Neurology最新文献

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: Neurofibrillary tangles (NFTs) progressively damage gray matter in Alzheimer disease (AD). Resulting cortical microstructural alterations might not be detectable using macrostructural metrics but may be studied using isotropic water diffusion, as it reflects extracellular free water content. The aim of this study was to examine the effect of NFTs on cortical microstructure by investigating whether cortical free water increases as a function of tau load. We also investigated whether phosphorylated tau in blood plasma also indicated cortical microstructural abnormalities.

Methods: For this cross-sectional study, we sampled participants with T1 MRI, multishell diffusion-weighted MRI, amyloid PET ([¹⁸F]AZD4694), tau PET, and plasma phosphorylated tau 217+ (p-tau217) from the Translational biomarkers in Aging and Dementia cohort at McGill University; participants were recruited between 2017 and 2024. We used the Neurite Orientation Dispersion and Density Imaging algorithm to calculate isotropic free water images ("free water"). FreeSurfer was used to calculate cortical thickness in the entorhinal, fusiform, inferior temporal, and middle temporal gyri regions of interest ("meta-ROI"); Automatic Segmentation of Hippocampal Subfields was used to calculate hippocampal volumes. We grouped participants by amyloid PET positivity (A), plasma p-tau217 positivity (T1), and tau PET positivity (T2). We performed voxel-wise correlation analyses between free water and these proteinopathy markers, as well as ROI-based analyses in the meta-ROI.

Results: A total of 303 participants (mean age 67 years, 58.7% female) were included in this study (168 cognitively normal individuals, 43 with mild cognitive impairment, 23 with AD dementia, 68 not diagnosed). Tau PET was positively correlated with free water in gray matter predominantly in the temporal lobe (partial R² = 0.39, p < 0.001), and the correlation of p-tau217 with the meta-ROI free water was entirely mediated by tau PET (p < 0.001). In addition, medial temporal and hippocampal free water was negatively correlated with Montreal Cognitive Assessment scores in the A-T₁+ and A+T₂+ groups. The strongest ROI-based multilinear models for predicting temporal gray matter and hippocampal tau PET burden used both cortical thickness and free water as predictors (temporal gray matter partial R² = 0.62; hippocampal partial R² = 0.64).

Discussion: In AD-relevant regions, increased free water correlates with tau load independently of macrostructural metrics or amyloid load. Free water may serve as an imaging marker for microstructural changes in gray matter resulting from NFT accumulation, complementary to macrostructural metrics.

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.

Background and objectives: Although etiology is considered central to outcomes in status epilepticus (SE), previous studies often lacked standardized classification and adjustment for confounders, particularly withdrawal of life-sustaining treatment (WLST). This study examined the association between SE etiology, mortality, and neurologic recovery using the International League Against Epilepsy (ILAE) classification while accounting for confounders and WLST.

Methods: This 2-center observational study included adults (≥18 years) with SE treated at the University Hospitals of Basel and Geneva from 2015 to 2023. Etiologies were classified as acute symptomatic, remote symptomatic-unprovoked, progressive CNS disorders, epilepsy without additional triggers, or cryptogenic. Demographics, SE type, SE severity score, Charlson Comorbidity Index, treatment data, complications, and WLST were assessed. The primary outcome was in-hospital mortality; secondary outcomes were 30-day mortality and recovery to premorbid neurologic function at discharge. Associations were assessed using Poisson regression with robust error variance, adjusted for age, nonconvulsive SE (NCSE) with coma, comorbidity, and center.

Results: Among 967 patients (median age 67 years, interquartile range 54-78; 46.5% female), SE was terminated in 95%, with 48.5% of patients recovering to premorbid function. Acute symptomatic SE accounted for 34.2%, remote symptomatic SE for 27.6%, SE due to progressive CNS disorders for 14.4%, epilepsy without additional triggers for 16.7%, and cryptogenic SE for 7.1%. In-hospital and 30-day mortality were 7.9% and 13.9%, respectively, while 48.5% recovered to premorbid function. Etiology was associated with neurologic recovery, with intracranial hemorrhage (relative risk [RR] 0.49, 95% CI 0.35-0.67) and acute symptomatic SE (RR 0.71, 95% CI 0.60-0.83) being associated with reduced likelihood of recovery, whereas known epilepsy was associated with increased likelihood of recovery (RR 1.40, 95% CI 1.23-1.60). NCSE with coma (11.9%) was independently associated with higher in-hospital and 30-day mortality and reduced recovery across all ILAE etiology groups. WLST did not significantly alter these associations.

Discussion: Etiology was associated with neurologic recovery but not with short-term mortality after adjustment for confounders and WLST. By contrast, NCSE with coma showed the strongest association with adverse outcomes. This suggests that while etiology informs prognosis for recovery, SE type, particularly NCSE with coma, is the more critical determinant of survival.

In 2025, international neurology celebrates the bicentenary of J.-M. Charcot's birth. As a major medical scientist in Paris and the founder of modern clinical neurology, Charcot became friends with the celebrated literary figure Alphonse Daudet. Discord subsequently intervened, as Daudet, afflicted with tabes dorsalis, was treated by Charcot without success and even underwent suspension therapy that led to serious side effects. Daudet's son, Léon, blamed Charcot for his own failure in medical school and became a bitter social critic of the French medical system, condemning the hospital hierarchy, including Charcot. Further family discord occurred when Léon married the granddaughter of Victor Hugo, instead of Charcot's own daughter. Within this background, after Charcot's death in 1893, Alphonse Daudet incorporated Charcot into a fictional account, A la Salpêtrière, one of 3 short stories in his Trois Souvenirs (3 Recollections). This study dissects Daudet's Charcot depiction where he presents Charcot as mostly silent, passive, and distant within a circus-like atmosphere of disruptive patients, foreign visitors, and interns. The portrait is a striking contrast to the many other first-hand descriptions of Charcot's domineering, autocratic, and patronizing manner. However, the depiction of a quiet and distantly bland master in the fictional office consultation setting is historically anchored in Daudet's life experiences, which included visits to the Salpêtrière, first-hand knowledge of Charcot over many years, and the experience of being a patient with unremitting neurologic disease. The veracity of the actual events is questionable, given the personal antagonism that colored the last years of their lives, but it is also conceivable to see in Charcot a Janus-like figure of dominance and theatrical authority in the teaching amphitheater interfaced with a more passive, reflective observer in the intimacy of an office setting.