Acute Infarction Research Articles

Acute Border Zone Infarcts in Hypereosinophilic Syndrome

Acute Border Zone Infarcts in Hypereosinophilic Syndrome

Mechanisms and Implications of Electrical Heterogeneity in Cardiac Function in Ischemic Heart Disease.

A healthy heart shows intrinsic electrical heterogeneities that play a significant role in cardiac activation and repolarization. However, cardiac diseases may perturb the baseline electrical properties of the healthy cardiac tissue, leading to increased arrhythmic risk and compromised cardiac functions. Moreover, biological variability among patients produces a wide range of clinical symptoms, which complicates the treatment and diagnosis of cardiac diseases. Ischemic heart disease is usually caused by a partial or complete blockage of a coronary artery. The onset of the disease begins with myocardial ischemia, which can develop into myocardial infarction if it persists for an extended period. The progressive regional tissue remodeling leads to increased electrical heterogeneities, with adverse consequences on arrhythmic risk, cardiac mechanics, and mortality. This review aims to summarize the key role of electrical heterogeneities in the heart on cardiac function and diseases. Ischemic heart disease has been chosen as an example to show how adverse electrical remodeling at different stages may lead to variable manifestations in patients. For this, we have reviewed the dynamic electrophysiological and structural remodeling from the onset of acute myocardial ischemia and reperfusion to acute and chronic stages post-myocardial infarction. The arrhythmic mechanisms, patient phenotypes, risk stratification at different stages, and patient management strategies are also discussed. Finally, we provide a brief review on how computational approaches incorporate human electrophysiological heterogeneity to facilitate basic and translational research.

Abstract 4117646: The Ultimate Test in Hemocompatibility: HeartMate3 Restart After Prolonged Pump Shut Down

Introduction: The HeartMate 3 (HM3) LVAD, was shown to have a higher survival free of hemocompatibility related adverse events (HRAE) compared to its predecessors (HM2, HVAD). Superior HM3 outcomes are attributed to wide blood flow pathways coupled with frictionless movement and intrinsic pulsatility, reducing shear stress and blood stasis. It is unknown if improved hemocompatibility can withstand pump restart after prolonged shutdown. We herein report a case of HM3 pump stoppage without subsequent HRAE. Case Presentation: A 41-year-old male underwent HVAD implant in 2019 for advanced non-ischemic cardiomyopathy. This was exchanged to HM3 for recurrent neurological events despite therapeutic anticoagulation. Ten months after exchange, he awakened one morning to find his LVAD had been off for an unknown period but had not heard any device alarms (85dB if on battery power, 165dB if on wall power). Since he felt well he changed to battery power resulting in immediate pump restart. Log file analysis showed pump stoppage 2 am – 10 am, without preceding low flow alarms or power elevations. Management and Outcomes: In the ER INR was 1.5 (2.8 one week prior) and systemic heparin was started. Evaluation included: 1) CT brain without acute infarcts 2) echocardiogram without intracardiac thrombus 3) CT Angiography with patency of the inflow cannula and outflow graft 4) stable serial LDH measurements. The controller was exchanged, and analysis noted normal function. 1-year later the patient is maintained on warfarin and aspirin 325mg without further HRAE. Given the patient’s neurologic history and pump stoppage event, we did not invoke ARIES trial guidance and thus continued aspirin. Conclusion: Pump stoppage occurs when there is complete battery depletion, disconnection of both power leads, or the percutaneous lead from system controller. Our case is unique in that the duration of pump shutdown was 8 hours and INR subtherapeutic, without HRAE in the background of neurologic events on HVAD support. It has been previously reported that complete outflow graft thrombosis can occur shortly after LVAD decommissioning. The HM3 User Manual recommends restarting the pump immediately if off for a few minutes and using clinical judgment for longer durations due to increased risk for thromboembolic events. Our case adds to the paucity of existing data on improved hemocompatibility of the HM3 during rare circumstances of the ultimate test in hemocompatibility: complete pump shut down.

Segmentation of infarct lesions and prognosis prediction for acute ischemic stroke using non-contrast CT scans

Background and PurposeIschemic stroke is the most common type of stroke and the second leading cause of global mortality. Prompt and accurate diagnosis is crucial for effective treatment. Non-contrast CT (NCCT) scans are commonly employed as the first-line imaging modality to identify the infarct lesion and affected brain areas, as well as to make prognostic predictions to guide the subsequent treatment planning. However, visual evaluation of infarct lesions in NCCT scans can be subjective and inconsistent due to reliance on expert experience. MethodsIn this study, we propose an automatic method using VB-Net with dual-channel inputs to segment acute infarct lesions (AIL) on NCCT scans and extract affected ASPECTS (Alberta Stroke Program Early CT Score) regions. Secondly, we establish a prediction model to distinguish reperfused patients from non-reperfused patients after treatment, based on multi-dimensional radiological features of baseline NCCT and stroke onset time. Thirdly, we create a prediction model estimating the infarct volume after a period of time, by combining NCCT infarct volume, radiological features, and surgical decision. ResultsThe median Dice coefficient of the AIL segmentation network is 0.76. Based on this, the patient triage model has an AUC of 0.837 (95 % confidence interval [CI]: 0.734–0.941), sensitivity of 0.833 (95 % CI: 0.626–0.953). The predicted follow-up infarct volume correlates strongly with the DWI ground truth, with a Pearson correlation coefficient of 0.931. ConclusionsOur proposed pipeline offers qualitative and quantitative assessment of infarct lesions based on NCCT scans, facilitating physicians in patient triage and prognosis prediction.

C-reactive protein after discharge and infarct size in patients with ST segment elevation myocardial infarction

Abstract Background C-reactive protein (CRP) peaks at 2 days in patients with ST-segment elevation myocardial infarction (STEMI) after percutaneous coronary intervention (PCI) and can predict final infarct size. It is, however, unknown whether CRP level after discharge, indicative of prolonged inflammation, plays a prognostic role in myocardial damage. Purpose To investigate the prevalence of high CRP level within 3 months after discharge in patients with STEMI and its association with myocardial damage. Methods In the current study, all patients were identified through the xx database and treated with timely PCI at xx hospital from 2011 to 2014. Blood samples were retrieved within 3 months after discharge. High CRP level was defined as CRP >=3 mg/L. Only patients with a cardiac magnetic resonance (CMR) at baseline or follow-up were recruited. The primary outcome was final infarct size. Multiple regression was performed to adjust for potential confounders using any baseline variable with P<0.10 for the difference between groups. Results Of the 1603 patients from xx, 273 patients had CRP measured following discharge and at least one CMR measured. Of them, 200 (73.3%) had high CRP level after discharge. There was no difference in period from PCI to CRP testing between patients with high CRP and those with low CRP [11 days, interquartile range (IQR) (4, 40) vs. 21 days, IQR (4, 42), P=0.31]. Patients with high CRP level showed larger final infarct size [12.5% left ventricle (LV) vs. 7.0% LV, P <0.001] and larger acute infarct size [15.2% LV vs. 10.6% LV, p=0.004] compared with those with low CRP level. Patients with high CRP level also had lower final myocardial salvage index (MSI) (0.67 vs. 0.75, P=0.003) and lower acute MSI (0.47 vs. 0.61, P=0.006). The results persisted after adjusting for potential confounders in multiple regression. Conclusions A large proportion of patients with STEMI undergoing PCI persisted high CRP within 3 months after discharge. High CRP level after discharge was associated with larger acute and final infarct size as well as lower acute and final MSI level.

Structural-informed functional MRI analysis of patients with empathy impairment following stroke.

The underlying functional alterations of brain structural changes among patients with empathy impairment following stroke remain unclear. We sought to investigate functional connectivity changes informed by brain structural abnormalities in multimodal magnetic resonance imaging (MRI) among patients with empathy impairment following stroke. We enrolled people who had experienced their first ischemic stroke, along with healthy controls. We assessed empathy 3 months after stroke using the Chinese version of the Empathy Quotient (EQ). During the acute phase, all patients underwent basic magnetic resonance imaging (MRI), followed by multimodal MRI during follow-up. Our MRI analyses encompassed acute infarction segmentation, volumetric brain measurements, regional quantification of diffusion parameters, and both region-of-interest-based and seed-based functional connectivity assessments. We grouped patients based on the severity of their empathy impairment for comparative analysis. We included 84 patients who had stroke and 22 healthy controls. Patients had lower EQ scores than controls. Patients with low empathy had larger left cortical infarcts (odds ratio [OR] 4.082, 95% confidence interval [CI] 1.183-14.088), more pronounced atrophy in the right cingulate cortex (OR 1.248, 95% CI 1.038-1.502), and lower scores on the Montreal Cognitive Assessment (OR 0.873, 95% CI 0.74-0.947). In addition, the cingulate cortex served as the seed in the seed-based analysis, which showed heightened functional connectivity between the anterior cingulate gyrus and the right superior parietal lobule, specifically in the low-empathy group. We did not evaluate the relationship between specific network involvement and empathy impairment among patients following stroke. Among patients with subacute ischemic stroke, reduced empathy was strongly associated with a more severe cognitive profile and atrophy of the right cingulate cortex. Our subsequent structural-informed functional MRI analysis suggests that the enhanced connectivity between the anterior cingulate gyrus and the superior parietal lobule may function as a compensatory mechanism for this atrophy.

Redefining Infarction Size for Small-Vessel Occlusion in Acute Ischemic Stroke: A Retrospective Case-Control Study.

Small-vessel occlusion, previously referred to as lacunar infarcts, accounts for approximately one-third of all ischemic strokes, using an axial diameter of less than 20 mm on diffusion-weighted imaging. However, this threshold may not adequately differentiate small-vessel occlusion from other pathologies, such as branch atheromatous disease (BAD) and embolism. This study aimed to assess the clinical significance and pathological implications of acute small subcortical infarctions (SSIs) based on infarct diameter. We conducted a retrospective case-control study using data from stroke patients recorded between 2016 and 2021 of the Stroke Registry in Chang Gung Healthcare System. Patients with acute SSIs in penetrating artery territories were included. Key variables such as patient demographics, stroke severity, and medical history were collected. Infarcts were categorized based on size, and the presence of early neurological deterioration (END) and favorable functional outcomes were assessed. Among the 855 patients with acute SSIs, the median age was 70 years and the median National Institutes of Health Stroke Scale (NIHSS) score at arrival was four. END occurred in 97 patients (11.3%). Those who experienced END were significantly less likely to achieve a favorable functional outcome compared to those who did not (18.6% vs. 59.9%, p < 0.001). The incidence of END increased progressively with infarct sizes of 15 mm or larger, with the optimal threshold for predicting END identified as 15.5 mm and for BAD, it was 12.1 mm. A multiple logistic regression analysis revealed that motor tract involvement [adjusted odds ratio (aOR) 2.3; 95% confidence interval (CI) 1.1-4.7], an initial heart rate greater than 90 beats per minute (aOR 2.3; 95% CI 1.2-4.3), and a larger infarct size (15 mm to less than 20 mm vs. 10 mm to less than 15 mm; aOR 3.0; 95% CI 1.4-6.3) were significantly associated with END. Our findings suggest that setting the upper limit for small-vessel occlusion at 15 mm would be more effective in distinguishing it from BAD. However, these findings should be interpreted in the context of the retrospective design and study population. Further multi-center research utilizing high-resolution vessel wall imaging is necessary to refine this threshold and enhance diagnostic accuracy.

Deep learning reconstruction of diffusion-weighted brain MRI for evaluation of patients with acute neurologic symptoms

Purpose: We aimed to evaluate whether the deep-learning (DL) accelerated diffusion weighted image (DWI) is clinically feasible for evaluating patients with acute neurologic symptoms, regarding its shorter study time and acceptable image quality. Materials and methods: In this retrospective study, brain images obtained at DWI with a b-value of 0 s/mm2 and DWI with a b-value of 1000 s/mm2 (DWI 1000) from 321 consecutive patients with acute stroke-like symptom were reconstructed with and without DL algorithm. We compare the diagnostic performance between DL-DWI and conventional DWI for detecting brain lesions, including acute infarction. We assessed the diagnostic accuracy of conventional DWI and DL-DWI and compared the results. Qualitative analysis based on image quality was assessed and compared using a five-point visual scoring system. Apparent diffusion coefficients (ADCs) from DWI with and without DL were also compared. Results: The mean acquisition time for the DL-DWI (49 s) was significantly shorter (P < 0.001) than conventional DWI (165 s). Both DWI with and without DL showed similar performance in diagnosing brain lesions especially sensitivity (98.8% in both DWI and DL-DWI) and specificity (99.5% in both DWI and DL-DWI). Overall image quality, gray-white matter and deep gray matter differentiation of two sequences were similar. DL DWI showed more artifacts than DWI. Lesion conspicuity, especially smaller than 5 mm, was better with DL DWI than conventional DWI (p = 0.03). ADC values of white matter, deep gray matter, and pons with DL were lower than conventional DWI. Conclusions: Compared to conventional DWI, DL-DWI achieved comparable image quality and brain lesion visualization for acute neurological symptoms, with a significantly shorter scan time.

Acute Cerebellar Infarct in A Patient with Undiagnosed Fahr’s Syndrome: A Case Report

Introduction: Fahr’s disease and Fahr’s syndrome represent clinical entities that result in diffuse intracranial brain calcification, either by way of genetic mutation in the case of the former or by secondary endocrine dysfunction in the latter. Case Report: We present a case of a middle-aged male with undiagnosed Fahr’s syndrome, identified during evaluation for symptoms of an acute posterior circulation cerebrovascular accident. Conclusion: Fahr’s syndrome is a clinical constellation of symptoms and radiographic findings often seen in late-stage hypoparathyroidism. The intracranial calcifications associated may be related to an increased risk for intracranial cerebrovascular disorders such as ischemic or hemorrhagic infarct. Keywords: Fahr’s syndrome; case report; posterior circulation stroke; cerebellar infarct.

The important role of ferroptosis in inflammatory bowel disease.

Ferroptosis is a type of regulated cell death that occurs due to the iron-dependent accumulation of lethal reactive oxygen species (ROS) from lipids. Ferroptosis is characterized by distinct morphological, biochemical, and genetic features that differentiate it from other regulated cell death (RCD) types, which include apoptosis, various necrosis types, and autophagy. Recent reports show that ferritin formation is correlated to many disorders, such as acute injury, infarction, inflammation, and cancer. Iron uptake disorders have also been associated with intestinal epithelial dysfunction, particularly inflammatory bowel disease (IBD). Studies of iron uptake disorders may provide new insights into the pathogenesis of IBD, thereby improving the efficacy of medical interventions. This review presents an overview of ferroptosis, elucidating its fundamental mechanisms and highlighting its significant involvement in IBD.

A diagnosis that’s hard to swallow: case report of delayed onset lateral medullary syndrome presenting with only dysphagia

BackgroundLateral Medullary Syndrome (LMS) is a posterior circulation stroke (PCS) that has a broad array of manifestations but most classically presents with Horner’s syndrome, ipsilateral ataxia, and ipsilateral hyperalgesia. Although dysphagia is also common, isolated and single presentation of this alone is rare and there are only a few case reports of this in the literature. This presentation can bias a clinician’s differential diagnosis and delay diagnosis.Case presentationA previously healthy 53-year-old-male presented with a complaint of dysphagia. He had no PCS symptoms, a National Institute of Health Stroke Scale (NIHSS) of zero, and an otherwise unremarkable neurological exam. Stroke imaging including non-contrast computed tomography (NCCT) scan of his head and computed tomography angiography (CTA) scan of his head and neck revealed no acute abnormalities. He was found to be positive for Influenza A, but otherwise all other etiologies for his dysphagia were worked up, including consultation with other specialty services, without resolve. Two days later, the patient subsequently developed new right sided sensory deficits and left sided Horner’s syndrome, in which a magnetic resonance imaging (MRI) scan of his head revealed an acute infarct of the left lateral medulla with likely thrombus in the left posterior inferior cerebellar artery (PICA).ConclusionsPCS is frequently missed due to the often-vague symptoms and reassuring negative imaging. This case highlights the variability of presentations that ED physicians may encounter. Nonetheless, a high index of suspicion for PCS should be maintained even in young patients without risk factors. Lastly, dysphagia is never normal, and this case demonstrates the need to reconsider neurogenic origin when other causes have been ruled out.

7087 An Unusual Movement Disorder, Case of Diabetic Striatopathy!

Abstract Disclosure: S. Azmat: None. O. Lodhi: None. R. Safi: None. H. harb: None. H. Ashok: None. M.F. Siddiqui: None. J.L. Gilden: None. Background: Non-ketotic Hyperglycemia Hemichorea-Hemiballismus Syndrome (NKH-CB) is rare complication of poorly controlled diabetes mellitus (DM) characterized by continuous, irregular jerky movements localized to one side of the body. It is commonly seen in type 2 DM and is often presented in females of East Asian descent. NKH-CB is often misdiagnosed due to its rarity and radiographic features easily mistaken for intracerebral hemorrhage.Case: A 70-year-old Latino male with type 2 diabetes mellitus, hypertension, bipolar disorder and past history of two cerebrovascular accidents presented to ED with non-radiating, midsternal chest pain. ACS was ruled out with negative serial troponins and normal EKG. Vital signs were significant for elevated blood pressure 151/64 mmHg. Labs showed blood glucose=447 mg/dL. Physical examination revealed large amplitude involuntary movements in left upper and lower extremities and facial region. He also veered to the left when ambulating. The patient reported that these abnormal movements were occurring for last three weeks although sensation was preserved bilaterally. Code stroke was called; non-contrast CT showed unilateral hyper density of the right caudate and putamen with no evidence of acute intracranial hemorrhage or large arterial territory infarction. CT Angiogram did not show any signs of stenosis or occlusion. He received intravenous fluids and 8 units lispro insulin in ED. Was admitted for further evaluation and received basal/bolus insulin therapy with target blood glucose of 140-160 mg%. He also received risperidone for his mental condition. Subsequent testing revealed hemoglobin A1C of 16.9% (reference range: &amp;lt; 5.7%). MRI Brian showed unilateral T1 hyperintensity involving right caudate and putamen corresponding to the hypodensity seen on CT. Neurology service was consulted. Based on clinical signs/symptoms coupled with neuroimaging, he was diagnosed with non-ketotic Hyperglycemia Hemichorea-Hemiballismus Syndrome. On day 2 with resolution of hyperglycemia, amplitude and frequency of involuntary arm movements were minimal. The patient was discharged with Lantus 7 and metformin 1000 mg for DM and risperidone for symptoms management. Conclusion: Diabetic neuropathy is commonly known to result in small and/or large fiber sensorimotor polyneuropathy, proximal motor, and acute mononeuropathies as well as entrapments, radiculopathies, autonomic neuropathies, and even cognitive disorders. This case describes rare case of simultaneous NKH-CB with history of CVA and antipsychotic medication use in a patient with poorly controlled DM which resolved with treatment of hyperglycemia. Thus offers valuable insights into the diagnostic challenges associated with this condition as well as potential links to other neurological complications. One should also remain vigilant of potential onset of seizures commonly seen with NKH. Presentation: 6/3/2024

8291 Graves’ Disease and Moyamoya Syndrome: A Complex Case of Thyroid Dysfunction and Neurovascular Abnormalities

Abstract Disclosure: A. Jamil: None. Q.V. Luong: None. A. Llorens Bonilla: None. A. Siddiqui: None. Background: Moyamoya disease is a cerebrovascular disease characterized by progressive stenosis and occlusion of cerebral arteries, particularly the internal carotid arteries, proximal anterior and middle cerebral arteries associated with a net-like collateral vessel formation. Moyamoya disease in association with certain systemic conditions (e.g. Graves’ disease, sickle cell anemia, neurofibromatosis type 1, and Down Syndrome) has been referred to as moyamoya syndrome. Graves’ disease is an autoimmune disease in which the development of thyroid-stimulating hormone (TSH) receptor autoantibodies leads to overproduction of thyroid hormones. Although the pathophysiology is unclear, Graves’ disease can adversely impact the clinical course of moyamoya syndrome.Clinical Case: A 26-year-old woman diagnosed with Graves’ disease at the age of 20 years who was in remission presented to the ED with right upper extremity weakness and headache. A stroke work-up was performed, and an initial CT head without contrast showed an acute infarct in the left temporal area. Extensive workup for hypercoagulability and cardiac causes were negative. MRI brain showed multiple infarcts of the left cerebral hemisphere with ivy sign, which are prominent linear or punctate high intensity areas in the subarachnoid space reflecting the development of collaterals that occurs in moyamoya disease. TSH at the time was noted to be &amp;lt;0.01 uIU/mL (range: 0.30-4.20 uIU/mL), indicating a thyrotoxic state. She was discharged on methimazole and antiplatelet therapies. However, the patient continued to have hypertension and headaches which did not resolve with the return to euthyroidism. At age 29, she again developed acute right upper and lower extremity weakness, and consequently presented to the ED. Imaging studies showed multiple punctate infarcts in her bilateral frontal lobes and bilateral ICA stenosis consistent with moyamoya disease. However, her biochemical studies showed euthyroidism. Ultimately, she underwent right frontotemporal craniotomy and direct parietal superficial temporal artery to middle cerebral artery bypass by neurosurgery to decrease her future stroke risk for her moyamoya syndrome, and her Graves’ disease remains in remission.Conclusions: The coexistence of Graves’ disease in moyamoya syndrome may suggest a pathophysiologic connection. It has been suggested that hemodynamic changes in cerebrovascular flow due to thyrotoxicosis might contribute to ischemic neurologic deficits. Surgical intervention for revascularization procedures should be attempted after optimal control of thyrotoxicosis, as this may help to prevent further ischemic events in the future and improve patient outcomes. Presentation: 6/1/2024

Baseline Blood Pressure Was Associated with Hemispheric Cerebral Blood Flow in Acute Small Subcortical Infarcts

Introduction: While increased baseline blood pressure (BP) is a prevalent comorbidity in the acute phase of ischemic stroke, the association between baseline BP and the state of hemispheric perfusion in patients with acute small subcortical infarcts (SSIs) has not been studied in detail. The aim of this study was to investigate the relationship between baseline BP and hemispheric cerebral blood flow (CBF) in acute SSIs. Methods: This retrospective study included 101 patients with acute SSIs. Baseline hemispheric CBF was assessed through co-registration of baseline CT perfusion imaging and follow-up diffusion-weighted imaging. The association between baseline BP, CBF, and different cerebral small vessel disease (CSVD) biomarkers was assessed. Results: Baseline systolic BP (SBP) and diastolic BP (DBP) were negatively associated with contralateral hemispheric CBF after multivariate-adjusted linear analysis (SBP: β = −0.001, 95% CI: −0.002 to 0.000, p = 0.030; DBP: β = −0.002, 95% CI: −0.003∼0.001, p = 0.006). Among other CSVD biomarkers, the presence of any cerebral microbleeds showed a significant association with lower CBF in the contralateral hemisphere of the infarct lesion (r = −0.270, p = 0.035). Conclusion: In patients with acute SSIs, increased baseline BP was associated with reduced CBF in the contralateral hemisphere of the infarct lesion, which probably could be interpreted by the exacerbation of the CSVD burden, suggesting a potential mechanistic link between BP autoregulation dysfunction and the aggravation of neurovascular impairment in SSIs.

68Ga-FAPI PET in Visualizing Acute Ischemic Stroke at Risk of Hemorrhagic Transformation.

Hemorrhagic transformation is a serious complication of ischemic stroke, which occurs at a rate of between 18% and 42%. 68Ga-FAPI PET can visualize acute cerebral infarction at risk of hemorrhagic transformation in the brain. We report a case of 68Ga-FAPI PET imaging in a patient with recurrent ischemic stroke. 68Ga-FAPI PET imaging revealed FAPI uptake in acute ischemic stroke with hemorrhagic transformation, but did not in some acute infarction and chronic infarction without hemorrhagic transformation. These findings suggest potential role of 68Ga-FAPI PET in the evaluation of acute ischemic stroke with the risk of hemorrhagic transformation.

Intraplaque hemorrhage volume in patients with carotid atherosclerosis: How informative is it?

Background and purposeIntraplaque hemorrhage (IPH) of carotid atherosclerosis is an important feature in complex lesions preceding acute stroke events. The current study aimed to determine the role played by IPH volume compared to that of carotid stenosis or maximal wall thickness in patients with carotid IPH. Materials and methodsThis retrospective study included 233 patients who presented with carotid IPH on vessel wall imaging (VWI). We divided the patients into symptomatic or asymptomatic groups based on territorial acute focal infarction. The IPH volume, degree of stenosis, and maximal wall thickness on VWI were analyzed. ResultsOf the 233 included patients with carotid IPH, 51 (21.9%) patients showed initial clinical symptoms and positive territorial findings on diffusion-weighted imaging (DWI). Moreover, 154 (66.1%) patients had low-grade stenosis below 50% (n = 19: symptomatic groups). Overall, carotid IPH volume, degree of stenosis, and maximal wall thickness were all significantly higher in the symptomatic groups (p = 0.001). The degree of stenosis, in all patients and especially in those with high-grade stenosis above 50%, was significantly correlated with territorial acute focal infarction on multivariate analysis (p < 0.01). In patients with low-grade stenosis below 50%, maximal wall thickness was associated with territorial acute focal infarction (p = 0.48). ConclusionCarotid IPH volume was a risk factor for territorial acute focal infarction. However, in patients with high-grade stenosis, the degree of stenosis was significantly linked to acute stroke. By contrast, in patients with low-grade stenosis, maximal wall thickness exhibited a significant association with acute stroke.

Unveiling Benedikt’s syndrome: A rare midbrain stroke presenting with oculomotor nerve palsy

A 34-year-old female presented to the neuro-ophthalmology outpatient department with the primary complaint of ptosis of the right eyelid experienced over the course of 3 days. Clinical evaluation unveiled a right oculomotor nerve palsy, accompanied by compromised motor function in the left upper and lower extremities. Neuroimaging studies subsequently revealed the presence of an acute non-hemorrhagic infarct localized within the right paramedian midbrain region, specifically encompassing the red nucleus and the oculomotor nerve fascicles, a presentation conclusively indicative of Benedikt’s syndrome.

Brown-Séquard syndrome after a. spinalis posterior infarction

Spinal cord infarction is an infrequent event, and the occurrence of Brown-Séquard syndrome resulting from spinal cord infarction is even rarer. In this case report, a 55-year-old woman presented with sudden onset of back pain and a right-sided Brown-Séquard syndrome. MRI of the spinal cord revealed acute infarction in the right posterior spinal artery at Th5-Th10. In case of sudden Brown-Séquard syndrome, the possibility of a spinal cord infarction should be considered.

Efficacy of Proprioceptive Neuromuscular Facilitation on Jaw Function in Bruxism Among Post Stroke Survivor: A Case Study

A 49-year-old male who was a known case of Type 2 diabetes mellitus and hypertensive had a history of an acute infarct in the left ganglia capsular region and a chronic infarct in the left parieto-occipital lobe, which was conservatively managed and was referred for physiotherapy rehabilitation for strengthening the right upper and lower limb. During the physiotherapy intervention, abnormal teeth grinding was observed, and the patient was asked about parafunctional behaviour. Upon examination, there was a restriction in the jaw range of motion assessed by measuring the jaw range using the vernier caliper and tightness in the masticatory muscle, as evidenced by palpating the masseter muscle. Proprioceptive neuromuscular facilitation and ultrasound therapy were given for 1 session per week for 2 weeks to treat bruxism along with standardized stroke protocol. At the end of 2 weeks after the intervention, there was an increase in jaw opening and reduced masticatory muscle activity. Jaw opening was measured using a vernier caliper, and masticatory activity was measured using electromyography of the masseter and temporalis muscles. This study suggests the importance of treating bruxism to prevent complications related to it. It concludes that proprioceptive neuromuscular facilitation and ultrasound therapy were effective in improving mouth opening and reducing the masticatory activity in bruxism among stroke patients with ganglia capsular involvement.

Diagnostic Challenges in Identifying Atrial Myxoma as a Cause of Transient Ischemic Attacks: A Case Report

Abstract Background A 67-year-old woman presented to hospital on multiple occasions with transient neurological symptoms over a period of 20 months. Initial diagnostics, including computed tomography (CT), carotid Dopplers, and electrocardiogram, were unremarkable. Magnetic resonance imaging (MRI) was arranged following the third neurological event which revealed multi-territory acute ischemic events, suggestive of a cardioembolic source. Transoesophageal echocardiography identified a large mobile atrial myxoma, histologically confirmed. Atrial myxoma, though rare, is an important cause of thromboembolic stroke, underscoring the need for comprehensive cardiac evaluation in cerebrovascular incidents. Methods The patient's case was reviewed, focusing on initial presentations, diagnostic workup, and subsequent management. Initial presentations included transient visual disturbances and transient leg weakness. Routine tests were conducted, including CT brain, carotid Dopplers, and blood tests. MRI and transoesophageal echocardiography were performed which ultimately identified the underlying cause of the patient’s neurological events. Results Initial evaluations (CT, carotid Dopplers) were normal. An MRI performed 20 months after her initial presentation revealed small acute infarcts in the right cerebellar hemisphere and left superior parietal lobe. Transoesophageal echocardiography subsequently detected a large atrial myxoma. The patient's transient symptoms and negative initial workup delayed the diagnosis, highlighting the necessity of including cardiac imaging early in the stroke workup, especially in cases of suspected cardioembolic events. Conclusion This case illustrates the critical role of thorough cardiac evaluation, including echocardiography, in diagnosing the cause of transient ischemic attacks (TIA) and strokes. The patient’s initial negative findings delayed the identification of a cardioembolic source, emphasizing the importance of comprehensive diagnostic protocols for suspected cerebrovascular events. Urgent surgical resection is essential for atrial myxoma to prevent recurrent embolic events. This report highlights the diagnostic and management challenges of cardiac myxomas, advocating for a more rigorous approach to stroke evaluation and timely intervention.