Holmes adie syndrome
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Holmes adie syndrome is a neurological disorder that affects the pupil of the eye and the autonomic nervous system.
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Nystagmus
This document provides an overview of nystagmus, including its definition, terminology, types, causes, and characteristics. Nystagmus is defined as a repetitive, to-and-fro movement of the eyes. It is classified as congenital or acquired, and includes types such as infantile nystagmus, spasmus nutans, end point nystagmus, vestibular nystagmus, optokinetic nystagmus, downbeat nystagmus, and nystagmus associated with strabismus. The document discusses the mechanisms, features, and treatments of different forms of nystagmus.
Approach to vision loss
1. The document provides an overview of approaches to evaluating vision loss, including determining whether it is monocular or binocular and transient or persistent.
2. Examinations should include visual acuity, color vision, visual fields, pupils, and examination of the eyes and optic discs.
3. Causes of transient and acute vision loss are discussed, including optic neuropathies, ischemic events, migraine, and PRES.
4. Progressive vision loss may be due to compressive lesions, glaucoma, or retinal disorders.
Horners syndrome
Horner's syndrome results from interruption of the sympathetic nerve supply to the eye, causing the classic triad of ptosis, miosis, and anhidrosis. It can occur from lesions anywhere along the three-neuron sympathetic pathway from the brainstem to the eye. Testing includes evaluating pupil response to light and pharmacologic tests like cocaine and apraclonidine to localize the lesion and guide further workup and treatment of the underlying cause when possible. The goal is to identify potentially serious underlying conditions causing Horner's syndrome.
Pupil
This document discusses the pupil in health and disease. It begins by describing the normal anatomy and function of the pupil, including its size, location, shape, and role in regulating light entry. It then covers various pupil reflexes and abnormalities such as anisocoria, mydriasis, miosis, light-near dissociation, Argyll Robertson pupils, and disorders of the third cranial nerve and sympathetic pathway. Causes, signs, and diagnostic tests for various pupil abnormalities are provided.
Approach to vision loss
This document discusses approaches to vision loss. It defines various patterns of vision loss including transient monocular, persistent monocular, and binocular vision loss. It describes causes of transient monocular vision loss such as amaurosis fugax which can be due to circulatory, ocular, or neurologic factors. Key factors in evaluating vision loss include whether it is monocular or binocular, the pattern and degree of loss, tempo of onset, and associated symptoms. Common causes of sudden monocular vision loss discussed include central retinal artery occlusion and optic neuritis.
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This document provides information about nystagmus, including its definition, mechanisms, causes, types, and clinical features. Some key points:
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- Causes can include lesions of the
Optic atrophy (b)
This document provides an overview of optic atrophy, including:
1. It defines optic atrophy as degeneration of the optic nerve due to damage to the visual pathways from the retina to the lateral geniculate body.
2. It classifies optic atrophy based on whether damage originates in the retina or more centrally, and by cause. Primary optic atrophy occurs without swelling, while secondary involves prior swelling.
3. Causes of primary optic atrophy include optic neuritis, compression, hereditary conditions, toxins, trauma, and multiple sclerosis. Secondary optic atrophy follows conditions like papilledema.
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Approach to vision loss
1. The document provides an overview of approaches to evaluating vision loss, including determining whether it is monocular or binocular and transient or persistent.
2. Examinations should include visual acuity, color vision, visual fields, pupils, and examination of the eyes and optic discs.
3. Causes of transient and acute vision loss are discussed, including optic neuropathies, ischemic events, migraine, and PRES.
4. Progressive vision loss may be due to compressive lesions, glaucoma, or retinal disorders.
Horners syndrome
Horner's syndrome results from interruption of the sympathetic nerve supply to the eye, causing the classic triad of ptosis, miosis, and anhidrosis. It can occur from lesions anywhere along the three-neuron sympathetic pathway from the brainstem to the eye. Testing includes evaluating pupil response to light and pharmacologic tests like cocaine and apraclonidine to localize the lesion and guide further workup and treatment of the underlying cause when possible. The goal is to identify potentially serious underlying conditions causing Horner's syndrome.
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This document discusses the pupil in health and disease. It begins by describing the normal anatomy and function of the pupil, including its size, location, shape, and role in regulating light entry. It then covers various pupil reflexes and abnormalities such as anisocoria, mydriasis, miosis, light-near dissociation, Argyll Robertson pupils, and disorders of the third cranial nerve and sympathetic pathway. Causes, signs, and diagnostic tests for various pupil abnormalities are provided.
Approach to vision loss
This document discusses approaches to vision loss. It defines various patterns of vision loss including transient monocular, persistent monocular, and binocular vision loss. It describes causes of transient monocular vision loss such as amaurosis fugax which can be due to circulatory, ocular, or neurologic factors. Key factors in evaluating vision loss include whether it is monocular or binocular, the pattern and degree of loss, tempo of onset, and associated symptoms. Common causes of sudden monocular vision loss discussed include central retinal artery occlusion and optic neuritis.
Nystagmus
This document provides information about nystagmus, including its definition, mechanisms, causes, types, and clinical features. Some key points:
- Nystagmus is a periodic rhythmic oscillation of the eyes, characterized by a slow drift in one direction followed by a fast corrective movement. It can be caused by disturbances of vision, eye movements, or the vestibulo-ocular reflex.
- Types of nystagmus include jerk nystagmus, pendular nystagmus, see-saw nystagmus, convergence-retraction nystagmus, and various forms of congenital or acquired nystagmus.
- Causes can include lesions of the
Optic atrophy (b)
This document provides an overview of optic atrophy, including:
1. It defines optic atrophy as degeneration of the optic nerve due to damage to the visual pathways from the retina to the lateral geniculate body.
2. It classifies optic atrophy based on whether damage originates in the retina or more centrally, and by cause. Primary optic atrophy occurs without swelling, while secondary involves prior swelling.
3. Causes of primary optic atrophy include optic neuritis, compression, hereditary conditions, toxins, trauma, and multiple sclerosis. Secondary optic atrophy follows conditions like papilledema.
4. Treatment focuses on the underlying cause, with vitamins sometimes used
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Horner Syndrome
This document discusses Horner syndrome, providing details on its features, diagnosis, and evaluation. Some key points:
- Horner syndrome is caused by disruption of the sympathetic pathway to the eye, resulting in ptosis, miosis, and other signs.
- Physical exam looks for subtle signs like ptosis, miosis, and dilation lag. Pharmacologic tests can help diagnose and localize the lesion.
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This document provides an overview of sixth nerve palsy, including:
- The sixth cranial nerve innervates the lateral rectus muscle to enable eye abduction. Sixth nerve palsy results in limited ability to turn the eye outward.
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SIXTH CRANIAL NERVE PALSY- Diagnosis and management
Cover the fixing eye
Examiner: Note movement of uncovered eye
- Esotropia in primary position
- Exotropia on looking towards affected side
- No movement on looking towards normal side
- Quantifies the deviation
- Helps in diagnosis and management
Past pointing test
- Patient asked to point with finger to target
- Deviation of finger from target indicates diplopia
- Helps in localizing the diplopia
Diplopia charting
- Patient asked to draw position of second image
- Helps in localizing and quantifying diplopia
Worth 4 dot test
- Assesses binocular single vision
- Loss of fusion indicates diplop
Supranuclear pathways and lesions
This document discusses supranuclear pathways and lesions that can affect eye movements. It begins with the fundamentals of extraocular movements and anatomy of cortical and brainstem centers that control eye movements. It then covers the basic types of eye movements like saccades, smooth pursuit, vestibular-ocular reflex, and vergence movements. It provides a step-wise approach to evaluating eye movement disorders and localizing lesions based on the type of eye movement affected. Supranuclear lesions can cause bilateral eye movement involvement, while specific brainstem lesions impact horizontal or vertical eye movements or specific eye movement types like saccades or vestibular-ocular reflex.
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The abducens nerve originates in the pons and contains motor neurons that innervate the lateral rectus muscle, allowing for eye movement outward. It exits the brainstem and travels through the cavernous sinus before entering the orbit through the superior orbital fissure to innervate the lateral rectus. Pathologies of the abducens nerve can occur at the nuclear, central, cisternal, petrous, cavernous, or orbital segments and result in lateral rectus palsy and limitations in abduction of the eye. Common causes include pontine hemorrhage, MS, meningiomas, and traumatic injuries.
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This document provides information on key anatomical structures of the fundus including:
1) It describes several structures that can be seen on examination of the fundus including the optic disc, macula, retinal blood vessels, and peripheral retina.
2) It explains features of the optic disc including that it is insensitive, round or oval in shape, and contains the lamina cribrosa through which ganglion cell axons exit the eye.
3) The macula is described as being located temporally from the optic disc, containing the highest concentration of cones, and responsible for photopic vision and color vision.
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mydriasis, nystagmus, papilledema.pptx
Mydriasis refers to the dilation of the pupil. It can occur normally in low light environments but prolonged or inappropriate mydriasis may indicate an underlying cause like injury, drugs, or conditions like Adie Syndrome. Treatment depends on the cause but may include medications. Mydriasis is a risk factor for angle closure glaucoma in individuals with narrow eye angles.
Nystagmus causes uncontrollable eye movements and can be congenital or acquired later in life due to conditions like MS, stroke or ear problems. Symptoms include blurred vision and dizziness. It is usually managed with glasses, contacts or rarely surgery but the underlying cause also needs to be addressed.
Papilledema refers to swelling of
Blindness and its management
The document discusses visually handicapped and visually challenged individuals. It defines different types of blindness from complete blindness to mild or moderate vision impairment. The leading causes of vision loss globally are uncorrected refractive errors and cataracts. Some key causes of blindness include glaucoma, macular degeneration, diabetic retinopathy, and certain eye diseases. Symptoms may include cloudy vision, inability to see shapes, or poor night vision. Blindness is diagnosed through eye exams and can sometimes be treated through glasses, surgery, medication or learning adaptive skills depending on the cause and severity of vision loss.
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This document discusses ocular signs in neurology. It outlines how to systematically examine the eyes including evaluating pupil size and reaction, ocular motor function, visual acuity and fields. It describes various neuro-ophthalmic disorders like Horner syndrome, third nerve palsy, and internuclear ophthalmoplegia that can be identified on examination. It also covers types of nystagmus including congenital, sensory deprivation, and motor imbalance nystagmus and discusses evaluating nystagmus to determine its cause.
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This document summarizes various types of gaze palsies, including their causes and clinical presentations. Supranuclear gaze palsies can result from lesions in areas that control eye movements, like the brainstem or cerebral cortex. Clinical exams help localize lesions and differentiate organic from functional disorders. Specific syndromes discussed include Parinaud's syndrome, progressive supranuclear palsy, internuclear ophthalmoplegia, and one-and-a-half syndrome. The document provides details on symptoms, locations of lesions, and distinguishing features of different supranuclear gaze palsy conditions.
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This document discusses Horner syndrome, providing details on its features, diagnosis, and evaluation. Some key points:
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- Physical exam looks for subtle signs like ptosis, miosis, and dilation lag. Pharmacologic tests can help diagnose and localize the lesion.
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The pupil is an opening in the iris that controls the amount of light entering the eye. It constricts and dilates under autonomic nervous system influence. The normal pupil diameter ranges from 2.5-4 mm in daylight and 1.3-10 mm in extremes. Unequal pupil sizes is called anisocoria. The pupil constricts in response to light and near vision. Abnormal pupils can be congenital, traumatic, inflammatory, or neurological in origin. Tests like cocaine, hydroxyamphetamine, and pilocarpine help localize lesions causing abnormalities like Horner's syndrome or Adie's tonic pupil.
Oculomotor nerve palsy
This document discusses the anatomy and function of the oculomotor nerve (cranial nerve 3). It describes the nucleus and course of the nerve, causes of lesions, clinical features of total oculomotor nerve palsy, treatment options which may include surgery or monitoring, and differential diagnoses. History, examination, and investigations are outlined to evaluate patients presenting with oculomotor nerve palsies.
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This document provides an overview of ocular myasthenia gravis (OMG), including pathophysiology, clinical presentation, diagnostic testing, and management. Key points include: OMG is caused by antibodies impairing acetylcholine receptors, causing muscle weakness that worsens with use. Common symptoms are fluctuating ptosis and diplopia. Diagnosis involves history, exam findings like fatigable ptosis, and may include tests like ice pack, Tensilon/neostigmine, EMG. Treatment focuses on pyridostigmine and immunosuppression with prednisone and azathioprine. Thymectomy may be considered for generalized cases under age 50.
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This document provides an overview of sixth nerve palsy, including:
- The sixth cranial nerve innervates the lateral rectus muscle to enable eye abduction. Sixth nerve palsy results in limited ability to turn the eye outward.
- Causes of sixth nerve palsy include idiopathic, vascular issues like hypertension and diabetes, trauma, and tumors. Symptoms include esotropia and diplopia.
- Diagnosis involves assessing eye movement limitations and diplopia. Treatment options include occlusion to control diplopia, botulinum toxin injection, or strabismus surgery if no spontaneous recovery occurs. Prognosis is generally good, with many cases recovering spontaneously in
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The document describes the anatomy and causes of various cranial nerve palsies. It discusses the third, fourth, sixth, and trochlear nerves. For each nerve, it outlines the nuclear location, anatomical course, common causes of palsy for adults and children, associated signs and symptoms, and important diagnostic considerations. Evaluation may include medical history, examination of eye movements and pupil function, and neuroimaging in certain cases to identify potentially compressive lesions.
SIXTH CRANIAL NERVE PALSY- Diagnosis and management
Cover the fixing eye
Examiner: Note movement of uncovered eye
- Esotropia in primary position
- Exotropia on looking towards affected side
- No movement on looking towards normal side
- Quantifies the deviation
- Helps in diagnosis and management
Past pointing test
- Patient asked to point with finger to target
- Deviation of finger from target indicates diplopia
- Helps in localizing the diplopia
Diplopia charting
- Patient asked to draw position of second image
- Helps in localizing and quantifying diplopia
Worth 4 dot test
- Assesses binocular single vision
- Loss of fusion indicates diplop
Supranuclear pathways and lesions
This document discusses supranuclear pathways and lesions that can affect eye movements. It begins with the fundamentals of extraocular movements and anatomy of cortical and brainstem centers that control eye movements. It then covers the basic types of eye movements like saccades, smooth pursuit, vestibular-ocular reflex, and vergence movements. It provides a step-wise approach to evaluating eye movement disorders and localizing lesions based on the type of eye movement affected. Supranuclear lesions can cause bilateral eye movement involvement, while specific brainstem lesions impact horizontal or vertical eye movements or specific eye movement types like saccades or vestibular-ocular reflex.
Clinical approach to optic neuritis
Discussion of clinical approach to typical (demyelnating) and atypical optic neuritis (immune/inflammatory/infectious) optic neuritis with evidence-based review.
Target: Ophthalmologists/Neurologists
Ptosis
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
Evaluation of a patient with diplopia
This document provides an overview of evaluating a patient presenting with diplopia (double vision). It discusses taking a thorough history and performing a physical exam to determine if the diplopia is monocular or binocular. A variety of tests are described to localize the cause and characterize the deviation, such as which muscles are affected and how the diplopia changes with different gazes or head positions. Causes can be supranuclear, nuclear, internuclear, infranuclear or myogenic/restrictive. Imaging may be needed to identify structural lesions.
Abducent nerve
The abducens nerve originates in the pons and contains motor neurons that innervate the lateral rectus muscle, allowing for eye movement outward. It exits the brainstem and travels through the cavernous sinus before entering the orbit through the superior orbital fissure to innervate the lateral rectus. Pathologies of the abducens nerve can occur at the nuclear, central, cisternal, petrous, cavernous, or orbital segments and result in lateral rectus palsy and limitations in abduction of the eye. Common causes include pontine hemorrhage, MS, meningiomas, and traumatic injuries.
Normal fundus
This document provides information on key anatomical structures of the fundus including:
1) It describes several structures that can be seen on examination of the fundus including the optic disc, macula, retinal blood vessels, and peripheral retina.
2) It explains features of the optic disc including that it is insensitive, round or oval in shape, and contains the lamina cribrosa through which ganglion cell axons exit the eye.
3) The macula is described as being located temporally from the optic disc, containing the highest concentration of cones, and responsible for photopic vision and color vision.
Orbital Apex Syndrome
This document provides information on orbital apex syndrome (OAS) and related conditions. It begins with an overview of applied anatomy of the superior orbital fissure and orbital apex. It then discusses the classification of OAS, cavernous sinus syndrome, and superior orbital fissure syndrome. The clinical presentation, etiology, and management of these conditions is summarized. Common causes include tumors, infections, inflammation, and vascular abnormalities. The document provides details on specific pathologies, treatments, and outcomes.
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Papilledema vs papillitis with notes timothy zagada
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SIXTH CRANIAL NERVE PALSY- Diagnosis and management
SIXTH CRANIAL NERVE PALSY- Diagnosis and management
Similar to Holmes adie syndrome
mydriasis, nystagmus, papilledema.pptx
Mydriasis refers to the dilation of the pupil. It can occur normally in low light environments but prolonged or inappropriate mydriasis may indicate an underlying cause like injury, drugs, or conditions like Adie Syndrome. Treatment depends on the cause but may include medications. Mydriasis is a risk factor for angle closure glaucoma in individuals with narrow eye angles.
Nystagmus causes uncontrollable eye movements and can be congenital or acquired later in life due to conditions like MS, stroke or ear problems. Symptoms include blurred vision and dizziness. It is usually managed with glasses, contacts or rarely surgery but the underlying cause also needs to be addressed.
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The document discusses visually handicapped and visually challenged individuals. It defines different types of blindness from complete blindness to mild or moderate vision impairment. The leading causes of vision loss globally are uncorrected refractive errors and cataracts. Some key causes of blindness include glaucoma, macular degeneration, diabetic retinopathy, and certain eye diseases. Symptoms may include cloudy vision, inability to see shapes, or poor night vision. Blindness is diagnosed through eye exams and can sometimes be treated through glasses, surgery, medication or learning adaptive skills depending on the cause and severity of vision loss.
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GLAUCOMA PRESENTATION.pptx
Glaucoma is a group of eye conditions that damage the optic nerve. The optic nerve sends visual information from your eye to your brain and is vital for good vision. Damage to the optic nerve is often related to high pressure in your eye. But glaucoma can happen even with normal eye pressure.
Glaucoma can occur at any age but is more common in older adults. It is one of the leading causes of blindness for people over the age of 60.
Many forms of glaucoma have no warning signs. The effect is so gradual that you may not notice a change in vision until the condition is in its later stages.
It's important to have regular eye exams that include measurements of your eye pressure. If glaucoma is recognized early, vision loss can be slowed or prevented. If you have glaucoma, you'll need treatment or monitoring for the rest of your life.
Products & Services
Book: Mayo Clinic Guide to Better Vision
Symptoms
The symptoms of glaucoma depend on the type and stage of your condition.
Open-angle glaucoma
No symptoms in early stages
Gradually, patchy blind spots in your side vision. Side vision also is known as peripheral vision
In later stages, difficulty seeing things in your central vision
Acute angle-closure glaucoma
Severe headache
Severe eye pain
Nausea or vomiting
Blurred vision
Halos or colored rings around lights
Eye redness
Normal-tension glaucoma
No symptoms in early stages
Gradually, blurred vision
In later stages, loss of side vision
Glaucoma in children
A dull or cloudy eye (infants)
Increased blinking (infants)
Tears without crying (infants)
Blurred vision
Nearsightedness that gets worse
Headache
Pigmentary glaucoma
Halos around lights
Blurred vision with exercise
Gradual loss of side vision
When to see a doctor
If you experience symptoms that come on suddenly, you may have acute angle-closure glaucoma. Symptoms include severe headache and severe eye pain. You need treatment as soon as possible. Go to an emergency room or call an eye doctor's (ophthalmologist's) office immediately.Causes
Glaucoma develops when the optic nerve becomes damaged. As this nerve gradually deteriorates, blind spots develop in your vision. For reasons that doctors don't fully understand, this nerve damage is usually related to increased pressure in the eye.
Elevated eye pressure happens as the result of a buildup of fluid that flows throughout the inside of the eye. This fluid also is known as the aqueous humor. It usually drains through a tissue located at the angle where the iris and cornea meet. This tissue also is called the trabecular meshwork. The cornea is important to vision because it lets light into the eye. When the eye makes too much fluid or the drainage system doesn't work properly, eye pressure may increase.
Open-angle glaucoma
This is the most common form of glaucoma. The drainage angle formed by the iris and cornea remains open.
Glaucoma | Glaucoma Surgery, Glaucoma Eye Surgery Centre | Glaucoma Centre in...
Glaucoma | Glaucoma Surgery, Glaucoma Eye Surgery Centre | Glaucoma Centre in...Vinayak Netralaya | Eye Hospital In Indore
Glaucoma treatment In Indore. Glaucoma treatment at Vinayak Netralaya With Laser for the different type of Glaucoma. Glaucoma Clinic with Latest Equipment for diagnosis and treatment of Glaucoma.
Glaucoma is the name for a group of eye conditions in which optic nerve is damaged at the point where it leaves the eye. This nerve carries information from the light sensitive layer, the retina, to the brain where it is perceived as a picture.
In some people, the glaucoma damage is caused by raised eye pressure. Others may have an eye pressure within normal limits but damage occurs because there is weakness in the optic nerve.
Different types of Glaucoma
Open angle glaucomas (chronic glaucoma): It is most common. The eye is anatomically normal, but blockage or malfunction of the drainage channels slowly over many years causes elevated eye pressure. There is no pain but the field of vision gradually becomes impaired. We need to use chemical cleaner (eye drops) to open the drain or turn down the faucet. If this is insufficient, we can stake the drain (laser trabeculoplasty) & if that doesn’t work. We need to put in new plumbing (surgery / implants)
Angle closure glaucoma (Acute glaucoma): The trabecular meshwork is normal, but the iris is pushed against the meshwork & there is sudden and more complete blockage to the flow of aqueous. It means the drainage channels are covered by a stopper & we need to remove the stopper (laser iridotomy). This glaucoma can be quite painful & will cause permanent damage to sight if not treated promptly. Glued iol surgery in indore with best doctors at glaucoma treatment hospital in indore.
Secondary and developmental glaucoma: When a rise in eye pressure is cause by another eye condition it is called secondary glaucoma. Glaucoma in childhood is called developmental or congenital which is caused by malformation in the eye.
Risk factors
> Hypertension
> Diabetes
> People over the age of 45.
> People with family history of glaucoma.
> People with myopia are more prone to develop open angle glaucoma & those with hyperopia are more prone to develop angle closure.
Warning Signs of Glaucoma
> Trouble adjusting to dark rooms
> Difficulty focusing on near or distant objects
> Squinting or blinking due to sensitivity to light or glare
> Recurrent pain in or around eyes
> Double vision
> Dark spot at the center of viewing
> Lines and edges appear distorted or wavy
> Excess “watery eyes”
> Dry eyes with itching or burning
Surgical facility includes
> Trabeculectomy with anti-fibrotic agents (MMC)
> Trabeculotomy for congenital glaucoma
> GLAUCOMA VALVE IMPLANT/ GLAUCOMA
> DRAINAGE DEVICE for complicated cases
Causes and Symptoms of Glaucoma in Dogs
Dr. Joel Todd Leroy Prince is a veterinarian who has treated many cases of glaucoma in dogs. Glaucoma occurs when the eye produces more fluid than it can drain, leading to increased pressure inside the eye. If not treated by reducing the pressure, glaucoma will cause vision loss. Symptoms can include a red eye, cloudy cornea, abnormal pupil size or response to light, bulging or recessed eyeball, blinking, head rubbing, and discomfort. A veterinarian can test for glaucoma by measuring intraocular pressure.
Common eye disease
This document summarizes several common eye disorders and diseases: refractive errors like myopia and presbyopia can usually be corrected with glasses or contacts; age-related macular degeneration damages central vision and has wet and dry forms; cataracts are the leading cause of blindness and can be treated surgically; diabetic retinopathy damages blood vessels in the retina due to diabetes; glaucoma damages the optic nerve and can cause vision loss; amblyopia is reduced vision in one eye caused by conditions like strabismus where the eyes do not align properly.
Genetic Disorders Toy Poodle
Genetic Disorders in Toy Poodles can affect the musculoskeletal system, eyes, blood, nervous system, reproductive/urinary systems, and skin. Common issues include patellar luxation, retinal dysplasia, cataracts, corneal dystrophy, entropion, progressive retinal atrophy, glaucoma, thrombocytopenia, hydrocephalus, epilepsy, deafness, cryptorchidism, and congenital hypotrichosis. Breeders should test for these conditions and buyers should have the puppy examined by a veterinarian to check for any health issues.
Pupils
The pupil is an opening in the iris that controls the amount of light entering the eye. When light hits the retina, signals are sent through the optic nerve and oculomotor nerve to the iris sphincter muscle, causing it to contract and reduce pupil size in the pupillary light reflex. Various conditions can cause the pupil to constrict (miosis) or dilate (mydriasis) abnormally. Adie's tonic pupil is characterized by a dilated pupil due to damage to parasympathetic innervation. The Argyll Robertson pupil constricts with accommodation but not light, indicating neurosyphilis. Parinaud and Marcus Gunn syndromes involve impaired light reflexes due to lesions in the
Second lecture neuro ophthalmology
This document discusses various conditions that affect the pupil, including Adie's tonic pupil, Argyll Robertson pupils, and pituitary adenomas. Adie's tonic pupil is caused by damage to the ciliary ganglion and results in a dilated, poorly reactive pupil. Argyll Robertson pupils are caused by neurosyphilis and show a dissociation between the light and near reflexes. Pituitary adenomas are tumors of the pituitary gland that can compress the optic chiasm and cause visual field defects such as bitemporal hemianopia. MRI is useful for evaluating these conditions.
Abnormalities of pupil
Abnormalities of pupil
Written By - Kh. Md .Imrul Morshed
B.Optom
Institute of community Ophthalmology, Chittagong , Bangladesh.
Amblyopia, Diagnosis and Management
The document discusses amblyopia, including its definition, causes, classification, risk factors, diagnosis, critical period of visual development, and management through eliminating obstacles to vision, correcting refractive errors, and forcing use of the amblyopic eye through occlusion of the better eye or use of cycloplegic drugs. Amblyopia is a potentially reversible reduction in visual acuity that develops due to abnormal visual experience during the critical period of visual development from birth to around age 8.
Abnormalities of the Pupil copy copy copy.pptx
Dr. Daniel Emediong Walter gave a presentation on abnormalities of the pupil. He discussed normal pupil size and shape. Abnormal pupils included anisocoria (unequal pupils) and abnormally large or small pupils. Causes of an abnormally large pupil included trauma, nerve palsy, drugs, and Adie's pupil. Causes of an abnormally small pupil included drugs, inflammation, and Horner's syndrome. Other topics included Marcus-Gunn pupil, congenital abnormalities like aniridia and iris coloboma, acquired issues like pseudoexfoliation and tears, and neurological conditions such as Horner's syndrome, Adie's tonic pupil, and Argyll-Robertson
Glaucoma
Glaucoma is a disease of the optic nerve that can cause vision loss and blindness. It is usually associated with elevated pressure in the eye, though some cases occur with normal pressure. There are five main types of glaucoma: open-angle glaucoma, which has no symptoms and is the most common type; angle-closure glaucoma, which is an emergency; congenital glaucoma present at birth; secondary glaucoma caused by other eye conditions or medications; and normal tension glaucoma of unknown cause. Worldwide, glaucoma is the second leading cause of blindness.
Glaucoma
This document provides information about glaucoma, including:
- Glaucoma is a disease of the optic nerve that can cause vision loss and blindness if left untreated. It has no symptoms in its early stages.
- The two main types are open-angle glaucoma, which accounts for 95% of cases, and closed-angle glaucoma, which develops more rapidly.
- Risk factors include family history, age over 40 for African Americans and 60 for others, high eye pressure, thin corneas, and certain medical conditions.
- Regular eye exams including tonometry to measure pressure and examination of the optic nerve are important for early detection and treatment to prevent vision loss. Glau
Abnormalities of the Pupil.pptx
This presentation discusses various abnormalities of the pupil. It begins by describing the normal anatomy and function of the pupil. It then discusses several types of abnormal pupils including anisocoria, abnormally large pupils, abnormally small pupils, and Marcus-Gunn pupil. It also covers several diseases that can affect the pupils, including congenital abnormalities like aniridia, iris coloboma, and leukocoria, as well as acquired structural abnormalities and various neurological abnormalities such as Horner's syndrome, Adie's tonic pupil, and Argyll-Robertson's pupil. For each abnormality, it provides details on signs and symptoms, causes, and potential treatments.
access-ms002-0115
This document provides information about age-related macular degeneration (AMD) including what it is, its symptoms, diagnosis and treatment. AMD affects the macula, which is responsible for central vision and can cause vision loss. There are two types, dry AMD and wet AMD. Wet AMD can be treated with injections if caught early, while dry AMD currently has no treatment. Risk factors include age, family history, smoking, diet and sunlight exposure. Maintaining a healthy lifestyle and diet rich in nutrients like lutein can help protect vision.
Presentation13
Amblyopia, also known as "lazy eye", is a condition where the eye and brain are not working together, reducing vision in one eye. Common causes include an inability to focus light on the retina in one eye. Treatment may involve patching the good eye to strengthen the weak eye. Diplopia, or double vision, can be caused by problems with binocular or monocular vision. Mydriatic eye drops dilate the pupil to treat some eye inflammations, while miotic drops cause pupil constriction. Presbyopia is age-related farsightedness that causes blurred close vision and may be treated with glasses, contacts, or surgery.
Causes Of Blurry Vision And Dizziness
Blurred vision and dizziness can be caused by several medical conditions:
1) A stroke decreases blood flow to the brain, which can cause blurred vision and dizziness.
2) Antihistamines used to treat allergies can cause angle-closure glaucoma in some people, resulting in blurred vision, headaches, and halos around lights.
3) Conditions like presbyopia (age-related blurred close vision), cataracts (cloudy vision and night halos), and retinal tears (sudden blurred vision) can be diagnosed and treated by an eye specialist.
Pilocarpine use in glaucoma
Pilocarpine is an eye drop medication used to treat glaucoma by reducing the pressure inside the eye. It works by stimulating muscarinic receptors in the eye, causing the iris sphincter muscle and ciliary muscle to contract. This contraction allows fluid to drain from the eye more easily, thereby lowering intraocular pressure. Pilocarpine should not be used by patients with uveitis or pupillary block glaucoma, or those with an allergy to pilocarpine. Common side effects include blurred vision, eye pain, headaches, and nausea.
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Macular Degeneration : causes, symptoms and treatment
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Holmes adie syndrome
- 2. Holmes Adie Syndrome Holmes-Adie Syndrome is a neurological disorder that affects the pupil of the eye and the autonomic nervous system. In Holmes-Adie Syndrome, the pupil of the affected eye is larger than the unaffected eye. The affected pupil constricts slowly when exposed to bright light. Patients with this disease also experience loss of deep tendon reflexes and excessive sweating. The symptoms of Holmes-Adie Syndrome may appear alone or along with other neurological disorders. Predominantly females between the ages of 20 and 40 seem to be affected by this eye disease.
- 3. Causes of Holmes-Adie Syndrome Holmes-Adie Syndrome cannot be classified as an inherited disease barring few cases. The disease is caused by a viral or a bacterial infection. The infection causes damage to the postganglionic fibers of the eye. Some eye experts believe that Holmes-Adie Syndrome is an autoimmune disorder. The immune system of the body makes antibodies that in turn affect those specific optic nerves. Arteritis, alcoholism, and diabetes can also cause the disease.
- 4. Symptoms People with Holmes-Adie Syndrome develop various distinct symptoms. The pupil of the affected eye first appears larger than the normal eye and reacts abnormally to light. At first, the pupil reacts slowly during close tasks such as reading because the eye begins to lose its close- range focusing power. Occasionally, the iris becomes de- pigmented, losing most or its entire colour. Blurred vision, especially at close range, is another common symptom of Holmes-Adie Syndrome, as well as excessive sweating.
- 5. Diagnosis of Holmes-Adie Syndrome Your ophthalmologist will ask questions to determine when your pupil size difference or blurry vision became noticeable. Your eye doctor will most likely to conduct an eye examination. This will include shining a very bright light into your eyes to test your pupil reactions. He/she may instil special diagnostic eye drops to assess the location in the nerve pathway that problems may be occurring.
- 6. Treatments Prescription of reading glasses is one of the options for the ophthalmologists. Reading glasses help in reducing the effects of the weakened vision of the affected eye. Pilocarpine drops must be applied at least 3 times daily or as prescribed by the eye doctor to the affected eye to constrict the dilated pupil. The ultimate treatment of excessive sweating is Thoracic Sympathectomy. Here, the involved nerve that causes the excessive sweating is severed. Holmes-Adie Syndrome is not a life-threatening disease. It does not lead to permanent disability. However, the loss of deep tendon reflexes seems to remain permanent. Sadly, Holmes-Adie Syndrome may progress with time. For most of the patients Pilocarpine drops and reading glasses seem to be enough for tackling the disease.
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