Cognitive changes associated with cerebral emboli during coronary intervention.

OBJECTIVE: To investigate factors influencing the frequency and type of microembolic signals (MES) detected using transcranial Doppler (TCD) in patients undergoing elective coronary intervention, and to correlate MES with silent stroke detected using magnetic resonance imaging (MRI) and cognitive dysfunction. METHODS: The subset study of a randomized clinical trial was conducted on 70 patients (58 males; mean age 59.9 ± 8.4 years) who underwent bilateral TCD monitoring of middle cerebral arteries (MCAs) during elective coronary interventions. Neurologic examination and brain MRI were performed prior to, and 24 h post­intervention. Cognitive function tests were performed prior to, and on day 30 post­intervention. RESULTS: The incidence of detected MES was 94.3 %. Eighteen (25.7 %) patients had new clinically asymptomatic ischemic lesions on MRI. The number of solid MES negatively correlated with changes in revised Addenbrooke's Cognitive Examination test (ACE-R) and, the number of solid MES and combinations of solid and gaseous MES negatively correlated with changes in Mini Mental­State Examination (MMSE) conducted on day 30 after the intervention (p < 0.05 in all cases). CONCLUSION: Cardiac catheterization was associated with a high risk of cerebral embolism in our patients. A higher number of solid MES and combinations of solid and gaseous MES was associated with the deterioration in cognitive tests (Tab. 5, Fig. 3, Ref. 30).

SARS-CoV-2 RNA in the Cerebrospinal Fluid of a Patient with Long COVID.

Over 10% of COVID-19 convalescents report post-COVID-19 complications, namely, 'long COVID' or 'post-COVID syndrome,' including a number of neuro-psychiatric symptoms. The pathophysiology of COVID-19 in the central nervous system is poorly understood but may represent post-COVID injury, ongoing sterile maladaptive inflammation, or SARS-CoV-2 persistence. We describe a long COVID patient with SARS-CoV-2 RNA in the cerebrospinal fluid, which seems important, specifically due to recent reports of gray matter volume loss in COVID-19 patients. Further studies of SARS-CoV2 RNA, markers of inflammation, and neuronal damage in the CSF of patients with long COVID would be useful and should address whether the CNS can serve as a reservoir of SARS-CoV-2, clarify the pathway by which COVID-19 contributes to CNS dysfunction, and how best to therapeutically address it.

The contribution of cerebrovascular risk factors, metabolic and inflammatory changes to cognitive decline in Parkinson's disease: preliminary observations.

To determine whether systemic medical factors, such as vascular risk factors, metabolic and inflammatory markers contribute to cognitive decline in Parkinson's disease (PD); if confirmed to determine whether a clinically applicable risk factor model can predict the conversion from normal cognition (NC) to mild cognitive impairment (MCI). 58 patients who met the UK Brain Bank Criteria for PD underwent clinical and laboratory assessment at study entry; 47 patients were re-assessed after 2 years. Medical history, vascular risk (QRISK2), blood metabolic and inflammatory factors, brain vessel examinations, activity of daily living, and neuropsychological testing were performed. Forty patients had NC and 18 patients had MCI at baseline. Patients with MCI had higher level of interleukin 6, folic acid below normal range and higher L-dopa equivalent dose compared to cognitive normal patients at baseline. Patients with NC at baseline were classified into two groups: patients who remained cognitively normal (non-converters, n = 23) and patients who progressed to MCI (converters, n = 11). MCI converters were older at baseline and had higher QRISK2 than the non-converters. Patients with higher QRISK2, lower uric acid level and lower activity of daily living scale at baseline had a higher risk of converting from NC to MCI with a sensitivity of 72.2%, a specificity of 87%, and an overall accuracy of 82.4%. Systemic medical factors are associated with cognitive impairment in PD both cross-sectionally and longitudinally. A risk factor model predicting the decline from NC to MCI could be constructed.

Sonolysis in risk reduction of symptomatic and silent brain infarctions during coronary stenting (SONOREDUCE): Randomized, controlled trial.

BACKGROUND: Silent brain infarcts can be detected on magnetic resonance imaging (MRI) in ~22% of patients after coronary angioplasty and stenting (CS). The effect of periprocedural sonolysis on the risk of new brain infarcts during CS was examined. METHODS: Patients undergoing elective CS were allocated randomly to a bilateral sonolysis group (70 patients, 58 men; mean age, 59.9 years) or a control group (74 patients, 45 men; mean age, 65.5 years). Neurologic examination, cognitive function tests, and brain MRI were performed prior to intervention and at 24 h after CS. Neurologic examination and cognitive function tests were repeated at 30 days after CS. RESULTS: No significant differences were observed in the number of patients with new infarcts (25.7 vs. 18.9%, P = 0.423), the number of lesions (1.3 ±â€¯1.0 vs. 2.9 ±â€¯5.3, P = 0.493), lesion volume (0.16 ±â€¯0.34 vs. 0.28 ±â€¯0.60 mL, P = 0.143), and the number of patients with new ischemic lesions in the insonated MCA territories (18.6vs. 17.6%, P = 0.958) between the sonolysis group and the control group. There were no cases of stroke, transient ischemic attack, myocardial infarction, or death in the two groups. Intracranial bleeding was reported only in 1 patient in the control group (0 vs. 1.4%, P = 0.888). Clock-drawing test scores at 30 days were significantly higher in the sonolysis group than in the control group (median 3.0 vs. 2.5, P = 0.031). CONCLUSIONS: Sonolysis does not reduce the risk of new brain infarcts after CS. The effect of sonolysis on number and volume of ischemic lesions and cognitive function should be assessed in further studies.

RNF213 Rare Variants in Slovakian and Czech Moyamoya Disease Patients.

RNF213/Mysterin has been identified as a susceptibility gene for moyamoya disease, a cerebrovascular disease characterized by occlusive lesions in the circle of Willis. The p.R4810K (rs112735431) variant is a founder polymorphism that is strongly associated with moyamoya disease in East Asia. Many non-p.R4810K rare variants of RNF213 have been identified in white moyamoya disease patients, although the ethnic mutations have not been investigated in this population. In the present study, we screened for RNF213 variants in 19 Slovakian and Czech moyamoya disease patients. A total of 69 RNF213 coding exons were directly sequenced in 18 probands and one relative who suffered from moyamoya disease in Slovakia and the Czech Republic. We previously reported one proband harboring RNF213 p.D4013N. Results from the present study identified four rare variants other than p.D4013N (p.R4019C, p.E4042K, p.V4146A, and p.W4677L) in four of the patients. P.V4146A was determined to be a novel de novo mutation, and p.R4019C and p.E4042K were identified as double mutations inherited on the same allele. P.W4677L, found in two moyamoya disease patients and an unaffected subject in the same pedigree, was a rare single nucleotide polymorphism. Functional analysis showed that RNF213 p.D4013N, p.R4019C and p.V4146A-transfected human umbilical vein endothelial cells displayed significant lowered migration, and RNF213 p.V4146A significantly reduced tube formation, indicating that these are disease-causing mutations. Results from the present study identified RNF213 rare variants in 22.2% (4/18 probands) of Slovakian and Czech moyamoya disease patients, confirming that RNF213 may also be a major causative gene in a relative large population of white patients.