Neurology最新文献

Background and objectives: Previous studies have indicated an increased risk of cerebrovascular and coronary events shortly after cancer diagnosis. However, whether cancer affects mortality outcomes after stroke and myocardial infarction (MI) remains unclear. We aimed to investigate the relationship between cancer diagnosis and mortality after stroke and MI.

Methods: Using linked nationwide databases from Taiwan, we conducted a population-based cohort study including 3 cohorts of patients with first-time ischemic stroke, hemorrhagic stroke, and MI between 2011 and 2019. The primary outcome was 90-day mortality, with follow-up beginning at the index stroke (for ischemic and hemorrhagic stroke cohorts) and MI (for the MI cohort) event date for all patients. Odds ratios (ORs) of 90-day mortality associated with all cancers combined and 15 cancer types were estimated through propensity score matching for potential confounding variables. Excess mortality rates (between patients with cancer and matched controls) were analyzed across time intervals after cancer diagnosis, stratified by age group, cancer stage, and cancer type.

Results: Overall, 440,664, 159,606, and 228,993 patients were included in ischemic stroke (mean age, 70.1 years; 40.7% female), hemorrhagic stroke (mean age, 65.4 years; 36.5% female), and MI (mean age, 67.8 years; 29.7% female) cohorts, respectively. Compared with matched controls, patients with cancer had higher risks of 90-day mortality in ischemic stroke (OR 2.71, 95% CI 2.63-2.79), hemorrhagic stroke (OR 2.20, 95% CI 2.11-2.29), and MI (OR 1.63, 95% CI 1.57-1.69). Across 3 cohorts, substantial variations existed among cancer types, with aggressive malignancies (e.g., pancreatic cancer) consistently presenting the highest risks. Excess mortality rates were highest during the first postdiagnosis year and declined progressively thereafter. This temporal pattern was consistent across age groups and cancer stages, with excess mortality rates highest among patients aged 18-59 years and those with stage 4 disease. Despite variability among cancer types, excess mortality typically peaked within 2 years.

Discussion: This population-based study showed that patients with cancer had higher risks of mortality after stroke and MI, with substantial variations by cancer type, although cause-specific mortality data were lacking. Excess mortality rates peaked shortly after diagnosis, particularly for early-onset cancer and advanced disease.

Background and objectives: Cerebral adrenoleukodystrophy (CALD) is a common manifestation of adrenoleukodystrophy (ALD) in men. Early detection of CALD lesions through MRI screening is critical to allow for therapeutic action preventing severe disability and death. While the frequency of brain MRI monitoring has been addressed by international recommendations, no consensus currently exists regarding which MRI sequences should be used in a real-world setting for screening and follow-up of CALD lesions. The aim of this study was to establish guidelines for the MRI protocol in clinical practice and to identify priority sequences for research use, thereby promoting intercenter harmonization.

Methods: A modified Delphi procedure was used to achieve consensus on MRI protocols for ALD screening, lesion monitoring, and research applications among experts with experience in brain imaging in ALD. Questionnaires allowed experts to indicate whether they considered sequences as core, optional, or research, or to express agreement (5-point scale ranging from completely disagree to completely agree) with specific statements. Topics where no agreement was reached were discussed during online consensus meetings.

Results: Thirty experts from 9 countries participated and agreed that the core screening protocol for ALD in adults and children should include at least 3D T1-weighted, spin-echo T2-weighted, 3D fluid-attenuated inversion recovery, and diffusion-weighted imaging (DWI). Postcontrast T1-weighted imaging should be performed systematically in specific clinical scenarios. Experts supported using DWI alongside the Loes score and postcontrast imaging to assess lesion progression. A research protocol was defined, prioritizing diffusion tensor imaging, MR perfusion, and quantitative volumetric analyses.

Discussion: This international project harmonizes the ALD MRI protocol, thus offering a practical framework to screen and monitor lesions, which will improve clinical decision making. It also identifies MRI sequences that should be prioritized in future research. Future research on MRI in ALD should focus on topics where no consensus has yet been reached in this project.

Background and objectives: There are significant differences in compensation between medical specialties. In this study, we analyzed neurologist compensation in the United States compared with other medical specialties and in relation to productivity metrics.

Methods: We evaluated data from the 2013-2023 editions of the SullivanCotter Physician Compensation and Productivity Survey, which collects compensation and productivity metrics directly from hospitals, hospital systems, and medical groups. We compared neurologists with 8 other specialties (internal medicine, pediatrics, family medicine, radiology, emergency medicine, neurosurgery, orthopaedic surgery, and interventional cardiology). The primary outcome was median compensation, defined as base salary and incentive pay, after being inflation-adjusted to 2023 dollars. The secondary outcome was median work relative value units (wRVUs), adjusted for modifiers and excluding technical components. The tertiary outcome was compensation per wRVU. Outcomes were standardized to a full-time effort equivalent.

Results: From 2013 to 2023, the average yearly number of physicians and neurologists in our cohort was 37,443 and 2,280, respectively. Inflation-adjusted median neurologist compensation started at $313,315 in 2013 and increased by 1.6% to $318,284 by 2023. In comparison, pediatrics remained the lowest compensated specialty, increasing by 4.9% from $258,073 to $270,666 and neurosurgery was the highest compensated, increasing by 5.0% from $790,336 to $829,527. Median neurologist wRVUs started at 4,475 in 2013 and increased by 12.3% to 5,024 by 2023. In 2023, neurologists received less compensation per wRVU ($65/wRVU) than neurosurgery ($90), orthopaedic surgery ($76), or interventional cardiology ($68), but more than pediatrics ($48), family medicine ($50), internal medicine ($54), radiology ($55), or emergency medicine ($56). Over time, neurologist compensation became less varied by geography of practice location or hospital vs medical group employment. Among neurologists, compensation increased for neurohospitalists and vascular neurologists, whereas it declined for those in epilepsy, neuromuscular, multiple sclerosis, and neurocritical care.

Discussion: Despite a 12% increase in wRVUs, inflation-adjusted neurologist compensation has remained stable since 2013. Compensation differences between neurologists and other medical specialties are not solely due to variance in wRVU generation. Future studies should explore factors contributing to these findings, including reimbursement models and governmental policies.

Background and objectives: In supratentorial intracerebral hemorrhage (ICH), hematoma location serves as a useful proxy for the underlying cerebral small vessel disease (cSVD) subtype, especially in the context of the Boston criteria. Whether this framework applies to spontaneous cerebellar ICH (cICH) remains unclear. We investigated whether hematoma location in cICH reflects distinct cerebral small vessel pathologies and explored an approach to support the diagnosis of underlying cerebral amyloid angiopathy (CAA) in this setting.

Methods: We performed a retrospective multicenter study of consecutive patients with spontaneous cICH admitted to 3 tertiary hospitals in Berlin, Germany, between 2010 and 2024. Clinical, neuroimaging (CT/MRI), and neuropathologic data were collected. cICH location was categorized as superficial, deep, or mixed. Deep and mixed cICH locations were grouped together. MRI-based cSVD markers and neuropathology-confirmed diagnoses were analyzed. CAA was categorized as probable vs no CAA (i.e., nonprobable) using the Boston criteria v2.0. Univariate regression analyses were performed for associations with cICH location. Subsequently, we proposed pilot clinical-MRI criteria that might support the presence of CAA as the cause of cICH.

Results: Among 221 patients with cICH (median age 75 years, interquartile range 65.5-84.5, 57% female), 31 (14%) had superficial and 190 (86%) had deep/mixed cICH. MRI was available in 100 and neuropathology in 35 patients. Superficial cICH location was associated with probable CAA per Boston criteria v2.0 (odds ratio [OR] 8.14, 95% CI 1.25-53.25), whereas deep/mixed cICH was linked to higher systolic blood pressure (OR 1.03, 95% CI 1.01-1.05 per mm Hg) and more severe cSVD burden on MRI (OR 5.37, 95% CI 1.97-14.58). Among patients with available pathology (n = 35), 33.3% of patients with superficial cICH had evidence of CAA vs 3.1% in deep/mixed cICH. Our exploratory construct-"Boston criteria v2.0-cICH with supporting CAA features"-showed a specificity of 94.4% and sensitivity of 60.0% against a probable CAA diagnosis (based on supratentorial findings) in the total patient sample.

Discussion: Superficial and deep/mixed cICH exhibit distinct clinical, neuroimaging, and neuropathologic profiles, suggestive of divergent cSVD etiologies. Limitations include the sample size and the retrospective design. Our proposed criteria represent a proof-of-concept tool to support CAA diagnosis in cICH within the Boston criteria v2.0 framework but require further validation.

Background and objectives: Traumatic brain injury (TBI) is a leading cause of long-term disability in working-age populations. Return to work is a key marker of recovery, yet most studies assess it as binary at fixed time points. We aimed to estimate transition probabilities to and from work disability during 5 years after TBI and how injury severity and preinjury sociodemographic and medical factors influence these probabilities.

Methods: We conducted a nationwide matched cohort study in Sweden using linked registers. Individuals aged 21-60 years with a TBI diagnosis between 2005 and 2016 were compared with up to 10 matched non-TBI individuals. TBI severity was proxied by care characteristics: TBI A (emergency visit or ≤2 days), TBI B (≥3 days), and TBI C (neurosurgery). Transition probabilities to and from work disability (>14 days sickness absence) were estimated with multistate models. Sociodemographic and medical factors were assessed with Cox regression.

Results: The cohort included 98,256 individuals with TBI and 981,191 matched non-TBI individuals (median age 39 years; 43% women). Transition probabilities to work disability were higher in all TBI groups: at 30 days, 5.5% (95% CI 5.4-5.7) for TBI A, 29% (28.0-30.7) for TBI B, and 43% (38.2-47.3) for TBI C, vs 0.5% (0.5-0.6) in non-TBI; at 5 years, 7.1% (7.0-7.3), 10.9% (10.2-11.7), and 12.9% (10.7-15.7), vs 4.0% (4.0-4.1). In TBI A and B, higher probability was predicted by older age (TBI A hazard ratio 1.23, 95% CI 1.20-1.26; TBI B 1.34, 1.21-1.48), female sex (TBI A 1.59, 1.56-1.62; TBI B 1.35, 1.26-1.44), and psychiatric disorders (TBI A 1.34, 1.30-1.39; TBI B 1.28, 1.11-1.48), while higher education (TBI A 0.83, 0.81-0.86) and city residence (TBI A 0.92, 0.90-0.95; TBI B 0.88, 0.80-0.95) were protective. In TBI C, only older age remained significant (1.59, 1.17-2.14).

Discussion: TBI was associated with persistently elevated transition probabilities to work disability across all severity groups, with early peaks in TBI B and C and a delayed increase in TBI A, influenced by sociodemographic and medical factors. However, the lack of standardized severity grading limits comparison with other studies. Still, these results suggest TBI increases long-term risk of work disability, supporting sustained individualized rehabilitation.

Background and objectives: The effects of lifetime cognitive enrichment on later-life cognitive outcomes are not comprehensively investigated. The aim of this study was to test the association of lifetime cognitive enrichment with Alzheimer disease (AD) dementia and cognitive decline and in an autopsied deceased subset to explore the association between lifetime enrichment and AD and related dementia (ADRD) pathologic indices and cognitive resilience that is, decline after adjusting for common ADRD pathologies.

Methods: This was a longitudinal clinicopathologic study involving older individuals from Northeastern Illinois who participated in the Rush Memory and Aging Project, were free of dementia at baseline, completed surveys reflecting lifetime enrichment, and had annual clinical evaluations. We constructed a composite measure reflecting lifetime cognitive enrichment and tested its association with incident AD dementia in proportional hazards models, mean age of AD dementia onset in an accelerated failure time model, and cognitive decline using linear mixed-effects models. In a deceased subset, we tested the association of lifetime cognitive enrichment with 9 ADRD pathologies and cognitive resilience.

Results: Participants (n = 1,939, 75% female, mean baseline age = 79.6) completed an average of 7.6 years of follow-up, during which 551 participants developed AD dementia. One unit higher in lifetime enrichment was associated with 38% lower hazards of developing AD dementia (hazard ratio 0.62, 95% CI 0.52-0.73, p < 0.001). High lifetime enrichment (90th percentile) compared with low (10th percentile) was associated with a mean of 5 years delayed onset of AD dementia. Lifetime enrichment was positively associated with cognitive function at baseline (estimate = 0.31, SE = 0.02, p < 0.001) and a slower rate of cognitive decline (estimate = 0.02, SE = 0.01, p = 0.002). In the deceased subset (n = 948), lifetime cognitive enrichment did not show meaningful associations with neuropathologic indices, but remained associated with higher cognitive function proximate to death (estimate = 0.32, SE = 0.06, p < 0.001) and a slower rate of cognitive decline after adjusting for pathology (estimate = 0.014, SE = 0.01, p = 0.02).

Discussion: Lifetime exposure to cognitive enrichment was related to lower risk of AD dementia and a slower rate of cognitive decline, including after adjustment for common ADRD pathologies, indicating higher resilience provided by lifetime enrichment. Our results suggest that cognitive health in later life is in part the product of lifetime exposure to cognitive enrichment.

The differentials for rapidly progressive dementia are broad, encompassing structural, infectious, inflammatory, neoplastic, and neurodegenerative etiologies. The presence of abnormal movements further complicates the diagnostic approach. We describe a 69-year-old man presenting with a diverse array of neurologic symptoms, starting with rapidly progressive cognitive impairment, later developing abnormal movements, sleep disruption, and constitutional symptoms. Despite extensive investigations and empirical treatment, the diagnosis remained elusive until postmortem evaluation. This case highlights the challenges inherent in neurologic diagnostic odysseys, offering insight into the diagnostic reasoning process and unveiling novel clinical findings that may aid earlier recognition of this rare disorder.