Inguinal Hernia in Premature Infants: To Operate Before or After Discharge from Hospital?

INTRODUCTION: This study aims to find out the optimal timing for herniotomy for premature infants with inguinal hernia (IH): early during hospitalisation or delayed after hospital discharge. METHOD: A retrospective cohort study was conducted on premature infants diagnosed with IH during their initial hospitalization between 2015 and 2020. Demographic data and clinical outcomes were compared between infants undergoing herniotomy before discharge ("early") and those who were discharged without herniotomy ("delayed"). Student's t-test or Mann-Whitney U test and Fisher's exact test were used for statistical analysis. RESULTS: Of 219 premature infants, 189 (86.3%) underwent early herniotomy, while 30 were discharged with unoperated IH. In the delayed group, 15 (50%) underwent planned delayed herniotomy, and the remaining 15 experienced spontaneous resolution (absence of inguinal bulge over at least 1-year follow-up). The gestational age and birth weight of both groups were similar. At surgery, the delayed group median (interquartile range) was significantly older (42.1[38-49] vs 37.7 [36-40] weeks, p < 0.001) and heavier (3.27 [2.21-4.60] vs 2.22 [2.00-2.70] kg, p < 0.001). Two infants (1%) in the early group presented with incarcerated IH requiring urgent operation. In the delayed group, no infant developed incarcerated IH while awaiting elective operation (time from diagnosis to operation 44 [21-85] days). There was no statistically significant difference in respiratory and surgical complications between the two groups, although the delayed group had lesser surgical complications (0% vs 9.5%). CONCLUSION: Deferring herniotomy after discharge for premature infants is safe with close monitoring and associated with a chance of spontaneous resolution. LEVEL OF EVIDENCE: Level III, treatment study.

The Longitudinal Impact of Excessive Daytime Somnolence on Motor and Nonmotor Symptoms of Parkinson's Disease in a Southeast Asian Cohort.

OBJECTIVE: Sleep-wake disturbances, such as excessive daytime somnolence (EDS), are nonmotor symptoms of Parkinson's disease (PD) and significantly affect the quality of life. This study aimed to examine the relationship between EDS and motor and nonmotor symptoms of PD. METHODS: Eighty-two patients with idiopathic mild PD were followed up twice a year for 2 years and assessed on sleep, mood, anxiety, cognition, function, and disease severity. Data were analyzed retrospectively, comparing motor and nonmotor outcomes between those with EDS and those without. RESULTS: At baseline, 27.9% had EDS and were similar in demographic and clinical characteristics to those without; 10% had persistent EDS during the first year of follow-up. Excessive daytime somnolence had a significant main effect on mood and anxiety as shown by consistently higher scores on the Geriatric Depression Scale (P = .022) and Hospital Anxiety and Depression Scale-Anxiety subscale scores (P = .011) throughout duration of follow-up. The group with persistent EDS showed greater rate of worsening Frontal Assessment Battery scores by the end of first-year follow-up (P = .025) and greater rate of worsening Apathy Scale scores by the end of 2-year follow-up (P = .002). No significant effects of EDS on motor symptoms and disease severity were found. CONCLUSIONS: In a Southeast Asian cohort of patients with PD, EDS had a negative longitudinal impact on mood, anxiety, apathy, and cognitive function but no impact on motor symptoms and disease severity. Excessive daytime somnolence is thus a potential therapeutic target to improve nonmotor outcomes.

Medial Temporal Atrophy in Amyloid-Negative Amnestic Type Dementia Is Associated with High Cerebral White Matter Hyperintensity.

BACKGROUND: Non-amyloid mechanisms behind neurodegeneration and cognition impairment are unclear. Cerebrovascular disease (CVD) may play an important role in suspected non-Alzheimer's pathophysiology (SNAP), especially in Asia. OBJECTIVE: To examine the association between CVD and medial temporal lobe atrophy (MTA) in amyloid-ß negative patients with mild amnestic type dementia. METHODS: Thirty-six mild dementia patients with complete neuropsychological, cerebrospinal fluid (CSF) biomarker, and neuroimaging information were included. Only patients with clinically significant MTA were recruited. Patients were categorized based on their CSF Aß levels. Neuroimaging and neuropsychological variables were analyzed. RESULTS: Despite comparable MTA between Aß positive and negative patients, Aß-negative patients had significantly greater white matter hyperintensities (WMH; Total Fazekas Rating) than their Aß-positive counterparts (6.42 versus 4.19, p = 0.03). A larger proportion of Aß-negative patients also had severe and confluent WMH. Regression analyses controlling for baseline characteristics yielded consistent results. CONCLUSION: Our findings demonstrate that MTA is associated with greater CVD burden among Aß-negative patients with amnestic type dementia. CVD may be an important mechanism behind hippocampal atrophy. This has implications on clinical management strategies, where measures to reduce CVD may slow neurodegeneration and disease progression.

Hippocampal subfield atrophy of CA1 and subicular structures predict progression to dementia in idiopathic Parkinson's disease.

BACKGROUND: Global hippocampal atrophy is a hallmark of Alzheimer's dementia and has been similarly reported in Parkinson's disease dementia (PDD). However, there is limited literature on the differential involvement of hippocampal subfields in predicting conversion to PDD. This study is an extension of previous findings on progression to mild cognitive impairment in Parkinson's disease (PD). METHODS: This cohort study recruited 73 non-demented participants with idiopathic PD (age 65.80±8.17, 75.3% male) from an outpatient neurology clinic. All participants underwent clinical assessment, neuropsychological testing and 3T MRI scans at baseline and 18 months while on prescribed dopaminergic medication. Hippocampal subfield volumes were obtained using automatic segmentation in FreeSurfer V.6.0. Participants who progressed to PDD and those who did not were compared on hippocampal subfield atrophy and cognitive change (episodic memory, attention, executive functions, language, visuospatial abilities). Subfields were further examined for their abilities to predict PDD conversion and distinguish PDD from non-demented PD using receiver operating characteristic analysis. RESULTS: Smaller baseline global hippocampal volume, cornu ammonis (CA) subfield CA1, subiculum and presubiculum volumes were observed in participants who went on to develop dementia, and predicted PDD conversion. Those who progressed to PDD saw greater decline in global hippocampal volume, granule cell layer of the dentate gyrus, presubiculum, parasubiculum and fimbria. Decline in subiculum and fimbria volume corresponded to cognitive decline in attention and executive functions, respectively. CONCLUSIONS: Early atrophy of CA1, subiculum and presubiculum preceded, and predicted, PDD conversion. Differential patterns of subfield atrophy were also observed among those who progressed to PDD and were associated with impaired executive functions.

Regional White Matter Hyperintensity Influences Grey Matter Atrophy in Mild Cognitive Impairment.

The association between cerebrovascular disease pathology (measured by white matter hyperintensities, WMH) and brain atrophy in early Alzheimer's disease (AD) remain to be elucidated. Thus, we investigated how WMH influence neurodegeneration and cognition in prodromal and clinical AD. We examined 51 healthy controls, 35 subjects with mild cognitive impairment (MCI), and 30 AD patients. We tested how total and regional WMH is related to specific grey matter volume (GMV) reductions in MCI and AD compared to controls. Stepwise regression analysis was further performed to investigate the association of GMV and regional WMH volume with global cognition. We found that total WMH volume was highest in AD but showed the strongest association with lower GMV in MCI. Frontal and parietal WMH had the most extensive influence on GMV loss in MCI. Additionally, parietal lobe WMH volume (but not hippocampal atrophy) was significantly associated with global cognition in MCI while smaller hippocampal volume (but not WMH volume) was associated with lower global cognition in AD. Thus, although WMH volume was highest in AD subjects, it had a more pervasive influence on brain structure and cognitive impairment in MCI. Our study thus highlights the importance of early detection of cerebrovascular disease, as its intervention at the MCI stage might potentially slow down neurodegeneration.

Progression of small vessel disease correlates with cortical thinning in Parkinson's disease.

OBJECTIVE: Cerebral small-vessel disease (SVD) is a risk factor for dementia in Parkinson's disease (PD), however the pathophysiological role of SVD in PD-dementia is unclear. We investigated the impact of baseline and progression of SVD on cortical thickness and the correlation to cognition. METHODS: Seventy-three mild PD patients with baseline and follow-up structural MRI scans, serial clinical and neuropsychological assessments were studied. SVD included the load of white matter hyperintensities (WMH), lacunes and perivascular spaces (PVS). WMH progression was assessed using the modified Rotterdam Progression scale, while for lacunes and PVS, development of new lesions was considered as lesion progression. Patients were classified as having SVD-progression and SVD-no-progression based on the longitudinal changes in their SVD measures. Freesurfer was used to measure baseline and follow-up regional cortical thickness and subcortical volumes and correlated to cognitive performance. RESULTS: Fourteen patients were classified as SVD-progression and 59 as SVD-no-progression. Over 18 months, PD SVD-progression demonstrated significant cortical thinning in the left frontal and bilateral parietal regions with associated decline in memory, executive function, and motor functions. PD SVD-progression also had reduced volumes in the nucleus accumbens and amygdala at baseline and greater atrophy in the caudate nucleus over 18 months. DISCUSSION: The extent and progression of SVD is associated with focal cerebral atrophy and domain-specific cognitive dysfunction. Measures to retard SVD may be potentially useful in preventing dementia in PD.