This document provides an overview of arterial anatomy in the brain and imaging of strokes. It discusses the anterior and posterior circulations, variants and anomalies like aberrant internal carotid arteries and persistent stapedial arteries. It also covers the circle of Willis and acute cerebral ischemia/infarction, including pathophysiology, CT findings like ASPECTS scoring, CTA, perfusion CT, and MRI findings in the hyperacute, subacute and chronic stages. Specific topics like watershed infarcts and artery of Percheron infarction are also mentioned.
1. The document discusses the anatomy and epidemiology of carotid atherosclerotic disease. It describes the anatomy of the aortic arch and its branches, including the common, external, and internal carotid arteries.
2. Pathophysiology sections cover the development of atherosclerosis in the carotid bulb and mechanisms by which plaques can cause TIAs or strokes via embolization and hypoperfusion.
3. Evaluation and management are discussed, including use of carotid duplex ultrasound, CTA, MRA, and angiography to diagnose stenosis. Medical management focuses on risk factor modification including smoking cessation and diabetes control.
Carotid ultrasound is used to detect plaque buildup in the carotid arteries, which can harden or rupture over time and increase the risk of stroke. Plaque can narrow the arteries and reduce blood flow to the brain. Ruptured plaque can also form blood clots, which may block or partially block the carotid artery and cause a stroke if pieces of plaque or clots break off and travel to the brain. Carotid ultrasound is recommended for those who have had a stroke or mini-stroke, have an abnormal carotid bruit sound, blood clots in the carotid arteries, or a dissection in the carotid artery wall. Ultrasound images show normal versus abnormal carotid arteries, including plaque buildup, ulcerations
This document discusses various types of vascular malformations. It begins by describing malformations with arteriovenous shunts, including arteriovenous malformations (AVMs), dural arteriovenous fistulas (DAVF), and pial arteriovenous fistulas. It then discusses malformations without shunts such as cavernous malformations, venous malformations, capillary telangiectasia, and Moyamoya disease. The document provides details on the characteristics, presentation, evaluation and treatment of different types of vascular malformations.
Magnetic Resonance Angiography and VenographyAnjan Dangal
Introduction to MR Angiography and Venography Procedure of Brain . Includes Indication, MRI protocol, planning and anatomy as well as brief intoduction to physics behind MRA and MRV principle.
This document provides an outline and overview of key topics related to stroke. It begins with definitions and classifications of stroke, including transient ischemic attack (TIA) and different types of stroke. It then covers risk factors, pathophysiology, signs and symptoms, investigations, and management approaches for stroke. Specific sections address hemorrhagic versus ischemic stroke, localization of stroke syndromes, and differentiating features between anterior and posterior circulation strokes. Differential diagnoses are also listed. The document aims to present essential information on stroke for medical education purposes.
This document provides an outline for a presentation on stroke. It begins with an introduction defining stroke and classifying it as either transient ischemic attack (TIA), progressive stroke, or completed stroke. It then covers the types and risk factors of stroke, including modifiable and non-modifiable risk factors. The pathophysiology of both ischemic and hemorrhagic stroke is explained. Signs and symptoms of stroke are outlined, including localization of symptoms based on hemisphere affected. Investigations, prognostic factors, and management of both acute stroke and long-term prevention are summarized.
This document provides an overview of arterial anatomy in the brain and imaging of strokes. It discusses the anterior and posterior circulations, variants and anomalies like aberrant internal carotid arteries and persistent stapedial arteries. It also covers the circle of Willis and acute cerebral ischemia/infarction, including pathophysiology, CT findings like ASPECTS scoring, CTA, perfusion CT, and MRI findings in the hyperacute, subacute and chronic stages. Specific topics like watershed infarcts and artery of Percheron infarction are also mentioned.
1. The document discusses the anatomy and epidemiology of carotid atherosclerotic disease. It describes the anatomy of the aortic arch and its branches, including the common, external, and internal carotid arteries.
2. Pathophysiology sections cover the development of atherosclerosis in the carotid bulb and mechanisms by which plaques can cause TIAs or strokes via embolization and hypoperfusion.
3. Evaluation and management are discussed, including use of carotid duplex ultrasound, CTA, MRA, and angiography to diagnose stenosis. Medical management focuses on risk factor modification including smoking cessation and diabetes control.
Carotid ultrasound is used to detect plaque buildup in the carotid arteries, which can harden or rupture over time and increase the risk of stroke. Plaque can narrow the arteries and reduce blood flow to the brain. Ruptured plaque can also form blood clots, which may block or partially block the carotid artery and cause a stroke if pieces of plaque or clots break off and travel to the brain. Carotid ultrasound is recommended for those who have had a stroke or mini-stroke, have an abnormal carotid bruit sound, blood clots in the carotid arteries, or a dissection in the carotid artery wall. Ultrasound images show normal versus abnormal carotid arteries, including plaque buildup, ulcerations
This document discusses various types of vascular malformations. It begins by describing malformations with arteriovenous shunts, including arteriovenous malformations (AVMs), dural arteriovenous fistulas (DAVF), and pial arteriovenous fistulas. It then discusses malformations without shunts such as cavernous malformations, venous malformations, capillary telangiectasia, and Moyamoya disease. The document provides details on the characteristics, presentation, evaluation and treatment of different types of vascular malformations.
Magnetic Resonance Angiography and VenographyAnjan Dangal
Introduction to MR Angiography and Venography Procedure of Brain . Includes Indication, MRI protocol, planning and anatomy as well as brief intoduction to physics behind MRA and MRV principle.
This document provides an outline and overview of key topics related to stroke. It begins with definitions and classifications of stroke, including transient ischemic attack (TIA) and different types of stroke. It then covers risk factors, pathophysiology, signs and symptoms, investigations, and management approaches for stroke. Specific sections address hemorrhagic versus ischemic stroke, localization of stroke syndromes, and differentiating features between anterior and posterior circulation strokes. Differential diagnoses are also listed. The document aims to present essential information on stroke for medical education purposes.
This document provides an outline for a presentation on stroke. It begins with an introduction defining stroke and classifying it as either transient ischemic attack (TIA), progressive stroke, or completed stroke. It then covers the types and risk factors of stroke, including modifiable and non-modifiable risk factors. The pathophysiology of both ischemic and hemorrhagic stroke is explained. Signs and symptoms of stroke are outlined, including localization of symptoms based on hemisphere affected. Investigations, prognostic factors, and management of both acute stroke and long-term prevention are summarized.
This document provides an overview of carotid Doppler ultrasound. It begins with the anatomy of the carotid arteries and their branches. It then discusses the technique of carotid Doppler ultrasound, including instrumentation, examination protocol, and interpretation of ultrasound findings. It provides details on evaluating the internal carotid, external carotid, and vertebral arteries for stenosis or occlusion. The document also covers characterizing carotid plaques and differentiating true findings from artifacts.
This document discusses stroke and conditions that can mimic stroke. It begins by defining stroke as a sudden neurological deficit caused by arterial ischemia or hemorrhage. While ischemic stroke diagnosis is often straightforward, clinical diagnosis is inaccurate 10-30% of the time as other conditions like infections, seizures, or tumors can appear similar. The document then discusses using a pattern-based approach to differentiate arterial ischemic strokes from stroke mimics based on imaging appearance over time from acute to chronic stages. Specific vascular territories, imaging sequences, and distinguishing features of common mimics like seizures and tumors are reviewed.
Radiologic Anatomy of the Blood Supply to the Brain.pptxWilliamsMusa1
The document summarizes the radiologic anatomy of the arterial blood supply to the brain using various imaging modalities. It describes the relevant gross anatomy of the major cerebral arteries, including branches and segments. MR angiography is discussed as the preferred noninvasive method for evaluating the cerebral vasculature. CT angiography and conventional angiography provide detailed images but are more invasive. Ultrasound can also be used to image intracranial vessels through various acoustic windows. Variations in anatomy, such as those seen in the circle of Willis, are commonly observed.
The subarachnoid space is located between the arachnoid membrane and pia mater in the brain. It contains cerebrospinal fluid and spongy connective tissue. Bleeding into this space is called a subarachnoid hemorrhage (SAH), which is often caused by the rupture of an intracranial aneurysm. CT and MRI are used to detect SAH. Treatment involves relieving vasospasm, removing blood, and clipping or coiling the aneurysm to prevent rebleeding. Complications include hydrocephalus, infarction, and herniation. The mortality rate of SAH is 30-60% even after reaching the hospital.
This document discusses various imaging modalities for stroke, focusing on their ability to assess the 4 P's: parenchyma, pipes, perfusion, and penumbra. CT techniques like non-contrast CT, CTA, and CTP can quickly detect hemorrhage, visualize vessels for clots, and assess perfusion/penumbra. MRI techniques like DWI, PWI, MRA provide highly sensitive visualization of acute ischemia and perfusion abnormalities to identify the ischemic core and penumbra. Imaging plays a crucial role in the early diagnosis and management of stroke by establishing the diagnosis, guiding therapy decisions, and identifying salvageable brain tissue.
The document discusses the cerebral vasculature and various pathologies related to cerebrospinal fluid circulation. It describes the internal carotid and vertebral-basilar arterial systems, including their major branches that supply different brain regions. Hydrocephalus is defined as a group of conditions resulting from impaired circulation and resorption of cerebrospinal fluid. A Chiari malformation involves the displacement of the cerebellar tonsils into the cervical canal, which can lead to progressive hydrocephalus.
Caroticocavernous fistula is an abnormal connection between the carotid artery and cavernous sinus, causing arterial blood to shunt into the sinus. It is usually caused by trauma but can also arise spontaneously. Patients typically present with pulsatile proptosis, orbital bruit, and chemosis, known as Dandy's triad. Diagnosis is made through imaging like CT, MRI, and catheter angiography. Treatment depends on the flow and involves conservative management, endovascular embolization, or radiosurgery to prevent complications like vision loss, glaucoma, and hemorrhage.
This document provides an overview of imaging in acute stroke. It discusses the goals of imaging evaluation for acute stroke which are to establish a diagnosis, guide treatment, assess location and size of involved territory, rule out hemorrhage and mimics, and obtain information about vasculature and perfusion. CT is the first-line test and can detect early signs of stroke within 6 hours. MRI, including DWI, is very sensitive for acute ischemia. CT angiography and perfusion can assess vessels, blood flow, and the ischemic penumbra. Different territories are discussed along with imaging findings and the physical basis of signs seen on various sequences.
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
This document discusses the anatomy, pathophysiology, clinical presentations, investigations, and management of various spinal cord vascular syndromes. It begins by describing the vascular supply and drainage of the spinal cord from segmental and radiculomedullary arteries. It then discusses various etiologies that can lead to spinal cord ischemia or hemorrhage including arterial occlusion, venous drainage abnormalities, vascular malformations, trauma, and surgery. Clinical syndromes are described based on the vascular territory involved. Imaging findings and treatment options are also summarized.
In this part of presentation we will discuss the role of Doppler Ultrasound in the Diagnosis of other causes of stenosis and variable pattern in circulation.
In my opinion this presentation will help u to identify even rare pathologies.
This document provides information about stroke, including:
1. Stroke is the sudden onset of neurological deficit due to vascular infarction of brain tissue, confirmed by neuroimaging. The two main types are ischemic (80%) and hemorrhagic (20%).
2. Risk factors for ischemic stroke include atherosclerosis, atrial fibrillation, smoking, hypertension, diabetes, and heart disease. Evaluation includes CT, MRI, ECG, and NIH stroke scale.
3. Early signs of ischemia on CT within 6 hours include hypoattenuation of over 1/3 of the MCA territory, loss of gray-white differentiation, and hyperattenuation of vessels. The ASPECTS score quantifies the
Spontaneous coronary artery dissection (SCAD) is a non-atherosclerotic separation of the coronary arterial walls, creating a false lumen. It predominantly affects young to middle-aged women and can lead to myocardial ischemia. Diagnosis is challenging as angiographic findings can mimic atherosclerosis. Intravascular ultrasound and optical coherence tomography provide better visualization of the dissection and intimal tears. Management involves antiplatelet therapy but thrombolysis and anticoagulation should be avoided due to risk of extension. Prognosis is generally good but recurrence risk remains.
This document discusses painful ophthalmoplegia, which presents as periorbital or hemicranial pain, ipsilateral ocular motor palsies, and sensory loss in the trigeminal nerve distribution. Causes include aneurysms, carotid cavernous fistulas, cavernous sinus thrombosis, tumors, and infections. Evaluation involves imaging like MRI/CT/angiography. Management depends on the underlying cause but may include antibiotics, anticoagulation, surgery, or steroids. Prognosis depends on early diagnosis and treatment, with potential for residual neurological deficits.
This document provides an overview of angiographic anatomy of intracranial and extracranial arteries. It discusses angiographic principles, phases of angiography, differences between CTA and cerebral angiography, sensitivity and specificity of the techniques, and anatomy of major arteries and their variations. It also covers collateral circulation, angiographic appearances of variations and anomalies, and sources used to compile the information.
1) The document discusses various types of intracranial aneurysms including their presentation, incidence, diagnosis, and radiographic features.
2) Saccular aneurysms are the most common type and can cause subarachnoid hemorrhage from rupture. They are often detected on CT/CTA or catheter angiography.
3) Other aneurysm types discussed include fusiform, dissecting, mycotic, oncotic, and traumatic pseudoaneurysms. These have different etiologies and features on imaging.
Brain arteriovenous malformations (bAVM) are abnormal connections of arteries and veins in the brain, forming a tangled web of vessels instead of a normal capillary network treated with multimodalities including, SRS, embolisation and Microneurosurgery.
This slides updates the management of AVM highlighting the importance of SM grading, Pollock radiation grading etc.
This document provides an overview of Moyamoya disease. It defines Moyamoya disease as a progressive stenosis of the intracranial arteries, typically the internal carotid arteries and proximal middle and anterior cerebral arteries, accompanied by a compensatory network of collaterals at the brain's base. The cause is unknown but genetic factors are believed to play a role. Clinically, it can present with transient ischemic attacks, strokes, or hemorrhage. Diagnosis is based on neuroimaging findings on MRI, MRA, CTA or DSA showing the characteristic vascular changes. Treatment involves medical management as well as surgical revascularization procedures. Prognosis depends on the extent of vascular involvement and collateral formation.
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
More Related Content
Similar to DIGITAL SUBTRACTION ANGIOGRAPHY IN CEREBROVASCULAR DISEASE AND PERSPECTIVE.pptx
This document provides an overview of carotid Doppler ultrasound. It begins with the anatomy of the carotid arteries and their branches. It then discusses the technique of carotid Doppler ultrasound, including instrumentation, examination protocol, and interpretation of ultrasound findings. It provides details on evaluating the internal carotid, external carotid, and vertebral arteries for stenosis or occlusion. The document also covers characterizing carotid plaques and differentiating true findings from artifacts.
This document discusses stroke and conditions that can mimic stroke. It begins by defining stroke as a sudden neurological deficit caused by arterial ischemia or hemorrhage. While ischemic stroke diagnosis is often straightforward, clinical diagnosis is inaccurate 10-30% of the time as other conditions like infections, seizures, or tumors can appear similar. The document then discusses using a pattern-based approach to differentiate arterial ischemic strokes from stroke mimics based on imaging appearance over time from acute to chronic stages. Specific vascular territories, imaging sequences, and distinguishing features of common mimics like seizures and tumors are reviewed.
Radiologic Anatomy of the Blood Supply to the Brain.pptxWilliamsMusa1
The document summarizes the radiologic anatomy of the arterial blood supply to the brain using various imaging modalities. It describes the relevant gross anatomy of the major cerebral arteries, including branches and segments. MR angiography is discussed as the preferred noninvasive method for evaluating the cerebral vasculature. CT angiography and conventional angiography provide detailed images but are more invasive. Ultrasound can also be used to image intracranial vessels through various acoustic windows. Variations in anatomy, such as those seen in the circle of Willis, are commonly observed.
The subarachnoid space is located between the arachnoid membrane and pia mater in the brain. It contains cerebrospinal fluid and spongy connective tissue. Bleeding into this space is called a subarachnoid hemorrhage (SAH), which is often caused by the rupture of an intracranial aneurysm. CT and MRI are used to detect SAH. Treatment involves relieving vasospasm, removing blood, and clipping or coiling the aneurysm to prevent rebleeding. Complications include hydrocephalus, infarction, and herniation. The mortality rate of SAH is 30-60% even after reaching the hospital.
This document discusses various imaging modalities for stroke, focusing on their ability to assess the 4 P's: parenchyma, pipes, perfusion, and penumbra. CT techniques like non-contrast CT, CTA, and CTP can quickly detect hemorrhage, visualize vessels for clots, and assess perfusion/penumbra. MRI techniques like DWI, PWI, MRA provide highly sensitive visualization of acute ischemia and perfusion abnormalities to identify the ischemic core and penumbra. Imaging plays a crucial role in the early diagnosis and management of stroke by establishing the diagnosis, guiding therapy decisions, and identifying salvageable brain tissue.
The document discusses the cerebral vasculature and various pathologies related to cerebrospinal fluid circulation. It describes the internal carotid and vertebral-basilar arterial systems, including their major branches that supply different brain regions. Hydrocephalus is defined as a group of conditions resulting from impaired circulation and resorption of cerebrospinal fluid. A Chiari malformation involves the displacement of the cerebellar tonsils into the cervical canal, which can lead to progressive hydrocephalus.
Caroticocavernous fistula is an abnormal connection between the carotid artery and cavernous sinus, causing arterial blood to shunt into the sinus. It is usually caused by trauma but can also arise spontaneously. Patients typically present with pulsatile proptosis, orbital bruit, and chemosis, known as Dandy's triad. Diagnosis is made through imaging like CT, MRI, and catheter angiography. Treatment depends on the flow and involves conservative management, endovascular embolization, or radiosurgery to prevent complications like vision loss, glaucoma, and hemorrhage.
This document provides an overview of imaging in acute stroke. It discusses the goals of imaging evaluation for acute stroke which are to establish a diagnosis, guide treatment, assess location and size of involved territory, rule out hemorrhage and mimics, and obtain information about vasculature and perfusion. CT is the first-line test and can detect early signs of stroke within 6 hours. MRI, including DWI, is very sensitive for acute ischemia. CT angiography and perfusion can assess vessels, blood flow, and the ischemic penumbra. Different territories are discussed along with imaging findings and the physical basis of signs seen on various sequences.
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
This document discusses the anatomy, pathophysiology, clinical presentations, investigations, and management of various spinal cord vascular syndromes. It begins by describing the vascular supply and drainage of the spinal cord from segmental and radiculomedullary arteries. It then discusses various etiologies that can lead to spinal cord ischemia or hemorrhage including arterial occlusion, venous drainage abnormalities, vascular malformations, trauma, and surgery. Clinical syndromes are described based on the vascular territory involved. Imaging findings and treatment options are also summarized.
In this part of presentation we will discuss the role of Doppler Ultrasound in the Diagnosis of other causes of stenosis and variable pattern in circulation.
In my opinion this presentation will help u to identify even rare pathologies.
This document provides information about stroke, including:
1. Stroke is the sudden onset of neurological deficit due to vascular infarction of brain tissue, confirmed by neuroimaging. The two main types are ischemic (80%) and hemorrhagic (20%).
2. Risk factors for ischemic stroke include atherosclerosis, atrial fibrillation, smoking, hypertension, diabetes, and heart disease. Evaluation includes CT, MRI, ECG, and NIH stroke scale.
3. Early signs of ischemia on CT within 6 hours include hypoattenuation of over 1/3 of the MCA territory, loss of gray-white differentiation, and hyperattenuation of vessels. The ASPECTS score quantifies the
Spontaneous coronary artery dissection (SCAD) is a non-atherosclerotic separation of the coronary arterial walls, creating a false lumen. It predominantly affects young to middle-aged women and can lead to myocardial ischemia. Diagnosis is challenging as angiographic findings can mimic atherosclerosis. Intravascular ultrasound and optical coherence tomography provide better visualization of the dissection and intimal tears. Management involves antiplatelet therapy but thrombolysis and anticoagulation should be avoided due to risk of extension. Prognosis is generally good but recurrence risk remains.
This document discusses painful ophthalmoplegia, which presents as periorbital or hemicranial pain, ipsilateral ocular motor palsies, and sensory loss in the trigeminal nerve distribution. Causes include aneurysms, carotid cavernous fistulas, cavernous sinus thrombosis, tumors, and infections. Evaluation involves imaging like MRI/CT/angiography. Management depends on the underlying cause but may include antibiotics, anticoagulation, surgery, or steroids. Prognosis depends on early diagnosis and treatment, with potential for residual neurological deficits.
This document provides an overview of angiographic anatomy of intracranial and extracranial arteries. It discusses angiographic principles, phases of angiography, differences between CTA and cerebral angiography, sensitivity and specificity of the techniques, and anatomy of major arteries and their variations. It also covers collateral circulation, angiographic appearances of variations and anomalies, and sources used to compile the information.
1) The document discusses various types of intracranial aneurysms including their presentation, incidence, diagnosis, and radiographic features.
2) Saccular aneurysms are the most common type and can cause subarachnoid hemorrhage from rupture. They are often detected on CT/CTA or catheter angiography.
3) Other aneurysm types discussed include fusiform, dissecting, mycotic, oncotic, and traumatic pseudoaneurysms. These have different etiologies and features on imaging.
Brain arteriovenous malformations (bAVM) are abnormal connections of arteries and veins in the brain, forming a tangled web of vessels instead of a normal capillary network treated with multimodalities including, SRS, embolisation and Microneurosurgery.
This slides updates the management of AVM highlighting the importance of SM grading, Pollock radiation grading etc.
This document provides an overview of Moyamoya disease. It defines Moyamoya disease as a progressive stenosis of the intracranial arteries, typically the internal carotid arteries and proximal middle and anterior cerebral arteries, accompanied by a compensatory network of collaterals at the brain's base. The cause is unknown but genetic factors are believed to play a role. Clinically, it can present with transient ischemic attacks, strokes, or hemorrhage. Diagnosis is based on neuroimaging findings on MRI, MRA, CTA or DSA showing the characteristic vascular changes. Treatment involves medical management as well as surgical revascularization procedures. Prognosis depends on the extent of vascular involvement and collateral formation.
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- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
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These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
2. INTRODUCTION
Fluoroscopic technique for visualization of blood vessels (Gold standard)
Accurately determine the size and location of vascular lesions, detecting tandem arterial lesions and assessing the
collateral circulation
Demonstration of vascular anatomy by direct injection of iodinated contrast medium into the vessel.
Radioopaque structures (eg. bones) are subtracted digitally from image
SIX VESSEL ANGIOGRAPHY
1. Right ICA
2. Left ICA
3. Right ECA
4. Left ECA
5. Right vertebral artery
6. Left vertebral artery
6. TECHNIQUE OF DSA
Adequate hydration with 4hr fasting prior to procedure
Informed consent
Sterilisation of site followed by local anesthesia
Site of puncture: Right femoral artery using Seldinger technique
Inject 2500U heparin (0.5ml) and flush sheath with saline
Desired catheter is taken and angiography is started
14. ACUTE CEREBRAL ISCHEMIA- INFARCTION
DSA used as a prelude to intraarterial thrombolysis or mechanical thrombectomy
Major vessel occlusion:
Interruption of contrast column
Abrupt vessel cut off
Meniscus sign
Tapered or rat tail narrowing
Tram track appearance with trickle of contrast around intraluminal thrombus
Less common signs:
Hyperemia with vascular blush around infracted zone (Luxury perfusion)
Early draining veins (AV shunting with contrast appearing in veins draining the infarct while
remainder of circulation is in later arterial or early capillary phase)
15. ACUTE CEREBRAL ISCHEMIA- INFARCTION
Early arterial phase: Abrupt vessel cut off (MCA) and Bare area of devascularised brain
16. ACUTE CEREBRAL ISCHEMIA- INFARCTION
Retrograde filling of distal MCA branches from collaterals from ACA and PCA
17. ACUTE CEREBRAL ISCHEMIA- INFARCTION
Capillary phase: Blush in
ACA/PCA territory
Venous phase: Persistent contrast in MCA
branches with Luxury perfusion at bare
area
19. VENOUS INFARCTION
DURAL SINUS THROMBOSIS
Occluded (non filling) sinus
Slow flow with or without clot in adjacent cortical veins
Delayed emptying of cortical veins: Hanging in space appearance
SUPERFICIAL VEIN THROMBOSIS
Thin round or tubular layer of contrast surrounding thrombus
DEEP CEREBRAL VENOUS THROMBOSIS
Absent opacification of deep venous system
25. MOYA MOYA DISEASE
Progressive bilateral stenosis of the distal internal carotid
arteries, extending to the proximal ACA and MCA, with
development of an extensive collateral (parenchymal,
leptomeningeal, and transdural) network at the base of the
brain like a cloud or puff of smoke
Suzuki’s 6 angiographic stages:
(1) stenosis of the carotid fork,
(2) appearance of moyamoya vessels at the base of the brain,
(3) intensification of moyamoya vessels,
(4) minimization of moyamoya vessels,
(5) reduction of moyamoya vessels
(6) disappearance of moyamoya vessels (collaterals only from
external carotid arteries)
1: Superior sagittal sinus 2: Transverse sinus 3: Superior petrous sinus 4: Bulb of internal jugular vein 5: Internal jugular vein 6: Confluence of sinuses 7: Sigmoid sinus
8: Inferior veins of cerebellar hemisphere 9: Inferior vermis vein 10: Inferior petrous sinus
1: Superior sagittal sinus 2: Superior cerebral veins 3: Great cerebral vein (Galen) 4: Basal vein (Rosenthal) 5: Superior petrous sinus 6: Cavernous sinus 7: Inferior petrous sinus
8: Bulb of internal jugular vein 9: Thalamostriate vein10: Internal cerebral vein11: Straight sinus 12: Transverse sinus 13: Sigmoid sinus
Acute thromboembolic occlusion. Left internal carotid angiogram, early arterial phase, AP view, shows abrupt "cut-off" of the MCA . Lateral view, early arterial phase, shows normal filling of both ACAs and the ipsilateral PCA via a large PCoA. The MCA distribution is not opacified, leaving a large "bare area" of devascularized brain.
Later image shows that the large "bare area" remains unopacified. Cortical branches are seen high over the left parietal convexity with early retrograde filling of the distal MCA branches via pial collaterals from the ACA and PCA. Collateral flow is also seen from the posterior temporal PCA branches into the MCA territory. (8-42D) Later image shows slow retrograde filling into the MCA territory from ACA and PCA collaterals.
Capillary phase shows diffuse brain "blush" in ACA/PCA territories; contrast with "bare area" normally supplied by the MCA. Some MCA branches are filling slowly via retrograde flow from ACA/PCA pial collaterals. (8-42F) Venous phase shows persisting contrast in some MCA branches that have filled in retrograde fashion via pial collaterals and are slowly emptying. Note "blush" at border of "bare area" caused by "luxury perfusion."
ICA Occlusion- Frontal projection from left cerebral angiogram delineates complete occlusion of left ICA to level of CCA. Normal opacification of ECA noted
Cortical vein occlusion is shown with dural sinus thrombosis. (L) Coronal NECT in a 62y woman with headache, left-sided weakness shows a hyperdense SSS st and thrombus in the adjacent vein of Trolard ſt. (R) CTV shows "empty delta" sign in the SSS , filling defects in the vein of Trolard. (9-31) Close-up view of lateral DSA in the same case shows thrombus in SSS and vein of Trolard .
Traumatic cervical ICA dissection. DSA shows the left ICA with greater than 50% luminal narrowing (arrows) with carotid terminus occlusion and lack of left anterior circulation filling (dashed circle).
Carotid web in a 47-yearold woman with left cerebral infarction. (a, b) Coronal maximum intensity projection CT angiogram (a) and preintervention DSA image (b) show a focal linear shelflike filling defect (arrow) along the wall of the left ICA origin, consistent with a carotid web. (c) Postintervention DSA image shows that the web is no longer present.
RCVS in a 30-year-old woman who presented with sudden-onset headache and no recent trauma. (a) DSA image shows multifocal narrowing (arrows) and beaded appearance of the anterior cerebral arteries and MCAs. (B) Follow-up DSA image at 10 days shows near-complete resolution.
Known moyamoya in a young patient with prior watershed infarcts. Anteroposterior DSA image shows right ICA and proximal MCA steno-occlusive disease of the carotid termini (arrowheads), with extensive small collateral lenticulostriate arteries (arrow).
Lateral left carotid angiogram in a patient with fibromuscular dysplasia. Note “string of pearls” appearance at around the C2 level.
Angiograms of a patient with Takayasu arteritis demonstrating long, smooth stenotic lesions of the left subclavian artery and involvement of other branches of the aortic arch vessels.
Lateral carotid angiogram demonstrates irregular beading appearance (arrowheads) of large and medium branches of the anterior, middle, and posterior cerebral arteries in a patient with systemic lupus erythematosus
Sagittal NECT reformatted from the axial source data shows dense thrombus ſt extending throughout the entire deep venous (Galenic) system. The SSS appears normal. (D) Venous phase of the lateral carotid DSA in the same case shows normal cortical veins and SSS , vein of Trolard . The ependymal veins, ICVs, vein of Galen, and straight sinus are unopacified because they are completely filled with thrombus.
Left MCA occlusion. (A) Initial lateral cerebral angiogram- Paucity of vessels in MCA distribution (B)- Repeat lateral angiogram after intra arterial lysis demonstrates recanalization of flow
Mechanical thrombectomy with recanalization of the basilar artery but the left posterior cerebral artery remains occluded. A, Axial and, B, sagittal noncontrast head CT images show hyperattenuated thrombus (arrow) in the distal basilar artery. C, Coronal CT angi- ography shows nonopacity of the distal basilar artery (arrow). Left vertebral arteriogram in frontal projection, D, before and, E, after mechanical thrombectomy demonstrate recanalization of the basilar artery but occlusion of the left posterior cerebral artery (arrows). F, Axial diffusion-weighted imaging and, G, apparent diffusion coefficient map show acute infarct in the bilateral posterior cerebral artery territories with increased susceptibility in the left posterior cerebral artery (arrow on H) and, H, axial susceptibility-weighted imaging, mitigating against further mechanical thrombectomy attempts.
Mechanical thrombectomy in intracranial atherosclerotic disease. A, Noncontrast head CT image on the axial plane shows multiple areas of subtle hypoattenuation in the right middle cerebral artery (MCA) distribution. B, Noncontrast head CT image on the axial plane shows calcified lesion in the right M1 middle cerebral artery (arrow). C, Time to maximum of residue function map on the axial plane shows large area of tissue at risk in the right MCA territory. Right common carotid arteriograms of, D, frontal and, E, lateral projections before attempted thrombectomy show occlusion of the distal M1 segment of the right MCA (arrow; thrombolysis in cerebral infarction score of 0). Right internal carotid arteriograms of, F, frontal and, G, lateral projections after three thrombectomy passes show antegrade flow through a high-grade stenosis (arrow) in the right distal M1 MCA
A: Initial DSA showing thromboembolic occlusion of the right distal internal carotid artery (ICA). B: Mechanical thrombectomy of the right distal ICA and middle cerebral artery (MCA), which achieved complete recanalization. C: Diffusion-weighted MRI revealing an acute infarction in the right insula and basal ganglia. E: The patient suffered a second stroke 6 days after the index stroke; DSA revealing embolic occlusion of the left proximal MCA. F: The left MCA was successfully reopened after mechanical thrombectomy G: Follow-up diffusion weighted MRI revealing a slightly increased signal intensity in the left basal ganglia.