�ݺ�ߣshows by User: AbnaJ1

�ݺ�ߣshows by User: AbnaJ1 / http://www.slideshare.net/images/logo.gif �ݺ�ߣshows by User: AbnaJ1 / Wed, 28 Feb 2024 16:34:03 GMT �ݺ�ߣShare feed for �ݺ�ߣshows by User: AbnaJ1 RADIATION PHYSICS ON BOLTZMANN EQUATION.pptx /slideshow/radiation-physics-on-boltzmann-equationpptx/266541984 boltzmannequation-240228163403-b8a87f2a
The BTE is a statement that in the steady state, there is no net change in the distribution function f (r , k ,t) Which determines the probability of finding an electron at position r→ , crystal momentum This equation expresses the continuity equation in real space in the absence of forces, fields and collisions. The differential form of the diffusion process can be substituted as follows: The forces and fields equation can be written as: The Boltzmann equation can be obtained from these. The BTE includes derivatives of all the variables of the distribution function on the left hand side and of the equation and the collision terms appear on the right hand side of this equation. The first term in the equation (4) gives the explicit time dependence of the distribution function. This is needed for the solution of the ac driving forces or for impulse perturbations. BTE is solved using the following approximations: – (1) The perturbations due to the external fields and forces is assumed to be small so that the distribution function can be linearized as: → → → → BTE is solved using the following approximations: – (1) The perturbations due to the external fields and forces is assumed to be small so that the distribution function can be linearized as: → → → → The BTE includes derivatives of all the variables of the distribution function on the left hand side and of the equation and the collision terms appear on the right hand side of this equation. The first term in the equation (4) gives the explicit time dependence of the distribution function. This is needed for the solution of the ac driving forces or for impulse perturbations. Where f0 (E)is – The equilibrium distribution function (Fermi function) which depends only on the energy E f1(r,k) is the perturbation term giving the departure from equilibrium. (2) the collision term in the BTE is written in the relaxation time so that the system returns to the equilibrium uniformly:Where τ - relaxation time, is in general a function of crystal momentum i.e. τ = τ(k).]]>
The BTE is a statement that in the steady state, there is no net change in the distribution function f (r , k ,t) Which determines the probability of finding an electron at position r→ , crystal momentum This equation expresses the continuity equation in real space in the absence of forces, fields and collisions. The differential form of the diffusion process can be substituted as follows: The forces and fields equation can be written as: The Boltzmann equation can be obtained from these. The BTE includes derivatives of all the variables of the distribution function on the left hand side and of the equation and the collision terms appear on the right hand side of this equation. The first term in the equation (4) gives the explicit time dependence of the distribution function. This is needed for the solution of the ac driving forces or for impulse perturbations. BTE is solved using the following approximations: – (1) The perturbations due to the external fields and forces is assumed to be small so that the distribution function can be linearized as: → → → → BTE is solved using the following approximations: – (1) The perturbations due to the external fields and forces is assumed to be small so that the distribution function can be linearized as: → → → → The BTE includes derivatives of all the variables of the distribution function on the left hand side and of the equation and the collision terms appear on the right hand side of this equation. The first term in the equation (4) gives the explicit time dependence of the distribution function. This is needed for the solution of the ac driving forces or for impulse perturbations. Where f0 (E)is – The equilibrium distribution function (Fermi function) which depends only on the energy E f1(r,k) is the perturbation term giving the departure from equilibrium. (2) the collision term in the BTE is written in the relaxation time so that the system returns to the equilibrium uniformly:Where τ - relaxation time, is in general a function of crystal momentum i.e. τ = τ(k).]]> Wed, 28 Feb 2024 16:34:03 GMT /slideshow/radiation-physics-on-boltzmann-equationpptx/266541984 AbnaJ1@slideshare.net(AbnaJ1) RADIATION PHYSICS ON BOLTZMANN EQUATION.pptx AbnaJ1 The BTE is a statement that in the steady state, there is no net change in the distribution function f (r , k ,t) Which determines the probability of finding an electron at position r→ , crystal momentum This equation expresses the continuity equation in real space in the absence of forces, fields and collisions. The differential form of the diffusion process can be substituted as follows: The forces and fields equation can be written as: The Boltzmann equation can be obtained from these. The BTE includes derivatives of all the variables of the distribution function on the left hand side and of the equation and the collision terms appear on the right hand side of this equation. The first term in the equation (4) gives the explicit time dependence of the distribution function. This is needed for the solution of the ac driving forces or for impulse perturbations. BTE is solved using the following approximations: – (1) The perturbations due to the external fields and forces is assumed to be small so that the distribution function can be linearized as: → → → → BTE is solved using the following approximations: – (1) The perturbations due to the external fields and forces is assumed to be small so that the distribution function can be linearized as: → → → → The BTE includes derivatives of all the variables of the distribution function on the left hand side and of the equation and the collision terms appear on the right hand side of this equation. The first term in the equation (4) gives the explicit time dependence of the distribution function. This is needed for the solution of the ac driving forces or for impulse perturbations. Where f0 (E)is – The equilibrium distribution function (Fermi function) which depends only on the energy E f1(r,k) is the perturbation term giving the departure from equilibrium. (2) the collision term in the BTE is written in the relaxation time so that the system returns to the equilibrium uniformly:Where τ - relaxation time, is in general a function of crystal momentum i.e. τ = τ(k). <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/boltzmannequation-240228163403-b8a87f2a-thumbnail.jpg?width=120&height=120&fit=bounds" /><br> The BTE is a statement that in the steady state, there is no net change in the distribution function f (r , k ,t) Which determines the probability of finding an electron at position r→ , crystal momentum This equation expresses the continuity equation in real space in the absence of forces, fields and collisions. The differential form of the diffusion process can be substituted as follows: The forces and fields equation can be written as: The Boltzmann equation can be obtained from these. The BTE includes derivatives of all the variables of the distribution function on the left hand side and of the equation and the collision terms appear on the right hand side of this equation. The first term in the equation (4) gives the explicit time dependence of the distribution function. This is needed for the solution of the ac driving forces or for impulse perturbations. BTE is solved using the following approximations: – (1) The perturbations due to the external fields and forces is assumed to be small so that the distribution function can be linearized as: → → → → BTE is solved using the following approximations: – (1) The perturbations due to the external fields and forces is assumed to be small so that the distribution function can be linearized as: → → → → The BTE includes derivatives of all the variables of the distribution function on the left hand side and of the equation and the collision terms appear on the right hand side of this equation. The first term in the equation (4) gives the explicit time dependence of the distribution function. This is needed for the solution of the ac driving forces or for impulse perturbations. Where f0 (E)is – The equilibrium distribution function (Fermi function) which depends only on the energy E f1(r,k) is the perturbation term giving the departure from equilibrium. (2) the collision term in the BTE is written in the relaxation time so that the system returns to the equilibrium uniformly:Where τ - relaxation time, is in general a function of crystal momentum i.e. τ = τ(k).

RADIATION PHYSICS ON BOLTZMANN EQUATION.pptx from Dr Abna J

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0 Basic Chest X ray Views - AP, PA & Lateral etc . pptx /slideshow/basic-chest-x-ray-views-ap-pa-lateral-etc-pptx/264960795 chestxrayviews-231227194202-501fbdd3
PA PROJECTION Sit or stand upright. Positioned to minimize magnification of the anteriorly positioned heart and consequent obscuration of the lungs. Make sure the patient is standing straight and is equally distributing the weight of the body on both feet. The upright position is preferred for the following reasons: It prevents engorgement (an excess of blood) of pulmonary vessels. It allows full expansion of the lungs To visualize possible air and fluid levels in the chest. An upright chest film is preferred over an upright abdominal film for the diagnosis of pneumoperitoneum (free air in the abdominal cavity). Ask the patient to move the shoulders forward and downward, so that the chest wall and both shoulders are in contact with the cassette. This helps to carry the clavicles below the lung apices. It is very important to minimize breast shadows. Ask the patient to pull the breasts upward and laterally (outwards), then remove her hands as she leans against the cassette holder to keep them in position. Rotation Even a small degree of rotation distorts the mediastinal borders, and the lung nearest the film will appear less translucent. The following points should be stressed to obtain a true PA view (without rotation): Ensure that the patient is standing evenly on both feet. Both shoulders should be rolled forward and downward. The chest radiograph should be well centred so that the medial ends of the clavicle are equidistant from the vertebral spinous processes at T4/5. CENTRAL RAY Over T7 vertebra SID: 72 inches Central ray Film holder (image receptor) placement The horizontal dimension of an average chest is greater than the vertical dimension. This requires that a 14 x 17-inch film holder or image receptor (IR) be placed crosswise. Or lengthwise depending on body type. Collimation The upper border of the illuminated field should be at the level of vertebra prominence (4 cm above the apex of lungs). This will result in a lower collimation border of 1-2 inches below the costophrenic angle, if the central ray was correctly centred. A general rule for average adult patients is to show a minimum of 10 ribs on a good PA chest radiograph. Evaluation criteria for a good PA projection Entire lung fields from apices to costophrenic angles should be clearly demonstrated. No rotation. (both the right and left sternal ends of the clavicle will be the same distance from the center line of the spine.) The direction of rotation can be determined by which sternal end of the clavicle is closest to the spine. Trachea is visible in midline. Scapula projected outside the lung fields. Ten posterior ribs are visible above the diaphragm. There is a sharp outline of the heart and diaphragm. A faint shadow of the ribs and superior thoracic vertebrae is visible through the heart shadow. Lung markings are visible from the hilum to the periphery of the lung. Variations An expiratory film may be helpful under some circumstances. ]]>
PA PROJECTION Sit or stand upright. Positioned to minimize magnification of the anteriorly positioned heart and consequent obscuration of the lungs. Make sure the patient is standing straight and is equally distributing the weight of the body on both feet. The upright position is preferred for the following reasons: It prevents engorgement (an excess of blood) of pulmonary vessels. It allows full expansion of the lungs To visualize possible air and fluid levels in the chest. An upright chest film is preferred over an upright abdominal film for the diagnosis of pneumoperitoneum (free air in the abdominal cavity). Ask the patient to move the shoulders forward and downward, so that the chest wall and both shoulders are in contact with the cassette. This helps to carry the clavicles below the lung apices. It is very important to minimize breast shadows. Ask the patient to pull the breasts upward and laterally (outwards), then remove her hands as she leans against the cassette holder to keep them in position. Rotation Even a small degree of rotation distorts the mediastinal borders, and the lung nearest the film will appear less translucent. The following points should be stressed to obtain a true PA view (without rotation): Ensure that the patient is standing evenly on both feet. Both shoulders should be rolled forward and downward. The chest radiograph should be well centred so that the medial ends of the clavicle are equidistant from the vertebral spinous processes at T4/5. CENTRAL RAY Over T7 vertebra SID: 72 inches Central ray Film holder (image receptor) placement The horizontal dimension of an average chest is greater than the vertical dimension. This requires that a 14 x 17-inch film holder or image receptor (IR) be placed crosswise. Or lengthwise depending on body type. Collimation The upper border of the illuminated field should be at the level of vertebra prominence (4 cm above the apex of lungs). This will result in a lower collimation border of 1-2 inches below the costophrenic angle, if the central ray was correctly centred. A general rule for average adult patients is to show a minimum of 10 ribs on a good PA chest radiograph. Evaluation criteria for a good PA projection Entire lung fields from apices to costophrenic angles should be clearly demonstrated. No rotation. (both the right and left sternal ends of the clavicle will be the same distance from the center line of the spine.) The direction of rotation can be determined by which sternal end of the clavicle is closest to the spine. Trachea is visible in midline. Scapula projected outside the lung fields. Ten posterior ribs are visible above the diaphragm. There is a sharp outline of the heart and diaphragm. A faint shadow of the ribs and superior thoracic vertebrae is visible through the heart shadow. Lung markings are visible from the hilum to the periphery of the lung. Variations An expiratory film may be helpful under some circumstances. ]]> Wed, 27 Dec 2023 19:42:02 GMT /slideshow/basic-chest-x-ray-views-ap-pa-lateral-etc-pptx/264960795 AbnaJ1@slideshare.net(AbnaJ1) Basic Chest X ray Views - AP, PA & Lateral etc . pptx AbnaJ1 PA PROJECTION Sit or stand upright. Positioned to minimize magnification of the anteriorly positioned heart and consequent obscuration of the lungs. Make sure the patient is standing straight and is equally distributing the weight of the body on both feet. The upright position is preferred for the following reasons: It prevents engorgement (an excess of blood) of pulmonary vessels. It allows full expansion of the lungs To visualize possible air and fluid levels in the chest. An upright chest film is preferred over an upright abdominal film for the diagnosis of pneumoperitoneum (free air in the abdominal cavity). Ask the patient to move the shoulders forward and downward, so that the chest wall and both shoulders are in contact with the cassette. This helps to carry the clavicles below the lung apices. It is very important to minimize breast shadows. Ask the patient to pull the breasts upward and laterally (outwards), then remove her hands as she leans against the cassette holder to keep them in position. Rotation Even a small degree of rotation distorts the mediastinal borders, and the lung nearest the film will appear less translucent. The following points should be stressed to obtain a true PA view (without rotation): �� Ensure that the patient is standing evenly on both feet. Both shoulders should be rolled forward and downward. The chest radiograph should be well centred so that the medial ends of the clavicle are equidistant from the vertebral spinous processes at T4/5. CENTRAL RAY Over T7 vertebra SID: 72 inches Central ray Film holder (image receptor) placement � The horizontal dimension of an average chest is greater than the vertical dimension. This requires that a 14 x 17-inch film holder or image receptor (IR) be placed crosswise. Or lengthwise depending on body type. Collimation The upper border of the illuminated field should be at the level of vertebra prominence (4 cm above the apex of lungs). This will result in a lower collimation border of 1-2 inches below the costophrenic angle, if the central ray was correctly centred. � A general rule for average adult patients is to show a minimum of 10 ribs on a good PA chest radiograph. Evaluation criteria for a good PA projection Entire lung fields from apices to costophrenic angles should be clearly demonstrated. No rotation. (both the right and left sternal ends of the clavicle will be the same distance from the center line of the spine.) The direction of rotation can be determined by which sternal end of the clavicle is closest to the spine. Trachea is visible in midline. Scapula projected outside the lung fields. Ten posterior ribs are visible above the diaphragm. There is a sharp outline of the heart and diaphragm. A faint shadow of the ribs and superior thoracic vertebrae is visible through the heart shadow. Lung markings are visible from the hilum to the periphery of the lung. Variations An expiratory film may be helpful under some circumstances. <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/chestxrayviews-231227194202-501fbdd3-thumbnail.jpg?width=120&height=120&fit=bounds" /><br> PA PROJECTION Sit or stand upright. Positioned to minimize magnification of the anteriorly positioned heart and consequent obscuration of the lungs. Make sure the patient is standing straight and is equally distributing the weight of the body on both feet. The upright position is preferred for the following reasons: It prevents engorgement (an excess of blood) of pulmonary vessels. It allows full expansion of the lungs To visualize possible air and fluid levels in the chest. An upright chest film is preferred over an upright abdominal film for the diagnosis of pneumoperitoneum (free air in the abdominal cavity). Ask the patient to move the shoulders forward and downward, so that the chest wall and both shoulders are in contact with the cassette. This helps to carry the clavicles below the lung apices. It is very important to minimize breast shadows. Ask the patient to pull the breasts upward and laterally (outwards), then remove her hands as she leans against the cassette holder to keep them in position. Rotation Even a small degree of rotation distorts the mediastinal borders, and the lung nearest the film will appear less translucent. The following points should be stressed to obtain a true PA view (without rotation): �� Ensure that the patient is standing evenly on both feet. Both shoulders should be rolled forward and downward. The chest radiograph should be well centred so that the medial ends of the clavicle are equidistant from the vertebral spinous processes at T4/5. CENTRAL RAY Over T7 vertebra SID: 72 inches Central ray Film holder (image receptor) placement � The horizontal dimension of an average chest is greater than the vertical dimension. This requires that a 14 x 17-inch film holder or image receptor (IR) be placed crosswise. Or lengthwise depending on body type. Collimation The upper border of the illuminated field should be at the level of vertebra prominence (4 cm above the apex of lungs). This will result in a lower collimation border of 1-2 inches below the costophrenic angle, if the central ray was correctly centred. � A general rule for average adult patients is to show a minimum of 10 ribs on a good PA chest radiograph. Evaluation criteria for a good PA projection Entire lung fields from apices to costophrenic angles should be clearly demonstrated. No rotation. (both the right and left sternal ends of the clavicle will be the same distance from the center line of the spine.) The direction of rotation can be determined by which sternal end of the clavicle is closest to the spine. Trachea is visible in midline. Scapula projected outside the lung fields. Ten posterior ribs are visible above the diaphragm. There is a sharp outline of the heart and diaphragm. A faint shadow of the ribs and superior thoracic vertebrae is visible through the heart shadow. Lung markings are visible from the hilum to the periphery of the lung. Variations An expiratory film may be helpful under some circumstances.

Basic Chest X ray Views - AP, PA & Lateral etc . pptx from Dr Abna J

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0 Cerebral Infarcts . pptx /slideshow/cerebral-infarcts-pptx/264958938 cerebralinfarcts-231227170410-e5a4535b
CEREBRAL INFARCTS Pathophysiology Significantly diminished blood supply to all parts(global ischemia) or selected areas(regional or focal ischemia) of the brain Focal ischemia- cerebral infarction Global ischemia-hypoxic ischemic encephalopathy(HIE), hypotensive cerebral infarction Infarct vs pneumbra In the central core of the infarct, the severity of hypoperfusion results in irreversible cellular damage Around this core, there is a region of decreased flow in which either: The critical flow threshold for cell death has not reached Or the duration of ischemia has been insufficient to cause irreversible damage. Current therapies attempt to rescue these ‘at risk’ cells Goal of imaging Exclude hemorrhage Identify the presence of an underlying structural lesion such as tumour , vascular malformation, subdural hematoma that can mimic stroke Identify stenosis or occlusion of major extra- and intracranial arteries Differentiate between irreversibly affected brain tissue and reversibly impaired tissue (dead tissue versus tissue at risk) Imaging modalities CT MRI Diffusion weighted imaging MRA MRS CT angiography CT perfusion imaging Perfusion-weighted MR Imaging Trans cranial doppler Cerebral angiography Classification Hyper acute infarct (2 weeks) Old infarct (> 8 to 10 weeks) CT-Hyperacute infarct Normal in 50 – 60% Hyperdense MCA sign-acute intraluminal thrombus Obscuration of lentiform nulei Dot sign-occluded MCA branch in sylvian fissure Insular ribbon sign –grey white interface loss along the lateral insula Hyperdense MCA sign Obscuration of lentiform nuclei Insular ribbon sign Insular ribbon sign MRI –Hyperacute infarct Absence of normal flow void with intra vascular arterial enhancement Anatomic changes in T1WI Sulcal effacement, Gyral edema, Loss of grey white interface Sulcal effacement CT- Acute infarct Low density basal ganglia Sulcal effacement Wedge shaphed parenchymal hypo density area that involves both grey and white matter Increasing mass effect Hemorrhagic transformation may occur -15 to 45% ( basal ganglia and cortex common site) in 24 to 48 hours Sulcal effacement MRI –Acute infarct T2WI-hyperintensity in affected area Meningeal enhancement adjacent to infarct(12 to 24 hours) Early parenchymal enhancement Hemorrhagic transformation becomes evident MRI –Acute infarct MRI –Acute infarct CT – sub acute infarct NECT Wedge-shaped area of decreased attenuation involving gray/white matter in typical vascular distribution Mass effect initially increases, then begins to diminish by 7-10 days HT of initially ischemic infarction occurs in 15-20% of MCA occlusions, usually by 48-72 hrs CECT Enhancement patterns typically patchy or gyral May appear as early as 2-3 days after ictus, persisting up to 8-10 weeks ]]>
CEREBRAL INFARCTS Pathophysiology Significantly diminished blood supply to all parts(global ischemia) or selected areas(regional or focal ischemia) of the brain Focal ischemia- cerebral infarction Global ischemia-hypoxic ischemic encephalopathy(HIE), hypotensive cerebral infarction Infarct vs pneumbra In the central core of the infarct, the severity of hypoperfusion results in irreversible cellular damage Around this core, there is a region of decreased flow in which either: The critical flow threshold for cell death has not reached Or the duration of ischemia has been insufficient to cause irreversible damage. Current therapies attempt to rescue these ‘at risk’ cells Goal of imaging Exclude hemorrhage Identify the presence of an underlying structural lesion such as tumour , vascular malformation, subdural hematoma that can mimic stroke Identify stenosis or occlusion of major extra- and intracranial arteries Differentiate between irreversibly affected brain tissue and reversibly impaired tissue (dead tissue versus tissue at risk) Imaging modalities CT MRI Diffusion weighted imaging MRA MRS CT angiography CT perfusion imaging Perfusion-weighted MR Imaging Trans cranial doppler Cerebral angiography Classification Hyper acute infarct (2 weeks) Old infarct (> 8 to 10 weeks) CT-Hyperacute infarct Normal in 50 – 60% Hyperdense MCA sign-acute intraluminal thrombus Obscuration of lentiform nulei Dot sign-occluded MCA branch in sylvian fissure Insular ribbon sign –grey white interface loss along the lateral insula Hyperdense MCA sign Obscuration of lentiform nuclei Insular ribbon sign Insular ribbon sign MRI –Hyperacute infarct Absence of normal flow void with intra vascular arterial enhancement Anatomic changes in T1WI Sulcal effacement, Gyral edema, Loss of grey white interface Sulcal effacement CT- Acute infarct Low density basal ganglia Sulcal effacement Wedge shaphed parenchymal hypo density area that involves both grey and white matter Increasing mass effect Hemorrhagic transformation may occur -15 to 45% ( basal ganglia and cortex common site) in 24 to 48 hours Sulcal effacement MRI –Acute infarct T2WI-hyperintensity in affected area Meningeal enhancement adjacent to infarct(12 to 24 hours) Early parenchymal enhancement Hemorrhagic transformation becomes evident MRI –Acute infarct MRI –Acute infarct CT – sub acute infarct NECT Wedge-shaped area of decreased attenuation involving gray/white matter in typical vascular distribution Mass effect initially increases, then begins to diminish by 7-10 days HT of initially ischemic infarction occurs in 15-20% of MCA occlusions, usually by 48-72 hrs CECT Enhancement patterns typically patchy or gyral May appear as early as 2-3 days after ictus, persisting up to 8-10 weeks ]]> Wed, 27 Dec 2023 17:04:10 GMT /slideshow/cerebral-infarcts-pptx/264958938 AbnaJ1@slideshare.net(AbnaJ1) Cerebral Infarcts . pptx AbnaJ1 CEREBRAL INFARCTS Pathophysiology Significantly diminished blood supply to all parts(global ischemia) or selected areas(regional or focal ischemia) of the brain Focal ischemia- cerebral infarction Global ischemia-hypoxic ischemic encephalopathy(HIE), hypotensive cerebral infarction Infarct vs pneumbra In the central core of the infarct, the severity of hypoperfusion results in irreversible cellular damage Around this core, there is a region of decreased flow in which either: The critical flow threshold for cell death has not reached Or the duration of ischemia has been insufficient to cause irreversible damage. Current therapies attempt to rescue these ‘at risk’ cells Goal of imaging Exclude hemorrhage Identify the presence of an underlying structural lesion such as tumour , vascular malformation, subdural hematoma that can mimic stroke Identify stenosis or occlusion of major extra- and intracranial arteries Differentiate between irreversibly affected brain tissue and reversibly impaired tissue (dead tissue versus tissue at risk) Imaging modalities CT MRI Diffusion weighted imaging MRA MRS CT angiography CT perfusion imaging Perfusion-weighted MR Imaging Trans cranial doppler Cerebral angiography Classification Hyper acute infarct (<12 hours) Acute infarct (12 to 48 hours) Subacute infarct (2 to 14 days) Chronic infarct (>2 weeks) Old infarct (> 8 to 10 weeks) CT-Hyperacute infarct Normal in 50 – 60% Hyperdense MCA sign-acute intraluminal thrombus Obscuration of lentiform nulei Dot sign-occluded MCA branch in sylvian fissure Insular ribbon sign –grey white interface loss along the lateral insula Hyperdense MCA sign Obscuration of lentiform nuclei Insular ribbon sign Insular ribbon sign MRI –Hyperacute infarct Absence of normal flow void with intra vascular arterial enhancement Anatomic changes in T1WI Sulcal effacement, Gyral edema, Loss of grey white interface Sulcal effacement CT- Acute infarct Low density basal ganglia Sulcal effacement Wedge shaphed parenchymal hypo density area that involves both grey and white matter Increasing mass effect Hemorrhagic transformation may occur -15 to 45% ( basal ganglia and cortex common site) in 24 to 48 hours Sulcal effacement MRI –Acute infarct T2WI-hyperintensity in affected area Meningeal enhancement adjacent to infarct(12 to 24 hours) Early parenchymal enhancement Hemorrhagic transformation becomes evident MRI –Acute infarct MRI –Acute infarct CT – sub acute infarct NECT Wedge-shaped area of decreased attenuation involving gray/white matter in typical vascular distribution Mass effect initially increases, then begins to diminish by 7-10 days HT of initially ischemic infarction occurs in 15-20% of MCA occlusions, usually by 48-72 hrs CECT Enhancement patterns typically patchy or gyral May appear as early as 2-3 days after ictus, persisting up to 8-10 weeks <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/cerebralinfarcts-231227170410-e5a4535b-thumbnail.jpg?width=120&height=120&fit=bounds" /><br> CEREBRAL INFARCTS Pathophysiology Significantly diminished blood supply to all parts(global ischemia) or selected areas(regional or focal ischemia) of the brain Focal ischemia- cerebral infarction Global ischemia-hypoxic ischemic encephalopathy(HIE), hypotensive cerebral infarction Infarct vs pneumbra In the central core of the infarct, the severity of hypoperfusion results in irreversible cellular damage Around this core, there is a region of decreased flow in which either: The critical flow threshold for cell death has not reached Or the duration of ischemia has been insufficient to cause irreversible damage. Current therapies attempt to rescue these ‘at risk’ cells Goal of imaging Exclude hemorrhage Identify the presence of an underlying structural lesion such as tumour , vascular malformation, subdural hematoma that can mimic stroke Identify stenosis or occlusion of major extra- and intracranial arteries Differentiate between irreversibly affected brain tissue and reversibly impaired tissue (dead tissue versus tissue at risk) Imaging modalities CT MRI Diffusion weighted imaging MRA MRS CT angiography CT perfusion imaging Perfusion-weighted MR Imaging Trans cranial doppler Cerebral angiography Classification Hyper acute infarct (2 weeks) Old infarct (> 8 to 10 weeks) CT-Hyperacute infarct Normal in 50 – 60% Hyperdense MCA sign-acute intraluminal thrombus Obscuration of lentiform nulei Dot sign-occluded MCA branch in sylvian fissure Insular ribbon sign –grey white interface loss along the lateral insula Hyperdense MCA sign Obscuration of lentiform nuclei Insular ribbon sign Insular ribbon sign MRI –Hyperacute infarct Absence of normal flow void with intra vascular arterial enhancement Anatomic changes in T1WI Sulcal effacement, Gyral edema, Loss of grey white interface Sulcal effacement CT- Acute infarct Low density basal ganglia Sulcal effacement Wedge shaphed parenchymal hypo density area that involves both grey and white matter Increasing mass effect Hemorrhagic transformation may occur -15 to 45% ( basal ganglia and cortex common site) in 24 to 48 hours Sulcal effacement MRI –Acute infarct T2WI-hyperintensity in affected area Meningeal enhancement adjacent to infarct(12 to 24 hours) Early parenchymal enhancement Hemorrhagic transformation becomes evident MRI –Acute infarct MRI –Acute infarct CT – sub acute infarct NECT Wedge-shaped area of decreased attenuation involving gray/white matter in typical vascular distribution Mass effect initially increases, then begins to diminish by 7-10 days HT of initially ischemic infarction occurs in 15-20% of MCA occlusions, usually by 48-72 hrs CECT Enhancement patterns typically patchy or gyral May appear as early as 2-3 days after ictus, persisting up to 8-10 weeks

Cerebral Infarcts . pptx from Dr Abna J

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0 Overuse syndromes of Ankle joint .ppt /slideshow/overuse-syndromes-of-ankle-joint-ppt/264957674 ankleoveruse-231227161817-57b440fa
Pain with disruption of cartilaginous synchondrosis between os trigonum & lateral tubercle of posterior talar process Anatomical variations: 1. normal tubercle 2.stedia’s process or enlarged tubercle 3.accessory bone or os trigonum 4.fused os trigonum via synchondrosis with talus. Fusion o os trigonum -- 8 to 11 yrs Ossification -- 2nd decade Pain syndrome -- 20 to 35 yrs PROTOCOL: sagittal view T1 , FS PD FSE MRI: T1: Hyointense sclerosis,edema b/w os trigonum & talus T2:Hyperintense marrow edema and edema posterior to talus & superior to os trigonum Differential diagnosis: Fracture lateral tubercle Posterior soft tissue impingement FHL tenosynovitis Dancer’s foot FHL checkrein deformity Accessory navicular: Unattached accessory bone or synchondrosis within medial navicular Types: 1. 4 to 6 mm 2. unossified zone of 1 to 3 mm 3.cornuate or enlarged navicular tuberosity Ossify at 9 to 11 yrs Symptoms after 5 yrs PROTOCOL: direct axial T1 & FS PD FSE or STIR MRI: T1: 1. small (4-6mm) marrow fat containing ossicle within TP tendon (seperated from navicle by 5-7 mm) 2. triangular or heart shaped ossicle with direct connection to medial navicular 3.cornuate extension of medial navicular with no synchondrosis T2: In types 1 & 2 – suppressed marrow fat signal in type 3 - normal marrow fat characteristics Differential diagnosis: Navicular tuberosity fracture TP tendon tear Midfoot arthritis Sesamoid dysfunction: Bipartite, fracture, turf toe , osteochondritis, sesamoiditis Altered signal & morphology of sesamoids Mc – within the double tendons of flexor hallucis brevis , articulating with 1st metatarsal head Bipartite- rounded edges Fracture- discrete hypointense frcture line Turf toe- capsular disruption Dd: stress fracture , synovitis Compartment syndrome: Compartments MRI: T1: intermediate signal in edematous muscle, loss of normal muscle striations T2:hyperintensity of involved muscles D/d: DVT Gastrocnemius-soleus muscle strain Cellulitis Tumour Myositis ossificans Gastro-soleus strain: Diffuse hyperintensity of medial head of gastro & soleus MRI: T1: intermediate signal edema laxity of intermuscular septum b/w the 2 muscles T2: hyperintense edematous muscle fibers GRADES: 1. no myofascial disruption edema,swelling + 2. weakness variable seperation of muscle from tendon orfascia 3. complete myofascial seper]]>
Pain with disruption of cartilaginous synchondrosis between os trigonum & lateral tubercle of posterior talar process Anatomical variations: 1. normal tubercle 2.stedia’s process or enlarged tubercle 3.accessory bone or os trigonum 4.fused os trigonum via synchondrosis with talus. Fusion o os trigonum -- 8 to 11 yrs Ossification -- 2nd decade Pain syndrome -- 20 to 35 yrs PROTOCOL: sagittal view T1 , FS PD FSE MRI: T1: Hyointense sclerosis,edema b/w os trigonum & talus T2:Hyperintense marrow edema and edema posterior to talus & superior to os trigonum Differential diagnosis: Fracture lateral tubercle Posterior soft tissue impingement FHL tenosynovitis Dancer’s foot FHL checkrein deformity Accessory navicular: Unattached accessory bone or synchondrosis within medial navicular Types: 1. 4 to 6 mm 2. unossified zone of 1 to 3 mm 3.cornuate or enlarged navicular tuberosity Ossify at 9 to 11 yrs Symptoms after 5 yrs PROTOCOL: direct axial T1 & FS PD FSE or STIR MRI: T1: 1. small (4-6mm) marrow fat containing ossicle within TP tendon (seperated from navicle by 5-7 mm) 2. triangular or heart shaped ossicle with direct connection to medial navicular 3.cornuate extension of medial navicular with no synchondrosis T2: In types 1 & 2 – suppressed marrow fat signal in type 3 - normal marrow fat characteristics Differential diagnosis: Navicular tuberosity fracture TP tendon tear Midfoot arthritis Sesamoid dysfunction: Bipartite, fracture, turf toe , osteochondritis, sesamoiditis Altered signal & morphology of sesamoids Mc – within the double tendons of flexor hallucis brevis , articulating with 1st metatarsal head Bipartite- rounded edges Fracture- discrete hypointense frcture line Turf toe- capsular disruption Dd: stress fracture , synovitis Compartment syndrome: Compartments MRI: T1: intermediate signal in edematous muscle, loss of normal muscle striations T2:hyperintensity of involved muscles D/d: DVT Gastrocnemius-soleus muscle strain Cellulitis Tumour Myositis ossificans Gastro-soleus strain: Diffuse hyperintensity of medial head of gastro & soleus MRI: T1: intermediate signal edema laxity of intermuscular septum b/w the 2 muscles T2: hyperintense edematous muscle fibers GRADES: 1. no myofascial disruption edema,swelling + 2. weakness variable seperation of muscle from tendon orfascia 3. complete myofascial seper]]> Wed, 27 Dec 2023 16:18:17 GMT /slideshow/overuse-syndromes-of-ankle-joint-ppt/264957674 AbnaJ1@slideshare.net(AbnaJ1) Overuse syndromes of Ankle joint .ppt AbnaJ1 Pain with disruption of cartilaginous synchondrosis between os trigonum & lateral tubercle of posterior talar process Anatomical variations: 1. normal tubercle 2.stedia’s process or enlarged tubercle 3.accessory bone or os trigonum 4.fused os trigonum via synchondrosis with talus. Fusion o os trigonum -- 8 to 11 yrs Ossification -- 2nd decade Pain syndrome -- 20 to 35 yrs PROTOCOL: sagittal view T1 , FS PD FSE MRI: T1: Hyointense sclerosis,edema b/w os trigonum & talus T2:Hyperintense marrow edema and edema posterior to talus & superior to os trigonum Differential diagnosis: Fracture lateral tubercle Posterior soft tissue impingement FHL tenosynovitis Dancer’s foot FHL checkrein deformity Accessory navicular: Unattached accessory bone or synchondrosis within medial navicular Types: 1. 4 to 6 mm 2. unossified zone of 1 to 3 mm 3.cornuate or enlarged navicular tuberosity Ossify at 9 to 11 yrs Symptoms after 5 yrs PROTOCOL: direct axial T1 & FS PD FSE or STIR MRI: T1: 1. small (4-6mm) marrow fat containing ossicle within TP tendon (seperated from navicle by 5-7 mm) 2. triangular or heart shaped ossicle with direct connection to medial navicular 3.cornuate extension of medial navicular with no synchondrosis T2: In types 1 & 2 – suppressed marrow fat signal in type 3 - normal marrow fat characteristics Differential diagnosis: Navicular tuberosity fracture TP tendon tear Midfoot arthritis Sesamoid dysfunction: Bipartite, fracture, turf toe , osteochondritis, sesamoiditis Altered signal & morphology of sesamoids Mc – within the double tendons of flexor hallucis brevis , articulating with 1st metatarsal head Bipartite- rounded edges Fracture- discrete hypointense frcture line Turf toe- capsular disruption Dd: stress fracture , synovitis Compartment syndrome: Compartments MRI: T1: intermediate signal in edematous muscle, loss of normal muscle striations T2:hyperintensity of involved muscles D/d: DVT Gastrocnemius-soleus muscle strain Cellulitis Tumour Myositis ossificans Gastro-soleus strain: Diffuse hyperintensity of medial head of gastro & soleus MRI: T1: intermediate signal edema laxity of intermuscular septum b/w the 2 muscles T2: hyperintense edematous muscle fibers GRADES: 1. no myofascial disruption edema,swelling + 2. weakness variable seperation of muscle from tendon orfascia 3. complete myofascial seper <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/ankleoveruse-231227161817-57b440fa-thumbnail.jpg?width=120&height=120&fit=bounds" /><br> Pain with disruption of cartilaginous synchondrosis between os trigonum & lateral tubercle of posterior talar process Anatomical variations: 1. normal tubercle 2.stedia’s process or enlarged tubercle 3.accessory bone or os trigonum 4.fused os trigonum via synchondrosis with talus. Fusion o os trigonum -- 8 to 11 yrs Ossification -- 2nd decade Pain syndrome -- 20 to 35 yrs PROTOCOL: sagittal view T1 , FS PD FSE MRI: T1: Hyointense sclerosis,edema b/w os trigonum & talus T2:Hyperintense marrow edema and edema posterior to talus & superior to os trigonum Differential diagnosis: Fracture lateral tubercle Posterior soft tissue impingement FHL tenosynovitis Dancer’s foot FHL checkrein deformity Accessory navicular: Unattached accessory bone or synchondrosis within medial navicular Types: 1. 4 to 6 mm 2. unossified zone of 1 to 3 mm 3.cornuate or enlarged navicular tuberosity Ossify at 9 to 11 yrs Symptoms after 5 yrs PROTOCOL: direct axial T1 & FS PD FSE or STIR MRI: T1: 1. small (4-6mm) marrow fat containing ossicle within TP tendon (seperated from navicle by 5-7 mm) 2. triangular or heart shaped ossicle with direct connection to medial navicular 3.cornuate extension of medial navicular with no synchondrosis T2: In types 1 & 2 – suppressed marrow fat signal in type 3 - normal marrow fat characteristics Differential diagnosis: Navicular tuberosity fracture TP tendon tear Midfoot arthritis Sesamoid dysfunction: Bipartite, fracture, turf toe , osteochondritis, sesamoiditis Altered signal & morphology of sesamoids Mc – within the double tendons of flexor hallucis brevis , articulating with 1st metatarsal head Bipartite- rounded edges Fracture- discrete hypointense frcture line Turf toe- capsular disruption Dd: stress fracture , synovitis Compartment syndrome: Compartments MRI: T1: intermediate signal in edematous muscle, loss of normal muscle striations T2:hyperintensity of involved muscles D/d: DVT Gastrocnemius-soleus muscle strain Cellulitis Tumour Myositis ossificans Gastro-soleus strain: Diffuse hyperintensity of medial head of gastro & soleus MRI: T1: intermediate signal edema laxity of intermuscular septum b/w the 2 muscles T2: hyperintense edematous muscle fibers GRADES: 1. no myofascial disruption edema,swelling + 2. weakness variable seperation of muscle from tendon orfascia 3. complete myofascial seper

Overuse syndromes of Ankle joint .ppt from Dr Abna J

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