1. The document discusses various neuroimaging problems and cases presented as learning objectives. It covers topics such as recognising perivascular spaces, measuring acoustic neuromas, spontaneous intracranial hypotension, vascular variants, intracranial cyst differential diagnosis, and conditions with restricted diffusion.
2. Measurement techniques for acoustic neuromas are described including perpendicular and parallel to the posterior petrous ridge and greatest craniocaudal dimension.
3. Criteria for diagnosing spontaneous intracranial hypotension are provided, including pachymeningeal enhancement and sagging of the brainstem and cerebellar tonsils.
Coloboma of the optic disc results from a failure in closure of the embryonic fissure. Medullated nerve fibers represent myelination of retinal nerve fibers that normally proceeds from the brain downwards but stops at the lamina cribrosa. Persistent hyaloid artery congenital remnants can take different forms like Bergmester's papilla or a vascular loop in the vitreous. Optic neuritis includes inflammatory and demyelinating disorders of the optic nerve that can be idiopathic, infectious, or toxic in etiology. Papilloedema is optic disc swelling associated with increased intracranial pressure that is usually bilateral.
1. Optic nerve hypoplasia is the most common optic disc anomaly and third leading cause of childhood blindness in the western world. It can cause reduced visual acuity and visual field defects.
2. Morning glory disc anomaly is characterized by a funnel-shaped enlarged dysplastic optic disc. It is often associated with visual impairment, retinal detachment, and occasionally brain anomalies.
3. Optic disc colobomas are typically bowl-shaped excavations of the optic disc that can be associated with microphthalmos, iris colobomas and other ocular issues as well as syndromic associations. Visual acuity is variably affected.
This document discusses various diseases of the skull and skull bones. It begins with an overview of imaging modalities used to evaluate the skull such as X-ray, CT scan, MRI, and 3D imaging. It then covers developmental disorders of the skull including craniosynostosis, anencephaly, and microcephaly. Infectious and neoplastic disorders of the skull base are also discussed. Finally, the document reviews traumatic injuries to the skull including fractures and neurotrauma.
1. Differential diagnosis of disc edema includes conditions like papilledema, optic neuritis, ischemic optic neuropathy, diabetic papillopathy, and hypertensive retinopathy.
2. Papilledema is caused by increased intracranial pressure and presents with bilateral disc swelling and normal vision, while optic neuritis typically causes unilateral vision loss and eye pain.
3. Diabetic papillopathy presents as transient unilateral or bilateral disc edema that resolves within months without vision loss, while malignant hypertension can lead to bilateral disc edema and vision changes as part of hypertensive retinopathy.
This document provides an overview of neuro-ophthalmic anatomy and examination. It discusses the anatomy of structures involved in eye movement like the skull base, orbital walls, and cranial nerves. It then covers topics like the neuro-ophthalmic exam approach, evaluating specific symptoms like vision changes and double vision, and testing cranial nerves. Key tests are described including Tensilon testing to help localize lesions. The goal of the neuro-ophthalmic exam is to localize lesions in the visual pathways and identify underlying pathologies.
This document provides information on ischemic optic neuropathy (ION), including its causes and types. It discusses non-arteritic anterior ischemic optic neuropathy (NAION) and arteritic anterior ischemic optic neuropathy (AION), noting the differences in symptoms, risk factors, and treatment approaches. Central retinal artery occlusion (CRAO) is also covered, outlining the pathophysiology, signs, imaging studies and prognosis. Central retinal vein occlusion (CRVO) is summarized as well.
Coloboma of the optic disc results from a failure in closure of the embryonic fissure. Medullated nerve fibers represent myelination of retinal nerve fibers that normally proceeds from the brain downwards but stops at the lamina cribrosa. Persistent hyaloid artery congenital remnants can take different forms like Bergmester's papilla or a vascular loop in the vitreous. Optic neuritis includes inflammatory and demyelinating disorders of the optic nerve that can be idiopathic, infectious, or toxic in etiology. Papilloedema is optic disc swelling associated with increased intracranial pressure that is usually bilateral.
1. Optic nerve hypoplasia is the most common optic disc anomaly and third leading cause of childhood blindness in the western world. It can cause reduced visual acuity and visual field defects.
2. Morning glory disc anomaly is characterized by a funnel-shaped enlarged dysplastic optic disc. It is often associated with visual impairment, retinal detachment, and occasionally brain anomalies.
3. Optic disc colobomas are typically bowl-shaped excavations of the optic disc that can be associated with microphthalmos, iris colobomas and other ocular issues as well as syndromic associations. Visual acuity is variably affected.
This document discusses various diseases of the skull and skull bones. It begins with an overview of imaging modalities used to evaluate the skull such as X-ray, CT scan, MRI, and 3D imaging. It then covers developmental disorders of the skull including craniosynostosis, anencephaly, and microcephaly. Infectious and neoplastic disorders of the skull base are also discussed. Finally, the document reviews traumatic injuries to the skull including fractures and neurotrauma.
1. Differential diagnosis of disc edema includes conditions like papilledema, optic neuritis, ischemic optic neuropathy, diabetic papillopathy, and hypertensive retinopathy.
2. Papilledema is caused by increased intracranial pressure and presents with bilateral disc swelling and normal vision, while optic neuritis typically causes unilateral vision loss and eye pain.
3. Diabetic papillopathy presents as transient unilateral or bilateral disc edema that resolves within months without vision loss, while malignant hypertension can lead to bilateral disc edema and vision changes as part of hypertensive retinopathy.
This document provides an overview of neuro-ophthalmic anatomy and examination. It discusses the anatomy of structures involved in eye movement like the skull base, orbital walls, and cranial nerves. It then covers topics like the neuro-ophthalmic exam approach, evaluating specific symptoms like vision changes and double vision, and testing cranial nerves. Key tests are described including Tensilon testing to help localize lesions. The goal of the neuro-ophthalmic exam is to localize lesions in the visual pathways and identify underlying pathologies.
This document provides information on ischemic optic neuropathy (ION), including its causes and types. It discusses non-arteritic anterior ischemic optic neuropathy (NAION) and arteritic anterior ischemic optic neuropathy (AION), noting the differences in symptoms, risk factors, and treatment approaches. Central retinal artery occlusion (CRAO) is also covered, outlining the pathophysiology, signs, imaging studies and prognosis. Central retinal vein occlusion (CRVO) is summarized as well.
After this presentation, the reader should be able to describe features of papilledema with main causes and investigations needed in the work up and differentiate it from pseudopapilledema.
The document discusses the anatomy, physiology, and various pathologies of the optic nerve. It begins with the anatomy of the optic nerve, describing its four parts and blood supply. It then discusses the physiology of axonal transport within the nerve. Several optic nerve disorders are examined in depth, including papilledema, optic neuritis, and optic atrophy. Papilledema is edema of the optic disc due to increased intracranial pressure and can be caused by various conditions. Optic neuritis is inflammation of the optic nerve that can result in vision loss and pain and is associated with multiple sclerosis or infections. Treatment involves corticosteroids. Optic atrophy involves nerve fiber loss and pallor of the disc.
This document discusses neuro-ophthalmology and is presented by Dr. Lee Ming Yueh. It covers various topics including visual pathway and visual field defects, the optic disc, pupils, and cranial nerve palsies with eye manifestations. For visual field defects, it describes different testing methods and lesion locations that can cause specific defect patterns. The optic disc section discusses conditions like edema, atrophy, and swelling. Pupils are described in terms of innervation, size, shape, and defects. Finally, different cranial nerve palsies are outlined, focusing on causes, clinical features, investigations, and management considerations for nerves III-VII.
This document provides an overview of neuro-ophthalmology topics including pupillary disorders, neuro-motility disorders, optic nerve disease, and visual field defects. It describes the anatomy and physiology related to these topics and discusses various conditions that can cause abnormalities, such as third nerve palsy, Horner's syndrome, optic neuritis, anterior ischemic optic neuropathy, papilledema, and visual field defects including arcuate scotomas. The document provides details on clinical features, causes, and treatments for these various neuro-ophthalmological conditions.
Speaker Name: Anjali
Topic: "Demystifying Nystagmus"
Hello Everyone, Namaste!! We would like to notify you all that Mero Eye Foundation is going to conduct an "EYE TALKS-Webinar", and we will be having our session live broadcast on YouTube (Session No. 118)
DATE: at, 07:300 PM NPT, 07:15 PM IST, 22nd May 2021.
YouTube links: https://youtu.be/b4G12rRvXFc
Papilloedema is swelling of the optic nerve head caused by increased intracranial pressure (ICP). It is nearly always bilateral and patients should be evaluated for an intracranial mass. Papilloedema can be caused by idiopathic intracranial hypertension, obstructive lesions, space occupying lesions, impaired CSF absorption, cerebral venous sinus thrombosis, cerebral edema from head trauma, or severe hypertension. Treatment involves reducing ICP through measures like mannitol infusion, CSF withdrawal, sedation, or surgery to remove masses. Complications can include visual loss or chronic headaches.
1. A 41-year-old man presented with blurred disc margins and was found to have reactive syphilis serology, indicating neurosyphilis presenting as asymptomatic optic perineuritis.
2. A 9-year-old boy presented with intermittent headaches and abdominal pain and was found to have bilateral optic disc swelling and markedly elevated blood pressure, leading to the diagnosis of a pheochromocytoma.
3. In both cases, the optic disc swelling was an unusual presenting sign that led to the diagnosis of an underlying systemic condition.
This document discusses three case studies and provides an overview of cranial nerves V, VII and VIII. The first case is about trigeminal neuralgia presenting with facial pain. The second case involves Bell's palsy causing facial droop and eye closure issues. The third case presents with hearing loss and vertigo, found to have cavernous sinus thrombosis. It then reviews radiological images of these cranial nerves and discusses various pathologies, including lesions, that can affect each nerve. Evaluation techniques and distinguishing features of different conditions like trigeminal neuralgia and Bell's palsy are also summarized.
Papilledema is swelling of the optic disc caused by increased intracranial pressure. It is characterized by blurred disc margins and retinal nerve fiber layer edema. Increased CSF pressure is transmitted through the subarachnoid space and causes axoplasmic stasis in the optic nerve head. Papilledema is graded based on degree of disc elevation and obscuration from Frisen scale 0-5. Treatment involves addressing the underlying cause of increased ICP through medications, repeated lumbar punctures, or neurosurgery.
This document discusses ptosis, or drooping of the eyelid. It begins by describing the functional anatomy of the levator palpebrae superioris muscle and other muscles involved in eyelid elevation. It then defines ptosis and classifies it as congenital or acquired, with the acquired category further divided into neurogenic, myogenic, aponeurotic, mechanical, and neurotoxic causes. Several types of congenital ptosis are described in detail, including blepharophimosis syndrome and Marcus Gunn jaw-winking syndrome. Evaluation of ptosis involves assessing history, appearance of eyelids at rest, levator function testing, and identifying associated signs. Investigations may include imaging or blood tests depending on
- Papilloedema is edema of the optic disc caused by increased intracranial pressure. It is a non-inflammatory condition where the optic nerve swells within the confined space of the optic nerve sheath.
- Increased intracranial pressure from brain tumors, abscesses, venous thrombosis, aneurysms or pseudotumor cerebri can cause papilloedema.
- On examination, the optic disc margins blur, the disc swells and veins become congested. Late stages show macular star/fan exudates and optic atrophy if untreated.
- Treatment is aimed at relieving intracranial pressure through tumor removal, shunting procedures or medication for pseud
Syringomyelia is a condition where a cyst, called a syrinx, develops in the spinal cord. It most commonly affects the lower cervical spine. It is often associated with abnormalities of the skull or spinal column. The majority of cases are linked to Chiari malformation type 1, where the cerebellar tonsils are displaced into the spinal canal. Symptoms vary depending on the location of the syrinx but can include pain, loss of sensation, muscle weakness or atrophy, and autonomic dysfunction. Diagnosis is made using imaging like MRI. Treatment involves surgery to decompress pressure on the spinal cord like laminectomy with the goal of resolving the syrinx.
Disc edema ,papilloedema & optic neuritisVinitkumar MJ
Optic neuritis, papilledema, and optic disc swelling can have various causes and presentations. Optic neuritis is inflammation of the optic nerve and can be idiopathic or associated with multiple sclerosis, infections, or other conditions. Papilledema refers specifically to bilateral disc swelling caused by increased intracranial pressure from conditions like brain tumors, infections, or idiopathic intracranial hypertension. Treatment involves identifying and treating the underlying cause, and corticosteroids may help reduce inflammation in optic neuritis. Prognosis depends on the severity and management of the specific condition involved.
Papilloedema is swelling of the optic disc caused by increased intracranial pressure. It is defined as disc swelling associated with raised ICP and is nearly always bilateral. The document discusses the anatomy of the optic disc, causes of papilloedema including tumors and idiopathic intracranial hypertension, pathogenesis related to alterations in pressure gradients, clinical features such as headache and diplopia, and epidemiology showing highest rates in obese women of childbearing age.
This document provides an overview of glaucoma, including its definition, types, symptoms, risk factors, diagnostic techniques, and treatment approaches. Primary open-angle glaucoma is the most common type of glaucoma. It is characterized by optic nerve damage and visual field loss associated with elevated intraocular pressure. While increased IOP is a major risk factor, some patients can have glaucoma despite normal IOP levels. Diagnosis involves measuring IOP, examining the optic nerve head and retinal nerve fiber layer, and testing visual fields. Treatment may involve eye drops or surgery to reduce IOP and prevent further optic nerve damage.
This document discusses papilledema, which is swelling of the optic disc due to increased intracranial pressure. It defines papilledema and outlines its causes, signs, symptoms, grading, histopathology, investigations, differential diagnosis, and treatment. The main points are that papilledema is caused by increased intracranial pressure, it can be graded on a scale from 0-5 based on severity, and treatment involves addressing the underlying cause of pressure increase as well as surgical decompression in severe cases to prevent vision loss.
This document discusses optic nerve disease and optic neuropathy. It covers the clinical features, examination, investigations, and various causes of optic nerve disease including optic neuritis, nutritional optic neuropathy, anterior ischemic optic neuropathy, papilledema, and Leber's hereditary optic neuropathy. Examinations discussed include visual acuity testing, color vision testing, visual field testing, ophthalmoscopy, fluorescein angiography, and visual evoked potentials. Causes covered in more depth include optic neuritis, anterior ischemic optic neuropathy, nutritional optic neuropathy, papilledema, and Leber's hereditary optic neuropathy.
Optic disc ( very good book by Dr . Kathleen B. Digre )Vinitkumar MJ
1. The document discusses the anatomy and variants of the optic disc, including normal anatomy, blood supply, congenital anomalies, acquired conditions, and imaging findings. Key points include the association between optic nerve hypoplasia and pituitary abnormalities, the double ring sign in optic disc hypoplasia, basal encephaloceles in morning glory disc, and renal dysplasia in papillorenal syndrome.
This document discusses the evaluation and classification of various optic nerve diseases. It covers clinical features of optic nerve dysfunction, optic disc changes, types of optic atrophy, signs of secondary optic atrophy, special investigations, classification of optic neuritis, associations between optic neuritis and demyelination diseases, clinical features and treatment of optic neuritis, and other causes of optic neuritis including infectious, parainfectious, and arteritic anterior ischemic optic neuropathy.
GRAND ROUNDS : Anterior ischemic optic neuropathy with empty sellaSumeet Agrawal
This document summarizes a case presentation of a 60-year-old woman who presented with sudden vision loss in her left eye. She was diagnosed with non-arteritic anterior ischemic optic neuropathy (NAION) based on her age, risk factors of hypermetropia and crowded discs, and clinical findings of unilateral optic disc edema and filling defects on fluorescein angiography. She was treated with intravenous steroids followed by a tapering oral steroid course, with some mild improvement in her vision. Factorial causes were thought to include possible sleep apnea, unknown systemic factors, and intermittent prolapse of the optic nerve into an empty sella.
This document discusses approaches to macrocephaly and microcephaly. Macrocephaly is defined as a head circumference over 2 standard deviations above the mean, while microcephaly is under 3 standard deviations below the mean. Causes of macrocephaly include genetic factors, hydrocephalus, tumors, and metabolic disorders. Hydrocephalus results from abnormal CSF accumulation and can be obstructive or communicating. Microcephaly can be primary/genetic due to syndromes or secondary from infections, drugs, or hypoxia that impact brain development prenatally or in the first two years. Evaluation and treatment depends on the underlying cause.
The document discusses cerebrospinal fluid (CSF) production and circulation. It notes that 70% of CSF is produced in the choroid plexuses of the ventricles and is secreted at a rate of 0.3-0.5 cc/kg/hr. The CSF has a lower concentration of proteins, glucose, and potassium compared to blood plasma. It circulates from the ventricles through the subarachnoid space surrounding the brain and spinal cord before being reabsorbed. The functions of CSF include mechanical protection, maintenance of brain environment, removal of waste, and nutrition of the brain.
After this presentation, the reader should be able to describe features of papilledema with main causes and investigations needed in the work up and differentiate it from pseudopapilledema.
The document discusses the anatomy, physiology, and various pathologies of the optic nerve. It begins with the anatomy of the optic nerve, describing its four parts and blood supply. It then discusses the physiology of axonal transport within the nerve. Several optic nerve disorders are examined in depth, including papilledema, optic neuritis, and optic atrophy. Papilledema is edema of the optic disc due to increased intracranial pressure and can be caused by various conditions. Optic neuritis is inflammation of the optic nerve that can result in vision loss and pain and is associated with multiple sclerosis or infections. Treatment involves corticosteroids. Optic atrophy involves nerve fiber loss and pallor of the disc.
This document discusses neuro-ophthalmology and is presented by Dr. Lee Ming Yueh. It covers various topics including visual pathway and visual field defects, the optic disc, pupils, and cranial nerve palsies with eye manifestations. For visual field defects, it describes different testing methods and lesion locations that can cause specific defect patterns. The optic disc section discusses conditions like edema, atrophy, and swelling. Pupils are described in terms of innervation, size, shape, and defects. Finally, different cranial nerve palsies are outlined, focusing on causes, clinical features, investigations, and management considerations for nerves III-VII.
This document provides an overview of neuro-ophthalmology topics including pupillary disorders, neuro-motility disorders, optic nerve disease, and visual field defects. It describes the anatomy and physiology related to these topics and discusses various conditions that can cause abnormalities, such as third nerve palsy, Horner's syndrome, optic neuritis, anterior ischemic optic neuropathy, papilledema, and visual field defects including arcuate scotomas. The document provides details on clinical features, causes, and treatments for these various neuro-ophthalmological conditions.
Speaker Name: Anjali
Topic: "Demystifying Nystagmus"
Hello Everyone, Namaste!! We would like to notify you all that Mero Eye Foundation is going to conduct an "EYE TALKS-Webinar", and we will be having our session live broadcast on YouTube (Session No. 118)
DATE: at, 07:300 PM NPT, 07:15 PM IST, 22nd May 2021.
YouTube links: https://youtu.be/b4G12rRvXFc
Papilloedema is swelling of the optic nerve head caused by increased intracranial pressure (ICP). It is nearly always bilateral and patients should be evaluated for an intracranial mass. Papilloedema can be caused by idiopathic intracranial hypertension, obstructive lesions, space occupying lesions, impaired CSF absorption, cerebral venous sinus thrombosis, cerebral edema from head trauma, or severe hypertension. Treatment involves reducing ICP through measures like mannitol infusion, CSF withdrawal, sedation, or surgery to remove masses. Complications can include visual loss or chronic headaches.
1. A 41-year-old man presented with blurred disc margins and was found to have reactive syphilis serology, indicating neurosyphilis presenting as asymptomatic optic perineuritis.
2. A 9-year-old boy presented with intermittent headaches and abdominal pain and was found to have bilateral optic disc swelling and markedly elevated blood pressure, leading to the diagnosis of a pheochromocytoma.
3. In both cases, the optic disc swelling was an unusual presenting sign that led to the diagnosis of an underlying systemic condition.
This document discusses three case studies and provides an overview of cranial nerves V, VII and VIII. The first case is about trigeminal neuralgia presenting with facial pain. The second case involves Bell's palsy causing facial droop and eye closure issues. The third case presents with hearing loss and vertigo, found to have cavernous sinus thrombosis. It then reviews radiological images of these cranial nerves and discusses various pathologies, including lesions, that can affect each nerve. Evaluation techniques and distinguishing features of different conditions like trigeminal neuralgia and Bell's palsy are also summarized.
Papilledema is swelling of the optic disc caused by increased intracranial pressure. It is characterized by blurred disc margins and retinal nerve fiber layer edema. Increased CSF pressure is transmitted through the subarachnoid space and causes axoplasmic stasis in the optic nerve head. Papilledema is graded based on degree of disc elevation and obscuration from Frisen scale 0-5. Treatment involves addressing the underlying cause of increased ICP through medications, repeated lumbar punctures, or neurosurgery.
This document discusses ptosis, or drooping of the eyelid. It begins by describing the functional anatomy of the levator palpebrae superioris muscle and other muscles involved in eyelid elevation. It then defines ptosis and classifies it as congenital or acquired, with the acquired category further divided into neurogenic, myogenic, aponeurotic, mechanical, and neurotoxic causes. Several types of congenital ptosis are described in detail, including blepharophimosis syndrome and Marcus Gunn jaw-winking syndrome. Evaluation of ptosis involves assessing history, appearance of eyelids at rest, levator function testing, and identifying associated signs. Investigations may include imaging or blood tests depending on
- Papilloedema is edema of the optic disc caused by increased intracranial pressure. It is a non-inflammatory condition where the optic nerve swells within the confined space of the optic nerve sheath.
- Increased intracranial pressure from brain tumors, abscesses, venous thrombosis, aneurysms or pseudotumor cerebri can cause papilloedema.
- On examination, the optic disc margins blur, the disc swells and veins become congested. Late stages show macular star/fan exudates and optic atrophy if untreated.
- Treatment is aimed at relieving intracranial pressure through tumor removal, shunting procedures or medication for pseud
Syringomyelia is a condition where a cyst, called a syrinx, develops in the spinal cord. It most commonly affects the lower cervical spine. It is often associated with abnormalities of the skull or spinal column. The majority of cases are linked to Chiari malformation type 1, where the cerebellar tonsils are displaced into the spinal canal. Symptoms vary depending on the location of the syrinx but can include pain, loss of sensation, muscle weakness or atrophy, and autonomic dysfunction. Diagnosis is made using imaging like MRI. Treatment involves surgery to decompress pressure on the spinal cord like laminectomy with the goal of resolving the syrinx.
Disc edema ,papilloedema & optic neuritisVinitkumar MJ
Optic neuritis, papilledema, and optic disc swelling can have various causes and presentations. Optic neuritis is inflammation of the optic nerve and can be idiopathic or associated with multiple sclerosis, infections, or other conditions. Papilledema refers specifically to bilateral disc swelling caused by increased intracranial pressure from conditions like brain tumors, infections, or idiopathic intracranial hypertension. Treatment involves identifying and treating the underlying cause, and corticosteroids may help reduce inflammation in optic neuritis. Prognosis depends on the severity and management of the specific condition involved.
Papilloedema is swelling of the optic disc caused by increased intracranial pressure. It is defined as disc swelling associated with raised ICP and is nearly always bilateral. The document discusses the anatomy of the optic disc, causes of papilloedema including tumors and idiopathic intracranial hypertension, pathogenesis related to alterations in pressure gradients, clinical features such as headache and diplopia, and epidemiology showing highest rates in obese women of childbearing age.
This document provides an overview of glaucoma, including its definition, types, symptoms, risk factors, diagnostic techniques, and treatment approaches. Primary open-angle glaucoma is the most common type of glaucoma. It is characterized by optic nerve damage and visual field loss associated with elevated intraocular pressure. While increased IOP is a major risk factor, some patients can have glaucoma despite normal IOP levels. Diagnosis involves measuring IOP, examining the optic nerve head and retinal nerve fiber layer, and testing visual fields. Treatment may involve eye drops or surgery to reduce IOP and prevent further optic nerve damage.
This document discusses papilledema, which is swelling of the optic disc due to increased intracranial pressure. It defines papilledema and outlines its causes, signs, symptoms, grading, histopathology, investigations, differential diagnosis, and treatment. The main points are that papilledema is caused by increased intracranial pressure, it can be graded on a scale from 0-5 based on severity, and treatment involves addressing the underlying cause of pressure increase as well as surgical decompression in severe cases to prevent vision loss.
This document discusses optic nerve disease and optic neuropathy. It covers the clinical features, examination, investigations, and various causes of optic nerve disease including optic neuritis, nutritional optic neuropathy, anterior ischemic optic neuropathy, papilledema, and Leber's hereditary optic neuropathy. Examinations discussed include visual acuity testing, color vision testing, visual field testing, ophthalmoscopy, fluorescein angiography, and visual evoked potentials. Causes covered in more depth include optic neuritis, anterior ischemic optic neuropathy, nutritional optic neuropathy, papilledema, and Leber's hereditary optic neuropathy.
Optic disc ( very good book by Dr . Kathleen B. Digre )Vinitkumar MJ
1. The document discusses the anatomy and variants of the optic disc, including normal anatomy, blood supply, congenital anomalies, acquired conditions, and imaging findings. Key points include the association between optic nerve hypoplasia and pituitary abnormalities, the double ring sign in optic disc hypoplasia, basal encephaloceles in morning glory disc, and renal dysplasia in papillorenal syndrome.
This document discusses the evaluation and classification of various optic nerve diseases. It covers clinical features of optic nerve dysfunction, optic disc changes, types of optic atrophy, signs of secondary optic atrophy, special investigations, classification of optic neuritis, associations between optic neuritis and demyelination diseases, clinical features and treatment of optic neuritis, and other causes of optic neuritis including infectious, parainfectious, and arteritic anterior ischemic optic neuropathy.
GRAND ROUNDS : Anterior ischemic optic neuropathy with empty sellaSumeet Agrawal
This document summarizes a case presentation of a 60-year-old woman who presented with sudden vision loss in her left eye. She was diagnosed with non-arteritic anterior ischemic optic neuropathy (NAION) based on her age, risk factors of hypermetropia and crowded discs, and clinical findings of unilateral optic disc edema and filling defects on fluorescein angiography. She was treated with intravenous steroids followed by a tapering oral steroid course, with some mild improvement in her vision. Factorial causes were thought to include possible sleep apnea, unknown systemic factors, and intermittent prolapse of the optic nerve into an empty sella.
This document discusses approaches to macrocephaly and microcephaly. Macrocephaly is defined as a head circumference over 2 standard deviations above the mean, while microcephaly is under 3 standard deviations below the mean. Causes of macrocephaly include genetic factors, hydrocephalus, tumors, and metabolic disorders. Hydrocephalus results from abnormal CSF accumulation and can be obstructive or communicating. Microcephaly can be primary/genetic due to syndromes or secondary from infections, drugs, or hypoxia that impact brain development prenatally or in the first two years. Evaluation and treatment depends on the underlying cause.
The document discusses cerebrospinal fluid (CSF) production and circulation. It notes that 70% of CSF is produced in the choroid plexuses of the ventricles and is secreted at a rate of 0.3-0.5 cc/kg/hr. The CSF has a lower concentration of proteins, glucose, and potassium compared to blood plasma. It circulates from the ventricles through the subarachnoid space surrounding the brain and spinal cord before being reabsorbed. The functions of CSF include mechanical protection, maintenance of brain environment, removal of waste, and nutrition of the brain.
This document provides an overview of neuro-ophthalmology topics including the pupil, ocular motor system, visual system, and visual fields. It discusses the anatomy and pathways of the light reflex and near reflex. It describes various causes of unequal pupil size and how to evaluate them. Common eye movement disorders like sixth nerve palsy are outlined along with treatment approaches. The anatomy and testing of the visual system is reviewed. Papilledema and its causes and stages are explained. Optic neuropathies like anterior ischemic optic neuropathy and giant cell arteritis are compared.
Hydrocephalus is an abnormal accumulation of cerebrospinal fluid in the brain ventricles that causes them to expand. It can be caused by obstruction of CSF flow or improper absorption. Common signs include an enlarged head size, bulging fontanelles, downward eye deviation, and irritability. Diagnosis involves imaging tests and lumbar puncture. Treatment is typically with a shunt system to drain excess CSF out of the brain ventricles. Complications can include infection, shunt malfunction, and bleeding.
This document provides information on vestibular schwannoma (VS), including:
- VS arises from schwann cells surrounding the vestibular nerve in the internal acoustic meatus.
- It is a benign, slow-growing tumor that initially causes hearing loss and tinnitus. As it expands, it can compress cranial nerves and cause symptoms like facial numbness.
- Diagnosis involves hearing tests showing asymmetric hearing loss and imaging like MRI showing a globular mass.
- Treatment depends on tumor size and hearing status. Surgery options include translabyrinthine, middle fossa, and retrosigmoid approaches.
hydrocephalus, clinical features in various age groups, investigations, treatment options to create a basic understanding of the underlying pathology and management
radiology ppt on mri sequences how to read basic mri sequences and basic path...drashish05
MRI of the brain showed abnormalities in a patient with dengue encephalitis including:
1. Hyperintensities in the bilateral basal ganglia on T1 and T2 FLAIR images.
2. Diffuse areas of diffusion restriction in both cerebral hemispheres, basal ganglia, and caudate nuclei, sparing the thalami and frontal white matter.
3. Increased cortical hyperintensities over time in the parieto-occipital lobes and thalami.
4. Diffusion restriction and hyperintensities in the pons, thalami, and hippocampi.
Robert is a 62-year-old man who recently fell from a ladder while picking mangoes in his backyard. He was found unconscious by his wife and appeared confused upon arrival to the emergency department. He is complaining of left arm pain and shows signs of right-sided weakness. A past medical history of hypertension is noted, as well as a family history significant for various conditions including hypertension, diabetes, and stroke. A physical exam reveals confusion, right-sided facial drooping, and weakness as well as a hematoma on the left side of his head and a swollen, bruised left arm. Differential diagnoses include head injury such as contusion, concussion, or hemorrhage as well as a potential cerebrovascular
Craniocerebral trauma is a leading cause of death and disability in children, most commonly resulting from road traffic accidents, falls, or assaults. Head injuries can cause skull fractures, hemorrhages such as epidural or subdural hematomas, and diffuse axonal injuries that may require neurosurgical intervention. Secondary injuries like increased intracranial pressure, edema, or hypotension can further damage the brain if not properly managed.
1. The document discusses the initial management of traumatic brain injury, including decompressive craniectomy to reduce ICP, hyperosmolar therapy with mannitol or HTS, CSF drainage with EVD, and sedation to control refractory ICP. Early enteral nutrition is recommended if no contraindications.
2. Spinal trauma management involves cervical spine clearance following the Canadian C-spine Rule or Nexus criteria. Imaging includes 3-view c-spine series and thoracolumbar films. Neurological exam uses the ASIA chart.
3. Common neurosurgical emergencies are discussed like raised ICP, stroke, seizures, and brainstem compression from posterior fossa
The document discusses various types of head injuries. It begins by describing assessment of head trauma patients using the Glasgow Coma Scale and managing the ABCs. It then covers specific types of injuries like epidural hematomas, which appear as hyperdense lenticular masses on CT. Surgical management may involve burr holes or craniotomy. Subdural hematomas are a common mass lesion seen in head injuries and the elderly on blood thinners. Signs include altered consciousness and focal deficits. Subarachnoid hemorrhage presents with a sudden, severe headache and may involve meningeal irritation signs. Treatment focuses on blood pressure control, preventing seizures and complications.
chiari or arnold chiari malformations, various types and pathophysiology, radiological and clinical presentation of the types, signs symptoms, investigations and treatment of these malformations both conservative and surgical. considerations and controversiies in management of chiari malformation associated with various conditions.
Subarachnoid haemorrhage occurs when there is bleeding into the subarachnoid space between the membranes surrounding the brain. The most common cause is rupture of a berry aneurysm. Patients typically experience a sudden and severe headache, vomiting, and may lose consciousness. Complications include rebleeding, hydrocephalus, cerebral vasospasm leading to ischemia, and hyponatremia. Prompt diagnosis and treatment are important to prevent neurological deficits and reduce mortality.
This document discusses cerebral herniation syndromes which occur when increased intracranial pressure causes brain tissue to be squeezed through openings in the skull. It describes the four main types of herniation - subfalcine, central/downward transtentorial, temporal transtentorial/uncal, and cerebellar tonsillar. Clinical signs and prognosis are provided for each type of herniation. The Monro-Kellie doctrine is also summarized, which states that the intracranial compartment has a fixed volume, and increases in any component can increase intracranial pressure.
This document discusses cranial nerves IX, X, XI, and XII. It begins with an overview of topics to be covered, including neuroradiology, nerve examination procedures, and pathology of individual cranial nerves. Lower cranial nerve syndromes are described, including intramedullary and extramedullary lesions. Specific conditions that may cause lower cranial nerve involvement are also outlined, such as glossopharyngeal neuralgia, glomus tumors, and accessory nerve lesions. Various case scenarios are presented to demonstrate clinical presentations associated with different cranial nerve pathologies. The levels and causes of lesions for each individual cranial nerve are detailed.
This document provides an overview of syringomyelia, including:
- It is a spinal cord cavity filled with cerebrospinal fluid, with a prevalence of 9 per 100,000 people.
- It can be caused by traumatic injury, Chiari malformation, or other craniovertebral junction anomalies.
- Symptoms depend on the location and extent of the syrinx and can include sensory loss, weakness, pain, and autonomic dysfunction.
- Magnetic resonance imaging is the best way to diagnose and assess syringomyelia.
- Treatment may involve surgery to decompress the craniovertebral junction, open the syrinx, or place a shunt
This document summarizes various neuro-ophthalmic manifestations of cerebrovascular diseases. It discusses atherosclerosis, strokes, raised intracranial pressure, cerebral aneurysms, cerebral venous thrombosis, migraines, embolisms, cervical arterial dissections, and effects on the internal carotid and vertebrobasilar arterial systems. Key signs involve visual field defects, transient vision loss, optic disc edema, retinal artery occlusions, and cranial nerve palsies. Imaging such as MRI and MRA are important for diagnosis and treatment involves managing risk factors, anticoagulation, and surgical intervention in some cases.
This document provides information on vascular disorders of the retina. It begins with the anatomy and blood supply of the retina. It then discusses diabetic retinopathy in detail, including pathogenesis, signs, diagnosis and treatment. It also briefly covers hypertensive retinopathy and retinal vein occlusion, describing their pathophysiology, classification systems, clinical presentation and management. The document focuses primarily on providing an overview of diabetic retinopathy and its various stages and complications.
Benign intracranial hypertension (BIH), also known as idiopathic intracranial hypertension or pseudotumor cerebri, is characterized by increased intracranial pressure without a tumor or other identifiable cause. Common symptoms include headache, nausea, visual disturbances, and papilledema which can cause vision loss if untreated. While the exact cause is unknown, theories include excess CSF production, increased blood flow to the brain, or impaired venous drainage from the brain. Treatment involves weight loss, medications like acetazolamide, and sometimes surgical procedures to relieve pressure like optic nerve sheath fenestration or CSF shunting.
Benign intracranial hypertension (BIH), also known as idiopathic intracranial hypertension or pseudotumor cerebri, is characterized by increased intracranial pressure without a tumor or other identifiable cause. Common symptoms include headache, nausea, visual disturbances, and papilledema which can cause vision loss if untreated. While the exact cause is unknown, theories include excess CSF production, increased blood flow to the brain, or impaired venous drainage from the brain. Treatment involves weight loss, medications like acetazolamide, and sometimes surgical procedures to relieve pressure like optic nerve sheath fenestration or CSF shunting.
Similar to Some problem solving in neuro imaging updated Oct 2021 (20)
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Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
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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
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Some problem solving in neuro imaging updated Oct 2021
1. Some problem solving in Neuro-
Imaging: a practical approach
• Dr. Vincent Batista Lemaire
• Locum Consultant Radiologist
• St. Richards Hospital ,West Sussex Hospitals Trust, NHS .
• Chichester , England , UK .
3. Some problem solving in Neuro-
Imaging : A practical Approach
• Learning Objectives :through some interesting cases :
• 1. Recognise perivascular spaces
• 2. Cut off for fluid in the optic nerve-sheath complex.
• 3. How to measure an acoustic neuroma
• 4. Spontaneous intracranial hypotension
• 5. Recognise some vascular anatomical variants and disease.
• 6. Intracranial cyst differential diagnosis .
• 7. Pathologic conditions with restricted diffusion .
• 8. Pathologic conditions with blooming or signal loss.
• 9. Hint for reporting Multiple Sclerosis .
• 10, Hint for reporting Dementia .
9. The optic nerve-sheath and CSF
• The orbital subarachnoid space surrounding the optic nerve is
continuous with the circulation system for cerebrospinal fluid (CSF).
• Patient with increased intracranial pressure (ICP) often develop
papilledema (swelling of the optic disc which is a ophthalmologic
diagnosis )is a vision -threatening condition . Apparently , the
increase in the CSF volume in the peri-optic space results in
unfolding of the optic nerve sheath , and it is believe that this, in
turn , compresses the nerve, causing stasis of the axonal transport
and producing swelling of the optic nerve axons . So thee is
widening of the optic nerve sheath and flattening of the posterior
sclera.
• Low CSF –pressure may be involved in the pathogenesis of the
glaucoma : the subarachnoid space is narrowed .
11. The optic nerve-sheath and CSF
• The optic nerve: homogeneous , dark , does not enhances:
enhances or become bright in neuritis , or larger in
tumours. Diameter 3 mm .
• The sheath has normal CSF , or narrow like in glaucoma or
increase , like in ecstatic or more conspicuous as in
Idiopathic intracranial hypertension or non idiopathic
intracranial hypertension .The sheath is 1 mm wide in each
side + 3 mm optic nerve =5 mm . When there is ICH =6 mm
, 1.5 mm in each side .
• The fat stranding or enhancement mean pathologic
conditions .
• Tram –track enhancement : optic nerve-sheath complex
peri-optic meningioma narrows the nerve.
12. Optic neuritis: STIR
• 59y/o M; decreased left vision, probable optic neuritis. Vision 6 x 36 in the
left eye and 6 x 6 in the right eye. Left afferent pupillary defect. Pain on
eye
movement. Previous leg numbness.
•
14. Optic gliomas and unidentified bright
object in NF1
• 13 y/o M ; headaches wakes from sleep.
• When confined to the optic nerves (Dodge stage 1 – see below), they can
safely be referred to as optic nerve gliomas. Often, however, they are
either centred on or extend to involve the chiasm and optic radiations. In
such cases, they are difficult to distinguish from hypothalamic
gliomas and such a distinction is in most instances artificial.
• Unidentified bright objects tends to receded after 10 years all and affect
mainly the Globus pallidus and the brainstem .
15.
16. At 10 mm the optic nerve-sheath complex =5 mm ,
if the optic nerve 3 mm and sheath > 2 mm ,we
need to think in abnormal enlargement of the
subarachnoid space
18. The optic nerve-sheath and CSF
:papilledema
• 19 y/o F ,5 weeks headache and bilateral papilledema .
• Flattening of the posterior eyeball at the optic disc and fluid surrounding
the optic nerve in patient with pineal glioma .Left , 4 months later after
endoscopic ventriculostomy .
Endoscopic ventriculostomy
20. The optic nerve-sheath and CSF
• Clinical History : 74 y/o , f , progressive field loss right eye, normal intra-
ocular pressure ; ? compressive optic nerve.
22. The optic nerve-sheath and CSF
• Clinical History : 63 y/o , M, background ophthalmoplegia migraine. 6/12
sudden onset worsening left gaze. O/E complete VI nerve palsy. ?structural
cause.
23. The optic nerve-sheath and CSF
• 1.There is CSF surrounding the optic nerve.
• 2. The cut off for abnormal CSF is 2 mm behind the globe .
• 3. Rule out brain tumor , dural sinus thrombosis or hydrocephalus.
• 4. Is there papilledema? Overweight patient?, Visual loss?, field defect ?
• 5. look for empty sella turcica , enlarged Meckel cave and prominent
arachnoid pits.
• think about: IDIOPATHIC INTRACRANIAL HYPERTENSION
24. The optic nerve-sheath and CSF
• Clinical History : 63 y/o M; pale optic disc left eye ; field of vision worse ;
r/o meningioma
25. 1.Prominent subarachnoid space around the left optic nerve.
2. Tortuosity of the left optic nerve.
3. Pale optic disc ; field of vision worsening
Asymmetrical idiopathic intracranial hypertension
26. How to measure an acoustic neuroma?
• 1. Perpendicular to the posterior petrous ridge
Ice cream cone
Thanks to Dr. Steve Connor
27. How to measure an acoustic neuroma
• 2. Parallel to the posterior petrous ridge
28. How to measures an acoustic neuroma
3. Greatest craniocaudal dimension
29. How to measure an acoustic neuroma
The acoustic neuroma measures 16.4 x 18 .6 mm perpendicular and parallel to the
petrous ridge x 14.5 mm in its greatest craniocaudal dimension .
30. How to measure an acoustic neuroma
Increased despite gamma knife
31. How to measures an acoustic neuroma
• More difficult task: intra-labyrinthine extending to the superior and lateral
semi-circular canal. Take the greatest diameter and describe the lesion .
normal
32. The low laying cerebellar tonsil
• The differential diagnosis :
• MR demonstration of less than 2 mm of tonsillar ectopia is probably
of no clinical significance in the absence of syringomyelia.
• The Chiari I malformation is defined as displacement of the
cerebellar tonsils into the cervical spinal canal . Unlike many
malformations of the central nervous system (CNS), this entity
manifests itself in early adulthood and middle age, often with a
confusing clinical picture . Additionally, a low degree of cerebellar
ectopia is often of no clinical significance .
• Arnold Chiari II to IV : tonsillar and cerebellar herniated.
• High intracranial pressure: expansive process .
• Low intracranial pressure : CSF leak
33. The low laying cerebellar tonsil
• Clinical History : 37 y/o , M, headache on sitting and standing, nausea,
neck pain, balance disturbance, negative CT .
53. 6 Years later
1. Not return to normal calibre
2.Discontinuous signal in SSS
3. Thickened nodular dura
54. The arteries
• Normal variant
• Aneurysm
• Arteritis
• Thrombosis
• Tiny arteries we must know: the inferior
anterior cerebellar artery :tinnitus and SNHL;
and the superior cerebellar artery :trigeminal
neuralgia .
55. Trigeminal artery
• The persistent trigeminal artery usually arises from the presellar ICA as it
exits the carotid canal and enters the cavernous sinus and it extends
posteriorly to join the distal third of the basilar artery usually between the
origins of the superior and anterior inferior cerebellar arteries.
68. Thrombosis
• 79 y/o M, slurred speech , left weakness.
• Right MCA hyperdense sign .
69. Thrombosis
• 56 y/o M; slurred speech ; left side weakness
• Right MCA hyperdense sign
70. Occlusion of the artery of Percheron
• Common trunk from posterior cerebral artery
with symmetrical infarcts in the paramedian
cerebral peduncle and thalami.
78. Vascular loop over the V cranial nerve
• 40 y/o M R trigeminal neuralgia.
• Superior cerebellar artery loop ; ? causing compression
79. Vascular loop over the V cranial nerve
• 68 y/o F ; recurrent R trigeminal neuralgia, shooting pain V2,V3.
• R trigeminal atrophy and 2 segments ( porus trigeminus and cisternal
segment)contacted by the superior cerebellar artery .
80.
81. Vascular loop over the V cranial nerve
• 59 y/o F , facial pain left side .
• Trigeminal nerve atrophy and vascular loop
82. Vascular loop over the trigeminal
nerve
• 68 y/o M; pain behind left eye
• Vertebrobasilar dolichoectasia abutting the left V cranial nerve.
83. Vascular loop over the VI cranial nerve
• 54 y/o F, internal strabism ,VI N palsy (abducens to rectus lateral muscle )
• The left vertebral artery joins the right to form the basilar artery to the
right of the midline at the level of the acoustic canal and then curves to
left left apparently abutting the R VI.
84. Vascular loop over the VII-VIII cranial
nerves
• 57y/o M , left side high frequency SNHL .
• Left AICA (anteroinferior cerebellar artery)abutting the left VII-VIII.
85. Vascular loop over the R VII-VIII cranial
nerves
• 68 y/o F ; asymmetrical SNHL + tinnitus .
• Right AICA abutting the statoacoustic nerve
86. Swirl sign
85 y/o woman :Lobar haemorrhage . Almost no surrounding
edema.The basal ganglia are spared. Low density in the core
In keeping with active bleeding . Severe edema effacing
the sulci and sylvian fissure.
88. Brain death
• 24 y/o woman ; cardiac arrest after allergic
reaction .
24 y/o woman cardiac arrest
Normal 12 y/o girl
89. Intracranial cysts : classification
according to Origin or Pathogenesis
• Normal and or variant: extra-axial :pineal ;
intra-axial :choroid plexus, ependymal , PVS
,neuroglial .
• Congenital :extra-axial: arachnoid, epidermoid
,dermoid , neurenteric , Rathke cleft; intra-
axial : colloid
• Note: intraventricular lesions are intra-axial
90. Intracranial cysts : classification
according to Origin or Pathogenesis
• Traumatic : post vascular event or surgery
intra-axial :porencephalic .
• Infectious : extra/intra-axial
:neurocysticercosis , hydatid , others.
• Tumor-associated : extra-axial: vestibular
schwannoma (true arachnoid cyst),
craniopharyngioma and pituitary macro-
adenoma ( enlarge the PVS), meningioma
( trapped CSF).
91. Classification of intracranial cysts according to
most common location : Osborn and Preece.
• Cyst Location
• Arachnoid middle cranial fossa
• Choroid plexus atria lateral ventricle
• Colloid pillar of fornix straddle the cyst ( Monro foramen).
• Craniopharyngioma (PVS) suprasellar
• Dermoid sellar , parasellar, midline
• Enlarged PVS basal ganglia/ midbrain
• Epidermoid cerebellopontine angle cistern
• Ependymal lateral ventricle
• Hydatid parietal lobe
• Meningioma with trapped CSF convexity or planum sphenoidale
• Neurenteric prepontine
• Nuerorocysticercosis convexity or basal subarachnoid spaces
• Neuroglial frontal lobe
• Pineal pineal gland
• Pituitary adenoma (PVS) parasellar
• Porencephalic cerebral hemispheres
• Rathke cleft sellar or suprasellar
• Schwannoma with arachnoid cyst cerebellopontine angle cistern
92. Dermoid cyst
• Origin : ectodermal, midline cyst
• Made of epithelium , collagen , dermis with hair follicles, sebaceous
glands , apocrine glands and liquid cholesterol . May contain teeth.
• Active production of hair and oils by the dermal appendages : early
rupture, which could cause chemical meningitis that may lead to
vasospasm , infarction , and even death .
• Capsule is thicker than that of epidermoid often contains plaques of
calcification .
• Well –defined; lobulated ; hyperintense on T1 , heterogeneous on t2,
suppress signal on STIR .
93. Dermoid cyst
• 59 y/o F; headaches , intermittent R hand weakness
• Epidermoid cyst resemble CSF ; craniopharyngioma high on t2 and
enhances .
94. Dermoid cyst
• 52 y/o F left migraine and hearing loss
Fatlike droplets is subarachnoid cistern : rupture
98. Neuroglial cyst ???
• 18 y/o M , Post viral ataxia; f/u t2; bottom 1 year later. ?low grade glioma ;
parasitic?
99. Arachnoid cyst
• Space occupying lesion that follows CSF in all sequences.
• Sharply demarcated , displace or deform the adjacent brain ; scalloping of
the calvarium .
• Occasionally : haemorrhage or proteinaceous content.
100. Arachnoid cyst
• 46 F ; right sided numbness + odd feeling
• Spinal arachnoid cyst
101. Arachnoid cyst
• 44 y/o F ; chronic headaches
• R ambient /perimesencephalic cistern
102. Arachnoid cyst
• 86 y/o F ; widened Silla turcica on CT .
• Intrasellar arachnoid cyst .
103. Arachnoid cyst
• 29 y/o M; infantile hemiparesis and seizures.
• Multilocular temporoparietal arachnoid cyst.
104. Arachnoid cyst
• 40 y/o M ; right leg dragging , head pain .
• Posterior fossa arachnoid cyst with Ommaya reservoir .
105. DWI: restricted water motion produces high signal
intensity on diffusion MR and hypointensity on
apparent diffusion coefficient (ADC)
Free water diffusion restricted diffusion
Facilitated diffusion
106. Restricted diffusion : mechanism
• 1. The brain shows restricted diffusion because is made of highly packed
cells with ADC values at 750. CSF values 3000-3050
• 2. cellular swelling in cytotoxic oedema : DWI: the extracellular space is
only 20% of the brain but dominant contributor to the ADC values. The
ADC reflect the state of the EXTRACELLULAR SPACE . In Ct the hypodensity
is due to water coming from the capillary to the extracellular space long
after the cytotoxic edema converts into ionic oedema with hypertonicity
in the extracellular space.
• 3. high cellularity in tumor ( lymphoma , medullablastoma );pus within
abscess; viscous fluid; blood products : the random ,fast-moving -moving
water protons to slow Brownian motion . The necrotic centre of a GBM
show high ADC .
108. Restricted diffusion
• acute stroke 500 x 10-6 mm2/
• White matter 750 x 10-6 mm2/s
• Oedema 1500 x 10 -6/s
• CSF 3200 x 10 -6/s
• S DWI = S b=0 x e (-bx D)
109. Restricted diffusion
• Disease Cause
• Hyper acute stroke (0-6hrs) cytotoxic oedema
• Acute stroke (6hrs -3days ) cytotoxic oedema
(sensibility > 90% in first 24hrs )
• Haemorrhage oxyhemoglobine intracellular
• Abscess increase viscosity and cellularity
• Tumour increase in cellularity
• Epidermoid tumour viscosity (debris , keratin , cholesterol )
• Encephalitis cytotoxic oedema
• Creutzfeldt -Jacob unknown
• Multiple sclerosis
( a few acute lesions) unknown
110. Restricted diffusion: acute ischaemia
• 76 y/o F ; sudden onset left side headache and vertigo; difficulty reading
and memory problems.
111. Restricted diffusion: acute ischaemia
• 73 y/o M; temp 41.c ; reduced GCS , intubated.
• External border zones of ACA, MCA and PCA + PICA: watershed ischaemia
114. Restricted diffusion: abscess
• Differential diagnosis of rim-enhancing lesions:
• - glioma
• - abscess
• - demyelinating disease
• - metastasis
• - radiation
• - infarct
• -evolving haematoma
• Demonstration of restricted diffusion within the central portion strongly
suggest abscess rather than a necrotic primary tumour or metastasis .It
will show high signal on DWI . T2 hypointense ring .
115. Restricted diffusion: abscess
• 1. point to ventricles.
• 2. daughter ring
• 3.homogeneous wall thickness but thicker
towards the cortex .
• 4. Fussy margins, no perfect sharp line .
• 5.T2/STIR superimposed dark line; low ADC .
• 6. If the lesion is not bright on DWI it is not
and abscess.
118. Restricted diffusion: tumour
• 73 y/o F ; solitary breast metastasis and 3 months f/u after cyber knife
therapy .
• Rim of restricted diffusion
f/u 3 months
119. Restricted diffusion: GBM
• If to much people in this party think about
GBM : traverse the grey-white matter junction ;single or multifocal ;
heterogeneous with irregular contour; annular contrast enhancement ,
central necrosis , haemorrhage; extends beyond enhancing rim ; over
corpus callosum butterfly wings ; dural extension ; mass over effect over
ventricles. (Dr.Mufudzi Maviki ; Jean-Louis Dietemann)
120. Restricted diffusion: GBM
• GBM:
• 1. rarely ring enhancement .
• 2. solitary , corpus callosum , deep white matter ,
irregular, random , ugly geographic necrosis ,
irregular peripheral enhancement recruiting new
vessels VS metastasis :no affecting the corpus
callosum , at the grey white matter junction ,
more spherical ,attention with haemorrhagic
mets which could be similar to and abscess.
122. Restricted diffusion: GBM
• 56 y/o M ; fall , right weakness an sensory changes .
• High grade multifocal GBM treated with dexamethasone; f/u 5 months
124. Restricted diffusion: lymphoma
• Deep settle: contact to the ventricles (juxta ventricular )and corpus
callosum , butterfly ; basal ganglia ,subependymal and gyral. Shows 1 mm
blurred along the margin, vividly homogeneous enhancement, no flow
void. Higly cellular , low ADC .
• 68 y/o F ; changes in personality , headaches .
125. Restricted diffusion: lymphoma
• 59 y/o F odd behaviour, seizure.
• Primary multifocal lymphoma
Multifocal :embedded or connected by Multicentric :not connected
129. Restricted diffusion: epidermoid tumor
• Fibrous capsule, containing keratohyalin and cholesterol crystal .
Lobulated, irregular , “cauliflower-like” mass with “fronds” .Surrounds,
engulfs vessels and nerves .
• Low heterogeneous signal on t1; t2/flair hyperintense ; high signal on DWI
and low on ADC .( same ADC as the brain tissue 735).High lactate on
spectroscopy .
• 49 y/o ; F ; asymmetrical sensorineural hearing loss
140. Susceptibility weighted imaging
• Previous know as BOLD venographic imaging . Differs significantly from a T2*-
weighted GE sequence, as SWI is based on a long echo-time(TE), with high
resolution, flow compensation , and filtered phase information in each voxel.
• Magnetic susceptibility is the relative ability of a substance to become
magnetized when exposed to a magnetic field: positive , ferromagnetic (Iron:
Fe2+,Fe3+) or paramagnetic (hemosiderin and deoxyhemoglobin + basal
ganglia calcification ; Gadolinium); negative, diamagnetic (free water and most
human tissue including cortical bone + calcification outside the basal ganglia).
• In a left handed system the iron deposition and haemorrhage
(paramagnetic) look bright on the phase and dark on SWI image relative to
the surrounding brain tissue and the calcium (diamagnetic) looks dark on
both phase and SWI image relative to brain tissue .
• Deoxyhemoglobin is paramagnetic. So the veins in the sulci and along the
lateral ventricle appear bright (positive phase) and are a marker of a left
handed system. Oxyhemoglobin is diamagnetic in nature, so arteries appear
dark (negative phase).
141. Data sets generated during the scan. 1. Magnitude. 2.
Filtered Phase image. 3. SWI. 4. SWI mIP. References:
Columbia Asia Hospital, Bengaluru.
Susceptibility weighted
imaging
1.Original Magnitude Image – shows
reduced anatomic differentiation.
2.Phase Mask Image - shows inverse
contrast behavior.
3.SWI data- is a combination of
magnitude and phase information.
4.Minimum intensity projections of
SWI(mIP SWI) with thickness of 3-
5mm.
In phase the blood is white and the calcium shows signal void
143. Susceptibility weighted imaging: SWI and
T2*gradient-echo hypointensities :blooming
• 1. Amyloid angiopathy : cortical subcortical microbleeds and spontaneous lobar
cerebral haemorrhage.
• 2. Hypertensive angiopathy : basal ganglia, thalamus , pons.
• 3. Diffuse axonal injury: grey /white matter junction in the frontal and temporal lobes ;
corpus callosum and posterolateral brainstem.
• 4. Multiple cavernomas :subcortical and cerebellar .
• 5. Venous angiomas
• 6. CADASIL : subcortical lacunar infarcts ,white matter lesions + foci in centrum
semiovale, thalamus , basal ganglia and pons. SWI subcortical . External capsule and
anterior temporal pole in patient with migraine, dementia and family history.
• 7. Tumor : haemorrhage and calcifications ; SWI used both , before and after the
administration of contrast could differentiated the vessels than change their signal
intensity from the regions of inactive haemorrhage which do not change.
• 8. Metastasis : melanoma , choriocarcinoma , lung ,breast and renal cell ca.
• 9. Multiples sclerosis : due to iron deposition ; central vein detection ;could detect near
50%more lesions .
• 10. Cerebral vasculitis , meningitis .
• 11. Dermoid : intracranial fat
153. SWI : multiple cavernous angiomas
• 69 y/o F ; right vocal cord palsy ; incidental finding of lesion at the base of the skull
.Multiple meningiomas and cavernous angiomas in neurofibromatosis type II
154. SWI : multiple cavernous angiomas
T2, t2+PD do not exhibit the classical “pop corn “ appearance. The cavernomas in
this case are well seen on SWI
156. SWI: CADASIL (Cerebral Autosomal –Dominant
Arteriopathy with Subcortical infarcts and
Leucoencephalopathy )
• 59 y/o M; progressive gait + cognitive disturbance.
157. SWI :tumour
• 85 y/o F ; road traffic accident ; confused, poor speech ; r/o subdural
• Too much people in this party : GBM
158. SWI :metastases
• Haemorrhagic intracranial metastases are considered to
represent between 3-14% of all cerebral metastases (c.f. 1-
3% of gliomas are haemorrhagic).
• Melanoma
• Choriocarcinoma
• Thyroid carcinoma: papillary carcinoma of the thyroid has
that highest rate .
• Renal cell carcinoma
• Lung carcinoma
• Breast carcinoma
• Hepatocellular carcinoma
• Mnemonic: MR CT BB
Dr. Maxime St-Amant and Prof. Frank Gaillard ; Radiopedia .
159. SWI :metastases
• 63 y/o previous resection met from RCC R frontal lobe; now seizure,
suspicious of recurrence.
160. Dermoid cyst
• 52 y/o F ; left migraine with aura ; clumsy , hearing loss.
• Ruptured dermoid cyst
162. Reporting Multiple Sclerosis
• I recommend The Radiologist Assistant :
multiple sclerosis by Frederik Barkhof, Robin
Smithuis and Marieke Hazewinkel.
• Highly recommended : post contrast scan at 5
or 15 minutes post injection .
163. Reporting Multiple Sclerosis
• For dissemination in space (DIS) lesions in two out of four typical areas of the
CNS are required: periventricular; juxtacortical ; infratentorial ; spinal cord.
• For dissemination in time (DIT) there are two possibilities: A new T2 and
/or gadolinium-enhancing lesion (s0 on follow-up MRI , with reference to a
baseline scan , irrespective of the timing or simultaneous presence of
asymptomatic gadolinium enhancing and non enhancing lesions at any
time .
165. Reporting Multiple Sclerosis
• Where are the lesions :
• 1.Juxtacortical : U fibers that touch the cortex
• 2.calloso-septal interphase : inferior surface of the
corpus callosum :cret –du-coq ; Dawson fingers : plaques
with perpendicular orientation at callososeptal
interphase along penetrating venules .
• 3. temporal lobe: juxtacortical or at the stem
• 4. brainstem , cerebellar peduncles and optic nerves .
166. Reporting Multiple Sclerosis
• Shape of the lesions:
• 1. ovoid
• 2. round
• 3. whorl , loop , coil : Balo’s concentric sclerosis
• 4. mass : tumefactive MS : open ring sign ; less oedema than
expected for the mass that we see.
167. Reporting Multiple Sclerosis
• Meaning :
• 1. low signal on T1W , low signal on FLAIR with
hyperintense halo , no enhancement : wet black holes,
permanent chronic demyelination ; axonal loss, matrix
destruction .
• 2. High signal on FLAIR: load lesion with demyelination .
• 3. Ring enhancement : old lesion or reactivation
• 4. Nodular enhancement : acute, recent lesion .
171. Reporting Multiple Sclerosis
• Interval scan :
• 1. new lesions : new focus , could be load lesion or acute
lesions .
• 2. enhancing to non enhancing lesions .
• 3. less conspicuous lesions / cleared lesions
• 4. acute lesion : contrast uptake
• 5. subacute lesions : early period , within 10 weeks and
reduce oedema ; late period: gliosis/re-myelination .
• 6. load lesion to wet lesions .
• 7. brain volume change 1% a year , in 10 year :
pseudoatrophy.
172. Hint reporting dementia
• Dementia: role of MRI updated version, The Radiologist Assistant by
Frederik Barkhof, Marieke Hazewinkel, Maja Binnewijzend and Robin
Smithuis Alzheimer Centre and Image Analysis Centre, Vrije Universiteit
Medical Center, Amsterdam and the Rijnland Hospital, Leiderdorp, The
Netherlands
• The Addenbrooke's Cognitive Examination-III (ACE-III) is a brief cognitive
test that assesses five cognitive domains: attention, memory, verbal
fluency, language and visuospatial abilities. ... The total score is 100 with
higher scores indicating better cognitive functioning.
• During the MMSE,Mini-Mental State examination , a health professional
asks a patient a series of questions designed to test a range of everyday
mental skills. The maximum MMSE score is 30 points. A score of 20 to 24
suggests mild dementia, 13 to 20 suggests moderate dementia, and less
than 12 indicates severe dementia.
173. Hint reporting dementia :type and
location .
• Alzheimer :hippocampus
• Fronto-temporal: (former Picks )more than parietal + genus of
corpus callosum .
• Lewy bodies: non-specific ; more white matter lesions than in
Alzheimer .
• Aphasia Progressive :severe anterior temporal atrophy .
• Posterior cortical atrophy (Benson’s syndrome): atrophy
parieto-occipital and posterior temporal B/L .
• Corticobasal degeneration : parasagittal frontoparietal, basal
ganglia , sustantia nigra and tegmentum .
• Vascular Cortical: ischaemic lesions corticosubcortical.
174. Hint reporting dementia :type and
location
• Vascular Subcortical :
- Binswanger, lacunar infarcts in the basal ganglia secondary to severe
hypertension ;
- leucoaraiose; white matter degeneration with progressive demyelination
secondary to small vessels disease.
- CADASIL ( Cerebral Autosomal Dominant Arteriopathy with Subcortical
Infarcts and Leucoencephalopathy ): lacunar infarcts in the basal ganglia and
brainstem + diffuse leucoaraiose predominant at the external capsule, anterior
insula and anterior temporal lobe; absent in the parietal and occipital lobes.
. Amyloid Angiopathy
. Infective encephalitis : Leucoencephalopathy Multifocal Progressive (LEMP),
virus JC; Creutzfeldt-Kakob .
. Toxic : Wernicke, lack of B1: periaqueductal high signal ; 3rd ventricle and
mammillary bodies.
.Korsakoff syndrome : ETOH; hippocampus-mammillary bodies-thalami with
severe atrophy of the mammillary bodies.
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