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33 results of 12 texts with exact phrase : 'inflammation'.

1. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 1, 2005, No. 2 , , ,

Noninvasive imaging of carotid plaque inflammation.
Trivedi R, King U, Graves M, et al. Noninvasive imaging of carotid plaque inflammation.
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2. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 3, 2007, No. 1 , , ,

Inflammation in stroke and focal cerebral ischemia.
Huang J, Upadhyay UM, Tamargo RJ. Inflammation in stroke and focal cerebral ischemia.
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3. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 5, 2009, No. 1 , , ,

Modern Aspects of Cutaneous Neurogenic Inflammation.
nder S, Seeliger S, Ansel JC, Schmelz M, Luger T. Modern Aspects of Cutaneous Neurogenic Inflammation.
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4. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 7, 2011, No. 2 , , ,

Furthermore, interleukin 17 (IL-17)-producing T cells (Th17 cells) believed to be key mediators of inflammation in MS, have been shown to be defined by a central memory T-cell phenotype and their numbers are reduced peripherally by fingolimod [13].
S1P1 [17], leads to selective retention in lymph nodes of circulating B cells and naive and central memory T lymphocytes that express CCR7, largely sparing effector memory T cells that do not express CCR7 [18]. The specific retention of central memory T cells is thought to be one of the key mechanisms of fingolimod’s therapeutic effect because more than 90% of T cells that accumulate in CSF in MS patients express a central memory phenotype [10]. Furthermore, interleukin 17 (IL-17)-producing T cells (Th17 cells) believed to be key mediators of inflammation in MS, have been shown to be defined by a central memory T-cell phenotype and their numbers are reduced peripherally by fingolimod [13]. Moreover, individuals receiving fingolimod 0.5 mg retain the capacity for clinically relevant increase in T-cell-dependent and T-cell-independent antibody levels in response to novel antigens [20]. The effect of fingolimod down-modulation in MS
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5. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 9, 2013, No. 1 , , ,

He coined the term “CCSVI” (chronic cerebrospinal venous insufficiency) in analogy to perivenous inflammation in chronic venous insufficiency of the legs.
In 2006, the vascular surgeon Paolo Zamboni re-introduced the pathophysiological concept of venous outflow pathology ultimately leading to multiple sclerosis (MS) [71]. He based this concept (or “the big idea”) on the well-known histopathologic features of a perivenous localization of inflammatory MS lesions. He coined the term “CCSVI” (chronic cerebrospinal venous insufficiency) in analogy to perivenous inflammation in chronic venous insufficiency of the legs. While Zamboni’s approach does not challenge the commonly accepted understanding of MS immunopathology [37], it does relegate it to the final stage in the disease cascade. According to the “CCSVI” concept, MS pathology starts with intracranial venous stasis based on a proximal obstruction of the main cervical and/or thoracic veins. This leads to perivenous diapedesis of erythrocytes in the white matter with subsequent release of iron, the actual catalyst of the widely known and accepted immune cascade [37]. The theory of venous outflow changes reaches back to the times of Charcot, who in 1868 provided an early histopathological description of perivenous inflammation in MS [16]. In 1947, Putnam, believing that thrombosis of the cerebral veins was a common finding in MS patients published preliminary results of treatment using dicoumarin in MS patients after experiments using induced sinus thrombosis in primates [50].
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The theory of venous outflow changes reaches back to the times of Charcot, who in 1868 provided an early histopathological description of perivenous inflammation in MS [16].
He based this concept (or “the big idea”) on the well-known histopathologic features of a perivenous localization of inflammatory MS lesions. He coined the term “CCSVI” (chronic cerebrospinal venous insufficiency) in analogy to perivenous inflammation in chronic venous insufficiency of the legs. While Zamboni’s approach does not challenge the commonly accepted understanding of MS immunopathology [37], it does relegate it to the final stage in the disease cascade. According to the “CCSVI” concept, MS pathology starts with intracranial venous stasis based on a proximal obstruction of the main cervical and/or thoracic veins. This leads to perivenous diapedesis of erythrocytes in the white matter with subsequent release of iron, the actual catalyst of the widely known and accepted immune cascade [37]. The theory of venous outflow changes reaches back to the times of Charcot, who in 1868 provided an early histopathological description of perivenous inflammation in MS [16]. In 1947, Putnam, believing that thrombosis of the cerebral veins was a common finding in MS patients published preliminary results of treatment using dicoumarin in MS patients after experiments using induced sinus thrombosis in primates [50]. However, his findings have not been validated or revisited since this time. In 1986, Schelling posed the hypothesis that venous intracranial or intraspinal reflux plays a significant role in the development of MS [53]. Subsequently, Zamboni and colleagues published several studies which were meant to support the “CCSVI” hypothesis [67,69,70]. They applied catheter angiographies in order to demonstrate various extracranial venous outflow obstructions in the internal jugular veins (IJVs) or azygos veins (AVs) [66], and re-
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The big idea: iron-dependent inflammation in venous disease and proposed parallels in multiple sclerosis.
Zamboni P. The big idea: iron-dependent inflammation in venous disease and proposed parallels in multiple sclerosis.
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The impact of inflammation on the athogenesis and prognosis of ischemic stroke.
Nakase T, Yamazaki N, Ogura A, SuzukiA, Nagata K. The impact of inflammation on the athogenesis and prognosis of ischemic stroke.
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6. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 9, 2013, No. 2 , , ,

These initial studies have shown the potential of USPIO -enhanced MRI, 18F-FDG PET, IL2 scintigraphy, and low-density lipoprotein scintigraphy to identify inflammation, the potential of annexin A5 scintigraphy to identify cell death, and platelet scintigraphy to depict plaque thrombosis.
Currently, there are few in vivo human studies on functional imaging of carotid plaques. These initial studies have shown the potential of USPIO -enhanced MRI, 18F-FDG PET, IL2 scintigraphy, and low-density lipoprotein scintigraphy to identify inflammation, the potential of annexin A5 scintigraphy to identify cell death, and platelet scintigraphy to depict plaque thrombosis. Biomarkers have been shown to improve prediction independent of conventional risk factors. High sensitivity C-reactive protein (hs-CRP) and lipoprotein-phospholipase A2 (PLA2) are two such candidates
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atherosclerosis, inflammation, vulnerable plaque.
atherosclerosis, inflammation, vulnerable plaque.
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7. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 11, 2015, No. 2 , , ,

The disease debuted with a general infectious syndrome, leftsided exophthalmos with transient visual disturbances and local inflammation of the conjunctiva.
The present report describes a 35-year-old man with a history of intermittent pain in the left retrobulbar area lasting approximately six months. The disease debuted with a general infectious syndrome, leftsided exophthalmos with transient visual disturbances and local inflammation of the conjunctiva. The condition was considered initially as conjunctivitis, and later – as TolosaHunt syndrome, which was successfully treated with eye drops, nonsteroidal anti-inflammatory drugs (NSAIDs), antibiotics and three courses of corticosteroids. For the final diagnosis prospective clinical and neuroimaging investigations (2D/3D/4D multimodal neurosonology, CT and MRI of the head) were performed.
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The multimodal neurosonology has a limited diagnostic value for imaging the retrobulbar granulomatous inflammation but contributes for the noninvasive assessment of the optic disc and optic nerve changes, associated with the disease.
Our study confirms that the diagnosis of Tolosa-Hunt syndrome is difficult and based on exclusion of other causes of painful ophthalmoplegia (e.g. orbital pseudotumor, thrombosis of the cavernous sinus, collagenosis, lymphoma, metastasis at al.). The complex use of clinical, laboratory and neuroimaging methods allowed prospective follow-up of the clinical evolution of the syndrome. The multimodal neurosonology has a limited diagnostic value for imaging the retrobulbar granulomatous inflammation but contributes for the noninvasive assessment of the optic disc and optic nerve changes, associated with the disease.
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8. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 12, 2016, No. 1 , , ,

The disease debuted with a general infectious syndrome, left-sided exophthalmos with transient visual disturbances and local inflammation of the conjunctiva.
The present report describes a 35-year-old man with a history of intermittent pain in the left retrobulbar area lasting approximately six months. The disease debuted with a general infectious syndrome, left-sided exophthalmos with transient visual disturbances and local inflammation of the conjunctiva. The condition was considered initially as conjunctivitis, and later – as Tolosa-Hunt syndrome, which was successfully treated with eye drops, nonsteroidal anti-inflammatory drugs (NSAIDs), antibiotics and corticosteroids. For the final diagnosis prospective clinical and neuroimaging investigations (2D/3D/4D multimodal neurosonology, CT and MRI of the head) were performed.
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Tolosa-Hunt syndrome is a rare condition characterized by episodic painful ophthalmoplegia caused by nonspecific granulomatous inflammation of the cavernous sinus, superior orbital fissure and/or orbit [4].
Tolosa-Hunt syndrome is a rare condition characterized by episodic painful ophthalmoplegia caused by nonspecific granulomatous inflammation of the cavernous sinus, superior orbital fissure and/or orbit [4]. It was written for the first time in 1954 by Tolosa [11]. In 1961, Hunt describes another 6 cases [6]. The diagnosis of Tolosa-Hunt syndrome is based on International Headache Society’s criteria [5]:
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The disease debuted with a general infectious syndrome, left-sided exophthalmos with transient visual disturbances and local inflammation of the conjunctiva [12].
retrobulbar area lasting approximately six months. The disease debuted with a general infectious syndrome, left-sided exophthalmos with transient visual disturbances and local inflammation of the conjunctiva [12]. The patient was hospitalized in the Clinic of Ophthalmology and diagnosed with acute inflammation of the orbit. There were performed parallel clinical, paraclinical and ophthalmic research. Afterward he was examined three times by performing control and neuroimaging studies. It was made a CT brain and orbits scan with contrast and MRI of the head with MR – angiography. Multimodal neuroophthalmo-sonography with 2D/3D/4D imaging of the vitreous body, optic disc was performed, standard measurement of the complex optic nerve/sheath diameters and their ratio in 3 mm behind the globe, retrobulbar space and B-flow imaging of the ophthalmic and central retinal artery [2].
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The patient was hospitalized in the Clinic of Ophthalmology and diagnosed with acute inflammation of the orbit.
retrobulbar area lasting approximately six months. The disease debuted with a general infectious syndrome, left-sided exophthalmos with transient visual disturbances and local inflammation of the conjunctiva [12]. The patient was hospitalized in the Clinic of Ophthalmology and diagnosed with acute inflammation of the orbit. There were performed parallel clinical, paraclinical and ophthalmic research. Afterward he was examined three times by performing control and neuroimaging studies. It was made a CT brain and orbits scan with contrast and MRI of the head with MR – angiography. Multimodal neuroophthalmo-sonography with 2D/3D/4D imaging of the vitreous body, optic disc was performed, standard measurement of the complex optic nerve/sheath diameters and their ratio in 3 mm behind the globe, retrobulbar space and B-flow imaging of the ophthalmic and central retinal artery [2]. The patient was treated successfully with eye drops, nonsteroidal anti-inflammatory drugs (NSAIDs), antibiotics and corticosteroids.
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Its relation to indolent inflammation of the cavernous sinus.
Hunt WE, Meagher JN, LeFever HE, Zeman W. Painful ophthalmoplegia. Its relation to indolent inflammation of the cavernous sinus.
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9. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 12, 2016, No. 2 , , ,

Most commonly SOVT is found in cases of orbital congestion such as orbital cellulitis, idiopathic orbital inflammation, thyroid-related orbitopathy, and
Superior ophthalmic vein thrombosis (SOVT) is an uncommon and very rare condition, occurring secondary to various etiologies. Risk factors for SOVT can be local or systemic, usually including at least one factor from the Virchow's triad: hypercoagulability, hemodynamic changes, and endothelial injury/dysfunction [9]. It usually presents with globe dystopia, proptosis, periorbital edema, ophthalmoplegia, and occasionally diminished visual acuity. Most commonly SOVT is found in cases of orbital congestion such as orbital cellulitis, idiopathic orbital inflammation, thyroid-related orbitopathy, and
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Also, no signs of inflammation were observed in carotid, axillary, and subclavian arteries.
sinus (fig. 1). MR angiography showed normal findings of arterial vessels. Temporal artery color Doppler ultrasound was normal. Also, no signs of inflammation were observed in carotid, axillary, and subclavian arteries. Based on this findings giant cell (temporal) arteritis was excluded.
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SOVT may occur as a result of infection and inflammation, trauma, hypercoagulable states, neoplasm, and orbital crowding [7].
The exact pathogenesis, etiology and risk factors for SOVT are unclear. SOVT may occur as a result of infection and inflammation, trauma, hypercoagulable states, neoplasm, and orbital crowding [7]. lnfection is probably the most common cause of SOVT [5]. ln our case the patient had a fever, with normal leukocyte count, and slightly elevated
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Although these investigations are recommended if there are no signs of inflammation and infection, we conducted a broad spectrum of analyses, and found only high values of vWfAg, as mentioned above.
1n cases of SOVT of unknown origin, different authors suggest evaluation for hypercoagulable conditions, including factor V Leiden, prothrombin gene mutation, antithrombin 111, and lupus anticoagulant [1]. Although these investigations are recommended if there are no signs of inflammation and infection, we conducted a broad spectrum of analyses, and found only high values of vWfAg, as mentioned above.
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10. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 13, 2017, No. 2 , , ,

Overall favorable effect is observed on: lipid profiles, threshold for arrhythmias, platelet activity, inflammation and endothelial function, atherosclerosis and hypertension.
-3 polyunsaturated fatty acids (LCn3PUFAs): eicosapentaenoic acids (EPA), docosapentaenoic acid (DPA), docosahexaenoic acid (DHA) in fish are the key nutrients responsible for the cardioprotective benefits and CVD prevention. Beneficial effects of fish consumption on the risk of CVD are derived from synergistic effects among nutrients in fish. Fish is considered to be an excellent source of proteins with low saturated fat (taurine, arginine, glutamine-known to regulate cardiovascular function)' and some nutritious trace elements (selenium and calcium) which may directly or indirectly provide cardiovascular benefits, alone or in combination with LCn3PUFAs and vitamins (vitamin D and B). Interactions between LCn3PUFAs and other nutrients, including nutritious trace elements and vitamins and amino acids are important in reducing the risk of CVD. Overall favorable effect is observed on: lipid profiles, threshold for arrhythmias, platelet activity, inflammation and endothelial function, atherosclerosis and hypertension. The American Heart Association recommends eating fish (particularly fatty fish) at least 2 times a week. Fish consumption may be inversely associated with ischemic stroke but not with hemorrhagic stroke, because of the potential antiplatelet aggregation property of LCn3PUFAs. A meta-analysis of 8 independent prospective cohort studies which included 200575 subjects and 3491 stroke events showed that individuals with higher fish intake had lower risk of total stroke, compared with those who never consumed fish or ate fish less than once per month. The reduction in risk of total stroke was statistically significant for fish intake once per week; for individuals who ate fish 5 times or more per week, the risk of stroke was lowered by 31%. The risk of ischemic stroke was also significantly reduced by eating fish twice per month.
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Hypothermia has been subject of research in experimental ICH models in the recent past and several rodent studies have reported reduction in inflammation, oxidative damage, blood brain barrier disruption and perihemorrhagic edema using prolonged therapeutic hypothermia [12, 24, 35].
Hypothermia has been subject of research in experimental ICH models in the recent past and several rodent studies have reported reduction in inflammation, oxidative damage, blood brain barrier disruption and perihemorrhagic edema using prolonged therapeutic hypothermia [12, 24, 35]. The clinical application of mild therapeutic hypothermia (35°C for up to 10 days) in patients with large ICH has been investigated by one research group from Erlangen, Germany [27, 52]. The authors of those studies describe a marked reduction of perihemorrhagic edema evolution and a lower mortality in treated patients as compared to historical controls. Hypothermia in ICH is currently being further investigated in ongoing trials [26].
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11. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 14, 2018, No. 2 , , ,

Although IPNV contributes to the progression and rupture of atherosclerotic lesions, some conflicting data exist in the literature for the temporal association of intraplaque inflammation and neovascularization.
Although IPNV contributes to the progression and rupture of atherosclerotic lesions, some conflicting data exist in the literature for the temporal association of intraplaque inflammation and neovascularization. The limited number of patients in cited reports and in our study and the multifaceted pathophysiology of the atherosclerotic plaque may explain the absence of statistically significant correlation between plaque echogenicity, inflammation and IPNV.
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The limited number of patients in cited reports and in our study and the multifaceted pathophysiology of the atherosclerotic plaque may explain the absence of statistically significant correlation between plaque echogenicity, inflammation and IPNV.
Although IPNV contributes to the progression and rupture of atherosclerotic lesions, some conflicting data exist in the literature for the temporal association of intraplaque inflammation and neovascularization. The limited number of patients in cited reports and in our study and the multifaceted pathophysiology of the atherosclerotic plaque may explain the absence of statistically significant correlation between plaque echogenicity, inflammation and IPNV.
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There was no information about previous injuries, inflammation, tumors and swelling in the elbow joint or systemic diseases (diabetes, chronic renal failure, rheumatologic disorder or malignancy).
A 26-year-old man complaining of unilateral stiffness and tingling of the small and ring finger of his right hand, hand weakness and inability to hold objects is described. There was no information about previous injuries, inflammation, tumors and swelling in the elbow joint or systemic diseases (diabetes, chronic renal failure, rheumatologic disorder or malignancy). Physical examination revealed a positive Tinel’s sign and a negative Phalen's test. The EMG recordings were normal; the CT-scan showed normal anatomy of the elbow, forearm and hand. According to these parameters, the patient was diagnosed with first-degree CTS. A conservative therapeutic approach was indicated. Resting and restriction of the limb movements were recommended.
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12. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 15, 2019, No. 1 , , ,

The inflammation of the vascular wall often leads to concentric thickening, development of fibrosis and formation of thrombi.
Takayasu arteritis is an inflammatory disease involving the aorta and its branches, pulmonary and coronary arteries. The inflammation of the vascular wall often leads to concentric thickening, development of fibrosis and formation of thrombi. Vessels involved in the process are remodeled, stenotic or dilated up to formation of aneurysms. We present a rare case of a patient with bilateral aneurysms and stenoses of the carotid arteries, diagnosed with computed tomography angiography and magnetic resonance tomography. We discuss the potential of different imaging methods in the assessment of changes in the vascular wall in patients with Takayasu arteritis.
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Takayasu arteritis (TA) is a chronic inflammatory disease that affects the walls of large vessels – the aorta and its branches, pulmonary and coronary arteries, and is characterized by granulomatous inflammation (panarteritis), with intimal proliferation and fibrosis of the media and the adventitia [7, 13].
Takayasu arteritis (TA) is a chronic inflammatory disease that affects the walls of large vessels – the aorta and its branches, pulmonary and coronary arteries, and is characterized by granulomatous inflammation (panarteritis), with intimal proliferation and fibrosis of the media and the adventitia [7, 13]. Changes in the vascular wall lead to stenoses and aneurysm formation of involved vessels. The disease affects predominantly women in the second and third decade of life and can also occur in individuals of practically any age [12]. The clinical picture is often nonspecific which can result in delay of diagnosis and to complications [7]. Immunological tests are often ambiguous, and biopsy of large vessels is a difficult and risky
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of inflammation) (Fig. 2).
of inflammation) (Fig. 2). Identical changes in the vascular wall were also found along the course of the thoracic and suprarenal abdominal aorta. The thoracic aorta is dilated to a varying degree along its entire course with a maximal dilatation in the thoraco-abdominal segment (Fig. 3). The dimensions and extent of the thrombosis of carotid aneurysms are identical to those depicted by the CTA (Fig. 3). On the dynamic contrast-enhanced MR angiography an asynchronous, delayed at the left, filling of the carotid arteries is observed (Fig. 4). The findings correspond to panvasculitis with involvement of the aorta, including the aortic arc and its branches and formation of aneurysms and segmental stenoses, probably
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In our case signs of active inflammation, stenotic and occlusive changes, and formation of aneurysms are observed simultaneously.
Inflammatory changes in the vascular wall in cases of TA include edema, thickening and enhancement of the wall in the acute phase of the disease, followed by stenoses up to complete occlusion of the affected vessels. The formation of an aneurysm is considered a late complication of TA and is a result of fibrotic changes in media and adventitia [7, 13]. The parallel development of stenotic and occlusive changes and aneurysms is rare, especially at the first clinical manifestation [6, 9]. In our case signs of active inflammation, stenotic and occlusive changes, and formation of aneurysms are observed simultaneously. We speculate that this can be a sign of an aggressive development of the disease, which is also supported by the progression of changes observed despite the course of treatment.
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In the venous phase a so-called "double ring" enhancement could be observed due to edema of the intima and active inflammation in the media and adventitia [4, 8].
Computed tomography allows a non-invasive and high-resolution imaging of the aorta and its branches and provides information about the changes in the vascular wall [15]. The examination protocol in cases of suspected Takayasu disease should not be limited only to the CTA but should also include a native and venous phase scan. The pre-contrast CT images in cases of Takayasu disease may show an increased density of the vascular wall; in up to 27% of the cases, fine transmural calcifications [4] are also found. In the venous phase a so-called "double ring" enhancement could be observed due to edema of the intima and active inflammation in the media and adventitia [4, 8]. In our case, the patient was referred to CTA to assess the aneurysms of the carotid arteries and therefore the full protocol was not used and the changes in the vascular wall were not characterized in detail. However, the diffuse thickening of the wall of the common carotid arteries, the proximal segments of the internal carotid arteries and the aortic arc suggest a systemic vascular inflammatory disease.
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The application of contrast allows seeing enhancement in the vascular wall, which is a sign of active inflammation [1].
The high sensitivity and specificity of the MRI in Takayasu disease has been confirmed by several studies [5, 11, 14]. Depending on the techniques used, the sensitivity, specificity and accuracy of the method ranges from 91%, 81% and 86% respectively in the non-contrast angiography and up to 100% for contrast-enhanced angiography. The assessment accuracy of the grade of stenotic lesions reaches 98% when the latter technique is used. The application of contrast allows seeing enhancement in the vascular wall, which is a sign of active inflammation [1]. Highresolution morphological images give information about the thickness of the vascular wall and the type of changes: edema, hemorrhages, thrombi, and calcifications. The individual layers of the wall are clearly distinguishable; it is also possible to localize the different types of changes. Our case demonstrates the whole spectrum of changes in Takayasu disease: intimal edema, inflammation, hemorrhages and fibrosis in the media and adventitia, and wall thrombosis in the lumen of the aneurysms. MRT provides coverage of a larger volume within one examination without ionizing
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Our case demonstrates the whole spectrum of changes in Takayasu disease: intimal edema, inflammation, hemorrhages and fibrosis in the media and adventitia, and wall thrombosis in the lumen of the aneurysms.
Depending on the techniques used, the sensitivity, specificity and accuracy of the method ranges from 91%, 81% and 86% respectively in the non-contrast angiography and up to 100% for contrast-enhanced angiography. The assessment accuracy of the grade of stenotic lesions reaches 98% when the latter technique is used. The application of contrast allows seeing enhancement in the vascular wall, which is a sign of active inflammation [1]. Highresolution morphological images give information about the thickness of the vascular wall and the type of changes: edema, hemorrhages, thrombi, and calcifications. The individual layers of the wall are clearly distinguishable; it is also possible to localize the different types of changes. Our case demonstrates the whole spectrum of changes in Takayasu disease: intimal edema, inflammation, hemorrhages and fibrosis in the media and adventitia, and wall thrombosis in the lumen of the aneurysms. MRT provides coverage of a larger volume within one examination without ionizing
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