Straube A, Büttner U (eds): Neuro-Ophthalmology.
Dev Ophthalmol. Basel, Karger, 2007, vol 40, pp 175–192
Therapeutic Considerations for Eye Movement Disorders
A. Straube
Department of Neurology, University of Munich, Munich, Germany
Abstract
Advances made in understanding the pathophysiology of eye movement disorders have only recently with the publication of the first well-planned studies been translated into better treatment strategies. The following chapter summarizes the pharmacological treatment options for a variety of oculomotor syndromes. Cortisone is useful, for example, for acute vestibular neuritis to improve the restitution of the labyrinthine function. For the widespread benign paroxysmal positioning nystagmus, a series of liberatory movements that free the semicircular canal from the causative otoconia is now a well-established therapy. Treatment for the central vestibular syndrome of upand downbeat nystagmus consists of drugs like the potassium canal blocker 4-aminopyridine, which influence the cerebellar circuits involved in the disorder’s pathophysiology. Acquired pendular nystagmus, one of the oculomotor syndromes often caused by multiple sclerosis, results in the severe impairment of reduced visual acuity. Memantine, a weak NMDA antagonist, has now been proven effective here. Finally, anticonvulsants like carbamazepine are the drugs of choice for disorders involving a nerve-blood vessel contact that induces symptoms of vestibular paroxysmia or superior oblique myokymia.
Copyright © 2007 S. Karger AG, Basel
The common goal of voluntary as well as most reflexive eye movements is to stabilize images on the retina (especially the central fovea, the area of the highest resolution) in order to prevent retinal slip. Abnormal involuntary eye movements may cause excessive motion of images on the retina, leading to blurred vision and to the illusion that the perceived world is moving (oscillopsia). Clinical examination of such pathological eye movements often allows the topological diagnosis of the lesion causing the abnormalities. Despite our extensive knowledge of the anatomy and physiology of eye movements, very little is known about pharmacological aspects of the ocular motor system. Thus, our treatment options for abnormal eye movements remain fairly limited. Most drug treatments are based on case reports. Only recently have a few controlled trials
Table 1. Practical treatment of oculomotor signs/syndromes
Ocular sign/disorder |
Substance |
Dosage |
Contraindications |
|
|
|
|
|
|
Vestibular neuritis |
Acute: dimenhydrinate |
50–100 mg |
General |
|
|
Prednisolone |
1 mg/kg body weight |
contraindications for |
|
|
|
per day for 5 days, |
cortisone and |
|
|
|
or starting with 100 mg |
dimenhydrinate |
|
Menière’s disease |
Acute: dimenhydrinate |
50–100 mg |
General |
|
|
Prophylaxis: betahistine |
8/16–32 mg/day |
contraindications for |
|
|
Gentamicin |
Locally in the middle ear |
dimenhydrinate and |
|
|
|
|
|
betahistine |
|
|
|
|
Ototoxic (hearing loss) |
Vestibular paroxysmia |
Carbamazepine |
2 |
200–600 mg slow- |
Drowsiness, ataxia |
|
|
release formulation |
Vertigo, dry mouth |
|
|
Gabapentin |
3–4 300–600 mg |
Enzyme induction |
|
Superior oblique |
Carbamazepine |
2 |
200–600 mg slow- |
Drowsiness, ataxia |
myokymia |
|
release formulation |
Vertigo, dry mouth |
|
|
Gabapentin |
3–4 300–600 mg |
Enzyme induction |
|
Downbeat nystagmus |
Clonazepam |
2 |
0.5–1 mg daily |
Sedation |
|
Baclofen |
3 |
5–10 mg daily |
Ataxia, weakness |
|
4-aminopyridine |
3 |
10 mg |
Seizures |
Upbeat nystagmus |
Baclofen |
3 |
5–10 mg |
Sedation; weakness |
|
4-aminopyridine |
|
|
Seizures |
Periodic alternating |
Baclofen |
3 |
5–10 mg |
Sedation |
nystagmus |
|
|
|
Ataxia, weakness |
Acquired pendular |
Memantine |
3–4 10 mg |
Somnolence, confusion, |
|
nystagmus |
Gabapentin |
3–4 300–600 mg |
dry mouth, edema |
|
|
|
|
|
|
been published (overview in [1–5]). Several drugs can themselves cause nystagmus, for example, anticonvulsants, sedatives, and antihistaminergic drugs induce gaze-evoked nystagmus; nicotinergic substances induce a nystagmus that can disclose an underlying vestibular tone imbalance; and intoxication due to lithium or phenytoin can lead to downbeat nystagmus as well as opsoclonus.
This chapter summarizes the most recent publications on pharmacological treatment options for the different eye movement syndromes and also gives a short overview of the clinical aspects and pathophysiology of these syndromes.
Eye movement syndromes are generally differentiated into those characterized by a pathological jerk nystagmus, pendular nystagmus, atypical nystagmus, or saccadic oscillations. All interfere with the normal foveal fixation of a target.
Straube |
176 |