Memon, Raima

Ectopic liver is a rare congenital anomaly characterized by the presence of liver tissue outside the normal liver without any direct connection to it. These lesions are usually detected incidentally during clinical evaluation for other issues. However, they sometimes mimic neoplastic lesions both clinically and radiologically, which poses diagnostic challenges. Here, we present 5 patients with ectopic liver, 4 of which mimicked neoplastic lesions. The first was a 54-year-old woman diagnosed with multiple liver lesions and an enlarged gastro-hepatic lymph node, suspected to be a primary hepatic neoplasm with metastasis. Upon resection, it was found to be a hepatocellular adenoma in the liver and intraabdominal ectopic liver tissue with a small hepatocellular adenoma. Patient 2 was a 36-year-old woman presenting with palpitations and shortness of breath. An echocardiogram revealed a right atrial mass, which was identified as ectopic liver upon microscopic examination. The third patient was a 57-year-old woman with intermittent abdominal pain who underwent cholecystectomy. Microscopy revealed ectopic liver tissue on the gallbladder's serosal surface, along with chronic cholecystitis. The fourth was a 36-year-old woman with a gallbladder polyp, which on microscopy revealed ectopic liver tissue with no other abnormalities in the gallbladder. The fifth patient was a 57-year-old woman presenting with shortness of breath, weakness, and right atrial mass, which was confirmed as ectopic liver. These patients illustrate varied presentations of ectopic liver, sometimes mimicking neoplasia. Hepatocellular adenomas arising in ectopic liver and ectopic liver in intracardiac locations are extremely rare and can be a diagnostic pitfall, as they can clinically, radiologically, and pathologically mimic serious conditions like neoplasia.

Background: Sleep disorders are common in Parkinson’s disease (PD) and include alterations in sleep-related EEG oscillations. Objective: This case-control study tested the hypothesis that patients with PD would have a lower density of Scalp-Slow Wave (SW) oscillations and higher slow-to-fast frequencies ratio in rapid eye movement (REM) sleep than non-PD controls. Other sleep-related quantitative EEG (qEEG) features were also examined, including SW morphology, sleep spindles, and Scalp-SW spindle phase-amplitude coupling. Methods: Polysomnography (PSG)-derived sleep EEG was compared between PD participants ( n = 56) and non-PD controls ( n = 30). Following artifact rejection, sleep qEEG analysis was performed in frontal and central leads. Measures included SW density and morphological features of SW and sleep spindles, SW-spindle phase-amplitude coupling, and spectral power analysis in Non-REM (NREM) and REM. Differences in qEEG features between PD and non-PD controls were compared using two-tailed Welch’s t-tests, and correction for multiple comparisons was performed per the Benjamini-Hochberg method. Results: SW density was lower in PD than in non-PD controls (F = 13.5, p’ = 0.003). The PD group also exhibited higher ratio of slow REM EEG frequencies (F = 4.23, p’ = 0.013), higher slow spindle peak frequency (F = 24.7, p’ < 0.002), and greater SW-spindle coupling angle distribution non-uniformity (strength) (F = 7.30, p’ = 0.034). Conclusion: This study comprehensively evaluates sleep qEEG including SW-spindle phase amplitude coupling in PD compared to non-PD controls. These findings provide novel insights into how neurodegenerative disease disrupts electrophysiological sleep rhythms. Considering the role of sleep oscillatory activity on neural plasticity, future studies should investigate the influence of these qEEG markers on cognition in PD.