Abstract 191: Selective Frontal Lobe Metabolic Dysfunction After Sub-arachnoid Hemorrhage

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Halinder S Mangat ◽  
Jana Ivanidze ◽  
Xiangling Mao ◽  
Dikoma Shungu ◽  
Malik Fakhar ◽  
...  
Keyword(s):  
Cerebral Infarction ◽  
Frontal Lobe ◽  
Ct Perfusion ◽  
Neurological Deficits ◽  
High Morbidity ◽  
Metabolic Dysfunction ◽  
Fisher Score ◽  
Csf Lactate ◽  
Occipital Lobes ◽  
Neurologically Intact

Aneurysmal SAH results in high morbidity. Patients who make a good neurological recovery report significant neuropsychological impairment such as loss of motivation, interests, and concentration, all of which are commonly associated with frontal lobe dysfunction. We hypothesize that subclinical frontal lobe injury occurs in neurologically intact SAH patients and may be identified by measuring brain energy metabolism using regional N-acetyl aspartate (NAA) as an imaging marker of neuronal integrity and mitochondrial function, and CSF lactate, as a marker of anaerobic metabolism. We utilized MR Spectroscopy (MRS) to measure regional NAA in SAH patients who had suffered neither cerebral infarction nor neurological deficits. Only patients who underwent endovascular aneurysm coiling were included. Measurements were made in frontal, temporal, occipital lobes, lateral ventricles, and averaged in each hemisphere from 3 slices. Matching ROIs were placed on the most proximate CT perfusion maps to measure corresponding rCBF. MR spectra were compared to controls from our data library (7 subjects) and to rCBF. Average age was 58 years, Hunt Hess score was 2.43±1.09, modified Fisher score was 2.79±1.05. 3 patients had DCI and none had cerebral infarction. Median GCS at discharge was 15. MRS was done at 9.93±7.73 days from admission. 1 patient had no MRS data, 3 patients had no CT perfusion. SAH patients demonstrated significantly reduced NAA/RMS in frontal lobes (16.18±4.96 vs. 20.93±5.56, p=0.042) but not in temporal (16.49±4.37 vs. 19.37±4.38, p=0.09) or occipital lobes (20.62±4.50 vs. 21.05±4.23, p=0.41). CSF lactate was significantly higher in SAH patients (7.74±2.27 vs. 4.02±0.76, p=0.001). NAA/RMS did not correlate with CBF in pooled data (R 2 =0.02, p=0.40) or in frontal lobe rCBF (R 2 =0.001, p=0.92); nor with CSF lactate (R 2 =0.02, p=0.53). Total frontal lobe NAA is selectively reduced and CSF lactate is elevated in neurologically intact survivors after SAH. This preliminary data is suggestive of energy depletion and subclinical brain injury, which appears to be independent of cerebral blood flow. In addition to validating this pilot data, we will study the association with cognitive impairment in these patients.

scholarly journals Cardio-Cerebral Infarction, Free-Floating Thrombosis and Hyperperfusion in COVID-19

2021 ◽  
Vol 13 (2) ◽  
pp. 266-268
Author(s):  
Sitara Koneru ◽  
Dinesh V. Jillella ◽  
Raul G. Nogueira
Keyword(s):  
Ischemic Stroke ◽  
Cerebral Infarction ◽  
Inflammatory Responses ◽  
Imaging Finding ◽  
Ct Perfusion ◽  
Hypercoagulable State ◽  
Left Internal Carotid Artery ◽  
Intraluminal Thrombus ◽  
Unique Case ◽  
Ct Perfusion Imaging

Cardio-cerebral infarction, which refers to an acute ischemic stroke (AIS) and acute myocardial infarction (AMI) that occur concurrently, is an uncommon phenomenon with a grave prognosis. Intraluminal carotid thrombus (ICT) is an infrequently encountered cause of ischemic stroke and can be associated with an underlying hypercoagulable state. One severe yet prevalent complication of infection with Coronavirus Disease 2019 (COVID-19) is thrombosis from multi-pathway inflammatory responses. Here, we present a unique case of cardio-cerebral infarction, with a free-floating intraluminal thrombus in the left internal carotid artery, in the setting of recent COVID-19 infection, and with the etiology of both events attributed to a COVID-19 hypercoagulable state. CT perfusion imaging also showed an interesting imaging finding of hyperperfusion, which is believed to be a form of dysfunctional cerebral autoregulation.

scholarly journals Intravenous Administration of Human Amniotic Mesenchymal Stem Cells in the Subacute Phase of Cerebral Infarction in a Mouse Model Ameliorates Neurological Disturbance by Suppressing Blood Brain Barrier Disruption and Apoptosis via Immunomodulation

2021 ◽  
Vol 30 ◽  
pp. 096368972110241
Author(s):  
Yasunori Yoshida ◽  
Toshinori Takagi ◽  
Yoji Kuramoto ◽  
Kotaro Tatebayashi ◽  
Manabu Shirakawa ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Mouse Model ◽  
Cerebral Infarction ◽  
Blood Brain Barrier ◽  
Brain Infarction ◽  
Brain Barrier ◽  
Neurological Deficits ◽  
Immunomodulatory Effects ◽  
Amniotic Mesenchymal Stem Cells

Neuro-inflammation plays a key role in the pathophysiology of brain infarction. Cell therapy offers a novel therapeutic option due to its effect on immunomodulatory effects. Amniotic stem cells, in particular, show promise owing to their low immunogenicity, tumorigenicity, and easy availability from amniotic membranes discarded following birth. We have successfully isolated and expanded human amniotic mesenchymal stem cells (hAMSCs). Herein, we evaluated the therapeutic effect of hAMSCs on neurological deficits after brain infarction as well as their immunomodulatory effects in a mouse model in order to understand their mechanisms of action. One day after permanent occlusion of the middle cerebral artery (MCAO), hAMSCs were intravenously administered. RT-qPCR for TNFα, iNOS, MMP2, and MMP9, immunofluorescence staining for iNOS and CD11b/c, and a TUNEL assay were performed 8 days following MCAO. An Evans Blue assay and behavioral tests were performed 2 days and several months following MCAO, respectively. The results suggest that the neurological deficits caused by cerebral infarction are improved in dose-dependent manner by the administration of hAMSCs. The mechanism appears to be through a reduction in disruption of the blood brain barrier and apoptosis in the peri-infarct region through the suppression of pro-inflammatory cytokines and the M2-to-M1 phenotype shift.

scholarly journals Herpes Zoster Ophthalmicus with Delayed Cerebral Infarction and Meningoencephalitis

1987 ◽  
Vol 14 (3) ◽  
pp. 312-314 ◽  
Author(s):  
Mark S. Freedman ◽  
Ronald D. Macdonald
Keyword(s):  
Herpes Zoster ◽  
Cerebral Infarction ◽  
Therapeutic Intervention ◽  
Morbidity And Mortality ◽  
High Morbidity ◽  
Herpes Zoster Ophthalmicus ◽  
Clinical Resolution ◽  
Cerebral Angiitis

ABSTRACT:Herpes zoster ophthalmicus can be complicated by a delayed ipsilateral cerebral angiitis which may cause infarction and a smoldering meningoencephalitis. We describe such a case treated successfully with steroids and acyclovir. It is important to consider the diagnosis of this disorder early since therapeutic intervention may prevent an otherwise high morbidity and mortality. Steroids may have to be continued for some time after clinical resolution, using the ESR as a guideline for decreasing dosages.

Early Stroke Detection in Perioperative Patients: A Simple Educational Intervention and Feasibility Study

2021 ◽  
Vol 104 (1) ◽  
pp. 150-158
Keyword(s):  
Neurological Deficit ◽  
Heart Surgery ◽  
Negative Impact ◽  
Open Heart Surgery ◽  
Neurological Deficits ◽  
Number Needed To Treat ◽  
High Morbidity ◽  
Neurological Assessment ◽  
Post Intervention ◽  
Perioperative Stroke

Background: Perioperative stroke is uncommon. However, it carries high morbidity and mortality. Unfortunately, the diagnosis is usually delayed resulting in reduced possibility for therapeutic intervention. Objective: To develop a protocol directed at shortening the time to detect neurological deficits in postoperative patients. Materials and Methods: By using a pre-post intervention design to evaluate the time to stroke recognition in post-open heart surgery patients. The intervention consisted of 1) A new protocol to evaluate new neurological deficits within 14 days after surgery, composed of six items of simple neurological assessment applied by CVT nurses during routine vital sign measurement. 2) An educational program for nurses, patients, and family focusing on postoperative stroke complications. Results: Between January 2014 and October 2015, the authors retrospectively reviewed 27 consecutive patients with acute neurological deficit within 14 days after surgery as the pre-intervention population. Twenty-seven consecutive patients with postoperative neurological deficits were enrolled during a post-intervention period, which was between November 2015 and September 2016. Comparing pre- and post-intervention periods, the authors found that stroke fast track activation was significantly increased from 4/27 (14.80%) to 15/27 (55.60%) (p=0.002). The median (min-max) duration from time last seen normal to first neurological deficit detection was reduced from 690 (19 to 9,190) to 130 (5 to 5,935) minutes (p=0.003). The number needed to treat for early detection when the protocol was used was 2.94. There was an increasing trend to endovascular treatment. Conclusion: Perioperative stroke is rare. However, it has negative impact to postoperative patients’ outcome. A simple protocol for postoperative neurological assessment after cardiac surgery is feasible to detect perioperative stroke. Keywords: Postoperative, In-hospital, Detection, Recognition, Stroke

Use of CT Perfusion to Differentiate between Brain Tumour and Cerebral Infarction

2004 ◽  
Vol 18 (1) ◽  
pp. 77-83 ◽  
Author(s):  
Raymond Lee ◽  
Raymond T.F. Cheung ◽  
Kwan N. Hung ◽  
Kai M. Au-Yeung ◽  
Lilian L.Y. Leong ◽  
...  
Keyword(s):  
Cerebral Infarction ◽  
Brain Tumour ◽  
Ct Perfusion

IM-12 activates the Wnt–β-catenin signaling pathway and attenuates rtPA-induced hemorrhagic transformation in rats after acute ischemic stroke

2019 ◽  
Vol 97 (6) ◽  
pp. 702-708 ◽  
Author(s):  
Ting Wang ◽  
Yu-Mei Duan ◽  
Qiao Fu ◽  
Tao Liu ◽  
Jin-Cheng Yu ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Acute Ischemic Stroke ◽  
Signaling Pathway ◽  
Glycogen Synthase ◽  
Hemorrhagic Transformation ◽  
Neurological Deficits ◽  
Control Group ◽  
High Morbidity ◽  
Sprague Dawley ◽  
Gsk 3Β

Hemorrhagic transformation (HT) is a devastating complication for patients with acute ischemic stroke (AIS) who are treated with tissue plasminogen activator (tPA). HT is associated with high morbidity and mortality, but no effective treatments are currently available to reduce the risk of HT. Therefore, methods to prevent HT are urgently needed. In this study, we used IM-12, an inhibitor of glycogen synthase kinase 3β (GSK-3β), to evaluate the role of the Wnt–β-catenin signaling pathway in recombinant tPA (rtPA)-induced HT. Sprague–Dawley rats were subjected to a middle cerebral artery occlusion (MCAO) model of ischemic stroke, and then were either administered rtPA, rtPA combined with IM-12, or the vehicle at 4 h after stroke was induced. Our results indicate that rats subjected to HT had more severe neurological deficits, brain edema, and blood–brain barrier (BBB) breakdown, and had a greater infarction volume than the control group. Rats treated with IM-12 had improved outcomes compared with those of rats treated with rtPA alone. Moreover, IM-12 increased the protein expression of β-catenin and downstream proteins while suppressing the expression of GSK-3β. These results suggest that IM-12 reduces rtPA-induced HT and attenuates BBB disruption, possibly through activation of the Wnt–β-catenin signaling pathway, and provides a potential therapeutic strategy for preventing tPA-induced HT after AIS.

scholarly journals Palliative Embolisation of Brain Arteriovenous Malformations Presenting with Progressive Neurological Deficit

2000 ◽  
Vol 6 (3) ◽  
pp. 177-183 ◽  
Author(s):  
M. Al-Yamany ◽  
K. G. terBrugge ◽  
R. Willinsky ◽  
W. Montanera ◽  
M. Tymianski ◽  
...  
Keyword(s):  
Neurological Deficit ◽  
Arteriovenous Malformations ◽  
Clinical Results ◽  
Neurological Deficits ◽  
Therapeutic Modality ◽  
High Morbidity ◽  
Progressive Neurological Deficit ◽  
Permanent Morbidity ◽  
Brain Avms

Large arteriovenous malformations (AVMs) located in eloquent areas of the brain are generally considered incurable because of the high morbidity and mortality associated with their treatment. When these patients develop a progressive neurological deficit they in time often become severely disabled. This report presents the results of palliative embolisation in this subgroup of patients. Analysis of our data-base of 714 patients with known brain AVMs revealed 17 patients who presented with progressive neurological deficit and who underwent palliative embolisation as the therapeutic modality of choice for management of their AVM. One patient was excluded due to lack of follow-up and two were excluded because they later received radiation therapy. Following embolisation 43% had improvement of their neurological deficit, 50% stabilized and 7% continued to deteriorate and these clinical results persisted for an average of more than 2 years follow-up. Transient neurological morbidity associated with embolisation treatment was 7% and there was no permanent morbidity and no mortality. Palliative embolisation of brain AVMs presenting with progressive neurological deficits arrested deterioration in more than 90% of patients and was associated with low morbidity and no mortality.

scholarly journals Sensitivity of CT perfusion for the diagnosis of cerebral infarction

2014 ◽  
Vol 61 (1.2) ◽  
pp. 41-45 ◽  
Author(s):  
Taijun Hana ◽  
Junya Iwama ◽  
Suguru Yokosako ◽  
Chika Yoshimura ◽  
Naoyuki Arai ◽  
...  
Keyword(s):  
Cerebral Infarction ◽  
Ct Perfusion

scholarly journals Formation of a meningoencephalocele after removal of a frontal lobe meningioma by transfrontal craniotomy in a cat

2020 ◽  
Vol 6 (2) ◽  
pp. 205511692095719
Author(s):  
Christian Günther ◽  
Katrin M Beckmann ◽  
Frank Steffen
Keyword(s):  
Frontal Lobe ◽  
Postoperative Recovery ◽  
Neurological Deficits ◽  
Anatomical Landmarks ◽  
En Bloc ◽  
Case Summary ◽  
Clonic Seizures ◽  
Definition Of ◽  
Neurological Progression

Case summary A 10-year-old castrated male domestic shorthair cat was referred for surgical treatment of a left-sided frontal lobe meningioma diagnosed by CT. Clinically, the cat had generalised tonic–clonic seizures, which reduced in frequency after treatment was started with prednisolone. After definition of the anatomical landmarks of the feline skull, a bilateral transfrontal craniotomy allowed en bloc removal of the meningioma. While postoperative recovery was uneventful, right-sided proprioceptive deficits were still present 6 months after surgery. MRI detected a probable meningoencephalocele herniating through the surgical bone defect in the frontal sinus. Because of the mild neurological deficits and good quality of life, the meningoencephalocele was not treated. Thirty-one months after meningioma removal the cat was alive without further neurological progression. Relevance and novel information To our knowledge, this is the first report to describe, in detail, the technique of transfrontal craniotomy in cats. Iatrogenic meningoencephalocele is a complication that has not previously been described after meningioma removal in cats, and should be considered as a potential complication after craniotomy.

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