Ocular flutter

By Marcello Cherchi, MD PhD

For patients

Ocular flutter (OF) is an eye movement abnormality in which both eyes move back and forth very quickly. OF is not a disease in itself, but can occur in the context of many diseases. If your doctor identifies OF, they may want to check several tests of balance function, and possibly brain imaging.

For clinicians

Overview

Ocular flutter (OF) is defined as back-to-back conjugate horizontal saccades with no inter-saccadic interval, and should be discernible on face-to-face examination. Presenting symptoms can include oscillopsia and blurry vision. OF is usually acquired, intermittent and involuntary. OF can occur in isolation, but it is more common for it to occur in conjunction with other findings, including other ocular motor abnormalities, and cerebellar signs. OF is more common in adults, but can occur at any age. It has been reported in association with a very broad range of disorders, including autoimmune disease, infectious, para-infectious, paraneoplastic, neurodegenerative, demyelinating, toxic, metabolic, intracranial hypertensive, and other pathologies. The underlying mechanism of OF is uncertain; several models have been proposed. Management and prognosis depend on the underlying etiology.

Introduction

Leigh and Zee describe, “back-to-back… saccades without an intersaccadic interval” and comment that, “If such oscillations occur only in the horizontal plane, they are termed ocular flutter; if they occur in all directions, the oscillation is called opsoclonus” (Leigh and Zee 2015), a classification echoed by other authors (Grossman and Rucker 2023).

Note that ocular flutter is different from square wave jerks, in that the latter is characterized by the presence of inter-saccadic intervals.

Horizontal ocular flutter can occur in isolation (Nasu et al. 2013), but it more commonly occurs in association with other findings. For example, horizontal ocular flutter can occur in conjunction with (multi-directional) opsoclonus, and often in association with cerebellar findings (such as truncal ataxia).

Most cases of ocular flutter are involuntary. There are case reports of individuals who can voluntarily produce short bursts of ocular flutter (Renard et al. 2009; Thomas et al. 2022; Yee et al. 1994), such as during convergence (Hotson 1984). Rosenberg suggests that ocular flutter may lie along a voluntary-involuntary continuum (Rosenberg 2021).

Historical background

Dr. David Cogan (1908 – 1993) is usually credited with having first described ocular flutter (Cogan 1954).

Epidemiology

Horizontal ocular flutter is rare, but no precise figures are available. Most cases of ocular flutter are described in adults, but it has also been reported in the pediatric population, with etiologies including:

  • Infectious:
    • Poliovirus (Asindi et al. 1988)
  • Autoantibodies:
    • Anti-sulphatide antibody positivity (Akcay et al. 2024)
    • Pediatric MOG (myelin-oligodendrocyte) antibody-associated demyelination (Breza et al. 2019)
  • Inborn errors of metabolism:
    • Ocular flutter in a 10-month old infant with carbohydrate-deficient glycoprotein syndrome type 1a (Stark et al. 2000)
  • Neurodegenerative:
    • Three children with infantile parkinsonism-dystonia exhibited ocular flutter and saccade initiation failure (Assmann et al. 2004)
  • Opsoclonus beginning at age 3 months, and resolving around 6 months, in an apparently otherwise healthy infant (Silverman et al. 2024)

Genetics

There is no literature describing particular genetic vulnerabilities to ocular flutter.

Pathophysiological mechanism of disease

The pathophysiologic mechanism of disease in ocular flutter is incompletely understood (but see the next section regarding proposed hypotheses).

At the cellular level, Shaikh and colleagues (Shaikh et al. 2008) suggest that ion channel abnormalities in burst cell membranes are responsible for saccadic oscillations.

Tsutsumi and colleagues (Tsutsumi et al. 2009) reported ocular flutter with a fairly focal lesion in the right upper pontine tegmentum that involved parts of the reticular formation, superior cerebellar peduncle and locus ceruleus.

Ibanez-Julia and colleagues (Ibáñez-Juliá et al. 2017) studied a series of six “adults with previous history of [undifferentiated] ocular flutter/opsoclonus and 12 health patients (paired by age and sex),” and reported that ocular flutter and opsoclonus may be associated with cortical and subcortical gray matter atrophy, as well as decreased cerebellar cortical volume.” Given the small number of patients and the undifferentiated nature of the series, we find these results too vague to clarify the mechanism of disease.

Given the very broad range of pathologies in which ocular flutter has been reported (see the section below on differential diagnosis), the articles cited above regarding specific lesions and broad anatomical findings seem unlikely to illuminate the mechanism of disease.

Models, while theoretical, at least offer testable hypotheses.

Theoretical considerations

We review several mechanisms that have been proposed as explanations for ocular flutter.

Hain and colleagues (Hain et al. 1986), reporting on a case of an unidentified progressive neurodegenerative disorder, hypothesize that:

“Experimental findings suggest that the pause cells tonically inhibit the burst cells of the brainstem (which lie in the paramedian reticular formation) that generate the immediate premotor commands for saccadic eye movements (Keller 1977). In this way, pause cells may prevent extraneous burst cell activity that might [otherwise] lead to saccadic oscillations (Zee and Robinson 1979)” (Hain et al. 1986).

In other words, failure of pause cells (“located in the midline of the caudal pons”) results in (inappropriate) disinhibition of burst neurons, which may drive ocular flutter.

Kudo and colleagues (Kudo et al. 2018), in a broader discussion of ocular flutter and opsoclonus, citing work by Zee and Robinson (Zee and Robinson 1979), Ramat and colleagues (Ramat et al. 2005) and Wong and colleagues (Wong et al. 2001) state that:

“The precise pathophysiologic mechanism of OF [ocular flutter] / OC [opsoclonus] is unknown… One of the most accepted mechanisms[s] involves disinhibition of the [cerebellar midline caudal] fastigial nucleus from the cerebellar cortex” (Kudo et al. 2018).

Optican and Pretegiani (Optican and Pretegiani 2017) review evidence reported by Yoshida and colleagues (Yoshida et al. 2004) regarding mutant mice with a deficiency in the delta-2 subunit of the glutamate receptor in cerebellar Purkinje neurons who exhibit opsoclonus, and evidence reported by Jen and colleagues (Jen et al. 2012) from humans with opsoclonus who were found to have anti-Purkinje cell antibodies and “proposed that those antibodies blocked the parallel fiber (PF) input to the PuC [Purkinje cells], allowing spontaneous oscillations generated in the inferior olives (IO) to be passed to the oculomotor vermis through the flocculus” (Optican et al. 2019). Although these studies pertained to opsoclonus (rather than strictly horizontal ocular flutter), Optican and Pretegiani view offer them as suggesting a plausible mechanism for an oscillatory signal.

Optican and Pretegiani (Optican and Pretegiani 2017), reviewing data from two previously reported patients (Pretegiani et al. 2017), propose another hypothesis, namely that abnormally increased activity of chloride channel function in GABAA receptors results in inappropriately enhanced inhibition of the oculomotor vermis (OMV), caudal fastigial nuclei (cFN) and omnipause neurons (OPN).

Ramat and colleagues (Ramat et al. 2005), starting with the observation that some people can voluntarily generate ocular flutter during convergence, developed a model, “based on (1) coupling of excitatory and inhibitory burst neurons in the brainstem, and (2) the hypothesis that burst neurons show post-inhibitory rebound discharge,” noting that, “When omnipause neurons are inhibited (as during saccades, saccade-vergence movement and blinks), this new model simulates oscillations with amplitudes and frequencies comparable to those in normal human subjects.”

In summary:

  • Hain and colleagues (Zee and Robinson 1979) hypothesize that horizontal ocular flutter results from malfunctioning pause neurons (in the midline caudal pons) whose dysfunction inappropriately disinhibit burst cells.
  • Kudo and colleagues (Kudo et al. 2018) hypothesize that opsoclonus and ocular flutter arise from malfunction in the cerebellar cortex which inappropriately disinhibits neurons in the cerebellar midline caudal fastigial nucleus.
  • According to Optican and Pretegiani (Optican and Pretegiani 2017), animal data (Yoshida et al. 2004) and human data (Jen et al. 2012) suggest that malfunctioning parallel fibers (that would normally modulate activity of Purkinje cells) inappropriately disinhibit Purkinje cells (that would normally modulate activity of neurons in the inferior olives), in turn inappropriately permitting spontaneous oscillations to be generated by the inferior olives and passed through the cerebellar flocculus to the oculomotor vermis.
  • Optican and Pretegiani (Optican and Pretegiani 2017) propose that inappropriately enhanced inhibition of the oculomotor vermis (OMV), caudal fastigial nuclei (cFN) and omnipause neurons (OPN).
  • Ramat and colleagues (Ramat et al. 2005) propose a model “based on (1) coupling of excitatory and inhibitory burst neurons in the brainstem, and (2) the hypothesis that burst neurons show post-inhibitory rebound discharge.”

All of these hypotheses (appropriately) postulate a mechanism for an oscillatory generator. Each hypothesis has some merit. Given that ocular flutter has been reported in association with a very broad range of pathologies (see the section below on differential diagnosis), it is certainly possible that multiple mechanisms are correct.

Clinical presentation

Ocular flutter in isolation can cause the symptom of blurred vision and disequilibrium (Seet and Lim 2006), and oscillopsia.

Physical examination

Horizontal ocular flutter should be visible on face-to-face examination. Depending on the etiological context, there may be other physical examination findings as well, such as truncal ataxia.

Ocular motor examination

Note that horizontal ocular flutter should be visible on face-to-face examination. This is different from the phenomenon of microsaccadic flutter, which is typically only identifiable on instrumented examination (Ashe et al. 1991; Galvez-Ruiz et al. 2018).

Some cases of ocular flutter appear only when in the supine position (Brodsky and Hunter 2011; Martins et al. 2019). A control systems analysis of this has been proposed (Optican et al. 2019).

Unusual variants include “unidirectional ocular flutter” (Kobayashi 2015; Verhaeghe et al. 2007). The “unidirectionality” in these cases really refers to the fact that the “ocular flutter” consists of a first saccade that is always in the same direction, followed by a contraversive saccade — in other words, a “single flutter” that always begins in the same direction, and may repeat after some delay. To us this description sounds more like a pulse-step mismatch.

Testing: auditory

Auditory assessment is generally not useful for the diagnoses in question.

Testing: vestibular

Instrumented ocular motor testing may quantify ocular flutter.

Other tests, such as rotatory chair testing (RCT), may identify other findings compatible with cerebellar dysfunction.

Studies such as cervical vestibular evoked myogenic potentials (cVEMP), ocular vestibular evoked myogenic potentials (oVEMP), video head impulse testing (vHIT), caloric testing and computerized dynamic posturography (CDP) do not clarify the cause of ocular flutter, but may help exclude competing diagnoses.

Testing: other

If there is reason to suspect an infectious or paraneoplastic etiology, then consultation with infectious disease or oncology may be appropriate.

Imaging

A patient with unexplained ocular flutter generally should be evaluated with brain MRI to assess for posterior fossa lesions.

Differential diagnosis

Ocular flutter has been described in an enormous range of central nervous system pathologies. A non-comprehensive list includes:

  • Isolated ocular flutter (Nasu et al. 2013)
  • Autoantibodies (not paraneoplastic):
    • Anti-sulphatide antibody positivity (Akcay et al. 2024)
    • Pediatric MOG (myelin-oligodendrocyte) antibody-associated demyelination (Breza et al. 2019)
    • Anti-GM2 antibody rhomboencephalitis (Daponte et al. 2021)
    • Anti-GAD (glutamic acid decarboxylase) antibody (Dubbioso et al. 2013)
    • Anti-GAD65 (glutamic acid decarboxylase) antibody “years after curative treatment of follicular thyroid carcinoma” (Fornari Caprara et al. 2024)
    • Ocular flutter, generalized myoclonus and ataxia occurring in a 6-year-old child with anti-GM1, anti-DG1a and anti-GD1b antibodies (Frattini et al. 2018)
    • Ocular flutter associated with generalized myoclonus and truncal ataxia in Graves’ ophthalmopathy (Kuwahara et al. 2013)
    • Ocular flutter, ataxia and encephalopathy in autoimmune thyroiditis (Lee et al. 2015)
    • DPPX (anti-dipeptidyl-peptidase-like protein 6) antibody-mediated encephalopathy (Soliman et al. 2025)
    • Ocular flutter and truncal ataxia in anti-amino-terminal of alpha-enolase antibody (Yamashita et al. 2023)
    • Ocular flutter, truncal ataxia and generalized myoclonus associated with anti-GQ1b antibodies (Zaro-Weber et al. 2008)
  • Paraneoplastic:
    • Anti-Ri antibody positive breast cancer (Cascone et al. 2025)
    • Presumably paraneoplastic in association with breast cancer and elevated levels of HVA (homovanillic acid) and VMA (vanillylmandelic acid) (Furman et al. 1988).
    • Presumably paraneoplastic, in association with lung adenocarcinoma (Kruger et al. 2014)
    • Ocular flutter and cerebellar ataxia in anti-Ma 1/2 antibody-mediated paraneoplastic syndrome in association with testicular seminoma (Newey et al. 2013)
    • Ocular flutter, opsoclonus-myoclonus ataxia and cerebellar cognitive affective syndrome associated with small cell lung carcinoma (Ohara et al. 2007)
    • Ocular flutter and spontaneous down beat nystagmus in anti-glutamic acid decarboxylase-associated paraneoplastic syndrome (Shivaram et al. 2022)
    • Ocular flutter, opsoclonus and myoclonus in Lambert-Eaton myasthenic syndrome associated with small-cell lung cancer (Simister et al. 2011)
  • Infectious:
    • Meningitis (Orimo et al. 1998)
    • Poliovirus (Asindi et al. 1988)
    • Lyme disease (Gyllenborg and Milea 2009)
    • Post-malaria ocular flutter and cerebellar ataxia (Idris and Sokrab 1999)
    • Lyme neuroborreliosis (Jäger et al. 2022)
    • Zika virus infection (Karam et al. 2017)
    • Scrub Typhus infection (Kasinathan et al. 2019)
    • Ocular flutter and truncal ataxia in Dengue fever (Mahale et al. 2017; Wiwanitkit 2017)
    • Ocular flutter in encephalopathy with COVID-19 (Umapathi et al. 2020)
    • Ocular flutter occurring in myoclonic encephalitis (Toupet et al. 1982)
  • Para-infectious:
    • Enteroviral rhomboencephalitis (Fong et al. 2017)
    • A post-infectious syndrome (pathogen not identified) manifesting with ocular flutter, postural tremulousness and CSF pleocytosis (Hankey and Sadka 1987)
    • “Cerebellar encephalitis” causing opsoclonus, ocular flutter, macro square wave jerks and generalized myoclonic jerks (Kömpf et al. 1985)
    • Ocular flutter following adenoviral conjunctivitis (Sira et al. 2011)
    • Ocular flutter occurring in an acute inflammatory polyneuropathy with cerebellar signs after cytomegalovirus infection (Toupet et al. 1982)
    • Ocular flutter and truncal ataxia with lymphocytic pleocytosis, believed to be a para-infectious cerebellitis (microbe not identified), that spontaneously resolved (Wang 1992)
    • Ocular flutter and truncal ataxia associated with enterovirus infection (Wiest et al. 1997)
  • Post-vaccination:
    • Ocular flutter, myoclonus and ataxia following an mRNA vaccine for COVID-19 (Poyraz et al. 2023)
  • Neurodegenerative:
    • Three children with infantile parkinsonism-dystonia exhibited ocular flutter and saccade initiation failure (Assmann et al. 2004)
    • Amyotrophic lateral sclerosis (Balaratnam et al. 2010)
    • Elicited by optokinetic stimulation in a patient with olivopontocerebellar atrophy (Koh and Kim 2006)
    • Friedreich ataxia (Monday et al. 1984)
    • Friedreich ataxia (Sohns et al. 2024)
    • Ocular flutter evoked by vestibular stimulation in multiple system atrophy, cerebellar subtype (So et al. 2024)
    • Ocular flutter in spinocerebellar degenerative disorders (Yamamoto et al. 1988)
  • Demyelination:
    • Multiple sclerosis (Francis and Heron 1985)
    • Positional ocular flutter associated with middle cerebellar peduncle demyelination (Martins et al. 2019)
    • Multiple sclerosis (Mukherjee et al. 2024)
    • Ocular flutter associated with a multiple sclerosis lesion in the paramedian pontine reticular formation (Schon et al. 2001)
  • Toxic:
    • Cyclosporine A toxicity (Apsner et al. 1997)
    • Vidaribine toxicity (Gizzi et al. 1990)
    • Toluene toxicity (Lazar et al. 1983)
    • Doxylamine toxicity (Li et al. 2021)
    • Ocular flutter and opsoclonus in phencyclidine toxicity (Shameer Nijam et al. 2019)
    • Ocular flutter in serotonin syndrome (Sim and Sun 2016)
    • Alcohol withdrawal (Dastjerdi et al. 2020)
  • Metabolic:
    • Ocular flutter and myoclonus in hyperosmolar hyperglycemic state (Nysten et al. 2021)
    • Opsoclonus in a cerebellar syndrome resulting from hypomagnesemia (Olmedo-Saura et al. 2023)
  • Inborn errors of metabolism:
    • Ocular flutter in a 10-month old infant with carbohydrate-deficient glycoprotein syndrome type 1a (Stark et al. 2000)
  • Intracranial hypertension:
    • Ocular flutter in intracranial hypertension following cerebral venous thrombosis (Ploner and Kupsch 2002; Shetty 2003)
  • Positional:
    • Ocular flutter appearing only in the supine position (Brodsky and Hunter 2011)
    • Positional ocular flutter associated with middle cerebellar peduncle demyelination (Martins et al. 2019)
  • Miscellaneous:
    • In association with essential tremor (Anagnostou et al. 2013)
    • Mild head trauma (Manta et al. 2018)
    • Ocular flutter and encephalitis in an “undifferentiated connective tissue disorder” (Maramattom and Thomas 2022)
    • Pregnancy (Roche and Alarcia 2020)
    • Opsoclonus beginning at age 3 months, and resolving around 6 months, in an apparently otherwise healthy infant (Silverman et al. 2024)
    • Ocular flutter was the initial manifestation of autoimmune glial fibrillary acidic protein astrocytopathy (Wada et al. 2022)
    • Ocular flutter evoked by vestibular stimulation (Yoon et al. 2024)

Management

When ocular flutter occurs in the context of an identifiable pathology, the management is treatment of the original disease. For example:

  • Ocular flutter occurring in the context of essential tremor responded to primidone (Anagnostou et al. 2013).
  • Ocular flutter occurring in the context of Lyme disease resolved with treatment (Jäger et al. 2022).

Some presumably para-infectious causes of ocular flutter may resolve spontaneously as the infectious illness resolves (Wang 1992).

Prognosis

The prognosis depends on the underlying etiology (if identifiable).

Curiously, some cases of what appear to be paraneoplastic ocular flutter arise but also spontaneously resolve before discovery of the neoplasm (Furman et al. 1988). Thus, spontaneous resolution does not guarantee benignity of this finding.

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Page first posted on November 30, 2025. Page last updated on November 30, 2025

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