Influenza viruses are important human pathogens that often cause respiratory tract infections, while neurological complications are rare.1 Secondary Parkinsonism following viral infections usually occur several years after encephalitis, but rarely during the acute encephalitic phase.2 A range of viruses are associated with acute and chronic Parkinsonism, such as the influenza virus, coxsackievirus, and human immunodeficiency virus (HIV).2 To our knowledge, Parkinsonism resulting from the influenza B virus has never been reported. Here, we describe an unusual encephalitis case, in which acute reversible Parkinsonism occurred when a influenza B virus infection affected the bilateral basal ganglia.
An unemployed 50‐year‐old man was admitted to our hospital complaining of progressively slower movement and a gait disturbance for half a month. Three weeks prior, he initially had a 38°C fever, sore throat, cough, and expectoration. A nasopharyngeal swab tested in another hospital showed the antigen and nucleic acid of the influenza B virus were positive. As the diagnosis was flu, anti‐infective drugs were used, including oseltamivir and cefuroxime. His symptoms were in remission one week later, but he developed progressively slower movement and a gait dysfunction. After being admitted to our hospital, he felt fatigued and was dull in response, being unable to do simple arithmetic. A neurological examination showed generalized bradykinesia (Video S1), and an intermittent resting tremor of the bilateral upper limbs was noted, as well as hypomimia. The modified Medical Research Council score for muscle strength was grade 4+ in all limbs. He had a history of kidney transplantation for 6 years, with immunosuppressant treatment with enteric‐coated mycophenolate sodium and tacrolimus. And he denied hypoxia and toxin exposure history. The patient explicitly agreed to his inclusion in this case report and gave written informed consent for publication.
Serological tests including full blood counts, blood glucose, thyroid function, liver and renal function, and tumor markers did not show any abnormity. Metabolic as well as endocrine dysfunctions were ruled out as the primary causes. A lumbar puncture was performed on the second day after admission, which found cerebrospinal fluid (CSF) pressure was normal (15 cm H2O), but an elevated protein concentration of 48.2 mg/dL was detected. Tests for antibodies mediating autoimmune encephalitis (anti‐NMDAR, ‐AMPAR, ‐LGI1, ‐CASPR2, ‐GABABR, ‐DPPX, ‐IgLON5, ‐GAD65) in CSF and paraneoplastic syndromes (anti‐Hu, ‐Yo, ‐Ri, ‐CV2, ‐PNMA2, ‐Amphiphysin) in serum were all negative. The test for influenza B viral RNA from the CSF was negative. Brain magnetic resonance imaging (MRI) revealed hypointensity in the bilateral caudate head and putamen on T1‐weighted sequences (Figure 1A) and hyperintensity on T2‐weighted sequences (Figure 1B) and fluid‐attenuated inversion recovery sequences (Figure 1C).