TREATMENT OF ABNORMAL EYE-MOVEMENTS THAT IMPAIR VISION - STRATEGIES BASED ON CURRENT CONCEPTS OF PHYSIOLOGY AND PHARMACOLOGY

被引:50
作者
LEIGH, RJ
AVERBUCHHELLER, L
TOMSAK, RL
REMLER, BF
YANIGLOS, SS
DELLOSSO, LF
机构
[1] UNIV CLEVELAND HOSP, DEPT VET AFFAIRS MED CTR, DEPT OPHTHALMOL, CLEVELAND, OH USA
[2] UNIV CLEVELAND HOSP, DEPT VET AFFAIRS MED CTR, DEPT NEUROSCI, CLEVELAND, OH USA
[3] UNIV CLEVELAND HOSP, DEPT VET AFFAIRS MED CTR, DEPT OPTOMETRY, CLEVELAND, OH USA
[4] CASE WESTERN RESERVE UNIV, MT SINAI MED CTR, CLEVELAND, OH USA
关键词
D O I
10.1002/ana.410360204
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
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.
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页码:129 / 141
页数:13
相关论文
共 105 条
[11]   CONTRAST SENSITIVITY AT HIGH VELOCITIES [J].
BURR, DC ;
ROSS, J .
VISION RESEARCH, 1982, 22 (04) :479-484
[12]   OCULOMOTOR EFFECTS OF GAMMA-AMINOBUTYRIC-ACID AGONISTS AND ANTAGONISTS IN THE VESTIBULAR NUCLEI OF THE ALERT MONKEY [J].
BUTTNER, U ;
STRAUBE, A ;
KURZAN, R .
ANNALS OF THE NEW YORK ACADEMY OF SCIENCES, 1992, 656 :645-659
[13]  
BUTTNERENNEVER JA, 1989, REV NEUROL-FRANCE, V145, P533
[14]   SACCADIC OMISSION - WHY WE DO NOT SEE A GREY-OUT DURING A SACCADIC EYE-MOVEMENT [J].
CAMPBELL, FW ;
WURTZ, RH .
VISION RESEARCH, 1978, 18 (10) :1297-1303
[15]   LOSS OF THE NEURAL INTEGRATOR OF THE OCULOMOTOR SYSTEM FROM BRAIN-STEM LESIONS IN MONKEY [J].
CANNON, SC ;
ROBINSON, DA .
JOURNAL OF NEUROPHYSIOLOGY, 1987, 57 (05) :1383-1409
[16]  
CARLOW TJ, 1986, NEUROOPHTHALMOLOGY, P251
[17]  
CARPENTER RHS, 1991, VISION VISUAL FUNCTI, V8, P1
[18]  
CIUFFREDA KJ, 1982, AM J OPTOM PHYS OPT, V59, P396
[19]   BACLOFEN AND VELOCITY STORAGE - A MODEL OF THE EFFECTS OF THE DRUG ON THE VESTIBULOOCULAR REFLEX IN THE RHESUS-MONKEY [J].
COHEN, B ;
HELWIG, D ;
RAPHAN, T .
JOURNAL OF PHYSIOLOGY-LONDON, 1987, 393 :703-725
[20]   VELOCITY STORAGE, NYSTAGMUS, AND VISUAL-VESTIBULAR INTERACTIONS IN HUMANS [J].
COHEN, B ;
HENN, V ;
RAPHAN, T ;
DENNETT, D .
ANNALS OF THE NEW YORK ACADEMY OF SCIENCES, 1981, 374 (NOV) :421-433