Cerebral small vessel diseases (CSVDs) are among the most common age-related pathologies of the brain. Arteriolosclerosis and cerebral amyloid angiopathy (CAA) are the most common CSVDs. In addition to causing stroke and dementia, CSVDs can have diverse covert radiological manifestations on computed tomography and magnetic resonance imaging including lacunes, T2-weighted white matter hyperintensities, increased density of visible perivascular spaces, microbleeds and cortical superficial siderosis. Because they cannot be visualized directly, research on the pathophysiology of CSVD has been difficult. However, advances in quantitative imaging methods, including physiological imaging such as measurement of cerebrovascular reactivity and increased vascular permeability, are beginning to allow investigation of the early effects of CSVD in living people. Furthermore, genomics, metabolomics and proteomics have the potential to illuminate previously unrecognized pathways to CSVD that could be important targets for new clinical trials.

Guillain-Barre syndrome (GBS) is the commonest cause of acute polyradiculoneuropathy that requires hospitalization. Many of these patients experience systemic and disease-related complications during its course. Notable among them is hyponatremia. Though recognized for decades, the precise incidence, prevalence, and mechanism of hyponatremia in GBS are not well known. Hyponatremia in GBS patients is associated with more severe in-hospital disease course, prolonged hospitalization, higher mortality, increased costs, and a greater number of other complications in the hospital and worse functional status at 6 months and at 1 year. Though there are several reports of low sodium associated with GBS, many have not included the exact temporal relationship of sodium or its serial values during GBS thereby underestimating the exact incidence, prevalence, and magnitude of the problem. Early detection, close monitoring, and better understanding of the pathophysiology of hyponatremia have therapeutic implications. We review the complexities of the relationship between hyponatremia and GBS with regard to its pathophysiology and treatment.

Background: Advanced parkinsonian syndromes represent a growing challenge for healthcare systems as their care needs are complex and costly. Current care models often lack integration of specialized neurology and palliative care, leading to suboptimal outcomes. The Advanced Care Team for Parkinson’s program (ACT-PD) addresses this gap by enhancing care quality and reducing costs. This study evaluates the cost-effectiveness of ACT-PD interventions compared to standard care (SC). Methods: A retrospective analysis compared 27 deceased ACT-PD patients (2022–2024) with 1,439 deceased SC patients (2011–2017). It assessed healthcare utilization, place of death, and patient Quality-Adjusted Life Years (QALYs). Healthcare utilization measures included hospitalizations, Intensive Care Unit (ICU) admissions, emergency department (ED) visits, and palliative care consultations. The analysis incorporated the incremental cost-effectiveness ratio (ICER) using Calgary Zone cost data from 2021–2022. Results: ACT-PD patients experienced fewer hospital deaths (33.33% vs. 45.90%) and more deaths at home (22.22% vs. 7.90%). They also had greater neurology (48.00% vs. 37.20%) and palliative care engagement (36.00% vs. 17.40%). ACT-PD avoided ICU admissions, saving $2.56 million annually, with total cost savings of $2.66 million. The ICER was $1,459 per QALY gained. Conclusions: Multidisciplinary palliative care interventions provided by ACT-PD are highly cost-effective, improving care quality while reducing healthcare costs.

This review looks back on our experience with acute middle cerebral artery embolectomies in the 1990s, frowned upon by stroke experts at the time, and no match for the newly introduced and proven treatment of acute ischemic stroke with intravenous recombinant tissue plasminogen activator (alteplase). The past several decades have seen dramatic developments in acute cerebral revascularization, the major paradigm shift being in the form of endovascular thrombectomy. Mechanical thrombectomy has moved from the operating room, where we performed it, to the interventional angiography suite armed with ever-improving clot aspiration and retrieval technologies.

Radiologic imaging has become integral in not only the detection and diagnosis of subdural hematoma (SDH) but also in guiding potential treatment options. This is especially true for chronic SDH, which has conventionally been managed via surgical drainage, but can now be treated with embolization of the middle meningeal artery (MMA). We review the imaging manifestations of SDH as a function of chronicity and standardized methods of measurement and identify the MMA and its clinically significant variant anatomy as it pertains to embolization planning. Equipped with a more comprehensive approach to characterizing SDH, the radiologist will be able to curate findings of greater utility to the clinician.

The carotid artery is unique; it is the only vessel to bifurcate into a bulb larger than itself. The history of its anatomic description, understanding of its pathophysiology and evolution of its imaging are relevant to current controversies regarding measurement of stenosis, surgical/endovascular therapies and medical management of carotid stenosis in stroke prevention. Treatment decisions on millions of symptomatic and asymptomatic patients are routinely based on information from clinical trials from over 30 years ago. This article briefly summarizes the highlights of past research in key areas and discuss how they led to current challenges of diagnosis and treatment.

Background: In multiple sclerosis (MS), soluble mediators of neuroinflammation are released by activated lymphocytes and resident immune cells, leading to demyelination and neurodegeneration. Radiologically isolated syndrome (RIS) is an entity in which white matter lesions fulfilling criteria for MS occur in individuals without any suggestive symptoms. The exact nature of pro- and anti-inflammatory cytokines in blood, and their association with disease activity in RIS/MS requires further clarification. Methods: Plasma was collected and cryopreserved from healthy controls (HCs), people with RIS and relapsing-remitting MS (RRMS) at the Barlo MS Centre. All samples were analyzed with OLink Target 96 Inflammation Multiplex Immunoassay Panel. Results: Individuals with RIS (p=0.0001; p= 0.0007; p= 0.0012) and RRMS (p<0.0001; p= 0.0003; p= 0.00112) had significantly higher concentrations of hepatocyte growth factor (HGF), interleukin-6 (IL-6), and chemokine ligand 23 (CCL23) in plasma compared to HCs, and patients with RRMS (p=0.0087) had significantly higher concentrations of HGF compared to individuals with RIS. Conclusions: Our study demonstrates that HGF, IL-6 and CCL23 are significantly increased in the plasma of patients with RIS and RRMS compared to HCs. Our observations suggest that the biology of MS is present in those with RIS, and these neuroinflammatory mediators may serve as a biomarker of disease activity.

Background: Tuberous Sclerosis Complex (TSC) is a multisystemic neurocutaneous disorder in which hamartomas confer significant medical risks, including mortality, by disruption of local tissues. However, only recently have multiple studies assessed specific aetiologies of mortality in TSC. Methods: A literature review of all available studies examining mortality in TSC was conducted until December 15, 2024. Results: We identified 13 studies reporting 411 deaths from 6735 individuals with TSC. Crude mortality per 100 individuals ranged from 1.4-13.8 over average intervals of 11-45 years. Mortality risk ranged from 3.0-4.9 (mean 4.3) versus the general population. Mean life expectancy was 66.2 years compared to 81.8 in the general population. In seven studies that reported specific aetiologies of mortality, 6/7 (85%) had renal (commonly renal failure or angiomyolipoma hemorrhage) or brain disease (most frequently sudden unexpected death in epilepsy or brain tumours) as the most common cause of mortality. Intellectual delay conferred increased mortality risk. Lymphangioleiomyomatosis conferred significant risk of mortality in adult women and cardiac rhabdomyomas were the dominant cause of neonatal mortality. Conclusions: Mortality in TSC is elevated compared to the general population, with brain and renal disease most frequently culpable. Future studies should assess the impact of disease modifying therapies on mortality in TSC.