Recent studies have demonstrated that atypical parkinsonism can be presented in autoimmune encephalitis and paraneoplastic neurological syndromes. However, it is unclear which anti-neural antibodies are involved and when these diseases should be suspected. To address these clinical questions, we conducted a scoping review and analyzed 38 articles. The literature shows that many anti-neural antibodies, including unknown ones, have been reported in progressive supranuclear palsy, corticobasal syndrome, and multiple system atrophy. Moreover, the following symptoms and signs suggest the possibility of autoimmune encephalitis and paraneoplastic neurological syndromes: early onset, acute or subacute progression, the presence of a neoplasm, significant weight loss, abnormal cerebrospinal fluid findings, the absence of typical brain magnetic resonance imaging findings, and the existence of atypical physical examination signs.

A 72-year-old male developed neurological symptoms such as difficulty in charging his electronic money card and making his mobile-phone call ten months before admission. On admission, neurological examination revealed extensive higher brain dysfunction such as impairment in recent memory, executive function disorders, constructional disturbance, agraphia and acalculia. Brain MRI revealed a low intensity lesion on the surface of the cerebral cortex diffusely and symmetrically on T₂*-weighted images. MRI images are consistent with superficial siderosis. However, the lack of hemosiderin deposition in the brain stem and cerebellar hemisphere was atypical of the classical type of superficial siderosis. ¹²³I-IMP-SPECT revealed hypoperfusion dominantly in the left hemisphere, particularly in the left frontal and parietal lobes. According to the Boston criteria, the patient with the cerebral microbleeds and cortical superficial siderosis was diagnosed with probable CAA (cerebral amyloid angiopathy).

An 83-year-old man presented with visual disturbance and right hemiparalysis, one month after daratumumab, bortezomib, and dexamethasone administration for multiple myeloma (MM). Blood screens revealed a CD4+ T-lymphocyte count of 132/μl. Diffusion weighted and fluid-attenuated inversion-recovery MR imaging showed high intensity signals in the both occipital lobes and left precentral area. The patient had no history of human immunodeficiency virus infection. Cerebrospinal fluid (CSF) JC virus (JCV) was positive (83 copies/ml), as indicated by PCR. The patient was diagnosed with progressive multifocal leukoencephalopathy (PML). MM treatment was discontinued, and mefloquine and mirtazapine therapy was started. However, the CSF JCV-DNA PCR count did not improve (111 copies/ml) after 30 days from starting mefloquine and mirtazapine therapy. The patient died six months after symptom onset. Conclusively, patients with decreased CD4+ T lymphocyte counts following DBd therapy for MM, the possibility of PML should be considered.

The patient is an 18-year-old female. She had a history of acute disseminated encephalomyelitis at the age of 6 and 7. She visited our hospital due to acute disturbance of consciousness, quadriplegia, and numbness of left upper and lower extremities. Brain MRI showed multiple DWI/FLAIR high-signal lesions in the bilateral cerebral hemispheres, cerebellum, and brainstem. Qualitative test indicated that serum anti-MOG antibodies was positive, and she was diagnosed with anti-MOG antibody-positive polyphasic disseminated encephalomyelitis. Intravenous mPSL pulse therapy was performed twice, but the symptoms worsened. As a second line treatment, plasma exchange was started. However, she developed transfusion related acute lung injury. Alternatively, she was treated with immunoadsorption plasmapheresis. Her symptoms were significantly improved. This case seems to be valuable because there are few reports showing effectiveness of immunoadsorption therapy on anti-MOG antibody-related diseases, especially for polyphasic disseminated encephalomyelitis.

We describe a case of behavioral variant frontotemporal dementia (bvFTD) presenting with frequent laughter during conversations. A 72-year-old male patient visited our hospital because of aspontaneity and abnormal behaviors. His medical history revealed epilepsy attacks approximately five years prior, which improved following administration of antiepileptic drugs. At the age of 67 years, the patient began exhibiting aspontaneity and abnormal behaviors, such as leaving a teahouse without paying for his coffee. Neurological examinations indicated moderate dementia and bradykinesia while walking. The patient frequently laughed during conversations with his wife and doctor, creating the impression that he was euphoric. His laughter was neither explosive nor obsessive, and did not involve loss of consciousness or seizures. MRI of the head revealed symmetrical atrophy of the bilateral frontal lobes. SPECT demonstrated decreased cerebral blood flow in the bilateral frontal lobes, particularly in the outer and inner frontal convexities. Based on the patient’s clinical history and imaging results, a diagnosis of bvFTD was established. Our literature review identified only one research paper discussing the frequency of laughter in frontotemporal dementia, which suggested that patients with bvFTD laugh less often. However, several reports indicated that patients with FTD exhibit euphoric behaviors more frequently compared to those with other forms of dementia. We hypothesize that euphoric patients with bvFTD may laugh more frequently during conversations, reflecting disorders of emotional expression and a loss of empathy.

Microbial tests are essential for appropriate management for acute meningitis and encephalitis, but it often takes several days to identify the results of culture tests or PCR. BioFire FilmArray^® meningitis/encephalitis panel (ME panel) is a rapid multiplex PCR assay that targets 14 bacteria, viruses, and yeast in 1 hour. In this single-center retrospective study, we reviewed adult patients who underwent ME panel test in parallel with conventional microbial tests from January to August 2021. Eighteen of 70 patients (26%) tested positive by ME panel, of which 8 patients (11%) were helpful in altering treatment strategy. Fifty-two patients (74%) could stop empirical treatment such as acyclovir or antibiotics due to negative results on ME panel. All results of ME panel were same as traditional assays. Use of ME panel can contribute to early diagnosis and treatment.

Among the abnormal kyudo movements (“yips”), “motare” is the inability to release the arrow at the intended timing if aiming the target. We hypothesized that “motare” is a task-specific focal dystonia (TSFD). We interviewed three participants with “motare,” three participants with “hayake”, and three controls without “motare” nor “hayake”. Moreover, we conducted a surface electromyography (sEMG) examination and found that “motare” was characterized by stereotypy, sensory tricks, and morning benefit; however, these findings were not observed in “hayake”. Abnormal co-contraction of the upper extremity antagonist muscles was observed in one of the three “motare” participants. Overall, these findings suggest that “motare” have the characteristics of TSFD not previously reported.