Bilateral Cerebral Infarction Research Articles

Decompressive Craniectomy for Bilateral Anterior Cerebral Artery Infarction: Case Report and Brief Literature Review

Decompressive craniectomy for “malignant” bilateral anterior cerebral artery infarction (BACAI) has not been reported in the literature. Here we present such a case in relation to its presentation, surgical management, outcome and anatomical basis.Bifronto-temporal decompressive craniectomy was performed on a patient diagnosed with acute infarction in bilateral anterior cerebral artery (ACA) territories and rapidly deteriorating having clinical and radiological signs of tonsillar herniation. Patient sustained several motor disabilities at sixth week following surgery, however, post-operative CT showed reversing of the “conning” with spaced basal cisterns which was compatible with clinical improvement.

Ischaemic strokes and myocardial infarctions in a young male cannabis user

Ischaemic cerebral infarctions are seen in young people but, under the age of 30, multiple bilateral infarcts are uncommon; genetic pre-disposition and co-morbidities often underlie them. There is growing awareness of the potential impact of modifiable risk factors, such as cannabis, for those experiencing stroke and other cardiovascular events. A case of a 29-year-old man is de­scribed who presented with sudden onset occipital headache and right eye vision loss. Computerised axial tomographic scanning (CT) of the brain dem­onstrated multifocal bilateral areas of low attenuation. A brain magnetic reso­nance imaging (MRI), confirmed bilateral acute cerebral infarctions. In view of a significant elevation in troponin levels at a previous admission, cardiac via­bility magnetic resonance imaging (cvMRI) was carried out and demonstrated acute infarction affecting the left ventricular apex and multiple smaller infarcts elsewhere within the myocardium. On this occasion he did not complain of chest pain. The electrocardiogram (ECG) showed ischaemic changes. The patient denied a family history of ischaemic heart disease, diabetes mellitus, hypertension and hypercholesterolaemia, but admitted to daily use of can­nabis and cigarette smoking. We considered the regular use of cannabis as a possible aetiology in the development of multi-territory cerebral and myocar­dial infarcts, previous myopericarditis and left ventricular dysfunction

Another cause of treatable dementia: rapid cognitive improvement after carotid endarterectomy. Illustrative case.

Revascularization techniques in cervical internal carotid artery (ICA) stenosis are indicated to prevent the onset or recurrence of ischemic events in the setting of atherosclerotic carotid artery disease. Recent reports, case series, and comparative studies have suggested that revascularization techniques may also improve cognitive outcome in both symptomatic and asymptomatic patients, thus raising the question of whether another surgically treatable dementia has presented itself. A 70-year-old right-handed female with a history of hypertension, diabetes, and bilateral silent cerebral infarcts was evaluated for progressive cognitive impairment over a 1-year period, which was associated with a severe left cervical ICA stenosis. Carotid endarterectomy (CEA) was indicated as a revascularization technique, and the patient showed significant neurocognitive improvement as early as one month postoperatively, consistent with blood flow restoration to the left hemisphere on control imaging. This case serves as a reminder that CEA may improve the cognitive outcome of patients previously impaired by uncomplicated severe cervical ICA atherosclerotic disease, which can be another cause of treatable dementia. Further prospective studies may help to assess this potential benefit.

Dide Botcazo Syndrome: An Atypical and Rare Presentation of Stroke

Dide-Botcazo syndrome is a very rare condition resulting from bilateral posterior cerebral infarction. The clinical presentation is atypical of cerebral infarction and is characterized by the association of cortical blindness and anosognosia associated with amnesia and topographical disorientation. We report the clinical case of a 65-year-old man consulting for confusion associated with amnesia, cortical blindness and right hemiparesis evolving for one week. The CT scan showed hypodensity in the territory of the bilateral posterior cerebral arteries. The scan also ruled out malformations such as aneurysms or cerebral masses, as well as hemorrhagic stroke. The patient was treated with antiplatelet drugs and early rehabilitation. Progression was marked by partial improvement in motor disorders and confusion. Cortical blindness and anosognosia were permanent.

Cortical blindness after percutaneous vertebroplasty: a case report and comprehensive review of the literature

ABSTRACT Objective Many complications but cortical blindness after percutaneous vertebroplasty has been rarely reported. Here, we describe a case who developed cortical blindness after percutaneous vertebroplasty. We also reviewed the literature to find the possible causes of this complication and its treatment. Methods Case report and literature review. Results A 71-year-old woman experienced cortical blindness after percutaneous vertebroplast. She developed dizziness, nausea, sweating, blood pressure changes, and vision loss during the procedure. MRI confirmed bilateral cerebral infarctions. The patient recovered with conservative treatment. Conclusions Percutaneous vertebroplasty, though helpful, carries a rare risk of cortical blindness. Surgeon awareness is crucial for informing patients of this potential complication.

Efficacy of Prolonged Impella 5.5 Support as Bridge to Heart Transplantation: Current Concepts and Future Direction.

To the Editor: Zaky et al.1 recently published an interesting article titled, “Impella 5.5 Support beyond 50 Days as Bridge to Heart Transplant in End-Stage Heart Failure Patients” that demonstrated efficacy of the Impella 5.5 regarding its ability to provide adequate prolonged hemodynamic support and maintain durability in four cases. The four patients presented in cardiogenic shock with a history of heart failure with or without chronic kidney disease. Due to contraindications to left ventricular assist device use, they received Impella 5.5 support for a mean duration of 70 days (range 54–83). All patients were able to ambulate by day 6, with the only device malfunction being loss of placement signal in one patient and the only complication being bilateral posterior cerebral artery infarcts of unknown cause in another patient. All four patients had devices with intact pump function on explantation and underwent successful heart transplantation. The authors note only one other report in the literature of prolonged Impella 5.5 support as bridge to heart transplantation and no reports in the existing literature of malfunctions or complications in patients with prolonged use (>50 days). Adding on to their discussion of the relevant literature, we wanted to note our published experience with a patient on prolonged Impella support beyond 50 days.2 The patient was a 51-year-old male with decompensated heart failure, chronic kidney disease, and cirrhosis who was sequentially supported with axillary intra-aortic balloon pump, Impella 5.5, and venoarterial extracorporeal membrane oxygenation (V-A ECMO) prior to triple organ, heart-liver-kidney transplantation. The patient was supported on Impella 5.5 for 79 days, comparable to the mean duration of support in the case series published by Zaky et al.1 Total length of temporary mechanical circulatory support (MCS) was 95 days prior to successful transplantation. During the period of Impella support in our patient, he had an episode of heparin-induced thrombocytopenia (HIT) at 30 days treated with argatroban and, subsequently, sepsis at 78 days, prompting Impella explant and initiation of V-A ECMO. Studies have evaluated the risk of these patterns of complications in patients supported with Impella and have shown an association between Impella support and HIT and sepsis.3–5 Our case report corroborates the findings of the reported case series.1 While our collective findings do demonstrate the efficacy of Impella 5.5 support for prolonged temporary MCS as a bridge to heart transplantation beyond the duration of less than or equal to 14 days as approved by the Food and Drug Administration, rates of complications during prolonged support have not been fully delineated. These potential complications do appear to be significant; however, they have not affected survival to transplantation based on our single-center experience. Multicenter, longitudinal studies are warranted to examine the risk and significance of complications of prolonged Impella support before prolonged use of this device becomes an established and widely applied bridging strategy.

Delayed-Onset Thalamic Dazzle and Homonymous Hemianopic Scotoma Following Bilateral Posterior Cerebral Artery Infarction.

Delayed-Onset Thalamic Dazzle and Homonymous Hemianopic Scotoma Following Bilateral Posterior Cerebral Artery Infarction.

Bilateral Cerebral Infarctions Secondary to Unilateral ICA Stenosis

A 76-year-old diabetic man presented to us with complaints of sudden-onset right-sided weakness for the last 4 days. On evaluation, he was found to have right hemiparesis (Modified Medical Research Council grade 4-/5) along with left leg weakness (4+/5). Neuroimaging revealed acute infarcts in the right anterior cerebral artery (ACA) territory and left cerebral external watershed territory. Magnetic resonance (MR) angiogram of the brain showed a hypoplastic right A1-ACA with bilateral A2-ACA arising from the left A1-ACA (bi-hemispheric A1-ACA). MR angiogram of the neck revealed significant left internal carotid artery (ICA) origin stenosis. It was concluded that the origin of right A2-ACA from left ACA was the probable because of right ACA infarcts, along with left cerebral watershed infarcts (embolic phenomenon). This represents a very important variation, as in these cases, even a unilateral ICA stenosis can lead to bilateral ACA stroke and thus necessitates urgent revascularization.

Clinical Symptoms, Etiology and Prognosis of Acute Bilateral Posterior Circulation Cerebral Infarction.

BackgroundAcute BPCCI was previously presented only as a case report. The prognosis of acute BPCCI is related to many factors, such as gender, age, NIHSS, Hypertension and so on. We first systematically analyzed the clinical symptoms, imaging, etiology and prognosis of acute BPCCI and identified a statistically significant factor.MethodsA total of 72 acute BPCCI patients admitted to the Department of Neurology, Beijing Friendship hospital, Capital Medical University were included. The demographics, risk factors, clinical manifestations, National Institute of Health stroke scale (NIHSS) on admission, imaging findings, and the modified Rankin Scale (mRS) at the third month after onset were collected. The mRS score greater than 3 indicated poor prognosis. The factors affecting their prognosis were analyzed.ResultsWe included 72 Chinese patients with acute BPCCI (82% male). The most common symptoms and signs of the patients were dizziness and unilateral limb weakness. Patients with acute BPCCI involving cerebellum accounted for 85% of the patients. The number of patients with large-artery atherosclerosis was 46 (64%), the number of patients with cardiogenic embolism was 12 (17%), and the number of patients with other causes and unknown causes was 14 (19%). After multivariate regression analyses, NIHSS score (odds ratio 0.725, 95% confidence interval 0.586–0.896, P = 0.003) was closely related with the prognosis of acute BPCCI.ConclusionOur study found that the symptoms and signs of acute BPCCI were nonspecific and mainly depended on imaging diagnosis. Acute BPCCI involving cerebellum was the most common case of acute BPCCI. The main cause of acute BPCCI was large-artery atherosclerosis. NIHSS score is identified as a statistically significant factor. The higher NIHSS score on admission showed the worse prognosis. Therefore, an acute BPCCI patient with a high NIHSS score should be paid more attention at the time of diagnosis.

Fetal-Type Variant of the Posterior Cerebral Artery and Concurrent Bilateral Cerebral Infarctions in a Korean Male Cadaver

Fetal-type variant of the posterior cerebral artery is a relatively common variant of the cerebral arterial circle (circle of Willis), but concurrent cerebral pathologies have not been well reported. We describe a case of fetal-type variant of the posterior cerebral artery and concurrent bilateral cerebral infarctions in the territories of the middle cerebral artery in a 78-year-old Korean male cadaver. Fetal-type variant of the posterior cerebral artery was found the right cerebral arterial circle, arose from the internal carotid artery with larger diameter than the pre-communicating segment from the basilar artery. Histopathological examination revealed that left supramarginal gyrus and right infraparietal lobule showed characteristic cerebral infarctions with chronological changes, respectively. Knowledge on the variation in the posterior cerebral artery combined with clinical features including cerebral infarction plays a pivotal role to anatomists and clinicians.

Bilateral posterior cerebral artery stroke following transtentorial herniation caused by a subependymal giant cell astrocytoma in a patient with tuberous sclerosis: a case report

Background: Acute increased intracranial pressure (IICP) is a life-threatening condition that requires urgent treatment. Rapid IICP with hydrocephalus may be complicated by ischemic stroke, convulsions, loss of consciousness, brain herniation, and death. Extremely rare complications include intracranial vessel entrapment and ischemic stroke due to sudden IICP in cases with benign tumors. Case Report: We report a case of bilateral posterior cerebral artery region infarction and complicated hydrocephalus with subependymal giant cell astrocytoma in a patient with tuberous sclerosis. Conclusion: We postulate that the temporary IICP induced by seizure led to transient bilateral posterior cerebral artery entrapment, causing ischemic stroke without vascular occlusion.

Editors' Note: Clinical Reasoning: A 70-Year-Old Man With Right Arm and Leg Shaking

Seizure-like activity is a common neurologic complaint among patients evaluated in the emergency department, and it may be due to a broad spectrum of epileptic and nonepileptic conditions. Drs. Frey and Seachrist navigated the case of a 70-year-old man with unilateral shaking, impaired consciousness, and generalized upper motor neuron signs in their case report. The patient failed to improve with intravenous lorazepam and was later found to have acute bilateral anterior cerebral artery infarctions. The authors postulate that the patient's anarthria and lethargy were a reflection of underlying akinetic mutism, although this is typically associated with preserved alertness in the setting of reduced speech output after frontal lobe injuries. Focal motor or complex partial seizures are also potential explanations for this patient's shaking movements and impaired speech output, and these findings are not uncommon after cortical infarction. Drs. Freund and Tatum emphasize that the patient's lack of response to lorazepam and unremarkable ictal/interictal EEG do not preclude the diagnosis of seizure. Ultimately, it is unclear if the patient's “seizure-like” movements were epileptic in origin, but the data suggest the patient's ongoing hypertonicity and mutism were more likely related to tissue injury rather than seizure. Early recognition (and treatment) of seizure in these cases is critical to prevent secondary brain injury. Seizure-like activity is a common neurologic complaint among patients evaluated in the emergency department, and it may be due to a broad spectrum of epileptic and nonepileptic conditions. Drs. Frey and Seachrist navigated the case of a 70-year-old man with unilateral shaking, impaired consciousness, and generalized upper motor neuron signs in their case report. The patient failed to improve with intravenous lorazepam and was later found to have acute bilateral anterior cerebral artery infarctions. The authors postulate that the patient's anarthria and lethargy were a reflection of underlying akinetic mutism, although this is typically associated with preserved alertness in the setting of reduced speech output after frontal lobe injuries. Focal motor or complex partial seizures are also potential explanations for this patient's shaking movements and impaired speech output, and these findings are not uncommon after cortical infarction. Drs. Freund and Tatum emphasize that the patient's lack of response to lorazepam and unremarkable ictal/interictal EEG do not preclude the diagnosis of seizure. Ultimately, it is unclear if the patient's “seizure-like” movements were epileptic in origin, but the data suggest the patient's ongoing hypertonicity and mutism were more likely related to tissue injury rather than seizure. Early recognition (and treatment) of seizure in these cases is critical to prevent secondary brain injury.

A RARE CAUSE OF PARAPLEGIA: DISTRIBUTIVE SHOCK CAUSING BORDER ZONE STROKES

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Simultaneous bilateral cerebrovascular infarction is relatively uncommon and is an entity seen rarely in watershed cerebral infarctions which occur at the border between cerebral vascular territories in the setting of severe hypotension. CASE PRESENTATION: 84-year-old male with history of CAD, cerebellar stroke, peripheral arterial disease was admitted to the ICU with distributive shock and intubated for toxic metabolic encephalopathy. Initial CT head on admission was unremarkable. On day 2 of hospitalization his neuro assessment was notable for bilateral lower extremity paresis with preservation of sensation, proprioception and temperature but had sluggish reflexes and loss of motor strength. Repeat CT head did not show a bleed and subsequently, MRI brain with MRA head and neck revealed bilateral acute anterior cerebral artery strokes. Given the location and duration of symptoms he was not a TPA candidate and was treated with medical management with aspirin and statin. Echocardiogram and carotid ultrasounds were done that were unremarkable for embolic cause of stroke. DISCUSSION: The anterior cerebral artery is a major vessel supplying blood to the interhemispheric region. ACA territory infarction accounts for only 0.3% to 4.4% of cerebral infarctions. Bilateral ACA infarction is even rarer. Twenty-seven cases of ACA territory infarction were reported among 1490 cases of cerebral infarction in the Lausanne Stroke Registry; among them, only two cases had bilateral ACA territory infarction. Bilateral ACA infarction can occur due to vasospasm in the setting of subarachnoid hemorrhage caused by a rupture of aneurysms of the anterior communicating arteries or distal ACAs, thrombosis or embolism in case of anomaly of circle of Willis or bilateral anaplastic ACAs. In our patient the area of infarction was in a watershed zone bilaterally, unfortunately affected by hypotension which is rare in the absence of any of the above-mentioned anomalies as predisposing factors. The true incidence of bilateral ACA infarction is unknown, with few cases reported in the literature. CONCLUSIONS: This case report highlights the possibility of developing simultaneous bilateral cerebral infarctions in the setting of profound systemic hypotension and shock, especially if the patient has baseline chronic small vessel changes. REFERENCE #1: Orlandi G, Moretti P, Fioretti C, Puglioli M, Collavoli P, Murri L. Bilateral medial frontal infarction in a case of azygous anterior cerebral artery stenosis. Ital J Neurol Sci. 1998;19:106–108. doi: 10.1007/BF02427567. [PubMed] [CrossRef] [Google Scholar] REFERENCE #2: Gacs G, Fox AF, Barnett HJ, Vinuela F. Occurrence and mechanisms of occlusion of the anterior cerebral artery. Stroke. 1983;14:952–959. [PubMed] [Google Scholar] REFERENCE #3: Bogousslavsky J, Regli F. Anterior cerebral artery territory infarction in the Lausanne Stroke Registry. Clinical and etiologic patterns. Arch Neurol. 1990;47:144–150. [PubMed] [Google Scholar] DISCLOSURES: No relevant relationships by Imama Ahmad, source=Web Response No relevant relationships by Christine Blaski, source=Web Response No relevant relationships by Sneha Lakshman, source=Web Response

Visual Diagnosis: Abnormal Behavior in a 2-month-old Boy.

Visual Diagnosis: Abnormal Behavior in a 2-month-old Boy.

Sequential pontine and bilateral cerebral peduncle infarction with resultant early Wallerian degeneration of the ponto‐cerebellar fibers

AbstractBilateral cerebral peduncular infarction (BCPI) is an extremely rare neurological disorder reportedly associated with locked‐in syndrome. A 60‐year‐old man represented with reduction in conscious level three weeks following a paramedian pontine infarction due to basilar artery thrombosis. Repeated MRI revealed subacute pontine infarction with new infarct involving bilateral cerebral peduncle. MRA showed absent flow‐related signal along the basilar artery consistent with occlusion. Additionally, Wallerian degeneration characterized by symmetrical hyperintense signal on MRI involving the ponto‐cerebellar fibers and both the middle cerebellar peduncles (MCPs) were seen. BCPI is an exceedingly rare type of stroke with characteristic symmetrical signal change involving the cerebral peduncles called “Mickey Mouse Ear” sign. Early Wallerian degeneration of the bilateral MCPs ensuing pontine infarction is also uncommon and is often detected incidentally and exhibits regular and symmetrical signal changes on MRI. Here, a rare encounter of early Wallerian degeneration following sequential pontine and BCPI is described.

Osteogenesis Imperfecta With Cerebral Atherosclerosis: A Family Report

Background: Osteogenesis imperfecta (OI) is a rare hereditary connective tissue disease. It is mainly associated with pathogenic variants in COL1A1 or COL1A2. Patients with OI usually have repeated history of bone fractures. Besides, osteogenesis imperfecta is associated with some cardiovascular complications, such as aortic and mitral valve dysfunction, aneurysm and aortic dissection. But the relationship between these diseases has not been well studied. Case Presentation: A 55-year-old man was admitted to our hospital mainly due to “dizziness for 2 hours”. He had a 4-month history of hypertension and a history of smoking for more than 20 years. He had no history of drinking alcohol. He had hunchback and O-type legs. Besides, the patient and some of his relatives had a history of repeated brittle fractures,which was considered as “osteogenesis imperfecta”. The clinical manifestation of OI in this family varies to a certain extent, from simple tooth disintegration to severe fracture deformity. The most serious patient of his family was unable to walk. CT and MRI revealed multiple systemic arteriosclerosis, including vertebral artery, posterior inferior cerebellar artery, cervical artery, and bilateral cerebellar multiple lacunar cerebral infarction. The blood sample of the patient was tested by whole exome sequencing, and the saliva samples of the patient’s family members were tested by Sanger sequencing. A mutation c.3159 + 2T > A was detected in COL1A2 gene associated with OI, also found in the other affected family members, which had not been reported before. It was a segregating mutation in the family. The clinical severity of the family members was heterogeneous.Discussion: This case is worth learning from the following aspects: 1. A pathogenic heterozygous mutation, c.3159 + 2T > A was detected in COL1A2 gene in the patient with OI, which is not reported in previous cases of OI. 2. The clinical manifestation of OI in this family varies to a certain extent, from simple tooth disintegration to severe fracture deformity. The most serious patient of his family was unable to walk. It presented the clinical heterogeneity of OI. Further basic researh on the mutation site of related gene of OI are needed. 3. We found the possibility of developing cerebral atherosclerosis in patients with OI. Therefore, patients with OI should give up smooking, exercise properly and keep on a low fat diet. They should pay attention to control blood pressure and blood lipid so as to reduce the risk of atherosclerosis. Conclusion: A c.3159 + 2T>A mutation in COL1A2 gene detected by whole exome sequencing was the causing reason of OI, the discovery enriched the gene mutation spectrum of OI. We also found that OI may have relationship with premature atherosclerosis, and the abnormal bones of the cervical spine may lead to vertebrobasilar ischemia.

Sigmoid colon obstruction due to Kaposiform Haemangioendothelioma

Kaposiform Haemangioendothelioma (KHE) is a very rare, benign but locally aggressive vascular tumour. Its incidence is 1/100000, and it is most commonly found in the cutaneous tissues of the extremities. A 6-month-old presented acutely after 2 days of increasing abdominal distension. Apart from distension, clinical examination was unremarkable. An abdominal x-ray demonstrated massive gaseous distension of bowel loops. A contrast enema demonstrated an irregular stenosis within the sigmoid colon. An urgent laparotomy was performed. A thick and very inflammatory stricture was resected. Histopathology confirmed this as Kaposiform Haemangioendothelioma with margin involvement. Patient had a complicated post-operative period due to prolonged sepsis resulting in a cardiac arrest and two return journeys to theatre. An MRI brain was performed after patient stabilisation, demonstrating bilateral cerebral infarcts – the patient went on to develop cerebral palsy. Mainstay management of KHE is primary resection. It is associated with Kasabach-Merritt Phenomenon – a consumptive coagulopathy, which is present in 70% of KHE patients and has an associated 10% mortality rate. There are a small number of cases of KHE with gastrointestinal involvement in the literature. A number of these presented with bowel obstruction but no other had such a complicated post-operative course.

A clinical characteristic analysis of five cases of rare bilateral cerebral peduncular infarction (BCPI) with the ‘Mickey Mouse ears’ sign

ABSTRACT Objective: To investigate the clinical manifestations, magnetic resonance imaging (MRI) features, and prognosis of patients diagnosed with bilateral cerebral peduncular infarction (BCPI) with the ‘Mickey Mouse ears’ sign. Methods: This study, retrospectively summarized the clinical features, MRI and magnetic resonance angiography (MRA) manifestations, and prognosis of 5 patients diagnosed with BCPI and with the ‘Mickey Mouse ears’ sign from our hospital. In the meantime, we also systematically analyzed and summarized the clinical and imaging features, and prognosis in combination with relevant cases from the national and international literature that had been reported. Results: In our study, five cases presented tetraplegia whereas 4 cases presented disturbance of consciousness. In all cases, the ‘Mickey Mouse ears’ sign was observed in the mid-brain level using a diffusion-weighted imaging (DWI) cross-section. The MRA images showed thrombosis on either the basilar artery (BA), posterior cerebral artery (PCA), or superior cerebellar artery (SCA). All the studied patients received standardized treatment for cerebral infarction. However, three patients died and the remaining two were left in a locked-in syndrome state. Conclusions: BCPI is a very rare stroke disease and its main clinical manifestations are locked-in syndrome and persistent vegetative states. However, the obtained imaging features on the brain-MRI of patients diagnosed with BCPI with the ‘Mickey Mouse ears’ sign can predict a bad prognosis.

Systemic thromboembolism including multiple cerebral infarctions with middle cerebral artery occlusion caused by the progression of adenomyosis with benign gynecological tumor: a case report

BackgroundAdenomyosis, a benign gynecological disease, causes cerebral infarction. Similar to Trousseau’s syndrome, it elevates cancer antigen 125 (CA125) and D-dimer levels; causes hypercoagulability; and results in cerebral infarction. However, no case of adenomyosis causing major cerebral artery occlusion and requiring endovascular thrombectomy has yet been reported. We report on a woman with middle cerebral artery occlusion caused by adenomyosis progression with a benign gynecological tumor and recurrent cerebral infarction. She was successfully treated by endovascular thrombectomy and hysterectomy.Case presentationA 48-year-old woman with heavy uterine bleeding was transported by ambulance to our hospital. Upon arrival, she presented with impaired consciousness. Laboratory test results revealed decreased hemoglobin (8.2 g/dL) and elevated D-dimer (79.3 µg/mL) levels. Radiological imaging revealed adenomyosis, a left ovarian tumor, multiple uterine myomas, and old and new bilateral renal infarctions. She experienced repeated episodes of excessive menstruation caused by adenomyosis and was scheduled for hysterectomy in 2 months at another hospital. After hospital admission, uterine bleeding stopped. However, 5 days after initial bleeding, she had another episode of heavy uterine bleeding and developed left hemiparesis and dysarthria 20 min later. Brain magnetic resonance imaging revealed bilateral multiple cerebral infarctions indicating right middle cerebral artery occlusion. Thus, endovascular thrombectomy was performed, and anticoagulant therapy was administered. Laboratory test results after thrombectomy revealed elevated CA125 (3536 U/mL) and CA19-9 (892 U/mL) levels. She was at a risk of recurrent heavy uterine bleeding leading to repeated cerebral infarction because of anticoagulant treatment. Therefore, we performed hysterectomy and ovariectomy 11 days after initial bleeding. Histopathological assessment revealed no malignancy. Although she developed asymptomatic pulmonary thromboembolism 14 days after initial bleeding, D-dimer and tumor marker levels returned to normal soon after gynecological surgery. At 15 months post-surgery, she had not experienced further ischemic events.ConclusionsAdenomyosis with benign gynecological tumors may be associated with elevated D-dimer and tumor marker levels; excessive menstruation; and anemia. It may cause systemic thromboembolism, including cerebral infarction. To our knowledge, no other study has reported that adenomyosis causes major cerebral artery occlusion requiring endovascular thrombectomy. Hysterectomy may be an effective radical treatment of this condition.

Dilated cardiomyopathy-related stroke mimicking large-artery atherosclerosis-related stroke: report of two cases

The clinical characteristics and treatment of stroke caused by dilated cardiomyopathy (DCM) are not clear, especially in patients with large-artery atherosclerosis (LAA)-related stenosis, which commonly causes acute ischemic stroke (AIS); therefore, the diagnosis and treatment of such patients are challenging. Herein, we summarize the clinical characteristics and suggest clues to guide the diagnosis and treatment of two cases. Case 1: A 67-year-old woman with a history of DCM presented with sudden-onset slurred speech and left limb weakness (>2 hours duration), which worsened after intravenous thrombolysis. Repeated brain computed tomography showed no hemorrhage; thus, cerebral artery occlusion or embolism was suspected. Emergency magnetic resonance imaging (MRI) and angiography (MRA) revealed acute multiple bilateral cerebral infarctions and severe left middle cerebral artery stenosis, respectively. We considered a DCM-related stroke and administered anticoagulation therapy. Subsequently, the patient’s symptoms improved significantly, and she was discharged on day 9, after showing no abnormal neurological signs. Case 2: A 49-year-old man with a history of DCM presented with acute headache and blurred vision for 4 days. MRI and MRA revealed multiple acute cerebral infarctions and left vertebral artery stenosis, respectively. We considered an LAA-related stroke and administered antiplatelet and cholesterol-lowering drugs. Eventually, the patient was discharged on day 13, after his right-sided hemianopia improved significantly. Both patients had LAA, which can be easily misdiagnosed as a stroke. LAA-related and DCM-related stroke need to be differentiated. DCM-related AIS lesions are often distributed in the areas supplied by the different cerebral arteries. It is necessary to carefully analyze the shape, location, and scope of the lesions, and identify the main causes of stroke. Anticoagulant therapy is preferred for DCM-related AIS.