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The main symptoms of Epstein–Barr virus encephalitis (EBV) encephalitis are fever, seizure, bizarre behaviour, headache, and metamorphosia.1 Bradykinesia, akathisia, involuntary hand movements, drooling, and torticollis are symptoms of Parkinson-like syndrome, which has never been described as a manifestation of EBV encephalitis. We report the case of a previously healthy boy who presented with Parkinson-like syndrome as the major symptom of EBV encephalitis.
A 12 year old, previously healthy boy was referred to our hospital because of severe cough with sputum and intermittent fever for seven days. Abdominal discomfort and vomiting were also noted one day before admission. On admission, his consciousness was clear with no focal neurological sign, no hepatosplenomegaly, no lymphoadenopathy, and no exudative tonsillitis or skin rash. There was no previous personal or family history of seizure disorder or migraine, and both the boy and his family denied being exposed to some possible hallucinogenic or neuroleptic drug. Blood analysis was normal except for a mild leucocytosis with a left shift (10 500/mm3; 84.6% neutrophils), and there were no atypical lymphocytes. C reactive protein (CRP) level was 0.17 mg/dl (normal <0.3 mg/dl).
After admission, mucolytic agents and bronchodilators were prescribed. Fever, abdominal discomfort, and vomiting subsided soon. Twenty four hours after admission, his condition deteriorated with drowsiness, involuntary rhythmic finger tapping movement, resting tremor, bradykinesia, photophobia, and staring eyes. But perceptual distortion was not noted. Cerebrospinal fluid (CSF) examination yielded yellow, clear fluid and normal opening pressure without microorganisms on Gram stain or culture. The cell count, protein, and sugar of CSF were all within normal limits. Table 1 lists laboratory evaluations for EBV and other possible pathogens of encephalitis. Brain magnetic resonance imaging (MRI) showed no abnormalities. Tc-99m HMPAO brain SPECT (Tc-99m hexamethylpropyleneamine oxime single photon emission tomography) showed diminished perfusion in the region of the right caudate nucleus . Electroencephalography (EEG) revealed diffuse slowing of background activity. His signs and symptoms showed gradual improvement under close observation in the following three weeks. He was then discharged in a stable condition. Follow up four months later showed no residual neurological sequelae.
Parkinson-like syndrome (extrapyramidal symptoms) is characterised by various neurological symptoms including akathisia, bradykinesia, torticollis, drooling, and involuntary hand movement. This syndrome develops in at least a quarter of children treated with neuroleptics due to disruption of the balance between the dopaminergic system and the cholinergic system within the basal ganglia. But Parkinson-like syndrome has also been recognised as a sequela of acute viral encephalitis, including coxsackie B, cytomegalovirus, measles, herpes simplex virus, Japanese B encephalitis virus, and encephalitis lethargica. Mycoplasma pneumoniae infection has also been recognised as a cause of Parkinson-like syndrome.2 In our patient, exposure to possible hallucinogenic or neuroleptic drugs was denied. Serological tests and culture for other possible pathogens were negative. EBV encephalitis was diagnosed by serological and CSF polymerase chain reaction findings which fulfilled the diagnostic criteria.
EBV encephalitis is generally considered to be a benign, self limited disease associated with few sequelae. However, an incidence of neurological sequelae after EBV encephalitis as high as 36% was reported by Domachowske and colleagues.3 The present case, therefore, not only draws attention to the role of EBV in infectious neurological disorders, but also suggests that an EBV aetiology should be considered in cases of Parkinson-like syndrome in childhood.