Introduction

Nystagmus is characterised by rapid, involuntary eye movements. If you have nystagmus, your eyes may move up and down, side to side, or in a circular motion, often described as “shaky vision”. Sometimes people are born with it; this is known as congenital nystagmus. Babies born with nystagmus usually show symptoms between 6 weeks and 3 months of age. It can also develop later in life, known as acquired nystagmus. Glasses, contact lenses, medications, and surgery are potential treatments.

Nystagmus itself isn’t considered dangerous, but it could indicate another eye problem, a neurological condition, or a problem with the parts of your inner ear that control balance and coordination, including: stroke, brain tumour, toxicity, head trauma (injury), and inflammatory diseases. This article will further discuss the triggers and associated conditions of acquired nystagmus in detail.

Understanding acquired nystagmus

The body has systems which regulate and stabilise normal vision, including the vestibulocular reflex, cerebellum and brainstem nuclei. These systems can be dysregulated by disease, trauma or exposure to toxins. However, acquired nystagmus is quite rare, which immediately raises a red flag and causes healthcare providers to investigate further in order to find the underlying cause.¹

Furthermore, patients with acquired nystagmus may experience a feeling that their surroundings are moving, which is called oscillopsia. This feeling can interfere with everyday activities such as reading and walking. In addition to this symptom, balance problems, light sensitivity, and dizziness are the biggest symptoms that are related to what causes it.¹

Triggers of acquired nystagmus

There are a myriad of triggers of acquired nystagmus. One of the most common is drug/substance-induced nystagmus. The excessive consumption of alcohol can cause intoxication, which is widely known to cause gaze-evoked nystagmus. In addition, many medications, including anticonvulsants, sedatives, lithium and a few anti-epileptic drugs can also be considered as triggers of acquired nystagmus. This can be due to the negative intervention on cerebellar or brainstem activity. However, with medication-induced nystagmus, it can potentially be reversible after the discontinuation of the medicine.²

Furthermore, metabolic and nutritional deficiencies can also cause acquired nystagmus. A major example of this is vitamin B12 deficiency, which mainly causes upbeat nystagmus. Vitamin B12 is paramount for normal neurological function as it is a primary component in myelin production in the nervous system. But due to the deficiency, there is a great interference with myelin production, leading to demyelination and therefore the compromise of neuronal signalling.³ Moreover, electrolyte imbalances or metabolic disease, especially mitochondrial diseases, can cause an Adenosine Triphosphate (ATP) deficit. ATP can break down into Adenosine Diphosphate (ADP) and Pi (inorganic phosphate group) and release energy for both myelin production and in the vestibulocular pathways.⁴

Trauma, particularly head injuries, can be a trigger of acquired nystagmus, especially if the injury affects cerebellar/brainstem activity. The vestibulocular system actually involves a network that spans the inner ear, brainstem, and cerebellum, so if a patient hits their head in a way that damages any of the aforementioned parts of the brain/ear, there is a high chance of acquired nystagmus occurring.⁵

Finally, acute vestibular insults frequently trigger nystagmus. Acute vestibular insults are sudden inner ear events that disrupt balance signals, including vestibular neuritis, labyrinthitis, or Meniere’s disease. These conditions disturb inner ear balance mechanisms, which causes patients to feel that the room is spinning (vertigo) alongside nystagmus. These episodes are typically sudden in onset and may be position-dependent, worsening when the patient lies on one side or changes posture.⁶

Neurological and systemic conditions associated with acquired nystagmus

While drugs, toxins, and trauma can act as immediate triggers, acquired nystagmus is frequently linked to deeper neurological or systemic disease. Identifying these associations is crucial because nystagmus often represents one of the first visible signs of underlying pathology.

The central nervous system causes

Multiple Sclerosis (MS) is one of the most important associations. MS is a chronic autoimmune disease where the immune system attacks the myelin sheath protecting nerve cells in the brain and spinal cord, disrupting communication between the brain and body. Hence, due to the demyelination, especially in the cerebellum and brainstem, there's a disruption to the vestibulocular pathways, which stabilise eye movement. In which the main 2 types of nystagmus it produces are pendular and gaze-evoked.⁷

The brain is supplied by two circulations, anterior and posterior. The posterior circulation supplies the cerebellum, brainstem and occipital lobes. So if there’s an occlusion/stoppage of one of the blood vessels, it can cause a stroke, damaging the area of supply, which then can lead to sudden onset nystagmus often accompanied by vertigo, diplopia or ataxia.^8,9

Similarly, brain tumours formed in a similar area of the posterior fossa, i.e. where the cerebellum and brainstem are situated, may potentially compress ocular motor circuits, causing persistent oscillations. Finally, inherited neurodegenerative diseases, such as spinocerebellar ataxias, are also associated with acquired nystagmus as part of a broader syndrome of imbalance and dysarthria.¹⁰

Vestibular disorders

Vestibular disorders such as vestibular neuritis, labyrinthitis or Meniere’s disease are also associated with acquired nystagmus. Vestibular neuritis and labyrinthitis produce acute vertigo with spontaneous horizontal nystagmus. Especially in vestibular neuritis, right vestibular neuritis causes nystagmus to the left side. This occurs because right vestibular neuritis damages the right vestibular nerve, creating an imbalance in vestibular input between the two sides. ¹¹ Meniere’s disease, characterised by endolymphatic hydrops, causes recurrent nystagmus attacks associated with fluctuating hearing loss and tinnitus. These problems usually start in the inner ear, but sometimes they look very similar to problems coming from the brain. Because of this, doctors need to check carefully to make sure they know where the problem is coming from.¹²

Ocular causes

Though less common, sometimes acquired nystagmus happens because of problems with the eyes themselves. If the optic nerve is damaged, e.g., from optic neuritis or ischaemic optic neuropathy, signals in the brain are not sent and received properly, i.e., poor visual input, which can cause sensory nystagmus. In adults, if vision in both eyes becomes very poor from severe scarring on the cornea or from dense cataracts, this may rarely induce nystagmus if binocular vision becomes severely impaired.¹³

Systemic/infectious causes

Finally, there are multiple systemic and infectious diseases which can be associated with acquired nystagmus. Firstly, Hashimoto's encephalopathy may lead to restrictive movements of the eye, and can sometimes be accompanied by nystagmus when the orbital muscles of the eyes are involved, and in severe cases with optic nerve compression.¹⁴ Secondly, infectious diseases such as syphilis, Lyme disease and HIV affect the central nervous system and/or vestibulocular pathways, which also give rise to abnormal eye movements.^15,16 Hence, when nystagmus shows up in these situations, it usually comes along with other neurological problems. This makes it a warning sign that there may be a more serious issue affecting the nervous system as a whole.

Diagnostic clues linking triggers to conditions

When diagnosing for acquired nystagmus, healthcare providers rely on a combination of patient history, investigation findings and clinical presentation of the eyes. In addition, the timings and circumstances of onset can reveal a lot about the underlying cause. For example, sudden nystagmus after a head injury, medication usage or illness can point to a specific trigger, whereas if it was developed over a longer period, the trigger could be due to an underlying neurological or systemic disease.

Since there are multiple types of acquired nystagmus, like upbeat, gaze-evoked, torsion, pendular, the direction, rhythm and amplitude can be essential in the process of diagnosis since it can point to where the underlying cause could originate from.

There's also a consideration of associated signs such as: balance problems, limb weakness, hearing changes, or visual deficits, which help distinguish between peripheral, central, and systemic causes. Laboratory tests, imaging, and vestibular assessments are then guided by these initial observations, focusing on the most likely sources suggested by the nystagmus pattern and history.

Why differentiation matters

Acquired nystagmus is a warning sign, not a standalone disease. The key point for clinicians and readers is that its presence signals the need for careful evaluation. Even subtle differences in eye movement patterns, onset, or context can provide crucial information about the urgency and type of underlying problem.

Understanding these distinctions allows healthcare providers to quickly identify treatable conditions, detect serious neurological or systemic diseases early, and avoid unnecessary testing. For patients, this means faster diagnosis, more appropriate care, and reduced risk of complications.

Recognising that nystagmus is a clue rather than the full story is essential: it guides the diagnostic process, helps prioritise investigations, and ensures that the right interventions are delivered at the right time.

Summary

Acquired nystagmus is an important clinical sign that can indicate a wide range of underlying issues, from peripheral vestibular disturbances to serious neurological or systemic conditions. Recognising it early is crucial, as it often precedes other symptoms and can guide timely evaluation.

Triggers such as medications, metabolic imbalances, trauma, or acute vestibular events provide context for when the nystagmus started, while careful observation of eye movement patterns and associated signs helps clinicians distinguish between peripheral and central causes. This differentiation is essential because management strategies and prognosis vary significantly depending on the origin.

By understanding the links between triggers, associated conditions, and diagnostic clues. For patients, accurate identification of the source of nystagmus means faster intervention, more effective care, and better overall outcomes. Acquired nystagmus is therefore a valuable diagnostic window, emphasising that even subtle eye movements can reveal significant underlying pathology.