasone, pentoxifylline, nitrazepam, and midazolam, and his signs and symptoms improved.
One month later, follow-up testing and examination were performed. No abnormalities on physical examination or laboratory test results were observed except pleocytosis in CSF (35 cells/microL). The patient reported aphasia and deterioration of memory. Six months later, results of CSF testing were within normal limits, and repeat MRI showed resolution of inflammatory lesions.
In this case, chorea occurred in the course of TBE. The neurologic phase of TBE was not preceded by the expected first-phase signs and symptoms. The diagnosis was confirmed with serologic test results, which were strongly positive in serum and CSF, and virus neutralization testing performed as described in Stiasny et al. showed a strongly positive titer of 1:320. We excluded hepatitis C virus; West Nile virus infection has not been reported in Poland. Because of his religious beliefs, the patient had not been vaccinated against TBE or yellow fever; he had not traveled abroad and had not been exposed to dengue virus. The differential diagnosis included Lyme disease, but the results of repeated serologic tests for B. burgdorferi were negative.
Chorea arises deep in the basal ganglia; high-definition MRI demonstrates caudate atrophy . In patients with TBE, MRI may reveal unilateral or bilateral thalamus lesions, as well as lesions in the cerebellum, brainstem, and nucleus caudalis . One case study presented a case of simultaneous lesions in the thalamus, stem, and spinal cord . Chorea developed in the patient reported here because of inflammatory lesions in the region of the thalamus. Supportive care is standard for patients with chorea, but after treatment for TBE, the lesions in this patient resolved, and the chorea abated.