Left Middle Cerebral Artery Research Articles

Simultaneous Multi-Vascular Bed Imaging in a Patient Supported by a Continuous-Flow LVAD

<h3>Introduction</h3> Patients supported with left ventricular assist devices (LVADs) are burdened by frequent hemocompatibility-related adverse events related to patient-pump interactions. These predominantly vascular events include stroke, gastrointestinal bleeding, and pump thrombosis. Our center performs routine, invasive hemodynamic ramp speed titrations in LVAD patients to determine the optimal rotational speed after implantation. We sought to interrogate changes in vascular hemodynamics during an exercise ramp study to understand the influence of pump speed and exercise on outflow graft and cerebrovascular flow. <h3>Case Report</h3> A 71-year-old male patient supported by Heartware HVAD operating at a baseline speed of 2700 RPM presented for LVAD ramp and exercise study with vascular imaging. A right heart catheterization, echocardiography with Doppler imaging of the patient's LVAD outflow graft, and vascular Doppler of the left common carotid artery and middle cerebral artery were performed. The patient's LVAD operating speed was reduced to 2400 RPM and then increased stepwise to a maximum speed of 3000 RPM. At each increment of operating speed, Doppler imaging was attempted and right heart catheterization was repeated. After reviewing data from the ramp study, the patient's operating speed was set to 2900 RPM and then a staged exercise protocol with bicycle ergometer was performed. Pertinent findings of vascular imaging include a blunting of peak systolic to end-diastolic velocity ratio in vascular beds with incremental speed increase and partial recovery of pulsatility with exercise (Figure). <h3>Summary</h3> This case demonstrates the influence LVAD speed adjustment and exercise have on carotid artery and outflow graft pulsatility. With exercise the outflow graft and carotid artery peak systolic and end-diastolic velocities were similar to those at the lowest LVAD pump speed, suggesting that intrinsic contractility and native LV unloading was restored with exercise despite a higher pump speed.

SMI-32 — a novel axonal injury marker for investigation of ischemic brain pathology

The relevance of this work is determined by the high prevalence and social significance of cerebrovascular diseases and the need to develop effective methods for verifying neuronal damage due to cerebral ischemia in experimental models.&#x0D; The aim of this study was to assess the possibility of immunohistochemical revealing of neurofilaments to detect axonal injury in cerebral ischemia models.&#x0D; Materials and methods. A model of transient focal cerebral ischemia by the left middle cerebral artery occlusion was reproduced in male Wistar, SHR and WKY rats. Axonal injury was assessed by immunohistochemical reactions for neurofilament proteins using SMI-32 and 2F11 antibodies.&#x0D; Results. In cerebral ischemia, damage to nerve fibers occurs, manifested by thickening of axons, their varicose expansion and segmental accumulation of neurofilament proteins. These changes are more noticeable with an immunohistochemical reaction to the SMI-32 marker of neurofilament heavy chain.&#x0D; Conclusions. The use of antibodies to the non-phosphorylated neurofilament heavy chain makes it easy to identify degenerating nerve fibers and can be recommended as an alternative method for detecting axonal injury.

An \u201cover-fused middle cerebral artery\u201d anomaly: a case report

BackgroundMCA has several anomalies, such as accessory MCA, duplicated MCA and twig-like MCA, up to now all these reported anomalies were hypothesized to due to the failure in fusion of the primitive arterial network. No anomaly of over fused MCA has been reported.Case presentationA 59- year- old male was hospitalized with a history of paroxysmal slurred speech and left side headache for a week, his blood pressure was 160/80 mmHg and he manifested mild incomplete motor aphasia at the time of admission. The head and neck CTA and DSA all presented a huge and tortuous left MCA, we diagnosed it an anomaly and termed it over-fused MCA. The patient’s speech impairment and headache were relieved by controlling his blood pressure.ConclusionsSuch an anomaly of over-fused MCA is reported for the first time, it’s not needed to put special intervention on the anomaly of the patient temporarily, but more observation are needed.

Assesment of Cerebral Blood Flow Velocities with Transcranial Doppler Ultrasonography in Heart Failure Patients with Reduced Ejection Fraction

BackgroundHeart and brain interaction is a well-known entity in heart failure (HF) and left ventricular systolic dysfunction poses an increased risk for stroke and cognitive impairment. Transcranial Doppler (TCD) provides valuable information on cerebral blood flow velocities (CBFV). However, less is known about CBFV in HF patients with reduced EF. So, we aimed to evaluate CBFV by means of TCD in patients with HF and reduced ejection fraction (HFrEF). MethodsThis study included 46 HFrEF patients (mean age 65.2±11 years, mean EF 20.1±3.8%) who underwent to TCD examination. In addition, 26 healthy individuals with sinus rhythm and EF >50% were included in the study as a control group. Peak systolic, mean and end diastolic flow velocities of the both right and left middle cerebral artery (RMCA and LMCA) were analyzed. In subgroup analysis, HFrEF patients compared according to rhythm. Correlation analyses was performed in HFrEF group between EF and TCD velocities. ResultsThe average of RMCA and LMCA peak systolic and mean flow velocities were significantly lower in HF patients than those in control group (76,06±23,7 cm/s and 48,49±16,4 cm/s in HF group vs 87,84±14,5 cm/s and 56,41±10,7 cm/s in control group, p=0,025 and p=0,016, respectively, for RMCA and 75,1±22,3 cm/s and 47,57±14.8 cm/s in HF group vs 88,73±17,7 cm/s and 57,15±12,4 cm/s in control group, p=0,009 and p=0,007, respectively, for LMCA). The average mean flow velocity of RMCA and LMCA was significantly lower in HFrEF patients with AF than HFrEF patients with sinus rhythm. (P=0.04 and P= 0.03, respectively) In correlation analysis, EF was significantly positively correlated with both LMCA and RMCA flow velocities in HFrEF group. ConclusionThis study showed that HFrEF patients have lower CBFV as compared to healthy controls and HFrEF patients with AF rhythm have lower CBFV compared to HFrEF with sinus rhythm which might be one of the explanations of the adverse interaction between heart and brain in HFrEF.

Ischemic Stroke

A patient with a history of chronic atrial fibrillation was diagnosed with sudden onset of right hemiparalysis in the hospital. The patient had been normal two hours prior and was referred to the cerebral vascular center. Images: Head CT images showed early ischemic changes in the left frontal lobe, insula, and temporal lobe(Alberta Stroke Program Early CT Score[ASPECTS]: 6 points). A hyperdense internal carotid artery(ICA)sign was found at the top of the left internal carotid artery. MRI DWI-ASPECTS was performed at 6 points. The MRA showed loss of the left internal carotid, anterior cerebral, and middle cerebral arteries. T2*WIs showed a susceptibility vessel sign(SVS)at the top of the left ICA and FLAIR vessel hyperintensity(FVH)in the left ICA to the middle cerebral artery. The patient was diagnosed with acute cerebral embolism with clinical-DWI mismatch and treated with endovascular therapy. Early CT signs are important in determining cerebral ischemic lesions, and hyperdense ICA/MCA signs are useful in identifying occluded vessels. Early ischemic changes can be seen more easily on MRI-DWI, and the location of the occluded vessel can be estimated by evaluating MRA, SVS, and FVH together.

Abstract P784: A Novel Rat Model of Embolic Cerebral Ischemia Using a Cell-Implantable Radiopaque Hydrogel Micro Fiber

Introduction: The failure of neuroprotective treatment-related clinical trials may be partially caused by unestablished animal models. We aimed to develop a novel focal stroke model using a cell-implantable radiopaque hydrogel micro fiber. The micro fiber is made of barium alginate hydrogel containing zirconia, and fabricated in a dual coaxial laminar flow microfluidic device. Methods: Using male Sprague Dawley rats (n=10), a catheter (ID 0.42mm, OD 0.55mm) was navigated from the caudal ventral artery to the left internal carotid artery using digital subtraction angiography. A radiopaque hydrogel micro fiber (0.4 mm in diameter, 1 mm in length) was advanced in the catheter by slow injection of heparinized physiological saline to establish local occlusion. 9.4-T MRI and 2% 2,3,5-triphenyl tetrazolium chloride staining were performed 24 hours after the creation of the stroke model. Results: The anterior cerebral artery-middle cerebral artery bifurcation was selectively embolized at all rats. The median operating time was 8.5 min (interquartile range; 6.25-12 min). The median infarct volume (mm 3 ) was 262 (interquartile range; 260-274) 24 hours after occlusion. Conclusions: We present a novel rat model for focal infarct only in the middle cerebral artery territory using a radiopaque hydrogel micro fiber. Furthermore, this model can be used for regeneration research of cerebral infarction because the hydrogel micro fiber can encapsulate stem cell.Figure Legends A: Puncture of the caudal ventral artery in a rat. B: Cerebral angiography of a rat. C: Occlusion of the anterior cerebral artery-middle cerebral artery bifurcation by a radiopaque hydrogel fiber (arrowhead). D: MR angiography detected selective occlusion of left middle cerebral artery. E: T2-weighted image showed infarct only in the middle cerebral artery after 24 hours occlusion. A radiopaque fiber did not affect the 9.4-T MRI. F: Radiopaque hydrogel fiber encapsulated HeLa cells.

ISCHEMIC STROKE IN COVID-19 PATIENT: A RARE CASE REPORT.

Background: COVID-19 is shown to be associated with hypercoagulable state which may cause neurological and cardiovascular complications. COVID-19 has been represented as an independent risk factor for acute ischemic stroke. Objective:We report a case of acute ischemic stroke as a COVID-19 complication. Material and methods: A 62-year-old known hypertensive male was diagnosed with COVID-19. He developed neurological symptoms 10 days after being tested positive. On doing an NC-CT head, a large acute ischemic stroke involving left Middle Cerebral Artery infarct was detected. Result and Conclusion: Our case represents the development of acute ischemic stroke as a neurological manifestation in patient with COVID-19. Early evaluation for acute neurological changes and timely management may reduce morbidity and mortality in such cases.

A CASE OF MIDDLE CEREBRAL ARTERY INFARCT FOLLOWING UNEVENTFUL CLIPPING OF ANTERIOR COMMUNICATING ARTERY ANEURYSM

Background: Aneurysms of the anterior communicating artery are the most frequently encountered intracerebral aneurysms in routine neurosurgical practice. Management of intracerebral aneurysm involves aneurysm clipping or endovascular coil aneurysm embolisation. However, to the best of our knowledge, there is no reported case of an isolated ipsilateral middle cerebral artery infarction following clipping of anterior communicating artery aneurysm. Case Description: A 65-year-old female with hypertension presented with a history of giddiness, fall and altered sensorium. The patient had a Glasgow Coma Scale (GCS) score of 12, and further investigation of the magnetic resonance imaging on suspicion of stroke revealed subarachnoid haemorrhage in the bilateral parietal sulcus, left Sylvain ssure, left ambient and quadrigeminal cisterns with intra-ventricular extension. The patient was subsequently referred for neurosurgery consultation. Computed tomography (CT) angiogram conrmed the presence of a ruptured anterior communicating artery aneurysm. The neurological assessment showed reduced responsiveness to verbal commands, with a Hunt and Hess score of 3. The patient underwent uneventful clipping of the aneurysm. Postoperatively, the patient did not wake up from anaesthesia and had persistently elevated blood pressure and right-sided hemiplegia. On the third day of postoperative care, a CT head scan revealed a left middle cerebral artery infarction with a midline shift. Decompressive craniotomy was performed, and following this procedure, the patient improved in sensorium with residual right-sided hemiplegia Conclusion: This case report presents an undetected new micro embolism or postoperative cerebral vasospasm as possible causes for the development of cerebral infarct in patients with subarachnoid haemorrhage following an aneurysm rupture.

Abstract P575: Impaired Distal Perfusion Predicts In-Hospital Outcome in Patients With Symptomatic Middle Cerebral Artery Stenosis

Background: Perfusion imaging is increasingly used to risk stratify patients with symptomatic intracranial stenosis. Length of hospital stay (LOS) in patients with ischemic stroke is a surrogate marker of increased morbidity. We aim to determine the association between perfusion delay on T max (&lt; 4 sec, 4-6 sec, and &gt; 6 sec) on perfusion weighted imaging and LOS in patients with symptomatic middle cerebral artery (MCA) stenosis. Methods: We included consecutive patients with left MCA stenosis admitted with ischemic stroke or TIA &lt;7 days from onset who underwent perfusion imaging (CT or MR perfusion) processed with RAPID software. We excluded patients with core infarct ≥ 30 mL. Perfusion mismatch was divided into three groups: mismatch volume ≥ 15 mL based on T max &gt; 6 sec delay, mismatch volume ≥ 15 mL based on T max 4-6 sec delay, and neither of the above mismatch patterns. The primary outcome was LOS, both as a continuous variable and categorical (≥ 7 days (prolonged LOS) vs. &lt;7 days). Results: 179 out of 194 patients met the inclusion criteria; mean age was 70.2 ± 15.4 years, 53.1% were women, median (IQR) NIHSS was 4 (1-9); 83.2% underwent MR perfusion; 38.5% had a mismatch volume ≥ 15 mL based on T max &gt; 6 sec and 31.3% had a mismatch volume ≥ 15 mL based on T max 4-6 sec and the median (IQR) LOS was 4 days (2-8). After adjusting for age and NIHSS, T max &gt; 6 sec mismatch definition was associated with prolonged LOS (OR 2.90 95% CI 1.06-8.18; p=0.039) but T max 4-6 sec definition was not (OR 1.45 95% CI 0.46-4.58, p=0.528), without any interaction based on perfusion imaging modality (p interaction = 0.568). We found similar associations when LOS was considered as a continuous variable for T max &gt; 6 sec (β coefficient=2.01, 95% CI 0.05-3.97, p=0.044) and T max 4-6 sec (β coefficient=1.24, 95% CI -0.85-3.34, p=0.244). In receiver operating curves, the optimal mismatch volume for T max &gt; 6 sec was 10 mL (sensitivity 0.61 and specificity 0.63) whereas for T max 4-6 sec it was 39 mL (sensitivity 0.61 specificity 0.56). Conclusion: In patients with recently symptomatic MCA stenosis, the T max &gt; 6 sec definition for mismatch, but not T max 4-6 sec, is associated with prolonged LOS. Prospective studies are needed to validate our findings and define the optimal mismatch threshold in patients with symptomatic MCA stenosis.

Abstract P380: Eloquence Mapping in Acute Ischaemic Stroke

Introduction: Patient selection for acute stroke revascularisation therapies is commonly based on clinical-imaging mismatch paradigms. Anatomical scores or total volumes of brain affected are assumed to correlate with clinical deficit without reference to the functional eloquence of the regions involved. In this study we used the relationship between presenting hypoperfusion abnormality and the corresponding NIHSS to generate functionally weighted atlases from patients with acute ischaemic stroke. Methods: Patients with acute large vessel occlusion (LVO) of the anterior circulation and with CTP at the time of presentation were included in this study. CTP was analysed with e-CTP (Brainomix Ltd., Oxford, UK) and hypoperfusion maps defined (Tmax &gt;6s). Voxelwise lesion to symptom mapping was used to generate probability maps associating regions of hypoperfusion with clinical deficit at presentation. Results: 58 patients with itemised NIHSS and CTP were included. Discrete patterns of deficit were associated with each NIHSS domain. Total NIHSS correlated most strongly with left MCA involvement, consistent with the weighting towards language in this clinical scale. Regions associated with upper and lower limb deficits identified the respective motor cortex regions and descending motor tracts. Example mapping is presented in the Figure (A: total NIHSS, B: left arm paresis, C: left leg paresis). Data from a larger cohort will be presented at the meeting. Conclusions: Functional mapping using associations between presenting NIHSS and hypoperfusion lesion can be used to create eloquence-weighted atlases. Such atlases from stroke patients may be helpful to develop tools to predict clinical deficit associated with a presenting ischemic core lesion defined on non-contrast CT or CTP. This approach could refine clinical-imaging mismatch concepts, expanding endovascular treatment to a wider group of patients who would not currently be treated.

Estrogen administration attenuates post-stroke depression by enhancing CREB/BDNF/TrkB signaling in the rat hippocampus.

A previous study demonstrated that 17β-estradiol (E2), which is an antidepressant, can ameliorate post-stroke depression (PSD); however, the underlying mechanisms governing this remain largely unknown. Therefore, the present study developed a PSD model in rats, which was induced by left middle cerebral artery occlusion followed by exposure to chronic mild stress for 2 weeks. The results revealed that the activity of the cAMP response element-binding protein (CREB), a cellular transcription factor, and the associated brain-derived neurotrophic factor (BDNF)/tyrosine kinase B (TrkB) signaling were all attenuated in the hippocampus in PSD rats. The depression-like behaviors were significantly improved after treatment with E2, along with increased CREB and the BDNF/TrkB signaling activity. These results provide novel insight into the molecular basis of PSD, and suggest the potential involvement of CREB/BDNF/TrkB signaling in E2-mediated improvement of PSD in rats.

Case Report: Decompressive Craniectomy for COVID-19 Malignant Cerebral Artery Infarction. Is Surgery a Good Option?

SARS-CoV2 infection can lead to a prothrombotic state. Large vessel occlusion, as well as malignant cerebral stroke have been described in COVID-19 patients. In the following months, given the increase in COVID-19 cases, an increase in malignant cerebral SARS-CoV2 associated strokes are expected. The baseline situation of the patients as well as the risk of evolution to a serious disease due to the virus, depict a unique scenario. Decompressive craniectomy is a life-saving procedure indicated in patients who suffer a malignant cerebral stroke; however, it is unclear whether the same eligibility criteria should be used for patients with COVID-19. To our knowledge seven cases of decompressive craniectomy and malignant cerebral stroke have been described to date. We report on a 39-year-old female with no major risk factors for cerebrovascular disease, apart from oral contraception, and mild COVID-19 symptoms who suffered from left hemispheric syndrome. The patient underwent endovascular treatment with stenting and afterward decompressive craniectomy due to a worsening neurological status with unilateral unreactive mydriasis. We present the case and provide a comprehensive review of the available literature related to the surgical treatment for COVID-19 associated malignant strokes, to establish whether the same eligibility criteria for non-COVID-19 associated strokes should be used. Eight patients, including our case, were surgically managed due to malignant cerebral stroke. Seven of these patients received decompressive craniectomy, and six of them met the eligibility criteria of the current stroke guidelines. The mortality rate was 33%, similar to that described in non-COVID-19 cases. Two patients had a left middle cerebral artery (MCA) and both survived after decompressive craniectomy. Our results support that decompressive craniectomy, using the current stroke guidelines, should be considered an effective life-saving treatment for COVID-19-related malignant cerebral strokes.

Well-Formed Segmental Cerebral Arteries Dampen the Peak Systolic Pressure Lowering the Chances of Aneurysms

Background: The segments of cerebral basal arterial network (CBAN) dampen the peak systolic pressure in blood flowing through these arteries. The number of aneurysms occurring in segments of CBAN will vary with the ability of each arterial segment to dampen the peak systolic pressure. Materials and Methods: Diameters of segments of CBAN were measured in cerebral computed tomography angiography images of 145 patients and the relative size of each vessel was calculated to standardise for differences in overall arterial sizes among patients. Relationships among sizes of CBAN components were statistically analysed. Presence of aneurysms in parts of internal carotid artery (ICA), middle cerebral artery (MCA), anterior cerebral artery (ACA), posterior cerebral artery (PCA), and vertebrobasilar (VB) arteries was recorded. Results: Forty-six aneurysms in right ICA and MCA and 32 aneurysms in left ICA and MCA segments were noted in 42 and 30 patients, respectively. Aneurysms in anterior communicating artery complex (AcomAC) and VB arterial segments were seen in 27 and 8 patients respectively, while they were not detected in parts of PCA. The significant (p<0·0001) inverse relationships between sizes of posterior communicating artery (PcomA) and the first segment of PCA on both sides indicated that blood inputs to the second part of PCA were similar. This smoothens vessels haemodynamics. Differences in means of the index of arterial size variation for people with aneurysms (0·96) and without aneurysms (0·86) was significant (p≤0·015). Aneurysms in ACA, PCA and VB arteries were less and was proposed that it is due to dampening of peak systolic blood pressures. The development of aneurysms occurring in CBAN depended on the degree of variation and asymmetry in its segments. Conclusion: Variation in segments of CBAN has been quantified. The peak pressure dampening mechanism in such arterial segments reduces the chances of development of aneurysms. Funding: None to declare Declaration of Interest: There is no conflict of interest with any of the authors. Ethical Approval: Randomly selected CCTA images of 145 patients archived in the Carestream data registry system at Royal Adelaide Hospital (RAH), South Australia between January 2011 and December 2019, were used in the study (male = 67, female = 78, mean age = 60·9 years) (Supplementary file 1). Human Research Ethics Board granted permission (approval number: H2014 -176) to access and use data from the Carestream data registry system (Vue RIS version 11·0·14·35).

Neuroimaging of Children With Takayasu Arteritis.

Takayasu arteritis is a rare granulomatous chronic vasculitis that affects the aorta and its main branches. Neurologic manifestations can accompany the disease; however, there is no study on neuroimaging in children with Takayasu arteritis. Therefore, we aimed to evaluate cranial magnetic resonance imaging (MRI) in pediatric Takayasu arteritis patients. Demographic, clinical, and laboratory data were obtained retrospectively. The study included 15 pediatric Takayasu arteritis patients. All patients presented with constitutional symptoms. Additionally, 6 patients suffered from headache, 2 had syncope, 1 had loss of consciousness, and 1 had convulsion. All patients underwent cranial and diffusion MRI a median 12 months after diagnosis. Cranial MRI findings were normal in 12 patients, whereas 3 patients had abnormal findings, as follows: stenosis in the M1 and M2 segments of the left middle cerebral artery (n = 1); diffuse thinning of the right internal carotid, middle cerebral, and right vertebral and basilar artery (n = 1); as a sequela, areas of focal gliosis in both the lateral ventricular and posterior periventricular regions (n = 1). Among these 3 patients, 1 had no neurologic complaints. Abnormal MRI findings can be observed in pediatric Takayasu arteritis patients, even those that are asymptomatic; therefore, clinicians should carefully evaluate neurologic involvement in all pediatric Takayasu arteritis patients.

Determinants of cerebral blood flow velocity change during squat-stand maneuvers.

The large changes in mean arterial blood pressure (MABP) and cerebral blood flow velocity (CBFV) induced by squat-stand maneuvers (SSM) make this approach particularly suited for studying dynamic cerebral autoregulation (CA). However, the role of other systemic determinants of CBFV has not been described and could provide alternative physiological interpretations of SSM results. In 32 healthy subjects (16 female), continuous recordings of MABP (Finometer), bilateral CBFV (transcranial Doppler, MCA), end-tidal CO2 (EtCO2; capnography), and heart rate (HR; electrocardiogram) were performed for 5 min standing at rest, and during 15 SSM at the frequency of 0.05 Hz. A time-domain, multivariate dynamic model estimated the CBFV variance explained by different inputs, corresponding to significant contributions from MABP (P < 0.00001), EtCO2 (P < 0.0001), and HR (P = 0.041). The autoregulation index (ARI; range 0-9) was estimated from the CBFV response to a step change in MABP. At rest, ARI values (typically 5.7) were independent of the number of model inputs, but during SSM, ARI was reduced compared with baseline (P < 0.0001), and the three input model yielded lower values for the right and left MCA (3.4 ± 1.2, 3.1 ± 1.3) when compared with the single-input MABP-CBFV model (4.1 ± 1.1, 3.9 ± 1.0; P < 0.0001). The high coherence of the MABP-CBFV transfer function at 0.05 Hz (typically 0.98) was considerably reduced (around 0.71-0.73; P < 0.0001) when the contribution of CBFV covariates was taken into account. Not taking into consideration other determinants of CBFV, in addition to MABP, could be misleading and introduce biases in physiological and clinical studies.

High-Dose Prednisolone for Treatment of Infantile Spasms After Presumed Perinatal Stroke.

BACKGROUND: High-dose prednisone and prednisolone have been increasingly studied as a lower-cost alternative to adrenocorticotropic hormone for the treatment of infantile spasms, but this treatment has not been well studied in children with infantile spasms due to perinatal stroke. METHODS: We identified a girl with new-onset infantile spasms due to presumed perinatal left middle cerebral artery stroke seen in our hospital's pediatric stroke clinic in 2019. RESULTS: This girl developed infantile spasms at 9 months old. She had right hemiplegic cerebral palsy due to her perinatal stroke but had been otherwise previously healthy. Modified hypsarrhythmia was confirmed on prolonged video-electroencephalography. High-dose prednisolone at 8 mg/kg per day was initiated on the sixth day of spasms. She was treated with this dose for 2 weeks and then tapered over 5 weeks. The girl became seizure-free after receiving her first dose of prednisolone and experienced no significant adverse effects during therapy. Routine electroencephalography after completion of prednisolone taper confirmed resolution of modified hypsarrhythmia and no epileptiform discharges. She continued to make excellent development progress during and after treatment. CONCLUSION: This case suggests high-dose prednisolone could be considered for first-line therapy for children with infantile spasms due to perinatal stroke; further study is needed.

The effect of fingolimod on regulatory T cells in a mouse model of brain ischaemia

BackgroundThe role of the immune system in stroke is well-recognised. Fingolimod, an immunomodulatory agent licensed for the management of relapsing-remitting multiple sclerosis, has been shown to provide benefit in rodent models of stroke. Its mechanism of action, however, remains unclear. We hypothesised fingolimod increases the number and/or function of regulatory T cells (Treg), a lymphocyte population which promotes stroke recovery. The primary aim of this study was to rigorously investigate the effect of fingolimod on Tregs in a mouse model of brain ischaemia. The effect of fingolimod in mice with common stroke-related comorbidities (ageing and hypercholesteremia) was also investigated.MethodsYoung (15–17 weeks), aged C57BL/6 mice (72–73 weeks), and ApoE−/− mice fed a high-fat diet (20–21 weeks) underwent permanent electrocoagulation of the left middle cerebral artery. Mice received either saline or fingolimod (0.5 mg/kg or 1 mg/kg) at 2, 24, and 48 h post-ischaemia via intraperitoneal injection. Another cohort of young mice (8–9, 17–19 weeks) received short-term (5 days) or long-term (10 days) fingolimod (0.5 mg/kg) treatment. Flow cytometry was used to quantify Tregs in blood, spleen, and lymph nodes. Immunohistochemistry was used to quantify FoxP3+ cell infiltration into the ischaemic brain.ResultsFingolimod significantly increased the frequency of Tregs within the CD4+ T cell population in blood and spleen post-ischaemia in all three mouse cohorts compared to untreated ischemic mice. The highest splenic Treg frequency in fingolimod-treated mice was observed in ApoE−/− mice (9.32 ± 1.73% vs. 7.8 ± 3.01% in young, 6.09 ± 1.64% in aged mice). The highest circulating Treg frequency was also noted in ApoE−/− mice (8.39 ± 3.26% vs. 5.43 ± 2.74% in young, 4.56 ± 1.60% in aged mice). Fingolimod significantly increased the number of FoxP3+ cells in the infarct core of all mice. The most pronounced effects were seen when mice were treated for 10 days post-ischaemia.ConclusionsFingolimod increases Treg frequency in spleen and blood post-ischaemia and enhances the number of FoxP3+ cells in the ischaemic brain. The effect of fingolimod on this regulatory cell population may underlie its neuroprotective activity and could be exploited as part of future stroke therapy.

Triggered by Covid-19? Large Vascular Occlusion Resulting in Cytokine Storm Syndrome and Kounis Syndrome: A Case Report

It has been widely reported that infections caused by coronaviruses, especially SARS-CoV-2 (Covid-19), can result in cytokine storm syndrome, one of the causes of acute cerebrovascular disease and ‘kounis syndrome’. An 87-year-old male patient, who did not have any chronic diseases apart from hypertensions, was admitted to our emergency department with mental fog and right-sided weakness in the absence of the typical symptoms of Covid-19 (such as fever, cough). In addition to evidence of left middle cerebral artery infarction in Computerized Tomography (CT) of the brain, there were infiltrative findings compatible with Covid-19 in thorax CT. Here, we discuss this case in the light of the literature, assuming that inflammation (cytokine storm) and hypercoagulopathy induced by Covid-19 may have presented with large vessel occlusion and kounis syndrome as a result of increased risk of arterial thrombosis.

A case of hemichorea in RNF213-related vasculopathy

BackgroundInternal carotid artery (ICA) stenosis has been recently reported to cause hemichorea, mainly in East Asia. The East Asian-specific p.R4810K variant of RNF213, a susceptibility gene for moyamoya disease (MMD), accounts for up to 25% of sporadic ischemic stroke with ICA stenosis cases in East Asia. However, as RNF213-related vasculopathy does not meet the diagnostic criteria for MMD, the creation of a new disease category has been suggested. Here, we report the first case of hemichorea in RNF213-related vasculopathy.Case presentationAn 81-year-old woman was admitted to our hospital with choreic movements in the periphery of the right extremities at rest. Though head magnetic resonance imaging showed no fresh or old cerebral infarction, 123I-iodoamphetamine-single photon emission computed tomography showed cerebral blood flow of < 80% in the anterior territory of the left middle cerebral artery (MCA) in a resting state and cerebrovascular reactivity of < 10% in the broader area supplied by the left MCA after acetazolamide challenge. Head magnetic resonance angiography and digital subtraction angiography revealed left ICA C1 portion stenosis with compromised collateral vessels. Involuntary movements resolved with haloperidol administration within 3 days, without apparent recurrence from continuation of the medication for a year. Genetic testing revealed the presence of the heterozygous RNF213 p.R4810K variant.ConclusionsChorea is thought to be caused by damage to circuitry connecting the basal ganglia with the cerebral cortex, as found in cases of MMD, which possess aberrant vessels in the basal ganglia. However, aberrant vessels and cerebral infarctions were not observed in the basal ganglia in the current case, decreasing the likelihood of a role in chorea. Alternatively, as RNF213 regulates vascular endothelial function and angiogenesis, dysregulation may impair the neurovascular unit and damage basal ganglia circuitry, contributing to the development of chorea. This case may renew interest in the concept of RNF213-related vasculopathy and the pathophysiological mechanisms behind chorea in ICA stenosis.

Post-stroke cognitive impairment on the Mini-Mental State Examination primarily relates to left middle cerebral artery infarcts.

BackgroundPost-stroke cognitive impairment can occur after damage to various brain regions, and cognitive deficits depend on infarct location. The Mini-Mental State Examination (MMSE) is still widely used to assess post-stroke cognition, but it has been criticized for capturing only certain cognitive deficits. Along these lines, it might be hypothesized that cognitive deficits as measured with the MMSE primarily involve certain infarct locations.AimsThis comprehensive lesion-symptom mapping study aimed to determine which acute infarct locations are associated with post-stroke cognitive impairment on the MMSE.MethodsWe examined associations between impairment on the MMSE (<5th percentile; normative data) and infarct location in 1198 patients (age 67 ± 12 years, 43% female) with acute ischemic stroke using voxel-based lesion-symptom mapping. As a frame of reference, infarct patterns associated with impairments in individual cognitive domains were determined, based on a more detailed neuropsychological assessment.ResultsImpairment on the MMSE was present in 420 patients (35%). Large voxel clusters in the left middle cerebral artery territory and thalamus were significantly (p < 0.01) associated with cognitive impairment on the MMSE, with highest odds ratios (>15) in the thalamus and superior temporal gyrus. In comparison, domain-specific impairments were related to various infarct patterns across both hemispheres including the left medial temporal lobe (verbal memory) and right parietal lobe (visuospatial functioning).ConclusionsOur findings indicate that post-stroke cognitive impairment on the MMSE primarily relates to infarct locations in the left middle cerebral artery territory. The MMSE is apparently less sensitive to cognitive deficits that specifically relate to other locations.