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A 38-year-old woman using hormonal contraception presented with right-sided abdominal and arm clonic seizures, right hemiparesis, hypesthesia, and nausea. She denied headache. D-dimers were 350 ng/mL (laboratory reference ≤500 ng/mL). CT showed a small left parietal hemorrhagic infarct with adjacent hyperdense cortical vein (figure 1). MRI 15 hours after onset showed magnetic susceptibility effect on susceptibility-weighted imaging (SWI, figure 2). Isolated cortical vein thrombosis is present in 5% of patients with cerebral venous thrombosis (CVT).1 Negative D-dimer and absence of headache does not exclude CVT1 and SWI is useful for confirmation of the diagnosis.2

Intracranial embolization usually arises from heart, precerebral artery or aorta but rarely the peripheral artery as retrograde upstream of embolus should be overcome. We encountered a woman who experienced a transient right acronumbness followed by a sudden onset of left hemiplegia and conscious change concurrently. Cranial computerized tomography revealed a hemorrhagic infarct at right lentiform nucleus. Angiography disclosed right axillary artery occlusion at the proximal portion without collateral circulation. Cardioaortic survey and coagulation profile were normal. Thrombectomy was done and radial flow was corrected rapidly. Post-thrombectomic heparinization did not bring complication. Therefore, a distant embolism from peripheral artery at the upper limb should be alerted for cerebral ischemia. A lower density of embolus and no-flow condition in her occluded axillary artery may facilitate the upstreamed embolization. Heparinization, under closed monitor, is not contraindicated for preventing restenosis after thrombectomy in case of hemorrhagic transformation in brain.

A 34-year-old woman with eclampsia and the hemolysis, elevated liver enzymes, and low platelets (HELLP) syndrome developed encephalopathy, cardiomyopathy, pulmonary edema, liver failure, and disseminated intravascular coagulation (DIC), all of which resolved. She also had retinal hemorrhages in both eyes and a hemorrhagic infarct in the left occipital lobe that resulted in a permanent right homonymous hemianopia and a persistently depressed acuity of 20/100 OS. This case is unusual in demonstrating permanent visual deficits. In nearly all cases of preeclampsia or eclampsia, visual deficits are reversible. The superimposition of the HELLP syndrome may create more neurologic damage. Clinicians should be alert to patients at risk for HELLP syndrome and manage them aggressively.

Invasive surgery brings with it a unique set of post-surgical risks that are directly dependent on various factors including the specific surgical approach used, pre-existing comorbidities and features such as gender and age. Pulmonary thromboembolism is one of the most feared complications following surgery, and diagnosis and treatment of this entity is a challenging task for the clinician. Here we describe a case of massive pulmonary thromboembolism and associated coronary artery thromboemboli status post spinal fusion surgery in a 68 year-old man with an undetected patent foramen ovale (PFO). Although the decedent was managed clinically with proper deep venous thrombosis prophylaxis protocols and physical rehabilitation, he went into cardiorespiratory arrest after experiencing acute oxygen desaturation and newly detected right bundle branch block. PFO can be incidentally found in 25% of the adult population. Several clinical syndromes including stroke, migraine headaches and obstructive sleep apnea have been associated in patients with PFO, the last two from which the decedent suffered. The pathology of this unique case of massive pulmonary thromboembolism resulting in coronary artery thromboemboli in the setting of an undetected PFO is discussed. The discovery of PFO in patients prior to surgery, if detected early, may improve post-surgical outcomes. Figure 1. Massive pulmonary artery thromboembolism in situ, gross examination. Figure 1. Massive pulmonary artery thromboembolism in situ, gross examination. Figure 2. Histology, hematoxylin and eosin. A. Pulmonary thromboembolus at the bifurcation of the pulmonary arteries and pulmonary trunk. B. Hemorrhagic infarct and thromboemboli in varying stages of organization, right lower lobe, lung. C. Cross section of the proximal left anterior descending coronary artery with thromboembolus. D. Cross section of the posterior descending coronary artery with thromboembolus. Figure 2. Histology, hematoxylin and eosin. A. Pulmonary thromboembolus at the bifurcation of the pulmonary arteries and pulmonary trunk. B. Hemorrhagic infarct and thromboemboli in varying stages of organization, right lower lobe, lung. C. Cross section of the proximal left anterior descending coronary artery with thromboembolus. D. Cross section of the posterior descending coronary artery with thromboembolus. Figure 3. Patent foramen ovale, gross examination. Figure 3. Patent foramen ovale, gross examination. Disclosures No relevant conflicts of interest to declare.

Background: Cerebral venous sinus thrombosis (CVST) is a rare form of stroke seen in young and middle aged group, especially in women due to thrombus of dural venous sinuses and can cause acute neurological deterioration with increased morbidity and mortality if not diagnosed in early stage. Neurological deficit occurs due to focal or diffuse cerebral edema and venous non-hemorrhagic or hemorrhagic infarct. Aim and Objectives: To assess/evaluate the role of Magnetic Resonance Imaging (MRI) and Magnetic Resonance Venography (MRV) as an imaging modality for early diagnosis of CVST and to study patterns of venous thrombosis, in detecting changes in brain parenchyma and residual effects of CVST using MRI. Materials and Methods: Retrospective descriptive analysis of 40 patients of CVST diagnosed on MRI brain and MRV was done. Results: 29/40 (72.5%) were males and 11/40 (27.5%) were females. Most of the patients were in the age group of 21-40 years (23/40-57.5%). Most of the patients 16/40 (40%) presented within 7 days. No definite cause of CVST was found in 24 (60%) patients in spite of detailed history. In 36/40 (90%) of cases major sinuses were involved, deep venous system were involved in 7/40 (17.5%) cases, superficial cortical vein was involved in 1/40 (2.5%) cases. Analysis of stage of thrombus (acute, subacute, chronic) was done based on its appearance on T1 and T2WI. 31/40 (77.5%) patients showed complete absence of flow on MRV, while 9/40 (22.5%) cases showed partial flow on MR venogram. Brain parenchyma was normal in 20/40 (50%) patients while 6/40 (15%) cases had non-hemorrhagic infarct and 14/40 (35%) patients presented with hemorrhagic infarct. Conclusion: Our study concluded that MRI brain with MRV is sensitive in diagnosing both direct signs (evidence of thrombus inside the affected veins) and indirect signs (parenchymal changes) of CVST and their follow up.

1H NMR imaging has been used to define zones of myocardial infarction (MI), which appear as areas of relatively increased signal intensity (SI). However, zones of decreased SI have been observed within or around the areas of infarction in NMR images acquired at high magnetic fields. To determine the cause of these areas of reduced SI, ex vivo spin-echo 1H NMR imaging at 1.5 T was performed in eight dogs following 72 h of coronary artery occlusion. In all dogs, a zone of increased SI (122 +/- 7% compared to control myocardium; P less than 0.01) was observed in the territory of the occluded coronary artery. In seven of the dogs, additional zones were also seen, within or around the central zone of increased SI, which displayed SI that was reduced in comparison with the local enhanced intensity, but was similar to the intensity of normal myocardium (97 +/- 7% compared to control; P = NS). Gross inspection and histological assessment of sliced myocardium disclosed hemorrhage in these regions characterized by locally decreased NMR SI. Image-derived calculation of T2 in the various infarct regions revealed a significant shortening of T2 in the hemorrhagic infarct zones characterized by decreased SI, in comparison with the nonhemorrhagic infarct zones characterized by increased SI (59 +/- 7 ms vs 73 +/- 10 ms, P less than 0.05). No difference was found, however, between the observed T2's of hemorrhagic infarct and of control tissue (57 +/- 4 ms). Using a biexponential analysis of T2 from the hemorrhagic infarct zones, the intrinsic T2 of water protons affected by hemorrhage was determined to be 43 +/- 9 ms, significantly reduced in comparison with the values obtained with the standard monoexponential fit. The reduction in T2 in the hemorrhagic zone is consistent with the paramagnetic effects of deoxyhemoglobin associated with intramyocardial hemorrhage. Thus the apparent T2, measured in hemorrhagic infarct tissue, represents the result of an averaging effect of infarct and hemorrhage on T2 relaxation times. These observations improve our understanding of the changes in NMR SI within the infarcted regions, and may provide a noninvasive method for the detection and quantitative assessment of intramyocardial hemorrhage.

A previously healthy 22-year-old Colombian man presented with recurrent fevers, cough, hemoptysis, and weight loss. He was treated with various antibiotics for presumed pneumonia without clinical response. Noncontrast high-resolution CT of the chest was performed (Fig 1.1). An empiric course of steroids produced only transient improvement. Multiple HIV tests and blood cultures were negative, as were bronchoscopy and bone marrow biopsy. Blood work demonstrated an elevated erythrocyte sedimentation rate (.90 mm/h). Lower extremity Doppler sonography revealed no evidence of deep venous thrombosis. Transesophageal echocardiography identified an 8 mm right atrial mass. Contrast-enhanced CT (Fig 1.2) was performed. The patient then underwent limited right thoracotomy with resection of the posterior segment of the right lower lobe. Pathologic examination revealed chronic pleuritis, hemorrhagic infarct, and organizing thrombus within the small pulmonary arteries. The right atrial mass was resected. Pathologic examination showed it to be composed entirely of thrombus. No organisms were seen and all cultures were negative. Postoperatively, the patient continued to experience fevers to 105°F that did not resolve with parenteral antibiotics. After receiving cyclosporine, his fever decreased and he experienced no further hemoptysis. Repeat CT showed no change in the size of the left pulmonary artery aneurysm, but the thickness of the wall diminished, and there was apparent improvement in the right pulmonary artery aneurysm, with a decrease in size and thickness of the aneurysm wall. He remained symptom-free for 3 months while undergoing empiric immunosuppression; however, he developed recurrent fevers and blood-tinged sputum, which progressed to frank hemoptysis, requiring hospitalization. Corticosteroid therapy was initiated and CT demonstrated an increase in the size of the left lower lobe pulmonary artery aneurysm with interim aneurysmal dilation of several sub

U The authors present a case of heparin-induced thrombocytopenia and thrombosis (HITT) that occurred after aneurysmal subarachnoid hemorrhage (SAH), and they review the relevant literature. An immune-mediated syndrome, HITT is characterized by moderate thrombocytopenia and paradoxical vascular thromboses. Although it has been estimated in prospective studies that HITT occurs in between 1 and 3% of patients receiving heparin, it is underrecognized in the neurosurgical literature. In the present case, a 49-year-old woman underwent clipping of a right posterior communicating artery aneurysm after suffering a Hunt and Hess Grade III SAH. She had an uncomplicated postoperative course with good clip positioning and no vasospasm observed on a cerebral angiogram obtained on Day 7.On Day 23, the patient developed a right hemiparesis and experienced a grand mal seizure. A head computerized tomography scan revealed a hemorrhagic infarct in the left middle cerebral artery distribution. Repeated cerebral angiograms did not show vasospasm. She was thrombocytopenic (platelet count as low as 46 × 109/L on Day 28 compared with 213 × 109/L on Day 1) and had been receiving heparin flushes to maintain intravenous catheter patency. An assay for HITT-associated antibodies was positive. The heparin flushes were discontinued and the platelet count recovered (121 × 109/L). She improved neurologically, but was left with a significant right hemiparesis at discharge. This patient had assay-proven heparin-induced thrombocytopenia despite minimal exposure to heparin. Because there was no evidence of vasospasm or other factors to account for her delayed hemorrhagic infarction, an HITT-related disorder seemed most likely. Despite a large body of literature describing HITT in nonneurosurgical patients, only three previous neurosurgical cases have been published. This case report may serve to heighten awareness of this disorder.

Cerebral sinus thrombosis associated with acquired free protein S deficiency is very rare. We report the case of an adult patient with acute lymphoblastic leukemia who presented with repeated transient ischemic attacks followed by a seizure during consolidation treatment with L-asparaginase. Magnetic resonance of the brain showed a small cortical hemorrhagic infarct. Superior sagittal sinus thrombosis was demonstrated by cerebral angiogram. A marked decrease of the free form of protein S was documented. One month later, when the patient was free of symptoms, the follow-up free protein S antigen level was restored to the normal range. We suggest that the sagittal sinus thrombosis in this patient was caused by acquired, transient free protein S deficiency. This case also extends the clinical spectrum of cerebral sinus thrombosis to include recurrent transient ischemic attacks alternating with seizures.

The very preterm infant is uniquely vulnerable to bleeding into the cerebral ventricles because of the numerous but unsupported blood vessels in the subependymal germinal matrix and unstable blood pressure and flow resulting from preterm delivery and respiratory distress. Approximately 25% of infants whose birthweights are 500 to 1,500 g have some intraventricular hemorrhage (IVH). Even a small IVH is associated with an increased risk of disability. A large IVH is sometimes complicated by hemorrhagic parenchymal infarction (also known as grade 4 IVH), which is believed to arise when venous occlusion from hematoma impairs perfusion in periventricular white matter. Large unilateral infarctions are usually associated with contralateral hemiparesis, but cognitive function may be less impaired. Prenatal glucocorticoid therapy reduces IVH by nearly 50% in randomized trials. Postnatal indomethacin reduces IVH, but reduced disability has not been consistently documented.

Symptomatic extralobar pulmonary sequestration in adults is thought to be extremely rare. We present a case of an extralobar pulmonary sequestration, with infarct, in a 28-year-old woman who complained abrupt onset of chest pain. Chest computed tomography and magnetic resonance imaging showed a mass in the left paraspinal area, medial to the left lower lobe, and serial chest radiographs revealed increasing pleural effusion. This was histopathologically confirmed to be a hemorrhagic infarct of the extralobar pulmonary sequestration.

A 25 year-old woman presented with left lower quadrant pain in the 11th week of gestation. Transvaginal sonography showed a 7 x 8 x 5 cm cystic-solid mass with an adjacent 9 mm echogenic structure on the left side corresponding to the adnexal stalk. Color Doppler sonography revealed the absence of central or peripheral flow within the mass suggestive of adnexal torsion and subsequent infarction. Laparoscopic detorsion of the left adnexa was not followed by restoration of perfusion ad a left adnexectomy was performed. Transvaginal color Doppler sonography is useful for preoperative diagnosis of adnexal torsion.

An 18-year-old woman presented with headache, right focal seizures, and diminished vision in the left eye for 20 days. Fundus examination revealed bilateral papilledema with large premacular sub–internal limiting membrane and subhyaloid bleeding in the left eye (figure 1A). MRI brain showed hemorrhagic infarct in the left temporal lobe (figure 2, A and B). Magnetic resonance venography showed left transverse and sigmoid sinus thrombosis (figure 2C). A diagnosis of Terson syndrome1 (vitreous hemorrhage) was made. Procoagulant workup was negative and the patient improved with conservative management2 (figure 1B). Even though Terson syndrome has been reported with subarachnoid hemorrhage, its occurrence with cortical venous sinus thrombosis is rare.

We describe the case of a 79-year-old woman with pulmonary infarction due to tumor emboli whose high-resolution CT (HRCT) scan demonstrated the reversed halo sign. The patient had gastric cancer and died because of cancer-related cerebral infarction. On autopsy, the central ground-glass area of the reversed halo sign on HRCT corresponded to pulmonary edema associated with alveolar septal capillary metastasis, whereas the peripheral ring-like consolidation consisted of a hemorrhagic infarct with tumor emboli. The present case is important because a detailed pathologic correlation with this unique HRCT appearance was revealed.

Despite an increased risk of stroke in pregnancy and puerperium, the overall incidence of the condition in this population is low. Therefore, there is limited data pertaining to these patients particularly from Asian countries. Our objective was to describe the risk factors and outcomes of 110 pregnancy-related ischemic strokes from 5 Asian countries.Data were collected by retrospective chart review in most cases and prospectively in the rest. Inclusion criteria for this subanalysis were women, pregnant or within 1-month postpartum, presenting to the study center with acute ischemic stroke (arterial or venous) confirmed by neuroimaging. Intracranial hemorrhages other than the ones associated with cerebral venous thrombosis or hemorrhagic infarct were excluded. Risk factors were diagnosed based on already published criteria. Outcomes were measured using modified Rankin score. Statistical analysis was done using Statistical Package for Social Sciences version 19.0.In all, 110 women with mean age of 27.94 years presented with pregnancy-related ischemic strokes; 58.2% of the strokes occurred postpartum and 49.1% were secondary to cerebral venous thrombosis. Venous strokes were significantly more likely to occur postpartum compared with arterial strokes (P=.01), to have abnormal "hypercoagulable panel result on admission" (P.001), less likely to have traditional stroke risk factors (P.001), to have hemorrhagic conversion of stroke (P.001), and to have lesser stroke severity and better functional outcome at 3 months (P.001 for each).Cerebral venous thrombosis is a significant contributor to pregnancy-related strokes in Asian women. Both traditional and pregnancy-specific risk factors should be addressed to control ischemic stroke risk in these women.

A forty-six-year-old premenopausal woman developed headache, nausea and vomiting, left hemiparesis, and seizure two days after parenteral use of progesterone and estradiol. Diabetes mellitus (DM) was found during admission. Computed tomography showed a hemorrhagic infarct in the right frontal lobe and increased density in the superior sagittal sinus (SSS). Left carotid angiography found occlusion of the left internal carotid artery (ICA). Right carotid angiograms failed to show the SSS and inferior sagittal sinus, suggestive of venous sinus thrombosis. Coexistence of the cerebral artery and the venous sinus occlusion has been described infrequently. In this case, the authors postulate that the use of estradiol and progesterone and the underlying DM increased vascular thrombogenicity, which provided a common denominator for thrombosis of both the ICA and the venous sinus.

We investigated 17 patients with 26 cerebellar hemorrhagic infarcts for their vascular anatomy, stroke mechanisms, and clinical course.Sixteen infarcts involved the superior cerebellar artery, nine the posterior inferior cerebellar artery, and one the anterior inferior cerebellar artery territories. The infarcts involved the full territory of the supplying arteries in 19 of 26 infarcts (73%). Sixteen of 17 patients were stable or improving when the hemorrhagic infarction was detected. All but one patient had an imaging study at the time of presentation that was negative for blood; hemorrhagic infarction was detected on routine serial scans performed during the first 15 days. Nine of the 17 patients were on anticoagulants when the cerebellar hemorrhagic infarct was detected; anticoagulation was maintained in eight of them with no clinical worsening. The stroke mechanism in all patients was considered embolic from cardiac and intraarterial sources. The causes, imaging findings, and consequences of hemorrhagic infarcts in the posterior circulation are similar to those in the anterior circulation. NEUROLOGY 1996;46: 346-349

Background: It is a well-known fact that very few patients of stroke arrive at the hospital within the window period of thrombolysis. Even among those who do, not all receive thrombolytic therapy. Objective: The objectives of this study were to determine the proportion of early arrival ischemic strokes (within 6 h of stroke onset) in our hospital and to evaluate the causes of nonadministration of intravenous and/or intraarterial thrombolysis in them. Materials and Methods: Data of all early arrival acute stroke patients between January 2010 and January 2015 were included. Factors determining nonadministration of intravenous and/or intraarterial thrombolysis in early arrival strokes were analyzed. Results: Out of 2,593 stroke patients, only 145 (5.6%) patients presented within 6 h of stroke onset and among them 118 (81.4%) patients had ischemic stroke and 27 (18.6%) patients had hemorrhagic stroke. A total of 89/118 (75.4%) patients were thrombolyzed. The reasons for nonadministration of thrombolysis in the remaining 29 patients were analyzed, which included unavoidable factors in 8/29 patients [massive infarct (N = 4), hemorrhagic infarct (N = 1), gastrointestinal bleed (N = 1), oral anticoagulant usage with prolonged international normalized ratio (INR) (N = 1), and recent cataract surgery (N = 1)]. Avoidable factors were found for 21/29 patients, include nonaffordability (N = 7), fear of bleed (N = 4), rapidly improving symptoms (N = 4), mild stroke (N = 2), delayed neurologist referral within the hospital (N = 2), and logistic difficulty in organizing endovascular treatment (N = 2). Conclusion: One-fourth of early ischemic stroke patients in our study were not thrombolyzed even though they arrived within the window period. The majority of the reasons for nonadministration of thrombolysis were potentially preventable, such as nonaffordability, intrahospital delay, and nonavailability of newer endovascular interventions.

Dear Sirs, Heparin is the primary acute therapy for cerebral venous thrombosis (CVT) [1], but in a subset of patients, endovascular treatment (ET) or decompressive craniotomy (DC) can be considered. ET is often reserved for patients with a severe course of the disease or who deteriorate despite heparin treatment, although data from randomised studies regarding its efficacy are lacking [2]. Small case series suggest that DC can be life-saving in patients with impending transtentorial herniation due to space-occupying lesions [3, 4]. The combined use of ET and DC in a single patient has only been described once [5]. This case report describes a second patient treated with both DC and ET. A 37-year-old woman was admitted with a generalized tonic-clonic seizure. She had been suffering from a progressive headache and vomiting since 1 week. On examination she was comatose [Glasgow Coma Scale (GCS) E1M5V1]. Her pupils were equal and responsive to light. Plantar reflexes were extensor bilaterally. CT-scan of the brain (Fig. 1a) revealed a left frontal hemorrhagic infarct surrounded by a zone of hypodensity and early signs of transtentorial herniation. CT-venography (CT-v) showed thrombosis of the left transverse and superior sagittal sinuses (Fig. 1b). The patient was started on low-molecular weight heparin (nadroparin, 5,700 IU twice daily). One hour later she deteriorated (E1M1V1). Because of impending herniation, an emergency left-sided decompressive hemicraniectomy was performed. Despite an uncomplicated procedure her clinical condition only slightly improved after surgery (E1M3Vtube) and she was transferred to a university hospital specialized in CVT. In the following 2 days she barely improved and, therefore, decision for endovascular treatment was made. Thrombolysis was considered too hazardous because of the recent operation, and therefore thrombosuction was performed using an Angiojet catheter. After the procedure, the sinuses were recanalised, but both the superior sagittal and transverse sinus reoccluded the next day. In the following days her consciousness gradually improved (E4M6V3). Initially she was severely disabled with aphasia and a hemiparesis. Three months later, however, she had only a mild aphasia and was independent in all daily activities (modified Ranking Scale 2). Fig. 1 a admission CT-scan showing left hemispheric haemorrhage surrounded by a zone of hypodensity due to venous infarction. b CT-venography showing occlusion of the superior sagittal sinus Evidence supporting the efficacy of endovascular thrombolysis or decompressive hemicraniectomy in CVT is limited. No randomised studies on ET were identified by the a authors of a Cochrane review [2]. A systematic analysis of 72 case series concluded that ET appears to be reasonably safe and can be considered in severe cases that do not respond to heparin therapy [6]. Patients with impending transtentorial herniation, however, do not appear to benefit from endovascular thrombolysis. Probably the effect of endovascular treatment comes too late and cannot prevent further brainstem compression [7]. In such cases, successful results of DC have been reported [3, 4, 8]. The combination of ET and DC has been reported once before in a case report [5]. Despite successful recanalisation of the major sinuses after local thrombolysis, the patient clinically deteriorated. Decompressive hemicraniectomy in that patient eventually resulted in improvement of the patient’s condition and at 3 months she had a favourable outcome. In a single center cohort of CVT patients, one patient also underwent both ET and DC, but no specific details on this patient are provided [9]. In our patient, hemicraniectomy was performed first to arrest impending herniation. Since she remained comatose after the procedure, mechanical thrombectomy was performed subsequently. The fact that the patient recovered despite reocclusion of the major sinuses is not easily explained. Possibly, the temporary opening of the sinuses may have restored venous flow sufficiently to prevent further infarction or haemorrhage. It is also possible that the endovascular treatment did not influence the clinical evolution after the hemicraniectomy. In patients treated with heparin only there is, surprisingly, no clear correlation between recanalisation and clinical outcome [10]. In summary, the combination of decompressive hemicraniectomy and endovascular thrombectomy in our patient appeared to be safe and resulted in a good clinical outcome.

Computed tomography (CT) was performed on an eleven-year-old dog four days after an acute onset of seizures and neurologic deficits. A ring-enhancing, intra-axial lesion associated with edema, falcial deviation and non-uniform ventricular compression was identified in the left frontal lobe. An area of ill-defined hyperdensity, compatible with hemorrhage, was noted on corresponding CT images prior to contrast enhancement. At post-mortem examination, a focal, hemorrhagic infarct, characterized by liquif ication necrosis, marked gliosis and neovascularization, was found. The etiology of the infarction could not be identified. The CT findings, however, were similar to those seen in humans with cerebral infarction due to embolic occlusion and subsequent hemorrhage. These findings and the pathophysi-ologic mechanisms behind them are discussed.

The management and outcome of cerebral venous thrombosis (CVT) may be different from that of arterial ischemic stroke (AIS). Clinically differentiating the 2 diseases on clinical grounds may be difficult. The main objective of this study was to identify predictors differentiating CVT from AIS in a large cohort of young Asian women, based on risk factors and investigations. Twelve centers in 8 Asian countries participated. Women aged 15-45 years were included if they had a diagnosis of first-ever symptomatic AIS or CVT confirmed by brain computed tomography scan or magnetic resonance imaging/magnetic resonance venography. Patients with head trauma, cerebral contusions, intracranial hemorrhage, and subarachnoid or subdural hemorrhage were excluded. Data, including demographic data, risk factor assessment, neuroimaging studies, blood tests, and cardiac studies, were collected by retrospective and then prospective chart review between January 2001 and July 2008. Outcome was based on the modified Rankin Scale (mRS) score at admission, discharge, and latest follow-up. A total of 958 patients (204 with CVT and 754 with AIS) were included in the study. Age under 36 years, anemia, pregnancy or postpartum state, and presence of hemorrhagic infarcts on computed tomography scan or magnetic resonance imaging were significant predictors of CVT on univariate analysis. Age over 36 years, diabetes, hypertension, dyslipidemia, recent myocardial infarction, electrocardiogram abnormalities, and blood glucose level >150 mg/dL were strong predictors of AIS. On multivariate analysis, postpartum state and hemorrhagic infarct were the strongest predictors of CVT (P < .001). Mortality was comparable in the 2 patient groups. Prognosis was significantly better for patients with CVT than for those with AIS (mRS score 0-2, 74% v 46%; P < .001). There was no difference in outcome between patients with obstetric and nonobstetric CVT. Our data indicate that in young Asian women, predictors of CVT differ from those for AIS. These findings could be useful in the early identification and diagnosis of patients with CVT.

Thrombolysis trials have recruited few patients aged ≥80 years, which has led to uncertainty about the likely risk-to-benefit profile in the elderly. Leukoaraiosis (LA) has been associated with hemorrhagic transformation (HT) and increases with advanced age. We tested whether there were any independent associations between age, LA and HT. Consecutive patients treated with intravenous (IV) tissue plasminogen activator (tPA) were identified from a prospective database. LA on baseline CT scans was assessed by two independent raters using the modified Van Swieten Score (mVSS) (maximum score 8, severe >4). HT was assessed on routine 24 hour to 48 hour CT /MRI scans using the European Cooperative Acute Stroke Study criteria for hemorrhagic infarct (HI) or parenchymal hematoma (PH) and judged symptomatic by the treating neurologist as per Safe Implementation of Thrombolysis in Stroke criteria. There were 206 patients treated with IV tPA (mean age: 71.0 years; range: 24-92 years), of whom 65/206 (32%) were aged ≥80 years. Overall, HT occurred in 41/206 patients (20%), HI in 31, PH1 in four (one symptomatic) and PH2 in six (three symptomatic). Age was not associated with HT (any HT: odds ratio [OR]=1.01; 95% confidence interval [CI]=0.5-2.08; p=0.99; PH: OR=0.53; 95% CI=0.12-2.3; p=0.51). There was one patient with PH1 and one patient with PH2 in 65 patients ≥80 years, both asymptomatic. LA was present in 112/208 (54%), and severe in 16.5%. LA increased with age (p

Marijuana, or cannabis, is one of the most commonly used illicit drugs worldwide. Although there are some case reports of stroke associated with cannabis use, there is no information on a causal role of cannabis in stroke. We identified 14 patients admitted to St Louis University Hospital between January 2004 and July 2007 with ischemic stroke who had documented clear exposure to cannabis during or before symptom onset and a positive urine screen for cannabis. We report this series, along with 3 cases previously reported by our group, for a total of 17 patients (13 men and 4 women), with a mean age of 41 years (range, 15-63 years). Nine patients were under age 45 years, 4 had a history of hypertension, and 10 sustained stroke in the posterior circulation. Headache, dysarthria, and ataxia were the most common presenting symptoms. Five patients had recurrent stroke with reexposure to cannabis. No patient had a prothrombotic state or cardiac source of embolism. Autopsy performed in 2 patients revealed hemorrhagic infarct with no evidence of vasculitis or embolus. The absence of other vascular risk factors in most of our patients, the temporal relation of symptom onset to cannabis exposure, and the recurrence of symptoms in a few patients with reexposure suggest a causal role of cannabis in these cases of ischemic stroke. However, this causal association cannot be definitely ascertained, given the descriptive nature of our series. More research is needed to explore this possible causal association.

Appendices epiploicae are adipose structures protruding from the serosal surface of the colon. They can be seen with abdominal radiography and cross-sectional imaging if the colonic wall is surrounded by intraperitoneal contrast material, ascites, or blood. Normal appendices epiploicae appear as lobulated masses of pericolic fat, usually 2-5 cm long and 1-2 cm thick. Their enlargement, deformity, or altered radiopacity may result from various pathologic processes that can originate locally or extend from adjacent viscera. In a series of 22 cases, appendices epiploicae were affected by spontaneous torsion and hemorrhagic infarct, calcification due to aseptic fat necrosis, primary or secondary inflammation, enlargement by lipomas or metastases, and incarceration in hernias. Disorders of appendices epiploicae are often manifested by nonspecific clinical signs and symptoms (eg, torsion is often mistaken for appendicitis or diverticulitis). These entities should be included in the differential diagnosis of any unexplained abdominal pain or pericolic lesions in adults.

We report the case of a 19-year-old woman who had developed obsessive-compulsive disorder after a hemorrhagic infarct in the left caudate nucleus after neurosurgery. Four years after the operation, her obsessive-compulsive disorder symptoms showed a remarkable reduction within a week of starting low-dose fluvoxamine, without any behavioral or psychological treatment.

Cerebral vasospasm continues to be the leading treatable cause of death and disability in patients with subarachnoid hemorrhage. Transluminal balloon angioplasty has been considered a safe and effective treatment for cerebral vasospasm resistant to maximal medical treatment. However, it should be performed in a timely manner, any delays could potentially increase the risk of hemorrhagic infarct. Angioplasty in the affected territory may be of benefit in improving not only the angiographic appearance but also the ultimate outcome for the patient, if performed in a timely fashion.

Consequences of neonatal cerebral venous infarct can be severe. However, we have identified a series of neonates with unilateral temporal lobe infarcts, suspected to be secondary to superficial cortical venous thrombosis, who have had relatively normal outcomes. Medical records were reviewed retrospectively. History, relevant studies, and outcomes for 7 patients are described. Most patients presented with neonatal seizures. Neuroimaging showed unilateral temporal lobe hemorrhage and surrounding ischemic change, which was initially attributed to thrombosis of the vein of Labbe; however, magnetic resonance venogram findings suggest that thrombosis of other superficial temporal lobe veins may also be involved. Seizure control was achieved in all cases. Development and neurologic examination at follow-up were usually normal. We conclude that neonatal temporal lobe hemorrhagic infarct secondary to suspected superficial temporal venous thrombosis appears to have a good clinical outcome. This is surprising, given the dramatic imaging and clinical presentations.

Background Self-retaining brain retractors are commonly used during intracranial surgery, and they are indispensable during microneurosurgery. There is a common severe complication due to the use of self-held retractors, that is, formation of a hemorrhagic infarct area in the brain region exposed to traction. All the more, present retractor systems are fixed and rigid and obstruct surgeons during surgery. Sometimes these retractors create glare in the microscope that distracts the surgeon. We hereby propose a simple and easy method of retraction of brain especially the temporal lobe using the transsylvian approach and vermis using the transvermian approach. Methods This is retrospective analysis of 47 patients in 4 years in which we have used our stitch retractor. We have analyzed their outcome, postoperative scan, and ease of performing surgery. Results In 47 patients, there was only 1 postoperative contusion, and the longest period it was kept for is 6 hours. The other advantage was that it does not obstruct in any way while doing dissections and surgery. There was no glare while operating under a microscope. Conclusion We hereby propose a simple and easy method of retraction of brain especially the temporal lobe using the transsylvian approach and vermis using the transvermian approach. It is minimally traumatic, reducing insult to the brain. It allows the surgeon to dissect without any obstruction and glare in the way. The biggest advantage of the present stitch retractor is that it is very cheap and simple to use.

Purpose: Optimal treatment strategies and neurologic outcome after stroke depend on an accurate characterization of the lesion. There is a need for high resolution noninvasive imaging for assessment of the infarct size, perfusion, and vascular territory. MRI at the ultra high field (UHF) of 8 T offers unprecedented resolution, but its utility for stroke evaluation has not been determined yet. Method: A 55-year-old man with hypertension experienced sudden onset of speech arrest and right-sided hemiparesis that resolved in

Plain and Gd-DTPA-enhanced MR images of the brain were obtained in 18 consecutive patients with meningitis (eight with tuberculous, five with bacterial, three with viral, and two with fungal infections); the MR images were compared with CT scans. MR images were obtained on a 2.0-T superconducting unit with both T1- and T2-weighted pulse sequences before injection and with a T1-weighted sequence after injection of Gd-DTPA (0.1 mmol/kg) in all patients. In tuberculous meningitis, MR imaging depicted ischemia/infarct, hemorrhagic infarct of basal ganglia, meningeal enhancement at either basal cistern or convexity surface of brain, and associated small granulomas in a few more patients than CT did. In bacterial meningitis, primary foci of extracranial inflammation (i.e., mastoid, paranasal sinuses) and adjacent intracranial lesions including localized dural inflammation, subdural fluid collection, and/or brain parenchymal lesions were demonstrated much better on MR than on CT. Otherwise, MR images generally matched the CT scan. Although the plain MR images, both T1- and T2-weighted, were the most sensitive in delineating ischemia/infarct, hemorrhage, and edema, they were not as specific as Gd-DTPA-enhanced T1-weighted images and postcontrast CT scans in defining the active inflammatory process of the meninges and focal lesions precisely. We conclude that if Gd-DTPA is used, MR imaging appears to be superior to CT in the evaluation of patients with suspected meningitis. Precontrast MR is needed to delineate ischemia/infarct, edema, and subacute hemorrhage.

Purpose To understand the biological basis of possible mechanisms responsible for increased fractional anisotropy (FA) in different stages of hemorrhage and hemorrhagic brain lesions. Materials and Methods A total of 19 patients with cerebral hemorrhage (CH), five patients with hemorrhagic infarct (HI), and nine patients with hemorrhagic brain tumor (HBT) were prospectively evaluated with diffusion tensor imaging (DTI) and the FA and mean diffusivity (MD) was quantified. Ex vivo DTI of blood clot and histology of the blood clot and HBT were performed to interpret the temporal changes in the DTI metrics. Results High FA (>0.20) with low MD in the acute and early subacute stage and low FA (

Awomaninher lateteenspresentedwithdystonicposturingofher left hand for 2 years and left foot for 3months. Dystonic posturing of her hand had started when she was 8 months pregnant, and it slowly worsened to involve her left lower limb, leading to difficulty in walking (Video). She was evaluated for left hemidystonia. Fluid-attenuated inversion recovery (FLAIR)magnetic resonance images (MRIs) of the brain gave the appearance of the eyeof-the-tiger sign in the right basal ganglia similar to what would be seenwithaneuroferritinopathy,butsusceptibility-weighted imaging revealed evidence of hemosiderin indicative of an old hemorrhagic infarct (Figure). The results ofmagnetic resonanceangiography for evaluation of intracranial vessels were normal. Mutation analysis for pantothenate kinase 2 was negative. Antinuclear antibody and anti–double-stranded DNAwere negative.

Zygomycosis is an uncommon but frequently fatal infection and occurs mostly in immunosuppressed hosts, whereas approximately 50% of zygomycosis occurs in diabetic patients. The current patient initially presented with persistent pulmonary edema secondary to renal failure. This was the last of four admissions within 1 year for this 68-year-old woman, for whom the chief complaints were shortness of breath and chest pain. Her past medical history included insulin-requiring type 2 diabetes and hypertension for 10 years, and chronic heart and renal failure. She was previously admitted to the hospital for what appeared to be pulmonary edema secondary to renal failure. In the last admission the patient developed pulmonary hemorrhage and metabolic acidosis. Transbronchial biopsy was performed, showing irregular fungal hyphae in the blood vessels, morphologically consistent with zygomycosis. Central nervous system computed tomography also revealed a large infarct in the cerebral hemisphere. The patient died on the seventh hospital day. At autopsy three organs were extensively involved by zygomycosis: (i) lungs were diffusely hemorrhagic with acute infarcts; (ii) pericardium had fibrotic inflammation; and (iii) the left cerebral hemisphere, cerebellum and pons had large hemorrhagic infarct by zygomycosis infection. Corticosteroid medication and hemodialysis triggered increasing hyperglycemia, metabolic acidosis and iron overload, which contributed to zygomycosis infection that subsequently spread to the heart and brain as a rare consequence.

We report on the case of a 2-year 5-month-old girl with congenital heart disease who developed left middle cerebral artery occlusion and cerebral hemorrhagic infarction a day after ventricular septal defect patch closure. Cranial computed tomography scan revealed an acute hemorrhagic infarct over the left middle cerebral artery territory with midline shift to the right. Since medical treatment failed, decompressive hemicraniectomy with duraplasty was performed, successfully reversing herniation. Decompressive surgery allows extracranial expansion of the swollen brain and relieves CSF space compression. We believe this to be the youngest reported patient to undergo decompressive hemicraniectomy for middle cerebral artery territory infarction. Although the patient survived, her functional outcome was poor. Decompressive hemicraniectomy can be lifesaving and should be considered as an alternative therapy for patients with brain swelling refractory to medical management.

Background MRI of the brain has facilitated the diagnosis of cerebellar infarction in the territory of the superior cerebellar artery (SCA). We analyzed the data on patients with SCA infarction who presented with only cerebellar symptoms in an attempt to define its underlying pathophysiology. Summary of Report Ten patients with SCA infarction who presented with cerebellar symptoms were studied by brain MRI, angiography, and underlying pathology. Brain MRI demonstrated an infarct in the SCA territory in the anterior rostral cerebellum of all patients. None had abnormalities in the brain stem. In four patients, a hemorrhagic infarct was present in the same region. Cerebral angiography revealed no obvious SCA occlusion or atherosclerotic vascular disease in any patient. Eight of the 10 patients had heart disease, such as atrial fibrillation or old myocardial infarction. The presumed diagnosis was occlusion of the SCA in its periphery due to cardiogenic embolism. Conclusions When a patient presents with only cerebellar symptoms and has cerebellar infarction demonstrated by brain MRI, the SCA branch is probably occluded by cardiogenic embolism.

A 1(1/2)-month-old baby with seizures, lethargy and refusal of feeds was diagnosed to have intracranial hemorrhage due to factor VII deficiency. MRI also demonstrated the unusual presence of a hemorrhagic infarct. The case underscores the importance of carrying out neuroimaging and appropriate hematological studies even in the absence of obvious external bleeding. Hypothesis for increased propensity for intra-cranial hemorrhage is discussed.

To the Editor, Splenic infarct may be observed during the course of several diseases; however, the incidence is quite low. Splenic infarct is related to thromboembolic events; various diseases, including sickle cell anemia, chronic myeloproliferative diseases, lymphoma, and leukemia, can also cause splenic infarct [1]. In patients with autoimmune hemolytic anemia (AIHA) massive hemolysis causes activation of the immune response, destruction of erythrocytes, and splenomegaly [2]. Splenic infarct is rarely observed in AIHA patients and to the best of our knowledge the literature contains only 3 cases of splenic infarct due to AIHA [3,4,5]. Herein we describe a 67-year-old female that presented to the emergency department with fatigue, tachycardia, and weakness. The patient’s vital signs were as follows: temperature: 37 °C; pulse: 120/min; blood pressure: 120/70 mmHg. Physical examination showed pale conjunctivas, icteric sclerae, and a spleen that was palpable 3 cm below the costa. Lymphadenopathy was not observed. Electrocardiography (ECG) and lung radiography results were normal. Complete blood count findings were as follows: Hb: 5.7 g/dL; MCV: 115 fL, WBC count: 6.4 x 109/L; Plt count: 157 x 109/L. Biochemical examination findings were as follows: total bilirubin: 2.0 mg/dL; indirect bilirubin: 1.5 mg/dL; LDH: 466 U/L. Her reticulocyte count was 6.38%, direct anti-globulin test with IgG and C3d complement was 4 positive, and the indirect anti-globulin test was 4positive. Erythrocyte agglutination, polychromasia, and spherocytes were observed in her peripheral blood smear. The patient was further examined to determine if there existed other secondary causes for her complaints; there were no signs of hepatitis, her IgG, IgA, and IgM levels were normal, and monoclonality was not observed on the serum protein electrophoresis. Mycoplasma pneumonia, ANA, anti-ds DNA, and HIV tests were negative. Lymphoma was eliminated via computed tomography (CT). Bone marrow aspiration showed the presence of erythroid hyperplasia. Based on these findings, the patient was diagnosed with AIHA. The patient was given erythrocyte suspension because of her symptomatic status. The patient was started on 1 mg/kg/d methylprednisolone and folic acid after the diagnosis of idiopathic mixed type AIHA. After 3 weeks of the steroid treatment, the patient developed left upper quadrant pain and and the abdominal ultrasonography revealed splenic infarct complicated by splenic hemorrhage. Upper abdominal MRI was performed to confirm the presence of splenic infarct. MRI showed that the spleen was 155 mm and that a wedge-shaped hemorrhagic infarct was present around the spleen (Figure). The patient was experiencing severe pain in the upper left quadrant and underwent splenectomy, a common treatment for AIHA. The patient’s pain disappeared following the splenectomy. To eliminate hypercoagulability causes protein C, protein S, antithrombin, factor VIII, factor V Leiden mutation, prothrombin mutation, lupus anticoagu-lant, anti-cardiolipin antibodies, and homocysteine were measured, all of which were normal. ECG showed a normal sinus rhythm. Transthoracic echocardiography did not show any cardiac valve pathology. Thromboemboli were not present during the observation. The patient was started on azathioprine for AIHA, as she was unresponsive to steroid treatment and splenectomy. Figure Axial T2-weighted fat-suppressed MRI shows a wedge shaped hyperintense area of infarction in the spleen (arrow), as well as decreased signal intensity of the liver The most common cause of splenic infarct is cardiovascular thromboembolism (22% of all cases), followed by thrombophilia[5]. In addition, the third most common cause of splenic infarct is hematological diseases, including sickle hemoglobinopathies, myelofibrosis, paroxysmal nocturnal hemoglobinuria, polycythemia vera, leukemia, and lymphoma, which account for 10% of all cases [1]; however, only 3 cases of splenic infarct due to AIHA have been reported [3,4,5]. Thrombogenic events and splenic vasculitis are not the only causes of splenic infarct. Other immune-mediated mechanisms related to cryoglobulin synthesis can cause splenic infarct [6]. In cases of cardiovascular thromboembolism or thrombophilia-induced infarct, the lungs, kidneys, heart, and intestine, together with splenic infarct, are affected by multiple emboli; however, in hematological diseases infarct is usually limited to the spleen [5]. The presented patient was evaluated for thrombophilia, but there was neither a laboratory evidence for hypercoagulability nor any cardiac cause. Moreover, the presented case only had an infarct that was localized in the spleen. Splenic infarct may have arisen in the present case due to splenomegaly or immune-mediated mechanisms caused by cold antibodies; the patient had both warm and cold antibodies. Medical treatment can be administered for uncomplicated splenic infarcts. Splenectomy is preferred in cases with persistent symptoms or complicated cases with a splenic pseudocyst, abscess, or hemorrhage; however, early splenectomy is required to prevent mortality [7]. The presented case had pain that was unresponsive to analgesic treatment, and her splenic infarct was complicated by the presence of a hemorrhage; therefore, splenectomy was performed with early intervention. Following the splenectomy the patient’s complaints disappeared. In conclusion, in patients with such hematological diseases as AIHA, hemoglobinopathies, polycythemia vera, myelofibrosis, leukemia, and lymphoma, and complaints of left upper quadrant pain, splenic infarct should be suspected and MRI or CT should be performed for diagnostic purposes. As thrombophilia can also cause infarct, patients should also be evaluated for thrombophilia. If a patient with splenic infarct complains of severe persistent pain and the case is complicated the patient should undergo splenectomy immediately to avoid mortality. Conflict of Interest Statement None of the authors have any conflicts of interest, including specific financial interests, relationships, and/or affiliations, relevant to the subject matter or materials included.

A clinicopathologic study was made in 28 patients who died after acute myocardial infarction (AMI) treated with coronary intervention (CI: Percutaneous transluminal coronary angioplasty (PTCA) or Stenting). Nineteen patients received PTCA (12 men and 7 women, 42 to 85 years of age, mean 71.4 years), and 9 patients received stenting after PTCA (8 men and 1 woman, 49 to 86 years of age, mean 67.7 years). Hemorrhagic infarction was found in 23 cases. Compared to direct PTCA, more severe hemorrhage was found in cases treated with PTCA after intracoronary thrombolytic therapy (rescue PTCA: r-PTCA). Also, severe hemorrhage in the infarct area was found in cases treated with percutaneous cardiopulmonary support (PCPS) after AMI. Hemorrhagic infarction was found even in patients treated with CI in the early phase after AMI, and also in some patients who recovered from initial heart failure after AMI. Compared to usual ischemic infarct, healing was greatly delayed in the hemorrhagic infarct area. We conclude that special care is required in the treatment of patients who received CI, because of a high possibility of hemorrhage in the infarct area after CI and the delay in healing in the hemorrhagic infarction area.

Sir, I read the report on an interesting case of beta-thalassemia/ hemoglobin E (b-thal/HbE) by Vineeta et al. with a great interest [1]. Vineeta et al. concluded that “Protein C and Protein S deficiency were the causative factor for developing hemorrhagic infarct in the HbE/ Beta thalassemia patient [1].” In fact, it can be confirmed that there existed a case of a combined genetic disorder between HbE and IVS1-5 mutation. However, the conclusion proposed by Vineeta et al. should be carefully considered. Firstly, a single case report is not a standard report to set any correlation in clinic. A systematic case control study must be performed to get the cause and outcome relationship. Secondly, the hemorrhagic infarct has no doubt related to abnormal Protein C and Protein S, but further referred linkage to b-thalassemia/HbE cannot be directly assumed. There must be a complete proposed biological process based on gene ontology principle to confirm this correlation.

Background and purpose After first-ever ischaemic stroke, to assess the risk and baseline factors associated with acute symptomatic seizure (ASS) (occurring within 7 days) and late post-stroke seizure (LPS) (>7 days). Methods All consecutive patients aged 15–49 with first-ever ischaemic stroke between 1994 and 2007 treated at the Helsinki University Central Hospital were included, using Cox proportional hazard models to identify factors associated with seizures. Adjustment was for age, gender, vascular risk factors, admission hyperglycemia (>6.1 mm) and hyponatremia (

Hyperintensities on T1-weighted magnetic resonance imaging (MRI) in the setting of brain ischemia are usually considered hemorrhagic transformations. Such changes can also be seen due to "incomplete infarction" with selective neuronal loss. Arguments regarding the cause of these T1 hyperintensities have shuttled between gemistocytic astrocyte accumulation, tissue calcification and paramagnetic substance deposition. Susceptibility weighted imaging (SWI), a sensitive modality for detecting paramagnetic agents and blood products, has never been used to resolve this issue. The study was aimed to evaluate the SWI signal changes of T1 hyperintense lesion in stroke patients and understand its usefulness in differentiating a hemorrhagic infarct and an incomplete infarct. All the seven patients with infarct, having hyperintensities on T1 weighted MR imaging seen over the last one year were subjected to SWI. In none of the patients SWI failed to show any blooming. By doing SWI for T1-weighted hyperintensities, we can differentiate hemorrhagic infarct and a non-hemorrhagic "incomplete infarct". This differentiation will immensely help in planning management strategy and prognostication.