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Ocular Pharmacology: What Drugs Affect Eye Movement?

4 min read

A 2025 analysis of the FDA Adverse Event Reporting System identified 30 drugs with significant associations to eye movement disorders (EMD), primarily central nervous system medications [1.3.5, 1.3.7]. Understanding what drugs affect eye movement is crucial for both patients and healthcare providers to mitigate potential risks.

Quick Summary

Numerous medications, especially those acting on the central nervous system, can alter ocular motor control. This includes anticonvulsants, antidepressants, sedatives, and lithium, which can cause nystagmus, diplopia, and saccadic dysfunction.

Key Points

  • CNS Drugs are Primary Culprits: A 2025 study confirmed that drugs acting on the central nervous system, such as antiseizure medications, antipsychotics, and antidepressants, are most frequently associated with eye movement disorders (EMD) [1.3.5, 1.3.7].

  • Anticonvulsants Pose High Risk: Medications like carbamazepine, phenytoin, and topiramate are widely known to cause nystagmus (involuntary eye movements), diplopia (double vision), and other EMDs [1.5.2].

  • Lithium and Nystagmus: The mood stabilizer lithium is strongly linked to downbeat nystagmus, an effect that can occur even at therapeutic doses and may sometimes persist after stopping the drug [1.2.6, 1.8.1].

  • Sedatives Slow Saccades: Sedatives such as benzodiazepines, propofol, and alcohol can significantly slow down saccadic eye movements, reducing their speed and accuracy [1.4.3, 1.6.2].

  • Antidepressants Cause Varied Effects: SSRIs and TCAs can cause blurred vision and pupil dilation (mydriasis), which may increase glaucoma risk, while rare cases of oculogyric crisis have been reported [1.7.1, 1.7.3].

  • Early Detection is Crucial: Many drug-induced eye movement changes are reversible if the offending medication is adjusted or stopped promptly [1.8.1]. Patients should report any new visual symptoms to their doctor [1.2.3].

  • Oculogyric Crisis is a Known Side Effect: Antipsychotic medications and, more rarely, some antidepressants and anticonvulsants, can trigger an oculogyric crisis, which is a prolonged, involuntary upward deviation of the eyes [1.2.2, 1.2.6].

In This Article

The Intricate Link Between Medications and Eye Control

Eye movements are complex processes controlled by a network of muscles and neural pathways originating in the brain [1.4.2]. Because the retina is ontogenically part of the brain, many systemic medications that cross the blood-brain barrier can have unintended consequences on visual function [1.5.1]. These effects, known as drug-induced eye movement disorders (EMD), can manifest as involuntary motions, slowed responses, or an inability to coordinate eye movements. A 2025 pharmacovigilance study analyzing over 6,000 EMD reports found that drug classes like antiseizure medications, antipsychotics, and antidepressants were primary contributors [1.3.5]. Common symptoms patients might experience include blurred vision, double vision (diplopia), or the illusion that stationary objects are moving (oscillopsia) [1.5.1, 1.5.2]. Understanding these potential side effects is vital for early detection and management to prevent lasting impairment [1.2.3].

Anticonvulsants and Seizure Medications

Anticonvulsant drugs are frequently cited as a cause of various EMDs [1.2.6]. Medications like phenytoin, carbamazepine, and lamotrigine are known to cause nystagmus (involuntary, rapid eye movements), diplopia, and ophthalmoplegia (paralysis or weakness of eye muscles) [1.5.2, 1.5.3]. Carbamazepine, for example, can affect saccadic eye movements and has been associated with downbeat nystagmus and oscillopsia [1.5.1]. Lamotrigine can also cause downbeat nystagmus, diplopia, and interfere with eye movements, particularly in overdose situations or when combined with other drugs like carbamazepine [1.2.6]. Topiramate (Topamax) is another anticonvulsant that can induce nystagmus and, more uniquely, acute myopia and angle-closure glaucoma due to transformations in the lens and ciliary body complex [1.2.2, 1.5.2]. A recent study identified the antiseizure medication zonisamide as having the highest risk for inducing EMD [1.3.5].

Psychiatric Medications: Antidepressants, Anxiolytics, and Mood Stabilizers

Psychotropic drugs work by altering neurotransmitter levels, which can also affect the neural pathways controlling the eyes [1.2.6].

  • Antidepressants: Selective Serotonin Reuptake Inhibitors (SSRIs) like fluoxetine and sertraline, as well as Tricyclic Antidepressants (TCAs), are associated with ocular side effects [1.7.1]. SSRIs can cause mydriasis (pupil dilation), which may increase the risk for angle-closure glaucoma in susceptible individuals [1.7.1, 1.7.3]. Rarely, medications like fluoxetine have been linked to oculogyric crises (prolonged, involuntary upward deviation of the eyes) and diplopia [1.7.1]. TCAs are known for anticholinergic effects that can lead to blurred vision and reduced accommodation [1.7.1].
  • Anxiolytics (Benzodiazepines): This class of drugs, including lorazepam and diazepam, can cause drowsiness, slurred speech, and horizontal gaze nystagmus [1.3.2]. They have been linked to dysfunction of saccades and smooth-pursuit eye movements [1.2.6]. The effects are often dose-dependent and can lead to a decrease in saccade peak velocity [1.4.3].
  • Lithium: Used as a mood stabilizer, lithium is well-documented to cause a variety of EMDs, even within its therapeutic range [1.8.1]. Downbeat nystagmus is a known side effect, and in some cases, it can persist even after the drug is discontinued [1.2.6, 1.8.3]. Other reported issues include impaired smooth pursuit eye movements, horizontal gaze palsy, and oculogyric crisis [1.8.2, 1.8.4].

Sedatives and Other CNS Depressants

Sedatives and hypnotics, including alcohol, have a pronounced effect on eye movements. Alcohol intoxication is a common cause of gaze-evoked nystagmus [1.3.1]. Barbiturates and benzodiazepines can also cause horizontal gaze nystagmus [1.3.2]. A study comparing different sedatives found that propofol and midazolam had strong effects on the dynamics and latency of saccades, causing them to become slower and less accurate (hypometric) [1.6.2, 1.6.3]. In contrast, dexmedetomidine, which has a different mechanism of action, had less impact on saccadic metrics [1.6.3].

Other Notable Medications

Many other classes of drugs can impact eye movement:

  • Antipsychotics: Both typical and atypical antipsychotics can cause oculogyric crisis [1.2.2, 1.2.6].
  • Antibiotics: Certain antibiotics like fluoroquinolones have been associated with ocular side effects, including rare instances of retinal detachment [1.2.3].
  • Antivirals: The antiviral drug acyclovir has been associated with nystagmus [1.3.5, 1.3.7].
  • Cardiovascular Drugs: Beta-blockers and calcium channel blockers have been reported in rare cases to cause diplopia [1.2.3].

Comparison of Drug Effects on Eye Movement

Drug Class Common Eye Movement Effects Specific Examples
Anticonvulsants Nystagmus, Diplopia, Saccadic Dysfunction, Ophthalmoplegia [1.5.2] Phenytoin, Carbamazepine, Lamotrigine, Topiramate [1.5.2]
Antidepressants Mydriasis, Blurred Vision, Oculogyric Crisis (rare) [1.7.1] SSRIs (Fluoxetine), TCAs (Amitriptyline) [1.7.1, 1.7.3]
Sedatives Nystagmus, Slowed Saccades, Saccadic Hypometria [1.3.2, 1.6.2] Alcohol, Benzodiazepines (Diazepam), Propofol [1.3.1, 1.3.2]
Mood Stabilizers Downbeat Nystagmus, Impaired Smooth Pursuit [1.2.6, 1.8.4] Lithium [1.2.6]
Antipsychotics Oculogyric Crisis, Slowed Saccadic Velocity [1.2.6, 1.4.3] Haloperidol, Risperidone, Aripiprazole [1.4.3, 1.3.5]

Conclusion: The Importance of Vigilance

The connection between systemic medications and eye movement is a critical area of pharmacology. While many of these side effects are reversible upon dose reduction or discontinuation of the offending drug, some can become permanent [1.2.6, 1.8.1]. Early recognition of symptoms like double vision, involuntary eye movements, or persistent blurred vision is crucial [1.2.3]. Patients starting a new medication, especially those in high-risk categories like anticonvulsants or lithium, should be informed of potential ocular side effects. Regular communication with both the prescribing physician and an eye care specialist can ensure that any adverse effects are managed promptly, preserving both systemic health and visual function.


Disclaimer: This article is for informational purposes only and does not constitute medical advice. Always consult with a qualified healthcare professional regarding any health concerns or before making any decisions related to your health or treatment.

For further reading, one authoritative source is the American Academy of Ophthalmology: https://www.aao.org

Frequently Asked Questions

Drug-induced nystagmus is an involuntary, rapid, and repetitive movement of the eyes caused as a side effect of certain medications. It is commonly associated with anticonvulsants (like phenytoin and carbamazepine), sedatives like alcohol, and the mood stabilizer lithium [1.2.5, 1.2.6].

While most ocular side effects of antidepressants, like blurred vision, are reversible upon discontinuation, they can increase the risk for conditions like acute angle-closure glaucoma in susceptible individuals [1.7.1, 1.7.3]. In rare instances, persistent issues have been reported, making regular eye exams important [1.7.5].

Many anti-seizure (anticonvulsant) drugs affect eye movement. A 2025 study identified zonisamide, vigabatrin, and tiagabine as having the highest risk [1.3.5]. More commonly used drugs like carbamazepine, phenytoin, and lamotrigine are also well-known for causing nystagmus and diplopia [1.5.2].

Not always, but eye movement disorders are a known side effect. Lithium can cause downbeat nystagmus and impair smooth pursuit eye movements even within the normal therapeutic range. In some cases, these effects can persist after the drug is stopped [1.2.6, 1.8.3].

An oculogyric crisis is a dystonic reaction characterized by a prolonged, involuntary upward deviation of the eyes. It is most commonly associated with antipsychotic medications but has also been linked to certain antidepressants and anticonvulsants like carbamazepine [1.2.2, 1.2.6].

Yes, benzodiazepines can affect vision by causing dysfunction in saccadic (quick) and smooth-pursuit eye movements. This can manifest as blurred vision, double vision (diplopia), or nystagmus. These effects are typically dose-dependent [1.2.6, 1.3.2].

If you experience new visual symptoms like double vision, involuntary eye movements, or significant blurring after starting a new medication, you should consult your prescribing doctor and an eye care professional promptly. Early intervention is key, as many of these side effects are reversible [1.2.3].

References

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Medical Disclaimer

This content is for informational purposes only and should not replace professional medical advice.