Evidence Of Acute Infarction Research Articles

Troponin levels in transient ischemic attack and ischemic stroke: does “transient” in your brain mean “better” for your heart?

PurposeTransient ischemic attack (TIA) is defined as a transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia, with clinical symptoms typically lasting less than one hour, and without evidence of acute infarction. In this type of ischemic event, there are no data about a possible cardiac injury tested with troponin. After a stroke, it is well established the cardiac involvement due to a neuro-inflammatory response (recently defined as Stroke Heart Syndrome). The aim of this study is to compare the troponin elevation after a stroke with the troponin elevation after a TIA. Materials and methodsThis is a retrospective, single center study on 565 patients (73 TIAs, 492 stroke). We collected demographic characteristics, cardiovascular risk factors, cardiac data such as troponin, NT-proBNP, left atrial dilatation, etiology of the ischemic event (TOAST classification). ResultsWe compare IS and TIA for each TOAST subtype. In all groups no substantial differences were found in demographic and past medical history (p > 0.05). However, the maximum troponin level reached were significantly lower in TIAs than IS (p < 0.05), except in lacunar etiology were troponin elevation was low also in IS group. We found a trend in favor to IS in the rise and fall troponin elevation over 30% in all the TOAST subgroups, but only in the cryptogenic etiology the difference was significant. About the others cardiac markers of injury, a significant higher rate of elevated NT-proBNP was found in the IS cohort. ConclusionsTroponin level after TIAs is significantly lower than after IS. Troponin elevation after an ischemic event may be more relevant in patients with higher NT-proBNP levels and older age. More studies are needed to better understand the pathophysiology of this phenomenon after an ischemic event.

FRI647 Hemiballismus - A Rare Presentation Of Uncontrolled Diabetes Mellitus Type 2

Abstract Disclosure: C.L. Macrohon: None. M.L. Kanapi: None. Background: Diabetic Striatopathy is a rare disease with a prevalence of 1 in 100,000 and is more commonly seen in elderly women with poor glycemic control. It is an acute movement disorder characterized by sudden, non-purposeful jerking movements secondary to non-ketotic hyperglycemia. This is associated with high-intensity signals on T1-weighted magnetic resonance imaging of the brain noted at the basal ganglia. Case: We have a case of an 80-year old female who came in due to a four-day history of persistent involuntary, non-purposeful jerking of her right upper extremity accompanied by episodes of agitation and visual hallucinations. She has Diabetes Mellitus Type 2 for the past 20 years on Glibenclamide and Metformin. However, self-monitoring of blood glucose revealed fasting glucose levels as high as 300mg/dl. She was asymptomatic hence did not have regular follow-up with her primary care physician. She had no history of previous cerebrovascular disease. Family history was unremarkable. Upon examination, she was disoriented to place but answers appropriately to questions and did not have any speech abnormalities. On inspection it was noted that she had high amplitude involuntary flailing of the right upper extremity accompanied by non-purposeful jerking of her right lower extremity. Initial blood glucose level was 354mg/dl with an Hba1c of 13.7%. Serum ketones was within normal limits with a value of 0.1mmol/L. A plain Magnetic Resonance Imaging of the brain was done which showed a region of T1 weighted hyperintensity with no corresponding abnormal restricted diffusion nor increased susceptibility signals involving the left lentiform nucleus with no evidence of acute infarction nor intracranial hemorrhage noted. At this time, patient was co-managed by Endocrinology and Neurology service with an impression of a Diabetic Striatopathy. For the hemiballism and other neurologic manifestations such as agitation, visual hallucinations and disorientation patient was given risperidone and clonazepam. Blood glucose was then managed through cautious insulin therapy as well as hydration. On the third hospital day, there was noted resolution of right-sided hemiballismus and at this time glycemic control was improved. Conclusion: Proper identification and diagnosis is essential in managing Diabetic striatopathy. Although this may be a rare presentation of uncontrolled diabetes mellitus, clinicians should be aware of the possibility of an acute movement disorder as an unveiling symptom. This shows the importance of prompt blood glucose measurement in these acute cases. Once identified, adequate glycemic control through insulin therapy remains to be the center and most effective therapeutic management for the resolution of these hyperkinetic symptoms. Presentation: Friday, June 16, 2023

Cerebral venous thrombosis and B12 deficiency

Infants with prematurity and necrotizing enterocolitis (NEC) are at increased risk for short bowel syndrome and subsequent nutritional deficiencies. In particular, ileal resection is associated with vitamin B12 malabsorption, which interferes with normal myelination and homocysteine metabolism.1, 2 Vitamin B12 deficiency is associated with neurodevelopmental delay as well as hyperhomocysteinemia, which increases the risk for venous thrombosis.2, 3 This eight-year-old boy presented with severe headache, dehydration, and lethargy. He developed acute onset severe frontal headache followed by decreased oral intake, decreased urine output, and recurrent vomiting. The headache was dull and radiating to the back of his head. At the same time, he appeared to be sleepy and less active. These symptoms lasted for two to three days before he was brought to the primary doctor's office and then referred to the emergency department. On assessment, he was tired-looking and exhibited mild microcephaly, but his neurological examination was normal, as was an examination by an ophthalmologist. He experienced mild global developmental delay. He was born at 25 weeks gestational age and had a prolonged stay in the neonatal intensive care unit, complicated by NEC and a hemicolectomy with ileostomy and removal of ileocecal valve. He had low normal levels of B12 for several years prior to presentation and was not treated (151 pg/ml after surgery [normal 160-950]). Brain magnetic resonance imaging and magnetic resonance venography (MRV) showed filling defects in the inferior sagittal, straight, torcula, and proximal transverse sinuses consistent with cerebral venous sinus thrombosis (CVST) with no evidence of acute infarction (Figure 1). Dehydration was initially considered to be the cause. Enoxaparin sodium was started at 1 mg/kg every 12 h with the goal of anti-Xa level between 0.5 and 1.0 U/ml. The hypercoagulation evaluation was normal. The B12 level was 86 pg/ml. His hematocrit was 33.3, and his mean corpuscular volume (MCV) was 87.4. He was not treated at that time. He was discharged within a week after the repeat imaging remained stable with the goal to continue enoxaparin sodium for three months. After three months, he again developed headache and lethargy, and MRV showed a new thrombus. Enoxaparin was switched to warfarin. After a year of warfarin, the clot resolved but he still had headaches. Two B12 levels were obtained, both below 200. His anemia worsened (hematocrit 24.7) and his MCV increased to 96.9. The homocysteine level was 184 μmol/L (normal <11.4). At this point, he began B12 injections (1000 mcg daily for one week followed by monthly and then quarterly injections thereafter). His B12 levels normalized and remained normal throughout his course. The warfarin was discontinued and thrombus has not recurred. Our patient had a difficult-to-treat CVST secondary to a condition predisposing to nutritional deficiency. His chronic B12 deficiency was overlooked by his treating physicians until he presented with a profound deficiency with megaloblastic anemia. The association between B12 deficiency and CVST has been described in children with nutritional deficiency and megaloblastic anemia.4 Previous authors suggested that testing for hyperhomocysteinemia and with B12 supplementation should be considered in pediatric patients with CVST.5 The diagnosis becomes even more crucial in patients with conditions known that promote nutritional deficiencies, such as a history of NEC and ileal surgery. In such children, early recognition of vitamin B12 deficiency and timely vitamin supplementation may prevent the occurrence of CVST as well as other manifestations of B12 deficiency, such as developmental delay.6, 7 In this patient, the B12 deficiency was chronic. While it is difficult to prove that the deficiency caused the CVST, it likley played a substantial role. Hyperhomocysteinemia can damage the vascular endothelium, predisposing to thrombus formation.8, 9 Consequently, vitamin B12 deficiency is a potential risk factor in children with CVST. Fatemeh Mohammadpour Touserkani: Conceptualization; supervision; writing – original draft; writing – review and editing. Theodora Andriotis: Conceptualization; investigation; writing – original draft; writing – review and editing. Yaoping Zhang: Conceptualization; supervision; writing – original draft; writing – review and editing. Steven Pavlakis: Conceptualization; supervision; writing – original draft; writing – review and editing. We would like to thank the patient's parents for their consent for this publication. The authors declare no conflict of interest.

Safety of 3 Tesla Magnetic Resonance Imaging in Patients with Sickle Cell Disease.

Sickle cell disease (SCD) is a well-characterized hemoglobinopathy affecting more than 20 million individuals worldwide and carries an increased risk of cerebral vasculopathy, cerebral infarct, and stroke. As mechanisms of cerebral infarction in SCD are partly attributable to microvascular vaso-occlusive crises, manifesting as altered cerebral blood flow and associated impaired oxygen delivery, magnetic resonance imaging (MRI) methods that can quickly provide a comprehensive perspective on structural and functional disease status, without exogenous contrast administration or ionizing radiation, have emerged as crucial clinical tools for surveillance. However, early ex vivo MRI work in suspended erythrocytes containing hemoglobin S at 0.35 Tesla (T) suggested that sickled erythrocytes can orient preferentially in the presence of an external magnetic field, and as such, it was suggested that MRI exams in sickle cell hemoglobinopathy could induce vaso-occlusion. While this observation has generally not impacted clinical imaging in individuals with SCD, it has led to resistance for some sickle cell studies within the engineering community among some imaging scientists as this early observation has never been rigorously shown to be unconcerning. Here, we performed MRI at the clinical field strength of 3 T in 172 patients with SCD, which included standard anatomical and angiographic assessments together with gold standard diffusion-weighted imaging (DWI; spatial resolution = 1.8 × 1.8 × 4 mm; b-value = 1000 s/mm2) for acute infarct assessment (performed approximately 20 min after patient introduction to the field isocenter). The presence of vasculopathy, as well as chronic and acute infarcts, was evaluated by two independent board-certified radiologists using standard clinical criteria. In these patients (52.3% female; mean age = 19.6 years; age range = 6–44 years), hematocrit (mean = 25.8%; range = 15–36%), hemoglobin phenotype (87.8% HbSS variant), presence of silent infarct (44.2%), and overt chronic infarct (13.4%) were consistent with a typical SCD population; however, no participants exhibited evidence of acute infarction. These findings are consistent with 3 T MRI not inducing acute infarction or vaso-occlusion in individuals with SCD and suggest that earlier low-field ex vivo work of erythrocytes in suspension is not a sufficient cause to discourage MRI scans in patients with SCD.

S2489 Tacrolimus-Induced Posterior Reversible Encephalopathy Syndrome With Seizures: A Rare Clinical Combination

INTRODUCTION: Tacrolimus, a calcineurin inhibitor, is a backbone of many liver transplant anti-rejection regimens. Posterior Reversible Encephalopathy Syndrome (PRES) is a rare clinical entity, with acute neurological symptoms and a classic MRI pattern. This case presents a recent liver transplant patient who developed PRES while on tacrolimus (TAC). CASE DESCRIPTION/METHODS: A 47-year-old woman s/p deceased donor liver transplant presented with 2 generalized tonic-clonic seizures. Her OLT 7 weeks prior for NASH with MELDNa 28 required retransplant day 2 for primary nonfunction. Immunosuppression included Basiliximab day 1 and day 4 induction, Mycophenolate Mofetil 1gm BID, Prednisone taper, and TAC with goal levels maintained 8–10 ng/mL. One week before presentation, she had progressive headaches, unsteady gait, hypertension, and hyperglycemia. Medications included unchanged doses of TAC 3 mg BID, prednisone 15 mg daily, TMP/SMX, 81mg ASA, and 20 mg omeprazole. She had 2 witnessed brief tonic- clonic seizures, which responded to lorazepam and leviteracetam, and was empirically treated with antimicrobials. Neurology evaluation revealed BP 176/86 mmHg and a postictal state without focal findings, and an encephalopathic EEG without seizure. CT head was negative for hemorrhage. Labs earlier that day showed normal CBC, INR, chemistry panel including renal and liver function except a glucose of 465mg/dL. Negative studies included: full respiratory viral panel including COVID-19, serum cryptococcus antigen and CMV PCR, UA, a LP with normal opening pressure and cell counts, and broad encephalitis PCR panels. TAC trough was 13.7 ng/mL. MRI revealed patchy focal T2-hyperintensities in bilateral cerebellar hemispheres and occipital lobes, consistent with PRES. DISCUSSION: PRES occurs in <1% of liver transplants, characterized by a typical brain edema pattern. Hypertension, encephalopathy, and seizures are frequent often without a seizure history. Of the few reports associating PRES with TAC, trough levels were not supratherapeutic. Presentation ranges days to months after drug initiation, with a more delayed PRES from TAC than cyclosporine at 26 vs. 12 days. MRI findings do not correlate with severity. The pathophysiology is unknown but may include blood-brain barrier damage and abnormal vascular autoregulation. Early recognition is key as management includes TAC discontinuation and aggressive blood pressure management. Most patients, including ours, have no major neurological sequelae if diagnosed and treated quickly.Figure 1.: MRI FLAIR images of Tacrolimus associated PRES. Multiple relatively symmetric patchy juxtacortical white matter abnormality in occipital lobes (A). Multiple patchy regions of abnormal focal T2-hyperintensity in the bilateral cerebellar hemispheres, right thalamus, centrum semiovale bilaterally (B). No evidence of acute infarction, hemorrhage, mass effect, hydrocephalus, vascular abnormality, nor any pathologic intracranial enhancement.

Safety of Triple Neuroprotection with Targeted Hypothermia, Controlled Induced Hypertension, and Barbiturate Infusion during Emergency Carotid Endarterectomy for Acute Stroke after Missing the 24 Hours Window Opportunity

The aim of this study is to establish the initial safety of triple neuroprotection (TNP) in an acute stroke setting in patients presenting outside the window for systemic tissue plasminogen activator (tPA). Over 12,000 patients were referred to our vascular services with carotid artery disease, of whom 832 had carotid intervention with a stroke rate of 0.72%. Of these, 25 patients presented (3%), between March 2015 and 2019, with acute dense stroke. These patients had either failed tPA or passed the recommended timing for acute stroke intervention. Fifteen (60%) had hemi-neglect with evidence of acute infarct on magnetic resonance imaging of the brain and a Rankin score of 4 or 5. Ninety-six percent had an 80-99% stenosis on the symptomatic side. Mean ABCD3-I score was 11.35. All patients underwent emergency carotid endarterectomy (CEA) with therapeutically induced hypothermia (32-34°C), targeted hypertension (systolic blood pressure 180-200mm Hg), and brain suppression with barbiturate. There were no cases of myocardial infarction, death, cranial nerve injury, wound hematoma, or procedural bleeding. Mean hospital stay was 8.4 (±9.5) days. All cases had resolution of neurological symptoms, except 3 who had failed previous thrombolysis. Eighty percent had a postoperative Rankin score of 0 on discharge and 88% of patients were discharged home with 3 requiring rehabilitation. Positive neurological outcomes and no serious adverse events were observed using TNP during emergency CEA in patients with acute brain injury. We recommend TNP for patients who are at an increased risk of stroke perioperatively, or who have already suffered from an acute stroke beyond the recommended window of 24hr. Certainly, the positive outcomes are not likely reproducible outside of high-volume units and patients requiring this surgery should be transferred to experienced surgeons in appropriate tertiary referral centers.

Self- or caregiver-delivered manual remote ischemic conditioning therapy in acute ischemic stroke is feasible: the Early Remote Ischemic Conditioning in Stroke (ERICS) trial

Background: Infarct growth and recurrent stroke may be responsible for early morbidity and mortality in patients with acute ischemic stroke. Remote ischemic conditioning (RIC) may reduce infarct growth and prevent recurrent stroke; however, the exact dose remains to be investigated. We hypothesized that self- or caregiver-delivered six cycles of RIC intervention in acute ischaemic stroke for the first 12 weeks is feasible and safe compared to the four cycles RIC intervention. Methods: Adult ischemic stroke patients presenting within the first 48 h of symptom onset were screened. Patients with magnetic resonance imaging (MRI) evidence of acute infarct were randomized (1:1) to receive either four or six cycles of RIC therapy sessions two times daily in both arms for 12 weeks. All patients underwent MRI for infarct volume assessment and endothelial-dependent flow-mediated dilation (EDFMD) testing at baseline, 7 days and 12 weeks. Results: A total of 57 patients with mean±SD age of 59.4±12.4 years and median National Institute of Stroke Scale, 4 (IQR, 3-7) were randomised at a median of 23 h 30 min (IQR, 10 h 20 min to 30 h) after symptom onset to either the four-cycle (n=27) or six-cycle group (n=30). A total of 18 (66%) patients completed ≥50% sessions in 12 weeks in the four-cycles group; 21 (69.7%) patients completed ≥50% sessions in 12 weeks in the six-cycle group (p=0.4). There was no between-group differences in infarct growth, early neurological deterioration, recurrent stroke, and EDFMD at 7 days and 90 days. Conclusion: Both four and six cycles of short-term self- or caregiver-delivered RIC therapy is safe and may be feasible in acute ischaemic stroke patients. Randomised clinical trials are needed to assess efficacy to decrease infarct growth and prevent early neurological deterioration. Registration: Clinical Trial Registry - India: CTRI/2016/11/007495; registered on 25/11/2016.

Anomalous Coronary Artery Origin and Sudden Cardiac Death: Clinical and Pathological Insights From a National PathologyRegistry.

This study sought to describe the clinical and pathological features of anomalous origin of a coronary artery (AOCA) in sudden cardiac death (SCD) victims. AOCA from the inappropriate sinus of Valsalva or from the pulmonary artery is increasingly diagnosed with current imaging techniques. AOCA is a possible cause of SCD. We reviewed a database of 5,100 consecutive cases of SCD referred to our specialist cardiac pathology center between January 1994 and March 2017 and identified a subgroup of 30 cases (0.6%) with AOCA. All cases underwent detailed post-mortem evaluation including histological analysis by an expert cardiac pathologist. Clinical information was obtained from referring coroners. The mean age was 28 ± 16 years and 23 individuals were male (77%). In 8 cases (27%), SCD occurred before 18 years of age. Cardiac symptoms were present in 11 individuals (37%), and syncope was the most common (n= 6, 20%). Anomalous left coronary artery arising from the right sinus of Valsalva (ALCA) with interarterial course (n= 11) and anomalous right coronary artery arising from the left sinus of Valsalva (ARCA) with interarterial course (n= 11) were the most common found. ALCA arising from pulmonary artery was present in 7 cases, whereas in 1 case, the left coronary artery arose from the noncoronary cusp. Left ventricular fibrosis was reported in 11 cases (37%) and was mainly subendocardial. There was evidence of acute infarction in 2 cases. Death occurred during exercise or emotional stress in 15 (50%) cases. The AOCA variant where death occurred more frequently during physical activity was ALCA (8 of 11, 73%), followed by ALCA arising from pulmonary artery (4 of 7, 57%) and ARCA (2 of 11, 18%). AOCA is a rare cause of SCD. ALCA and ARCA with interarterial course are the most common anatomical variants recognized at the postmortem of SCD victims. ALCA is more commonly associated with death during exercise. Cardiac arrhythmias causing sudden death seem most likely in the cases without overt myocardial damage.

Abstract WP50: Potential Impact of Triage Using Non-Contrast Head CT and Stroke Severity on a Regional Stroke System of Care: A Population-Based Study

Background and Purpose: Acute ischemic stroke (AIS) patients may benefit from endovascular therapy (EVT) up to 24 hours since last known normal (LKN). Advanced imaging, including CT or MR angiography and perfusion studies, is required for patient selection. Large non-thrombectomy centers may be able to obtain and interpret these images quickly, but smaller hospitals may not have sufficient real-time CT technician and radiology support. We estimated transfer rates using non-contrast head CT and stroke severity to select patients to be transferred to larger centers for evaluation. Methods: We identified all AIS among residents of the Greater Cincinnati/Northern Kentucky Stroke Study region in 2010 comprising approximately 1.3 million people. Study nurses abstracted relevant information from the medical record, including times of symptom onset, LKN, and ED arrival, and all cases were verified by study physicians. Only cases age ≥18 with baseline mRS 0-2 that presented to an ED were included. Among cases that presented between 6 and 24 hours from LKN, those without evidence of acute infarct on head CT and with initial NIHSS ≥6 or ≥10 were identified. Results: Of 1359 AIS cases at local EDs, 448 (33.0%) presented between 6 and 24 hours, of which s383 (85.5%) showed no evidence of acute infarct on CT. Of cases with no acute infarct on CT, 89/383 (23.2%) had NIHSS ≥6, of which 66 (74.2%) initially presented to a hospital without thrombectomy capabilities; and 51/383 (13.3%) had NIHSS ≥10, of which 40 (78.4%) presented to a non-thrombectomy hospital. Conclusions: From 6 to 24 hours after stroke onset within our population, 40-66 AIS patients annually (0.8-1.3/week, or 3-5 patients per 100,000 persons per year) may present to non-thrombectomy hospitals and need to be transferred using non-contrast CT and stroke severity as screening tools. Such an approach may sufficiently mitigate the impact of delays in treatment on outcomes, without overburdening the referring nor accepting hospitals.

Outpatient management of transient ischaemic attack.

Stroke is a significant cause of death and disability in Singapore; in 2014, it was the fourth most common cause of death. Transient ischaemic attack (TIA) is defined as a transient episode of neurological dysfunction caused by focal brain, spinal cord or retinal ischaemia without evidence of acute infarction. The diagnosis of TIA/acute stroke needs to be considered in all patients who present with sudden focal neurological dysfunction. Prompt referral for assessment, neuroimaging and intervention provides the best chance for neurological recovery and/or minimising further neurological damage. Primary care physicians have a crucial role in TIA/stroke prevention and management. This includes referring patients with suspected acute TIA/stroke to hospitals with stroke treatment facilities immediately; managing the modifiable risk factors of cerebral ischaemia; continuing prescription of antiplatelet agents and/or anticoagulation where indicated; and teaching patients to recognise and respond to suspected cerebral ischaemia using the FAST (face, arm, speech, time) acronym.

Dabigatran Therapy in Acute Ischemic Stroke Patients Without Atrial Fibrillation.

Acute ischemic stroke patients are at risk of early recurrence. We tested the feasibility and safety of initiating dabigatran in patients, within 24 hours of minor stroke in patients without atrial fibrillation. Minor stroke patients (National Institutes of Health Stroke Scale score ≤3) without atrial fibrillation and evidence of acute infarction on magnetic resonance imaging were treated with dabigatran. Treatment began within 24 hours of onset and was continued for 30 days. The primary end point was symptomatic hemorrhagic transformation. A total of 53 patients with median (interquartile range) age of 68 (57-77) years and National Institutes of Health Stroke Scale score of 1 (0-2) were enrolled. Baseline diffusion-weighted imaging volume was 0.8 (0.3-2.4) mL. No patients experienced symptomatic hemorrhagic transformation. Three patients had evidence of asymptomatic petechial hemorrhagic transformation on day 7, which remained stable at day 30, while continuing dabigatran. Dabigatran treatment within 24 hours of minor stroke is feasible. A larger randomized trial is required to confirm the safety and efficacy of this treatment approach. URL: http://www.clinicaltrials.gov. Unique identifier: NCT 01769703.

Emergency placement of stent-graft for symptomatic acute carotid artery occlusion after endarterectomy

A patient underwent a left-sided carotid endarterectomy (CEA) for an asymptomatic 80% carotid artery (CA) stenosis. There were no signs of intolerance during the carotid cross-clamping and an initially uneventful...

Abstract W P185: Clinical Predictors of Stroke, TIA and Mimic among Patients with Transient Neurological Dysfunction Admitted to an Emergency Department Observation Unit

Background: In patients with resolved symptoms, transient ischemic attack (TIA) is distinguished from ischemic stroke by neuroimaging evidence of acute infarction. DW-MRI has been shown to be more sensitive at detecting infarction than CT, but is not uniformly available in the acute setting. Hypothesis: We sought to identify predictors of stroke diagnosis among a cohort of clinically suspected TIA patients undergoing an accelerated diagnostic protocol in an emergency department observation unit (EDOU). Methods: We prospectively studied 189 patients treated in the EDOU of a single tertiary care academic medical center. Patients underwent DW-MRI of the brain (unless contraindicated), and bedside neurologist evaluation. A CT scan of the brain was considered optional prior to EDOU admission. We compared the odds of extremity weakness, sensory loss, facial droop, visual disturbance, slurred speech, aphasia, dizziness, and headache between patients with final diagnosis of stroke, TIA and mimic. This study was approved by the hospital IRB. Results: Thirty-one patients (16%) were diagnosed with an acute ischemic stroke, 85 (45%) TIA, and 73 (39%) mimic. Mean age was 64.8 years (SD = 15.5; range = 30-90). DW-MRI was performed on 92% of patients. A CT scan was also performed in 80% of patients diagnosed with stroke and 0 were diagnostic. Median ABCD2 scores were 4 for stroke and TIA (IQR 3-5) and 3 for mimic (IQR 2-4). Only headache symptoms predicted lower odds of stroke (OR 0.22; 95% CI: 0.05-0.96). Both headache (OR 1.44; 95% CI: 1.03-2.03) and visual disturbance (OR 3.14; 95% CI: 1.49-6.65) increased the odds of mimic diagnosis, but were also present in 13% and 10% of stroke patients respectively. Slurred speech (OR 0.48: 95% CI: 0.25-0.93); aphasia (OR 0.34 95% CI: 0.15-0.76) and facial droop (OR 90.36: 95% CI: 0.14-0.94) significantly predicted lower odds of mimic diagnosis. Conclusions: In our investigation of patients with transient neurologic dysfunction in an EDOU, stroke diagnosis was common and could not be predicted by clinical variables alone. Early DW-MRI should be considered in all TIA patients, especially those reporting slurred speech, aphasia or facial droop.

Magnetic resonance imaging in patients with transient ischemic attack.

Magnetic resonance imaging in patients with transient ischemic attack.

A blood-making lung mass

Dear Editor, An 81-year-old woman presented to us with right arm weakness and slurred speech. She had a history of rheumatoid arthritis, chronic renal insufficiency, hypertension, and a monoclonal gammopathy of undetermined significance. Her vital signs and physical examination were unremarkable. A complete blood count with differential showed hemoglobin 10.7 g/dL, platelets 493,000/μL, 68 % neutrophils, 12 % lymphocytes, 19 % monocytes, 1 % eosinophils, 0 % basophils, and 0.3 % immature granulocytes. Peripheral blood smear was notable for excessive platelets, frequent platelet clumping, giant platelets, normochromic normocytic red blood cells, and normal-appearing white blood cells. A leukoerythroblastic picture was not present. The majority of her platelet counts had been greater than 500,000/μL for the past 6 months. A comprehensive metabolic panel showed creatinine 1.7 mg/dL. A CT scan of head showed no evidence of acute infarct or hemorrhage. A carotid Doppler showed no evidence of hemodynamically significant stenosis. The patient’s right arm weakness and slurred speech resolved in 3 h. This episode was diagnosed with transient ischemic attack (TIA). She was given Plavix and aspirin. Subsequently, a chest X-ray incidentally revealed a mass in her right lung (Fig. 1a). A CT scan of chest showed an 8.4× 5.4×7.3 cm heterogeneous mass in her right hemithorax (Fig. 1b). A CT scan-guided percutaneous biopsy of the lung mass showed cellular hematopoietic elements within the trilineage maturation (Fig. 1c), indicating that the mass was due to extramedullary hematopoiesis (EMH). The bone marrow aspiration and biopsy were obtained without difficulty. Bone marrow specimens revealed maturing trilineage hematopoiesis with a marked myeloid predominance, megakaryocytic atypia (Fig. 1d), and minimal reticulin fibrosis (Fig. 1e). Her JAK-2 mutation analysis was positive, and the presence of JAK-2 mutation ruled out secondary myelofibrosis caused by toxin, infection, and other hematological malignancies. Bone marrow biopsy findings and presence of JAK-2 mutation were consistent with the diagnosis of prefibrotic phase of idiopathic myelofibrosis. The patient was started on hydroxyurea, continued on Plavix, and discharged after 4 days; at the last follow-up in August, 2012, she had no further similar TIA, platelet counts were normal, and she was well. Other than in the liver and spleen, EMH is exceptionally rare. To date, there have been a few reported cases of pulmonary EMH. Rumi et al. presented a case of dyspnea secondary to pulmonary EMH [1]. Hsu et al. reported a case of EMH mimicking metastatic lung carcinoma [2]. In another case report, Pandit et al. described a pulmonary EMH induced by chronic allergen challenge [3]. Here, we report a case of a patient with a pulmonary EMH in the setting of prefibrotic phase of idiopathic myelofibrosis. The presence of JAK-2 mutation in our patient ruled out secondary myelofibrosis caused by toxin, infection, and other hematological malignancies. Decision regarding management of pulmonary EMH depends on symptoms, coexisting conditions, and underlying causes. There are no set guidelines on the treatment of pulmonary EMH. Cytoreduction with hydroxyurea, steroids, allogenic stem cell transplantation, and radiation therapy have been documented in some case reports with varying success [4]. Our patient received cytoreductive treatment (hydroxyurea). Her platelets counts came down to normal, and her clinical course was stable. J. Wang (*) Department of Internal Medicine, St. Luke’s Hospital, 232 South Woods Mill Road, Chesterfield, MO 63017, USA e-mail: Jianbo310@gmail.com

The incidence and clinical predictors of acute infarction in patients with transient ischemic attack using MRI including DWI

According to the most recent definition of transient ischemic attack (TIA) and the recommendations of the American Heart Association, magnetic resonance imaging (MRI) including diffusion-weighted imaging (DWI) is considered a mandatory tool in evaluating and treating patients with TIA. This study aims to determine the incidence of TIA-related acute infarction, identify the independent predictors of acute infarction, and investigate the correlation between acute infarction detected by DWI-MRI and stroke risk during hospitalization. Over a 36-month period (starting November 2007), all TIA patients (symptom duration of <24 h) who were admitted to hospital within 48 h of symptom onset and who underwent DWI-MRI were included in this population-based prospective study. The incidence of acute infarction, clinical predictors, and association with stroke recurrence during hospitalization were studied. Of 1,910 patients (mean age, 66.7 ± 13 years; 46 % women), 1,862 met the inclusion criteria. A TIA-related acute infarction was detected in 206 patients (11.1 %). Several independent predictors were identified with logistic regression analysis: motor weakness [odds ratio (OR), 1.5], aphasia (OR, 1.6), National Institutes of Health Stroke Scale (NIHSS) score of ≥10 at admission (OR, 3.2), and hyperlipidemia (OR, 0.6). Of 24 patients (1.3 %) who suffered a stroke during hospitalization (mean, 6 ± 4 days), five had positive DWI. Stroke rate during hospitalization was nonsignificantly higher in patients with positive DWI than those with negative DWI (2.4 vs 1.1 %, respectively; P = 0.12). The evidence of acute infarction by DWI-MRI in TIA patients was detected in 11.1 % of patients and associated with motor weakness, aphasia, and NIHSS score of ≥10 at admission.

How to identify stroke mimics in patients eligible for intravenous thrombolysis?

Since decision-making for thrombolysis in acute stroke settings is restricted to a limited time window and based on clinical assessment and CT findings only, thrombolysis is sometimes applied to patients with a final diagnosis other than a stroke. From a prospectively collected stroke/MRI data bank (2004-2010) with 648 suspected ischemic stroke patients treated with rtPA, we identified patients without evidence of acute infarction on follow-up MRI and a final diagnosis other than a stroke or acute cerebrovascular event. We compared demographics, symptoms, complications, and outcome of patients with stroke mimics (SM) to those with acute infarction. In 42 patients, an SM was diagnosed: seizures in 20, conversion disorder in seven, dementia in six, migraine in three, brain tumor in two, and others in four patients. Patients with SM less often had typical stroke symptoms like dysarthria (p < 0.01), facial palsy (p < 0.001), hemiparesis (p < 0.001), horizontal gaze palsy (p < 0.001), and visuospatial neglect (p = 0.03), while aphasia (p = 0.004) and accompanying convulsions (p = 0.01) occurred more often. Independent predictors of SM were known cognitive impairment, aphasia, and accompanying convulsions. Thrombolysis-related complications (orolingual angioedema) occurred in one SM patient and none of the SM patients deteriorated clinically. Stroke mimics comprise neurological/psychiatric disorders and differ from ischemic stroke patients with regard to the clinical presentation at onset. This might be helpful in deciding which patients should undergo acute stroke MRI to rule out SM, facilitate treatment decisions, and reduce the risk of unnecessary therapy.

Plasma glial fibrillary acidic protein levels in children with sickle cell disease

To determine if glial fibrillary acidic protein (GFAP) is associated with brain injury in children with sickle cell disease (SCD), we measured plasma GFAP among cross-sectional groups of unselected children with SCD, subsets of children with SCD and normal brain MRI or MRI evidence of cerebral infarct, healthy pediatric controls, and adults with brain injury. Children with SCD had higher plasma GFAP than healthy pediatric controls (mean concentrations 0.14 ± 0.37 vs. 0.07 ± 0.08 ng/mL; P 5 0.003); also, 16.0% (16/100) of children with SCD and cerebral infarct had GFAP elevations above the 95th percentile of healthy pediatric controls (P 5 0.04). Although not statistically significant, children with SCD and cerebral infarct had more elevated GFAP levels than with SCD and no infarct (16/100, 16.0% vs. 14/168, 8.3%; P 5 0.07). Children with SCD and acute brain ischemia had a higher proportion of elevated GFAP than SCD children with normal MRI (3/6, 50% vs.8.3%; P 5 0.01). GFAP was associated with elevated systolic blood pressure in the preceding year and correlated positively with white blood cell count and negatively with age and performance IQ. Plasma GFAP is elevated among children with SCD and may be associated with subclinical brain injury.

Part One: For the Motion Carotid Disease is Rarely Responsible for Stroke after Coronary Bypass Surgery

Part One: For the Motion Carotid Disease is Rarely Responsible for Stroke after Coronary Bypass Surgery

How Much Would Performing Diffusion-Weighted Imaging for All Transient Ischemic Attacks Increase MRI Utilization?

The American Heart Association recently redefined TIA to exclude patients with infarction on neuroimaging. Given its advantages, MRI/diffusion-weighted imaging (DWI) was recommended as the preferred imaging modality. We determined how frequently MRI/DWI was performed for TIA and ascertained the proportion of clinically defined TIA patients who had ischemic lesions on DWI in our community in 2005. All clinically defined TIA cases among residents of a 5-county region around Cincinnati who presented to emergency departments were identified during 2005. Demographics and medical history, whether MRI/DWI was performed, and DWI findings were recorded. Generalized estimating equations were used to compare groups to account for the design of the study and multiple events per patient. Of 834 TIA events in 799 patients, 323 events (40%) had MRI/DWI performed. Patients who had MRI/DWI were younger (mean, 66 vs 70 years; P=0.03), had less severe prestroke disability (baseline modified Rankin Scale score, 0; 44% vs 34%; P=0.02), were less likely to have previous stroke or TIA (42% vs 56%; P=0.002), and were less likely to have atrial fibrillation (10% vs 16%; P=0.01). Of the 323 events with DWI, 51 (15%) had evidence of acute infarction. Patients with positive DWI were older (75 vs 64 years; P=0.0001) and more likely to have atrial fibrillation (21% vs 7%; P=0.002). Performing MRI/DWI on all clinically defined TIA patients in our community would reveal more cases of actual infarction but would more than double current use. Future studies should assess whether MRI/DWI is warranted for all TIA patients.