1. The document presents a case of a 20-year-old male with involuntary eye movements since birth, blurry distant vision for 5 years, and recurrent eye pain and discomfort for 7 years. Examination found nystagmus and a diagnosis of infantile nystagmus syndrome was made. 2. The discussion section defines nystagmus and its mechanisms, describes features like waveforms and territories, and covers types of nystagmus including congenital sensory deficit nystagmus, congenital motor nystagmus, and spasmus nutans. 3. Congenital nystagmus is often idiopathic but can be hereditary, and genetic factors like mutations

1. CONGENITAL NYSTAGMUS-
CASE PRESENTATION
PRESENTER: DR. KRATI GUPTA
MODERATOR: DR. DAMARIS MAGDELENE

2. CHEIF COMPAINTS:
• 20 year old male presented to OPD on 06/10/2016.
• C/O Blurring of distant vision since 5 years – painless(OU).
• Recurrent episodes of ocular pain and discomfort since 7 years.
• Involuntary movement of the eyes since birth.
 PAST HISTORY:
• No H/O ocular trauma.
 SYSTEMIC HISTORY:
• No H/O DM, HTN, IHD, Asthma

3. ON SLE : OD OS
Vision 6/12, N8 6/9P, N8
Pinhole vision NI NI
Flash -0.50DS/-2.25DC X90 +-/-0.75DCx130
Acceptance +-/-2.00DC X 90, 6/9 N6 +-/ -0.50 DC X 130, 6/7.5 N6
Extraocular Movements Full , orthophoric Full, orthophoric
Lids normal normal
Conjunctiva quiet quiet
Cornea clear clear
Anterior chamber VH grade IV VH grade IV
Iris WNL WNL
Pupil R/R/RTL R/R/RTL
Lens Clear Clear
Intraocular Pressure with NCT
@12:24pm
16mm of Hg 20mm of Hg
Other OU - Nystagmus

4.  DIAGNOSIS :
Infantile Nystagmus Syndrome
 TREATMENT
• Glasses.
• Review after one year.
 FUNDUS EXAMINATION
WNL

5. DISCUSSION
INTRODUCTION
• Nystagmus and nystagmoid eye movements in the pediatric age group can be :
 Congenital
 Acquired
• Nystagmus in the pediatric population can be :
 Of benign origin.
 Associated with abnormal visual development
 Associated with underlying neurologic disorder.

6. DEFINITION
• Nystagmus is derived from a Greek word ‘nystagmos’ meaning ‘to nod’ and
‘nystazein’ meaning ‘to doze’.
• Nystagmus is a repetitive to and fro, involuntary eye movement initiated by slow
drifts of eyes away from the desired direction of gaze.
• It is characterized by rhythmic succession of eye movements, which are more or
less regular, change alternately in direction, and may be pendular or jerky in
character.
• The movements may be spontaneous or provoked, physiological or pathological,
unconscious and almost always involuntary.
• It can be defined as a disturbance of ocular stability, characterized by stimulation
or alteration of the elements of the system that controls the eye position.

7. INCIDENCE AND PREVALENCE
• The prevalence of nystagmus according to some studies could be stipulated to be about
1 in 1000.
• Eighty percent of nystagmus is congenital, and the remaining twenty percent is
acquired.
• Amongst males, the prevalence of nystagmus is 1/5,032 and amongst females it is
1/10,596.
• However, other studies have reported an annual incidence of 1 in 350 to 1 in 6550.
• The occurrence of nystagmus in pediatric strabismic population is higher, up to 50%.

8. MECHANISM OF NYSTAGMUS
Aim of ocular movements :
• To maintain foveal centration of an object of interest.
Nystagmus due to distubance of:
1. Visual fixation
2. Ocular movements - Neural integrator.
3. Vestibulo-ocular reflex.

9. FIXATION
This has two distinct components:
• The ability of the visual system to detect retinal image drift and program
corrective eye movements accordingly.
• The suppression of unwanted saccades that would take the eye off the target.

10. VESTIBULO OCULAR REFLEX
• Mechanism by which , the eye
movements compensate for head
posture changes at short latencies,
thus maintaining clear vision during
normal activities, especially those
associated with locomotion.
• Thus, vestibular system perceives
head movement and makes the
eyeball move in the opposite
direction.

11. NEURAL INTEGRATOR
• Ability of the CNS (neural integrator) to
hold the eye at an eccentric position in
the orbit against the elastic pull of the
suspensory ligament and extraocular
muscles(EOM), which tend to return it
towards the central position.
• It is a gaze- holding network :
Complex integration between
Cortical centers
Cerebellum
Ascending vestibular pathways and
Ocular motor nuclei

12. • A disorder affecting any of the
three mechanisms that control
eye movements can result in
nystagmus.
Thus, nystagmus can be said
to result from the instability or
impairment of the system
responsible for controlling eye
position or its movements.

13. FEATURES OF NYSTAGMUS
• Nystagmus is a repetitive, involuntary to and fro movement of the eyes (horizontal,
vertical or torsional)
• It can be physiological
(e.g. following the rotation of an optokinetic drum)
• It can be pathological phenomenon. In pathological nystagmus, there are 2 phases
1. Involuntary defoveating drift of the eye from the target of interest followed by,
2. Corrective refixation saccade back to the target.

14. TERMINOLOGIES
• Saccade/ Pursuit
• Jerk / Pendular
• Amplitude
• Frequency
• Intensity
• Null zone
• Foveation period
• Neutral zone
• Conjugate/disconjugate
• Dissociated

15. SACCADE/ PURSUIT
• Saccades are sudden, simultaneous movements of both eyes in the same
direction to place the object of interest on to the fovea.
• Pursuit eye movements allow the eyes to closely follow a moving object
located by the saccadic system.
• Pursuit differs from the vestibulo-ocular reflex, which only occurs during
movements of the head and serves to stabilize gaze on a stationary object.

16. JERK / PENDULAR
JERK NYSTAGMUS PENDULAR NYSTAGMUS
Jerk nystagmus is saccadic with a slow
defoveating ‘drift’ movement and a fast
corrective refoveating saccadic movement.
• Sinusoidal oscillation with slow phase in
both directions and no corrective saccade.
• In pendular nystagmus both the foveating
and defoveating movements are slow (i.e.
the velocity of nystagmus is equal in both
directions).
Direction of jerk nystagmus = direction of the
fast component.
Pendular nystagmus may be horizontal or
vertical.
• Right or left beating nystagmus
• Upbeat or downbeat nystagmus
• Rotatory
Not characterised by right,left,up,down beating
as there is no fast phase.

19. AMPLITUDE
• Amplitude is the extent of excursion of the nystagmus
• Fine/ small : less than 50
• Medium/ moderate : 50-150
• Coarse/ large : greater than 150

20. FREQUENCY
• Frequency is the number of complete to and fro movements in one second.
• Described an cycles/sec or Hertz (Hz)
• Slow : (1-2 Hz)
• Medium : (3-4 Hz)
• Fast: (5 Hz or more)

21. INTENSITY
• This is mathematically denoted by the amplitude of the nystagmus
multiplied by frequency.
INTENSITY = AMPLITUDE X FREQUENCY

22. NULL ZONE
• This is the field of gaze in which the intensity of the nystagmus is minimal.
• In most individuals with jerk nystagmus, the severity of the eye movements can be
reduced by positioning their eyes in a particular gaze.
• The patient with nystagmus adopts a position of the head such that the field of
gaze of the eyes falls in the null zone.
• This provides the patient with an increased foveation period and better visual
acuity in that gaze.

23. FOVEATION PERIOD
• The period for which the image of an object of regard rests on the fovea only
when the visual line is directed at the target, during the time of nystagmus
oscillations is called the foveation period.
• The foveation period increases with decrease in the intensity of the nystagmus,
which is maximally demonstrated when the eyes are in the null position of gaze.
• It is an important concept to remember while describing the clinical features of
the nystagmus being examined because it is of paramount relevance from the
management point of view.
• Usually the foveation period correlates well with the best visual acuity of the
patient.

24. NEUTRAL ZONE
• The neutral zone is that eye position in which a reversal of direction of jerk
nystagmus occurs and in which none of the several bidirectional waveforms, or
pendular nystagmus is present.
• It is not synonymous with the null zone.
• The null and neutral zones usually overlap.
• However, several cases have been recorded where they do not.

25. CONJUGATE AND DISCONJUGATE NYSTAGMUS
• While it is generally true that the oscillatory movements in both eyes in a patient
with nystagmus is symmetrical and in the same direction, there are cases where this
is not true.
• Thus, depending on the direction and the amplitude of the nystagmus in both eyes,
it can be clinically subclassified as:
 Conjugate nystagmus: This implies that the nystagmus is symmetrical in direction,
amplitude and frequency in both eyes.
 Disconjugate nystagmus: This implies that the direction of nystagmus is different in
the two eyes. The amplitude may be the same or it may be different.

26. DISSOCIATED NYSTAGMUS
• The amplitude of the nystagmus is different in the two eyes while the direction
remains the same.
• This clinical entity basically refers to unidirectional but asymmetrical nystagmus in
both eyes.
• The most classical cause of this is internuclear ophthalmoplegia associated with
either multiple sclerosis or other cerebrovascular disease.
• However, there are considerable overlaps between the terms disconjugate and
dissociated nystagmus, and the terms should be used judiciously.

27. SCHEMATIC FOR DOCUMENTING NYSTAGMUS
(Courtesy of JJ Kanski, Signs in Ophthalmology: Causes and Differential Diagnosis, Mosby 2010)

28. ALEXANDER’S LAW
• This is a generalized observational regimen related to jerk nystagmus which states that
the amplitude of the nystagmus increases or is largest when the eye moves in the
direction of the fast phase.
• Grade I : Nystagmus only in the direction of the fast component.
• Grade II : Nystagmus in primary gaze position .
• Grade III : Nystagmus evident in all positions of the eyes.

29. CLASSIFICATION
• Optokinetic
• Vestibular
• End-point
Physiological
• Congenital nystagmus
• latent nystagmus
• Spasmus nutans
Early onset
(childhood)
• Gaze-evoked
• Vestibular
• Upbeat/downbeat
• Dissociated nystagmus
• Periodic alternating nystagmus
Pathological

30. INFANTILE NYSTAGMUS SYNDROME (INS)
Old term: Congenital nystagmus; Motor and sensory nystagmus.
• This is classically a form of conjugate, uniplanar, horizontal nystagmus .
• It appears by the age of zero to six months.
• It progresses from pendular to jerk type and stabilizes in a particular pattern by the age of
about five to six years.
• It may be associated with anomalies of afferent visual pathways such as albinism,
congenital cataract, or optic atrophy, or may appear where no visual or neurological
impairment is detected.

31. • Nystagmus can occur secondary to poor vision or to a motor deficit with the nystagmus
itself causing poor vision, though the distinction is not always clear.
• Certain clinical features help to differentiate congenital nystagmus from other ocular
oscillations.
• In congenital nystagmus, eye movements are usually conjugate and horizontal even on
upgaze and downgaze.
• Torsional and vertical components are rare and even if present are difficult to identify
clinically.
• The most common waveforms are jerk, pendular, and asymmetric pendular. Of these
three, the most common waveform is the jerk variety.

32. • In studies of infants with congenital nystagmus, the initial waveforms are of the
pendular variety.
• Shortly thereafter the waveform changes to a predominantly jerk type allowing for
better visual acuity through improved foveation around 1 year of age.

33. CHARACTERISTICS
• Horizontal nystagmus ( mixed pendular and jerk)
• Bilateral conjugate movements of the eyes.
• Uniplanar -direction of oscillation remains constant regardless of direction of gaze
• With or without normal visual acuity.
• Head turn to achieve null point.
• Accentuation with distant fixation and decreased by convergence.
• Abolished in sleep.

34. • In patients with nystagmus, with the chromosome X being affected, dampening of the
nystagmus can often be achieved by sleep, sedation, increased fusion,convergence,
contact lenses and extraocular muscle surgery.
• In contrast to adults with acquired nystagmus, oscillopsia is not experienced even by
adults with congenital nystagmus .
• There is a strong family predisposition .
• Strabismus present in 15% -30% of patients.

35. • Reverse response to OKN stimulus ( fast phase in direction of moving OKN drum)
• Exponential increase in velocity of slow phase with distance from fixation.

36. SENSORY DEFICIT (AFFERENT) NYSTAGMUS
• Sensory deprivation nystagmus is the more common form of infantile nystagmus.
• It is caused by impairment of central vision in early life due to
 Congenital cataract
 Macular hypoplasia
 Albinism
Leber congenital amaurosis
 Optic nerve hypoplasia
Achromatopsia
• In general, children with bilateral poor vision by 2 years of age develop nystagmus,
the severity of which is associated with the degree of visual loss.

37. ETIOLOGY

38. CONGENITAL MOTOR (EFFERENT) NYSTAGMUS
• A family history is common, with X-linked (dominant or recessive) inheritance the
common mode.
• Presentation is about 2–3 months after birth and persists throughout life.
• VA is generally better than with sensory deficit nystagmus, at 6/12–6/36.
• In the primary position there is low-amplitude pendular nystagmus that may
convert to jerk nystagmus on side gaze .

39. (Courtesy of JJ Kanski, Signs in Ophthalmology: Causes and
Differential Diagnosis, Mosby 2010)
Congenital motor (efferent)
nystagmus,
• In this case pendular in the
primary position and on vertical
gaze,
• but converting to a gaze-
evoked jerk nystagmus on left
and right gaze

40. GENETIC ASPECTS OF NYSTAGMUS
• Congenital idiopathic nystagmus is genetically heterogeneous.
• Autosomal dominant, autosomal recessive and X-linked patterns of inheritance have
been reported.
• Several genes are found to be responsible for congenital motor nystagmus.
• A family with nystagmus and a balanced 7;15 translocation has been identified.

41. • Autosomal dominant form of transmission to 6p12 in a large pedigree of
congenital nystagmus has been found.
• Missense mutations in the Pax6 gene have been associated with autosomal
dominant congenital nystagmus and aniridia.
• More recently, the FRMD7 gene has been identified as a specific genetic defect in
X-linked idiopathic congenital nystagmus.

42. SPASMUS NUTANS
Triad of symptoms:
• Pendular Nystagmus
• Head nodding
• Torticollis (head tilt or head turn)

43. SPASMUS NUTANS
• Presentation of this rare condition is between 3 and 18 months.
• It presents with unilateral or bilateral small-amplitude high-frequency horizontal
nystagmus .
• It is frequently asymmetrical, with increased amplitude in abduction.
• Vertical and torsional components may be present.
• An idiopathic form spontaneously resolves by age 3 years, but glioma of the anterior
visual pathway, empty sella syndrome and porencephalic cyst can also be causative.

44. (Courtesy of JJ Kanski, Signs in Ophthalmology: Causes
and Differential Diagnosis, Mosby 2010)
Spasmus nutans – the nystagmus
in this patient is pendular,
uniplanar and of equal amplitude
in all directions of
gaze

45. FUSION MALDEVELOPMENT NYSTAGMUS SYNDROME
Old term: Latent/Manifest latent nystagmus
• Latent nystagmus is associated with infantile esotropia
• There is dissociated vertical deviation .
• With both eyes open there is no nystagmus.
• Horizontal nystagmus becomes apparent on covering one eye.
• The fast phase is in the direction of the uncovered fixating eye.
• An element of latency may be superimposed on a manifest nystagmus so that when one
eye is covered the amplitude of nystagmus increases (manifest-latent nystagmus).

46. A and B:
• Accelerating show phase waveforms are
characteristic of congenital nystagmus
(idiopathic infantile nystagmus)
• while decelerating slow phase waveforms
are typical of manifest latent nystagmus
(Fusion maldevelopment nystagmus
syndrome)

47. PERIODIC ALTERNATING NYSTAGMUS
• Periodic alternating nystagmus (PAN) is a conjugate horizontal jerk nystagmus that
periodically reverses direction.
• During the active phase, the amplitude and frequency of nystagmus first progressively
increase then decrease.
• This is followed by an interlude lasting 4–20 s during which time the eyes are steady and may
show low-intensity, often pendular movements.
• A similar sequence in the opposite direction occurs thereafter, the whole cycle lasting
between 1 and 3 minutes.
• PAN can be congenital or due to cerebellar disease, ataxia telangiectasia and drugs such as
phenytoin.

48. EVALUATION AND TREATMENT OF CONGENITAL
NYSTAGMUS
• The goal of evaluation in an infant presenting with nystagmus is to exclude sensory causes
of nystagmus.
• A detailed clinical interview and examination is necessary including history, visual acuity,
pupil examination, orthoptic assessment, slit-lamp examination, and dilated fundoscopic
examination.
• Ancillary tests such as electroretinogram, potentials, and neuroimaging are ordered when
there is clinical suspicion for sensory cause for the nystagmus.
• Patients suspected of spasmus nutans should have neuroimaging to exclude a mass lesion.
• Electroretinogram should be considered in the presence of photophobia, myopia, or with
paradoxic pupillary reactions in order to exclude retinal dystrophies.

49. HISTORY
• The presence of neurological disorder, developmental delay, and hereditary metabolic
diseases should be elicited.
• A family history of nystagmus, and the timing of onset should be sought from the
parents.
• Any history of refractive treatments, and medical or surgical interventions should be
elicited.
• In an older child, questions regarding the presence of oscillopsia, worsening of
nystagmus in any particular gaze, and the presence of dizziness should be asked.
• The family should also be questioned whether the child turns or tilts his or her head .

50. CLINICAL EXAMINATION
• Any abnormality of head posture should be noted.
• Visual acuity.
• Color vision.
• Stereopsis.
• Visual fields should be tested.
• Dilated funduscopic examination should be performed.

51. MOTILITY AND ALIGNMENT
• Motility should be tested by recording ductions.
• Direction of nystagmus whether horizontal, vertical, torsional, or mixed should be
observed.
• Covering one eye will reveal the presence of Latent Nystagmus.
• Nystagmus should be observed in all gazes and also during convergence.
• The effect of removing fixation on nystagmus should also be noted using Frenzel goggles.
• Cancellation of vestibuloocular reflex .

52. MEASUREMENT OF NYSTAGMUS WAVEFORM
• In order to characterize nystagmus it is important to measure eye position and velocity
as well as target position during attempted fixation in different gaze angles.
• Nystagmus is measured in terms of amplitude, frequency, direction, and waveform that
is pendular or jerk

53. ANTERIOR SEGMENT EXAMINATION
Examination of the pupils
• Bilaterally sluggish pupils or presence of relative afferent pupillary defect suggests
anterior visual pathway disease.
• Pupillary dilation in response to light, the so-called ‘paradoxical pupil’, is often seen in
patients with :
Congenital photoreceptor abnormalities such as achromatopsia.
Leber congenital amaurosis
Cone dystrophy
Congenital stationary night blindness

54. Examination of the iris
• The iris should also be examined for transillumination defects.
• Iris transillumination defects are universally present in oculocutaneous albinism.

55. POSTERIOR SEGMENT EVALUATION
• Ophthalmoscopic examination to look for optic nerve anomalies and macular hypoplasia
should be carried out.
• The macula should be assessed for normal pigment and vascular pattern surrounding a
well-delineated fovea.
• Lack of a normal foveal reflex is indicative of macular hypoplasia, as in ocular albinism.

56. • It is not unusual to find a completely normal fundus in infants who present with
infantile nystagmus.
• In such instances retinal dystrophies such as:
 Leber’s congenital amaurosis
 Congenital stationery night blindness
 Cone dystrophy
• Should be considered in the differential diagnosis and an electroretinogram should
be ordered to evaluate for these conditions.

57. INVESTIGATIONS
• Electroretinogram-
ERG should be performed when the suspicion of sensory nystagmus .
• Visual-Evoked Response-
Visual-evoked response (VER) has limited use in the evaluation of infantile
nystagmus due to the inability of infants to perform pattern VER.
Flash VER provides little insight into visual pathway dysfunction but may be of
some value in documenting abnormal chiasmal crossing in albinism.

58. • Neuroimaging-
Infants and children with nystagmus and reduced vision with abnormal optic nerves
will need neuroimaging.
Atypical congenital waveforms such as seesaw nystagmus and periodic alternating
nystagmus should also undergo neuroimaging.
Children in whom the timing of onset of nystagmus is uncertain should have
neuroimaging performed to exclude any structural lesion in the brain.
Neuroimaging is unnecessary in Latent Nystagmus.
Examination under anesthesia may be required in some patients to adequately
evaluate ocular structures in the work-up of infantile nystagmus.

59. • Eye Movement Recordings
As a research tool, eye movement recordings are invaluable.
They elegantly characterize the waveforms of all types of nystagmus.
 Recordings performed over several decades have led to remarkable advances in
the understanding of the physiology of normal and abnormal eye movements.

61. MANAGEMENT OF CONGENITAL NYSTAGMUS
BEHAVIORAL INTERVENTIONS
• Parents and teachers need to be aware of preferred head positions and to be
reminded that this is a useful adaptation in affected children and should not be
discouraged.
• Vision enhancing adjustments at school include orienting the chalkboard, teacher,
and television in the favored direction of gaze for the child.
MEDICAL MANAGEMENT
• Medications such as baclofen and gabapentin may be helpful.

62. OPTICAL MANAGEMENT
• Spectacle Correction
Children with congenital nystagmus often have significant ametropia.
 Careful cycloplegic refraction and prescribing glasses to maximize visual potential is
the initial step in the management of children with congenital nystagmus.
• Contact Lenses
Some patients with congenital nystagmus experience damping of nystagmus and
consequent improvement in visual acuity when using contact lenses.
• Prisms
Prisms can help in two ways to improve visual function in
children with nystagmus:
1. Correction of anomalous horizontal or vertical head turn, and
2. Base-out/base-in prisms to improve visual acuity by stimulating vergence eye
movements.

63. CORRECTION OF HEAD POSTURE
• Prisms minimize head turn by reorienting the line of sight toward the primary gaze.
• The eyes remain in the preferred gaze position to maximize visual function.
• Prisms help to redirect the line of sight so that the head can assume a more natural
relationship with the environment.

64. LASER IN SITU KERATOMILIEUSIS
• One recent study reported the beneficial effect of laser in situ keratomilieusis
(LASIK) in myopic patients with congenital nystagmus.
• Although the mechanism for improvement is not clear, selected patients with
myopia and congenital nystagmus may benefit from laser refractive surgery.

65. BOTULINUM TOXIN CHEMODENERVATION
• Injection of botulinum toxin into the extraocular muscles or the retrobulbar space to
abolish eye movements due to nystagmus.
• Amplitude and intensity of nystagmus is reduced in all reported cases.
• Side effects and complications of this procedure that has limited its usefulness include:
 Ptosis
 Diplopia
Ophthalmoplegia
 Temporary nature of the injection
Need for repeated injections
Risk of infection
Potential for sight-threatening complications

66. SURGICAL THERAPIES FOR CONGENITAL
NYSTAGMUS
Surgical treatment for nystagmus is performed for two main reasons:
• To correct anomalous head postures.
• To improve visual acuity.

67. TREATMENT MODALITIES FOR HORIZONTAL
ANOMALOUS HEAD POSTURES
• In the various procedures that can be employed to correct anomalous head postures,
the aim of surgery is to move the null zone closer to the primary position .
• The most popular procedure for correction of horizontal head postures is the recess-
resect operation on the extraocular muscle is:
• Kestenbaum Anderson procedure (classic maximum)
• Other variations of Kestenbaum–Anderson procedure

68. • Vertical anomalous head postures
These include various combinations of recessions and resections of involved
vertical muscles.

69. SURGERY TO IMPROVE VISUAL ACUITY
The surgical principles of the procedures described below involve decreasing the eye
movements, thereby increasing the foveation time leading to improvement in visual acuity
• Horizontal muscle recessions
It involves placing the rectus muscles behind the equator to decrease the rotational
effect on a given eye movement.
The nystagmus gets damped and the foveation fraction increases thereby improving the
visual acuity.

70. • Tenotomy of horizontal rectus muscles
A recently introduced surgical treatment of congenital nystagmus is tenotomy of
horizontal rectus muscles which has shown encouraging results thus far in a dog
model and in humans with INS without eccentric null points.
• Combining Tenotomy with Other Procedures
If tenotomy proves to be an effective treatment for congenital nystagmus, it can also
be combined with nystagmus procedures aimed at damping congenital nystagmus or
with strabismus procedures in patients with congenital nystagmus.

71. • Artificial divergence
Artificial divergence procedures may be effective in those patients with congenital
nystagmus in whom the nystagmus damps during convergence.

72. COMPLICATIONS OF NYSTAGMUS SURGERY
• Three important complications of the surgical procedures discussed above for
treatment of congenital nystagmus are as follows:
1. With all the procedures there is a chance of creating a heterotropia.
2. Many patients with nystagmus may eventually require surgery on all their rectus
muscles, thereby increasing the risk of anterior segment ischemia.
3. All procedures are associated with a significant chance of undercorrection.