Acute Ischemic Stroke AIS
Conditions
Keywords
Stroke, Neuroinflammation, Palmitoylethanolamide, Luteolin
Brief summary
Acute ischemic stroke is caused by reduced blood supply to the brain associated with neuroinflammation. This mechanism contributes to acute neuronal death and persists even after reopening of the closed vessel, with consequent limitation of clinical and functional improvement. Experimental and clinical evidence demonstrated the anti-inflammatory and neuroprotective effect of micronized and ultramicronized Palmitoylethanolamide (PEA). The aim of this study is to evaluate the effect of co-ultramicronized PEA and luteolin (700 mg + 70 mg in 10 ml) on the clinical outcomes of patients with acute ischemic stroke undergoing mechanical thrombectomy.
Interventions
DIETARY_SUPPLEMENTco-ultramicronized Palmitoylethanolamide + Luteolin (770 mg)
oral suspension, 10 ml twice a day (every 12 hours) for 7 days
OTHERPlacebo
oral suspension,10 ml twice a day (every 12 hours) for 7 days
PROCEDUREThrombectomy
Endovascular Thrombectomy in all eligible patients, according to national acute stroke treatment guidelines
Sponsors
Ospedali Riuniti Trieste
Study design
Allocation
RANDOMIZED
Intervention model
PARALLEL
Primary purpose
SUPPORTIVE_CARE
Masking
QUADRUPLE (Subject, Caregiver, Investigator, Outcomes Assessor)
Eligibility
Sex/Gender
ALL
Age
60 Years to No maximum
Healthy volunteers
No
Inclusion criteria
* age ≥ 60 years * both genders * first acute ischemic stroke in the middle cerebral artery area confirmed by angio-CT and CTP, eligible for mechanical thrombectomy according to national guidelines * NIHSS \> 6 * compliant patients * signed informed consent
Exclusion criteria
* hemorrhagic stroke * previous stroke (TIA, ischemic or hemorrhagic stroke) * presence of clinically evident neurodegenerative diseases (Alzheimer's disease, Parkinson's disease) * presence of psychiatric comorbidity (schizophrenia, bipolar disorder, depressive syndrome) * presence of chronic inflammatory diseases (chronic inflammatory bowel disease, vasculitis etc.) * current or previous neoplasia * uncontrolled diabetes mellitus (glycemia on admission \>400 mg/dL or \<50 mg/dL) * dysphagia, with inability to feed orally * inability to provide informed consent * pre-existing disability (pre-stroke mRS \>2) * allergy or hypersensitivity to the study treatment
Design outcomes
Primary
| Measure | Time frame | Description |
|---|---|---|
| Change from baseline in the mean neurological disability score assessed by National Institutes of Health Stroke Scale (NIHSS), at 3 and 7 days (end of treatment) after hospitalization, between the two groups | Baseline-hospitalization, 3 and 7 days | NIHSS score ranges from 0 to 42, with higher scores indicating more severe neurological deficit |
| Change from baseline in the mean functional disability score assessed by modified Rankin Scale (mRS), at 7 days after hospitalization, between the two groups | Baseline-hospitalization and 7 days | mRS consists of 6 grades from 0 to 5, with 0 corresponding to no symptoms and 5 corresponding to severe disability |
Secondary
| Measure | Time frame | Description |
|---|---|---|
| Volume of restored penumbra | Baseline-hospitalization, 3 days | Volume of initial penumbra on admission CT perfusion scans not evolved to ischemic lesion on follow-up CT scan at 72 hrs since stroke onset |
| Incidence of death and/or major vascular events (recurrent strokes, myocardial ischemia or peripheral arterial ischemia) from baseline to 7 days after hospitalization, between the two groups | From baseline to 7 days | — |
| Change from baseline of inflammatory and brain damage mediators [interleukin- 6 (IL-6), matrix metalloproteinase- 9 (MMP-9) and neurofilament light (NfL)] plasma levels at 3 and 7 days after hospitalization, between the two groups | Baseline-hospitalization, 3 and 7 days | — |
Countries
Italy
Contacts
Primary ContactMarcello Naccarato, MD, PhD
Backup ContactPaola Caruso, MD
Outcome results
None listed