Objective: Chronic subdural hematoma (CSDH) is a common form of intracranial hemorrhage with a substantial recurrence rate. Atorvastatin may reduce CSDH via its anti-inflammatory and pro-angiogenesis effects, but its effectiveness for preventing recurrent CSDH has never been explored. We hypothesized that atorvastatin is effective in reducing recurrence of CSDH after surgery and identified determining factors predictive of hematoma recurrence.

Methods: A prospective study was conducted in 168 surgical cases of CSDH.All patients were randomly assigned to the group treated with atorvastatin or control group. Clinically relevant data were compared between two groups, and subsequently between the recurrence and non-recurrence patients. Multiple logistic regression analysis of the relationship between atorvastatin treatment and the recurrence using brain atrophy, septated and bilateral hematoma was performed.

Results: Atorvastatin group conferred an advantage by significantly decreasing the recurrence rate (P = 0.023), and patients managed with atorvastatin also had a longer time-to-recurrence (P = 0.038). Admission brain atrophy and bilateral hematoma differed significantly between the recurrence and non-recurrence patients (P = 0.047 and P = 0.045). The results of logistic regression analysis showed that atorvastatin significantly reduced the probability of recurrence; severe brain atrophy and bilateral hematoma were independent risk factors for recurrent CSDH.

Conclusions: Atorvastatin administration may decrease the risks of recurrence.Patients with severe brain atrophy and bilateral CSDH are prone to the recurrence.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4923224PMC
http://dx.doi.org/10.3389/fnins.2016.00303DOI Listing

Publication Analysis

Top Keywords

brain atrophy
16
bilateral hematoma
12
atrophy bilateral
12
atorvastatin
9
recurrence
9
chronic subdural
8
subdural hematoma
8
recurrence rate
8
recurrence non-recurrence
8
non-recurrence patients
8

Similar Publications

Introduction: Alzheimer's disease (AD) patients with higher educational attainment (EA) often exhibit better cognitive function. However, the relationship among EA status, AD pathology, structural brain reserve, and cognitive decline requires further investigation.

Methods: We compared cognitive performance across different amyloid beta (Aβ) positron emission tomography (A ±) statuses and EA levels (High EA/Low EA).

View Article and Find Full Text PDF

NOTCH3 Mutation Causes Glymphatic Impairment and Promotes Brain Senescence in CADASIL.

CNS Neurosci Ther

January 2025

Department of Neurology, Mental and Neurological Disease Research Center, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.

Aims: The aim of this study is to investigate the role of glymphatic function of cerebral autosomal dominant arteriopathy, subcortical infarcts, and leukoencephalopathy (CADASIL), the most common monogenic small vessel disease caused by NOTCH3 mutation, and to explore potential therapeutic strategies to improve glymphatic function.

Methods: We assessed glymphatic influx and efflux function in CADASIL mouse models (Notch3) and correlated these findings with brain atrophy in CADASIL patients. We also investigated the underlying mechanisms of glymphatic impairment, focusing the expression of AQP4 in astrocytic endfeet.

View Article and Find Full Text PDF

The cytoskeleton, composed of microtubules, intermediate filaments and actin filaments is vital for various cellular functions, particularly within the nervous system, where microtubules play a key role in intracellular transport, cell morphology, and synaptic plasticity. Tubulin-specific chaperones, including tubulin folding cofactors (TBCA, TBCB, TBCC, TBCD, TBCE), assist in the proper formation of α/β-tubulin heterodimers, essential for microtubule stability. Pathogenic variants in these chaperone-encoding genes, especially TBCD, have been linked to Progressive Encephalopathy with Brain Atrophy and Thin Corpus Callosum (PEBAT, OMIM #604,649), a severe neurodevelopmental disorder.

View Article and Find Full Text PDF

Clinical Diagnosis and Differential Diagnosis Between CSF1R- and AARS2-Related Leukoencephalopathy.

J Mol Neurosci

January 2025

Department of Neurology, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Science/Peking Union Medical College, Beijing, 100730, China.

CSF1R-related leukoencephalopathy (CSF1R-L) and AARS2-related leukoencephalopathy (AARS2-L) were two disease entities sharing similar phenotype and even pathological changes. Although clinically, radiologically, and pathologically similar, they were caused by mutation of two different genes. As the rarity of the two diseases, the differential diagnosis of them was difficult.

View Article and Find Full Text PDF

Sarcopenia and cancer cachexia are two life-threatening conditions often misdiagnosed. The skeletal muscle is one of the organs most adversely affected by these conditions, culminating in poor quality of life and premature mortality. In addition, it has been suggested that chemotherapeutic agents exacerbate cancer cachexia, as is the case of doxorubicin.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!