MeVO

MeVo - Clinical Trials

Definition

Occlusions beyond proximal LVO: M2/M3, A2/A3, P2/P3

Typically: Lower NIHSS & Smaller infarct core

Trials

DISCOUNT (2024)

-No fx benefit, possible ↑ complications

DISTALS (2024)

-No fx benefit

ESCAPE-MeVO (2025)

-No fx benefit

DISTAL (2025)

-No fx benefit

Direct-to-Angio

Direct-to-Angio - Clinical trials

Basics

-Test workflow speed

(🚑 → Angio) vs (🚑 → ED → CT → decision → Angio)

-Goal: ⬇️ Door-to-puncture time→ improve outcomes (time-dependent EVT benefit)

Trials

Pfaff et al. (2020)

↓ DTP time, no fx benefit

ANGIOCAT (2021)

↓ DTP, improved fx outcome

DIRECT ANGIO (2026)

↓ DTP, no fx benefit

↑ ICH (safety sign)→ Stopped early (methodologic concerns)

DIRECT (Ongoing)

Cooper is a center

IV Fluids

IV Fluids

NS (NaCl 0.9%)

0.9% = 0.9 g NaCl per 100 mL

Molecular weight: Na = 23; Cl = 35.5; NaCl = 58.5

So sodium fraction: 23/58.5 = 0.39

1L NS has 0.39% of Na = 3.54g

LR

Total amount Na⁺ = 130 mEq/L

1 mEq Na = 23 mg

130 mEq/L x 23 = 3000 mg

1L LR has 0.30% Na = 3.0g

Summary

In sum, 1L

NS has 3.54g Na

LR has 3.0g Na

AHA recommendation

< 2300 mg sodium/day

Ideal goal: 1500 mg/day for most adults

Delirium

Delirium

"to leave the furrow"

Important

-Problem list, delirium itself alone cannot be billed

#Acute encephalopathy, 'cause' (delirium, 'delirum type')

-Mortality, 3y is 75% in hospitalized

Pathophysiology

-Constellation of sx suggesting global brain dysfx

-Imbalance DA vs ACh

Risk factors

-↑% → ↑age (especially >65yo)
-Medical conditions

-Modifiable: meds, immobility, metabolic disturb, poor O2

Inpatient Monitoring

CAM (Confusion Assessment Method)

-Usual screen by nurse, criteria:

1. Acute onset and fluctuating course

2. Inattention

3. Disorganized thinking

4. Altered level of consciousness

-Dx req: 1 + 2 + (3 or 4)

1:1

Pending

6 Dx criteria (DSM-V)

A- Attention & Awareness

B- Baseline change

C- Cognitive deficit

D- Duration

E- Etiology

F- Fluctutate

Neuro-exam

-Look for: multifocal MCL (metab disturb) & frontal release

-Mental status exam

>Orientation & attention (months backwards [<25 sec, n mistakes])

>Luria test

Classification

-Based on motor: hyperactive, hypoactive, and mixed

-Althoux hypoactive occurs 80%, does not bother, so no consults

Work-up

-Check med list

>Diphenhydramine (sleep-aid) and opiates (post-op) 

-If no baseline, cEEG (diffuse background slow)

>POC EEG was approved for differ delirium ≠ szs

Management

-Delirium always has a cause, reverse the underlying cause!

Delirium Precautions

-Minimize sleep disturbances (lab draws, nursing care, etc), blood draws, restraints, catheterization etc as medically appropriate

-Maintain proper sleep/wake cycle (open and close shades, lights off at night)

-Frequent reorientation to place, date, and time

-Facilitate family communication/visitation as possible

-Ensure patient has glasses, hearing aids, etc

-Ensure appropriate analgesia

-Ensure appropriate fluid input and output

Prevention

- no spsfic med

>Antipsychotic do not treat delirium, do not ↓length

Sx management of agitation

-Propranolol no evidence

*Contraindication if, QTc > 500

*For hypoactive, methylphenidate (nut no clear evidence)

Abstract - Donanemab in Early Alzheimer’s Disease: Greater Benefit in Lower Tau Burden (P2-12.011)

Title: Donanemab in Early Alzheimer’s Disease: Greater Benefit in Lower Tau Burden (P2-12.011)

Authors: Aswathi Sajeendran, Jamir Pitton Rissardo, Omar Elmandouh, and Ana Leticia Fornari Caprara

Conference: 2026 AAN, Chicago, IL

Objective

To evaluate the effect of donanemab compared to placebo on cognitive and functional outcomes in Alzheimer’s disease (AD) patients stratified by tau burden (low/medium [L/M] vs. high [H]).

Background

Donanemab, an anti-amyloid monoclonal antibody, has shown promise in slowing cognitive decline in early AD. Tau pathology may influence treatment response, but subgroup effects remain unclear.

Design/Methods

We systematically reviewed placebo-controlled trials of donanemab in AD reporting outcomes by tau burden. Standardized mean differences (SMD) with 95% confidence intervals (CI) were pooled using inverse-variance methods under fixed- and random-effects models. Outcomes included the integrated Alzheimer’s Disease Rating Scale (iADRS), Clinical Dementia Rating–Sum of Boxes (CDR-SB), ADAS-Cog13, ADCS-iADL, and MMSE. The between-study variance was estimated using REML, and SMDs were calculated as Hedges’ g.

Results

Donanemab significantly improved iADRS (g = 3.28; 95% CI 2.09–4.48; p < 0.01) and favored treatment on CDR-SB (g = –0.61; 95% CI –0.82 to –0.40), ADAS-Cog13 (g = –1.54; 95% CI –2.21 to –0.86), ADCS-iADL (g = 1.70; 95% CI 0.93–2.47), and MMSE (g = 0.53; 95% CI 0.18–0.89). Subgroup analysis showed greater benefit in L/M tau versus H tau across most outcomes: iADRS (L/M: g = 3.80; 95% CI 2.37–5.23; H: g = 0.94; 95% CI –2.16 to 4.04), CDR-SB (L/M: g = –0.67; 95% CI –0.94 to –0.40; H: g = –0.69; 95% CI –1.18 to –0.20), ADAS-Cog13 (L/M: g = –1.72; 95% CI –2.52 to –0.92; H: g = –0.40; 95% CI –2.11 to 1.31), ADCS-iADL (L/M: g = 2.00; 95% CI 1.06–2.94; H: g = 0.99; 95% CI –0.81 to 2.79), and MMSE (L/M: g = 0.57; 95% CI 0.14–1.00; H: g = 0.33; 95% CI –0.47 to 1.13). Between-group differences were not statistically significant (p > 0.25). Heterogeneity was low (I² ≤ 26%).

Conclusions

Donanemab demonstrates clinically meaningful benefits in early AD, particularly among patients with lower tau burden. While high-tau patients showed attenuated responses, subgroup differences were not statistically significant, warranting further investigation.

Citation

Sajeendran A, Rissardo JP, Elmandouh O, Caprara AL. Donanemab in Early Alzheimer’s Disease: Greater Benefit in Lower Tau Burden (P2-12.011). Neurology 2026;106(11_suppl_1):868. doi: 10.1212/WNL.0000000000213161.

Figure 1. Forest plot of iADRS showing significant benefit of donanemab, with greater effect in low/intermediate tau burden and attenuated response in high tau patients.

Figure 2. Forest plot of CDR-SB demonstrating improved clinical progression with donanemab, consistent across tau strata with low heterogeneity.

Figure 3. Forest plot of ADAS-Cog13 showing cognitive improvement favoring donanemab, with stronger effects in low/medium tau and attenuated benefit in high tau.

Abstract - Do SGLT2 Inhibitors Influence Parkinson’s Disease Risk? A Meta-analysis of Randomized Trials (P6-17.012)

Title: Do SGLT2 Inhibitors Influence Parkinson’s Disease Risk? A Meta-analysis of Randomized Trials (P6-17.012)

Authors: Theres Boby Alexander, Jamir Pitton Rissardo, Ana Leticia Fornari Caprara, and Ian M. Walker

Conference: 2026 AAN, Chicago, IL

Objective

To evaluate whether sodium-glucose cotransporter-2 (SGLT2) inhibitors influence the risk of Parkinson’s disease (PD) in patients with diabetes, heart failure, or chronic kidney disease.

Background

SGLT2 inhibitors have transformed the management of type 2 diabetes and heart failure by reducing cardiovascular events and slowing kidney disease progression. Preclinical studies suggest neuroprotective effects. Given shared metabolic and inflammatory pathways between diabetes and PD, SGLT2 inhibitors may influence PD risk.

Design/Methods

A systematic search of ClinicalTrials.gov identified randomized controlled trials reporting PD incidence in SGLT2 inhibitor versus placebo arms. No eligible data were found for ertugliflozin, enavogliflozin, henagliflozin, ipragliflozin, luseogliflozin, or tofogliflozin. Pooled odds ratios (OR) with 95% confidence intervals (CI) were calculated using a random-effects Mantel-Haenszel model, and heterogeneity was assessed with the I² statistic.

Results

Fourteen trial arms from 12 unique studies (n ≈ 64,000; follow-up 7–50 months) were included. Two arms were excluded from pooled analysis due to zero events in both groups. The pooled OR for PD was 0.55 (95% CI: 0.27–1.12; p = 0.20). Heterogeneity was negligible (I² = 0%), and the prediction interval ranged from 0.23 to 1.50. Subgroup analyses showed no significant effect for individual agents: empagliflozin 10 mg (OR 0.64, 95% CI 0.17–2.43), empagliflozin 25 mg (OR 0.33, 95% CI 0.01–8.15), dapagliflozin 10 mg (OR 0.33, 95% CI 0.09–1.23), sotagliflozin (OR 0.25, 95% CI 0.03–2.24), canagliflozin 100 mg (OR 3.00, 95% CI 0.31–28.81), and bexagliflozin (OR 1.50, 95% CI 0.06–36.99). No evidence of publication bias was detected (Egger’s p = 0.96).

Conclusions

SGLT2 inhibitors do not significantly alter the risk of PD. These findings support their neurological safety, though longer follow-up and dedicated neurodegenerative outcome trials are warranted.

Citation

Alexander TB, Rissardo JP, Caprara AL, Walker IM. Do SGLT2 Inhibitors Influence Parkinson’s Disease Risk? A Meta-analysis of Randomized Trials (P6-17.012). Neurology 2026;106(11_suppl_1):862. doi: 10.1212/WNL.0000000000213157.

Figure 1. Forest plot of randomized trials evaluating SGLT2 inhibitors and Parkinson’s disease risk, showing no significant association (OR 0.55; 95% CI 0.27–1.12) with negligible heterogeneity.

Abstract - Responsive Neurostimulation Targeting Thalamic Nuclei in Lennox-Gastaut Syndrome: A Systematic Review of Clinical Outcomes and Programming Parameters (P1-10.002)

Title: Responsive Neurostimulation Targeting Thalamic Nuclei in Lennox-Gastaut Syndrome: A Systematic Review of Clinical Outcomes and Programming Parameters (P1-10.002)

Authors: Ana Leticia Fornari Caprara, Jamir Pitton Rissardo, Salman Assad, Evren Burakgazi-Dalkilic, and Eric P. Nagele

Conference: 2026 AAN, Chicago, IL

Objective

To summarize clinical outcomes, stimulation parameters, and safety of thalamic responsive neurostimulation (RNS) in patients with Lennox-Gastaut syndrome (LGS).

Background

LGS is a severe developmental and epileptic encephalopathy often refractory to medications and vagus nerve stimulation. Deep brain stimulation of the centromedian (CM) nucleus has shown promise, but data on closed-loop RNS targeting thalamic nuclei remain limited. Understanding programming strategies and outcomes is critical for optimizing therapy.

Design/Methods

We performed a structured review of PubMed and clinical trial registries through September 2025 for studies reporting RNS in LGS or LGS phenotype. Extracted variables included demographics, seizure outcomes (≥50% responder rate), stimulation parameters, lead configuration, follow-up duration, and adverse events.

Results

Nine studies (n=30 LGS patients) were identified: 2 case reports, 4 case series, 1 multicenter cohort, and 2 feasibility trials. Mean age at implant ranged from 12–17 years; follow-up ranged 5–24 months. Targets included CM (most common), anterior nucleus, and pulvinar. Reported programming typically used high-frequency stimulation (100–200 Hz), pulse width 160 μs, and current 1–3 mA, with individualized titration. ≥50% responder rates varied widely across studies (0%–100%), with a pooled weighted estimate of 56.7% (95% CI: 38.9%–74.4%). Adverse events were rare; one case of myasthenia gravis and two infections requiring intervention were reported. Concurrent neuromodulation (e.g., active VNS) was feasible without device interference. Ongoing IDE trials (NCT05339126) aim to clarify long-term efficacy and biomarker-driven programming.

Conclusions

Thalamic RNS is a promising adjunctive therapy for LGS, offering individualized, closed-loop modulation with favorable safety. Early evidence suggests clinically meaningful seizure reduction in most patients, though heterogeneity in targets and programming underscores the need for prospective trials and standardized protocols.

Citation

Caprara AL, Rissardo JP, Assad S, Burakgazi-Dalkilic E, Nagele EP. Responsive Neurostimulation Targeting Thalamic Nuclei in Lennox-Gastaut Syndrome: A Systematic Review of Clinical Outcomes and Programming Parameters (P1-10.002). Neurology 2026;106(11_suppl_1):689. doi: 10.1212/WNL.0000000000213061.

Figure 1. Summary of included studies on thalamic responsive neurostimulation in Lennox–Gastaut syndrome, detailing targets, stimulation parameters, responder rates, and safety outcomes across reported cohorts.

Abstract - To Anticoagulate or Not? Stroke Prevention in Atrial Fibrillation Patients with a Single Additional Stroke Risk Factor (P3-5.001)

Title: To Anticoagulate or Not? Stroke Prevention in Atrial Fibrillation Patients with a Single Additional Stroke Risk Factor (P3-5.001)

Authors: Arthur Gribachov, Jamir Pitton Rissardo, Ana Leticia Fornari Caprara, and Vishnu Vardhan Byroju

Conference: 2026 AAN, Chicago, IL

Objective

To compare ischemic stroke (IS) risk between oral anticoagulant (OAC) and no-OAC, and new-oral anticoagulants (NOACs) and vitamin K antagonists (VKAs) in atrial fibrillation (AF) patients with a non-sex-related CHA2DS2-VASc score of 1.

Background

The benefit of OAC in AF patients with a single additional stroke risk factor remains uncertain. Evidence comparing NOACs and VKAs in this intermediate-risk group is limited.

Design/Methods

A systematic PubMed search identified studies evaluating stroke prevention in this population. A meta-analysis of four observational studies (six arms) was performed using Mantel-Haenszel methods. Odds ratios with 95% confidence intervals were pooled under fixed- and random-effects models. Tau estimator: DerSimonian-Laird. Heterogeneity was assessed with I² and Cochran’s Q. Publication bias was evaluated using trim-and-fill and fail-safe N. Subgroup analyses were stratified by follow-up duration.

Results

For OAC versus no-OAC, fixed-effect analysis showed a significant reduction in IS risk (OR 0.78; 95% CI 0.69 to 0.87; p < 0.01), whereas random-effects analysis was nonsignificant (OR 0.82; 95% CI 0.62 to 1.09). Subgroup estimates favored OAC at 1.5-year follow-up (OR 0.69) and 2.5-year follow-up (OR 0.74). For NOAC versus VKA, both fixed-effect and random-effect analyses were non-significant, with similar findings at 1-year (OR 0.50; 95% CI 0.19–1.33) and 2-year (OR 0.65; 95% CI 0.30–1.38) follow-up. Heterogeneity was low for OAC versus no OAC (I² = 1%) but moderate for NOAC versus VKA (I² = 36%).

Conclusions

In AF patients with a single additional stroke risk factor, OAC may reduce IS risk compared with no-OAC, particularly with longer follow-up. NOACs and VKAs appear similarly effective in this population.

Citation

Gribachov A, Rissardo JP, Caprara AL, Byroju VV. To Anticoagulate or Not? Stroke Prevention in Atrial Fibrillation Patients with a Single Additional Stroke Risk Factor (P3-5.001). Neurology 2026;106(11_suppl_1):943. doi: 10.1212/WNL.0000000000213209.

Figure 1. Forest plot comparing oral anticoagulation strategies in atrial fibrillation with CHA₂DS₂-VASc = 1, showing reduced stroke risk with OAC versus no-OAC and no difference between NOACs and VKAs.

Abstract - Virtual Reality Meets Reality: Wii-based Rehabilitation Shows Comparable Effects in Parkinson’s Disease (P6-17.007)

Title: Virtual Reality Meets Reality: Wii-based Rehabilitation Shows Comparable Effects in Parkinson’s Disease (P6-17.007)

Authors: Omar Elmandouh, Jamir Pitton Rissardo, Ana Leticia Fornari Caprara, and Ian M. Walker

Conference: 2026 AAN, Chicago, IL

Objective

To evaluate the clinical impact of Wii-based interventions on balance, mobility, gait, and quality of life in individuals with Parkinson’s disease.

Background

Conventional physical therapy remains the cornerstone of rehabilitation in PD, but adherence can be limited by monotony and accessibility barriers. Exergaming platforms, such as the Nintendo Wii, offer an interactive and attractive alternative by combining physical exercise with real-time visual feedback. These systems aim to enhance motor learning and neuroplasticity through task-specific, repetitive practice in a stimulating environment. However, the clinical effectiveness of Wii- based interventions compared to standard therapy remains uncertain, warranting systematic evaluation.

Design/Methods

A meta-analysis of randomized controlled trials comparing Wii-based interventions to conventional therapy. Outcomes included Berg Balance Scale (BBS), 10-Meter Walk Test (10-MWT), Timed Up and Go (TUG), Dynamic Gait Index (DGI), and Parkinson’s Disease Questionnaire-39 (PDQ-39). Pooled estimates were calculated using random-effects models and expressed as mean differences (MD) or standardized mean differences (SMD) with 95% confidence intervals (CI).

Results

Seven trials were included. Wii-based therapy showed no significant advantage over conventional therapy for balance (BBS MD −0.06; 95% CI −1.49 to 1.37; I²=0%) or gait speed (10-MWT SMD −0.22; 95% CI −0.64 to 0.20; I²=0%). Mobility improvements were small and not statistically significant (TUG SMD −0.12; 95% CI −0.36 to 0.13; I²=36%). Gait adaptability showed a non-significant trend favoring control (DGI MD −0.65; 95% CI −1.71 to 0.40; I²=55%). Quality of life changes were minimal (PDQ-39 MD −1.71; 95% CI −5.34 to 1.92; I²=0%). Overall, Wii-based interventions were comparable to conventional therapy across all outcomes, with low to moderate heterogeneity.

Conclusions

Wii-based rehabilitation offers similar benefits to conventional therapy for balance, mobility, and quality of life in Parkinson’s disease. While not superior, its engaging nature may enhance adherence, supporting its role as an alternative or adjunct in rehabilitation programs.

Citation

Elmandouh O, Rissardo JP, Caprara AL, Walker IM. Virtual Reality Meets Reality: Wii-based Rehabilitation Shows Comparable Effects in Parkinson’s Disease (P6-17.007). Neurology 2026;106(11_suppl_1):622. doi: 10.1212/WNL.0000000000213023.

Figure 1. Forest plot of Berg Balance Scale showing no difference between Wii-based and conventional therapy in Parkinson’s disease (MD −0.06; 95% CI −1.49 to 1.37).

Figure 2. Forest plot of 10-Meter Walk Test showing no significant difference in gait speed between Wii-based and conventional therapy (SMD −0.22; 95% CI −0.64 to 0.20).

Figure 3. Forest plot of Timed Up and Go demonstrating small, non-significant mobility differences between Wii-based and conventional therapy (SMD −0.12; 95% CI −0.36 to 0.13).

Abstract - Inverse Association Between Parkinson’s Disease and Rheumatoid Arthritis: A Meta-analysis of Observational Studies (P11-17.004)

Title: Inverse Association Between Parkinson’s Disease and Rheumatoid Arthritis: A Meta-analysis of Observational Studies (P11-17.004)

Authors: Theres Boby Alexander, Jamir Pitton Rissardo, Ana Leticia Fornari Caprara, and Ian M. Walker

Conference: 2026 AAN, Chicago, IL

Objective

To evaluate the association between Parkinson’s disease (PD) and rheumatoid arthritis (RA) using a systematic meta-analysis of observational studies.

Background

PD and RA are chronic disorders with distinct clinical phenotypes but overlapping immunological and inflammatory pathways. Clarifying this relationship is critical for understanding shared pathophysiology and identifying potential therapeutic targets.

Design/Methods

We systematically searched PubMed and Embase for observational studies reporting RA incidence in PD patients (PD→RA) or PD incidence in RA patients (RA→PD). Twelve studies met inclusion criteria (4 PD→RA; 8 RA→PD). Data were pooled using a binary outcome meta-analysis with the Mantel-Haenszel method under a random-effects model (DerSimonian-Laird estimator). Risk ratios (RR) with 95% confidence intervals (CI) were calculated. Between-study heterogeneity was assessed using τ², I², and Cochran’s Q test. Publication bias was evaluated using Egger’s regression, Begg’s rank correlation, and trim-and-fill analysis.

Results

The overall random-effects model showed no significant association (RR 0.99; 95% CI: 0.77 to 1.28; p = 0.95), with high heterogeneity (τ² = 0.15; I² = 95%). Subgroup analysis revealed non-significant association with PD and risk of RA (RR = 0.81; 95% CI: 0.48–1.35), as well as the association with RA and risk of PD (RR = 1.09; 95% CI: 0.79–1.50). Publication bias tests were non-significant (Egger’s p = 0.68; Begg’s p = 0.58), although trim-and-fill suggested one potentially missing study.

Conclusions

PD was not associated with RA risk, and RA was not linked to PD risk. Further studies are needed to elucidate possible association between RA and PD.

Citation

Alexander TB, Rissardo JP, Caprara AL, Walker IM. Inverse Association Between Parkinson’s Disease and Rheumatoid Arthritis: A Meta-analysis of Observational Studies (P11-17.004). Neurology 2026;106(11_suppl_1):861. doi: 10.1212/WNL.0000000000213156.

Figure 1. Forest plot of observational studies assessing bidirectional associations between Parkinson’s disease and rheumatoid arthritis, showing no significant overall relationship and substantial interstudy heterogeneity across subgroups.