Relationships of Hematocrit With Chronic Covert and Acute Symptomatic Lacunar Ischemic Lesions.

BACKGROUND AND OBJECTIVES: Red blood cell (RBC) concentrations are known to associate with ischemic stroke. It is unclear whether RBC concentrations associate specifically with small vessel disease lacunar infarcts. We investigated the hypothesis that RBC concentrations associate with both chronic covert and acute symptomatic brain MRI lacunar infarcts. METHODS: A cross-sectional observational analysis was performed across 2 cohorts with available hematocrit (as the assessment of RBC concentration exposure) and MRI outcome data. The primary setting was a population-based cohort of stroke-free, older adult (>50 years) participants from the Northern Manhattan Study (NOMAS) enrolled between 2003 and 2009. A second replication sample consisted of patients admitted with acute stroke and enrolled into the Columbia Stroke Registry (CSR) between 2005 and 2020. Associations of hematocrit with (1) chronic, covert lacunar infarcts and (2) symptomatic (i.e., acute) lacunar strokes were separately assessed from the NOMAS and CSR cohorts, respectively, using general additive models after adjusting for relevant covariates. RESULTS: Of 1,218 NOMAS participants analyzed, 6% had chronic, covert lacunar infarcts. The association between hematocrit and these covert lacunar infarcts was U-shaped (χ2 = 9.21 for nonlinear associations; p = 0.03), with people with hematocrit extremes being more likely to have covert lacunar infarcts. Of the 1,489 CSR patients analyzed, 23% had acute lacunar strokes. In this sample, only the relationships of increased hematocrit concentrations and lacunar strokes were replicated (adjusted coefficient ß = 0.020; SE = 0.009; p = 0.03). DISCUSSION: We identified relationships of hematocrit with MRI lacunar infarcts in both stroke-free and ischemic stroke cohorts, respectively. The relationship between increased hematocrit concentrations with lacunar infarcts was replicated in both cohorts. Further studies are required to clarify the mechanisms behind the relationships of hematocrit with ischemic cerebral small vessel disease.

Duration of Heightened Risk of Acute Ischemic Stroke After Hospitalization for Acute Systolic Heart Failure.

Background The duration and magnitude of increased stroke risk after a hospitalization for acute systolic heart failure (HF) remains uncertain. Methods and Results The authors performed a retrospective cohort study using claims (2008-2018) from a nationally representative 5% sample of Medicare beneficiaries aged ≥66 years. Cox regression models were fitted separately for the groups with and without acute systolic HF to examine its association with the incidence of ischemic stroke after adjustment for demographics, stroke risk factors, and Charlson comorbidities. Corresponding survival probabilities were used to compute the hazard ratio (HR) in each 30-day interval after discharge. The authors stratified patients by the presence of atrial fibrillation (AF) before or during the hospitalization for acute systolic HF. Among 2 077 501 eligible beneficiaries, 94 641 were hospitalized with acute systolic HF. After adjusting for demographics, stroke risk factors, and Charlson comorbidities, the risk of ischemic stroke was highest in the first 30 days after discharge from an acute systolic HF hospitalization for patients with AF (HR, 2.4 [95% CI, 2.1-2.7]) and without AF (HR, 4.6 [95% CI, 4.0-5.3]). The risk of stroke remained elevated for 60 days in patients with AF (HR, 1.4 [95% CI, 1.2-1.6]) and was not significantly elevated afterward. The risk of stroke remained significantly elevated through 330 days in patients without AF (HR, 2.1 [95% CI, 1.7-2.7]) and was no longer significantly elevated afterward. Conclusions A hospitalization for acute systolic HF is associated with an increased risk of ischemic stroke up to 330 days in patients without concomitant AF.

Transcirculation Embolization to New Territory During Mechanical Thrombectomy for Acute Ischemic Stroke.

Embolization in new territories (ENT) is a known complication of mechanical thrombectomy with incidence dependent upon a variety of procedural factors. We present 2 cases of anterior circulation to posterior circulation ENT. These cases were managed with manual aspiration thrombectomy with excellent radiographic and clinical outcome. We present the available literature involving ENT along with our experience in management.

Breakthrough Seizure Associated With Kratom Use in Patients With Epilepsy.

PURPOSE OF REVIEW: Kratom (mitragynine) is a commercially available herbal supplement that is gaining popularity in the United States. Kratom is associated with a variety of neurologic effects. This review will discuss kratom's association with seizure through 3 cases and highlight what neurologists should know about kratom's clinical effects and legal status. RECENT FINDINGS: Kratom is currently commercially available, unscheduled by the US Drug Enforcement Administration, and a topic of regulatory debate in the United States. Large poison center reviews have suggested that kratom use is associated with seizure. There have been limited case studies to corroborate this finding. We present 3 cases in which seizures were associated with kratom use in patients treated for epilepsy. SUMMARY: Since 2008, kratom use is rising in prevalence in the United States aided by lack of regulation. Neurologists need to be aware of its association with seizure and other neurologic side effects.

Bruxism in Acute Neurologic Illness.

PURPOSE OF REVIEW: While traditionally encountered in ambulatory settings, bruxism occurs in patients with a variety of acute neurologic illnesses including encephalitis, intracerebral hemorrhage, traumatic brain injury, hypoxic-ischemic encephalopathy, and acute ischemic stroke. Untreated bruxism in acute neurologic illness can lead to tooth loss, difficulty in mouth care resulting in recurrent aspiration pneumonia, endotracheal tube dislodgement, and even tongue laceration or amputation. Inpatient clinicians should be aware of the etiologies and management strategies for bruxism secondary to acute neurologic illness. RECENT FINDINGS: Management strategies for bruxism are varied and include pharmacologic and non-pharmacologic therapies in addition to onabotulinumtoxinA (BoNT-A). Bruxism impacts patients with a variety of acute neurologic illnesses, and emerging evidence suggests successful and safe treatment strategies.

Cavernous Thrombophlebitis Secondary to Cavernous Internal Carotid Mycotic Aneurysm.

We report a case of a 22-year-old male with a history of intravenous drug use presenting with cavernous sinus syndrome secondary to cavernous thrombophlebitis. The source of the thrombophlebitis was from a mycotic aneurysm in the setting of fungal endocarditis. With antifungal therapy and aortic valve replacement, the patient had full resolution of cranial nerve deficits. Descriptions of mycotic aneurysms of the cavernous portion of the internal carotid artery are limited to case reports and case series. Most have been nonendocarditic in etiology with poor prognosis. We present a unique case with endocarditic etiology and an excellent prognosis.

Peroxiredoxin 6 (Prdx6) supports NADPH oxidase1 (Nox1)-based superoxide generation and cell migration.

Nox1 is an abundant source of reactive oxygen species (ROS) in colon epithelium recently shown to function in wound healing and epithelial homeostasis. We identified Peroxiredoxin 6 (Prdx6) as a novel binding partner of Nox activator 1 (Noxa1) in yeast two-hybrid screening experiments using the Noxa1 SH3 domain as bait. Prdx6 is a unique member of the Prdx antioxidant enzyme family exhibiting both glutathione peroxidase and phospholipase A2 activities. We confirmed this interaction in cells overexpressing both proteins, showing Prdx6 binds to and stabilizes wild type Noxa1, but not the SH3 domain mutant form, Noxa1 W436R. We demonstrated in several cell models that Prdx6 knockdown suppresses Nox1 activity, whereas enhanced Prdx6 expression supports higher Nox1-derived superoxide production. Both peroxidase- and lipase-deficient mutant forms of Prdx6 (Prdx6 C47S and S32A, respectively) failed to bind to or stabilize Nox1 components or support Nox1-mediated superoxide generation. Furthermore, the transition-state substrate analogue inhibitor of Prdx6 phospholipase A2 activity (MJ-33) was shown to suppress Nox1 activity, suggesting Nox1 activity is regulated by the phospholipase activity of Prdx6. Finally, wild type Prdx6, but not lipase or peroxidase mutant forms, supports Nox1-mediated cell migration in the HCT-116 colon epithelial cell model of wound closure. These findings highlight a novel pathway in which this antioxidant enzyme positively regulates an oxidant-generating system to support cell migration and wound healing.