Distinct Clinical Implications of Patient- Versus Clinician-Rated Motor Symptoms in Parkinson's Disease.

BACKGROUND: Patient-rated motor symptoms (PRMS) and clinician-rated motor symptoms (CRMS) often differ in Parkinson's disease (PD). OBJECTIVE: Our goal was to investigate the determinants and clinical implications of PRMS compared with CRMS in PD. METHODS: This retrospective, observational cohort study analyzed the cross-sectional associations and longitudinal impacts of PRMS as assessed by the Movement Disorders Society-sponsored Unified PD Rating Scale (MDS-UPDRS) part 2, while controlling for CRMS measured by MDS-UPDRS part 3. Longitudinal analyses used Cox proportional hazards models and multiple linear mixed-effects random intercepts/slope models, adjusting for many clinical predictors. We conducted propensity score matching (PSM) to reinforce our analyses' robustness and surface-based morphometry to investigate neural correlates. RESULTS: We enrolled 442 patients with early-stage PD. At baseline, regardless of CRMS, PRMS were associated with the severity of postural instability and gait disturbance (PIGD). Notably, PRMS independently and more accurately predicted faster long-term deterioration in motor function than CRMS (Hoehn and Yahr 4, adjusted hazard ratio per +1 point = 1.19 [95% confidence intervals, 1.08-1.32]), particularly in PIGD (PIGD subscore, ß-interaction = 0.052 [95% confidence intervals, 0.018-0.086]). PSM confirmed these findings' robustness. Surface-based morphometry suggested that enhanced sensory processing was distinctively associated with PRMS. CONCLUSIONS: In early-stage PD, PRMS weighed different aspects of symptoms and more effectively predicted motor deterioration compared to CRMS, with distinctive brain structural characteristics. The superior sensitivity of PRMS to subtle declines in drug-refractory symptoms like PIGD likely underlie our results, highlighting the importance of understanding the differential clinical implications of PRMS to prevent long-term motor deterioration. © 2024 The Author(s). Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.

Postoperative cerebral air embolism with delayed abnormal brain MRI findings.

Cerebral air embolism (CAE) is a rare but well-known complication resulting from invasive medical procedures; however, previous studies have not examined the postoperative longitudinal MRI changes in CAE. In particular, the likelihood that such changes may be observed after an initial delay when using magnetic resonance imaging (MRI) has not been explored. We herein report a case of CAE with no MRI abnormalities 4 h after a pulmonary vein isolation (PVI) procedure and where the first abnormality was found 22 h after the procedure. A 65-year-old man underwent PVI for paroxysmal atrial fibrillation and showed no signs of recovery from anesthesia after the procedure; thus, he was transferred to our emergency department for further examination. Neurological examination revealed conjugate eye deviation to the right and quadriplegia. Although initial computed tomography (CT) and MRI revealed no abnormalities, CAE was suspected, and a high-concentration oxygen treatment was administered. MRI performed 22 h after the procedure revealed restricted diffusion affecting the cortical areas. At the same day, he was transferred for hyperbaric­oxygen chamber treatment. After 7 days of treatment, the patient recovered clinically and neurologically. He regained consciousness and was able to communicate. As suggested by this case, CT and MRI findings may fail to reveal CAE abnormalities initially. In such cases, as urgent treatment is necessary, it is important to consider diagnosing CAE based on the patient's history and administering a high concentration of oxygen. Finally, to reach a correct diagnosis, repeated brain MRI should be considered for patients with suspected CAE.

A Case of Invasive Aspergillus Rhinosinusitis Presenting with Unilateral Visual Loss and Subsequently Associated with Meningitis, Subarachnoid Hemorrhage, and Cerebral Infarction.

Visual impairment can occur because of several mechanisms, including optic nerve disease and occasionally fungal sinusitis. An 87-year-old man presented with the loss of right visual acuity; he was diagnosed with optic neuritis. Steroid pulse therapy was not effective. One month later, he became unconscious because of meningitis, following which treatment with ceftriaxone and acyclovir was initiated. However, his consciousness deteriorated because of a subarachnoid hemorrhage caused by a ruptured aneurysm. Meningitis and vascular invasion caused by fungal rhinosinusitis were suspected, and the sinus mucosa was biopsied. He was pathologically diagnosed with invasive Aspergillus rhinosinusitis. Despite continuous liposomal amphotericin B administration, he died of cerebral infarction, following a right internal carotid artery occlusion. It is important to consider the possibility of Aspergillus as an etiological agent, especially when cerebrovascular events are associated with visual impairment.