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Background Elevated cardiac troponin (cTn) is detected in 10% to 30% of patients with acute ischemic stroke (AIS) and correlates with poor functional outcomes. Serial cTn measurements differentiate a dynamic cTn pattern (rise/fall >20%), specific for acute myocardial injury, from elevated but stable cTn levels (nondynamic), typically attributed to chronic cardiac/noncardiac conditions. We investigated if the direction of the cTn change (rising versus falling) affects mortality and outcome. Methods and Results We retrospectively screened consecutive patients with AIS admitted to 5 stroke centers for elevated cTn at admission and at least 1 additional cTn measurement within 48 hours. The pattern of cTn was defined as rising if >20% increase from baseline, falling if >20% decrease, or nondynamic if ≤20% change in either direction. Logistic regression analyses were performed to assess the association of cTn patterns and 7‐day mortality and unfavorable discharge disposition. Of 3789 patients with AIS screened, 300 were included. Seventy‐two had a rising pattern, 66 falling, and 162 nondynamic. In patients with AIS with rising cTn, acute ischemic myocardial infarction was present in 54%, compared with 33% in those with falling cTn (P

Introduction Arteriovenous shunting has been described in glioblastoma multiforme (GBM), also known as WHO grade 4 astrocytoma. This case report demonstrates the diagnostic dilemma of GBM, which was subsequently found to have macrovascular arteriovenous shunting. The lesion was initially treated as an ischemic stroke for months. Methods A 65‐year‐old‐man with a past medical history of hypertension, hyperlipidemia, and diabetes presented to a community hospital in February 2023 with worsening left‐sided weakness. The patient started having left‐sided weakness around December 2023, but no work‐up had been completed. The exam was notable for spastic hemiparesis. Results At the time of initial presentation, a non‐contrasted head computed tomography (NCHCT) was interpreted as normal. Magnetic resonance imaging (MRI) of the brain showed diffusion restriction and fluid attenuated inversion recovery (FLAIR) hyperintensity in the right corona radiata and was interpreted as a subacute right corona radiata and gangliocapsular infarct. Computed tomography angiogram (CTA) of the head and neck was unremarkable. He was discharged on aspirin and a high‐intensity statin. He re‐presented in April 2023 with sepsis and was found to have multiple pressure ulcers; his left‐sided weakness had worsened despite a course of inpatient rehabilitation. A repeat NCHCT demonstrated hyperdensity within the suspected infarct, interpreted as hemorrhagic transformation. The next day, he was found to be difficult to arouse and dysarthric. He was subsequently transferred to our institution for further management. On arrival, a CTA of the head and neck was performed, which suggested that the previously described hyperdensity was possibly a venous varix, and a thrombosed developmental venous anomaly or arteriovenous malformation was suggested. The patient then underwent an MRI brain with and without contrast, which noted that there was an increase in size of a heterogeneously enhancing mass centered in the posterior right basal ganglia/corona radiata with extension into right thalamus, right cerebral peduncle, and posterior right body of corpus callosum. The MRI findings were most consistent with GBM. Given the diagnostic uncertainty, the patient underwent a cerebral angiogram, which demonstrated a hypervascular posterior right basal ganglia mass with arteriovenous shunting from the middle cerebral artery to the internal cerebral veins. Shortly after, the patient underwent a brain biopsy, which demonstrated GBM (IDH‐wildtype, WHO grade 4). The patient was ultimately transitioned to hospice. Conclusion This case highlights the presence of macrovascular shunting in GBM. Intratumoral arteriovenous shunting in GBM has been described, and when present, can lead to delay in treatment due to the broadened differential diagnosis. This patient was first treated for an ischemic stroke with subsequent hemorrhagic transformation. Further imaging suggested a venous varix, thrombosed developmental venous anomaly, or arteriovenous malformation, but the combination of the cerebral angiogram and MRI led to the definitive diagnosis in a patient with a short survival period.

Introduction Bow Hunter’s Syndrome (BHS) is a rare etiology of vertebrobasilar insufficiency that usually occurs with head turn, which causes compression of the vertebral artery by an osteophyte. There is subsequent hypoperfusion of brain tissue, but thromboembolism and ischemic stroke is rare. Timely diagnosis is imperative, as decompressive surgery can be curative. This unique case highlights the diagnostic and therapeutic challenges of a patient with multiple vascular risk factors who suffered from strokes secondary to BHS. Methods A 79‐year‐old man with a past medical history of peripheral artery disease, abdominal aortic aneurysm, myocardial infarction with drug eluding stents (on dual antiplatelet therapy (DAPT)), complete heart block with pacemaker, heart failure with reduced ejection fraction, hypertension, hyperlipidemia, and diabetes mellitus presented to an outside hospital with recurrent episodes of right‐sided weakness every 1‐2 days over the previous 3 weeks. Episodes always occurred after activity and only upon sitting. He had previously undergone non‐contrasted head computed tomography (NCHCT) (magnetic resonance imaging (MRI) was unable to be performed secondary to pacemaker), which did not reveal strokes. His initial computed tomography angiogram (CTA) of the head and neck was unremarkable. However, CTA head and neck 4 days later demonstrated 90 percent stenosis of the mid left V2 at the C3‐4 level and a 75‐90 percent stenosis of the left mid V2 segment at the C5‐6 level (hard and soft plaque in these areas). He was switched from DAPT to aspirin and warfarin because he was considered a “DAPT failure.” He continued to have episodes, so he was transferred to our institution for a second opinion. Results On arrival, the exam was notable for right‐sided hemiparesis and dysmetria. Repeat CTA head and neck demonstrated multifocal intracranial atherosclerosis with marked stenosis of the left V4 segment. However, marked stenosis at V2 appeared to be owed to external compression from facet arthrosis rather than atherosclerosis. He also had moderate stenosis of the right V4 segment. Eventually, he underwent an MRI brain, which demonstrated acute to subacute infarcts in the left pons. He was taken for a cerebral angiogram on the same day, which demonstrated stenosis of the distal V2 segment of the left vertebral artery (at the level of C3‐C4) with interval development of marked stenosis following neck flexion and occlusion of the left vertebral artery following leftward head rotation. Findings were most consistent with rotational occlusion of the left vertebral artery, which is also known as BHS. The patient underwent surgery, but suffered from a gastrointestinal bleed and developed post‐operative atrial fibrillation; after a risks/benefits discussion, he was discharged on anticoagulation only. He had no further strokes. Conclusion This patient suffered from ischemic strokes, which occur in less than 10% of BHS cases. Contralateral vertebral artery stenosis, which is unable to supply retrograde flow during compression, is the likely etiology of this patient's strokes. Recurrent posterior circulation strokes in the setting of optimal medical management should clue clinicians to consider other etiologies of stroke. Dynamic angiography is the gold standard for BHS and decompressive surgery is often curative.

Background Cardiovascular complications after acute ischemic stroke (AIS) can be related to chronic/comorbid cardiac conditions or acute disruption of the brain–heart autonomic axis (stroke‐heart syndrome). Women are known to be more vulnerable to certain stress‐induced cardiac complications, such as Takotsubo cardiomyopathy. We investigated sex differences in cardiac troponin (cTn) elevation, cardiac events, and outcomes after AIS. Methods and Results We retrospectively analyzed consecutive patients with AIS from 5 stroke centers. Patients with AIS with elevated baseline cTn and at least 2 cTn measurements were included, while patients with acute comorbid conditions that could impact cTn levels were excluded. Poststroke acute myocardial injury was defined as the presence of a dynamic cTn pattern (rise/fall >20% in serial measurements) in the absence of acute atherosclerotic coronary disease (type 1 myocardial infarction) or cardiac death (type 3 myocardial infarction). From a total cohort of 3789 patients with AIS, 300 patients were included in the study: 160 were women (53%). Women were older, had a lower burden of cardiovascular risk factors, and more frequently had cardioembolic stroke and right insula involvement (P values all

Abstract Background Acute liver failure resulting from drug-induced liver injury can lead to the development of neurological complications called hepatic encephalopathy (HE). Hepatic transforming growth factor beta 1 (TGFβ1) is upregulated due to liver failure in mice and inhibiting circulating TGFβ reduced HE progression. However, the specific contributions of TGFβ1 on brain cell populations and neuroinflammation during HE are not known. Therefore, the aim of this study was to characterize hepatic and brain TGFβ1 signaling during acute liver failure and its contribution to HE progression using a combination of pharmacological and genetic approaches. Methods C57Bl/6 or neuron-specific transforming growth factor beta receptor 2 (TGFβR2) null mice (TGFβR2ΔNeu) were treated with azoxymethane (AOM) to induce acute liver failure and HE. The activity of circulating TGFβ1 was inhibited in C57Bl/6 mice via injection of a neutralizing antibody against TGFβ1 (anti-TGFβ1) prior to AOM injection. In all mouse treatment groups, liver damage, neuroinflammation, and neurological deficits were assessed. Inflammatory signaling between neurons and microglia were investigated in in vitro studies through the use of pharmacological inhibitors of TGFβ1 signaling in HT-22 and EOC-20 cells. Results TGFβ1 was expressed and upregulated in the liver following AOM injection. Pharmacological inhibition of TGFβ1 after AOM injection attenuated neurological decline, microglia activation, and neuroinflammation with no significant changes in liver damage. TGFβR2ΔNeu mice administered AOM showed no effect on liver pathology but significantly reduced neurological decline compared to control mice. Microglia activation and neuroinflammation were attenuated in mice with pharmacological inhibition of TGFβ1 or in TGFβR2ΔNeu mice. TGFβ1 increased chemokine ligand 2 (CCL2) and decreased C-X3-C motif ligand 1 (CX3CL1) expression in HT-22 cells and reduced interleukin-1 beta (IL-1ß) expression, tumor necrosis factor alpha (TNFα) expression, and phagocytosis activity in EOC-20 cells. Conclusion Increased circulating TGFβ1 following acute liver failure results in activation of neuronal TGFβR2 signaling, driving neuroinflammation and neurological decline during AOM-induced HE.