Parkinson’s disease (PD) has undergone significant advancements in diagnosis and treatment over the past century, with apparent dopaminergic cell degeneration on dopamine transporter scans and a strong response to medication being key features. However, the etiology remains complex, involving various pathogenic mechanisms beyond alpha-synuclein accumulation. The recent brain-first versus body-first hypothesis, emerging from advances in functional imaging and clinical symptom clustering, suggests distinct starting points of alpha-synuclein pathology-either in the brain or the body, with subsequent spread via neural connections. This theory, exemplified by the alpha-synuclein origin site and connectome (SOC) model, proposes that body-first PD may originate in the enteric nervous system and spread to the brain, while brain-first PD starts within the central nervous system, such as the olfactory bulb or amygdala. While the SOC model offers valuable insights into the progression of PD, it raises several controversies. Critics argue that the model may oversimplify the disease’s complexity, failing to account for overlapping symptoms and the varying progression rates observed in different subtypes. Furthermore, there are concerns about the lack of longitudinal data and the potential for reclassification of PD subtypes over time. Despite these challenges, the ongoing development of imaging techniques that reflect in-vivo pathology holds promise for resolving these controversies and advancing the selection of patients for disease-modifying therapies.

Background
The premotor cortex plays a role in the planning of movement. Previous transcranial magnetic stimulation (TMS) studies have shown ipsilateral premotor-to-motor inhibition in healthy subjects at rest. Moreover, this premotor-to-motor inhibition has been found to be modulated during preparation for movement, such as precision grip and whole hand grasp. Cooperation between the bilateral ventral premotor cortices may play a functional role. We aimed to investigate the influence of the contralateral on the ipsilateral ventral premotor cortex.
Methods
Fourteen right-handed healthy subjects (six women and eight men; mean age, 37 years; standard deviation, 14 years) completed the study. We used a three single-pulse TMS paradigm (preconditioning, conditioning and test pulse) to sequentially stimulate the right ventral premotor cortex, left ventral premotor cortex and left primary motor cortex.
Results
We found that in healthy subjects at rest, stimulating the contralateral ventral premotor cortex resulted in reversal of the resting premotor-to-motor inhibition.
Conclusions
Our results suggest that the contralateral ventral premotor cortex exerts an inhibitory influence on the ipsilateral ventral premotor cortex, which may be a component of bi-hemispheric control of manual tasks. This is the first study to evaluate the functional connectivity between the bilateral ventral premotor cortices.

Rituximab (RTX) is a monoclonal antibody that targets CD20 on B cells and is used to reduce the relapse risk in neuromyelitis optica spectrum disorder (NMOSD). Some patients experience relapse or exacerbation shortly after RTX treatment. We report a 54-year-old female with seronegative NMOSD who relapsed soon after RTX treatment.

Complete surgical resection is a well-known therapeutic gold standard for spinal ependymoma, but it is associated with high postoperative morbidity. Intraoperative neuromonitoring (INM) is important for detecting and reducing the rate of surgical complications during this operative procedure. We report a case of postoperative paraplegia due to tumor bleeding during the operation. INM of the patient revealed abrupt loss of waveforms during the operation. This finding suggested that INM is helpful for detecting intraoperative hematomyelia and minimizing postoperative neurologic sequelae.

Excessive daytime sleepiness (EDS), with or without an excessive need for sleep, is a primary reason for patients seeking consultation at the sleep unit. EDS is observed in ~5% of the general population. Common causes of EDS include obstructive sleep apnea, sleep deprivation, effects of medication, psychiatric disease (especially depression), and circadian rhythm disorders. Coronavirus disease 2019 (COVID-19) infection is a rare cause of EDS. We present a case of mild COVID-19 infection as an unusual cause of hypersomnolence.