This document discusses blepharospasm and hemifacial spasm, focusing on blepharospasm. It defines blepharospasm as involuntary contractions of the periocular muscles, resulting in forceful eye closure and impaired opening. Blepharospasm is primarily idiopathic and classified as a focal dystonia. While the exact cause is unknown, it is thought to involve basal ganglia dysfunction and overactivity of the seventh nerve. Treatment involves conservative measures, botulinum toxin type A injections, and occasionally surgery. Botulinum toxin injections into the pretarsal portion of the orbicularis oculi muscle are most effective for treating blepharospasm symptoms.
Botulinum toxin type A is produced by Clostridium botulinum and is used commercially as Botox. It works by inhibiting the release of acetylcholine at neuromuscular junctions, causing localized muscle weakness. In ophthalmology, it is used to treat blepharospasm, hemifacial spasm, strabismus, dry eye, and for cosmetic purposes to reduce wrinkles. Complications are usually minor and transient.
Glaucoma drainage devices are implants used to drain aqueous humor from the anterior chamber to control intraocular pressure. They consist of a silicone tube extending from the anterior chamber to a plate beneath the conjunctiva. Open tube designs like Molteno and Baerveldt and flow-restricted designs like Ahmed are commonly used. GDDs are generally used when filtering surgeries have failed or are likely to fail. While they effectively lower IOP, complications can include hypotony, elevated IOP, migration or erosion of the device, and diplopia. Long-term studies show success rates of 65-85% in maintaining IOP control.
This document summarizes newer treatment modalities for glaucoma. It discusses how lowering intraocular pressure remains the primary treatment but may not stop disease progression. It then outlines several novel treatment approaches being investigated, including cannabinoids, cellular cytoskeletal modulators, memantine, and Rho kinase inhibitors. Clinical trials have been conducted or are ongoing for some of these alternative therapies to potentially treat glaucoma through neuroprotective mechanisms rather than solely lowering pressure. However, many of these novel agents have shown toxicity or failed to meet efficacy endpoints to date.
Cataract surgery in special situations by Dr. Iddi.pptxIddi Ndyabawe
This document discusses cataract surgery in special situations. It covers considerations for combined cataract extraction and glaucoma surgery, cataract surgery in patients with high myopia, uveitis, small pupils, mature cataracts, diabetes, and Fuchs endothelial dystrophy. Key factors include preoperative evaluation, managing increased risks during surgery such as weak zonules or poor visibility, and postoperative care to prevent complications related to the underlying conditions. Surgical techniques are adapted based on the situation, such as using pupil expansion devices, minimizing phaco power, or coating the endothelium with viscoelastic.
Minimally Invasive Glaucoma Surgery (MIGS)Meironi Waimir
Minimally invasive glaucoma surgery (MIGS) is a group of procedures that minimizes the invasive rate of glaucoma with five characteristics: ab interno microincision, minimal trauma, more effective, high safety profile, and quick recovery.
MIGS is a surgery that uses an incision in a clear cornea and is indicated in patients with mild to moderate open angle glaucoma.
The technique of MIGS is based on several mechanisms, namely trabecular meshwork bypass stents including iStent, trabectome, and Hydrus microstent; Suprachoroidal implant using Cypass microstent; And subconjungtiva filtration using XEN gel stent.
MIGS technology has potential advantages in glaucoma management by reducing the burden of treatment, improving patients quality of life, and cutting or delaying more invasive surgeries.
Autonomic innervation of ocular strucures and Pupillary reflexesDhanyasree Nair
The document discusses the autonomic innervation of ocular structures and pupillary reflexes. It notes that the autonomic nervous system innervates structures like the iris, ciliary muscle, eyelids, blood vessels and lacrimal gland. The sympathetic system prepares the body for emergencies and supplies structures like the iris dilator and parasympathetic restores resting state and supplies the iris sphincter. Pupillary reflexes like light, near and darkness are discussed along with their pathways. Abnormalities in afferent pathways can cause total or relative afferent defects while efferent defects affect the light reflex. Conditions like Adie's tonic pupil and Argyll Robertson pupil that cause diss
The document discusses recent advances in the management of obstruction of the lacrimal drainage system. It describes the history and evolution of various surgical techniques for treating this obstruction, including external dacryocystorhinostomy (DCR), endoscopic endonasal DCR, ultrasonic endoscopic DCR, non-laser endonasal DCR, endocanalicular laser DCR, and balloon-assisted DCR. It then provides details on the surgical procedure for external DCR, including patient preparation, instrumentation, osteotomy creation, flap formation, flap anastomosis, wound closure, and post-operative management. Potential complications are also briefly mentioned.
1) Research into using ROCK inhibitors to treat glaucoma began in the late 1990s and focused on their role in regulating the aqueous humour outflow pathways and lowering intraocular pressure.
2) Several ROCK inhibitors have been studied including SNJ-1656, AR-12286, Ripasudil, and Netarsudil. They lower IOP by decreasing outflow resistance but Netarsudil also lowers production and episcleral venous pressure.
3) Netarsudil was approved by the FDA in 2017 and clinical trials found it lowers IOP similarly to latanoprost, especially in patients with lower baseline pressures.
Botulinum toxin type A is produced by Clostridium botulinum and is used commercially as Botox. It works by inhibiting the release of acetylcholine at neuromuscular junctions, causing localized muscle weakness. In ophthalmology, it is used to treat blepharospasm, hemifacial spasm, strabismus, dry eye, and for cosmetic purposes to reduce wrinkles. Complications are usually minor and transient.
Glaucoma drainage devices are implants used to drain aqueous humor from the anterior chamber to control intraocular pressure. They consist of a silicone tube extending from the anterior chamber to a plate beneath the conjunctiva. Open tube designs like Molteno and Baerveldt and flow-restricted designs like Ahmed are commonly used. GDDs are generally used when filtering surgeries have failed or are likely to fail. While they effectively lower IOP, complications can include hypotony, elevated IOP, migration or erosion of the device, and diplopia. Long-term studies show success rates of 65-85% in maintaining IOP control.
This document summarizes newer treatment modalities for glaucoma. It discusses how lowering intraocular pressure remains the primary treatment but may not stop disease progression. It then outlines several novel treatment approaches being investigated, including cannabinoids, cellular cytoskeletal modulators, memantine, and Rho kinase inhibitors. Clinical trials have been conducted or are ongoing for some of these alternative therapies to potentially treat glaucoma through neuroprotective mechanisms rather than solely lowering pressure. However, many of these novel agents have shown toxicity or failed to meet efficacy endpoints to date.
Cataract surgery in special situations by Dr. Iddi.pptxIddi Ndyabawe
This document discusses cataract surgery in special situations. It covers considerations for combined cataract extraction and glaucoma surgery, cataract surgery in patients with high myopia, uveitis, small pupils, mature cataracts, diabetes, and Fuchs endothelial dystrophy. Key factors include preoperative evaluation, managing increased risks during surgery such as weak zonules or poor visibility, and postoperative care to prevent complications related to the underlying conditions. Surgical techniques are adapted based on the situation, such as using pupil expansion devices, minimizing phaco power, or coating the endothelium with viscoelastic.
Minimally Invasive Glaucoma Surgery (MIGS)Meironi Waimir
Minimally invasive glaucoma surgery (MIGS) is a group of procedures that minimizes the invasive rate of glaucoma with five characteristics: ab interno microincision, minimal trauma, more effective, high safety profile, and quick recovery.
MIGS is a surgery that uses an incision in a clear cornea and is indicated in patients with mild to moderate open angle glaucoma.
The technique of MIGS is based on several mechanisms, namely trabecular meshwork bypass stents including iStent, trabectome, and Hydrus microstent; Suprachoroidal implant using Cypass microstent; And subconjungtiva filtration using XEN gel stent.
MIGS technology has potential advantages in glaucoma management by reducing the burden of treatment, improving patients quality of life, and cutting or delaying more invasive surgeries.
Autonomic innervation of ocular strucures and Pupillary reflexesDhanyasree Nair
The document discusses the autonomic innervation of ocular structures and pupillary reflexes. It notes that the autonomic nervous system innervates structures like the iris, ciliary muscle, eyelids, blood vessels and lacrimal gland. The sympathetic system prepares the body for emergencies and supplies structures like the iris dilator and parasympathetic restores resting state and supplies the iris sphincter. Pupillary reflexes like light, near and darkness are discussed along with their pathways. Abnormalities in afferent pathways can cause total or relative afferent defects while efferent defects affect the light reflex. Conditions like Adie's tonic pupil and Argyll Robertson pupil that cause diss
The document discusses recent advances in the management of obstruction of the lacrimal drainage system. It describes the history and evolution of various surgical techniques for treating this obstruction, including external dacryocystorhinostomy (DCR), endoscopic endonasal DCR, ultrasonic endoscopic DCR, non-laser endonasal DCR, endocanalicular laser DCR, and balloon-assisted DCR. It then provides details on the surgical procedure for external DCR, including patient preparation, instrumentation, osteotomy creation, flap formation, flap anastomosis, wound closure, and post-operative management. Potential complications are also briefly mentioned.
1) Research into using ROCK inhibitors to treat glaucoma began in the late 1990s and focused on their role in regulating the aqueous humour outflow pathways and lowering intraocular pressure.
2) Several ROCK inhibitors have been studied including SNJ-1656, AR-12286, Ripasudil, and Netarsudil. They lower IOP by decreasing outflow resistance but Netarsudil also lowers production and episcleral venous pressure.
3) Netarsudil was approved by the FDA in 2017 and clinical trials found it lowers IOP similarly to latanoprost, especially in patients with lower baseline pressures.
Ptosis, or abnormally low position of the upper eyelid, can be congenital or acquired. Congenital ptosis is caused by weakness of the levator palpebrae superioris muscle. Acquired ptosis has many causes including neurogenic (e.g. third nerve palsy), myogenic (e.g. myasthenia gravis), aponeurotic/involutional, mechanical (e.g. tumors), or pseudoptosis. Ptosis is evaluated through history, examination of lid position and ocular motility, and measurements including marginal reflex distance 1 (MRD1) and 2 (MRD2). Management depends on the underlying cause and severity of ptosis
The document discusses bionic eyes and their technological components. It describes how a bionic eye works by having electrodes implanted on the retina that are connected to a camera, video processing unit, and wireless transmitter. The Argus II is highlighted as the most advanced retinal prosthesis currently. It summarizes the key components of a bionic eye like the camera sensor technology, video processing unit, wireless transmission, and microelectrode array. The document also outlines improvements in resolution, material biocompatibility, wireless efficiency, and decreasing costs and size over time as important future opportunities to enhance bionic eye technology.
Medical treatment of primary open angle glaucomaAdithya Phadnis
The document discusses goals and approaches for treating glaucoma. The primary goal is lowering intraocular pressure to reduce risk of vision loss. Medical approaches include various drug classes that decrease aqueous production or increase outflow, while surgical options are considered when pressure cannot be controlled through medical therapy alone. Follow-up care involves regular exams and testing to monitor pressure and disease stability.
This document discusses various causes of optic disc edema. It begins by defining disc edema as swelling of the optic disc that can be caused by active or passive factors other than papilledema. Several pseudoedemas are described including drusen, myelinated fibers, tilted discs, and hypoplastic discs. True disc edemas can result from inflammation, vascular issues like CRVO, infiltrative diseases, or papilledema from increased intracranial pressure. Papilledema is usually bilateral non-inflammatory swelling caused by conditions that raise ICP like brain tumors, infections, pseudotumor cerebri, or venous sinus thrombosis. The pathogenesis and features of optic neuritis, multiple sclerosis, and papille
The document summarizes eyelid anatomy and physiology of the lacrimal pump. It describes the embryology, gross anatomy, structures, muscles, glands, blood supply and lymphatic drainage of the eyelids. The key structures discussed include the tarsal plates, septum orbitale, orbicularis oculi muscle, levator palpebrae superioris muscle, and meibomian glands. The document also briefly outlines the functions of the meibomian glands and arterial blood supply to the eyelids.
This document discusses automated perimetry and the interpretation of visual field tests. It covers perimeter logic and identifying field defects, criteria for glaucomatous defects, and detecting glaucomatous progression. Key points include interpreting visual fields systematically using total and pattern deviation plots in 8 zones, criteria for identifying glaucomatous defects including abnormalities in the pattern deviation plot, global indices, and techniques for detecting progression such as the overview program and Glaucoma Progression Analysis. Interpretation requires correlating results with clinical findings and considering factors like learning effects and fluctuation.
Dry eye is a disease characterized by unstable tear film and ocular surface inflammation. It results in eye discomfort, visual disturbance, and potential ocular surface damage. Dry eye is caused by factors that interrupt normal tear production or function like lacrimal gland damage, meibomian gland dysfunction, or neurological issues. Diagnosis involves evaluating symptoms, ocular surface staining, and tear film breakup time. Management includes artificial tears, punctal plugs, cyclosporine drops, and procedures like LipiFlow that target meibomian glands.
This document discusses masquerade syndromes caused by neoplasms that mimic inflammatory conditions of the eye. It defines masquerade syndromes and notes they are rare. Primary examples discussed include primary intraocular lymphoma, which can present with blurred vision, floaters, and vitreous inflammation. Diagnosis requires identifying malignant cells in ocular specimens. Other primary neoplasms mentioned are choroidal lymphomas and melanomas. Secondary neoplasms and metastases that can cause masquerade syndromes include lymphomas, leukemias, and cancers such as lung and breast that metastasize to the choroid. Paraneoplastic syndromes without tumor cells in the eye are also discussed. Early recognition of the underlying malignancy
Corneal edema after cataract surgery - MALEK AL KOTTMalek Al Kott
This document summarizes the structure and function of the cornea, with a focus on the endothelium and causes of corneal edema. It discusses the cornea's five layers, with details on the endothelium and its pump functions. Causes of corneal edema include loss of endothelial cells from aging, surgery, diseases like Fuchs endothelial dystrophy, intraoperative injuries from instruments or ultrasound, and postoperative issues like glaucoma or toxic anterior segment syndrome. The document also outlines examination techniques for the cornea like slit lamp, specular microscopy, and pachymetry.
1) A 58-year-old male office worker with keratoconus presented with irritation and dryness when wearing RGP lenses. He had a history of extended computer use in an air-conditioned environment.
2) Examination found punctate staining, neovascularization, nasal dellen, and hyperemia in both eyes. Corneal topography showed increased steepening. Fitting a new scleral lens provided better cone clearance and movement.
3) The patient continued having discomfort from dryness likely caused by his medications, work environment, mild MGD, and tight-fitting lenses. Scleral lenses or modifying the RGP lens parameters were recommended to improve comfort.
Glaucoma refers to a group of eye disorders characterized by optic nerve damage and vision loss. It is classified as primary or secondary. Primary open-angle glaucoma is the most common type. Elevated intraocular pressure damages the optic nerve, though pressure can be elevated without damage. Risk factors include age, family history, race, and central corneal thickness. Treatment aims to lower pressure and prevent further vision loss through medications, laser treatments, or surgery. Medications work by reducing fluid production or increasing outflow, and include prostaglandins, beta-blockers, alpha-agonists, and carbonic anhydrase inhibitors. Long-term monitoring is needed to evaluate treatment effectiveness.
This document discusses various minimally invasive glaucoma surgery (MIGS) procedures and devices. MIGS procedures are minimally traumatic, avoid complications of traditional glaucoma surgery, and provide rapid recovery with minimal impact on quality of life. Devices discussed include the Trabectome, iStent, CyPass microstent, Hydrus microstent, Aquasys stent, canaloplasty, Ex-PRESS shunt, and Gold Microshunt. Laser procedures like cyclophotocoagulation are also summarized.
This document discusses astigmatism, presbyopia, and aphakia. It defines these conditions and describes their causes, symptoms, diagnosis, and treatment options. For astigmatism, it covers the different types including regular, irregular, and mixed astigmatism. It discusses optical correction using lenses, refractive surgery options like LASIK, and intraocular lenses. For presbyopia, it defines the condition, describes the age-related decline in accommodation, symptoms, and treatments like multifocal lenses, contact lenses, and refractive surgery options.
Pseudoexfoliation syndrome is a systemic condition characterized by grey-white fibrillar deposits that can lead to open-angle glaucoma. It involves the trabecular meshwork, lens, ciliary body and other ocular tissues, and is a major risk factor for glaucoma. Treatment involves managing elevated intraocular pressure through medications, laser trabeculoplasty, trabeculectomy or cataract surgery due to the increased risk of complications from zonular weakness.
This document summarizes several studies and clinical trials related to the treatment of diabetic retinopathy and diabetic macular edema. It discusses the Diabetic Retinopathy Study (DRS) and Early Treatment Diabetic Retinopathy Study (ETDRS) which established laser photocoagulation as the standard treatment for proliferative diabetic retinopathy and diabetic macular edema. It also summarizes the Diabetic Retinopathy Clinical Research Network (DRCR.Net) which conducted several clinical trials comparing treatments for diabetic macular edema such as anti-VEGF injections and laser photocoagulation. The document provides high-level overviews of many landmark studies that helped advance the treatment of diabetic eye disease.
This document discusses ophthalmic viscosurgical devices (OVDs), including their history, properties, composition, classification, and uses. It begins by describing the introduction of sodium hyaluronate as the first OVD used in ophthalmic surgery in 1972. It then covers the ideal properties of an OVD and the rheological properties of viscosity, elasticity, coatability, and others. OVDs are classified as cohesive, dispersive, or viscoadaptive based on their molecular structure and behavior. The document discusses the advantages and uses of OVDs in cataract surgery, glaucoma surgery, keratoplasty, and other ophthalmic procedures. It concludes by outlining complications like
This document discusses various vitreous substitutes and intraocular gases used to replace the vitreous humor after surgery. It describes the anatomy and composition of the natural vitreous and ideal properties for substitutes. Common substitutes discussed include gases like air, sulfur hexafluoride and perfluorocarbons; liquids like silicone oil, perfluorocarbon liquids and semi-fluorinated alkanes; and experimental polymers and implants. The document compares different options and provides details on how each works, associated complications, and appropriate uses.
This document discusses recent advances in the management of Bell's palsy. It begins with the anatomy of the facial nerve and describes its intracrannial and extracranial course. It then discusses Bell's palsy itself, including causes, clinical features, prognosis, and treatment options. The mainstay treatments are corticosteroids, antiviral drugs like acyclovir, and sometimes combined steroid and antiviral therapy. Surgery is generally not indicated unless there is not complete recovery with medical treatment. Overall advances include better understanding of Bell's palsy etiology and more evidence supporting combined steroid and antiviral therapy.
Ptosis, or abnormally low position of the upper eyelid, can be congenital or acquired. Congenital ptosis is caused by weakness of the levator palpebrae superioris muscle. Acquired ptosis has many causes including neurogenic (e.g. third nerve palsy), myogenic (e.g. myasthenia gravis), aponeurotic/involutional, mechanical (e.g. tumors), or pseudoptosis. Ptosis is evaluated through history, examination of lid position and ocular motility, and measurements including marginal reflex distance 1 (MRD1) and 2 (MRD2). Management depends on the underlying cause and severity of ptosis
The document discusses bionic eyes and their technological components. It describes how a bionic eye works by having electrodes implanted on the retina that are connected to a camera, video processing unit, and wireless transmitter. The Argus II is highlighted as the most advanced retinal prosthesis currently. It summarizes the key components of a bionic eye like the camera sensor technology, video processing unit, wireless transmission, and microelectrode array. The document also outlines improvements in resolution, material biocompatibility, wireless efficiency, and decreasing costs and size over time as important future opportunities to enhance bionic eye technology.
Medical treatment of primary open angle glaucomaAdithya Phadnis
The document discusses goals and approaches for treating glaucoma. The primary goal is lowering intraocular pressure to reduce risk of vision loss. Medical approaches include various drug classes that decrease aqueous production or increase outflow, while surgical options are considered when pressure cannot be controlled through medical therapy alone. Follow-up care involves regular exams and testing to monitor pressure and disease stability.
This document discusses various causes of optic disc edema. It begins by defining disc edema as swelling of the optic disc that can be caused by active or passive factors other than papilledema. Several pseudoedemas are described including drusen, myelinated fibers, tilted discs, and hypoplastic discs. True disc edemas can result from inflammation, vascular issues like CRVO, infiltrative diseases, or papilledema from increased intracranial pressure. Papilledema is usually bilateral non-inflammatory swelling caused by conditions that raise ICP like brain tumors, infections, pseudotumor cerebri, or venous sinus thrombosis. The pathogenesis and features of optic neuritis, multiple sclerosis, and papille
The document summarizes eyelid anatomy and physiology of the lacrimal pump. It describes the embryology, gross anatomy, structures, muscles, glands, blood supply and lymphatic drainage of the eyelids. The key structures discussed include the tarsal plates, septum orbitale, orbicularis oculi muscle, levator palpebrae superioris muscle, and meibomian glands. The document also briefly outlines the functions of the meibomian glands and arterial blood supply to the eyelids.
This document discusses automated perimetry and the interpretation of visual field tests. It covers perimeter logic and identifying field defects, criteria for glaucomatous defects, and detecting glaucomatous progression. Key points include interpreting visual fields systematically using total and pattern deviation plots in 8 zones, criteria for identifying glaucomatous defects including abnormalities in the pattern deviation plot, global indices, and techniques for detecting progression such as the overview program and Glaucoma Progression Analysis. Interpretation requires correlating results with clinical findings and considering factors like learning effects and fluctuation.
Dry eye is a disease characterized by unstable tear film and ocular surface inflammation. It results in eye discomfort, visual disturbance, and potential ocular surface damage. Dry eye is caused by factors that interrupt normal tear production or function like lacrimal gland damage, meibomian gland dysfunction, or neurological issues. Diagnosis involves evaluating symptoms, ocular surface staining, and tear film breakup time. Management includes artificial tears, punctal plugs, cyclosporine drops, and procedures like LipiFlow that target meibomian glands.
This document discusses masquerade syndromes caused by neoplasms that mimic inflammatory conditions of the eye. It defines masquerade syndromes and notes they are rare. Primary examples discussed include primary intraocular lymphoma, which can present with blurred vision, floaters, and vitreous inflammation. Diagnosis requires identifying malignant cells in ocular specimens. Other primary neoplasms mentioned are choroidal lymphomas and melanomas. Secondary neoplasms and metastases that can cause masquerade syndromes include lymphomas, leukemias, and cancers such as lung and breast that metastasize to the choroid. Paraneoplastic syndromes without tumor cells in the eye are also discussed. Early recognition of the underlying malignancy
Corneal edema after cataract surgery - MALEK AL KOTTMalek Al Kott
This document summarizes the structure and function of the cornea, with a focus on the endothelium and causes of corneal edema. It discusses the cornea's five layers, with details on the endothelium and its pump functions. Causes of corneal edema include loss of endothelial cells from aging, surgery, diseases like Fuchs endothelial dystrophy, intraoperative injuries from instruments or ultrasound, and postoperative issues like glaucoma or toxic anterior segment syndrome. The document also outlines examination techniques for the cornea like slit lamp, specular microscopy, and pachymetry.
1) A 58-year-old male office worker with keratoconus presented with irritation and dryness when wearing RGP lenses. He had a history of extended computer use in an air-conditioned environment.
2) Examination found punctate staining, neovascularization, nasal dellen, and hyperemia in both eyes. Corneal topography showed increased steepening. Fitting a new scleral lens provided better cone clearance and movement.
3) The patient continued having discomfort from dryness likely caused by his medications, work environment, mild MGD, and tight-fitting lenses. Scleral lenses or modifying the RGP lens parameters were recommended to improve comfort.
Glaucoma refers to a group of eye disorders characterized by optic nerve damage and vision loss. It is classified as primary or secondary. Primary open-angle glaucoma is the most common type. Elevated intraocular pressure damages the optic nerve, though pressure can be elevated without damage. Risk factors include age, family history, race, and central corneal thickness. Treatment aims to lower pressure and prevent further vision loss through medications, laser treatments, or surgery. Medications work by reducing fluid production or increasing outflow, and include prostaglandins, beta-blockers, alpha-agonists, and carbonic anhydrase inhibitors. Long-term monitoring is needed to evaluate treatment effectiveness.
This document discusses various minimally invasive glaucoma surgery (MIGS) procedures and devices. MIGS procedures are minimally traumatic, avoid complications of traditional glaucoma surgery, and provide rapid recovery with minimal impact on quality of life. Devices discussed include the Trabectome, iStent, CyPass microstent, Hydrus microstent, Aquasys stent, canaloplasty, Ex-PRESS shunt, and Gold Microshunt. Laser procedures like cyclophotocoagulation are also summarized.
This document discusses astigmatism, presbyopia, and aphakia. It defines these conditions and describes their causes, symptoms, diagnosis, and treatment options. For astigmatism, it covers the different types including regular, irregular, and mixed astigmatism. It discusses optical correction using lenses, refractive surgery options like LASIK, and intraocular lenses. For presbyopia, it defines the condition, describes the age-related decline in accommodation, symptoms, and treatments like multifocal lenses, contact lenses, and refractive surgery options.
Pseudoexfoliation syndrome is a systemic condition characterized by grey-white fibrillar deposits that can lead to open-angle glaucoma. It involves the trabecular meshwork, lens, ciliary body and other ocular tissues, and is a major risk factor for glaucoma. Treatment involves managing elevated intraocular pressure through medications, laser trabeculoplasty, trabeculectomy or cataract surgery due to the increased risk of complications from zonular weakness.
This document summarizes several studies and clinical trials related to the treatment of diabetic retinopathy and diabetic macular edema. It discusses the Diabetic Retinopathy Study (DRS) and Early Treatment Diabetic Retinopathy Study (ETDRS) which established laser photocoagulation as the standard treatment for proliferative diabetic retinopathy and diabetic macular edema. It also summarizes the Diabetic Retinopathy Clinical Research Network (DRCR.Net) which conducted several clinical trials comparing treatments for diabetic macular edema such as anti-VEGF injections and laser photocoagulation. The document provides high-level overviews of many landmark studies that helped advance the treatment of diabetic eye disease.
This document discusses ophthalmic viscosurgical devices (OVDs), including their history, properties, composition, classification, and uses. It begins by describing the introduction of sodium hyaluronate as the first OVD used in ophthalmic surgery in 1972. It then covers the ideal properties of an OVD and the rheological properties of viscosity, elasticity, coatability, and others. OVDs are classified as cohesive, dispersive, or viscoadaptive based on their molecular structure and behavior. The document discusses the advantages and uses of OVDs in cataract surgery, glaucoma surgery, keratoplasty, and other ophthalmic procedures. It concludes by outlining complications like
This document discusses various vitreous substitutes and intraocular gases used to replace the vitreous humor after surgery. It describes the anatomy and composition of the natural vitreous and ideal properties for substitutes. Common substitutes discussed include gases like air, sulfur hexafluoride and perfluorocarbons; liquids like silicone oil, perfluorocarbon liquids and semi-fluorinated alkanes; and experimental polymers and implants. The document compares different options and provides details on how each works, associated complications, and appropriate uses.
This document discusses recent advances in the management of Bell's palsy. It begins with the anatomy of the facial nerve and describes its intracrannial and extracranial course. It then discusses Bell's palsy itself, including causes, clinical features, prognosis, and treatment options. The mainstay treatments are corticosteroids, antiviral drugs like acyclovir, and sometimes combined steroid and antiviral therapy. Surgery is generally not indicated unless there is not complete recovery with medical treatment. Overall advances include better understanding of Bell's palsy etiology and more evidence supporting combined steroid and antiviral therapy.
SSPE, dr. amit vatkar, pediatric neurologistDr Amit Vatkar
Subacute sclerosing pan encephalitis (SSPE) also known as Dawson Disease, Dawson encephalitis, and measles encephalitis is a rare and chronic form of progressive brain inflammation caused by a persistent infection with measles virus.
In this presentaion i will a case a sspe and give u some information regarding daignosis and treatment
This document provides an overview of cerebral palsy, including its definition, classification, clinical assessment, goals of management, and treatment approaches. Cerebral palsy is a non-progressive brain disorder resulting from injury to the developing brain, with an incidence of 2-5 per 1000 live births. It is classified based on type of motor dysfunction and pattern of limb involvement. Physical examination aims to determine muscle strength, tone, and degree of deformity. Management goals target communication, daily living skills, mobility, and focus on the individual's needs as an adult. Treatment includes physical therapy, orthotics, spasticity management, and orthopedic surgery.
The document discusses several neuromuscular disorders including cerebrovascular accident, epilepsy, Bell's palsy, Parkinson's disease, and multiple sclerosis. It covers the etiology, clinical presentation, investigations, management, and dental considerations for treating patients with these conditions. Special precautions are needed during dental procedures to minimize stress and prevent injury due to issues like paralysis, seizures, tremors, spasticity, and altered sensation or swallowing.
This document provides information on physiotherapy treatment for Bell's palsy. It begins with an overview of Bell's palsy, including its causes, symptoms, and grading scales. It then discusses specific assessments, including cranial nerve and facial muscle testing. Treatment approaches covered include corticosteroids, antiviral medications, eye care, facial exercises, electrical stimulation, massage, and rarely, surgery. Outcome measures used to evaluate recovery are also outlined.
The document provides an overview of benign paroxysmal positional vertigo (BPPV). It defines BPPV as short episodes of dizziness associated with changes in head position, caused by dislodged crystals from the inner ear settling in the semicircular canals. It describes the most common symptoms of BPPV and explains the mechanisms of canalithiasis and cupulolithiasis. The document outlines the diagnostic Hallpike test and various treatment options for BPPV including canal repositioning procedures, exercises, and occasionally surgery if more conservative treatments are ineffective. It aims to educate on the characteristics, causes, diagnosis, and management of BPPV.
This document contains a neurologist's presentation on epilepsy. It discusses:
1) The causes, risk factors, classification, diagnosis, and management of seizures. The three main causes of transient loss of consciousness are syncope, psychogenic non-epileptic seizures, and epilepsy.
2) The importance of taking a detailed history from both the patient and collateral sources. Features of the pre-ictal, ictal, and post-ictal periods are important for diagnosis.
3) Treatment involves lifestyle counseling, first aid, anti-epileptic medications, and consideration of surgical options if medications fail. Managing epilepsy requires a holistic approach and partnership between the patient and care providers.
This document provides an overview of the approach to evaluating a patient presenting with headache. It discusses classifying headaches as primary or secondary and identifying red flags that suggest an underlying condition. The evaluation involves taking a thorough history including description of pain, associated symptoms, aggravating/relieving factors, medications, and performing a neurological exam to identify potential causes and guide further investigation or treatment.
The document discusses guidelines for determining brain death in children. It outlines the criteria, including: 1) excluding reversible causes of coma through clinical examination and testing, 2) confirming absence of brainstem reflexes and apnea through a clinical examination and apnea test, and 3) declaring death after two examinations show findings consistent with brain death. Special considerations for newborns are discussed, as the diagnosis in this age group is more uncertain. Ancillary tests may be used but are not required to determine brain death.
This document discusses ptosis, which is a drooping of the upper eyelid. It describes the functional anatomy of the levator palpebrae superioris muscle, which is responsible for eyelid elevation, as well as Muller's muscle and other muscles that can modify eyelid position. The document then covers evaluation of ptosis, including measurements of eyelid position, levator function testing, and classification of ptosis as congenital, acquired neurogenic, myogenic, aponeurotic, mechanical or pseudoptosis. Surgical management options are then briefly mentioned depending on the type and severity of ptosis.
This document provides information on consciousness and coma:
- Consciousness has two components - arousal from the reticular activating system and awareness from the cerebral cortex. Stimulation of the RAS produces arousal while its destruction causes coma.
- The Glasgow Coma Scale and newer scales like FOUR are used to evaluate patients in comatose or reduced states of consciousness. The FOUR scale assesses eye, motor, brainstem, and respiratory responses.
- Causes of coma can be structural/focal brain injuries or non-structural/diffuse issues like hypoxia, infections, or toxic exposures. An approach is outlined to initially stabilize an unconscious patient and guide further examination and investigations.
231125 Group 6 Sedation and Regional Anesthesia.pptxDakaneMaalim
The document discusses sedation and regional anesthesia. It begins by introducing sedation as a continuum between consciousness and general anesthesia, allowing patients to maintain protective reflexes and respond to stimuli. It then describes the levels of sedation from minimal to general anesthesia. Regional anesthesia techniques are also discussed, including neuraxial methods like epidural and spinal anesthesia, as well as peripheral nerve blocks and topical anesthesia. Specific drugs, procedures, indications, contraindications and complications are outlined for both sedation and regional anesthesia.
an inner ear disorder that cause episodes of vertigo
(spining) . this sildeshare contained detailed information about definition, causes, types, medical and nursing management.
Vertigo is a subtype of dizziness in which a patient inappropriately experiences the perception of motion (usually a spinning motion) due to dysfunction of the vestibular system.
The document discusses the embryology, anatomy, components, causes of injury, grading systems, evaluation, and treatment of the facial nerve. It covers the development of the facial nerve from the embryonic stage through maturity and describes the various parts of the nerve and their functions. The document also outlines different classification systems for nerve injuries, approaches for evaluating facial nerve paralysis, and surgical and non-surgical techniques for treating injuries or reanimating paralysis of the facial nerve.
The document discusses pupil function and abnormal pupil reactions. It covers:
1. The physiology of pupil constriction and dilation which is controlled by the parasympathetic and sympathetic nervous systems respectively.
2. How to examine pupils including observing size and shape, light reflex testing, swinging flashlight test, and near reflex testing.
3. Various diseases and conditions that can cause abnormal pupil reactions like Horner's syndrome, third nerve palsy, Adie's tonic pupil, and Argyll Robertson pupils.
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4. Disclosure Information
• In the past 12 months, I have no relevant financial
relationships with the manufacturer(s) of any commercial
product(s) and/or provider(s) of commercial services
discussed in this CME activity.
• I do not intend to discuss an unapproved/investigative use of
a commercial product/device in my presentation.
5. In 1985, Professors Stanley Fahn and David
Marsden created a new society, now known
as the International Parkinson and
Movement Disorders Society (MDS)..
This term was suggested by Professor Lewis
Rowland to Professor Fahn, to encompass
all disorders hypokinetic and hyperkinetic,
which were previously known as
extrapyramidal syndromes.
Source: Camargo CHF, Teive HAG. Drugs in Context 2019; 8: 212586. DOI: 10.7573/dic.212586 2
of 14 ISSN: 1740-4398
What is movement disorder?
6. What is dystonia?
Involuntary muscle contractions
Sustained contraction vs intermittent contraction
(tonic vs clonic)
→ abnormal postures or repetitive movements
Can affect 1 muscle, groups of muscles, or muscles throughout
the body
Thought to be caused by damage or abnormalities in basal
ganglia
Can be idiopathic, genetic, or acquired
10. Clinical definition
• PRIMARY Blepharospasm1,2
– Benign Essential Blepharospasm (BEB). Also
known as Essential Bleharospasm
• Mostly Idiopathic
• Form of focal dystonia
– Involuntary contractions of the periocular
muscles resulting in forceful eye closure, and
impairing normal opening and closing of the
eyes
1. Cillino S, et al. Eye 2010; 24: 600–607.
2. Berardelli et al., (1985). Brain, 108(Pt 3), 593–608.
11. Clinical definition
• SECONDARY Bleharospasm1
– Ophthalmological cause
• Usually acute and obvious e.g. corneal abrasion
– Drug induced (side effect)
• Dopaminergic antagonists (e.g. neuroleptics)
– Can also occur in the setting of secondary
dystonia (e.g. Cerebral Palsy)
1. Simon GJB, et al. Int Ophtalmol Clin 2005: 49-75.
12. History
• First record of
blepharospasm is
from a 16th century
painting by a Flemish
artist Brueghel called
“De Gaper”
• These patients were
considered mentally
unstable and spasms
were regarded as
psychogenic in origin
13. Primary Blepharospasm
• Adult onset (5th to 7th decade of life) but
younger cases are also seen
• More common in females (~75%)
• Prevalence 1.2-5 cases per 100,000
14. Primary Blepharospasm
• Burden
– Interference with daily tasks
– ~12% incapacitated or functionally blind
– Can cause occupational disability and
depression
1. McCann JD, et al. Int Ophtalmol Clin 2005: 113-21.
15. Blepharospasm
neurophysiology1,2
Tonic or phasic contractions of the orbicularis oculi muscles
May also be associated with levator palpebrae muscle inhibition
Abnormal responsiveness of the blink reflex to sensory stimuli
In patients with blepharospasm, the recovery cycle of the R2
component of the blink reflex is enhanced, presumably owing to
a lack of brain stem interneuronal inhibition
1. Berardelli, A., et al. (1998). Brain, 121(Pt 7), 1195–212.
2. Jankovic, J. (2006). Lancet Neurol, 5, 864–72.
16. Blepharospasm
pathophysiology
• Mutual inhibition of protractors and retractors is
lost
• Spams of the Orbicularis oculi with or without
Corrugator supercilli, procerus and frontalis
muscles results in involuntary forceful blinking
• Muscles innervated by the temporal division of
the Facial Nerve
• Sensory tricks can temporarily relieve symptoms
– Whistling, singing, finger touch of face etc.
17. Etiology
• Cause of BEB (multifactorial) is still debated but consists
of sensory, motor, and central nervous components1
1. Simon GJB, et al. Int Ophtalmol Clin 2005: 49-75.
Genetics?
Sensory Trigger?
Reduced CNS
inhibition
Hyperactive circuit in
the cortical/ sub-
cortical areas
Motor: Periocular
muscle contractions
Hyper-active motor nerve branches of the
facial nucleus, facial nerve, orbicularis oculi,
corrugator and procerus muscles
CNS activates control
center
(Basal ganglia, mid-
brain, or brain-stem)
Sensory nerves respond to stimuli: light,
corneal/eyelid irritation, pain, emotion, stress,
or other trigeminal stimulants
18. Diagnosis
• Early symptoms of Blepharospasm include:
– Increased involuntary blink rate and Eyelid or uppr-
face spasms
– Eye irritations and perception of dry eye
– Eyelid tightness
– Light sensitivity
– Increased wrinkles around the eyes
1. Boyd B, Drews R. Highlights Ophthalmol 1995. 23(4): 39-43.
19. Diagnosis
• Diagnosis of BEB is one of exclusion
– Based on clinical exam
– Rule out secondary blepharospasm due to
ophthalmological causes
– Review history for secondary dystonias including
medication
– Rule out neurological disorders such as Parkinson’s,
Huntington’s, and motor tics
1. Simon GJB, et al. Int Ophtalmol Clin 2005: 49-75.
20. Treatment
• Conservative
• Treatment of choice: Botulinum Toxin Type A
• Oral Medications (limited efficacy)
– Benzodiazepines, anticholinergics, dopaminergic
blocking agents
• Surgery
– Myectomy
1. Simon GJB, et al. Int Ophtalmol Clin 2005: 49-75.
21. Role of BoNT-A in BEB
• Botulinum toxin type A, used in the treatment of
blepharospasm since 1983, has become the
treatment of choice, and is very successful in
controlling eyelid spasms.
• Average doses of toxin type A are 12.5--25 U per eye
for BOTOX®, injected just beneath the skin into the
orbicularis muscle.
22. • Basal ganglia dysfunction
• Overactivity of the seventh nerve
leading to simultaneous forceful
contractions of the eyelid
protractors and retractors
• Ion channelopathy
• Sensitization of the trigeminal
system by photophobia
The mechanism
underlying benign
essential
blepharospasm is
not yet clearly
understood.
Some of the
proposed
mechanisms
https://eyewiki.aao.org/Blepharospasm
Pathophysiology
24. • Sphincter muscle around the eye: pars orbitalis and pars palpebralis
(preseptal and pretarsal part)
• Orbital part originates in the nasal part of frontal bone, frontal process
of maxilla, lacrimal bone (medial part of the orbit), medial palpebral
ligament, runs around the eye via the upper eye cover fold and lid and
returns in the lower eyelid to the lateral palpebral ligament
• Preseptal or palpebral part originates in the medial palpebral ligament
lacrimal sac, runs above and below the eye to the lateral palpebral
ligament
• The orbital and the preseptal muscles form concentric circles around
the eye
• Pretarsal part lies just around the palpebral margin
Orbicularis oculi. Most commonly involved
Anatomy of the periocular muscles
25. Levator
palpebrae
superioris
• arises from the inferior
surface of the sphenoid
bone
• From this point, it diverges
anteriorly to insert into the
skin of the upper eyelid and
the superior tarsal plate
• elevates and retracts the
upper eyelid
Anatomy of the periocular muscles
26. • Originates in the fascia of the nasal bone and upper
nasal cartilage
• Runs through the area of the root of the nose and fans
upward to insert in the skin in the center of the
forehead between the eyebrows
• It acts to pull the skin of the center of the forehead
down, forming transverse wrinkles in the glabella region
and bridge of the nose
• It usually acts together with corrugator or orbicularis
oculi or both
Procerus
Anatomy of the periocular muscles
27. Frontalis
• A thin and quadrilateral muscle adherent to
the superficial fascia
• The frontalis muscle passes through and
inserts into the bundles of the orbicularis
oculi muscle on the superior border of the
eyebrow at the middle and medial side of
the upper eyelid
• The frontalis muscle intermixes with the
bundle of the orbicularis oculi muscle
Anatomy of the periocular muscles
32. BEB Injection Dos and Donts
• Avoid:
– Levator Palabrae Superioris (ptosis)
– Medial lower lid injections (Dilopia)
– Injection very close to lid margin
– Injury to eye (needle should point away from
pupil)
• Total initial dose of BOTOX ® should not be
more than 25 u per eye
1. Allergan Data on File.
33. Pretarsal vs. preseptal
injections
• Data suggest better outcomes with
pretarsal injections
– Aramideh M et al. 1995:
• Significantly more clinical success (81 to 95%)
• Significant decrease in ptosis
• Significant increase in duration (8.5 to 12.5 weeks)
– Cakmur R et al. 2002:
• Significantly higher response rate (97% vs 90%)
• Significantly longer duration (11.4 vs. 8.19 weeks)
34. Recommended units Site of muscle
2.5 -5 units
Volume:
0.05-0.1 ml at each site
Medial and lateral pre tarsal orbicularis
oculi of upper lid
Lateral pre tarsal orbicularis oculi of lower
lid
Medial and lateral pre septal orbicularis
oculi of upper lid
Lateral pre septal orbicularis oculi of lower
lid
Medial and lateral pars orbitalis orbicularis
oculi of upper lid
Lateral pars orbitalis orbicularis oculi of
lower lid
Dosage and Adverse Reactions
35. Comparison of (a) preseptal and (b) pretarsal injection points in
Blepharospasm
• Four injections are usually given in the orbital or preseptal portion of the orbicularis oculi muscle,
can also be injected into the pretarsal portion of the orbicularis oculi.
• Avoid injection into the medial part of pre septal portion to avoid ptosis
• Injection in pretarsal portion of the orbicularis oculi muscle is considered the best method for
treating involuntary eyelid closure due to contractions of this muscle
• Side effects after botulinum toxin injection, including ptosis, diplopia, dry eyes, epiphora, keratitis,
lid edema, entropion/ectropion, and facial weakness, are transient and usually mild
36.
37. Meige Syndrome
• Blepharospasm + oromandibular dystonia
(lower facial spasm)
• BOTH sides affected
British Journal of Ophthalmology 1997;81:439–442
38. Meige Syndrome
• Population
30-70 years old, mean age 55 years old
Female > males (2:1)
5/100,000
• Can start as blepharospasm and then spread
to involve lower face
• Spread is more common early in disease
39. Meige syndrome
• Cause: dopaminergic and cholinergic
hyperactivity
• Decreased functioning of inhibitory neurons
• Abnormal sensorimotor processing
• Abnormal control of CN nuclei in brainstem by
basal ganglia
• Can be primary or secondary
40. Meige Syndrome
• Treatment:
“Sensory tricks”
• 1st line systemic medication
• 2nd line botulinum toxin
– Reserved for blepharospasm component
• Deep brain stimulation
41.
42.
43.
44.
45. Hemifacial spasm: clinical
overview
• What is it?
– A common adult-
onset non-dystonic
disorder
– Involuntary tonic or
clonic spasms of one
side of face
– Severity is variable
46. Clinical features
• Ususally unilateral but may be bilateral
– Bilateral cases have asynchronous
contractions of both sides
• Involuntary contractions start usually in
the periocular muscles but spread to
involve all muscles supplied by the 7th
nerve
• There may or may not be antecedent
history of Bell’s palsy
1. Cillino S, et al. Eye 2010; 24: 600–607.
2. Berardelli et al., (1985). Brain, 108(Pt 3), 593–608.
48. Epidemiology
• Adult onset (4th to 5th decade of life)
usually in the periocular muscles
– May spread slowly to involve other muscles
over months to years
• More common in females
• Prevalence
– 14.5 cases per 100,000 in women
– 7.4 cases per 100,000 in men
49. Epidemiology
• Burden
– Interference with daily tasks
– Can cause occupational/ social disability and
depression
– Facial assymmetry
• Commoner in women but men more likely
to seek treatment
• More common in Asian than in Caucasian
populations
Kemp LW et al. Curr Treat Options Neurol 2004; 175-9.
50.
51.
52.
53. Neurophysiology
• Tonic or phasic contractions of the muscles supplied by
7th nerve
• Spasms continue during sleep: sleep may be disturbed
• May also be associated with spasms of stapedius
• Sensory tricks provide temporary relief
• Worsening seen with increased stress, chewing,
speaking, bright light, and cold
1. Berardelli, A., et al. (1998). Brain, 121(Pt 7), 1195–212.
2. Jankovic, J. (2006). Lancet Neurol, 5, 864–72.
54. Neurophysiology
• Theories of causation
– Vascular compression by
aberrant loop (of a branch of
the Posterior Inferior Cerebellar
Artery, [PICA])
– Compression may even be due
to tumors, local infections, or
other vascular malformations
– Focal secondary demyelination
– Ephaptic transmission
1. Kemp LW et al. Curr Treat Options Neurol 2004; 175-9.
2. Tan NC et al. Q J Med 2002; 95: 493-500.
55. Diagnosis
• Early symptoms include:
– Increased involuntary blink rate and Eyelid or
uppr-face spasms
– Eye closure along with synchronous lower face
symptoms such as angle of mouth deviations or
latysmal contractions or clicking noise due
stapedial contractions
• In severe cases there may be sustained
contractions of the affected side of face
1. Boyd B, Drews R. Highlights Ophthalmol 1995. 23(4): 39-43.
62. Treatment
• Conservative
• Treatment of choice: Botulinum Toxin Type A
• Oral Medications (limited efficacy)
– Benzodiazepines, Carbamazepine, Baclofen, Phenytoin
etc.
• Surgery
– Janetta’s operation (Microvascular decompression)
• Some patients may experience recurrence of HFS
• Complications include hearing loss and facial weakness
1. Simon GJB, et al. Int Ophtalmol Clin 2005: 49-75.
63. Role of BoNT A In HFS
• Botulinum toxin type A, used in the treatment of
blepharospasm since 1983, has become the
treatment of choice, and is very successful in
controlling eyelid spasms.
• Average doses of toxin type A are 12.5--25 U per eye
for BOTOX ®, injected just beneath the skin into the
orbicularis muscle.
64.
65.
66.
67. Injection sites Average dose per
injection site
Medial and lateral pre – tarsal part of pars palpebralis
part of orbicularis oculi of upper lid
2.5 5 U
Lateral pre – tarsal part of pars palpebralis part of
orbicularis oculi of lower lid
2.5 5 U
Medial and lateral pre – septal part of pars palpebralis
part of orbicularis oculi of upper lid
2.5 5 U
Lateral pre – septal part of pars palpebralis part of
orbicularis oculi of lower lid
2.5 5 U
Medial and lateral pars orbitalis part of orbicularis oculi
of upper lid
2.5 5 U
Lateral pars orbitalis pars orbicularis part of orbicularis
oculi of lower lid
2.5 5 U
Dose and site of Botulinum toxin injection
68. Injection sites Average dose per
injection site
Procerus 1.25 – 5 U
Corrugator 1.25 – 5 U
Frontalis 1.25 – 5 U
Nasalis 1.25 – 5 U
Levator labii superioris 2.5 – 5 U
Zygomaticus major 2.5 – 12 U
Orbicularis oris 1.5 – 5 U
Risorius 1.25 – 5 U
Depressor anguli oris 2.5 – 5 U
Mentalis 2.5 – 5 U
Platysma 5 – 20 U
Dose and site of Botulinum toxin injection
72. Jordan DR et al. (1989). Essential blepharospasm and related dystonias. Survey of
Ophthalmology, 34(2), 123–132.
73.
74. Key Messages
• Hemifacial spasm is a movement disorder affecting the muscles innervated by the facial nerve. The result
is involuntary tonic or clonic contractions of the facial muscles, which are almost always unilateral.
• The cause in most cases is a compression of the facial nerve in its root-exit zone from the brainstem by a
vessel with an aberrant or ectatic blood vessel.
• The diagnosis is led by the clinical features. Important in deciding treatment is the differential diagnostic
differentiation from other craniofacial movement disorders. Magnetic resonance imaging using CISS
sequence is helpful for diagnosing a possible vascular compression or other intracranial cause.
• The most important symptomatic treatment is local injection of botulinum toxin. In more than 85% of
patients this leads to a notable alleviation of symptoms. The disadvantage associated with his procedure is
the fact that repeated administration at intervals of several months is necessary.
• Microvascular decompression surgery is the only causal treatment option with a success rate of about 85%
in terms of permanent freedom of symptoms.
Figure: Simplified classification of movement disorders.
Decrease dopamine by 30% at substansia nigra pars compacta…Trigeminal circuit inhibition…orbicularis oculi weakness…imbalance and compensation to increase blinking…eye dryness… increase blinking
Palpebralis- closes the eyelid….. Orbitalis- squeezes the eye shut
Alexandra Sifferlin Jan. 5, 2017
Forget wrinkles. Botox is now being used to treat migraines, depression, twitching eyes, overactive bladders, sweaty palms and more. Some call it a marvel of medicine; others caution the risks are still unknown. Inside the exploding business and strange science of Botox
Optional- corrugators, procerus, nasalis, medial frontalis- 1.25 to 2.5 U each
Up to 20U per eye
Abstract
AIMS To determine the relation between dry eye and Meige’s syndrome.
METHODS 325 patients with dry eye were divided into those responsive to topical and other forms of treatment (n=276) and those who were not (n=49). A neuropsychiatric examination was performed to check for Meige’s syndrome in the latter group.
RESULTS Twenty eight (57%) of the treatment unresponsive patients were diagnosed with Meige’s syndrome.
CONCLUSIONS There is a subgroup of patients with dry eye who do not respond to simple therapy. More than half of these patients have Meige’s syndrome and need psychiatric, as well as ophthalmic, care
Spasm ofjaw opening and mouth retraction in
a 65 year old lady with symptoms for four years.
Spasm ofjaw opening, with
dystonic posturing of left arm and
spasms offlexion of right fingers in a
65 year old man. His illness started
with dystonic writer's cramp, which
was followed 10 years later by the
oromandibular dystonia
In addition to a comprehensive review of the literature on hemifacial spasm, medical records and videos of consecutive patients referred to the Movement Disorders Clinic at Baylor College of Medicine for hemifacial spasm between 2000 and 2010 were reviewed, and videos of illustrative cases were edited. Among 215 patients referred for evaluation of hemifacial spasm, 133 (62%) were classified as primary or idiopathic hemifacial spasm (presumably caused by vascular compression of the ipsilateral facial nerve), and 4 (2%) had hereditary hemifacial spasm. Secondary causes were found in 40 patients (19%) and included Bell's palsy (n = 23, 11%), facial nerve injury (n = 13, 6%), demyelination (n = 2), and brain vascular insults (n = 2). There were an additional 38 patients (18%) with hemifacial spasm mimickers classified as psychogenic, tics, dystonia, myoclonus, and hemimasticatory spasm. We concluded that although most cases of hemifacial spasm are idiopathic and probably caused by vascular compression of the facial nerve, other etiologies should be considered in the differential diagnosis, particularly if there are atypical features.
Among 215 patients referred for evaluation of hemifacial spasm, 133 (62%) were classified as primary or idiopathic hemifacial spasm (presumably caused by vascular compression of the ipsilateral facial nerve), and 4 (2%) had hereditary hemifacial spasm. Secondary causes were found in 40 patients (19%) and included Bell's palsy (n = 23, 11%), facial nerve injury (n = 13, 6%), demyelination (n = 2), and brain vascular insults (n = 2). There were an additional 38 patients (18%) with hemifacial spasm mimickers classified as psychogenic, tics, dystonia, myoclonus, and hemimasticatory spasm. We concluded that although most cases of hemifacial spasm are idiopathic and probably caused by vascular compression of the facial nerve, other etiologies should be considered in the differential diagnosis, particularly if there are atypical features.
The axial-plane CISS sequence shows a loop of the posterior inferior cerebellar artery (Arrow A) which compresses the facial nerve (Arrow B), where it exists the brainstem
Endoscopic image—taken using a 30°endoscope—shows the proximal part of the cochlear nerve (VIII) and the facial nerve with its root-exit zone (VII), which is compressed by a loop of the posterior inferior cerebellar artery (PICA) (same patient as in Figure 2)
After microsurgical dissection of the vessel from the facial nerve, a teflon sponge is placed between brainstem and vessel, in order to permanently prevent vascular compression (VII = facial nerve, PICA = posterior inferior cerebellar artery)
Different forms of vascular compression
In this case the compression is caused by a vein (V) in close proximity to the brainstem (VII = facial nerve, VIII = cochlear nerve)
Here, the compression is caused by a combination of the vertebral artery (VA) and posterior inferior cerebellar artery (PICA). (VII = facial nerve)
The compression is caused by a combination of vertebral artery (VA), the descending posterior inferior cerebellar artery (PICA), and the anterior inferior cerebellar artery (AICA)
Background
Hemifacial spasm (HFS) is a debilitating disorder characterized by intermittent involuntary movement of muscles innervated by the facial nerve. HFS is caused by neurovascular compression along the facial nerve root exit zone and can be treated by microvascular decompression (MVD). The goal was to determine rates and predictors of spasm freedom after MVD for HFS.
Methods
A literature search using the key terms “microvascular decompression” and “hemifacial spasm” was performed. The primary outcome variable was spasm freedom at last follow-up. Analysis was completed to evaluate for variables associated with spasm-free outcome.
Results
A total of 39 studies including 6249 patients were analyzed. Overall spasm freedom rate was 90.5% (5652/6249) at a follow-up of 1.25 ± 0.04 years. There was no significant relationship between spasm freedom versus persistent spasm and age at surgery, timing of follow-up, gender, disease duration, side of disease, or vessel type. Spasm freedom was more likely after an initial surgery versus a redo MVD (odds ratio 4.16, 95% confidence interval 1.99–8.68; P < 0.01).
Conclusions
MVD works well for HFS with cure rates >90% at 1-year follow-up in 6249 patients from 39 studies. A significant predictor of long-term spasm freedom at 1 year was an initial MVD as compared to repeat MVD. The majority of published manuscripts on MVD for HFS are heterogeneous single-institutional retrospective studies. As such, a large-scale meta-analysis reporting outcome rates and evaluating significant predictors of spasm freedom provides utility in the absence of randomized controlled studies.