Definition/Introduction

Nystagmus is derived from Greek nustagmos (nodding, drowsiness) and nystazein (be sleepy or doze). It is a rhythmic, involuntary, rapid, oscillatory movement of the eyes. It may have a slow, fast, or a combination of both. It can be continuous, paroxysmal, with positional or gaze or head positioning triggers. It can be distinguished from saccades, oscillations, and other abnormal involuntary eye movements that are fast-acting and mimickers. These movements can reduce vision, affect depth perception, balance, and coordination. Often, nystagmus can be seen transiently, which may indicate some underlying pathology. Nystagmus can also be labeled as manifest (omnipresent), latent (when covering one eye), or both.[1] 

The Classification Committee of the Bárány Society established the different classification of nystagmus for clinical and research purposes, with special emphasis on a common language for vestibular disorders worldwide. Pathologic nystagmus results from diseases affecting the cortex, anterior visual tracts, brainstem, cerebellum, and peripheral vestibular apparatus.

Physiological nystagmus- normal nystagmus variant of oculomotor function 

• Physiologic end-point nystagmus- horizontal jerks nystagmus results from testing oculomotor movements too far laterally 
• Per-rotational nystagmus- horizontal jerk nystagmus that occurs with sustained head rotations, with fast phases ipsilateral to the rotation
• Post-rotational nystagmus- reflexive horizontal nystagmus that occurs with a rapid brake to a unidirectional head rotation, with a contralateral fast phase and a subjective rocking boat sensation
• Optokinetic or pendular nystagmus- multi-direction (e.g.vertical, torsional, or horizontal) nystagmus in response to moving or rotating visual fields or objects, the slow phase is ipsilateral to the visual stimuli, and it does not have a fast phase. [2] 

  • Asymmetry is abnormal, and the lesion can localize to the parietal-occipital cortex.
• Optokinetic after-nystagmus- persisting ipsilateral optokinetic nystagmus after the visual stimulus has extincted, can persist for seconds and dissipates.
• Vestibular ocular reflex- reflex controlled by semicircular canals in the inner ear,  seen when the patient sees a fixed image, and a rapid head rotation is elicited bilaterally.
• Caloric nystagmus- VOR reflex elicited by stimulating the tympanic membrane and horizontal semicircular canals with either warm or cold water.

  • Cold stimulus-eyes will turn slowly towards the cold water stimulation with rapid nystagmus away. Absence may indicate brain death.
  • Warm stimulus- eyes will turn slowly away with rapid nystagmus toward the side of the stimulus. Absence may indicate brain death.
• Magnetic vestibular stimulation-induced nystagmus-nystagmus that occurs while the patient is undergoing an MRI depends on the strength and direction of the field. It results from an interaction between the MRI field currents with the ionic currents in the endolymph fluid.

Etiology

• Infantile nystagmus usually develops by three months of age. It is characterized by a horizontal movement and has correlations with conditions such as albinism, congenital iris absence, underdeveloped optic nerves, or congenital cataract. Children aged 6 months to 3 years can have a form of nystagmus known as spasmus nutans.[3] This form usually improves without intervention between ages 2 through 8 years. Characteristically, children will often nod or tilt their heads with this type of nystagmus, and the eyes may move in any direction.[4]
• Acquired causes of nystagmus require exploration if the eye movements develop later in life.

Issues of Concern

Nystagmus, in some patients, can be asymptomatic. However, in most, nystagmus causes vertigo, oscillopsia, blurred vision, or abnormal head positioning. Vertigo is the primary symptom and occurs most commonly with vestibular problems. Oscillopsia, which is a sensation of the environment moving back and forth, depends on the type of nystagmus present but can be continuous, intermittent, or gaze-evoked.[5]  Blurred vision usually occurs due to the retinal image being affected by the motion. This blurred vision can lead to abnormal head positioning, which is when patients compensate for their vision changes by finding gaze positions that minimize their symptoms.

Clinical Significance

A major concern with finding pathological nystagmus is localizing the abnormal brain or ear apparatus structures affected and what is the underlying etiology. For instance, acquired nystagmus, which develops later in adolescence or adulthood, can indicate a central nervous system issue like multiple sclerosis, head injury, brain tumor, metabolic disorder, medication side effect, hyperventilation, or even alcohol or drug toxicity.[6][7][8][9][10] The differential diagnosis of nystagmus also includes oculogyric crises and ocular bobbing. Oculogyric crises are distinguishable from nystagmus by noting a lack of a specific rhythm or slow phase with the eye movements. This type of eye movement most commonly presents with phenothiazine intoxication. Ocular bobbing is more irregular than nystagmus and usually occurs in locked-in syndrome.

Pathological nystagmus- abnormal nystagmus from central or peripheral nervous system damage to the vestibular-oculocephalic  and/or cortical areas affecting the oculomotor function

• Spontaneous nystagmus- occurs consistently with fixed central gaze position stationary, upright, and neutral positions.
• Spontaneous peripheral vestibular nystagmus- occurs due to abnormal vestibular tone between vestibular nerves and the labyrinth; it is strictly unilateral and can be subclassified based on the direction.

  • Horizontal-torsional nystagmus
  • Vertical-torsional nystagmus
  • Horizontal-vertical-torsional nystagmus
  • Peripheral vestibular nystagmus, inhibitory type
  • Peripheral vestibular nystagmus, excitatory type
  • Recovery nystagmus
• Spontaneous central vestibular nystagmus

  • Predominantly horizontal central vestibular nystagmus

    • Direction-fixed horizontal central vestibular nystagmus
    • Latent nystagmus
    • Periodic alternating nystagmus
  • Predominantly vertical or torsional central vestibular nystagmus

    • Downbeat nystagmus
    • Upbeat nystagmus
    • Torsional nystagmus
  • Infantile nystagmus
  • Acquired pendular nystagmus
• Oculomasticatory myorhythmia
• Seesaw nystagmus
• Epileptic nystagmus
• Pursuit-paretic nystagmus
• Gaze-evoked nystagmus

  • Unilateral
  • Bilateral
  • Vertical
  • First-degree vestibular
  • Vestibular plus gaze-holding nystagmus
  • Rebound nystagmus
  • Centripetal nystagmus
• Triggered nystagmus

  • Positional nystagmus

    • Benign paroxysmal positional nystagmus (BPPN)

      • Anterior semicircular canal BPPN 
      • Posterior semicircular canal BPPN
      • Horizontal semicircular canal BPPN
      • Pseudo-spontaneous nystagmus
    • Central positional nystagmus
• Headshaking-induced nystagmus
• Cross-coupled nystagmus
• Sound-induced nystagmus
• Valsalva-induced nystagmus
• Pressure-induced nystagmus
• Vibration-induced nystagmus
• Hyperventilation-induced nystagmus
• Pursuit-induced nystagmus
• Vertical nystagmus 

  • Vertical nystagmus

    • Posterior fossa lesions
    • Medication side effects
    • Vitamin deficiencies
    • Inflammatory and autoimmune/paraneoplastic conditions
    • Hereditary and degenerative cerebellar ataxias.

Nursing, Allied Health, and Interprofessional Team Interventions

All interprofessional healthcare team members should be aware of the nature of nystagmus and, depending on specialty, be capable of varying degrees of interpretation. However, the ability to recognize the condition is essential so that the patient can be referred to the appropriate clinician for further workup and diagnosis. It must be charted in the patient's record so that all healthcare team members are aware and appropriate action can take place, leading to a more accurate diagnosis and improved patient outcomes.

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References

1.

Dell'Osso LF, Schmidt D, Daroff RB. Latent, manifest latent, and congenital nystagmus. Arch Ophthalmol. 1979 Oct;97(10):1877-85. [PubMed: 485910]

2.

Gresty MA, Ell JJ, Findley LJ. Acquired pendular nystagmus: its characteristics, localising value and pathophysiology. J Neurol Neurosurg Psychiatry. 1982 May;45(5):431-9. [PMC free article: PMC1083123] [PubMed: 7086456]

3.

Young TL, Weis JR, Summers CG, Egbert JE. The association of strabismus, amblyopia, and refractive errors in spasmus nutans. Ophthalmology. 1997 Jan;104(1):112-7. [PubMed: 9022113]

4.

ANDERSON JR. Causes and treatment of congenital eccentric nystagmus. Br J Ophthalmol. 1953 May;37(5):267-81. [PMC free article: PMC1324101] [PubMed: 13042022]

5.

Rushton D, Cox N. A new optical treatment for oscillopsia. J Neurol Neurosurg Psychiatry. 1987 Apr;50(4):411-5. [PMC free article: PMC1031874] [PubMed: 3585351]

6.

Masucci EF, Kurtzke JF. Downbeat nystagmus secondary to multiple sclerosis. Ann Ophthalmol. 1988 Sep;20(9):347-8. [PubMed: 3190116]

7.

Tilikete C, Jasse L, Pelisson D, Vukusic S, Durand-Dubief F, Urquizar C, Vighetto A. Acquired pendular nystagmus in multiple sclerosis and oculopalatal tremor. Neurology. 2011 May 10;76(19):1650-7. [PubMed: 21555732]

8.

Schmidt D, Kommerell G. [Seesaw nystagmus with bitemporal hemianopia following head traumas]. Albrecht Von Graefes Arch Klin Exp Ophthalmol. 1969;178(4):349-66. [PubMed: 5307804]

9.

Hübner J, Sprenger A, Klein C, Hagenah J, Rambold H, Zühlke C, Kömpf D, Rolfs A, Kimmig H, Helmchen C. Eye movement abnormalities in spinocerebellar ataxia type 17 (SCA17). Neurology. 2007 Sep 11;69(11):1160-8. [PubMed: 17846415]

10.

Fish DJ, Rosen SM. Epidural opioids as a cause of vertical nystagmus. Anesthesiology. 1990 Oct;73(4):785-6. [PubMed: 2221451]

Disclosure: Rupinder Sekhon declares no relevant financial relationships with ineligible companies.

Disclosure: Franklyn Rocha Cabrero declares no relevant financial relationships with ineligible companies.

Disclosure: Jonathon Deibel declares no relevant financial relationships with ineligible companies.