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Farrher E, Chiang CW, Cho KH, Grinberg F, Buschbeck RP, Chen MJ, Wu KJ, Wang Y, Huang SM, Abbas Z, Choi CH, Shah NJ, Kuo LW. Spatiotemporal characterisation of ischaemic lesions in transient stroke animal models using diffusion free water elimination and mapping MRI with echo time dependence. Neuroimage 2021; 244:118605. [PMID: 34592438 DOI: 10.1016/j.neuroimage.2021.118605] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/10/2020] [Revised: 09/14/2021] [Accepted: 09/19/2021] [Indexed: 11/16/2022] Open
Abstract
BACKGROUND AND PURPOSE The excess fluid as a result of vasogenic oedema and the subsequent tissue cavitation obscure the microstructural characterisation of ischaemic tissue by conventional diffusion and relaxometry MRI. They lead to a pseudo-normalisation of the water diffusivity and transverse relaxation time maps in the subacute and chronic phases of stroke. Within the context of diffusion MRI, the free water elimination and mapping method (FWE) with echo time dependence has been proposed as a promising approach to measure the amount of free fluid in brain tissue robustly and to eliminate its biasing effect on other biomarkers. In this longitudinal study of transient middle cerebral artery occlusion (MCAo) in the rat brain, we investigated the use of FWE MRI with echo time dependence for the characterisation of the tissue microstructure and explored the potential of the free water fraction as a novel biomarker of ischaemic tissue condition. METHODS Adult rats received a transient MCAo. Diffusion- and transverse relaxation-weighted MRI experiments were performed longitudinally, pre-occlusion and on days 1, 3, 4, 5, 6, 7 and 10 after MCAo on four rats. Histology was performed for non-stroke and 1, 3 and 10 days after MCAo on three different rats at each time point. RESULTS The free water fraction was homogeneously increased in the ischaemic cortex one day after stroke. Between three and ten days after stroke, the core of the ischaemic tissue showed a progressive normalisation in the amount of free water, whereas the inner and outer border zones of the ischaemic cortex depicted a large, monotonous increase with time. The specific lesions in brain sections were verified by H&E and immunostaining. The tissue-specific diffusion and relaxometry MRI metrics in the ischaemic cortex were significantly different compared to their conventional counterpart. CONCLUSIONS Our results demonstrate that the free water fraction in FWE MRI with echo time dependence is a valuable biomarker, sensitive to the progressive degeneration in ischaemic tissue. We showed that part of the heterogeneity previously observed in conventional parameter maps can be accounted for by a heterogeneous distribution of free water in the tissue. Our results suggest that the temporal evolution of the free fluid fraction map at the core and inner border zone can be associated with the pathological changes linked to the evolution of vasogenic oedema. Namely, the homogeneous increase in free water one day after stroke and its tendency to normalise in the core of the ischaemic cortex starting three days after stroke, followed by a progressive increase in free water at the inner border zone from three to ten days after stroke. Finally, the monotonous increase in free fluid in the outer border zone of the cortex reflects the formation of fluid-filled cysts.
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Affiliation(s)
- Ezequiel Farrher
- Institute of Neuroscience and Medicine 4, INM-4, Forschungszentrum Jülich, Germany.
| | - Chia-Wen Chiang
- Institute of Biomedical Engineering and Nanomedicine, National Health Research Institutes, Miaoli, Taiwan
| | - Kuan-Hung Cho
- Institute of Biomedical Engineering and Nanomedicine, National Health Research Institutes, Miaoli, Taiwan
| | - Farida Grinberg
- Institute of Neuroscience and Medicine 4, INM-4, Forschungszentrum Jülich, Germany
| | - Richard P Buschbeck
- Institute of Neuroscience and Medicine 4, INM-4, Forschungszentrum Jülich, Germany
| | - Ming-Jye Chen
- Institute of Biomedical Engineering and Nanomedicine, National Health Research Institutes, Miaoli, Taiwan
| | - Kuo-Jen Wu
- Center for Neuropsychiatric Research, National Health Research Institutes, Miaoli, Taiwan
| | - Yun Wang
- Center for Neuropsychiatric Research, National Health Research Institutes, Miaoli, Taiwan
| | - Sheng-Min Huang
- Institute of Biomedical Engineering and Nanomedicine, National Health Research Institutes, Miaoli, Taiwan
| | - Zaheer Abbas
- Institute of Neuroscience and Medicine 4, INM-4, Forschungszentrum Jülich, Germany
| | - Chang-Hoon Choi
- Institute of Neuroscience and Medicine 4, INM-4, Forschungszentrum Jülich, Germany
| | - N Jon Shah
- Institute of Neuroscience and Medicine 4, INM-4, Forschungszentrum Jülich, Germany; Department of Neurology, RWTH Aachen University, Aachen, Germany; JARA - BRAIN - Translational Medicine, Aachen, Germany; Institute of Neuroscience and Medicine 11, INM-11, JARA, Forschungszentrum Jülich, Germany
| | - Li-Wei Kuo
- Institute of Biomedical Engineering and Nanomedicine, National Health Research Institutes, Miaoli, Taiwan; Institute of Medical Device and Imaging, National Taiwan University College of Medicine, Taipei, Taiwan.
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Deddens LH, van Tilborg GAF, van der Marel K, Hunt H, van der Toorn A, Viergever MA, de Vries HE, Dijkhuizen RM. In Vivo Molecular MRI of ICAM-1 Expression on Endothelium and Leukocytes from Subacute to Chronic Stages After Experimental Stroke. Transl Stroke Res 2017; 8:10.1007/s12975-017-0536-4. [PMID: 28509283 PMCID: PMC5590030 DOI: 10.1007/s12975-017-0536-4] [Citation(s) in RCA: 18] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/21/2016] [Revised: 04/17/2017] [Accepted: 04/24/2017] [Indexed: 11/26/2022]
Abstract
Molecular MRI allows in vivo detection of vascular cell adhesion molecules expressed on inflamed endothelium, which enables detection of specific targets for anti-neuroinflammatory treatment. We explored to what extent MR contrast agent targeted to intercellular adhesion molecule-1 (ICAM-1) could detect endothelial- and leukocyte-associated ICAM-1 expression at different stages after experimental stroke. Furthermore, we assessed potential interfering effects of ICAM-1-targeted contrast agent on post-stroke lesion growth. Micron-sized particles of iron oxide (MPIO) functionalized with control IgG (IgG-MPIO) or anti-ICAM-1 antibody (αICAM-1-MPIO) were administrated at 1, 2, 3, 7, and 21 days after unilateral transient middle cerebral artery occlusion in mice, followed by in vivo MRI and postmortem immunohistochemistry. αICAM-1-MPIO induced significant contrast effects in the lesion core on post-stroke days 1, 2, and 3, and in the lesion borderzone and contralesional tissue on post-stroke day 2. αICAM-1-MPIO were confined to ICAM-1-positive vessels and occasionally co-localized with leukocytes. On post-stroke day 21, abundant leukocyte-associated αICAM-1-MPIO was immunohistochemically detected in the lesion core. However, MRI-based detection of αICAM-1-MPIO-labeled leukocytes was confounded by pre-contrast MRI hypointensities, presumably caused by phagocytosed blood remains. IgG-MPIO did not induce significant MRI contrast effects at 1 h after injection. Lesion development was not affected by injection of αICAM-1-MPIO or IgG-MPIO. αICAM-1-MPIO are suitable for in vivo MRI of ICAM-1 expression on vascular endothelium and leukocytes at different stages after stroke. Development of clinically applicable MPIO may offer unique opportunities for MRI-based diagnosis of neuroinflammation and identification of anti-inflammatory targets in acute stroke patients.
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Affiliation(s)
- Lisette H Deddens
- Biomedical MR Imaging and Spectroscopy Group, Center for Image Sciences, University Medical Center Utrecht, Utrecht, The Netherlands
| | - Geralda A F van Tilborg
- Biomedical MR Imaging and Spectroscopy Group, Center for Image Sciences, University Medical Center Utrecht, Utrecht, The Netherlands
| | - Kajo van der Marel
- Biomedical MR Imaging and Spectroscopy Group, Center for Image Sciences, University Medical Center Utrecht, Utrecht, The Netherlands
| | - Hedi Hunt
- Biomedical MR Imaging and Spectroscopy Group, Center for Image Sciences, University Medical Center Utrecht, Utrecht, The Netherlands
| | - Annette van der Toorn
- Biomedical MR Imaging and Spectroscopy Group, Center for Image Sciences, University Medical Center Utrecht, Utrecht, The Netherlands
| | - Max A Viergever
- Biomedical MR Imaging and Spectroscopy Group, Center for Image Sciences, University Medical Center Utrecht, Utrecht, The Netherlands
| | - Helga E de Vries
- Department of Molecular Cell Biology and Immunology, VU University Medical Center, Amsterdam, The Netherlands
| | - Rick M Dijkhuizen
- Biomedical MR Imaging and Spectroscopy Group, Center for Image Sciences, University Medical Center Utrecht, Utrecht, The Netherlands.
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Sparacia G, Anastasi A, Speciale C, Agnello F, Banco A. Magnetic resonance imaging in the assessment of brain involvement in alcoholic and nonalcoholic Wernicke’s encephalopathy. World J Radiol 2017; 9:72-78. [PMID: 28298967 PMCID: PMC5334504 DOI: 10.4329/wjr.v9.i2.72] [Citation(s) in RCA: 10] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/24/2016] [Revised: 10/14/2016] [Accepted: 12/28/2016] [Indexed: 02/06/2023] Open
Abstract
AIM To present the typical and atypical magnetic resonance (MR) imaging findings of alcoholic and non-alcoholic Wernicke’s encephalopathy.
METHODS This study included 7 patients with Wernicke’s encephalopathy (2 men, 5 women; mean age, 52.3 years) that underwent brain MR examination between January 2012 and March 2016 in a single institution. Three patients were alcoholics and 4 patients were non-alcoholics. MR protocol included a T2-weighted sequence, a fluid attenuation inversion recovery (FLAIR) sequence, a diffusion-weighted sequence (b = 0 and 1000 s/mm2), and a contrast-enhanced MR sequence. All MR images were retrospectively reviewed at baseline and follow-up by two radiologists.
RESULTS All patients with Wernicke’s encephalopathy had bilateral areas showing high signal intensity on both T2-weighted and FLAIR MR images in the typical sites (i.e., the periaqueductal region and the tectal plate). Signal intensity abnormalities in the atypical sites (i.e., the cerebellum and the cerebellar vermis) were seen in 4 patients, all of which had no history of alcohol abuse. Six patients had areas with restricted diffusion in the typical and atypical sites. Four patients had areas showing contrast-enhancement in the typical and atypical sites. Follow-up MR imaging within 6 mo after therapy (intravenous administration of thiamine) was performed in 4 patients, and demonstrated a complete resolution of all the signal intensities abnormalities previously seen in all patients.
CONCLUSION MR imaging is valuable in the diagnosis of Wernicke’s encephalopathy particularly in patients presenting with atypical clinical symptoms, or with no history of alcohol abuse.
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Abstract
Supratentorial glioblastoma is the most frequent primary intracranial tumor in adults. Its localization in the cerebellum is extremely rare and such tumor presenting as cerebellopontine angle (CPA) mass in an adult is even rarer. We report the case of primary cerebellar glioblastoma in a 52-year-old woman who presented clinically and radiologically as CPA mass. Its clinical presentation, radiological findings, and treatment instituted are discussed in view of pertinent literature.
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Affiliation(s)
- Souvagya Panigrahi
- Department of Neurosurgery, S. C. B. Medical College and Hospital, Cuttack, Odisha, India
| | - Sudhansu S Mishra
- Department of Neurosurgery, S. C. B. Medical College and Hospital, Cuttack, Odisha, India
| | - Srikant Das
- Department of Neurosurgery, S. C. B. Medical College and Hospital, Cuttack, Odisha, India
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Göb E, Bittner S, Bobak N, Kraft P, Göbel K, Langhauser F, Homola GA, Brede M, Budde T, Meuth SG, Kleinschnitz C. The two-pore domain potassium channel KCNK5 deteriorates outcome in ischemic neurodegeneration. Pflugers Arch 2014; 467:973-87. [PMID: 25315980 DOI: 10.1007/s00424-014-1626-8] [Citation(s) in RCA: 10] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/01/2014] [Revised: 09/29/2014] [Accepted: 10/01/2014] [Indexed: 01/05/2023]
Abstract
Potassium channels can fulfill both beneficial and detrimental roles in neuronal damage during ischemic stroke. Earlier studies have characterized a neuroprotective role of the two-pore domain potassium channels KCNK2 (TREK1) and KCNK3 (TASK1). Protective neuronal hyperpolarization and prevention of intracellular Ca(2+) overload and glutamate excitotoxicity were suggested to be the underlying mechanisms. We here identify an unexpected role for the related KCNK5 channel in a mouse model of transient middle cerebral artery occlusion (tMCAO). KCNK5 is strongly upregulated on neurons upon cerebral ischemia, where it is most likely involved in the induction of neuronal apoptosis. Hypoxic conditions elevated neuronal expression levels of KCNK5 in acute brain slices and primary isolated neuronal cell cultures. In agreement, KCNK5 knockout mice had significantly reduced infarct volumes and improved neurologic function 24 h after 60 min of tMCAO and this protective effect was preserved at later stages of infarct development. KCNK5 deficiency resulted in a significantly reduced number of apoptotic neurons, a downregulation of pro-apoptotic and upregulation of anti-apoptotic factors. Results of adoptive transfer experiments of wild-type and Kcnk5 (-/-) immune cells into Rag1 (-/-) mice prior to tMCAO exclude a major role of KCNK5 in poststroke inflammatory reactions. In summary, KCNK5 expression is induced on neurons under ischemic conditions where it most likely exerts pro-apoptotic effects. Hence, pharmacological blockade of KCNK5 might have therapeutic potential in preventing ischemic neurodegeneration.
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Affiliation(s)
- Eva Göb
- Department of Neurology, University Clinics Würzburg, Würzburg, Germany
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Lakičević G, Arnautović K, Mužević D, Chesney T. Cerebellar glioblastoma multiforme presenting as hypertensive cerebellar hemorrhage: case report. J Neurol Surg Rep 2014; 75:e117-21. [PMID: 25097829 PMCID: PMC4110145 DOI: 10.1055/s-0034-1376198] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/30/2013] [Accepted: 03/15/2014] [Indexed: 11/06/2022] Open
Abstract
Background Cerebellar glioblastoma multiforme (GBM) is rare and presents with increased intracranial pressure and cerebellar signs. The recommended treatment is radical resection, if possible, with radiation and chemotherapy. Clinical Presentation A 53-year-old man presented with hypertensive cerebellar bleeding and a 2-day history of severe headaches, nausea, vomiting, gait instability, and elevated blood pressure. Computed tomography (CT) showed a left cerebellar hematoma with no obstruction of cerebrospinal fluid and no hydrocephalus. CT angiography showed no signs of pathologic blood vessels in the posterior cranial fossa. The patient was observed in the hospital and discharged. Subsequent CT showed complete hematoma resorption. Two weeks later, he developed headaches, nausea, and worsening cerebellar symptoms. Magnetic resonance imaging (MRI) showed a 4-cm diameter tumor in the left cerebellar hemisphere where the hemorrhage was located. The tumor was radically resected and diagnosed as GBM. The patient underwent radiation and chemotherapy. At a follow-up of 1.5 years, MRIs showed no tumor recurrence. Conclusion Hypertensive cerebellar hemorrhage may be the first presentation of underlying tumor, specifically GBM. Patients undergoing surgery for cerebellar hemorrhage should have clot specimens sent for histologic examination and have pre- and postcontrast MRIs. Patients not undergoing surgery should have MRIs done after hematoma resolution to rule out underlying tumor.
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Affiliation(s)
- Goran Lakičević
- Department of Neurosurgery, University Hospital, Mostar, Bosnia and Herzegovina
| | - Kenan Arnautović
- Semmes-Murphey Clinic, and Department of Neurosurgery, University of Tennessee Health Science Center, Memphis, Tennessee, United States
| | - Dario Mužević
- Department of Neurosurgery, Osijek University School of Medicine, Osijek, Croatia
| | - Thomas Chesney
- Pathology Group of Midsouth, Memphis, Tennessee, United States
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Regulatory T cells are strong promoters of acute ischemic stroke in mice by inducing dysfunction of the cerebral microvasculature. Blood 2012; 121:679-91. [PMID: 23160472 DOI: 10.1182/blood-2012-04-426734] [Citation(s) in RCA: 289] [Impact Index Per Article: 22.2] [Reference Citation Analysis] [Abstract] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/14/2022] Open
Abstract
We have recently identified T cells as important mediators of ischemic brain damage, but the contribution of the different T-cell subsets is unclear. Forkhead box P3 (FoxP3)-positive regulatory T cells (Tregs) are generally regarded as prototypic anti-inflammatory cells that maintain immune tolerance and counteract tissue damage in a variety of immune-mediated disorders. In the present study, we examined the role of Tregs after experimental brain ischemia/reperfusion injury. Selective depletion of Tregs in the DEREG mouse model dramatically reduced infarct size and improved neurologic function 24 hours after stroke and this protective effect was preserved at later stages of infarct development. The specificity of this detrimental Treg effect was confirmed by adoptive transfer experiments in wild-type mice and in Rag1(-/-) mice lacking lymphocytes. Mechanistically, Tregs induced microvascular dysfunction in vivo by increased interaction with the ischemic brain endothelium via the LFA-1/ICAM-1 pathway and platelets and these findings were confirmed in vitro. Ablation of Tregs reduced microvascular thrombus formation and improved cerebral reperfusion on stroke, as revealed by ultra-high-field magnetic resonance imaging at 17.6 Tesla. In contrast, established immunoregulatory characteristics of Tregs had no functional relevance. We define herein a novel and unexpected role of Tregs in a primary nonimmunologic disease state.
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Kininogen deficiency protects from ischemic neurodegeneration in mice by reducing thrombosis, blood-brain barrier damage, and inflammation. Blood 2012; 120:4082-92. [PMID: 22936662 DOI: 10.1182/blood-2012-06-440057] [Citation(s) in RCA: 99] [Impact Index Per Article: 7.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/31/2022] Open
Abstract
Thrombosis and inflammation are hallmarks of ischemic stroke still unamenable to therapeutic interventions. High-molecular-weight kininogen (KNG) is a central constituent of the contact-kinin system which represents an interface between thrombotic and inflammatory circuits and is critically involved in stroke development. Kng(-/-) mice are protected from thrombosis after artificial vessel wall injury and lack the proinflammatory mediator bradykinin. We investigated the consequences of KNG deficiency in models of ischemic stroke. Kng(-/-) mice of either sex subjected to transient middle cerebral artery occlusion developed dramatically smaller brain infarctions and less severe neurologic deficits without an increase in infarct-associated hemorrhage. This protective effect was preserved at later stages of infarction as well as in elderly mice. Targeting KNG reduced thrombus formation in ischemic vessels and improved cerebral blood flow, and reconstitution of KNG-deficient mice with human KNG or bradykinin restored clot deposition and infarct susceptibility. Moreover, mice deficient in KNG showed less severe blood-brain barrier damage and edema formation, and the local inflammatory response was reduced compared with controls. Because KNG appears to be instrumental in pathologic thrombus formation and inflammation but dispensable for hemostasis, KNG inhibition may offer a selective and safe strategy for combating stroke and other thromboembolic diseases.
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Changes in T2 relaxation time after stroke reflect clearing processes. Neuroimage 2012; 61:780-5. [DOI: 10.1016/j.neuroimage.2012.04.023] [Citation(s) in RCA: 18] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/20/2012] [Accepted: 04/04/2012] [Indexed: 11/18/2022] Open
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Neuroimaging findings in acute Wernicke's encephalopathy: review of the literature. AJR Am J Roentgenol 2009; 192:501-8. [PMID: 19155417 DOI: 10.2214/ajr.07.3959] [Citation(s) in RCA: 190] [Impact Index Per Article: 11.9] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/16/2022]
Abstract
OBJECTIVE Wernicke's encephalopathy is an acute neurological syndrome resulting from thiamine (vitamin B1) deficiency. Early recognition is important because timely thiamine supplementation can reverse the clinical features of the disease. The aim of this article is to provide an update on the typical and atypical neuroimaging findings of the acute phase of the disease. CONCLUSION Wernicke's encephalopathy is characterized by a quite distinct pattern of MR alterations, which include symmetrical alterations in the thalami, mamillary bodies, tectal plate, and periaqueductal area, but atypical alterations may also been seen. A thorough knowledge of the neuroimaging findings of Wernicke's encephalopathy will assist in arriving at an early diagnosis, thus reducing the morbidity and mortality associated with this disease.
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Zuccoli G, Santa Cruz D, Bertolini M, Rovira A, Gallucci M, Carollo C, Pipitone N. MR imaging findings in 56 patients with Wernicke encephalopathy: nonalcoholics may differ from alcoholics. AJNR Am J Neuroradiol 2008; 30:171-6. [PMID: 18945789 DOI: 10.3174/ajnr.a1280] [Citation(s) in RCA: 176] [Impact Index Per Article: 10.4] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/16/2022]
Abstract
BACKGROUND AND PURPOSE Wernicke encephalopathy (WE) is a severe neurologic disorder resulting from dietary vitamin B(1) deficiency. This study was undertaken to analyze and compare MR imaging findings and neurologic manifestations at clinical presentations of patients with WE with and without a history of alcohol abuse. MATERIALS AND METHODS WE patients were identified using diagnostic neurologic data bases. Fifty-six patients (29 females, 27 males) diagnosed between 1999 and 2008 with WE who improved within 1 month from the onset of thiamine administration were included in the analysis. Patients' records were reviewed for clinical manifestations and imaging studies' findings. MR imaging was performed in the acute phase of the disease at a field strength of 1T (16 patients) and 1.5T (40 patients). All MR images were of acceptable to good quality and were retrospectively reviewed. We compared imaging findings and clinical presentation in the alcoholic (AL) group versus the non-alcoholic (NA) group using the 2-tailed Fisher exact test and the Phi coefficient as appropriate. RESULTS Forty-three percent of the patients were in the AL group, whereas 57% were in the NA group. Eighty-nine percent showed changes in consciousness, 75% had ocular manifestations, and 54% had ataxia. On MR imaging, 80% of the patients had evidence of symmetric lesions in the medial thalami and in the periventricular region of the third ventricle; 59%, in the periaqueductal area; 45%, in the mamillary bodies; 36%, in the tectal plate; and 7%, in the periventricular gray matter located anteriorly to the fourth ventricle. Signal-intensity alterations in areas considered atypical for the disease were noted only in the NA group and always in association with the typical findings. Contrast enhancement of the thalamus and mamillary bodies was significantly associated with alcohol abuse. CONCLUSIONS Contrast enhancement in the mamillary bodies and thalamus is a typical finding of the disease in AL patients. Atypical MR imaging findings characterize NA patients.
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Affiliation(s)
- G Zuccoli
- Department of Radiology, Arcispedale Santa Maria Nuova, Reggio Emilia, Italy.
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Hur H, Jung S, Jung TY, Kim IY. Cerebellar glioblastoma multiforme in an adult. J Korean Neurosurg Soc 2008; 43:194-7. [PMID: 19096643 DOI: 10.3340/jkns.2008.43.4.194] [Citation(s) in RCA: 22] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/02/2007] [Accepted: 04/07/2008] [Indexed: 11/27/2022] Open
Abstract
Primary cerebellar glioblastoma multiforme (GBM) is a rare tumor in adults that accounts for just 1% of all cases of GBM. Due to their rarity, cerebellar GBMs are not yet completely understood about the pathogenesis and the prognosis. Here, we present a case of GBM in a 69-year-old man. Neurologic examination revealed the presence of cerebellar signs. Magnetic resonance imaging (MRI) showed a 4.5 x 3.6 cm-sized, ill-defined, heterogeneously enhancing mass in the left cerebellum and two patchy hyperintense lesions in the right cerebellum with minimal enhancement. After operation, glioblastoma was histologically confirmed. Postoperative radiotherapy with concomitant and adjuvant temozolomide chemotherapy was subsequently followed. Here, a case of unusual GBM in the cerebellum is reported with review of literature regarding the pathogenesis, the differential diagnosis and prognosis. There was no evidence of recurrence during postoperative one year. This patient showed a good prognosis in spite of the multiple lesions.
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Affiliation(s)
- Hyuk Hur
- Department of Neurosurgery, Chonnam National University Hwasun Hospital & Medical School, Hwasun, Korea
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13
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Zuccoli G, Gallucci M, Capellades J, Regnicolo L, Tumiati B, Giadás TC, Bottari W, Mandrioli J, Bertolini M. Wernicke encephalopathy: MR findings at clinical presentation in twenty-six alcoholic and nonalcoholic patients. AJNR Am J Neuroradiol 2007; 28:1328-31. [PMID: 17698536 PMCID: PMC7977668 DOI: 10.3174/ajnr.a0544] [Citation(s) in RCA: 114] [Impact Index Per Article: 6.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/18/2022]
Abstract
BACKGROUND AND PURPOSE Wernicke encephalopathy is a severe neurologic disorder that results from a dietary vitamin B1 deficiency. It is characterized by changes in consciousness, ocular abnormalities, and ataxia. This study was undertaken to analyze and compare findings on MR imaging and neurologic symptoms at clinical presentations of patients with Wernicke encephalopathy with and without a history of alcohol abuse. MATERIALS AND METHODS A multicenter study group retrospectively reviewed MR brain imaging findings, clinical histories, and presentations of 26 patients (14 female, 12 male) diagnosed between 1999 and 2006 with Wernicke encephalopathy. The age range was 6-81 years (mean age, 46 .6+/-19 years). RESULTS Fifty percent of the patients had a history of alcohol abuse, and 50% had no history of alcohol abuse. Eighty percent showed changes in consciousness, 77% had ocular symptoms, and 54% had ataxia. Only 38% of the patients showed the classic triad of the disease at clinical presentation. At MR examination, 85% of the patients showed symmetric lesions in the medial thalami and the periventricular region of the third ventricle, 65% in the periaqueductal area, 58% in the mamillary bodies, 38% in the tectal plate, and 8% in the dorsal medulla. Contrast enhancement of the mamillary bodies was statistically positively correlated with the alcohol abuse group. CONCLUSIONS Our study confirms the usefulness of MR in reaching a prompt diagnosis of Wernicke encephalopathy to avoid irreversible damage to brain tissue. Contrast enhancement in the mamillary bodies is a typical finding of the disease in the alcoholic population.
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Affiliation(s)
- G Zuccoli
- Department of Radiology, Intensive Care Unit, Arcispedale Santa Maria Nuova, Reggio Emilia, Italy, and Magnetic Resonance Unit, University Hospital of Badalona, Barcelona, Spain.
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Danchaivijitr N, Wakeham NR, Patel MC, McEvoy AW, Van Dellen J, Waldman AD. Subacute cerebellar infarct mimicking meningioma. Clin Radiol 2004; 59:531-3. [PMID: 15145724 DOI: 10.1016/j.crad.2004.01.003] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/26/2022]
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Lin SP, Schmidt RE, McKinstry RC, Ackerman JJH, Neil JJ. Investigation of mechanisms underlying transient T2 normalization in longitudinal studies of ischemic stroke. J Magn Reson Imaging 2002; 15:130-6. [PMID: 11836767 DOI: 10.1002/jmri.10052] [Citation(s) in RCA: 17] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/06/2022] Open
Abstract
PURPOSE To determine if the phenomenon of transient normalization of T2 relaxation in the subacute stage of ischemic stroke is associated with either magnetic susceptibility effects secondary to hemorrhage or changes in tissue water content. MATERIALS AND METHODS We utilized a rat model of transient, focal, cerebral ischemia. The possibility of hemorrhage was evaluated with T2*-weighted (T2*W) imaging and histology. Changes in water content were assessed by brain wet-to-dry weight. RESULTS Susceptibility effects were not evident in T2*W images, and neither red blood cells nor unchelated Fe(III) was found in hematoxylin and eosin (H-E)- or Prussian Blue-stained sections, respectively. However, between the peak of T2 contrast and the point of transient T2 normalization, water content consistently decreased by an average of 3%. CONCLUSION Transient T2 normalization is associated with normalization of water content and can occur without evidence of hemorrhage.
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Affiliation(s)
- Shao-Pow Lin
- Washington University School of Medicine, St. Louis, Missouri 63110, USA
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16
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Pereira AC, Doyle VL, Clifton A, Howe FA, Griffiths JR, Brown MM. Case reports. The transient disappearance of cerebral infarction on T(2)Weighted MRI. Clin Radiol 2000; 55:725-7. [PMID: 10988057 DOI: 10.1053/crad.2000.0118] [Citation(s) in RCA: 11] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/11/2022]
Affiliation(s)
- A C Pereira
- Division of Clinical Neuroscience, Institute of Neurology, University College London, UK
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Neumann-Haefelin T, Kastrup A, de Crespigny A, Yenari MA, Ringer T, Sun GH, Moseley ME. Serial MRI after transient focal cerebral ischemia in rats: dynamics of tissue injury, blood-brain barrier damage, and edema formation. Stroke 2000; 31:1965-72; discussion 1972-3. [PMID: 10926965 DOI: 10.1161/01.str.31.8.1965] [Citation(s) in RCA: 259] [Impact Index Per Article: 10.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/16/2022]
Abstract
BACKGROUND AND PURPOSE With the advent of thrombolytic therapy for acute stroke, reperfusion-associated mechanisms of tissue injury have assumed greater importance. In this experimental study, we used several MRI techniques to monitor the dynamics of secondary ischemic damage, blood-brain barrier (BBB) disturbances, and the development of vasogenic edema during the reperfusion phase after focal cerebral ischemia in rats. METHODS Nineteen Sprague-Dawley rats were subjected to transient middle cerebral artery occlusion of 30 minutes, 60 minutes, or 2.5 hours with the suture occlusion model. MRI, including diffusion-weighted imaging (DWI), T2-weighted imaging, perfusion-weighted imaging, and T1-weighted imaging, was performed 5 to 15 minutes before reperfusion, as well as 0.5, 1.5, and 2.5 hours and 1, 2, and 7 days after withdrawal of the suture. Final infarct size was determined histologically at 7 days. RESULTS In the 30-minute ischemia group (and partially also after 60 minutes), DWI abnormalities reversed transiently during the early reperfusion period but recurred after 1 day, probably due to secondary ischemic damage. After 2.5 hours of ischemia, DWI abnormalities no longer reversed, and signal intensity on both DWI and T2-weighted images increased rapidly in the previously ischemic region due to BBB damage (enhancement on postcontrast T1-weighted images) and edema formation. Early BBB damage during reperfusion was found to be predictive of relatively pronounced edema at subacute time points and was probably related to the increased mortality rates in this experimental group (3 of 7). CONCLUSIONS Reperfusion after short periods of ischemia (30 to 60 minutes) appears to be mainly complicated by secondary ischemic damage as shown by the delayed recurrence of the DWI lesions, whereas BBB damage associated with vasogenic edema becomes a dominant factor with longer occlusion times (2.5 hours).
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Affiliation(s)
- T Neumann-Haefelin
- Department of Radiology, Lucas MRS/MRI Center, Stanford Stroke Center, Stanford University, CA, USA.
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Okamoto K, Ito J, Furusawa T, Sakai K, Watanabe M, Tokiguchi S. Small cortical infarcts mimicking metastatic tumors. Clin Imaging 1998; 22:333-8. [PMID: 9755395 DOI: 10.1016/s0899-7071(98)00025-4] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/30/2022]
Abstract
Small cortical enhancing lesions mimicking metastases were demonstrated on contrast imaging in three patients without specific neurologic deficits corresponding to the lesions. One patient had a long carcinoma. However, all had cardiac arrhythmias known as major sources of cerebral emboli. Two had early cerebral infarcts and ischemic heart diseases. The lesions disappeared spontaneously on follow-up studies. They were subsequently presumed to be small infarcts. Clinical information and follow-up examinations are important to differentiate these small cortical lesions from metastases.
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Affiliation(s)
- K Okamoto
- Department of Radiology, School of Medicine, Niigata University, Japan
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Gröhn OH, Lukkarinen JA, Oja JM, van Zijl PC, Ulatowski JA, Traystman RJ, Kauppinen RA. Noninvasive detection of cerebral hypoperfusion and reversible ischemia from reductions in the magnetic resonance imaging relaxation time, T2. J Cereb Blood Flow Metab 1998; 18:911-20. [PMID: 9701353 DOI: 10.1097/00004647-199808000-00012] [Citation(s) in RCA: 76] [Impact Index Per Article: 2.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/26/2022]
Abstract
The hypothesis was tested that hypoperfused brain regions, such as the ischemic penumbra, are detectable by reductions in absolute transverse relaxation time constant (T2) using magnetic resonance imaging (MRI). To accomplish this, temporal evolution of T2 was measured in several models of hypoperfusion and focal cerebral ischemia in the rat at 9.4 T. Occurrence of acute ischemia was determined through the absolute diffusion constant D(av) = 1/3 TraceD, while perfusion was assessed by dynamic contrast imaging. Three types of regions at risk of infarction could be distinguished: (1) areas with reduced T2 (4% to 15%, all figures relative to contralateral hemisphere) and normal D(av), corresponding to hypoperfusion without ischemia; (2) areas with both reduced T2 (4% to 12%) and D(av) (22% to 49%), corresponding to early hypoperfusion with ischemia; (3) areas with increased T2 (2% to 9%) and reduced D(av) (28% to 45%), corresponding to irreversible ischemia. In the first two groups, perfusion-deficient regions detected by bolus tracking were similar to those with initially reduced T2. In the third group, bolus tracking showed barely detectable arrival of the tracer in the region where D(av) was reduced. We conclude that T2 reduction in acute ischemia can unambiguously identify regions at risk and potentially discriminate between reversible and irreversible hypoperfusion and ischemia.
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Affiliation(s)
- O H Gröhn
- NMR Research Group, A.I. Virtanen Institute, University of Kuopio, Finland
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Mathews VP, Caldemeyer KS, Ulmer JL, Nguyen H, Yuh WT. Effects of contrast dose, delayed imaging, and magnetization transfer saturation on gadolinium-enhanced MR imaging of brain lesions. J Magn Reson Imaging 1997; 7:14-22. [PMID: 9039589 DOI: 10.1002/jmri.1880070104] [Citation(s) in RCA: 37] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/03/2023] Open
Abstract
This paper discusses the types of paramagnetic agents available for clinical brain imaging and reviews investigations that have sought to optimize the use of these agents by varying the administered dose, delaying the imaging time after contrast administration, and altering image contrast by using magnetization transfer saturation pulses.
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Affiliation(s)
- V P Mathews
- Department of Radiology, Indiana University School of Medicine, Indianapolis, USA
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Cinnamon J, Viroslav AB, Dorey JH. CT and MRI diagnosis of cerebrovascular disease: going beyond the pixels. Semin Ultrasound CT MR 1995; 16:212-36. [PMID: 7654410 DOI: 10.1016/0887-2171(95)90019-5] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/26/2023]
Abstract
Cerebrovascular disease is one of the leading causes of morbidity and mortality in the United States, with an incidence of approximately 500,000 cases of stroke per year. Tremendous strides in the diagnosis of stroke have been made in recent years, although the main diagnostic tools available remain CT, MRI, and MR angiography. Because new treatment options are being developed, it has become imperative to analyze these anatomic studies more intensively and critically, with an eye toward eliciting vital pathophysiological information. This article reviews various imaging findings in that light and offers a perspective on the radiologist's role in the management of patients with these conditions.
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Affiliation(s)
- J Cinnamon
- Department of Radiology, Emory University School of Medicine, Atlanta, GA, USA
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Asato R, Okumura R, Miki Y, Konishi J. MR T2-weighted image of subacute cerebral infarct can be isointense to the surrounding brain: MR fogging in cerebral infarct. ACTA ACUST UNITED AC 1994. [DOI: 10.1007/bf01766089] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/01/2022]
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