Explore the vast range of titles available.

Parkinson's disease or parkinsonism have been described after infections by viruses, such as influenza A, Epstein-Barr virus, varicella zoster, hepatitis C virus, HIV, Japanese encephalitis virus, or West Nile virus.1 We report a patient with probable Parkinson's disease, who was diagnosed after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Because of the worsening of tremor in his right extremities, in a follow-up visit on June 29, biperiden was added at a dose of 2 mg daily, and increased to 4 mg daily after 1 week, which resulted in improvement of the tremor. Other researchers have proposed the so-called multiple hit hypothesis, by which the combination of toxic stress and an inhibition of neuroprotective responses can lead to neuronal death.4 Parkinson's disease is often preceded by anosmia, which is a common feature of SARS-CoV-2 infection.5 Immune activation in the olfactory system might eventually lead to the misfolding of α-synuclein and the development of Parkinson's disease.6 This mechanism is supported by post-mortem studies, showing increased levels of TNF,7 IL1, and IL6.8 Moreover, patients with Parkinson's disease had an elevated CSF antibody response to seasonal coronaviruses, compared with age-matched healthy controls.9 In Ashkenazi-Jewish people with Parkinson's disease, about a third are carriers of either a GBA or a LRRK2 mutation.10 A genetic analysis for these mutations and 62 other mutations associated with the disease was negative and our patient had no previous family history of Parkinson's disease.

In this international registry study of patients who had a transient ischemic attack or minor stroke and who were evaluated on an urgent basis by stroke specialists, the 1-year risk of recurrent stroke was 5.1%, which is lower than the risk reported in historical cohorts. Previous studies conducted between 1997 and 2003 estimated that the risk of stroke or an acute coronary syndrome was 12 to 20% during the first 3 months after a transient ischemic attack (TIA) or minor stroke. 1 , 2 Since then, there have been major changes in the management of TIA, including urgent management in specialized units, implementation of immediate investigations, and rapid treatment with antithrombotic agents and other stroke-prevention strategies. 1 – 4 Given these changes, the current prognosis of patients who have had a TIA and the role of risk-scoring systems in patients receiving urgent care are unclear. 5 – 11 Current guidelines recommend . . .

Whether surgery is beneficial for patients with asymptomatic carotid stenosis is controversial. Better methods of identifying patients who are likely to develop stroke would improve the risk–benefit ratio for carotid endarterectomy. We aimed to investigate whether detection of asymptomatic embolic signals by use of transcranial doppler (TCD) could predict stroke risk in patients with asymptomatic carotid stenosis. The Asymptomatic Carotid Emboli Study (ACES) was a prospective observational study in patients with asymptomatic carotid stenosis of at least 70% from 26 centres worldwide. To detect the presence of embolic signals, patients had two 1 h TCD recordings from the ipsilateral middle cerebral artery at baseline and one 1 h recording at 6, 12, and 18 months. Patients were followed up for 2 years. The primary endpoint was ipsilateral stroke and transient ischaemic attack. All recordings were analysed centrally by investigators masked to patient identity. 482 patients were recruited, of whom 467 had evaluable recordings. Embolic signals were present in 77 of 467 patients at baseline. The hazard ratio for the risk of ipsilateral stroke and transient ischaemic attack from baseline to 2 years in patients with embolic signals compared with those without was 2·54 (95% CI 1·20–5·36; p=0·015). For ipsilateral stroke alone, the hazard ratio was 5·57 (1·61–19·32; p=0·007). The absolute annual risk of ipsilateral stroke or transient ischaemic attack between baseline and 2 years was 7·13% in patients with embolic signals and 3·04% in those without, and for ipsilateral stroke was 3·62% in patients with embolic signals and 0·70% in those without. The hazard ratio for the risk of ipsilateral stroke and transient ischaemic attack for patients who had embolic signals on the recording preceding the next 6-month follow-up compared with those who did not was 2·63 (95% CI 1·01–6·88; p=0·049), and for ipsilateral stroke alone the hazard ratio was 6·37 (1·59–25·57; p=0·009). Controlling for antiplatelet therapy, degree of stenosis, and other risk factors did not alter the results. Detection of asymptomatic embolisation on TCD can be used to identify patients with asymptomatic carotid stenosis who are at a higher risk of stroke and transient ischaemic attack, and also those with a low absolute stroke risk. Assessment of the presence of embolic signals on TCD might be useful in the selection of patients with asymptomatic carotid stenosis who are likely to benefit from endarterectomy. British Heart Foundation.

Stroke remains a major global health concern, ranking as the second most common cause of death and the third leading cause of disability worldwide. Despite advances in therapy and management, ischemic stroke patients continue to face high risks of recurrence, cardiovascular events, and mortality. Effective secondary stroke prevention is critical, encompassing antithrombotic therapy, management of vascular risk factors such as hypertension, dyslipidemia, and diabetes mellitus, and conducting healthy lifestyle. Approximately 80% of strokes are ischemic, with a significant proportion attributable to large-artery atherosclerosis of the extra- and intracranial arteries, particularly in the internal carotid artery. Atherothrombotic strokes, linked to plaque rupture and thrombus formation, present a notably high risk of recurrence. Inflammatory and immune mechanisms play pivotal roles in both the initiation and progression of atherosclerosis and stroke. Colchicine, an anti-inflammatory agent, has shown potential in managing cardiovascular disease, though its effects on stroke reduction and prevention have been inconsistent across studies. Its possible protective role against stroke is attributed to its anti-inflammatory actions, which include disrupting microtubule dynamics, inhibiting immune cell movement, and lowering inflammatory markers like L-Selectin and E-Selectin, while also suppressing interleukin release. Glucagon-like peptide-1 receptor agonists (GLP-1RA) agents have emerged as effective therapies for type 2 diabetes with notable cardiovascular benefits. These agents enhance glucose control while also providing protective effects against atherosclerosis and stroke. GLP-1RA drugs work by mimicking the effects of GLP-1, a peptide that regulates insulin release and glucose metabolism. They also exhibit anti-inflammatory properties, potentially reducing stroke risk through mechanisms such as improved endothelial function and reduced plaque formation. Clinical trials have indicated that GLP-1RA agents can significantly lower the incidence of nonfatal strokes and major adverse events. This narrative review underscores the importance of targeting inflammation to reduce the risk of recurrent stroke, emphasizing recent studies on colchicine and GLP-1RA. It consolidates evidence regarding the efficacy of these agents in secondary stroke prevention; however, future studies are needed to further explore their mechanisms and roles in comprehensive stroke management strategies.

Stroke is a major cause of cognitive impairment and dementia in adults, however the role of the ischemic lesions themselves, on top of other risk factors known in the elderly, remains controversial. This study used structural equation modeling to determine the respective impact of the new ischemic lesions' volume, preexisting white matter lesions and white matter integrity on post stroke cognitive state. Consecutive first ever mild to moderate stroke or transient ischemic attack patients recruited into the ongoing prospective TABASCO study underwent magnetic resonance imaging scans within seven days of stroke onset and were cognitively assessed one year after the event using a computerized neuropsychological battery. The volumes of both ischemic lesions and preexisting white matter lesions and the integrity of the normal appearing white matter tissue were measured and their contribution to cognitive state was assessed using structural equation modeling path analysis taking into account demographic parameters. Two models were hypothesized, differing by the role of ischemic lesions' volume. Structural equation modeling analysis of 142 patients confirmed the predominant role of white matter lesion volume (standardized path coefficient β =  -0.231) and normal appearing white matter integrity (β =  -0.176) on the global cognitive score, while ischemic lesions' volume showed no such effect (β = 0.038). The model excluding the ischemic lesion presented better fit to the data (comparative fit index 0.9 versus 0.092). Mild to moderate stroke patients with preexisting white matter lesions are more vulnerable to cognitive impairment regardless of their new ischemic lesions. Thus, these patients can serve as a target group for studies on cognitive rehabilitation and neuro-protective therapies which may, in turn, slow their cognitive deterioration.

A naturally occurring loss-of-function mutation in the gene for C-C chemokine receptor type 5 (CCR5-Δ32) has recently been reported as a protective factor in post-stroke motor and cognitive recovery. We sought to examine whether this mutation also prevented the development of depressive symptoms up to 2 years after a stroke. Participants were survivors of a first-ever mild to moderate ischemic stroke or transient ischemic attack from the TABASCO prospective study who underwent a 3 T MRI at baseline and were examined by a multiprofessional team 6, 12 and 24 months after the event, including an evaluation of depressive symptoms using the Geriatric Depression Scale. CCR5-Δ32 status and a baseline depression evaluation were available for 435 patients. Compared with noncarriers, CCR5-Δ32 carriers (16.1%) had fewer depressive symptoms at admission (p = 0.035) and at 6 months (p < 0.001), 12 months (p < 0.001) and 24 months (p = 0.006) after the index event. This association remained significant at 6 and 12 months after adjustment for age, sex, education, antidepressant use, ethnicity and the presence of cortical infarcts. These findings were more robust in women. Compared to baseline, depressive symptoms in CCR5-Δ32 noncarriers tended to remain stable or grow worse over time, but in CCR5-Δ32 carriers, symptoms tended to improve. A limitation of this study was the exclusion of patients who had a severe stroke or who had pre-stroke depression. Carriers of the CCR5-Δ32 allele had a lower tendency to develop depressive symptoms post-stroke, and this phenomenon was more prominent in women. These findings could have clinical implications; they suggest a mechanism-based treatment target for post-stroke depression. Drugs mimicking this loss-of-function mutation exist and could serve as a novel antidepressant therapy.

In 2014, the definition of embolic strokes of undetermined source (ESUS) emerged as a new clinical construct to characterize cryptogenic stroke (CS) patients with complete vascular workup to determine nonlacunar, nonatherosclerotic strokes of presumable embolic origin. NAVIGATE ESUS, the first phase III randomized-controlled, clinical trial (RCT) comparing rivaroxaban (15 mg daily) with aspirin (100 mg daily), was prematurely terminated for lack of efficacy after enrollment of 7213 patients. Except for the lack of efficacy in the primary outcome, rivaroxaban was associated with increased risk of major bleeding and hemorrhagic stroke compared with aspirin. RE-SPECT ESUS was the second phase III RCT that compared the efficacy and safety of dabigatran (110 or 150 mg, twice daily) to aspirin (100 mg daily). The results of this trial have been recently presented and showed similar efficacy and safety outcomes between dabigatran and aspirin. Indirect analyses of these trials suggest similar efficacy on the risk of ischemic stroke (IS) prevention, but higher intracranial hemorrhage risk in ESUS patients receiving rivaroxaban compared to those receiving dabigatran (indirect HR = 6.63, 95% CI: 1.38–31.76). ESUS constitute a heterogeneous group of patients with embolic cerebral infarction. Occult AF represents the underlying mechanism of cerebral ischemia in the minority of ESUS patients. Other embolic mechanisms (paradoxical embolism via patent foramen ovale, aortic plaque, nonstenosing unstable carotid plaque, etc.) may represent alternative mechanisms of cerebral embolism in ESUS, and may mandate different management than oral anticoagulation. The potential clinical utility of ESUS may be challenged since the concept failed to identify patients who would benefit from anticoagulation therapy. Compared with the former diagnosis of CS, ESUS patients required thorough investigations; more comprehensive diagnostic work-up than is requested in current ESUS diagnostic criteria may assist clinicians in uncovering the source of brain embolism in CS patients and individualize treatment approaches.

Background Study aimed at investigation of pathogenic role and prognostic value of several selected cerebrospinal fluid acute phase factors that can reflect the severity of ischemic brain damage. Methods Ninety five acute ischemic stroke patients were investigated. Ischemic region visualized at the twenty fourth hour by conventional Magnetic Resonance Imaging. Stroke severity evaluated by National Institute Health Stroke Scale. One month outcome of disease was assessed by Barthel Index. Cerebrospinal fluid was taken at the sixth hour of stroke onset. CSF pro- and anti-inflammatory cytokines were studied by Enzyme Linked Immunosorbent Assay. Nitric Oxide and Lipoperoxide radical were measured by Electron Paramagnetic Resonance. CSF Nitrate levels were detected using the Griess reagent. Statistics performed by SPSS-11.0. Results At the sixth hour of stroke onset, cerebrospinal fluid cytokine levels were elevated in patients against controls. Severe stroke patients had increased interleukin-6 content compared to less severe strokes (P < 0.05). Cerebrospinal fluid Electron Paramagnetic Resonance signal of nitric oxide was increased in patients against controls. Severe stroke group had an elevated Electron Paramagnetic Resonance signal of lipoperoxiradical compared to less severe stroke. Cerebrospinal fluid nitrate levels in less severe stroke patients were higher than those for severe stroke and control. Positive correlation was established between the initial interleukin-6 content and ischemic lesion size as well as with National Institute Health Stroke Scale score on the seventh day. Initial interleukin-6 and nitrate levels in cerebrospinal fluid found to be significant for functional outcome of stroke at one month. Conclusion According to present study the cerebrospinal fluid contents of interleukin-6 and nitrates seem to be the most reliable prognostic factors in acute phase of ischemic stroke.

Background: Despite declining age-adjusted stroke mortality rates, the disease remains the third most common cause of death in Israel. Based on a national survey, we examined mortality rates during the first 3 years after a first-ever acute ischemic stroke (IS) and the major predictors of short-term (1 month) and long-term (3 years) mortality. Methods: In the National Acute Stroke Israeli Survey (NASIS 2004), data were collected on all hospitalized stroke patients in Israel during a 2-month period. Mortality rates for first-ever IS were assessed at 1 month and 3 years and predictors of death were evaluated using the Cox proportional hazard model. Results: A total of 1,079 first-ever IS patients were included. Survival data were complete for over 99% of patients. Cumulative mortality rates were 9.9% at 1 month and 31.1% at 3 years. Of the survivors at 1 month, 23.5% did not survive for 3 years. At 1 month, the hazard ratio (HR) for death significantly increased with stroke severity. One-month mortality was also associated with a decreased level of consciousness (HR 2.9, 95% CI 1.7–5.1), total anterior circulation infarction (TACI); HR 4.9, 95% CI 1.6–15.2), temperature on admission (HR 1.5, 95% CI 1.1–2.1 per 1°C), age (HR 1.04, 95% CI 1.02–1.07 per year) and glucose levels on admission (HR 1.003, 95% CI 1.001–1.006 per 1 mg/dl). Age-adjusted proportions of diabetes and chronic heart failure were considerably higher in the deceased compared with survivors at 3 years (48 vs. 38 and 21 vs. 9%, respectively). In the multivariate survival analyses, predictors of death at 1 month also predicted death at 3 years; however, history of dementia (HR 1.5, 95% CI 1.0–2.4), diabetes (HR 1.6, 95% CI 1.0–2.4), peripheral artery disease (HR 1.7, 95% CI 1.1–2.8), chronic heart failure (HR 1.6, 95% CI 1.1–2.4) and malignancy (HR 1.7, 95% CI 1.1–2.7) were additional predictors of long-term mortality for patients surviving the first month after stroke. Conclusions: Approximately one third of patients did not survive 3 years after the first-ever IS. While age and markers of severe stroke were the major predictors of death at 1 month, comorbidities and variables associated with atherosclerotic vascular disease predicted long-term mortality. Improved control of these factors can potentially reduce long-term mortality in stroke victims.

In a large trial, the estimated incidence of stroke, systemic embolism, hemorrhage, or death was 2.8 percentage points lower to 0.5 percentage points higher with early than with later use of direct oral anticoagulants.