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Journal of Neurosciences in Rural... 2024Cerebral microbleeds (MBs) are recently described entity on magnetic resonance (MR) neuroimaging and are considered one of the markers of small vessel disease. We aimed...
OBJECTIVES
Cerebral microbleeds (MBs) are recently described entity on magnetic resonance (MR) neuroimaging and are considered one of the markers of small vessel disease. We aimed to study the clinicoradiological features of cerebral MBs that were diagnosed in MR neuroimaging.
MATERIALS AND METHODS
We studied 109 South Indian patients, who presented to a tertiary care institution for MR neuroimaging with cerebral MBs as diagnosed on MR neuroimaging based on either the gradient T2* imaging or susceptibility-weighted imaging. The clinical details and coexisting MR features of infarcts, macrohemorrhages, lacunar infarcts, and white matter leukoaraiosis were evaluated and analyzed.
RESULTS
Of 109 patients, 79 were males and 30 were females. Associated clinical comorbidities noted include hypertension (62.39%), diabetes (23.85%), and alcoholism (31.19%) apart from the history of anti-platelet/anti-coagulant usage (15.5%), previous cardiac disease (12.84%), and previous stroke/transient ischemic attacks (9.17%). Other co-existing neuroimaging abnormalities noted include cortical infarcts (27.52%), old hemorrhages (29.36%), lacunar infarcts (56.88%), and white matter leukaraiosis (67.89%).
CONCLUSION
The clinicoradiological features of cerebral MBs in South Indian patients are similar to other Asian and Western studies with significant coexistence of clinical comorbidities and imaging features of small vessel changes. Further studies with a larger sample are needed to correlate the grade of MBs to the individual risk of these clinicoradiological characteristics.
PubMed: 38746508
DOI: 10.25259/JNRP_331_2023 -
Revista de Neurologia May 2024Basilar artery dolichoectasia (BADE) refers to abnormal enlargement or displacement of the basilar artery (BA). The previously reported prevalence of BADE among patients...
INTRODUCTION
Basilar artery dolichoectasia (BADE) refers to abnormal enlargement or displacement of the basilar artery (BA). The previously reported prevalence of BADE among patients with stroke is 0.3 to 33.1%, however, it might vary among studied populations. We aim is to determine the prevalence of BADE in patients presenting with acute ischemic stroke (AIS) or transient ischemic attack (TIA) in a Stroke Unit in a single center in Spain.
PATIENTS AND METHODS
Patients 50 years old or older presenting with AIS or TIA were eligible for inclusion. Demographic and clinical data were prospectively collected. Two neuroradiologists, blind to each other, assessed BA morphology.
RESULTS
Among 126 patients, 34.1% fulfilled the criteria for BADE (ectasia or dolichosis). BADE was associated with advanced age (p = 0.04). Patients with fetal-type circle of Willis presented smaller BA diameters (2.9 ± 0.1 vs. 3.5 ± 0.1; p < 0.001), whereas patients with lacunar strokes presented a greater diameter than other stroke subtypes (3.8 ± 0.3 mm vs. 3.3 ± 0.1 mm; p = 0.04).
DISCUSSION AND CONCLUSIONS
In this single-center study of patients presenting with AIS or TIA, the prevalence of BADE (ectasia or dolichosis) is high. Further studies focusing on Spaniards should confirm our results.
Topics: Humans; Spain; Vertebrobasilar Insufficiency; Ischemic Attack, Transient; Female; Male; Prevalence; Aged; Middle Aged; Ischemic Stroke; Prospective Studies; Aged, 80 and over
PubMed: 38743020
DOI: 10.33588/rn.7810.2023298 -
Brain Communications 2024White matter hyperintensities (WMH), a common feature of cerebral small vessel disease, are related to worse clinical outcomes after stroke. We assessed the impact of...
White matter hyperintensities (WMH), a common feature of cerebral small vessel disease, are related to worse clinical outcomes after stroke. We assessed the impact of white matter hyperintensity changes over 1 year after minor stroke on change in mobility and dexterity, including differences between the dominant and non-dominant hands and objective in-person assessment versus patient-reported experience. We recruited participants with lacunar or minor cortical ischaemic stroke, performed medical and cognitive assessments and brain MRI at presentation and at 1 year. At both time points, we used the timed-up and go test and the 9-hole peg test to assess mobility and dexterity. At 1 year, participants completed the Stroke Impact Scale. We ran two linear mixed models to assess change in timed-up and go and 9-hole peg test, adjusted for age, sex, stroke severity (National Institutes of Health Stroke Scale), dependency (modified Rankin Score), vascular risk factor score, white matter hyperintensity volume (as % intracranial volume) and additionally for 9-hole peg test: Montreal cognitive assessment, hand (dominant/non-dominant), National Adult Reading Test (premorbid IQ), index lesion side. We performed ordinal logistic regression, corrected for age and sex, to assess relations between timed-up and go and Stroke Impact Scale mobility, and 9-hole peg test and Stroke Impact Scale hand function. We included 229 participants, mean age 65.9 (standard deviation = 11.13); 66% male. 215/229 attended 1-year follow-up. Over 1 year, timed-up and go time increased with aging (standardized β [standardized 95% Confidence Interval]: 0.124[0.011, 0.238]), increasing National Institutes of Health Stroke Scale (0.106[0.032, 0.180]), increasing modified Rankin Score (0.152[0.073, 0.231]) and increasing white matter hyperintensity volume (0.176[0.061, 0.291]). Men were faster than women (-0.306[0.011, 0.238]). Over 1 year, slower 9-hole peg test was related to use of non-dominant hand (0.290[0.155, 0.424]), aging (0.102[0.012, 0.192]), male sex (0.182[0.008, 0.356]), increasing National Institutes of Health Stroke Scale (0.160 [0.094, 0.226]), increasing modified Rankin Score (0.100[0.032, 0.169]), decreasing Montreal cognitive assessment score (-0.090[-0.167, -0.014]) and increasing white matter hyperintensity volume (0.104[0.015, 0.193]). One year post-stroke, Stroke Impact Scale mobility worsened per second increase on timed-up and go, odds ratio 0.67 [95% confidence interval 0.60, 0.75]. Stroke Impact Scale hand function worsened per second increase on the 9-hole peg test for the dominant hand (odds ratio 0.79 [0.71, 0.86]) and for the non-dominant hand (odds ratio 0.88 [0.83, 0.93]). Decline in mobility and dexterity is associated with white matter hyperintensity volume increase, independently of stroke severity. Mobility and dexterity declined more gradually for stable and regressing white matter hyperintensity volume. Dominant and non-dominant hands might be affected differently. In-person measures of dexterity and mobility are associated with self-reported experience 1-year post-stroke.
PubMed: 38715716
DOI: 10.1093/braincomms/fcae133 -
Journal of Clinical Medicine Mar 2024Exercise has shown beneficial effects on neuronal neuroplasticity; therefore, we want to analyze the influence of high-intensity interval training (HIIT) on... (Review)
Review
Exercise has shown beneficial effects on neuronal neuroplasticity; therefore, we want to analyze the influence of high-intensity interval training (HIIT) on neuroplasticity markers in post-stroke patients. A systematic review of RCTs including studies with stroke participants was conducted using the following databases (PubMed, LILACS, ProQuest, PEDro, Web of Science). Searches lasted till (20/11/2023). Studies that used a HIIT protocol as the main treatment or as a coadjutant treatment whose outcomes were neural plasticity markers were used and compared with other exercise protocols, controls or other kinds of treatment. Studies that included other neurological illnesses, comorbidities that interfere with stroke or patients unable to complete a HIIT protocol were excluded. HIIT protocol, methods to assess intensity, neuroplasticity markers (plasmatic and neurophysiological) and other types of assessments such as cognitive scales were extracted to make a narrative synthesis. Jadad and PEDro scales were used to assess bias. Eight articles were included, one included lacunar stroke (less than 3 weeks) and the rest had chronic stroke. The results found here indicate that HIIT facilitates neuronal recovery in response to an ischemic injury. This type of training increases the plasma concentrations of lactate, BDNF and VEGF, which are neurotrophic and growth factors involved in neuroplasticity. HIIT also positively regulates other neurophysiological measurements that are directly associated with a better outcome in motor learning tasks. We conclude that HIIT improves post-stroke recovery by increasing neuroplasticity markers. However, a limited number of studies have been found indicating that future studies are needed that assess this effect and include the analysis of the number of intervals and their duration in order to maximize this effect.
PubMed: 38610750
DOI: 10.3390/jcm13071985 -
Radiology Case Reports Jun 2024Cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy (CADASIL) is caused by mutations in the NOTCH3 gene. Clinical manifestations...
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy (CADASIL) is caused by mutations in the NOTCH3 gene. Clinical manifestations of CADASIL include lacunar infarcts, transient ischemic attacks, dementia, migraine, and psychiatric disorders. Cerebral MRI can show signal abnormalities in the basal ganglia and white matter, especially characteristic when located in the anterior part of the temporal lobe and external capsules. We report CADASIL patient treated with intravenous tenectelase for acute ischemic stroke, and we present a review of literature aimed to report effectiveness and safety of intravenous thrombolysis in CADASIL patients.
PubMed: 38596173
DOI: 10.1016/j.radcr.2024.03.006 -
Thrombosis Journal Apr 2024Older individuals and, in particular, individuals at risk of recurrent stroke, may be susceptible to thrombosis when participating in exercise, however, this aspect has...
INTRODUCTION
Older individuals and, in particular, individuals at risk of recurrent stroke, may be susceptible to thrombosis when participating in exercise, however, this aspect has not been well investigated.
METHODS
Clot microstructure and conventional markers of thrombotic risk were determined in twenty lacunar stroke patients and fifteen healthy age-matched controls before, immediately after and 1 h after a bout of moderate intensity cycling exercise. Data were analyzed using a linear mixed model approach.
RESULTS
At rest, clot microstructure (1.69 ± 0.07 vs. 1.64 ± 0.05, corresponding to a difference of ~ 50% in normalized clot mass; p = 0.009) and thrombocyte count (73%; p < 0.0001) were higher, and activated partial thromboplastin time was lower (18%; p = 0.0001) in stroke patients compared to age-matched controls. Acute exercise increased thrombogenic markers similarly in the two groups: incipient clot microstructure (1.69 ± 0.07 vs. 1.74 ± 0.05; p = 0.0004 and 1.64 ± 0.05 vs. 1.71 ± 0.04; p < 0.0001, for stroke and controls respectively), plasma fibrinogen (12%; p < 0.0001 and 18%; p < 0.0001, for stroke and controls respectively) and the combined coagulation factors II, VII and X (p = 0.0001 and p < 0.0001, for stroke and controls respectively).
CONCLUSION
The results show that exercise transiently increases the risk of blood clot formation in both stroke patients and controls, however, due to the higher baseline thrombogenicity in stroke patients, the post exercise risk of forming blood clots may be higher in this group.
TRIAL REGISTRATION
Registered at ClinicalTrials.gov (NCT03635177).
PubMed: 38581046
DOI: 10.1186/s12959-024-00604-9 -
Stroke and Vascular Neurology Apr 2024Cerebral small vessel disease (cSVD) causes lacunar stroke (25% of ischaemic strokes), haemorrhage, dementia, physical frailty, or is 'covert', but has no specific... (Review)
Review
Cerebral small vessel disease (cSVD) causes lacunar stroke (25% of ischaemic strokes), haemorrhage, dementia, physical frailty, or is 'covert', but has no specific treatment. Uncertainties about the design of clinical trials in cSVD, which patients to include or outcomes to assess, may have delayed progress. Based on experience in recent cSVD trials, we reviewed ways to facilitate future trials in patients with cSVD.We assessed the literature and the LACunar Intervention Trial 2 (LACI-2) for data to inform choice of Participant, Intervention, Comparator, Outcome, including clinical versus intermediary endpoints, potential interventions, effect of outcome on missing data, methods to aid retention and reduce data loss. We modelled risk of missing outcomes by baseline prognostic variables in LACI-2 using binary logistic regression.Imaging versus clinical outcomes led to larger proportions of missing data. We present reasons for and against broad versus narrow entry criteria. We identified numerous repurposable drugs with relevant modes of action to test in various cSVD subtypes. Cognitive impairment is the most common clinical outcome after lacunar ischaemic stroke but was missing more frequently than dependency, quality of life or vascular events in LACI-2. Assessing cognitive status using Diagnostic and Statistical Manual for Mental Disorders Fifth Edition can use cognitive data from multiple sources and may help reduce data losses.Trials in patients with all cSVD subtypes are urgently needed and should use broad entry criteria and clinical outcomes and focus on ways to maximise collection of cognitive outcomes to avoid missing data.
PubMed: 38569894
DOI: 10.1136/svn-2023-003022 -
Frontiers in Neurology 2024Thalamic pain syndrome is a distressing type of central post-stroke pain (CPSP) that occurs in up to 10% of cases following a cerebrovascular accident, typically with a...
Thalamic pain syndrome is a distressing type of central post-stroke pain (CPSP) that occurs in up to 10% of cases following a cerebrovascular accident, typically with a delayed onset of signs and symptoms, and is often chronic or even life-long. Thalamic pain syndrome, as is the case for other CPSPs, is difficult to treat, and the response is typically moderate at best. Central pain also occurs after vascular insults in parts of the CNS other than the thalamus. Only a few patients present with the classic "Dejerine and Roussy syndrome," so the term CPSP is preferred for describing neuropathic pain after stroke. There are no pathognomonic features of this syndrome. The thalamus probably has a substantial role in some patients with central pain, either as a pain generator or by abnormal processing of ascending input. Long-term post-stroke pain disorders can reduce the quality of life, affect mood, sleep, and social functioning, and can lead to suicide. Hemi-body pain is common in patients with thalamic lesions. Hyperbaric oxygen has known physiologic and pharmacologic effects with documented benefits in brain-related hemorrhages, acute and chronic stroke, traumatic brain injury, mild cognitive impairment, neurodegenerative diseases, and neuroprotection, but has never been reported as a treatment for thalamic pain syndrome. A 55-year-old man with a history of migraines suffered a right thalamic lacunar infarction following a brain angiogram to investigate a suspected AVM found on prior imaging that resulted in immediate left-sided weakness and numbness, evolving to severe chronic pain and subsequent stiffness. Diagnosed with thalamic pain syndrome, multiple pharmacologic therapies provided only partial relief for a year after the stroke. The patient's symptoms resolved and quality of life markedly improved with hyperbaric oxygen therapy, as assessed by multiple validated questionnaires, thus it may be a treatment option for thalamic pain syndrome.
PubMed: 38545283
DOI: 10.3389/fneur.2024.1364716 -
Stroke Apr 2024The importance of thromboembolism in the pathogenesis of lacunar stroke (LS), resulting from cerebral small vessel disease (cSVD), is debated, and although antiplatelets...
BACKGROUND
The importance of thromboembolism in the pathogenesis of lacunar stroke (LS), resulting from cerebral small vessel disease (cSVD), is debated, and although antiplatelets are widely used in secondary prevention after LS, there is limited trial evidence from well-subtyped patients to support this approach. We sought to evaluate whether altered anticoagulation plays a causal role in LS and cSVD using 2-sample Mendelian randomization.
METHODS
From a recent genome-wide association study (n=81 190), we used 119 genetic variants associated with venous thrombosis at genome-wide significance (<5*10) and with a linkage disequilibrium r<0.001 as instrumental variables. We also used genetic associations with stroke from the GIGASTROKE consortium (62 100 ischemic stroke cases: 10 804 cardioembolic stroke, 6399 large-artery stroke, and 6811 LS). In view of the lower specificity for LS with the CT-based phenotyping mainly used in GIGASTROKE, we also used data from patients with magnetic resonance imaging-confirmed LS (n=3199). We also investigated associations with more chronic magnetic resonance imaging features of cSVD, namely, white matter hyperintensities (n=37 355) and diffusion tensor imaging metrics (n=36 533).
RESULTS
Mendelian randomization analyses showed that genetic predisposition to venous thrombosis was associated with an increased odds of any ischemic stroke (odds ratio [OR], 1.19 [95% CI, 1.13-1.26]), cardioembolic stroke (OR, 1.32 [95% CI, 1.21-1.45]), and large-artery stroke (OR, 1.41 [95% CI, 1.26-1.57]) but not with LS (OR, 1.07 [95% CI, 0.99-1.17]) in GIGASTROKE. Similar results were found for magnetic resonance imaging-confirmed LS (OR, 0.94 [95% CI, 0.81-1.09]). Genetically predicted risk of venous thrombosis was not associated with imaging markers of cSVD.
CONCLUSIONS
These findings suggest that altered thrombosis plays a role in the risk of cardioembolic and large-artery stroke but is not a causal risk factor for LS or imaging markers of cSVD. This raises the possibility that antithrombotic medication may be less effective in cSVD and underscores the necessity for further trials in well-subtyped cohorts with LS to evaluate the efficacy of different antithrombotic regimens in LS.
Topics: Humans; Cerebral Small Vessel Diseases; Diffusion Tensor Imaging; Embolic Stroke; Fibrinolytic Agents; Genome-Wide Association Study; Mendelian Randomization Analysis; Stroke; Stroke, Lacunar; Thrombosis; Venous Thrombosis
PubMed: 38527140
DOI: 10.1161/STROKEAHA.123.044937 -
Molecular Genetics and Metabolism... Mar 2024Fabry disease (FD) is a life-limiting disorder characterized by intracellular globotriaosylceramide (Gb3) accumulations. The underlying α-galactosidase A (α-GAL A)...
Fabry disease (FD) is a life-limiting disorder characterized by intracellular globotriaosylceramide (Gb3) accumulations. The underlying α-galactosidase A (α-GAL A) deficiency is caused by variants in the gene . Variants of unknown significance (VUS) are frequently found in and challenge clinical management. Here, we investigated a 49-year old man with cryptogenic lacunar cerebral stroke and the chance finding of the VUS S126G, who was sent to our center for diagnosis and initiation of a costly and life-long FD-specific treatment. We combined clinical examination with investigations of dermal fibroblasts (HDF), induced pluripotent stem cells (iPSC), and iPSC-derived sensory neurons. We analyzed α-GAL A activity in iPSC, Gb3 accumulation in all three cell types, and action potential firing in sensory neurons. Neurological examination and small nerve fiber assessment was normal except for reduced distal skin innervation. S126G iPSC showed normal α-GAL A activity compared to controls and no Gb3 deposits were found in all three cell types. Baseline electrophysiological characteristics of S126G neurons showed no difference compared to healthy controls as investigated by patch-clamp recordings. We pioneer multi-level cellular characterization of the VUS S126G using three cell types derived from a patient and provide further evidence for the benign nature of S126G in , which is of great importance in the management of such cases in clinical practice.
PubMed: 38469097
DOI: 10.1016/j.ymgmr.2023.101029