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At least 973 records · Page 54Linked to original sources
PubMed1990

Pallor of the optic disc in children.

This report discusses the subject of pallor of the optic disc from the viewpoint of a paediatric neurologist. The paper is divided into two sections, one on optic atrophy in childhood and the second on optic nerve hypoplasia. Optic atrophy in children is a topic which is very poorly covered in standard textbooks either of neurology or ophthalmology. This review attempts to develop a working approach to the management of children who present with optic nerve atrophy as their primary neurological finding.

Child↗
PubMedDate not supplied

[Effectiveness of magnetotherapy in optic nerve atrophy. A preliminary study].

Magnetotherapy effects on visual functions (vision acuity and field), on retinal bioelectric activity, on conductive vision system, and on intraocular circulation were studied in 88 patients (160 eyes) with optic nerve atrophy. A Soviet Polyus-1 low-frequency magnetotherapy apparatus was employed with magnetic induction of about 10 mT, exposure 7-10 min, 10-15 sessions per course. Vision acuity of patients with its low (below 0.04 diopters) values improved in 50 percent of cases. The number of patients with vision acuity of 0.2 diopters has increased from 46 before treatment to 75. Magnetotherapy improved ocular hemodynamics in patients with optic nerve atrophy, it reduced the time of stimulation conduction along the vision routes and stimulated the retinal ganglia cells. The maximal effect was achieved after 10 magnetotherapy sessions. A repeated course carried out in 6-8 months promoted a stabilization of the process.

Adolescent↗
PubMed1984

Acute anterior and posterior ischemic optic neuropathy.

Criteria for diagnosis of acute ischemic optic neuropathy (acute ION) were proposed: acute ION was divided into two groups, ie, acute anterior ischemic optic neuropathy (acute AION) and acute posterior ischemic optic neuropathy (acute PION). Acute AION is characterized by pale or sometimes hyperemic papilledema in the early stage, followed by postneuritic optic atrophy. In contrast, acute PION shows normal optic disk in the early stage followed by development of simple optic atrophy. We analyzed 31 eyes of 24 cases with acute AION and 20 eyes of 18 cases with acute PION. The diagnostic criteria and clinical findings in both types were compared. Through analyses of the etiological factors, acute PION was thought to be acute retrobulbar optic neuritis caused by ischemic changes in the optic nerve. Laboratory examinations of serum lipids, hemostatic and fibrinolytic activities in cases of acute ION did not reveal significant differences from the findings in cases with retinal vein occlusion and diabetic retinopathy. In the early stage of acute ION, steroid therapy gave rise to some improvement of the visual function but showed no effect in the late stage of the disease.

Adult↗
PubMed2002

Optic nerve degeneration and mitochondrial dysfunction: genetic and acquired optic neuropathies.

Selective degeneration of the smallest fibers (papillo-macular bundle) of the human optic nerve occurs in a large number of optic neuropathies characterized primarily by loss of central vision. The pathophysiology that underlies this peculiar pattern of cell involvement probably reflects different forms of genetic and acquired mitochondrial dysfunction. Maternally inherited Leber's hereditary optic neuropathy (LHON), dominant optic atrophy (Kjer disease), the optic atrophy of Leigh's syndrome, Friedreich ataxia and a variety of other conditions are examples of inherited mitochondrial disorders with different etiologies. Tobacco-alcohol amblyopia (TAA), the Cuban epidemic of optic neuropathy (CEON) and other dietary (Vitamins B, folate deficiencies) optic neuropathies, as well as toxic optic neuropathies such as due to chloramphenicol, ethambutol, or more rarely to carbon monoxide, methanol and cyanide are probably all related forms of acquired mitochondrial dysfunction. Biochemical and cellular studies in LHON point to a partial defect of respiratory chain function that may generate either an ATP synthesis defect and/or a chronic increase of oxidative stress. Histopathological studies in LHON cases and a rat model mimicking CEON revealed a selective loss of retinal ganglion cells (RGCs) and the corresponding axons, particularly in the temporal-central part of the optic nerve. Anatomical peculiarities of optic nerve axons, such as the asymmetric pattern of myelination, may have functional implications on energy dependence and distribution of mitochondrial populations in the different sections of the nerve. Histological evidence suggests impaired axonal transport of mitochondria in LHON and in the CEON-like rat model, indicating a possible common pathophysiology for this category of optic neuropathies. Histological evidence of myelin pathology in LHON also suggests a role for oxidative stress, possibly affecting the oligodendrocytes of the optic nerves.

Animals↗
PubMed1980

Computer densitometry of retinal nerve fibre atrophy. A pilot study.

Lack of nerve fibre layer opacity and a granular appearance of the retina are important funduscopic signs in optic atrophy. In this pilot study serially obtained fundus photographs from a case with developing optic atrophy where subjected to computer densitometry. A monotonic increase in local density variations was found during evolution of optic atrophy. The change in density variations closely followed the funduscopic change in nerve fibre layer opacity. This method makes it possible to detect and quantify diffuse atrophy of the retinal nerve fibre layer.

Adult↗
PubMed1987

A subhyaloid haemorrhage as the presenting symptom of bilateral optic neuropathy.

A 28 year-old man with a spontaneous vitreous haemorrhage as the first sign of Leber's optic atrophy is presented. The blood collected in a central retrohyaloid area covering the left macula. The exact starting point of the haemorrhage was never positively identified, but it seemed to originate from an area of microangiopathy adjacent to the optic disc. For 8-10 months the vision of the left eye gradually decreased to counting fingers. A year later the visual acuity dropped to the same level on the right eye. The picture was compatible with Leber's optic atrophy. Other disorders causing bilateral optic neuropathy were excluded. A careful family history revealed several cases of visual problems for several generations. Vitreous haemorrhage as the first sign of Leber's optic atrophy has not previously been reported. Peripapillar microangiopathy, however, has been described in the asymptomatic stage of the disease.

Adult↗
PubMed2005

Ocular and systemic manifestations of PHACES (Posterior fossa malformations, Hemangiomas, Arterial anomalies, Cardiac defects and coarctation of the Aorta, Eye abnormalities, and Sternal abnormalities or ventral developmental defects) syndrome.

INTRODUCTION: PHACES syndrome (Posterior fossa malformations, Hemangiomas, Arterial anomalies, Cardiac defects and coarctation of the aorta, Eye abnormalities, and Sternal abnormalities or ventral developmental defects) is a rare neurocutaneous syndrome with only 2 case reports published in the ophthalmic literature. This study was conducted to identify ocular and systemic manifestations of PHACES syndrome. METHODS: A retrospective chart review was performed on 8 children with a diagnosis of PHACES syndrome. Information recorded included age at first visit, length of follow-up, gender, race, vision, need for glasses, strabismus, amblyopia, ptosis, proptosis, anterior and posterior segment abnormalities, need for treatment of the hemangioma, type of treatment of the hemangioma, and systemic manifestations. RESULTS: Periocular and ocular findings in patients with PHACES syndrome included hemangioma involving ocular structures (n = 6), strabismus (n = 4), amblyopia (n = 5), proptosis (n = 2), ptosis (n = 5), anterior polar cataract (n = 1), optic atrophy from optic neuropathy (n = 1), heterochromia (n = 1), and refractive error requiring glasses (n = 2). All patients were treated with steroids for the hemangioma. Systemic manifestations of PHACES syndrome included posterior fossa malformation (n = 4), hemangioma (n = 8), arterial anomalies (n = 3), cardiac abnormalities (n = 3), and sternal or ventral deformities (n = 3). CONCLUSION: Children with PHACES syndrome may have significant ocular and systemic abnormalities and are at increased risk for strabismus and amblyopia. They often require steroid therapy of the hemangioma to prevent and/or treat ocular complications. These patients require careful monitoring by a pediatric ophthalmologist in addition to other subspecialists.

Abnormalities, Multiple↗
PubMed2006

Familial Madras motor neuron disease (FMMND): study of 15 families from southern India.

Madras motor neuron disease (MMND) and Madras motor neuron disease variant (MMNDV) have an unique geographic distribution with concentration of majority of cases in the southern states of India. They have the characteristic features of onset in young, weakness and wasting of the limbs, multiple cranial nerve palsies particularly involving the 7th, 9th to 12th and sensorineural hearing impairment. In addition, all patients with MMNDV have bilateral optic atrophy. During the past 32 years, a total of 104 patients were diagnosed to have MMND and among these 25 patients with the familial form were further evaluated. In this report, we describe the clinical features of these 25 patients diagnosed to have familial Madras motor neuron disease (FMMND) or familial Madras motor neuron disease variant (FMMNDV), belonging to 15 families hailing from southern India. There were 10 patients diagnosed to have FMMND and 15 with FMMNDV. There were 14 males and 11 females with mean age at onset of 13.0+/-6.2 years and mean duration of illness of 73.6+/-74.0 months. Notably, the occurrence of MMNDV in the familial group (15 of 25 patients) was significantly more as compared to occurrence in the group with sporadic MMND (SMMND) [12 of 79 patients] (p=0.0002).

Adolescent↗
PubMed2002

Developmental neurogenetics and neuro-ophthalmology.

The field of developmental neurogenetics has burgeoned over the past decade. Through the combined efforts of developmental biologists, geneticists, and clinicians, genetic defects resulting in neuro-ophthalmic disorders such as holoprosencephaly, microphthalmia, dominant optic atrophy, and optic nerve colobomas have been identified and characterized at the molecular level. Experimental studies in model organisms are continuing to identify novel genes critical for ocular and central nervous system development. Mutations in some of these genes have revealed a spectrum of pathology similar to that observed in septo-optic dysplasia, Möebius syndrome, and Duane retraction syndrome. This review examines our current knowledge of the molecular genetics of neuro-ophthalmic disease and focuses on several candidate genes for afferent and efferent visual system disorders.

Developmental Biology↗
PubMedDate not supplied

Bilateral glaucomatous optic neuropathy in Takayasu's disease without cervical arterial stenosis.

PURPOSE: Although significant decrease in retinal perfusion is usually not observed before all of the cervical arteries became markedly narrowed in patients with Takayasu's disease (TD), we present bilateral glaucomatous optic neuropathy in a patient with TD without any cervical arterial stenosis. METHODS: Ophthalmoscopic examination disclosed glaucomatous optic neuropathy in both eyes with 7/10-cup/disc ratio in the right eye and 9/10 in the left eye. Left subclavian selective arteriographic examination demonstrated segmental high-grade stenosis, namely 90 percent stenosis in the mid portion of the left subclavian artery. Arteriography, digital subtraction angiography (DSA), magnetic resonance angiography (MRA) and color Doppler sonography revealed patent cervical, carotid interna, ophthalmic, retinal and posterior ciliary arteries. RESULTS: Patient was followed up for 48 months with frequent intervals and there was no deterioration of visual acuity, visual field and optic neuropathy without any antiglaucomatous treatment. CONCLUSIONS: Although it is a known fact that classical ophthalmic manifestations of the TD occur only when major cervical arteries are occluded, no occlusion was observed in this patient with bilateral optic atrophy. The optic nerve damage is caused by various factors, but these factors require much elucidation before the optic neuropathy can be understood.

Adult↗
PubMed1975

Drusen of the optic disc. A histopathological study.

A retrospective study of autopsy and surgically enucleated eyes yielded eighteen autopsy and four surgically enucleated eyes harbouring drusen of the optic disc. The average age of the patients in this series was 58-6 years. Various histopathological changes were noted in the optic nerve head and adjacent retina; these comprised compression of nerve fibres, partial optic atrophy, elevation of the optic disc, cytoid bodies, disc haemorrhage, sequelae of haemorrhage, and juxtapapillary retinal scarring. All optic disc drusen were calcified and five of the ten disc drusen stained positively for the presence of iron.

Eye Diseases↗
PubMedDate not supplied

Regressed retinopathy of prematurity in children aged 5-8 years in Sivas, Turkey.

In this present study regressed retinopathy of prematurity has been investigated in children born prematurely (< 2300 g birth weight and < 34 weeks gestational age) in Sivas, Turkey during January 1989-January 1992. At the age of 5-8 years, 55 children born prematurely were examined; eye fundus information could be obtained by indirect ophthalmoscopy in all of them. The frequency of regressed retinopathy of prematurity was 35.45 percent for the whole group. Severe forms with optic atrophy, dragged optic disk, vitreoretinal scarring, retinal traction and temporal avascular retina were seen in 13.63 percent of cases. Moderate forms with pigmentary changes, vitreoretinal interphase changes and lattice degeneration were seen in 21.81 percent of cases. While the severe and moderate regressed premature retinopathy findings in premature children with gestational ages of 30-34 weeks were observed to be 12.0 and 14.0 percent, respectively, those in the 25-29 week-gestational-aged premature children were determined to be 5.0 and 28.33 percent, respectively. Although the incidence of both severe and moderate regressed premature retinopathy was higher in the 25-29 week gestational-aged group when compared to that of the 30-34-week-gestational-aged group, the difference was not found to be statistically significant (p > 0.05). In conclusion, premature retinopathy should not only be followed up in the early stage with active changes but also later in infancy and childhood because of regressed premature retinopathy findings that may require treatment.

Child↗
PubMed2000

[Changes to visual acuity and the visual field in a case of meningioma operated at the anterior level].

It's presented a midline meningioma of anterior level case which preoperative has an importance affectation of the visual acuity and visual field, and postoperative in dynamic is founded the important improvement of visual acuity and visual field. It's discussed visual field topography and atrophy optic pathophysiology. It's a neuro-ophthalmology case example, where the cooperation neurosurgery-ophthalmology permit medical solution and restored in social life of the patient.

Female↗
PubMed2002

[Optic nerve lesions in diabetes mellitus].

The present paper is a retrospective study revealing some optic nerve lesions on a group of 1.700 diabetic patients which belonged to the common casuistry of the Ophthalmologic Clinic and Diabetic and Nutrition Diseases Clinic in Craiova. A reduced frequency of optic neuropathy in diabetic persons was established such as: 27 patients (1.58%). Affected optic nerve may present various clinical aspects among which ischemic optic neuropathy is predominant (59.20%) followed by secondary optic atrophy, ischemic optic post neuropathy (33.40%) and juxtabulbar optic neuritis (7.40%).

Adult↗
PubMed1991

Ophthalmic findings in maple syrup urine disease.

Maple Syrup Urine Disease is an autosomal recessive disorder of branched chain amino acid metabolism with an incidence in Ireland of one in 140,154 births. Ocular complications in untreated or late diagnosed patients includes optic atrophy, grey optic papilla, nystagmus, ophthalmoplegia, strabismus and cortical blindness. Seven patients with maple syrup urine disease were studied. All were diagnosed with the aid of newborn screening and commenced on early dietary treatment (mean age at diet introduction = 5 days). All remain physically well, with average intellectual performance, three having minor neurological defects and one strabismus. Early diagnosis, proper therapy and subsequent vigilant management may reduce substantially the risks of ophthalmic complications in this rare disease.

Child↗
PubMed1985

Retinal potentials in patients with primary open-angle glaucoma: physiological evidence for temporal frequency tuning deficits.

The pattern-reversal retinal potential is a bio-electrical signal which can be recorded from the cornea of the human eye when a phase-alternating (contrast-reversing) pattern is viewed. The PRRP is correlated with activity of the retinal ganglion cells and visual diseases which affect the proximal retinal layers (such as optic atrophy and optic neuritis) and cause significant alterations in the waveform of the human PRRP. This study examined the PRRP in 32 patients with primary open-angle glaucoma (POAG) and 32 age-matched visual normals (AMVNs). Counterphasing (2, 4, 8 and 16 reversals/sec) checkerboard patterns (15', 30', 60', and 120' checks) were used as visual stimuli. PRRP amplitude was significantly reduced in patients with POAG. When temporal frequency was held constant, the magnitude of the observed PRRP amplitude reductions was identical for all check sizes. However, the magnitude of the observed amplitude reductions increased as temporal frequency increased. Therefore, in patients with POAG, the shape of the PRRP spatial tuning function was normal (although uniformly reduced for all check sizes), while the temporal tuning function was attenuated for high frequencies. Statistically significant increases in PRRP latency were also observed in the POAG patients, but these increases were quite small (mean = 3.6 ms).

Aged↗