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Ischaemic optic neuropathy. The clinical profile and natural history
147
CUURENTOPHTHALMOLOGY
Correction of Enophthaimos in the Anophthalmic Orbit, by R.E. Iverson, L.M. Vistnes and R.J. Siegel, Plast Reconstr Surg 51:545-554, 1973, The Anophthalmic Orbit Surgical Correction of Lower Lid Ptosis, by L.M. Vistnes, R.E. Iverson and D.R. Laub. Plast Reconstr Surg 52:346-351, 1973, and Mechanism of Upper Lid Ptosis in the Anophthalmic Orbit, by L.M. Vistnes. Plast Reconstr Surg 58:539-545, 1976 These three papers present the evolvement in thinking about the various cosmetic problems SO frequently seen in the anophthalmic orbit, as the senior author (Dr. Vistnes) has seen and treated some 100 patients with such problems over the past 5 years. The papers read together summarize the pathomechanical factors thought to be responsible for the common findings which in the last paper are placed together as the anophthalmic orbit syndrome: 1) superior sulcus depression, 2) enophthalmos, 3) lower lid ptosis, 4) upper lid ptosis. The key factor is thought to be loss of the globe, which is replaced with an implant of lesser diameter and volume. Even when added to the volume of the average prosthesis, the total volume is less than that of the globe, causing both enophthalmos and depression of the superior sulcus. Due to the anatomy of the levator apparatus, the salient features of which are described in the third paper, this volume deficit also produces upper lid ptosis in that the balance and pivot point of a carefully balanced levator apparatus over a normal globe is altered. The weight of a normal prosthesis, many times that of a normal globe, by its constant unrestrained pressure, causes ptosis of the lower lid so frequently seen in many of these patients. This allows the other features (enophthalmos, superior sulcus depression and upper lid ptosis) to become more pronounced, as the prosthesis follows the lower lid in its downward path. Surgical solutions to the problems are indicated, with results of such surgery compared to other methods. The authors have successfully corrected enophthalmos and superior sulcus depression by the placement of room temperature vulcanizing (RTV) silicone along the floor and lateral aspect of the orbit under the periorbita, thus augmenting orbital volume. Similarly, the placement of a strip of fascia lata as a sling along the ciliary margin of the lower lid, with the ends sutured securely to the medial canthal tendon and an opening in the lateral orbital rim respectively, has provided firm and permanent support for the lower lid at a higher and normal level. Correction of upper lid ptosis has been by standard methods of lid shortening or levator shortening, depending on the severity of the problem. (Abstract by L. M. Vistnes)
Comment For the anophthalmic orbit syndrome, Vistnes first corrects the volume deficit (which is the cause of superior sulcus depression and enophthalmos of the prosthetic eye) with RTV silicone along the floor and lateral orbital wall. There is no doubt but that correcting volume deficit along the floor and walls of the orbit, without interfering with the action of the rectus muscles, is the best (and only) way to correct superior sulcus depression. Inserting materials, even autogenous fascia lata, in the upper lid for this deformity is improper and obsolete; it gives a poor correction at best and may result in ptosis of the lid which then must be corrected. David Sol1 has devised expandable implants for the floor and for the muscle cone (manufactured by Dow Corning) which solves the same problem in another excellent way. Still another method of replacing the deficit, reported in the September-October I977 issue of the Transactions ofthe American Academy of Ophthalmology consists of determining the precise volume needed with a cast of the upper face. From the wax pattern developed, an acrylic implant is made which is placed within the orbit. If lower lid sag is present, Vistnes corrects this in a second procedure, as he has described. Ptosis of the upper lid can be corrected then, or at a later operation. Vistnes is one of the plastic surgeons who has been making significant contributions to the solution of many orbital adnexal problems. We hope that this able investigator and his associates will continue their work for many decades. ALSTONCALLAHAN
Ischaemic Optic Neuropathy. The Clinical Profile and Natural History, by D.R. Boghen
and J.S. Glaser.
Brain 98:689-708,
1975
The clinical profiles of 50 patients with ischemic optic neuropathy were reviewed to analyze and contrast data related to visual function, general morbidity and prognosis in non-arteritic (37) versus arteritic
148
SurvOphthalmol 22 (2) September-October1977
CURRENT OPHTHALMOLOGY
(13) cases. Data were analyzed for age/sex, visual symptoms at onset, medical symptoms at onset, concurrent medical conditions, ophthalmological findings, diagnostic procedures and efficacy of treatment. The salient features of idiopathic (non-arteritic) optic neuropathy may be summarized as follows. (1) The syndrome occurs primarily in 5%70-year-old patients who, for the most part, are otherwise well. (2) Mild hypertension is present in about half of the cases, but does not determine a separate variant of the disorder. (3) There is no significant association with extracranial carotid occlusive disease. (4) Over long follow-up periods, there appears to be no increased incidence of stroke. (5) The syndrome should be easily recognized on clinical grounds, consisting of sudden or rapidly progressive monocular visual deficit associated with optic disc swelling, with stable visual defects of variable degree. (6) After an interval of months to many years, the second eye is involved in about 40 per cent of cases (old optic atrophy coupled with contralateral fresh disc infarction may be confused with the Foster-Kennedy syndrome). (7) No form of therapy has proved efficacious. (8) Pathophysiological mechanisms remain speculative. It is the responsibility of the physician, whether ophthalmologist or neurologist, to distinguish the patient with occult arteritis (history, physical examination, sedimentation rate, arterial biopsy) and institute immediate high-dosage corticosteroid therapy. It is also incumbent upon the clinician to desist from unnecessary and unrewarding diagnostic procedures, in particular cerebral angiography, when confronted with an instance of non-arteritic ischaemic optic neuropathy. (Abstract by JS Glaser)
Comment This article describes in great detail a significant syndrome in neuroophthalmology, so-called ischemic optic neuropathy. The syndrome has distinct clinical characteristics and can be diagnosed without the necessity of any invasive tests. It is frequently confused with papilledema from increased intracranial or intraorbital pressure, and occasionally it is confused with so-called Foster-Kennedy Syndrome. The clue is the sudden onset of loss of vision in an elderly individual with swelling of the optic nerve head and no ancillary neurological signs or symptoms. A frequent tragedy is the occurrence of the syndrome in the remaining eye, which occurs in about half of the patients. Secondary optic atrophy almost always follows the obstruction and compression of the neural elements of the optic disc caused by the disease. The cause is unknown, but it is probably caused by small vessel disease of the optic nerve head. It is not associated, however, with any other distinct systemic vascular disease. This article is worth reading in its entirety so that awareness of this entity becomes established in the minds of ophthalmic practitioners. ROBERT S. JAMPEL
Combined Contactoptical System, by M. Dutescu, E.M. Hanrath and C. Boeck. Klin Monatsbl Augenheilk 168.51 l-518, 1976 The indications and the adaptation of a combined contactoptical system called a “piggyback” system, are discussed. This system comprises the adaptation of a soft contact lens upon which a hard one is applied. Careful measurements of the soft lens surface are combined with trial lens procedure in determining the base curve of the hard lens. The optical and the therapeutic results obtained in seven groups of patients (56 eyes) are discussed together with the results of the adaptation of the lenses, The 56 eyes were classified in the following groups, representing the indications of this combined system: high cornea1 astigmatism (17 eyes), aphakia (6 eyes), keratoconus (3 eyes), keratoplasty (6 eyes), injuries (14 eyes), chronic lesions of the epithelium (7 eyes) and hyposecretion of the tear fluid (3 eyes). The optical results were very good. The residual astigmatism which remains after setting up the soft contact lens is almost fully compensated for by the hard contact lens even on high cornea1 astigmatism. The great advantage of this system is that it allows a_good centrical seat of the piggy-back lens and the diminuation of the spectacle blur. A good seat of the contact lens was also obtained with very irregular corneas (aphakia, keratoconus, injuries, keratoplasty). The soft contact lenses have proven valuable therapy for a number of cornea1 diseases, such as chronic lesions of the epithelium, recent cornea1 transplants, and hyposecretion of the tear fluid, whereas the hard
CUURENTOPHTHALMOLOGY
Correction of Enophthaimos in the Anophthalmic Orbit, by R.E. Iverson, L.M. Vistnes and R.J. Siegel, Plast Reconstr Surg 51:545-554, 1973, The Anophthalmic Orbit Surgical Correction of Lower Lid Ptosis, by L.M. Vistnes, R.E. Iverson and D.R. Laub. Plast Reconstr Surg 52:346-351, 1973, and Mechanism of Upper Lid Ptosis in the Anophthalmic Orbit, by L.M. Vistnes. Plast Reconstr Surg 58:539-545, 1976 These three papers present the evolvement in thinking about the various cosmetic problems SO frequently seen in the anophthalmic orbit, as the senior author (Dr. Vistnes) has seen and treated some 100 patients with such problems over the past 5 years. The papers read together summarize the pathomechanical factors thought to be responsible for the common findings which in the last paper are placed together as the anophthalmic orbit syndrome: 1) superior sulcus depression, 2) enophthalmos, 3) lower lid ptosis, 4) upper lid ptosis. The key factor is thought to be loss of the globe, which is replaced with an implant of lesser diameter and volume. Even when added to the volume of the average prosthesis, the total volume is less than that of the globe, causing both enophthalmos and depression of the superior sulcus. Due to the anatomy of the levator apparatus, the salient features of which are described in the third paper, this volume deficit also produces upper lid ptosis in that the balance and pivot point of a carefully balanced levator apparatus over a normal globe is altered. The weight of a normal prosthesis, many times that of a normal globe, by its constant unrestrained pressure, causes ptosis of the lower lid so frequently seen in many of these patients. This allows the other features (enophthalmos, superior sulcus depression and upper lid ptosis) to become more pronounced, as the prosthesis follows the lower lid in its downward path. Surgical solutions to the problems are indicated, with results of such surgery compared to other methods. The authors have successfully corrected enophthalmos and superior sulcus depression by the placement of room temperature vulcanizing (RTV) silicone along the floor and lateral aspect of the orbit under the periorbita, thus augmenting orbital volume. Similarly, the placement of a strip of fascia lata as a sling along the ciliary margin of the lower lid, with the ends sutured securely to the medial canthal tendon and an opening in the lateral orbital rim respectively, has provided firm and permanent support for the lower lid at a higher and normal level. Correction of upper lid ptosis has been by standard methods of lid shortening or levator shortening, depending on the severity of the problem. (Abstract by L. M. Vistnes)
Comment For the anophthalmic orbit syndrome, Vistnes first corrects the volume deficit (which is the cause of superior sulcus depression and enophthalmos of the prosthetic eye) with RTV silicone along the floor and lateral orbital wall. There is no doubt but that correcting volume deficit along the floor and walls of the orbit, without interfering with the action of the rectus muscles, is the best (and only) way to correct superior sulcus depression. Inserting materials, even autogenous fascia lata, in the upper lid for this deformity is improper and obsolete; it gives a poor correction at best and may result in ptosis of the lid which then must be corrected. David Sol1 has devised expandable implants for the floor and for the muscle cone (manufactured by Dow Corning) which solves the same problem in another excellent way. Still another method of replacing the deficit, reported in the September-October I977 issue of the Transactions ofthe American Academy of Ophthalmology consists of determining the precise volume needed with a cast of the upper face. From the wax pattern developed, an acrylic implant is made which is placed within the orbit. If lower lid sag is present, Vistnes corrects this in a second procedure, as he has described. Ptosis of the upper lid can be corrected then, or at a later operation. Vistnes is one of the plastic surgeons who has been making significant contributions to the solution of many orbital adnexal problems. We hope that this able investigator and his associates will continue their work for many decades. ALSTONCALLAHAN
Ischaemic Optic Neuropathy. The Clinical Profile and Natural History, by D.R. Boghen
and J.S. Glaser.
Brain 98:689-708,
1975
The clinical profiles of 50 patients with ischemic optic neuropathy were reviewed to analyze and contrast data related to visual function, general morbidity and prognosis in non-arteritic (37) versus arteritic
148
SurvOphthalmol 22 (2) September-October1977
CURRENT OPHTHALMOLOGY
(13) cases. Data were analyzed for age/sex, visual symptoms at onset, medical symptoms at onset, concurrent medical conditions, ophthalmological findings, diagnostic procedures and efficacy of treatment. The salient features of idiopathic (non-arteritic) optic neuropathy may be summarized as follows. (1) The syndrome occurs primarily in 5%70-year-old patients who, for the most part, are otherwise well. (2) Mild hypertension is present in about half of the cases, but does not determine a separate variant of the disorder. (3) There is no significant association with extracranial carotid occlusive disease. (4) Over long follow-up periods, there appears to be no increased incidence of stroke. (5) The syndrome should be easily recognized on clinical grounds, consisting of sudden or rapidly progressive monocular visual deficit associated with optic disc swelling, with stable visual defects of variable degree. (6) After an interval of months to many years, the second eye is involved in about 40 per cent of cases (old optic atrophy coupled with contralateral fresh disc infarction may be confused with the Foster-Kennedy syndrome). (7) No form of therapy has proved efficacious. (8) Pathophysiological mechanisms remain speculative. It is the responsibility of the physician, whether ophthalmologist or neurologist, to distinguish the patient with occult arteritis (history, physical examination, sedimentation rate, arterial biopsy) and institute immediate high-dosage corticosteroid therapy. It is also incumbent upon the clinician to desist from unnecessary and unrewarding diagnostic procedures, in particular cerebral angiography, when confronted with an instance of non-arteritic ischaemic optic neuropathy. (Abstract by JS Glaser)
Comment This article describes in great detail a significant syndrome in neuroophthalmology, so-called ischemic optic neuropathy. The syndrome has distinct clinical characteristics and can be diagnosed without the necessity of any invasive tests. It is frequently confused with papilledema from increased intracranial or intraorbital pressure, and occasionally it is confused with so-called Foster-Kennedy Syndrome. The clue is the sudden onset of loss of vision in an elderly individual with swelling of the optic nerve head and no ancillary neurological signs or symptoms. A frequent tragedy is the occurrence of the syndrome in the remaining eye, which occurs in about half of the patients. Secondary optic atrophy almost always follows the obstruction and compression of the neural elements of the optic disc caused by the disease. The cause is unknown, but it is probably caused by small vessel disease of the optic nerve head. It is not associated, however, with any other distinct systemic vascular disease. This article is worth reading in its entirety so that awareness of this entity becomes established in the minds of ophthalmic practitioners. ROBERT S. JAMPEL
Combined Contactoptical System, by M. Dutescu, E.M. Hanrath and C. Boeck. Klin Monatsbl Augenheilk 168.51 l-518, 1976 The indications and the adaptation of a combined contactoptical system called a “piggyback” system, are discussed. This system comprises the adaptation of a soft contact lens upon which a hard one is applied. Careful measurements of the soft lens surface are combined with trial lens procedure in determining the base curve of the hard lens. The optical and the therapeutic results obtained in seven groups of patients (56 eyes) are discussed together with the results of the adaptation of the lenses, The 56 eyes were classified in the following groups, representing the indications of this combined system: high cornea1 astigmatism (17 eyes), aphakia (6 eyes), keratoconus (3 eyes), keratoplasty (6 eyes), injuries (14 eyes), chronic lesions of the epithelium (7 eyes) and hyposecretion of the tear fluid (3 eyes). The optical results were very good. The residual astigmatism which remains after setting up the soft contact lens is almost fully compensated for by the hard contact lens even on high cornea1 astigmatism. The great advantage of this system is that it allows a_good centrical seat of the piggy-back lens and the diminuation of the spectacle blur. A good seat of the contact lens was also obtained with very irregular corneas (aphakia, keratoconus, injuries, keratoplasty). The soft contact lenses have proven valuable therapy for a number of cornea1 diseases, such as chronic lesions of the epithelium, recent cornea1 transplants, and hyposecretion of the tear fluid, whereas the hard