Acute Cerebellar Infarction Research Articles

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.

Acute Obstructive Hydrocephalus and Acute Cerebellar Ischemic Stroke as a Complication of Takayasu Arteritis in a Young Male Patient: A Rare Case Report

Introduction: Takayasu arteritis is a rare type of vasculitis associated with various neurological manifestations. Multiple components, including thrombosis, embolism, stenosis, and vascular inflammation, are involved in the underlying pathophysiology. Case Presentation: A 21-year-old male patient presented with vomiting, difficulty speaking, disorientation, and seizures. On examination, pinpoint pupils and blood pressure discrepancies among four limbs were noted. Imaging findings supported the diagnosis of acute obstructive hydrocephalus, acute cerebellar infarction, and Takayasu arteritis. The patient was treated with IV antibiotics and steroids and underwent a ventriculoperitoneal shunt. Case discussion: Takayasu arteritis with cerebellar ischemia and obstructive hydrocephalus is quite a rare case. It presents with headache, dizziness, disorientation, and rarely with stroke. The diagnostic process includes computed tomography angiography (CTA) and imaging of the brain. It is mostly treated with pharmacological therapy; however, in some cases, surgery is required. Conclusion: This case highlights the rare but serious neurological adverse effects of Takayasu arteritis in young male patients, as well as the importance of interdisciplinary care. To prevent neurological degeneration, Takayasu arteritis patients must be identified and treated as soon as possible.

Cholecystitis in older patients following hip fracture: a case series and literature review

ObjectiveThis study’s aim is to describe the characteristics of perioperative acute cholecystitis in older patients with hip fracture.MethodsFrom January 1, 2018, to April 30, 2023, 7,746 medical records were retrospectively collected for patients aged ≥ 65 years who were hospitalised for hip fracture in Beijing Jishuitan Hospital, Capital Medical University. We reviewed 10 cases with confirmed diagnoses of acute cholecystitis.ResultsOf these 10 cases, five femoral neck fractures and five intertrochanteric fractures received orthopaedic surgery. The ratio of males to females was 2:8, the median age was 83.1 years (71–91 years), and there was a median BMI of 25.35 (15.56–35.16). 50% of cases had a poor functional capacity before fracture of below four metabolic equivalents. The median onset time of acute cholecystitis was five days (2–14 days) after fracture, including five cases before orthopaedic surgery and five cases after orthopaedic surgery. All patients had anorexia and fever during the course of the disease. In seven cases of calculous cholecystitis, two underwent percutaneous transhepatic biliary drainage, and one underwent percutaneous cholecystostomy. Two cases of calculous cholecystitis had poor prognosis; one died 49 days after fracture operation, and the reason for death was multiple organ failure caused by severe infection. The other one developed acute cerebellar infarction after gallbladder surgery through treatment in an intensive care unit and neurology department. The case was discharged with dysphasia, and the duration from fracture to discharge was 92 days.ConclusionThis is the first study on the characteristics of acute cholecystitis in older patients with hip fracture in China. The incidence of acute cholecystitis in our study was 0.13%, with a high risk of in-hospital mortality and elevated hospitalisation costs. Our 10 cases with hip fractures accompanied by acute cholecystitis have common characteristics of poor-to-moderate functional capacity before fracture, increased blood glucose levels and enhanced protein metabolism after fracture. The death and the severe case have similar characteristics of low BMI, multiple underlying diseases, high plasma osmotic pressure and calculous cholecystitis, which occurred after orthopaedic surgery. These issues require attention and prompt, active intervention. Related issues require further research.

Safe and time-saving treatment method for acute cerebellar infarction: Navigation-guided burr-hole aspiration - 6-years single center experience.

While patients with medically intractable acute cerebellar infarction typically undergo suboccipital craniectomy and removal of the infarcted tissue, this procedure is associated with long operating times and postoperative complications. This study aimed to investigate the effectiveness of minimally invasive navigationguided burr hole aspiration surgery for the treatment of acute cerebellar infarction. Between January 2015 and December 2021, 14 patients with acute cerebellar infarction, who underwent navigation-guided burr hole aspiration surgery, were enrolled in this study. The preoperative mean Glasgow Coma Scale (GCS) score was 12.7, and the postoperative mean GCS score was 14.3. The mean infarction volume was 34.3 cc at admission and 23.5 cc immediately following surgery. Seven days after surgery, the mean infarction volume was 15.6 cc. There were no surgery-related complications during the 6-month follow-up period and no evidence of clinical deterioration. The mean operation time from skin incision to catheter insertion was 28 min, with approximately an additional 13 min for extra-ventricular drainage. The mean Glasgow Outcome Scale score after 6 months was 4.8. Navigation-guided burr hole aspiration surgery is less time-consuming and invasive than conventional craniectomy, and is a safe and effective treatment option for acute cerebellar infarction in selected cases, with no surgery-related complication.

Patient with Recurrent Acute Ischemic Strokes Found to have Cryptococcal Meningitis: A Case Report (P12-5.023)

<h3>Objective:</h3> n/a <h3>Background:</h3> Cryptococcal meningitis is a rare cause of ischemic stroke. Infections most often present in immunocompromised patients, classically AIDS or transplant patients. We present a case of a seemingly immunocompetent patient who presented with recurrent strokes found to have cryptococcal meningitis. <h3>Design/Methods:</h3> n/a <h3>Results:</h3> The patient was a 55-year-old male construction worker with hypertension. A year prior to admission, he was hospitalized for a week with mild SARS-COVID-19 infection. He had received two doses of the mRNA Covid vaccines. One month prior to admission, he developed headaches initially treated as sinus infection with oral antibiotics and steroids. Two weeks later, there was concern for acute-onset aphasia. He was afebrile with mild leukocytosis (13.6 B/L). MRI brain showed multiple, bilateral, scattered lacunar infarcts and left cerebellar infarcts. Transthoracic and transesophageal echocardiography were unremarkable. A loop recorder was placed. He was started on dual antiplatelet and statin therapy. A week later, he was encephalopathic and lethargic. Repeat MRI brain showed new acute lacunar and bilateral cerebellar infarcts. The loop recorder was negative for arrhythmias. A lumbar puncture (LP) was deferred for unclear reasons. Patient was transferred to our stroke service, where he was febrile (102.3°F) with leukocytosis (17.4 B/L). He was encephalopathic and had nuchal rigidity. LP showed elevated opening pressure (55 cm H2O) and tested positive for Cryptococcal antigen. Liposomal amphotericin B and flucytosine were initiated. Diagnostic angiogram was negative for vasculitis. His CD4 count was 332 (normal 410–1,590), however HIV testing was negative and pan-CT scan showed no signs of underlying malignancy. His prolonged hospital course was complicated by elevated intracranial pressure, further strokes, and poor mental status requiring placement of tracheostomy and enteral tube access. <h3>Conclusions:</h3> It is important to keep infection, including cryptococcal meningitis, in the differential for the cause of recurrent strokes even in seemingly immunocompetent patients. <b>Disclosure:</b> Lauren Thaete has nothing to disclose. Dr. Azuma has nothing to disclose.

Use of doxorubicin-eluting bead transarterial chemoembolization for unresectable hepatocellular carcinoma with portal vein invasion: a prospective study.

To evaluate the applicability of transarterial chemoembolization (TACE) treatment with doxorubicin drug-eluting beads (DEBs) in advanced hepatocellular carcinoma (HCC) patients with portal vein invasion (PVI). This prospective study was approved by the institutional review board and informed consent was obtained from all participants. A total of 30 HCC patients with PVI received DEB-TACE between 2015 and 2018. The following parameters were evaluated: complications during DEB-TACE, abdominal pain, fever, and laboratory outcomes, including liver function change. Overall survival (OS), time to progression (TTP), and adverse events were also analyzed and assessed. DEBs measuring 100-300 μm in diameter were loaded with doxorubicin (150 mg per procedure). There were no complications during DEB-TACE and no significant differences in the levels of prothrombin time, serum albumin, or total bilirubin at follow-up compared to baseline. The median TTP was 102 days (95% confidence interval [CI], 42-207 days) and the median OS was 216 days (95% CI, 160-336 days). Three patients (10%) had severe adverse reactions, including transient acute cholangitis (n=1), cerebellar infarction (n=1), and pulmonary embolism (n=1), but no treatment-related death occurred. DEB-TACE may be a therapeutic option for advanced HCC patients with PVI.

椎骨動脈狭窄による小脳梗塞によって浮動性めまいと一過性に視界の上下逆転を来した1例(Dizziness and reversal of vision metamorphopsia due to cerebellum infarction caused by a vertebral artery stenosis: a case report)

要旨 椎骨動脈狭窄による小脳梗塞によって一過性に視界が上下逆転する現象（reversal of vision metamorphopsia: RVM）を呈した症例を経験した。症例は狭心症，高血圧，糖尿病の既往がある71歳の男性で，浮動性めまいを主訴に救急搬送された。受診2日前と受診前日に突然誘因なく浮動性めまいが出現したが，それぞれ1時間の安静で改善した。受診当日も同様の症状が再燃し悪心も伴うため発症1時間後に救急要請した。来院時のバイタルサインは安定していた。めまいや嘔気の症状が強く可能な範囲での診察では，明らかな脳神経所見の異常はなく運動麻痺や小脳失調も認めなかったが，診察中に患者が「上下が逆に見える」と訴えた。各種画像検査から椎骨動脈狭窄を伴う急性期小脳梗塞と診断し，加療目的に脳神経外科に入院した。入院後にRVMの再燃はなかった。RVMの機序は明らかでないが，本症例では後下小脳動脈領域の梗塞により，視覚と前庭系の情報を統合する前庭小脳繊維が障害されたことが原因と考えた。またRVMの症状は一過性であることが多いとされるが，後頭葉や頭頂葉，残存した正常小脳などが持つ代償機構と，視覚的錯覚からの回復が複合的に機能しているためと考えた。RVMはとくに急性期診療を担う救急外来で遭遇しうるため救急医にとって有用な訴えとなる。RVMを認めた場合は，積極的に中枢性疾患を疑い画像検査を行うべきである。

Abstract Number ‐ 113: A Lateral Medullary Infarct Complicated by Central Hypoventilation Syndrome

Introduction A 43‐year‐old male with no known past medical history presented to a primary stroke center for sudden onset headache, nausea, vomiting, and dizziness while driving. A computed tomography angiogram of the head and neck revealed a left vertebral artery occlusion, and the patient was transferred to our comprehensive stroke center for further evaluation and treatment. Upon arrival at our facility, the patient was noted to have a national institute of health stroke scale score of 7 with left facial droop, dysarthria, and right upper extremity dysmetria. A cerebral angiogram revealed a tortuous left vertebral artery with dissection in the V4 segment. Subsequent brain diffusion weighted imaging revealed an acute infarct in the right lateral medulla measuring 1.4cm and several acute cerebellar infarcts. (fig. 1) In the postangiography period, the patient had dysphagia, sialorrhea, multiple aspiration episodes, and oral secretions requiring early tracheostomy and percutaneous endoscopic gastrostomy on hospital day (HD) #6. The subsequent hospital course was complicated by prolonged singultus lasting until HD #23 and repetitive vomiting requiring a transition from a gastric to a gastro‐jejunal feeding tube. Methods A central hypoventilation syndrome (CHS) prolonged ventilator weaning. Despite preserved ability to take large‐volume voluntary breaths, the patient experienced multiple episodes of sleep‐associated apnea and rapid shallow breathing pattern during daily spontaneous breathing trials (SBT). The apnea episodes were registered with ventilator apnea alarms set at 20 seconds. This pattern continued when attempting an SBT utilizing a T‐piece adaptor. The ability to maintain adequate minute ventilation in an asleep state subsequently improved, and the patient was able to tolerate 48 hours of spontaneous breathing with no apnea on HD #35. Results Few cases of CHS secondary to lateral medullary infarction (LMI) have been documented in the literature.(1‐3) As the respiratory drive originates from neurons in the latero‐rostro‐ventral medulla, infarcts in this brainstem region may lead to respiratory failure. More specifically to our patient, ataxic breathing may result from lesions in the rostro‐ventral medulla with yawning and hiccups being seen in lesions to the posterolateral medulla.(4) As our patient presented with a sizable 1.4cm lesion, likely impairing these brainstem centers, it is expected that his symptoms would account for multiple respiratory symptoms. The unique feature of the acquired CHS in the setting of LMI is its unilateral location implying lateralization of the respiratory control. In addition to the aforementioned symptoms, his lesion likely led to prolonged weaning from the ventilator as has been described previously.(5) Conclusions This case raises awareness regarding potentially disastrous complications of the lateral medullary syndrome like central hypoventilation syndrome. We urge caution and careful evaluation of patients with lateral medullary infarctions for disorders of the respiratory control system.

Dynamics of Cerebral Function in Patients with Acute Cerebellar Infarction.

Few studies were devoted to investigating cerebral functional changes after acute cerebellar infarction (CI). The purpose of this study was to examine the brain functional dynamics of CI using electroencephalographic (EEG) microstate analysis. And the possible heterogenicity in neural dynamics between CI with vertigo and CI with dizziness was explored. Thirty-four CI patients and 37 age- and gender-matched healthy controls(HC) were included in the study. Each included subject underwent a 19-channel video EEG examination. Five 10-s resting-state EEG epochs were extracted after data preprocessing. Then, microstate analysis and source localization were performed using the LORETA-KEY tool. Microstate parameters such as duration, coverage, occurrence, and transition probability are all extracted. The current study showed that the duration, coverage, and occurrence of microstate(Ms) B significantly increased in CI patients, but the duration and coverage of MsA and MsD decreased. Compared CI with vertigo to dizziness, finding a decreasedtrend in the coverage of MsD and the transition from MsA and MsB to MsD. Taken together, our study sheds new light on the dynamics of cerebral function after CI, mainly reflecting increased activity in functional networks involved in MsB and decreased activity in functional networks involved in MsA and MsD. Vertigo and dizziness post-CI may be suggested by cerebral functional dynamics. Further longitudinal studies are needed to validate and explore the alterations in brain dynamics to what extent depict the clinical traits and their potential applications in the recovery of CI.

The frequency and characteristics of saccadic dysmetria in isolated cerebellar infarction.

To investigate the frequency and pattern of horizontal saccadic dysmetria in unilateral cerebellar infarction and identify the responsible region for horizontal saccadic dysmetria. From the acute stroke registry of Keimyung University Dongsan Medical Center between July 2016 and October 2020, 43 patients with acute unilateral cerebellar infarction were enrolled. Eye movements were recorded during the acute period and the lesion was mapped using MRIcron software for subtraction analysis. Saccadic dysmetria was marked as hypometric when the gain is < 0.85 and hypermetric when > 1.0. Among the 43 participants, 30 patients (69.8%) demonstrated saccadic dysmetria. The age was significantly higher in patients with dysmetria (66.87 ± 12.82 vs. 53.54 ± 14.09, p = 0.004). Type of dysmetria showed a significant difference according to the vascular territory of the lesion. The posterior inferior cerebellar artery (PICA) infarction group presented ipsiversive saccadic dysmetria, while the superior cerebellar artery (SCA) group showed contraversive dysmetria (p < 0.001). In the SCA group, the culmen, fastigium, and dentate were the most frequently damaged regions, while the tonsil and inferior semilunar lobule were in the PICA group. Saccadic dysmetria was observed in a large proportion of cerebellar stroke patients, and the types of saccades were distinctive according to the vascular territory of the lesion.

Woman With Fever, Headache, and Ataxia

A 53-year-old woman with an unremarkable medical history presented to the emergency department with 2 weeks of right-sided frontal headache and right-sided neck pain and 3 days of fever, dizziness, nausea, vomiting, and inability to ambulate. Her vital signs revealed a temperature of 38 °C (100.4 °F). Physical examination revealed pain with neck flexion, inability to ambulate without assistance, and significant right-sided dysmetria on finger-nose-finger testing. Brain magnetic resonance imaging revealed an acute right cerebellar infarct secondary to nonocclusive right sigmoid sinus and internal jugular vein thrombosis, also confirmed on computed tomography (Figure 1, Figure 2).

PSAT032 Metoclopramide Induced Pheochromocytoma Multisystem Crisis: An Unusual Initial Presentation of Pheochromocytoma

Abstract Introduction Pheochromocytoma is a rare catecholamine secreting tumor arising from the adrenal medulla. It presents with hypertension and symptoms of catecholamine excess (episodic headache, sweating, palpitations). Pheochromocytoma crisis (PC) can encompass multiple organ failure, lactic acidosis, elevated temperature, encephalopathy, and hypertension and/or hypotension. Metoclopramide is a D2 receptor blocker and is known to precipitate pheochromocytoma crisis. It is commonly used in the emergency department (ED) for nausea and is often used as part of the "migraine cocktail". Case presentation 41-year-old female with primary hypothyroidism and hypertension diagnosed 5 months prior on two anti-hypertensive agents, presented to the ED with a severe headache. She recently had been placed on a Holter monitor for evaluation of episodes of palpitation/tachycardia. She was hemodynamically stable. Intravenous metoclopramide was administered as part of a "migraine cocktail". Shortly thereafter, she developed tachycardia with heart rate (HR) in the 130s, hypertension with blood pressure (BP) in the 180s/120s and proceeded to have generalized tonic-colonic seizures that lasted for 3 minutes. She was treated with lorazepam and was intubated for airway protection. Initial labs were only significant for mild leukocytosis. The urine drug screen was unrevealing. Due to the unexpected rapid clinical deterioration, computed tomography (CT) of the head, chest, abdomen, and pelvis were obtained. CT abdomen revealed a large 6.4×5.7×5.2 cm right adrenal mass. HR and BP remained elevated in the 170s and 200s/100s respectively. Given CT findings, a PC was suspected. She was started on doxazosin and labetalol. Phenoxybenzamine was later started. Biochemical testing was consistent with pheochromocytoma with elevated normetanephrine (NE) &amp;gt;20,000 pg/mL (&amp;lt;=148 pg/mL), metanephrine (M)&amp;gt;20,000 pg/mL (&amp;lt;=60 pg/mL), and total urinary metanephrines (TM) &amp;gt;40,000 pg/mL (&amp;lt;=205 pg/mL). HR and BP stabilized with treatment and the patient was subsequently extubated. She was noted to have new dysarthria and visual field deficits. Magnetic resonance imaging and CT angiography revealed findings consistent with posterior reversible encephalopathy syndrome (PRES) and acute cerebellar infarct. Dotatate scan was negative for metastasis. She later underwent right adrenalectomy; pathology report confirmed the diagnosis of nonmalignant pheochromocytoma. Repeat NE, M, and TM 10 days post-op were unremarkable. The patient follows with endocrinology clinic outpatient and has been doing well. Conclusion Multiple cases of metoclopramide-induced pheochromocytoma crisis have been reported in the literature. These accounts indicate that the empiric use of metoclopramide for individuals presenting with headaches/nausea is not without risk especially for those with a history of hypertension and other symptoms of catecholamine excess. This case also highlights the importance of suspecting pheochromocytoma crisis in patients who develop rapid onset hypertensive crisis and other symptoms of catecholamine excess immediately after administering metoclopramide. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.

急性单发小脑小梗死的临床特征 Clinical Features of Acute Single Small Cerebellar Infarction

急性单发小脑小梗死的临床特征 Clinical Features of Acute Single Small Cerebellar Infarction

Incidence and clinical features of acute multiple small cerebellar infarction

ObjectiveTo investigate the clinical and imaging features and to identify possible etiology of acute multiple small cerebellar infarction (MSCI). MethodsWe retrospectively enrolled 220 patients with acute cerebellar infarction, divided them into MSCI and large cerebellar infarction (LCI) groups, according to the quantity and size of lesions confirmed by MRI analysis. Clinical and imaging features were compared between the two groups to explore the possible etiology and pathogenesis. ResultsAmong 220 patients, 90 patients presented MSCI symptoms. The proportions of extracerebellar lesions (P = 0.001) and bilateral infarction (P = 0.001) in the MSCI group were higher than those in the LCI group. No significant differences were found in terms of age, gender, and common vascular risk factors between the two groups. The proportions of vertigo and headache in the MSCI group were significantly lower than those in the LCI group (P < 0.000 and 0.034, respectively), and limb weakness was significantly higher (P = 0.039) in the MSCI patients. Moreover, the proportions of nystagmus and ataxia in the MSCI group were significantly lower than those in the LCI group (P < 0.043 and 0.003, respectively). The MSCI group had higher proportions of ACA and MCA stenosis, while the proportion of posterior circulation stenosis was similar between the two groups. Infarctions involving the posterior inferior cerebellar (PICA) region and mixed territories were far more frequent than those involving the anterior inferior cerebellar artery (AICA) region and superior cerebellar artery (SCA) territory (P < 0.05). Large-artery atherosclerosis and multiple plus undetermined etiology were the main etiological factors of MSCI. ConclusionIn patients with acute cerebellar infarction, 30% of patients presented with MSCI. MSCI and LCI showed similar vascular risk factors and vascular stenosis in the posterior circulation system. Patients with MSCI should pay more attention to evaluating anterior circulation vessels’ anatomy. Large-artery atherosclerosis was the main pathogenesis of acute MSCI. Assessment of cerebral vessels might be critically required in patients with MSCI complicated atrial fibrillation.

Disrupted topological properties of the structural brain network in patients with cerebellar infarction on different sides are associated with cognitive impairment.

PurposeTo explore changes in the brain structural network in patients with cerebellar infarction on different sides and their correlations with changes in cognitive function.MethodsNineteen patients with acute left posterior cerebellar infarction and 18 patients with acute right posterior cerebellar infarction seen from July 2016 to September 2019 in the Department of Neurology, Affiliated Brain Hospital of Nanjing Medical University, were selected. A total of 27 healthy controls matched for sex, age, and years of education were recruited. The subjects underwent head diffusion magnetic resonance imaging examination and neuropsychological cognitive scale evaluation, and we analyzed changes in brain structural network properties in patients with cerebellar infarction and their correlation with changes in patients' cognitive function.ResultsThe Mini-Mental Status Examination (MMSE), Montreal Cognitive Assessment (MOCA) and the Rey auditory verbal learning test (RAVLT) scores in the left and right cerebellar infarction groups were significantly lower than those in the healthy control group (p < 0.05). In addition, the digit span test (DST) scores were lower in the left cerebellar infarction group (p < 0.05); the trail-making test (TMT) times in the right cerebellar infarction group were significantly higher than those in the left cerebellar infarction group (p < 0.05). Meanwhile, the left and right cerebellar infarction groups had abnormal brain topological properties, including clustering coefficient, shortest path length, global efficiency, local efficiency and nodal efficiency. After unilateral cerebellar infarction, bilateral cerebral nodal efficiency was abnormal. Correlation analysis showed that there was a close correlation between decreased processing speed in patients with left cerebellar infarction and decreased efficiency of right cerebral nodes (p < 0.05), and there was a close relationship between executive dysfunction and decreased efficiency of left cerebral nodes in patients with right cerebellar infarction (p < 0.05).ConclusionPatients with cerebellar infarction have cognitive impairment. Unilateral cerebellar infarction can reduce the network efficiency of key regions in the bilateral cerebral hemispheres, and these abnormal changes are closely related to patient cognitive impairment. The results of this study provide evidence for understanding the underlying neural mechanisms of cerebellar cognitive impairment and suggest that brain topological network properties may be markers of cerebellar cognitive impairment.

Topography and etiologies of cerebellar infarcts presenting as isolated acute vestibular syndrome

To investigate the topography and etiologies of acute cerebellar infarcts (ACIs) that presented as isolated acute vestibular syndromes (AVSs). ACI was ascertained on magnetic resonance diffusion-weighted imaging combined with apparent diffusion coefficient sequence and was categorized into the simple (territory and small infarct) and the complicated (concomitant infarcts in territories of posterior circulation besides cerebellum). Infarct topography and etiologies were compared between ACI patients with isolated AVS and non-isolated AVS (general and/or local neurological symptoms and/or signs with or without AVS). We enrolled 129 ACI patients, and 53 patients (53/129, 41.1%) had isolated AVS. In isolated AVS, the infarct lesions could be territory infarcts, small infarcts involving cortical, subcortical, and areas directly related to vestibular structures, and the primary etiologies were of large artery atherosclerosis and small vessel disease. Compared with the patients with non-isolated AVS, those with isolated AVS had more prevalence of small vessel disease (OR 6.30, 2.16-18.39; p = 0.001) and more probability of small infarcts (OR 6.04, 95%CI 2.31-15.76; p < 0.0001). In isolated AVS patients, the small infarct located more frequently in cerebellar hemispheres than the areas directly related to vestibular structures (27/35 vs 8/35), and the territory infarct located more frequently in the area supplied by posterior inferior cerebellar artery than the other areas (9/13 vs 4/13). Our study found that ACI could be presented as isolated AVS, which occurred more frequently in patients with small hemisphere infarct or infarct in the territory supplied by posterior inferior cerebellar artery.

Analysis of Factors Associated with Hemorrhagic Transformation in Acute Cerebellar Infarction

ObjectivesHemorrhagic transformation (HT) is a frequent and severe complication of ischemic stroke. This study aimed to evaluate the factors associated with the occurrence of HT in patients with acute cerebellar infarction. Materials and methodsA total of 190 patients, 141 male (74.2%) and 49 female (25.8%) with mean age 61.84 ± 12.16 years, who were admitted within 72 h of acute cerebellar infarction onset from January 2017 to March 2021 were retrospectively recruited. The multivariate logistic regression analysis was used to evaluate the independent influent factors for HT and receiver-operating characteristic (ROC) curve was applied to calculate the predictive value of those factors for HT in patients with acute cerebellar infarction. Results37 out of 190 recruited patients (19.47%) had HT within 14 days after acute cerebellar infarction onset. The incidence rates of HT occurring within 3 days, 3–7 days and 7–14 days were 13.5%, 40.5% and 45.9%, respectively. Results of the multivariable logistic regression analysis indicated that atrial fibrillation (AF) (OR 6.196, 95% CI 1.357-28.302, P = 0.019), infarct diameter (OR 5.813, 95% CI 2.932-11.526, P < 0.001), white matter hyperintensity (WMH) (OR 2.44, 95% CI 1.134–5.252, P = 0.023) were independent risk factors for HT in acute cerebellar infarction, while lymphocyte count (OR 0.319, 95% CI 0.142-0.716, P = 0.006) showed an independently protective effect. ConclusionsInfarct diameter, AF and WMH are independent risk factors for HT in patients with acute cerebellar infarction, while the lymphocyte count is a protective factor.

An optimal scale for predicting gait independence in patients with acute cerebellar infarction

An optimal scale for predicting gait independence in patients with acute cerebellar infarction

Rate of Infarct–Edema Growth on CT Predicts Need for Surgical Intervention and Clinical Outcome in Patients with Cerebellar Infarction

BackgroundUp to 20% of patients with cerebellar infarcts will develop malignant edema and deteriorate clinically. Radiologic measures, such as initial infarct size, aid in identifying individuals at risk. Studies of anterior circulation stroke suggest that mapping early edema formation improves the ability to predict deterioration; however, the kinetics of edema in the posterior fossa have not been well characterized. We hypothesized that faster edema growth within the first hours after acute cerebellar stroke would be an indicator for individuals requiring surgical intervention and those with worse neurological outcomes.MethodsConsecutive patients admitted to the neurological intensive care unit with acute cerebellar infarction were retrospectively identified. Hypodense regions of infarct and associated edema, “infarct–edema”, were delineated by using ABC/2 for all computed tomography (CT) scans up to 14 days from last known well. To examine how rate of infarct–edema growth varied across clinical variables and surgical intervention status, nonlinear and linear mixed-effect models were performed over 2 weeks and 2 days, respectively. In patients with at least two CT scans, multivariable logistic regression examined clinical and radiological predictors of surgical intervention (defined as extraventricular drainage and/or posterior fossa decompression) and poor clinical outcome (discharge to skilled nursing facility, long-term acute care facility, hospice, or morgue).ResultsOf 150 patients with acute cerebellar infarction, 38 (25%) received surgical intervention and 45 (30%) had poor clinical outcome. Age, admission National Institutes of Health Stroke Scale (NIHSS) score, and baseline infarct–edema volume did not differ, but bilateral/multiple vascular territory involvement was more frequent (87% vs. 50%, p < 0.001) in the surgical group than that in the medical intervention group. On 410 serial CTs, infarct–edema volume progressed rapidly over the first 2 days, followed by a subsequent plateau. Of 112 patients who presented within two days, infarct–edema growth rate was greater in the surgical group (20.1 ml/day vs. 8.01 ml/day, p = 0.002). Of 67 patients with at least two scans, after adjusting for baseline infarct–edema volume, vascular territory, and NIHSS, infarct–edema growth rate over the first 2 days (odds ratio 2.55; 95% confidence interval 1.40–4.65) was an independent, and the strongest, predictor of surgical intervention. Further, early infarct–edema growth rate predicted poor clinical outcome (odds ratio 2.20; 95% confidence interval 1.30–3.71), independent of baseline infarct–edema volume, brainstem infarct, and NIHSS.ConclusionsEarly infarct–edema growth rate, measured via ABC/2, is a promising biomarker for identifying the need for surgical intervention in patients with acute cerebellar infarction. Additionally, it may be used to facilitate discussions regarding patient prognosis.

A RARE PRESENTATION OF A RARE DISEASE: HYPEREOSINOPHILIC SYNDROME PRESENTING WITH ACUTE CORONARY AND CEREBROVASCULAR OCCLUSIVE DISEASE

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Hypereosinophilic Syndrome (HES) is defined by the presence of peripheral eosinophilia of 1.5 x 10*9 /L for at least one month resulting in end organ damage in the absence of secondary causes of eosinophilia[1]. The most common organs involved at presentation are skin and lungs. Early cardiovascular and cerebrovascular involvement is rare[2]. CASE PRESENTATION: A 59 year old female with Diabetes Mellitus and hypertension presented with non-ST segment elevation myocardial infarction of the inferior wall. A few days later the patient developed acute right cerebral and cerebellar infarction confirmed by MRI of the brain.She had leukocytosis with an eosinophil count 79 x 10*3/mcL. Tests for parasitic infection, drug allergy, mast cell dyscrasias, and autoimmune process were negative. Bone marrow biopsy showed hypercellular bone marrow with dysplastic eosinophils suggestive of HES. In the absence of skin disease, negative PDGFRA 2 translocation, and normal vitamin B12 levels, a diagnosis of Idiopathic HES was made. She was treated with high dose steroids, hydroxyurea, and leukapheresis followed by imatinib, with no benefit.Over the next week MRI revealed multiple new bilateral infarcts in the cerebellum and cerebrum. Concomitantly she developed STEMI of the inferior wall. Echocardiogram on day three was normal. On days 6, 11, and 23, echocardiogram revealed worsening restrictive cardiomyopathy with infiltrative disease in both ventricles extending from apex to lateral wall and obliterating the left ventricular cavity resulting in cardiogenic shock and pulmonary edema. Rapidly progressing neurologic, as well as cardiac complications, were attributed to HES. Interleukin-5 receptor antibody, Benralizumab, was started without benefit and the patient died. DISCUSSION: In primary HES, eosinophilic expansion occurs due to underlying stem cell, myeloid, or eosinophilic neoplasm. In secondary HES, polyclonal eosinophilic expansion is driven by eosinophilopoietic cytokines. Neurological and cardiovascular involvement is well described but rare and presents usually in the form of parenchymal involvement and not vascular occlusive disease as in our patient[2]. CONCLUSIONS: HES syndrome typically presents with features of gastrointestinal, pulmonary, and skin involvement[1]. Neurological involvement, when seen, is in the form of parenchymal involvement and later in disease course. Our patient instead had arterial occlusive disease involving coronary, cerebral, and vertebral basilar system as the primary manifestation of the disease, which is unique. Similarly, cardiac involvement occurs as a restrictive/infiltrative cardiomyopathy not as coronary artery occlusion. A striking feature was the rapid progression of infiltrative disease of the left ventricle leading to near occlusion of the LV cavity resulting in cardiogenic shock and death within 2 weeks. REFERENCE #1: Shomali, W., Gotlib, J. World Health Organization defined eosinophilic disorders: 2019 update on diagnosis, risk stratification and management. American Journal of Hematology. 2019; 94: 1149-1167. https://www.ncbi.nlm.nih.gov/pubmed/31423623 REFERENCE #2: Ogbogu, P., Rosing, D., Horne, M. Cardiovascular Manifestations of Hypereosinophilic Syndromes. Immunology and Allergy Clinics of North America. 2007; 7: 457 - 475. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2048688/# DISCLOSURES: No relevant relationships by Aaron Douen, source=Web Response No relevant relationships by Padmanabhan Krishnan, source=Web Response No relevant relationships by Nikisha Pandya, source=Web Response No relevant relationships by Valeriia Shnayder, source=Web Response No relevant relationships by Nikolas St.Cyr, source=Web Response No relevant relationships by Ayla Zubair, source=Web Response