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LETTER TO THE EDITOR
Dementia and Neurocognitive Disorders 2023: 22: 2: 81-83

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Post COVID-19 Vaccination Encephalitis as a Cause of Subacute Progressive Dementia: A Case Report and Literature Review
Heui-Seop Jung, Yun Jeong Hong , Seong Hoon Kim, Yun Sang Oh, Si Baek Lee, Myung Ah Lee, Jeong Wook Park
Department of Neurology, Uijeongbu St. Mary’s Hospital, The Catholic University of Korea, Seoul, Korea
Post COVID-19 Vaccination Encephalitis as a Cause of Subacute Progressive Dementia: A Case Report and Literature Review
Heui-Seop Jung, Yun Jeong Hong , Seong Hoon Kim, Yun Sang Oh, Si Baek Lee, Myung Ah Lee, Jeong Wook Park
Department of Neurology, Uijeongbu St. Mary’s Hospital, The Catholic University of Korea, Seoul, Korea
The coronavirus disease 2019 (COVID-19) pandemic has caused more than 500 million
infected cases, causing a new public health crisis.1
Many people are vaccinated against
COVID-19 to prevent infection and bring an end to the pandemic. However, various
complications have been reported.1,2
Autoimmune encephalitis is a progressive
encephalopathy that can develop rapidly (usually in less than 6 weeks) caused by brain
inflammation.3
In this case report, we present a rare case of a 59-year-old woman who
visited an outpatient clinic because of subacute onset cognitive decline. She was diagnosed
with post COVID-19 vaccination encephalitis. We observed 1-year cognitive outcomes and
neuroimaging changes of the patient. Clinical, neuroimaging, and cerebrospinal fluid (CSF)
findings of the patient are described below.
A 59-year-old woman visited our outpatient clinic due to subacute cognitive impairments and
abnormal behaviors for 3 weeks. She had diabetes mellitus, hypertension, hyperlipidemia, and
hypothyroidism on stable medications. She had received the second COVID-19 vaccination
(BNT162b2, BioNTech and Pfizer). She suffered from generalized weakness and mild frontal
headache without any other symptoms such as nausea or fever. At one month after the
vaccination, she showed memory impairments and disorientation and started to get lost in
familiar places. Her younger sister reported that the patient had inappropriate self-talking and
aggressive behaviors. These symptoms were progressive for a few weeks. However, they had
become stationary before the admission. On admission, physical examination and vital signs
were normal. On neuropsychological tests, the Mini-Mental State Examination (MMSE) score
was 13 (7 years of education) and the clinical dementia rating (CDR) score was 2, suggesting
moderate to severe dementia. She showed cognitive impairments in naming, verbal and visual
memory encoding, visuospatial, and frontal executive functions (Table 1). Brain magnetic
resonance (MR) imaging revealed high signal intensities in left anterior & medial temporal lobe
in fluid attenuated inversion recovery imaging with gyral enhancements in T1-weighted contrast
enhancement (Fig. 1). MR angiography showed no large vessel stenosis. On CSF examination,
total protein was slightly increased to 47.3 mg/dL, while other findings (1 WBC/mm3
, 0 RBC/
mm3
) were normal. CSF cytology, antibodies for autoimmune encephalitis, infection markers
(including viral markers), and serologic paraneoplastic antibodies were unremarkable. An
electroencephalography also showed normal findings. Considering her stable course and
refusal to an intravenous steroid therapy, the patient received conservative treatment without
any immunosuppressive agents. Her symptoms were stable during admission.
Her cognitive function was improved to mild to moderate dementia (MMSE 14, CDR 1 [sum
of boxes: 6]) at 3 months after discharge (Table 1). According to her sister, she could perform
everyday housework independently without any help and go out to meet other people just
before re-admission due to a pontine infarction after 16 months. At the re-admission, left
temporal lesions disappeared and became atrophic (Fig. 1).
Our patient visited a hospital due to cognitive decline. She was diagnosed as encephalitis.
On laboratory tests, there was no positive result in autoimmune antibody markers or
plausible provoking event/signs suggesting central nervous system (CNS) infection. Thus, we
assumed that her encephalitis might be induced by COVID-19 vaccination. Our case fulfilled
the criteria for possible autoimmune encephalitis suggested by Graus et al.3
Autoimmune
encephalitis might be associated with antibodies against neuronal cell surface or synaptic
proteins. It can develop with symptoms resembling infectious encephalitis. It can also
show neurological and psychiatric manifestations without fever or CSF pleocytosis.3
After
vaccination, antigens are recognized as potential pathogens and activate circulating immune
cells. Peripheral proinflammatory cytokines expressed after vaccination are important
because they might partly cause neuroinflammatory reactions by microglial activation.4
These processes exhibit cognitive impairments of autoimmune encephalitis.4
The incidence
of post-vaccination encephalitis associated with Pfizer-BioNTech mRNA vaccine has been
reported to be 2 per 10 million doses of vaccinations. Complications due to such encephalitis
are very rare.4
The Pfizer vaccine is based on mRNA. Although there are a variety of CNS
symptoms, cognitive impairments are easily underdiagnosed due to its non-specificity.1,2,4,5
Our case report has a few limitations in that we cannot prove a cause-and-effect relationships
between the vaccine and encephalitis. Because vaccination-induced encephalitis is
considered a reversible cause of dementia, her remnant cognitive declines after 1 year should
be re-evaluated further due to a possibility of underlying neurodegenerative disorders.
In summary, we report a rare case of vaccination induced encephalitis in a patient presented
with dementia. Thus, we should carefully examine and undergo history takings for elderly
patients with cognitive impairments to exclude reversible causes. Clinicians should consider
autoimmune encephalitis as a possible diagnosis when assessing post-vaccination neurologic
symptoms and subacute dementia.
Key Words:
대한치매학회지 (Dementia and Neurocognitive Disorders)