Journal of Neuro-Ophthalmology:
Therapy for Nystagmus
Thurtell, Matthew J MBBS, FRACP; Leigh, R John MD
Department of Neurology, University Hospitals Case Medical Center, Cleveland, Ohio; and Neurology Service and Daroff-Dell'Osso Ocular Motility Laboratory, Veterans Affairs Medical Center, Cleveland, Ohio.
Supported by the National Institutes of Health R01-EY06717, the Office of Research and Development, the Medical Research Service, the Department of Veterans Affairs, and the Evenor Armington Fund.
Address correspondence to Dr. R. John Leigh, MD, Department of Neurology, University Hospitals Case Medical Center, 11100 Euclid Avenue, Cleveland, OH 44106-5040; E-mail: firstname.lastname@example.org
Pathological forms of nystagmus and their visual consequences can be treated using pharmacological, optical, and surgical approaches. Acquired periodic alternating nystagmus improves following treatment with baclofen, and downbeat nystagmus may improve following treatment with aminopyridines. Gabapentin and memantine are helpful in reducing acquired pendular nystagmus due to multiple sclerosis. Ocular oscillations in oculopalatal tremor may also improve following treatment with memantine or gabapentin. The infantile nystagmus syndrome (INS) may have only a minor impact on vision if “foveation periods” are well developed, but symptomatic patients may benefit from treatment with gabapentin, memantine, or base-out prisms to induce convergence. Several surgical therapies are also reported to improve INS, but selection of the optimal treatment depends on careful evaluation of visual acuity and nystagmus intensity in various gaze positions. Electro-optical devices are a promising and novel approach for treating the visual consequences of acquired forms of nystagmus.
Rational therapy of nystagmus rests on several basic principles (1). A clear percept of an object requires that its image be held steadily within about 0.5 degrees of the center of the fovea. For objects with higher spatial frequencies, such as Snellen optotypes, retinal image slip should be less than 5 degrees per second.
Patients with infantile nystagmus syndrome (INS), formerly called congenital nystagmus, often have a brief epoch of stillness called the “foveation period” during each cycle of the nystagmus, which is sufficient to provide clear vision (Fig. 1). It appears that they can suppress the visual consequences of rapid image motion at times other than during the foveation period, and therefore seldom complain of oscillopsia (2).
There are 3 gaze-holding mechanisms that promote clear vision. Visual fixation mechanisms reduce eye drifts that take the eyes away from the target and suppress unwanted saccades. The vestibulo-ocular reflex (VOR) generates eye movements to compensate for head perturbations at short latency, being especially important for stabilizing gaze during locomotion. An eccentric gaze-holding mechanism is important to withstand the elastic pull of the orbital fascia that tends to bring the eye back to the center position. Malfunction of each of these gaze-holding mechanisms, as well as other abnormal inputs to the ocular motor system, may cause drifts of the eye away from the target (slow phases) with interspersed corrective quick phases (saccades) that constitute pathological nystagmus.
Based on these principles, one goal of therapy is to abolish abnormal ocular oscillations and leave normal gaze-holding eye movements intact. For example, treatments to stop the eyes from moving altogether, such as botulinum toxin injections, may abolish the ocular oscillations, but provide no net improvement, since patients then complain of blurred vision when they move their head (due to absent VOR) and diplopia (due to absent vergence, which normally aligns the eyes). Treatments that suppress the abnormal ocular oscillations without affecting normal eye movements are therefore preferred. Furthermore, some forms of nystagmus, such as the gaze-evoked nystagmus common with drug intoxications and cerebellar disease (1,3), do not usually cause sufficient visual disturbance to require treatment. It should be noted that inappropriate saccades, including intrusions and oscillations, may also impair vision, but treatments for these are reviewed elsewhere (1,4-6).
We will review, in turn, drug treatments for pathological nystagmus, optical devices that negate the visual consequences of ocular oscillations, and surgical procedures. We will briefly discuss botulinum toxin and alternative methods to treat nystagmus (Table 1). We caution that although many treatments have been proposed for nystagmus, few have been evaluated with controlled clinical trials (7-9).
Nystagmus of Peripheral Vestibular Imbalance
This form of nystagmus usually resolves over the course of a few days. Medications, mainly used to treat associated vertigo, nausea, and vomiting, are helpful only during the acute phase of the illness (1,10). Nystagmus associated with benign paroxysmal positional vertigo is better treated with repositioning procedures, such as the Epley maneuver (11), than with medications.
This type of nystagmus is largely a feature of diseases affecting the vestibulocerebellum. Several hypotheses have been proposed for its pathogenesis, most invoking an up-down asymmetry that affects the inhibition of projections of the vertical semicircular canals, vertical smooth pursuit, or otolithic influences (1). Many medications have been reported to improve downbeat nystagmus, including the GABAA agonist clonazepam (12,13) and the GABAB agonist baclofen (14,15). However, a double-masked comparison of baclofen and gabapentin showed that neither drug produced a consistent improvement and that, in some patients, the nystagmus was made worse (16).
An interest in using anticholinergic agents was generated by the observation that intravenous scopolamine reduces downbeat nystagmus (17). However, a controlled trial of the oral anticholinergic agent trihexyphenidyl produced only modest improvement and side effects that were poorly tolerated (18).
The potassium channel blockers 3,4-diaminopyridine and 4-aminopyridine are promising for the treatment of downbeat nystagmus. Both medications have been shown to suppress downbeat nystagmus in some patients (19-22). Although they are generally well tolerated, they can cause seizures. How do they suppress nystagmus? Because potassium channels are abundant on cerebellar Purkinje cells, the aminopyridines may increase their discharge. The enhanced Purkinje cell activity could then restore normal levels of inhibition of vertical vestibular eye movements, leading to suppression of the nystagmus (22). However, 4-aminopyridine suppresses upbeat nystagmus in some patients (23), and it may occasionally cause downbeat nystagmus to convert to upbeat nystagmus (24). Alternatively, 4-aminopyridine could modulate otolithic mechanisms that influence vertical nystagmus (24). Whatever the mechanism, many patients are likely to benefit from treatment with 4-aminopyridine, which is generally better tolerated than 3,4-diaminopyridine (21,25,26).
This form of nystagmus usually occurs with brainstem lesions. Although it may produce pronounced visual symptoms during the acute period, upbeat nystagmus often resolves spontaneously or converts to downbeat nystagmus. There are few clinical trials evaluating pharmacological treatments for this form of nystagmus, although 1 recent study has shown that it may be suppressed with memantine (8). Treatments similar to those for downbeat nystagmus, such as the aminopyridines (23), are also worth considering in patients with persistent upbeat nystagmus.
Periodic Alternating Nystagmus
This form of nystagmus consists of spontaneous horizontal nystagmus that reverses direction approximately every 100-120 seconds. The acquired form of periodic alternating nystagmus (PAN) is a rare but well understood form of central vestibular nystagmus. A monkey model has been produced following surgical lesions of the cerebellar nodulus and ventral uvula (27). Such lesions may cause excessive vestibular responses (velocity storage), which, in turn, stimulate adaptive mechanisms that cause the ocular oscillations (28). The nystagmus of most patients (and the monkey model) is decreased following treatment with the GABAB agonist baclofen (29-32). Improvement following treatment with memantine has also been reported (33). The infantile form of PAN, which has a more variable cycle length, probably has a different pathogenesis and only occasionally improves with baclofen treatment (34-37).
Acquired Pendular Nystagmus Associated With Multiple Sclerosis
This form of nystagmus usually causes visual impairment and oscillopsia, for which most affected patients seek therapy. These patients often have coexisting internuclear ophthalmoparesis and impaired visual function due to optic neuropathy. Indeed, the amplitude of the nystagmus is often greater in the eye with poorer vision, prompting the hypothesis that delays in visual pathway conduction give rise to the oscillations (38). However, other investigations have suggested that an instability in the gaze-holding mechanism (neural integrator) may be responsible (39-41). Suspicion of neural integrator dysfunction led to the testing of medications with presumed effects on GABA-mediated and glutamate-mediated mechanisms (41,42). In early studies, GABAergic agents, such as clonazepam, valproate, and isoniazid, were found to decrease the nystagmus in some patients (43,44). In a multicenter double-masked study of 15 patients with acquired pendular nystagmus (APN) (16), gabapentin, an anticonvulsant initially thought to have GABAergic action, was compared to baclofen, a GABAB agonist. Visual acuity improved significantly with gabapentin, but not with baclofen. Gabapentin reduced median eye speed in all 3 planes, but baclofen did so only in the vertical plane. In 10 of the 15 patients, the suppression of nystagmus with gabapentin was substantial, and 8 patients chose to continue taking the drug. However, some patients in the study showed no response to either medication. An important side effect of gabapentin was increased ataxia. Three subsequent trials, 1 comparing gabapentin with the anticonvulsant Vigabatrin (45) and the other 2 comparing it with memantine (8,9), have confirmed that gabapentin is an effective treatment for APN. Vigabatrin, which is more purely GABAergic than gabapentin, was ineffective in the first of these trials (45), suggesting that gabapentin suppresses APN by a non-GABAergic mechanism. Gabapentin is now known to exert its effect by binding to the calcium channel subunit α2δ-1 (46).
Memantine, a noncompetitive N-methyl-D-aspartate receptor antagonist that has been used for more than 25 years in Germany as a therapy for a variety of neurological symptoms, including treatment of spasticity in multiple sclerosis (MS), was recently approved by the United States Food and Drug Administration at a dose of 20 mg/d for the treatment of memory failure in Alzheimer disease. At doses of 40 mg/d, memantine has been reported to reduce or abolish APN in patients with MS (8,9,47). Memantine also shows some antagonistic effects at 5-hydroxytryptamine and nicotinic acetylcholine receptors (48). Memantine may reduce nystagmus in some patients in whom gabapentin has proven ineffective (8,9,49). However, at doses of 30 mg/d, patients with MS may develop blurred vision, fatigue, severe headache, increased muscle weakness, or gait instability (50), so that gabapentin may be the preferred treatment when APN is due to MS.
While recent clinical trials have compared the relative efficacy of gabapentin and memantine for APN (8,9), further trials are required to determine if combinations of gabapentin and memantine have an additive effect and to establish whether these drugs may be useful adjuncts to surgical treatments for APN, as suggested in case reports (51,52). The same is true for other medications that have been reported to suppress nystagmus in individual patients with APN, but have not been studied in controlled trials (Table 1).
Previously called oculopalatal myoclonus, oculopalatal tremor (OPT) usually develops in the weeks following brainstem or cerebellar strokes that interrupt projections from the deep cerebellar nuclei. These projections run in the superior cerebellar peduncle, bending (but not synapsing) near the red nucleus, before descending in the central tegmental tract to contact the inferior olivary nuclei (53). In health, inferior olivary neurons, which possess gap junctions (connexins) on their dendrites, discharge asynchronously. Following degenerative hypertrophy of the inferior olives, gap junctions also develop on the cell bodies of olivary neurons (54), producing electrotonic coupling between them. Thereafter, ensembles of inferior olivary neurons begin to fire in synchrony at a frequency of about 2 Hz and serve as “pacemakers” projecting via climbing fibers to the cerebellum, where maladaptive learning takes place (55,56). The entire process results in spontaneous oscillations of the eyes, palate, and other branchial muscles at a frequency of about 2 Hz.
Nystagmus may be the only clinical manifestation of OPT. Some patients show partial suppression of their nystagmus with gabapentin (16) or memantine (Fig. 2) (8). However, neither drug noticeably suppresses the palatal tremor, which is usually asymptomatic. While the nystagmus of OPT can respond dramatically to gabapentin or memantine in occasional patients (8), it is generally more refractory to treatment than is APN secondary to MS.
The hypertrophied inferior olivary nucleus of patients with OPT also shows increased acetylcholinesterase activity (57), prompting trials of anticholinergic agents. Some patients with pendular nystagmus may show a response to trihexyphenidyl (58,59), but a clinical trial of this medication showed only modest effects (18). A discrepancy between the effects of intravenous scopolamine (17) and oral trihexyphenidyl in certain pendular forms of nystagmus might be due to the more selective antagonism of muscarinic receptors by trihexyphenidyl (60). Intravenous scopolamine clouds consciousness and is not a practical therapy for pendular forms of nystagmus. Furthermore, transdermal scopolamine is not a reliable therapy for pendular forms of nystagmus and can make the nystagmus worse or induce confusion (61).
Novel therapies for OPT may target the unusual electrotonic coupling of the inferior olivary neurons by connexins (62-64). These connexins can be inhibited by certain antimalarial agents (65). Other medications reported to aid patients with OPT are listed in Table 1.
Familial Episodic Vertigo and Ataxia Type 2
Nystagmus in this disorder, which is due to a calcium channelopathy, usually responds to acetazolamide (66-68), although associated cerebellar symptoms are occasionally made worse (69). The potassium channel blocker 4-aminopyridine is also an effective treatment for episodic ataxia type 2 in some patients (70). Some patients with spinocerebellar ataxia type 6 who have episodic attacks of vertigo and nystagmus benefit from acetazolamide (71). Studies of animal models for these channelopathies are likely to produce a clearer rationale for therapy (72).
This form of nystagmus may be suppressed by alcohol (73,74) and clonazepam (75). We have observed improvement of hemiseesaw nystagmus in single patients treated with gabapentin or memantine (8).
This ocular motor disorder, which consists of slow-and sometimes symptomatic-vertical oscillations in an eye with visual loss (1), may be improved with gabapentin (76).
Nystagmus of Early Childhood
The nystagmus of some patients with INS has improved with gabapentin or memantine. In a randomized, controlled, double-masked trial comparing the 2 medications, nystagmus intensity and visual acuity improved in both treatment groups (77). However, there was only a small effect in patients with abnormal afferent visual system function or structure compared to those with normal afferent visual systems. INS may also be reduced by smoking cannabis (78,79).
Gene therapy holds the potential for treatment of nystagmus associated with retinal disorders. For example, in an animal model of Leber congenital amaurosis, successful gene therapy restored vision and reduced the associated nystagmus (80-83).
Correction of refractive error is worthwhile in most patients with infantile or acquired forms of nystagmus and may produce an appreciable improvement in vision (84,85). Contact lenses may suppress INS (86), suggesting a mechanism beyond refractive correction (discussed further in the final section of this review). The main therapy for latent nystagmus (fusional maldevelopment nystagmus syndrome) consists of measures to improve vision, such as patching for amblyopia (87).
Patients whose nystagmus is suppressed by convergence may benefit from wearing spectacle prisms that require convergence for single vision of far targets (88). Adequate convergence may be produced by a pair of 7 prism-diopter base-out prisms with −1 diopter spherical power added to compensate for the accommodation that accompanies the induced convergence (89). (The spherical correction may not be required in individuals with presbyopia.) With base-out prisms, some individuals with INS experience an improvement of vision that is sufficient to qualify them for a driving license. Occasional patients with acquired nystagmus may benefit from prisms (90). Those whose nystagmus is worse during near viewing may respond to base-in prisms, which reduce convergence effort (91). Patients with INS whose nystagmus is of lower amplitude when the eyes are placed in an eccentric null position rarely report a benefit from conjugate prisms that shift gaze.
An alternative approach has been to develop optical devices that negate the visual effects of the nystagmus. One approach consists of using high-plus spectacle lenses in combination with high-minus contact lenses (92). The underlying principle is that stabilization of images on the retina can be achieved if the power of the spectacle lens focuses the primary image close to the center of rotation of the eye. However, such images are defocused, requiring a contact lens to extend the focus back onto the retina. Because the contact lens moves with the eye, it does not negate the effect of retinal image stabilization due to the spectacle lens. With such high-positive spectacle lens and high-negative contact lens combinations, it is possible to negate about 90% of the visual effects of eye movements (93). However, this approach impairs all eye movements, including the VOR and vergence, so that it is only useful when the patient is stationary and viewing monocularly. Other disadvantages are that the field of view is limited and patients with ataxia may have difficulty inserting the contact lens. Gas-permeable or even soft contact lenses may, however, achieve lesser degrees of image stabilization that are beneficial to the patient (94,95). Thus, in selected patients, this approach may prove useful for limited periods of time, such as for the duration of a movie.
A more recent approach is to develop an electro-optical device that measures the ocular oscillations and negates their effects (96). This approach is best suited for pendular nystagmus, which can be electronically distinguished from normal eye movements, such as voluntary saccades. Figure 3 summarizes the image-shifting optics that are being used to develop a portable battery-driven device (97,98), a prototype of which is shown in Figure 4.
Surgical procedures for the treatment of nystagmus have mainly been developed for patients with INS. The Anderson-Kestenbaum operation aims to move the attachments of the extraocular muscles, so that the null point is shifted to the straight-ahead gaze position (99,100). Selection of patients who will benefit most entails measuring visual acuity and nystagmus intensity in different gaze positions (101). The surgeon can then calculate what is required surgically to shift the position of the null point (102,103). The Anderson-Kestenbaum procedure not only shifts and broadens the null zone, it decreases nystagmus intensity outside of the null zone, and may improve head posture (104-106).
A second surgical approach, suitable for patients whose nystagmus suppresses with convergence, aims to diverge the eyes, thereby requiring the patient to converge during far viewing (107,108). Some surgeons have reported that combining the Anderson-Kestenbaum operation with a divergence procedure may produce a better visual outcome than either alone (102,107,109).
A third approach involves large recessions (weakening) of the horizontal rectus muscles, which may cause improvement of vision and head posture (110-115). However, experimental procedures to weaken the extraocular muscles induce adaptive changes that restore muscle force (116). Such changes might cause the nystagmus to increase in severity following an initial improvement. Thus, controlled studies are required to evaluate the long-term effects of this recession approach.
An observation of Dell'Osso (117), that some suppression of nystagmus and broadening of the null zone follows almost every surgical procedure for INS, led to the suggestion that simply detaching the muscles, dissecting the perimuscular fascia, and reattaching them (“tenotomy and reattachment”) at the same site on the globe might suppress INS. Experimental studies using a canine model support this hypothesis (118). The operation may have its effects by disrupting extraocular proprioceptive feedback signals (119). Recent work has shown that the brain not only receives proprioceptive inputs from extraocular muscles (120), but appears to use that information at a cortical level (121). Clinical trials have indicated that some patients treated with tenotomy and reattachment show improvement in some measures of visual and ocular motor function following horizontal rectus surgery (122-124), but not all reports agree (125).
Aside from the need to conduct masked trials, other challenges to evaluate the effectiveness of surgical therapies for INS arise from the inherent variability of the nystagmus waveform and the complex relationship between waveform and visual acuity in any 1 individual. Thus, measurements of the duration of the foveation period from eye movement records (126) may appear to improve more with surgery than do conventional measurements of visual acuity, which is highly variable in INS. Carefully selected patients with INS may benefit from surgical treatments that are geared to their individual visual and ocular motor findings: 1) if there is a narrow eccentric null zone, then the Anderson-Kestenbaum operation should be considered; 2) if the nystagmus is greatly reduced with convergence, then a bilateral medial rectus recession procedure often damps the nystagmus; and 3) if neither of these conditions apply, then tenotomy and reattachment may help some patients by broadening the null zone. Patients with INS and associated afferent visual system abnormalities, such as oculocutaneous albinism, are less likely to benefit from surgery (127).
Extraocular muscle surgery has also been tried as a treatment for acquired nystagmus, either alone or in combination with medication therapy, sometimes with success (52,128-131). However, formal clinical trials are needed to determine whether surgery has a role in the treatment of acquired nystagmus.
Botulinum toxin has been injected into the extraocular muscles or retrobulbar space to temporarily reduce or abolish acquired nystagmus (132,133). Although some patients have reported improved vision (134-137), common side effects include ptosis and diplopia, which are usually more troublesome to the patient than were the visual consequences of the nystagmus itself. Less often, botulinum toxin has been used to treat infantile or latent nystagmus (138,139).
Another drawback of botulinum toxin treatment for nystagmus is that it also impairs normal eye movements (140,141). Compromised function of the VOR causes patients to complain of blurred vision or oscillopsia when they walk. In patients who habitually view with their injected (paretic) eye, adaptive changes may take place such that the nystagmus increases in the noninjected eye (135).
Thus, botulinum toxin may abolish nystagmus and improve vision in some patients and may be acceptable to patients who are prepared to view monocularly. However, its limited period of action and side effects limit its therapeutic value.
OTHER TREATMENT APPROACHES
After the observation that wearing contact lenses may suppress INS (86), it was documented that electrical stimulation or vibration over the forehead may suppress the oscillations in some patients (142). Such effects may be exerted via the trigeminal system, which receives afferent (proprioceptive) signals from the extraocular muscles (143). Acupuncture to the neck muscles may suppress INS in some patients, perhaps by a similar mechanism (144,145). Biofeedback has also been reported to help some patients with this condition (146,147), but without sustained effects (148). At present, a definite benefit from any of these treatments is yet to be demonstrated via controlled trials.
As more becomes known about the pharmacology of the ocular motor system, new medications may emerge for the treatment of acquired and infantile forms of nystagmus. Ideally, these drugs should be evaluated in controlled masked trials. Better understanding of the proprioceptive control of eye movements may make it possible to hone surgical treatments, such as tenotomy and reattachment (149), or even develop medication therapies that act at the insertions of the extraocular muscles (119). Since INS appears to be genetically determined in many individuals (150), specific treatment directed toward the abnormal protein or channel may be effective. Gene therapy offers great promise for those individuals with hereditary retinal disorders that are associated with nystagmus (83). In refractory acquired forms of nystagmus, electro-optical devices may negate the visual consequences of the nystagmus if individualized digital filtering of nystagmus waveforms can be achieved and the devices can be miniaturized (97).
1. Leigh RJ,
Zee DS. The Neurology of Eye Movements, 4th edition. New York, NY: Oxford University Press, 2006.
2. Abadi RV,
Whittle JP, Worfolk R. Oscillopsia and tolerance to retinal image movement in congenital nystagmus. Invest Ophthalmol Vis Sci. 1999;40:339-345.
3. Hogan RE,
Collins SD, Reed RC, Remler BF. Neuro-ophthalmological signs during rapid intravenous administration of phenytoin. J Clin Neurosci. 1999;6:494-497.
4. Shaikh AG,
Miura K, Optican LM, Ramat S, Leigh RJ, Zee DS. A new familial disease of saccadic oscillations and limb tremor provides clues to mechanisms of common tremor disorders. Brain. 2007;130:3020-3031.
5. Serra A,
Liao K, Martinez-Conde S, Optican LM, Leigh RJ. Suppression of saccadic intrusions in hereditary ataxia by memantine. Neurology. 2008;70:810-812.
6. Shaikh AG,
Ramat S, Optican LM, Miura K, Leigh RJ, Zee DS. Saccadic burst cell membrane dysfunction is responsible for saccadic oscillations. J Neuroophthalmol. 2008;28:329-336.
7. Straube A,
Leigh RJ, Bronstein A, Heide W, Riordan-Eva P, Tijssen CC, Dehaene I, Straumann D. EFNS task force-therapy of nystagmus and oscillopsia. Eur J Neurol. 2004;11:83-89.
8. Thurtell MJ,
Joshi AC, Leone AC, Tomsak RL, Kosmorsky GS, Stahl JS, Leigh RJ. Cross-over trial of gabapentin and memantine as treatment for acquired nystagmus. Ann Neurol. 2010;67:676-680.
9. Starck M,
Albrecht H, Pollmann W, Dieterich M, Straube A. Acquired pendular nystagmus in multiple sclerosis: an examiner-blind cross-over treatment study of memantine and gabapentin. J Neurol. 2010;257:322-327.
10. McLean RJ,
Gottlob I. The pharmacological treatment of nystagmus: a review. Expert Opin Pharmacother. 2009;10:1805- 1816.
11. von Brevern M,
Seelig T, Radtke A, Tiel-Wilck K, Neuhauser H, Lempert T. Short-term efficacy of Epley's manoeuvre: a double-blind randomised trial. J Neurol Neurosurg Psychiatry. 2006;77:980-982.
12. Currie JN,
Matsuo V. The use of clonazepam in the treatment of nystagmus-induced oscillopsia. Ophthalmology. 1986;93:924-932.
13. Young YH,
Huang TW. Role of clonazepam in the treatment of idiopathic downbeat nystagmus. Laryngoscope. 2001;111:1490-1493.
14. Dieterich M,
Straube A, Brandt T, Paulus W, Büttner U. The effects of baclofen and cholinergic drugs on upbeat and downbeat nystagmus. J Neurol Neurosurg Psychiatry. 1991;54:627-632.
15. Kastrup O,
Maschke M, Keidel M, Diener HC. Presumed pharmacologically induced change from upbeat- to downbeat nystagmus in a patient with Wernicke's encephalopathy. Clin Neurol Neurosurg. 2004;107:70-72.
16. Averbuch-Heller L,
Tusa RJ, Fuhry L, Rottach KG, Ganser GL, Heide W, Büttner U, Leigh RJ. A double-blind controlled study of gabapentin and baclofen as treatment for acquired nystagmus. Ann Neurol. 1997;41:818-825.
17. Barton JJ,
Huaman AG, Sharpe JA. Muscarinic antagonists in the treatment of acquired pendular and downbeat nystagmus-a double-blind, randomized trial of three intravenous drugs. Ann Neurol. 1994;35:319-325.
18. Leigh RJ,
Burnstine TH, Ruff RL, Kasmer RJ. The effect of anticholinergic agents upon acquired nystagmus. A double-blind study of trihexyphenidyl and tridihexethyl chloride. Neurology. 1991;41:1737- 1741.
19. Strupp M,
Schuler O, Krafczyk S, Jahn K, Schautzer F, Büttner U, Brandt T. Treatment of downbeat nystagmus with 3,4-diaminopyridine: a placebo-controlled study. Neurology. 2003;61:165-170.
20. Kalla R,
Glasauer S, Schautzer F, Lehnen N, Büttner U, Strupp M, Brandt T. 4-aminopyridine improves downbeat nystagmus, smooth pursuit, and VOR gain. Neurology. 2004;62:1228-1229.
21. Strupp M,
Kalla R, Glasauer S, Wagner J, Hüfner K, Jahn K, Brandt T. Aminopyridines for the treatment of cerebellar and ocular motor disorders. Prog Brain Res. 2008;171:535-541.
22. Glasauer S,
Rossert C. Modelling drug modulation of nystagmus. Prog Brain Res. 2008;171:527-534.
23. Glasauer S,
Kalla R, Buttner U, Strupp M, Brandt T. 4-aminopyridine restores visual ocular motor function in upbeat nystagmus. J Neurol Neurosurg Psychiatry. 2005;76:451-453.
24. Helmchen C,
Sprenger A, Rambold H, Sander T, Kompf D, Straumann D. Effect of 3,4-diaminopyridine on the gravity dependence of ocular drift in downbeat nystagmus. Neurology. 2004;63:752-753.
25. Halmagyi GM,
Leigh RJ. Upbeat about downbeat nystagmus. Neurology. 2004;63:606-607.
26. Leigh RJ.
Potassium channels, the cerebellum, and treatment for downbeat nystagmus. Neurology. 2003;61:158-159.
27. Waespe W,
Cohen B, Raphan T. Dynamic modification of the vestibulo-ocular reflex by the nodulus and uvula. Science. 1985;228:199-202.
28. Leigh RJ,
Robinson DA, Zee DS. A hypothetical explanation for periodic alternating nystagmus: instability in the optokinetic-vestibular system. Ann N Y Acad Sci. 1981;374:619-635.
29. Halmagyi GM,
Rudge P, Gresty MA, Leigh RJ, Zee DS. Treatment of periodic alternating nystagmus. Ann Neurol. 1980;8:609-611.
30. Furman JM,
Wall C III, Pang DL. Vestibular function in periodic alternating nystagmus. Brain. 1990;113:1425-1439.
31. Garbutt S,
Thakore N, Rucker J, Han Y, Kumar AN, Leigh RJ. Effects of visual fixation and convergence in periodic alternating nystagmus due to MS. Neuroophthalmology. 2004;28:221-229.
32. Cohen B,
Dai M, Yakushin SB, Raphan T. Baclofen, motion sickness susceptibility and the neural basis for velocity storage. Prog Brain Res. 2008;171:543-553.
33. Kumar A,
Thomas S, McLean R, Proudlock FA, Roberts E, Boggild M, Gottlob I. Treatment of acquired periodic alternating nystagmus with memantine: a case report. Clin Neuropharmacol. 2009;32:109-110.
34. Gradstein L,
Reinecke RD, Wizov SS, Goldstein HP. Congenital periodic alternating nystagmus. Diagnosis and management. Ophthalmology. 1997;104:918-928.
35. Solomon D,
Shepard N, Mishra A. Congenital periodic alternating nystagmus: response to baclofen. Ann N Y Acad Sci. 2002;956:611-616.
36. Hertle RW,
Reznick L, Yang D. Infantile aperiodic alternating nystagmus. J Pediatr Ophthalmol Strabismus. 2009;46:93-103.
37. Comer RM,
Dawson EL, Lee JP. Baclofen for patients with congenital periodic alternating nystagmus. Strabismus. 2006;14:205-209.
38. Barton JJ,
Cox TA. Acquired pendular nystagmus in multiple sclerosis-clinical observations and the role of optic neuropathy. J Neurol Neurosurg Psychiatry. 1993;56:262-267.
39. Averbuch-Heller L,
Zivotofsky AZ, Das VE, DiScenna AO, Leigh RJ. Investigations of the pathogenesis of acquired pendular nystagmus. Brain. 1995;118:369-378.
40. Das VE,
Oruganti P, Kramer PD, Leigh RJ. Experimental tests of a neural-network model for ocular oscillations caused by disease of central myelin. Exp Brain Res. 2000;133:189-197.
41. Arnold DB,
Robinson DA, Leigh RJ. Nystagmus induced by pharmacological inactivation of the brainstem ocular motor integrator in monkey. Vision Res. 1999;39:4286-4295.
42. Straube A,
Kurzan R, Büttner U. Differential effects of bicuculline and muscimol microinjections into the vestibular nuclei on simian eye movements. Exp Brain Res. 1991;86:347-358.
43. Lefkowitz D,
Harpold G. Treatment of ocular myoclonus with valproic acid. Ann Neurol. 1985;17:103-104.
44. Traccis S,
Rosati G, Monaco MF, Aiello I, Agnetti V. Successful treatment of acquired pendular elliptical nystagmus in multiple sclerosis with isoniazid and base-out prisms. Neurology. 1990;40:492-494.
45. Bandini F,
Castello E, Mazzella L, Mancardi GL, Solaro C. Gabapentin but not vigabatrin is effective in the treatment of acquired nystagmus in multiple sclerosis: how valid is the GABAergic hypothesis? J Neurol Neurosurg Psychiatry. 2001;71:107-110.
46. Bauer CS,
Nieto-Rostro M, Rahman W, Tran-Van-Minh A, Ferron L, Douglas L, Kadurin I, Sri Ranjan Y, Fernandez-Alacid L, Millar NS, Dickenson AH, Lujan R, Dolphin AC. The increased trafficking of the calcium channel subunit alpha2delta-1 to presynaptic terminals in neuropathic pain is inhibited by the alpha2delta ligand pregabalin. J Neurosci. 2009;29:4076-4088.
47. Starck M,
Albrecht H, Pollmann W, Straube A, Dieterich M. Drug therapy for acquired pendular nystagmus in multiple sclerosis. J Neurology. 1997;244:9-16.
48. Rogawski MA,
Wenk GL. The neuropharmacological basis for the use of memantine in the treatment of Alzheimer's disease. CNS Drug Rev. 2003;9:275-308.
49. Shery T,
Proudlock FA, Sarvananthan N, McLean RJ, Gottlob I. The effects of gabapentin and memantine in acquired and congenital nystagmus: a retrospective study. Br J Ophthalmol. 2006;90:839-843.
50. Villoslada P,
Arrondo G, Sepulcre J, Alegre M, Artieda J. Memantine induces reversible neurologic impairment in patients with MS. Neurology. 2009;72:1630-1633.
51. Jain S,
Proudlock F, Constantinescu CS, Gottlob I. Combined pharmacologic and surgical approach to acquired nystagmus due to multiple sclerosis. Am J Ophthalmol. 2002;134:780-782.
52. Tomsak RL,
Dell'Osso LF, Jacobs JB, Wang ZI, Leigh RJ. Eye muscle surgery for acquired forms of nystagmus. In: Leigh RJ, Devereaux MW, eds. Advances in Understanding Mechanisms and Treatment of Infantile Forms of Nystagmus. New York, NY: Oxford University Press, 2008:112-116.
53. Deuschl G,
Toro C, Valls-Solo J, Zee DS, Hallett M. Symptomatic and essential palatal tremor. 1. Clinical, physiological and MRI analysis. Brain. 1994;117:775-788.
54. Ruigrok TJ,
de Zeeuw CI, Voogd J. Hypertrophy of inferior olivary neurons: a degenerative, regenerative or plasticity phenomenon. Eur J Morphol. 1990;28:224-239.
55. Hong S,
Leigh RJ, Zee DS, Optican LM. Inferior olive hypertrophy and cerebellar learning are both needed to explain ocular oscillations in oculopalatal tremor. Prog Brain Res. 2008;171:219-226.
56. Liao K,
Hong S, Zee DS, Optican LM, Leigh RJ. Impulsive head rotation resets oculopalatal tremor: examination of a model. Prog Brain Res. 2008;171:227-234.
57. Koeppen AH.
Olivary hypertrophy: histochemical demonstration of hydrolytic enzymes. Neurology. 1980;30:471-480.
58. Herishanu Y,
Louzoun Z. Trihexyphenidyl treatment of vertical pendular nystagmus. Neurology. 1986;36:82-84.
59. Jabbari B,
Rosenberg M, Scherokman B, Gunderson CH, McBurney JW, McClintock W. Effectiveness of trihexyphenidyl against pendular nystagmus and palatal myoclonus: evidence of cholinergic dysfunction. Mov Disord. 1987;2:93-98.
60. Buckley NJ,
Bonner TI, Buckley CM, Brann MR. Antagonist binding properties of five cloned muscarinic receptors expressed in CHO-K1 cells. Mol Pharmacol. 1989;35:469-476.
61. Kim JI,
Averbuch-Heller L, Leigh RJ. Evaluation of transdermal scopolamine as treatment for acquired nystagmus. J Neuroophthalmol. 2001;21:188-192.
62. Condorelli DF,
Parenti R, Spinella F, Trovato Salinaro A, Belluardo N, Cardile V, Cicirata F. Cloning of a new gap junction gene (CX36) highly expressed in mammalian brain neurons. Eur J Neurosci. 1998;10:1202-1208.
63. Devor A,
Yarom Y. Electrotonic coupling in the inferior olivary nucleus revealed by simultaneous double patch recordings. J Neurophysiol. 2002;87:3048-3058.
64. Shaikh AG,
Hong S, Liao K, Tian J, Solomon D, Zee DS, Leigh RJ, Optican LM. Oculopalatal tremor explained by model of inferior olivary hypertrophy and cerebellar plasticity. Brain. 2010;133:923-940.
65. Cruikshank SJ,
Hopperstad M, Younger M, Connors BW, Spray DC. Potent block of Cx36 and Cx50 gap junction channels by mefloquine. Proc Natl Acad Sci U S A. 2004;33:12364-12369.
66. Griggs RC,
Moxley R III, Lafrance RA, McQuillen J. Hereditary paroxysmal ataxia: response to acetazolamide. Neurology. 1978;28:1259-1264.
67. Baloh RW,
Jen JC. Genetics of familial episodic vertigo and ataxia. Ann N Y Acad Sci. 2002;956:338-345.
68. Jen JC.
Recent advances in the genetics of recurrent vertigo and vestibulopathy. Curr Opin Neurol. 2008;21:3-7.
69. Marti S,
Baloh RW, Jen JC, Straumann D, Jung HH. Progressive cerebellar ataxia with variable episodic symptoms-phenotypic diversity of R1668W CACNA1A mutation. Eur Neurol. 2008;60:16-20.
70. Strupp M,
Kalla R, Dichgans M, Freilinger T, Glasauer S, Brandt T. Treatment of episodic ataxia type 2 with the potassium channel blocker 4-aminopyridine. Neurology. 2004;62:1623-1625.
71. Jen JC,
Yue Q, Karrim J, Nelson SF, Baloh RW. Spinocerebellar ataxia type 6 with positional vertigo and acetazolamide responsive episodic ataxia. J Neurol Neurosurg Psychiatry. 1998;65:565-568.
72. Stahl JS.
Eye movements of the murine P/Q calcium channel mutant rocker, and the impact of aging. J Neurophysiol. 2004;91:2066- 2078.
73. Frisén L,
Wikkelso C. Posttraumatic seesaw nystagmus abolished by ethanol ingestion. Neurology. 1986;36:841-844.
74. Lepore FE.
Ethanol-induced reduction of pathological nystagmus. Neurology. 1987;37:887.
75. Cochin JP,
Hannequin D, Do Marcolino C, Didier T, Augustin P. Intermittent see-saw nystagmus abolished by clonazepam. Rev Neurol (Paris). 1995;151:60-62.
76. Rahman W,
Proudlock F, Gottlob I. Oral gabapentin treatment for symptomatic Heimann-Bielschowsky phenomenon. Am J Ophthalmol. 2006;141:221-222.
77. McLean R,
Proudlock F, Thomas S, Degg C, Gottlob I. Congenital nystagmus: randomized, controlled, double-masked trial of memantine/gabapentin. Ann Neurol. 2007;61:130-138.
78. Pradeep A,
Thomas S, Roberts EO, Proudlock FA, Gottlob I. Reduction of congenital nystagmus in a patient after smoking cannabis. Strabismus. 2008;16:29-32.
79. Dell'Osso LF.
Suppression of pendular nystagmus by smoking cannabis in a patient with multiple sclerosis. Neurology. 2000;54:2190-2191.
80. Narfstrom K,
Katz ML, Bragadottir R, Seeliger M, Boulanger A, Redmond TM, Caro L, Lai CM, Rakoczy PE. Functional and structural recovery of the retina after gene therapy in the RPE65 null mutation dog. Invest Ophthalmol Vis Sci. 2003;44:1663-1672.
81. Acland GM,
Aguirre GD, Ray J, Zhang Q, Aleman TS, Cideciyan AV, Pearce-Kelling SE, Anand V, Zeng Y, Maguire AM, Jacobson SG, Hauswirth WW, Bennett J. Gene therapy restores vision in a canine model of childhood blindness. Nat Genet. 2001;28:92-95.
82. Jacobs JB,
Dell'osso LF, Hertle RW, Acland GM, Bennett J. Eye movement recordings as an effectiveness indicator of gene therapy in RPE65-deficient canines: implications for the ocular motor system. Invest Ophthalmol Vis Sci. 2006;47:2865-2875.
83. Bennicelli J,
Wright JF, Komaromy A, Jacobs JB, Hauck B, Zelenaia O, Mingozzi F, Hui D, Chung D, Rex TS, Wei Z, Qu G, Zhou S, Zeiss C, Arruda VR, Acland GM, Dell'Osso LF, High KA, Maguire AM, Bennett J. Reversal of blindness in animal models of leber congenital amaurosis using optimized AAV2-mediated gene transfer. Mol Ther. 2008;16:458-465.
84. Anderson J,
Lavoie J, Merrill K, King RA, Summers CG. Efficacy of spectacles in persons with albinism. J AAPOS. 2004;8:515-520.
85. Hertle RW.
Examination and refractive management of patients with nystagmus. Surv Ophthalmol. 2000;45:215-222.
86. Dell'Osso LF,
Traccis S, Abel LA, Erzurum SI. Contact lenses and congenital nystagmus. Clin Vis Sci. 1988;3:229-232.
87. von Noorden GK,
Campos EC. Binocular Vision and Ocular Motility: Theory and Management of Strabismus, 6th edition. St Louis, MO: Mosby, 2001.
88. Serra A,
Dell'osso LF, Jacobs JB, Burnstine RA. Combined gaze-angle and vergence variation in infantile nystagmus: two therapies that improve the high-visual-acuity field and methods to measure it. Invest Ophthalmol Vis Sci. 2006;47:2451-2460.
89. Dell'Osso LF.
Improving visual acuity in congenital nystagmus. In: Smith JL, Glaser JS, eds. Neuro-Ophthalmology: Symposium of the University of Miami and the Bascom Palmer Eye Institute, Volume 7. St Louis, MO: Mosby, 1973:98-106.
90. Lavin PJ,
Traccis S, Dell'Osso LF, Abel LA, Ellenberger C Jr. Downbeat nystagmus with a pseudocycloid waveform: improvement with base-out prisms. Ann Neurol. 1983;13:621-624.
91. Averbuch-Heller L,
Leigh RJ. Medical treatments for abnormal eye movements. Pharmacological, optical and immunological strategies. Aust N Z J Ophthalmol. 1997;25:7-13.
92. Rushton D,
Cox N. A new optical treatment for oscillopsia. J Neurol Neurosurg Psychiatry. 1987;50:411-415.
93. Leigh RJ,
Rushton DN, Thurston SE, Hertle RW, Yaniglos SS. Effects of retinal image stabilization in acquired nystagmus due to neurologic disease. Neurology. 1988;38:122-127.
94. Yaniglos SS,
Leigh RJ. Refinement of an optical device that stabilizes vision in patients with nystagmus. Optom Vis Sci. 1992;69:447-450.
95. Yaniglos SS,
Stahl JS, Leigh RJ. Evaluation of current optical methods for treating the visual consequences of nystagmus. Ann N Y Acad Sci. 2002;956:598-600.
96. Stahl JS,
Lehmkuhle M, Wu K, Burke B, Saghafi D, Pesh-Imam S. Prospects for treating acquired pendular nystagmus with servo-controlled optics. Invest Ophthalmol Vis Sci. 2000;41:1084-1090.
97. Smith RM,
Oommen BS, Stahl JS. Image-shifting optics for a nystagmus treatment device. J Rehabil Res Dev. 2004;41:325-336.
98. Smith RM,
Oommen BS, Stahl JS. Application of adaptive filters to visual testing and treatment in acquired pendular nystagmus. J Rehabil Res Dev. 2004;41:313-324.
99. Anderson JR.
Causes and treatment of congenital eccentric nystagmus. Br J Ophthalmol. 1953;37:267-281.
100. Kestenbaum A.
Nouvelle operation de nystagmus. Bull Soc Ophtalmol Fr. 1953;6:599-602.
101. Spielmann A.
Clinical rationale for manifest congenital nystagmus surgery. J AAPOS. 2000;4:67-74.
102. Zubcov AA,
Stark N, Weber A, Wizov SS, Reinecke RD. Improvement of visual acuity after surgery for nystagmus. Ophthalmology. 1993;100:1488-1497.
103. Dell'Osso LF,
Flynn JT. Congenital nystagmus surgery: a quantitative evaluation of the effects. Arch Ophthalmol. 1979;97:462-469.
104. Lee IS,
Lee JB, Kim HS, Lew H, Han SH. Modified Kestenbaum surgery for correction of abnormal head posture in infantile nystagmus: outcome in 63 patients with graded augmentaton. Binocul Vis Strabismus Q. 2000;15:53-58.
105. Chang YH,
Chang JH, Han SH, Lee JB. Outcome study of two standard and graduated augmented modified Kestenbaum surgery protocols for abnormal head postures in infantile nystagmus. Binocul Vis Strabismus Q. 2007;22:235-241.
106. Gupta R,
Sharma P, Menon V. A prospective clinical evaluation of augmented Anderson procedure for idiopathic infantile nystagmus. J AAPOS. 2006;10:312-317.
107. Sendler S,
Shallo-Hoffmann J, Mühlendyck H. Die Artifizielle-Divergenz-Operation beim kongenitale Nystagmus. Fortschr Ophthalmol. 1990;87:85-89.
108. Cüppers C.
Probleme der operativen Therapie des okularen Nystagmus. Klin Monbl Augenheilkd. 1971;159:145-157.
109. Kaufmann H,
Kolling G. Therapie bei Nystagmuspatienten mit Binokularfunktionen mit und ohne Kopfzwangshaltung. Ber Deutsch Ophthalmol Ges. 1981;78:815-819.
110. von Noorden GK,
Sprunger DT. Large rectus muscle recession for the treatment of congenital nystagmus. Arch Ophthalmol. 1991;109:221-224.
111. Helveston EM,
Ellis FD, Plager DA. Large recession of the horizontal recti for treatment of nystagmus. Ophthalmology. 1991;98:1302-1305.
112. Alio JL,
Chipont E, Mulet E, De La Hoz F. Visual performance after congenital nystagmus surgery using extended hang back recession of the four horizontal rectus muscles. Eur J Ophthalmol. 2003;13:415-423.
113. Atilla H,
Erkam N, Isikcelik Y. Surgical treatment in nystagmus. Eye. 1999;13(pt 1):11-15.
114. Erbagci I,
Gungor K, Bekir NA. Effectiveness of retroequatorial recession surgery in congenital nystagmus. Strabismus. 2004;12:35-40.
115. Arroyo-Yllanes ME,
Fonte-Vazquez A, Perez-Perez JF. Modified Anderson procedure for correcting abnormal mixed head position in nystagmus. Br J Ophthalmol. 2002;86:267-269.
116. Optican LM,
Robinson DA. Cerebellar-dependent adaptive control of primate saccadic system. J Neurophysiol. 1980;44:1058-1076.
117. Dell'Osso LF.
Development of new treatments for congenital nystagmus. Ann N Y Acad Sci. 2002;956:361-379.
118. Dell'Osso LF,
Hertle RW, Williams RW, Jacobs JB. A new surgery for congenital nystagmus: effects of tenotomy on an achiasmatic canine and the role of extraocular proprioception. J AAPOS. 1999;3:166-182.
119. Dell'Osso LF,
Wang ZI. Extraocular proprioception and new treatments for infantile nystagmus syndrome. Prog Brain Res. 2008;171:67-75.
120. Eberhorn AC,
Horn AK, Fischer P, Buttner-Ennever JA. Proprioception and palisade endings in extraocular eye muscles. Ann N Y Acad Sci. 2005;1039:1-8.
121. Zhang M,
Wang X, Goldberg ME. Monkey primary somatosensory cortex has a proprioceptive representation of eye position. Prog Brain Res. 2008;171:37-45.
122. Hertle RW,
Dell'Osso LF, FitzGibbon EJ, Thompson D, Yang D, Mellow SD. Horizontal rectus tenotomy in patients with congenital nystagmus: results in 10 adults. Ophthalmology. 2003;110:2097-2105.
123. Hertle RW,
Dell'Osso LF, FitzGibbon EJ, Yang D, Mellow SD. Horizontal rectus muscle tenotomy in children with infantile nystagmus syndrome: a pilot study. J AAPOS. 2004;8:539-548.
124. Wang ZI,
Dell'Osso LF. Tenotomy procedure alleviates the “slow to see” phenomenon in infantile nystagmus syndrome: model prediction and patient data. Vision Res. 2008;48:1409-1419.
125. Boyle NJ,
Dawson EL, Lee JP. Benefits of retroequatorial four horizontal muscle recession surgery in congenital idiopathic nystagmus in adults. J AAPOS. 2006;10:404-408.
126. Dell'Osso LF,
Jacobs JB. An expanded nystagmus acuity function: intra- and intersubject prediction of best-corrected visual acuity. Doc Ophthalmol. 2002;104:249-276.
127. Hertle RW,
Anninger W, Yang D, Shatnawi R, Hill VM. Effects of extraocular muscle surgery on 15 patients with oculo-cutaneous albinism (OCA) and infantile nystagmus syndrome (INS). Am J Ophthalmol. 2004;138:978-987.
128. Depalo C,
Hertle RW, Yang D. Eight eye muscle surgical treatment in a patient with acquired nystagmus and strabismus: a case report. Binocul Vis Strabismus Q. 2003;18:151-158.
129. Castillo IG,
Reinecke RD, Sergott RC, Wizov S. Surgical treatment of trauma-induced periodic alternating nystagmus. Ophthalmology. 2004;111:180-183.
130. Wang ZI,
Dell'Osso LF, Tomsak RL, Jacobs JB. Combining recessions (nystagmus and strabismus) with tenotomy improved visual function and decreased oscillopsia and diplopia in acquired downbeat nystagmus and in horizontal infantile nystagmus syndrome. J AAPOS. 2007;11:135-141.
131. Spielmann AC.
Large recession of the four vertical rectus muscles for acquired pendular vertical nystagmus and oscillopsia without a null zone. J AAPOS. 2009;13:102-104.
132. Crone RA,
de Jong PT, Notermans G. Behandlung des Nystagmus durch Injektion von Botulinustoxin in die Augenmuskeln. Klin Monbl Augenheilkd 1984;184:216-217.
133. Helveston EM,
Pogrebniak AE. Treatment of acquired nystagmus with botulinum A toxin. Am J Ophthalmol. 1988;106:584-586.
134. Leigh RJ,
Tomsak RL, Grant MP, Remler BF, Yaniglos SS, Lystad L, Dell'Osso LF. Effectiveness of botulinum toxin administered to abolish acquired nystagmus. Ann Neurol. 1992;32:633-642.
135. Tomsak RL,
Remler BF, Averbuch-Heller L, Chandran M, Leigh RJ. Unsatisfactory treatment of acquired nystagmus with retrobulbar injection of botulinum toxin. Am J Ophthalmol. 1995;119:489-496.
136. Ruben ST,
Lee JP, Oneil D, Dunlop I, Elston JS. The use of botulinum toxin for treatment of acquired nystagmus and oscillopsia. Ophthalmology. 1994;101:783-787.
137. Repka MX,
Savino PJ, Reinecke RD. Treatment of acquired nystagmus with botulinum neurotoxin A. Arch Ophthalmol. 1994;112:1320-1324.
138. Liu C,
Gresty M, Lee J. Management of symptomatic latent nystagmus. Eye. 1993;7:550-553.
139. Carruthers J.
The treatment of congenital nystagmus with Botox. J Pediatr Ophthalmol Strabismus. 1995;32:306-308.
140. Inchingolo P,
Optican LM, FitzGibbon EJ, Goldberg ME. Adaptive mechanisms in the monkey saccadic system. In: Schmid R, Zambarbieri D, eds. Oculomotor Control and Cognitive Processes. Amsterdam, The Netherlands: Elsevier, 1991:147-162.
141. Acheson JF,
Bentley CR, Shallo-Hoffmann J, Gresty MA. Dissociated effects of botulinum toxin chemodenervation on ocular deviation and saccade dynamics in chronic lateral rectus palsy. Br J Ophthalmol. 1998;82:67-71.
142. Sheth NV,
Dell'Osso LF, Leigh RJ, van Doren CL, Peckham HP. The effects of afferent stimulation on congenital nystagmus foveation periods. Vision Res. 1995;35:2371-2382.
143. Porter JD.
Brainstem terminations of extraocular muscle primary afferent neurons in the monkey. J Comp Neurol. 1986;247:133-143.
144. Ishikawa S,
Ozawa H, Fujiyama Y. Treatment of Nystagmus by Acupuncture. Highlights in Neuro-Ophthalmology: Proceedings of the Sixth Meeting of the International Neuro-ophthalmology Society (INOS). Amsterdam, The Netherlands: Aeolus Press, 1987:227-232.
145. Blekher T,
Yamada T, Yee RD, Abel LA. Effects of acupunture on foveation charactersitics in congenital nystagmus. Br J Ophthalmol. 1998;82:115-120.
146. Abadi RV,
Carden D, Simpson J. A new treatment for congenital nystagmus. Br J Ophthalmol. 1980;64:2-6.
147. Ciuffreda KJ,
Goldrich SG, Neary C. Use of eye movement auditory biofeedback in the control of nystagmus. Am J Optom Physiol Opt. 1982;59:396-409.
148. Sharma P,
Tandon R, Kumar S, Anand S. Reduction of congenital nystagmus amplitude with auditory biofeedback. J AAPOS. 2000;4:287-290.
149. Dell'Osso LF,
Tomsak RL, Thurtell MJ. Two hypothetical nystagmus procedures: augmented tenotomy and reattachment and augmented tendon suture (sans tenotomy). J Pediatr Ophthalmol Strabismus. 2009;46:337-344.
150. Thomas S,
Proudlock FA, Sarvananthan N, Roberts EO, Awan M, McLean R, Surendran M, Kumar AS, Farooq SJ, Degg C, Gale RP, Reinecke RD, Woodruff G, Langmann A, Lindner S, Jain S, Tarpey P, Raymond FL, Gottlob I. Phenotypical characteristics of idiopathic infantile nystagmus with and without mutations in FRMD7. Brain. 2008;131:1259-1267.
151. Gresty MA,
Ell JJ, Findley LJ. Acquired pendular nystagmus: its characteristics, localising value and pathophysiology. J Neurol Neurosurg Psychiatry. 1982;45:431-439.
152. Ferro JM,
Castro-Caldas A. Palatal myoclonus and carbamazepine. Ann Neurol. 1981;10:402-403.
153. Sakai T,
Shiraishi S, Murakami S. Palatal myoclonus responding to carbamazepine. Ann Neurol. 1981;9:199-200.
154. Nathanson M,
Bergman PS, Bender MB. Visual disturbances as the result of nystagmus on direct forward gaze. AMA Arch Neurol Psychiatry. 1953;69:427-435.
155. Schon F,
Hart PE, Hodgson TL, Pambakian AL, Ruprah M, Williamson EM, Kennard C. Suppression of pendular nystagmus by smoking cannabis in a patient with multiple sclerosis. Neurology. 1999;53:2209-2210.
156. Devogelaere T,
Gobin C, Casaer P, Spileers W. Repeated bilateral retrobulbar injection of botulinum toxin in a blind patient with retinitis pigmentosa and incapacitating nystagmus. Binocul Vis Strabismus Q. 2006;21:235-238.
© 2010 Lippincott Williams & Wilkins, Inc.