Normal eyes, abnormal eyes, and 20/20 vision.
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Eye Diseases↗
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Ocular bobbing: abnormal eye movement or eye movement's abnormality?
Ocular bobbing is classified as an abnormal eye movement, resulting from pathological neuronal activity of the brain stem after bilateral pontine lesions. Clinical oculographic study of 5 patients suffering from ocular bobbing shows that upwards voluntary eye movements are abnormal. We suggest that ocular bobbing should not to be regarded as an abnormal eye movement, but, rather, as the only residual movement of patients which are totally deprived of both horizontal and upward movements.
Arterial Occlusive Diseases↗
[Abnormal eye movements].
Abnormal eye movements constitute a pathological entily characterized by the inability to maintain an immobile gaze, gazing being unwillingly disturbed by displacement of the eyes. The semiology of abnormal eye movements is very accurate. It is based on clinical analysis and on eye movements recording. It is important to study abnormal eye movements, since many of them have localizing or pathological value.
Eye Movements↗
[Diagnosis and clinical assessment of abnormal eye movements].
Abnormal eye movements and nystagmus are, when present, useful for diagnosis of localization of the lesion. Observations of mortality and range of eye movements, pursuit and saccadic eye movements, ability of visual fixation, nystagmus and involuntary eye movements as well as head and eye position, palpebral fissures, ptosis, pupils are important for assessment of eye movements. Anatomical pathways important for horizontal eye movements locate in the caudal pons and for vertical eye movements, in the rostral mesencephalon. In those structures two types of saccade related neurons--burst cells and pause cells-are present and generate premotor saccadic commands. The gaze directed nystagmus results from the central vestibular disorder, not from the peripheral labyrinthine lesion. Bruns' nystagmus characterized by low-frequency, large amplitude nystagmus on looking ipsilaterally and high-frequency, small-amplitude nystagmus on looking contralaterally, is seen in the brainstem lesion. Ocular bobbing consists of rapid downward movement of the eyes followed by a slower return to the primary position and is a sign of pontine lesion. Opsoclonus, multidirectional saccadic oscillation with out intersaccadic interval and flatter-like oscillation, purely horizontal saccadic oscillation are seen in patients with cerebellar and brainstem lesions and may be due to dysfunction of pause cells.
Eye Movements↗
[CHROMOSOME RESEARCH IN EYE ABNORMALITIES].
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Chromosome Aberrations↗
Inheritance of two new eye mutants in a mosquito. Brown and abnormal eye in Culex tritaeniorhynchus.
The genetic analysis of two new mutants, brown and abnormal eye, is presented. The data indicate that both mutants are recessive and under the control of loci in linkage group III. The gene sequence for linkage group III is cl-Adh-s-bw-ae. The total length of linkage group III is now approximately 48 map units. Mosquitoes homozygous for both brown and rose, another eye-color mutant in linkage group I, exhibit a third new phenotype, yellow-orange eye.
Animals↗
Tandem duplication of 11p12-p13 in a child with borderline development delay and eye abnormalities: dose effect of the PAX6 gene product?
We report on a girl with a duplication of chromosome band 11p12-->13, which includes the Wilms tumor gene (WT1) and the aniridia gene (PAX6). The girl had borderline developmental delay, mild facial anomalies, and eye abnormalities. Eye findings were also present in most of the 11 other published cases with partial trisomy 11p, including 11p12-->13. Recently, it was shown that introduction of additional copies of the PAX6 gene into mice caused very variable eye abnormalities. Therefore, a PAX6 gene dosage effect is likely to be present in mice and humans. The central nervous system may be less sensitive to an altered PAX6 gene dosage, which is consistent with the borderline developmental delay in the present patient. Urogenital abnormalities were absent in this patient and in most of the other patients with partial trisomy of 11p. Therefore, the effect of a WT1 gene duplication on the embryological development of the urogenital tract remains uncertain.
Chromosome Aberrations↗
Abnormal eye movements in blepharospasm and involuntary levator palpebrae inhibition. Clinical and pathophysiological considerations.
We report on four patients with involuntary eyelid closure and eye movement disorders. Three were healthy until the onset of their illness and one had a mild generalized choreoathetosis and dystonia due to kernicterus. Electromyographic recording revealed solely blepharospasm in two patients and blepharospasm in combination with involuntary levator palpebrae inhibition in the other two. The eye movement abnormalities were clinically characterized by inability to fix gaze and short or prolonged episodes of uncontrollable eye deviations accompanied, in two patients, by diplopia in horizontal or vertical directions. These episodes occurred independently of a disorder of eyelid movement. Eye movement recordings with a double magnetic induction technique showed saccadic intrusions in horizontal directions. They consisted of highly frequent square wave jerks in three and sporadic macro-square wave jerks in two patients. There were also episodes of extraocular muscle dystonia, commonly known as oculogyric crises, resulting in involuntary upward eye deviation in all patients and lateral deviation in three patients. In one patient, nasal-ward deviations were sometimes restricted to one eye. We conclude that these abnormal eye movements do not necessarily point to a symptomatic form of dystonia and that they may limit the beneficial effect of botulinum toxin or surgical intervention in the therapeutic management of involuntary eyelid closure. We suggest that either basal ganglia, especially substantia nigra pars reticularis and the brainstem structures, especially the paramedian pontine reticular formation, or both, may be involved in the pathogenesis of these abnormal movements.
Adult↗
[Clinical aspects of abnormal eye movements].
This paper reviews a variety of abnormal eye movements which include abnormal ocular positions, restricted eye motions, impairment of conjugated eye movements, abnormal smooth pursuit, abnormal saccade, gaze-evoked nystagmus, down-beat nystagmus, internuclear ophthalmoplegia, supranuclear ophthalmoplegia, square wave jerks, roving eye movement, ocular bobbing, ocular dipping, reverse ocular bobbing, and ping-pong gaze. Abnormal eye movements occur from stroke, spinocerebellar degeneration, Parkinson disease, multiple system atrophy, progressive supranuclear palsy, multiple sclerosis, Miller Fisher syndrome, myasthenia gravis, opsoclonus-polymyoclonia syndrome, and Creutzfeldt-Jakob disease. In neurological practice, it is important to observe abnormal eye movements accurately and enthusiastically, to make appropriate anatomical and etiological diagnosis.
Adult↗
Congenital abnormal eye movement without gaze nystagmus.
Ten cases with congenital abnormal eye movements were reported. Eye movement abnormalities were confined to horizontal pursuit, OKN, and visual suppression. Horizontal saccade and VOR, and vertical eye movements were normal in most cases. Gaze nystagmus was not observed in any case. No serious lesion in the CNS concerning eye movements was detected. Although the cause of abnormal eye movements was not clear, congenital origin was postulated. Similar cases reported in the literature were discussed. These cases may be called "congenital nystagmus without gaze nystagmus."
Audiometry↗
Unilateral eye abnormalities in reared Mediterranean gilthead sea bream.
Eye abnormalities in reared gilthead sea bream (Sparus aurata) were investigated clinically and by histological techniques. A significant number of fish had a cataract in one eye and ocular inflammation including gross exophthalmos. In a small number of fish gas bubbles were observed in the anterior chamber of the eye. Histological examination provided no evidence of an infectious process and a possible behavioural aetiology is discussed.
Animals↗
Treatment of abnormal eye movements that impair vision: strategies based on current concepts of physiology and pharmacology.
Certain abnormal eye movements, especially pathological nystagmus, degrade vision and cause illusory motion of the seen environment. These symptoms are due to excessive movement of images of stationary objects on the retina. Recently, the pathophysiology underlying several types of nystagmus and saccadic oscillations was better defined by the development of animal models and by experimental pharmacological studies. Despite this, few reliable therapies are currently available for these abnormal eye movements. In clinical studies, a number of drugs reportedly helped individual patients, but few drugs have been subjected to double-blind trials. An alternative approach to pharmacological suppression of abnormal eye movements is optical stabilization of images on the retina, which is helpful in selected patients. Weakening of the extraocular muscles, using botulinum toxin or surgery, is prone to cause diplopia and may induce plastic-adaptive changes that render the effect temporary. In some patients, treatment of an underlying condition, such as the Arnold-Chiari malformation, reduces nystagmus and improves vision. There is a need for multicenter trials to evaluate systematically potential treatments of abnormal eye movements that impair vision.
Animals↗
Positron emission tomography in diagnosing brainstem vascular lesions that cause abnormal eye movements.
PURPOSE: To evaluate the efficacy of positron emission tomography (PET) in aiding in the diagnosis of brainstem infarctions that cause abnormal eye movements. METHOD: Cerebral glucose metabolism was examined by PET with 18F-fluorodeoxyglucose as a tracer in five normal control subjects and six patients with abnormal eye movements. The PET images were registered to and superimposed on magnetic resonance images (MRIs). RESULTS: All control subjects showed little asymmetry of glucose metabolism in the brainstem, whereas all six patients demonstrated areas of low glucose metabolism in the brainstem. Areas of low metabolism seen by PET were wider than they appeared to be by MRI; MRIs even appeared normal in some patients. Asymmetry index measurements at the level of the ischemic lesion ranged between 19% and 45%. CONCLUSIONS: Positron emission tomography detected metabolic abnormality in patients with brainstem lesions that caused abnormal eye movements. Superimposing PET images on MRIs accurately localized abnormally low metabolism in the brainstem. Combined imaging with PET and MRI can be used to diagnose ischemic lesions in the brainstem from functional (PET) and morphologic (MRI) viewpoints.
Adult↗
[Developmental mechanisms of congenital eye abnormalities].
Experimental teratology in mice was studied to clarify the developmental mechanisms of congenital eye abnormalities. Pregnant Jcl: ICR mice were treated intraperitoneally with ochratoxin A on day 7 of pregnancy. The offspring were grossly observed on day 9, 10, 11, 12, 13, 14, 16 or 18 of gestation, or at the second or fourth week after birth. Then, the eyes were histologically examined in serial sections. Mother mice were injected with ochratoxin A on day 8, 9, 10 or 11 of pregnancy, and the eyes of fetuses were examined on day 16 of gestation to determine the critical periods for the congenital eye abnormalities. Pregnant C57BL/6NJcl mice were also given an intraperitoneal injection of ochratoxin A on day 7 of pregnancy, and the eyes of offspring were observed grossly and histologically on day 16 or 18 of gestation, or at the second or fourth week after birth. Fetal and postnatal eyes showed various kinds and degrees of developmental abnormalities histologically. They included anophthalmia, microphthalmia, aphakia, mesenchymal dysgenesis of the anterior segment, faulty separation of the lens vesicle, developmental abnormalities of the vitreous, faulty closure of the embryonic fissure, retinal rosette formation and aberrant optic nerve fiber. Since anophthalmia, microphthalmia and aphakia caused by the developmental disturbances of the optic and lens vesicles were not established in the fetuses whose mothers were treated with ochratoxin A after day 9 of pregnancy, the critical periods for these abnormalities were considered to be on day 8 of gestation or earlier. Mesenchymal dysgenesis of the anterior segment, faulty separation of the lens vesicle and developmental abnormalities of the vitreous were frequently observed in the fetuses whose mothers were injected with ochratoxin A on day 7, 8 or 9 of pregnancy. It was considered that there was a correlation between the critical periods for these three abnormalities and the stage of the neural crest cell migration around the optic vesicle. Mesenchymal dysgenesis of the anterior segment observed in mice corresponded to the Axenfeld-Rieger syndrome or Peters' anomaly encountered clinically. Processes of production of these abnormalities based on the faulty migration of the neural crest cells which form the ocular anterior segment were demonstrated.(ABSTRACT TRUNCATED AT 400 WORDS)
Animals↗
Abnormal eye, a new eye mutant in the mosquito, Anopheles culicifacies.
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Animals↗
Visual impairment and eye abnormalities in Oklahoma Indians.
OBJECTIVE: To determine the prevalence of visual impairment and eye abnormalities in Oklahoma Indians. METHODS: The cross-sectional study included 1019 Oklahoma Indians, aged 48 to 82 years; 60.2% were women. All participants gave a personal interview, and all underwent an eye examination, including the determination of best-corrected visual acuity and an ophthalmoscopic examination. In addition, two 45 degrees fundus photographs were taken of each eye, and these photographs were graded by the Fundus Photography Reading Center at the University of Wisconsin, Madison. RESULTS: Among the 1019 participants, 77.4% had a visual acuity of 20/20 or better, 19.5% and 2.5% had visual acuities of between 20/25 and 20/40 and between 20/50 and 20/190, respectively; and 0.6% were legally blind, all in the better eye. Cataract was the most frequent contributing cause and age-related macular degeneration the second most frequent contributing cause of visual impairment. The overall prevalence proportions of age-related macular degeneration, cataract, diabetic retinopathy, and definite glaucoma were 33.6%, 39.6%, 20.1%, and 5.6%, respectively. Most of the other eye abnormalities were rare in the study participants, except for pinguecula (42.4%) and dermatochalasis (30.1%). CONCLUSIONS: Oklahoma Indians have a higher prevalence of visual impairment, age-related macular degeneration, and diabetic retinopathy than other ethnic groups. The implementation of adequate treatment and prevention programs for eye diseases is indicated.
Aged↗
Eye abnormalities in the mentally handicapped.
In 1987, a survey of eye abnormalities was undertaken of the mentally handicapped patients in Stoke Park Hospital, Bristol. The total population was 367 patients (262 females and 105 males). Of the 367 patients reviewed, 218 were found to have one or more eye anomalies (including the Down's Syndrome group), which shows that more than half the patients suffered from eye disorders (59%). The prevalence of the following anomalies is presented in detail: strabismus, refractive errors and cataracts. Corneal anomalies, nystagmus, retinopathy, glaucoma and other eye pathologies associated with various syndromes are noted. Eye anomalies in 31 patients suffering from Down's syndrome in the sample are recorded. Preventative measures to ameliorate the defects of eyesight, particularly in the aging population, relevance of regular eye examination and medical or surgical treatment of eye disorders are discussed.
Adolescent↗
Abnormal eye movements in Gerstmann-Sträussler-Scheinker disease.
Gerstmann-Sträussler-Scheinker disease is a familial disorder of progressive ataxia and dementia in adulthood with extrapyramidal signs in some families. Neuro-ophthalmic examinations and eye movement recordings were performed in members of a large Indiana kindred. Five affected members and 11 members at risk were studied. Eye movements were recorded with videotape, electro-oculography, and/or magnetic scleral search coil. All affected members had abnormal eye movements characteristic of extrapyramidal diseases and cerebellar disorders. Nine members at risk had normal eye movements, but two others had slightly abnormal eye movements. Neuro-ophthalmic examination and eye movement recordings might be helpful in detecting early signs of Gerstmann-Sträussler-Scheinker disease in persons at risk.
Adolescent↗