Saccade (Saccadic Eye Movement)

Key Points at a Glance

Highlights of this disease

• Saccades are conjugate eye movements that rapidly shift the point of fixation, reaching a maximum velocity of approximately 700°/s.
• Voluntary saccades are primarily initiated by the frontal eye field (FEF), while involuntary saccades are mainly initiated by the superior colliculus (SC).
• Horizontal saccades are generated via the pathway: PPRF → abducens nucleus → MLF → oculomotor nucleus; vertical saccades via riMLF → trochlear nucleus and oculomotor nucleus.
• In progressive supranuclear palsy (PSP), slowing of vertical saccades is an early diagnostic clue; in Huntington disease, impaired saccade initiation is an early sign.
• Saccadic intrusions such as square-wave jerks (SWJ), ocular flutter, and opsoclonus are abnormal movements consisting of rapid eye movements that occur transiently, unlike nystagmus.
• The antisaccade task is being studied as a biomarker for differentiating mild cognitive impairment (MCI) and Alzheimer disease. ³⁾

1. What is a saccade?

A saccade is a conjugate eye movement that rapidly shifts the point of fixation from one part of the visual field to another. Examples include eye movements while reading, the fast phase of nystagmus, and eye movements during REM sleep.

Functional significance

The fovea is a region approximately 1.0 mm in diameter (about 3° of visual angle) with the highest density of cone photoreceptors. By rapidly shifting the line of sight via saccades, it becomes possible to quickly assess the surrounding environment.

Classification of saccades

• Voluntary saccades: Intentionally performed, such as reading text or looking at a designated target.
• Involuntary saccades: Occur unintentionally, such as the fast phase of nystagmus or during REM sleep.
• Prosaccades: A task in which a saccade is made toward a visual stimulus that appears.
• Antisaccades: A task in which a saccade is directed opposite to the appearing stimulus. Requires two processes: suppression of reflexive prosaccades and generation of voluntary saccades.
• Memory-guided saccades: A task in which a saccade is made with a delay to a remembered location after the visual stimulus disappears.

Key Parameters of Saccades

The following parameters are used in clinical evaluation.

Parameter	Description
Amplitude	Angle of eye movement (°)
Latency	Time from stimulus presentation to saccade onset (approximately 200 ms)
Peak velocity	Approximately 300–350°/s at 15°, approximately 475–525°/s at 35°
Duration	Linear relationship with amplitude. Amplitude and velocity also have a linear relationship.
Gain	Ratio of actual amplitude to target amplitude

Saccade initiation takes about 200 milliseconds, and the maximum velocity reaches approximately 700°/second. Once initiated, the trajectory is fixed and cannot be corrected mid-flight (ballistic nature).

Q How fast do saccades move per second?

A

Peak velocity depends on amplitude: about 300–350°/second for a 15° saccade, 475–525°/second for 35°, and up to about 700°/second at maximum. There is a linear relationship between amplitude and velocity.

2. Main Symptoms and Clinical Findings

Subjective Symptoms

Saccade abnormalities themselves are often difficult for patients to notice. They may be noticed through the following symptoms.

• Oscillopsia: Patients may report a sensation of the visual field shaking due to saccadic intrusions.
• Difficulty reading: Reduced saccade velocity impairs the ability to follow lines of text.
• Difficulty fixating or double vision: Reflects impaired control of eye movements.

Clinical Findings (Findings Confirmed by Physician Examination)

Standard Evaluation Items

• Delayed saccade initiation: Whether saccades are generated promptly after a command. Delay is characteristic of ocular motor apraxia and Huntington disease.
• Range of motion and conjugacy: Check for limitation of eye movement range and velocity mismatch between the two eyes.
• Slowed saccade velocity: Slowing of vertical saccades is characteristic of PSP, and horizontal saccades in SCA2.
• Saccade dysmetria: Hypometric saccades (undershoot) are characteristic of Parkinson disease, while hypermetric saccades (overshoot) are characteristic of cerebellar disease.
• Independent assessment of horizontal and vertical directions: Because different diseases affect each direction independently, both directions must be examined separately.

Types of saccadic intrusions and oscillations

Saccadic intrusions are abnormal eye movements distinct from nystagmus. Nystagmus primarily involves slow-phase drift, whereas saccadic intrusions primarily involve rapid eye movements. ²⁾

Square-wave oscillations

Square-wave jerks (SWJ): Horizontal conjugate saccades during fixation (typically <2°). Caused by dysfunction of the superior colliculus, omnipause neurons, or the cerebellar fastigial nucleus. ²⁾

Macro square-wave jerks (MSWJ): Amplitude >5°. Occur in cerebellar disease, PSP, MS, and hydrocephalus. Associated with brief intersaccadic intervals. ¹⁾

Macrosaccadic oscillations: Oscillations around the fixation point with a crescendo-decrescendo pattern. Caused by damage to the cerebellar fastigial nucleus/vermis. ²⁾

Sinusoidal oscillations

Ocular flutter: High-frequency horizontal saccadic bursts without intersaccadic intervals. Caused by damage to the PPRF or cerebellar fastigial nucleus. Occurs in paraneoplastic syndromes and viral encephalitis. ²⁾

Opsoclonus: Multidirectional, irregular, high-frequency saccades without intersaccadic intervals. Representative condition is opsoclonus-myoclonus syndrome (neuroblastoma in children). ²⁾

Saccadic pulses: A brief saccade away from the fixation point followed immediately by a corrective saccade. The difference from SWJ is the absence of an intersaccadic interval. ²⁾

Q How are square-wave jerks (SWJ) different from nystagmus?

A

SWJ are saccadic intrusions where rapid eye movements transiently take the eyes away from the fixation point. In nystagmus, the slow-phase drift is primary, and the fast phase is a corrective movement. SWJ are rhythmic but do not involve slow-phase drift, which distinguishes them from nystagmus. ²⁾

3. Causes and Risk Factors

Saccadic abnormalities appear as symptoms of various neurological diseases. Below are representative diseases and abnormal patterns.

Movement Disorders

• Progressive supranuclear palsy (PSP): Slowing of vertical saccades appears early, preceding ophthalmoplegia. Due to burst neuron damage in the riMLF (rostral interstitial nucleus of the medial longitudinal fasciculus). SWJ are also frequently observed.
• Parkinson’s disease: Hypometric horizontal and vertical saccades.
• Multiple system atrophy (MSA): SWJ, saccadic dysmetria.
• Huntington’s disease: Saccade initiation failure is the main ocular finding. Saccadic slowing is also present.
• Spinocerebellar ataxia (SCA): In SCA2, horizontal saccadic slowing is typical. SCA with saccadic intrusions (SCASI) presents with macrosaccadic oscillations.
• Friedreich’s ataxia: Macrosaccadic oscillations, continuous SWJ.
• Ocular motor apraxia: Characterized by head thrusts and blinks to compensate for saccade initiation.
• Ataxia telangiectasia: Hypometric saccades, alternating skew deviation, SWJ.

Neuropsychiatric Disorders

• Alzheimer’s disease (AD): Hypometric saccades, prolonged latency, reduced peak velocity, impaired antisaccades.
• ADHD: Reduced ability to suppress unnecessary saccades.
• Autism: Increased antisaccade errors.
• Schizophrenia (childhood-onset): Increased predictive saccades and intrusive saccades.

Main causative diseases leading to saccadic intrusions

Type of intrusion	Representative causative diseases
SWJ	Parkinson’s disease, PSP, cerebellar ataxia, MS, paraneoplastic encephalitis
Macrosaccadic oscillations	Spinocerebellar degeneration, cerebellar tumor, hereditary cerebellar degeneration
Saccadic pulses	Toxic/metabolic encephalopathy, MS, brainstem lesions
Ocular flutter	Paraneoplastic (anti-Ri), MS, post-viral encephalitis
Opsoclonus	OMS, neuroblastoma (children), anti-Hu, anti-Ri encephalitis

Daily Care and When to See a Doctor

Preventing saccadic abnormalities themselves is difficult. However, early diagnosis and treatment of the underlying disease directly affect prognosis. If you experience letters shaking while reading or a sensation of involuntary eye movements, we recommend consulting a neuro-ophthalmologist.

Q What neurological diseases may be suspected from saccadic abnormalities?

A

Slowing of vertical saccades is an early sign of PSP and may precede ophthalmoplegia. In Huntington’s disease, impaired saccade initiation is characteristic. In SCA2, slowing of horizontal saccades is typically observed.

4. Diagnosis and Examination Methods

Clinical Evaluation (Bedside)

The five-item evaluation by Termsarasab provides a basic framework.

1. Saccade initiation: Check the promptness of initiation after command.
2. Range of motion and conjugacy: Evaluate limitations in range and differences in velocity between the two eyes.
3. Saccade velocity: Check for slowing.
4. Saccade accuracy: Check for hypometria, hypermetria, and corrective saccades.
5. Saccadic intrusions/oscillations: Identify SWJ, macrosaccadic oscillations, flutter/opsoclonus.

It is important to evaluate horizontal and vertical directions independently, as different diseases affect each direction separately.

Eye Movement Recording

• Electronystagmography (ENG): Eye movement recording using the corneo-retinal potential difference. It allows quantitative evaluation of saccades, pursuit, and fixation. ²⁾
• Video-oculography (VOG): Enables quantitative assessment using high-speed eye tracking. ²⁾
• Video analysis software (e.g., Kinova): Applied for simple quantitative assessment of eye movements at the bedside. ¹⁾

Differential diagnosis based on saccade velocity

If the abduction saccade velocity is normal, an apparent abduction limitation can be judged as an apparent deficit of abduction (ADAD) rather than a sixth cranial nerve palsy. ⁵⁾

Clinical application of the antisaccade task

• Perform prosaccade and antisaccade tasks under gap/overlap conditions. ³⁾
• The antisaccade task is more effective than the prosaccade task in differentiating MCI/AD from healthy controls. ³⁾
• Evaluation metrics: saccade latency, directional error rate, amplitude, peak velocity. ³⁾⁴⁾

5. Standard treatment

Saccadic abnormalities often appear as symptoms of an underlying disease. Therefore, diagnosis and treatment of the primary disease are the highest priority.

Treatment of the primary disease

Disease-specific treatment for each neurodegenerative or psychiatric disorder is fundamental. Direct intervention for saccadic abnormalities is secondary.

Treatment of MSWJ associated with hydrocephalus

MSWJ can appear reversibly due to hydrocephalus. With improvement of hydrocephalus after ventricular drainage or VP shunt, MSWJ disappears. ¹⁾

Tanaka et al. (2021) reported a case of a 54-year-old man with right thalamic hemorrhage and acute hydrocephalus. After emergency ventricular drainage, MSWJ (rightward intrusive saccades, 2–3 Hz, amplitude >5°, median corrected latency 200 ms) appeared and disappeared on day 2 with improvement of hydrocephalus. On day 36, MSWJ reappeared after drainage clamping, but disappeared again on day 39 after VP shunt, with no recurrence at 6 months. ¹⁾

Pharmacotherapy

No specific pharmacotherapy for saccadic intrusions has been established. For some eye movement disorders, baclofen, gabapentin, memantine, etc. have been tried. ²⁾

Saccadic Adaptation

Normal saccadic accuracy is the result of a continuous adaptation process. Unconscious corrections are made in response to changes due to aging or disease.

Clinical Considerations

Saccadic abnormalities are often a phenotype of the underlying disease. Symptomatic treatment alone is insufficient; diagnosis and treatment of the underlying disease are most important.

6. Pathophysiology and Detailed Mechanisms

Neural Circuitry of Saccade Generation

• Frontal eye field (FEF): Triggers most voluntary saccades. Projects directly to the contralateral PPRF and superior colliculus.
• Superior colliculus (SC): Primarily initiates involuntary saccades. Fixation neurons in the rostral pole of the SC excite omnipause neurons to maintain fixation. ¹⁾
• Parietal lobe: The superior parietal lobule and parietal eye field directly connect to the superior colliculus. Parietal lobe damage increases prosaccade latency.
• Basal ganglia: The striatum is involved in the generation and suppression of reflexive saccades. Pharmacological inhibition of GABAergic projections from the substantia nigra pars reticulata results in uncontrollable saccadic intrusions. ¹⁾
• Cerebellum: The vermis and fastigial nucleus are involved in saccadic accuracy. Damage to the fastigial nucleus/cerebellar outflow pathway causes macrosaccadic oscillations (repetitive hypermetria). ²⁾
• FEF and SC are complementary; damage to one still allows horizontal saccade generation, but damage to both results in significant deficits.

Pathway of Horizontal Saccades

FEF → SC → PPRF (paramedian pontine reticular formation) → abducens nucleus → MLF → oculomotor nucleus

The abducens nucleus contains two types of neurons: (1) lower motor neurons that directly innervate the ipsilateral lateral rectus muscle, and (2) internuclear neurons that cross the midline, join the MLF, and terminate on oculomotor nucleus neurons that innervate the contralateral medial rectus muscle.

Vertical saccade pathway

FEF → SC → riMLF (rostral interstitial nucleus of the medial longitudinal fasciculus) → trochlear nucleus and oculomotor nucleus → superior oblique, inferior oblique, superior rectus, inferior rectus muscles

The riMLF sends axons to the trochlear and oculomotor nuclei on both sides. Damage to burst neurons in the riMLF causes slowing of downward saccades in early PSP. The interstitial nucleus of Cajal (iC) is involved in maintaining vertical gaze holding, and unilateral iC lesions cause ocular tilt reaction.

Neural mechanism of antisaccades

Correct antisaccade generation requires two processes: (1) suppression of reflexive prosaccades, and (2) generation of voluntary saccades to the mirror image location of the target. ⁴⁾

• Fixation neurons and movement neurons in the SC modulate their discharge antagonistically. ⁴⁾
• The DLPFC and ACC send top-down inhibitory signals to the SC. ⁴⁾
• The SEF sends supplementary motor commands to the SC and FEF, contributing to successful voluntary antisaccades. ⁴⁾
• The antisaccade task recruits a fronto-parietal-subcortical network consisting of the DLPFC, SEF, FEF, ACC, posterior parietal cortex, thalamus, and striatum. ³⁾

Neural mechanism of saccadic oscillations

Saccades are generated by a pulse-step stimulus. High-frequency firing from burst neurons (pulse signal) moves the eye, tonic neuron stimulation for gaze holding (step signal) maintains eye position, and pause neurons maintain fixation. Disruption of local brainstem neural circuits leads to saccadic intrusions. They are broadly classified into square-wave oscillations (with intersaccadic intervals) and sinusoidal oscillations (without intervals).

Reversible mechanism of MSWJ (hydrocephalus)

Hydrocephalus due to obstruction of the fourth ventricle outlet → dilation of the third ventricle and cerebral aqueduct → mechanical stretching of the superior colliculus → decreased fixation neuron activity → decreased omnipause neuron activity → development of MSWJ. Reversible improvement with hydrocephalus treatment suggests a functional rather than destructive mechanism. ¹⁾

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7. Latest Research and Future Perspectives (Research-stage Reports)

For Patients: Please Read Carefully

The following content is currently at the research stage or under clinical trial and is not standard treatment available at general hospitals. It is reference information for professionals regarding future medical developments.

Saccade Biomarkers for Alzheimer’s Disease and MCI

Opwonya et al. (2022) ³⁾ systematically reviewed 35 original articles and conducted 27 meta-analyses. Prosaccade latency was significantly longer in the AD group than in the MCI group (under gap and overlap conditions), and antisaccade error rate was significantly higher in the AD group than in the MCI group (under gap condition). The antisaccade paradigm was more effective than prosaccade in differentiating patients from healthy controls, suggesting that selection of specific saccade paradigms and conditions can distinguish MCI, AD, and healthy individuals. Eye-tracking technology has potential as a non-invasive, inexpensive AD biomarker.

Assessment of Alcohol Use Disorder Using Antisaccade Tasks

Si et al. (2022) showed that chronic alcohol use causes impairment of inhibitory control. Both high-dose (0.8 g/kg) and low-dose (0.4 g/kg) increased antisaccade latency and reduced speed. It was suggested that antisaccade inhibitory control may serve as an early biomarker for alcohol use disorder (AUD), and the possibility of saccade assessment using VR technology and mobile devices was discussed. ⁴⁾

Q Can saccade testing detect Alzheimer's disease early?

A

Antisaccade tasks are useful for differentiating MCI and AD, and research is progressing as a non-invasive biomarker. ³⁾ However, at present, it is still at the research stage as an aid to clinical diagnosis and is not used as an established standard test.

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8. References

1. Tanaka K, Ando D, Irie K, et al. Macrosquare-wave jerks subsiding after hydrocephalus treatment in a thalamic hemorrhage patient. Intern Med. 2021;60:2487-2490.
2. Gurnani B, et al. Nystagmus and nystagmoid movements review. Clin Ophthalmol. 2025;19:1617-1650.
3. Opwonya J, Doan DNT, Kim SG, et al. Saccadic eye movement in mild cognitive impairment and Alzheimer’s disease: a systematic review and meta-analysis. Neuropsychol Rev. 2022;32:193-227.
4. Si Y, Wang L, Zhao M. Anti-saccade as a tool to evaluate neurocognitive impairment in alcohol use disorder. Front Psychiatry. 2022;13:823848.
5. Lam D, Blah TR, Lau FS, et al. Apparent defective abduction without diplopia. Cureus. 2022;14(9):e29155.