Palinopsia and polyopia in the absence of
drugs or cerebral disease
Howard D. Pomeranz, MD, PhD; and Simmons Lessell, MD

Article abstract—Objective: To report the occurrence of palinopsia and polyopia in patients who neither used drugs nor
had diseases of the cerebral hemispheres, a group in which these visual symptoms have not been reported. Method: The
patient records in the database of an academic neuro-ophthalmology unit were reviewed. Results: Seventeen patients were
identified in the database with the diagnosis of palinopsia or polyopia, of whom eight had diseases of the cerebral
hemispheres, leaving nine patients for analysis. No patients with a history of drug toxicity were identified. In one patient
the symptoms presented during an initial episode of demyelinative optic neuritis in the absence of clinical or laboratory
evidence of cerebral lesions. In another patient they developed immediately after laser treatment of diabetic macular
edema. A third patient developed the symptoms in association with visual loss from Leber’s hereditary optic neuropathy.
The other six patients were healthy individuals. Conclusion: Palinopsia and related visual symptoms can occur in
otherwise healthy individuals and in patients with disease apparently confined to the eye or the optic nerve. Key words:
Palinopsia—Polyopia—Visual hallucinations—After-image.
NEUROLOGY 2000;54:855–859

Palinopsia is a symptom distinct from the physiologic after-image in which images of an object persist
or reappear after the patient has stopped looking at
the object.1-3 In some cases patients see a series of
“echoes” of the object, separate from but in proximity
and identical to the actual object, giving the impression of polyopia (cerebral polyopia). Eye movement
may make the original object appear to leave a trail.
These abnormal positive visual phenomena may occur in the same patient and may well be related
pathophysiologically. Palinopsia, cerebral polyopia,
and visual trailing are usually reported by patients
with neurologic and psychiatric disorders or by individuals who have used or abused certain drugs.
However, we have encountered these symptoms in
healthy individuals who presumably had not and
were not using illicit drugs, and in patients with
diseases apparently limited to the retina or optic
nerve. They were identified in the computerized database of the neuro-ophthalmology unit of the Massachusetts Eye and Ear Infirmary. Their case
histories are the basis of this report.
Case reports. Patients with reduced vision. Patient
1. Two days after grid laser treatment for diabetic macular edema of her right eye, a 70-year-old woman began to
notice “repetition of images.” She would see a scene repeated if she looked away. For example, on one occasion
she looked across the street at a blond woman and then on
looking elsewhere toward a man, was startled to see the
image of the blond woman in front of the man. She also
noticed that when she looked at a television screen everything appeared “cracked.” The symptoms cleared after several weeks only to reappear spontaneously 2 weeks later.

Her vision had been decreasing for 5 years from diabetic
retinopathy and she had experienced two vitreous hemorrhages in her left eye. Glaucoma recognized 1 year earlier
had been treated with a laser trabeculoplasty. She also
had drug-controlled hypertension and unexplained normochromic, normocytic anemia. At the time of her palinopsia
she could see only 20/100 with her right eye and hand
motions with her left. Her neurologic history was positive
only for 1 hour of slurred speech a year earlier. No abnormalities were found on neurologic examination. Her medications were levothyroxine, Glyburide, Clonazepam,
Metformin, Metoprolol, and Enalapril.
Several months later the patient developed occlusion of
the left middle cerebral artery, which rendered her aphasic
and hemiplegic and prevented us from learning if her palinopsia had persisted. MRI performed after the stroke
showed no lesions other than the recent brain infarction.
Patient 2. A 41-year-old woman first noticed blurred
vision in both eyes while driving. Her vision gradually
worsened and she realized that her color vision was impaired. There was a history of alcohol abuse but she ate
well and denied using illicit drugs. Her family history was
negative for eye and neurologic disorders. Shortly after her
vision failed, she started to notice prolonged after-images,
especially when she was tired or when she was seated in a
moving vehicle. She stated that the images appeared to be
“following me all the way” for up to an hour. As an example she reported that the image of a pink automobile that
she had seen as she passed a parking lot remained in view
for half an hour as her vehicle traveled to other areas. This
symptom occurred infrequently.
Eighteen months after the onset of her visual problem
her visual acuity was best corrected to 20/400 bilaterally
with central scotomas and optic atrophy. Neurologic examination showed an anxious and depressed woman with

From the Department of Ophthalmology, Harvard Medical School and the Neuro-Ophthalmology Unit, Massachusetts Eye and Ear Infirmary, Boston, MA.
Received August 5, 1999. Accepted in final form October 1, 1999.
Address correspondence and reprint requests to Dr. Howard D. Pomeranz, University of Maryland, Department of Ophthalmology, 419 West Redwood Street,
4th Floor, Baltimore, MD 21201.
Copyright © 2000 by the American Academy of Neurology

855

minimal signs of a peripheral polyneuropathy. Cranial
MRI and CT, EEG, and examination of the CSF gave negative results. There was a nonrecordable visual evoked
response but her brainstem auditory and somatosensory
evoked responses were within normal limits. Tests on the
patient’s blood showed that she was homoplasmic for the
11778 mitochondrial DNA mutation associated with Leber’s hereditary optic neuropathy. No follow-up information
is available.
Patient 3. A 39-year-old woman who was well psychiatrically, ophthalmologically, and neurologically developed
pain in her left eye that was aggravated by eye movement.
Within days the vision in that eye failed to the extent that
she could only count fingers, but her right eye retained
normal visual acuity and both of her fundi were unremarkable. Her medical history was notable for asthma and
thrombophlebitis. She was being treated with Warfarin.
She denied ever using illicit drugs. The patient’s brother
had MS. Brain MRI showed no abnormalities. Within 2
months her visual function had recovered spontaneously
and completely; however, she reported that she had been
seeing abnormally persistent after-images. For example
she related an incident in which, “I looked at my foot, I
looked away and still saw my foot.” The palinoptic images
were seen as a black-and-white outline. When she experimented by alternately closing each eye she found that she
only saw after-images when she looked with her right eye
(the unaffected eye).
The palinopsia stopped spontaneously and never recurred despite several additional attacks of optic neuritis
in each eye. Several years later the development of spinal
cord symptoms and signs, and the appearance of spinal cord
lesions on MRI led to a diagnosis of MS. She has been stable
neurologically and free of palinopsia for the past decade.
Patients with normal vision. Patient 4. A 32-yearold psychiatrically and neurologically healthy woman
whose only previous eye problem was myopia noticed an
enhanced after-image. This occurred only after viewing an
illuminated stimulus, especially on her computer screen.
The image of the object would persist for several seconds
and could be reestablished by blinking. Sometimes the object would appear to leave a trail if she moved. On one
occasion she saw multiple images of the stimulus. The
after-images were always isochromatic to the stimulus,
and the size of the after-image was the same as that of the
stimulus, not expanding in proportion to the distance from
the surface on which it was projected. She denied using
medications or illicit drugs currently or previously.
Examination 6 months after the onset of her symptoms
showed that her best corrected visual acuities were 20/30
in the right eye and 20/25 in the left eye with normal color
vision (Ishihara), full visual fields, and normal fundi. Her
neurologic examination showed no abnormalities.
Patient 5. A 42-year-old healthy man with a negative
psychiatric and neurologic history whose only eye problem
had been congenital color blindness, had three 15-minute
episodes in which he hallucinated a wavy line. The hallucinations began in the right paracentral area and expanded to form a pattern of scintillating, concentric,
angulated lines. There were no headaches then or since.
After the third episode he saw colorless, pulsating dots in
the left inferior quadrant of his visual field that disappeared with eye closure. Evaluation by an ophthalmologist
856 NEUROLOGY 54

February (2 of 2) 2000

failed to demonstrate any abnormalities and the episodes
of wavy lines continued to occur several times a year.
At age 46 he became aware that he had abnormally
persistent after-images especially after awakening in the
morning. They would remain for several seconds and reproduce only a portion of the previous scene. Sometimes he
would see multiple after-images if he moved his eyes. The
size of the images expanded in proportion to the distance
from the surface against which it was projected. The images were black and white (“like a photographic negative”)
unless precipitated by a brightly colored stimulus, in
which case the colors were “reversed.” Wearing sunglasses
helped.
He denied using any medications or ever using illicit
drugs. A neurologic examination, several neuro-ophthalmologic examinations, and two CT scans of the brain failed to
demonstrate any abnormalities. Trials of phenytoin and propranolol therapy did not relieve the symptoms.
His uncorrected visual acuity at age 47 was 20/15 in
each eye. Visual fields were full and his fundi were normal.
When interviewed by telephone at age 63, 17 years after
onset, the patient reported that his symptoms were unchanged and that his general health had remained normal.
Patient 6. A 28-year-old woman whose previous psychiatric, neurologic, and ophthalmologic health had been
good developed daily, severe, throbbing left-side headaches. At the same time she started to have multiple visual disturbances. She saw numerous small bright lights
“moving like fireflies” whenever she went into a brightly lit
environment. In dim light she saw “snow—like watching a
television channel that isn’t broadcasting.” She also had
daily episodes in which she would see reduplications of
images (“like vibrations”). The headache improved but the
visual symptoms persisted. She denied using medications
or illicit drugs currently or in the past. A neurologic examination revealed no abnormalities.
Examination 6 months after onset showed that her uncorrected visual acuity was 20/15 in each eye with normal
color vision (Ishihara), full visual fields, and normal fundi.
During the next year the repetitive images appeared
with increasing frequency and a trial of therapy with phenytoin failed to help. Neuro-ophthalmologic and neurologic
examinations continued to give unremarkable results, and
no abnormalities were found on cranial CT and MRI. Neither Clonazepam nor carbamazepine therapy lessened the
symptoms.
Patient 7. A 28-year-old man whose only psychiatric,
ophthalmologic, or neurologic problem had been fully correctable myopia became aware of small brown spots in the
visual fields of both eyes and a throbbing, mild, left supraorbital headache. Shortly thereafter he noted additional visual symptoms. After prolonged gazing at a scene,
certain portions would disappear. In daylight he would see
images “like sparks or fireflies” and at night he would see
what resembled “particles of snow floating around.” He
also became aware of unusual after-images. When he
looked at something he would see several adjacent ghost
images. Sometimes an object at which he was looking
would reappear in another area of his visual field after a
short interval (figure 1).
He denied drug use or abuse. A retinal evaluation and
complete neurologic examination revealed no abnormalities. Cranial CT showed only that he had a smaller right

Figure 1. Patient 7. Patient’s sketch of
examples of abnormal images.
hemisphere. No abnormalities were seen on EEG. A trial
of phenytoin therapy did not prove helpful.
Examination at age 29 showed that his corrected visual
acuities were 20/15 in each eye with normal color vision
(Ishihara) and full visual fields. Slit-lamp inspection
showed normal anterior segments with clear media, and
his fundi were unremarkable. His only ophthalmic abnormality was ocular hypertension with applanation intraocular pressures of 23 mm Hg in the right eye and 22 mm Hg
in the left eye.
When he was reevaluated at the age of 35 he reported
that all of his symptoms had persisted. His findings on
examination were unchanged.
Patient 8. A 42-year-old man developed abnormal
after-images. During the initial episode, which occurred
while driving, he noticed that the headlights of passing
vehicles left a peculiar and prolonged “trail.” He stopped to
eat at a restaurant, and on redirecting his gaze from his
dinner plate to a window, he saw a clear and distinct
image of his French-fries fried potatoes superimposed on
the window. This experience caused him to drive home
immediately from Maine to Massachusetts in a panic. Similar episodes continued with increasing frequency. He described moving objects as leaving “a trail.” For seconds a
ghost image would follow a moving stimulus and would
merge with the stimulus when it stopped (figure 2). His
persistent or recurrent images were isochromatic to the
stimulus. He was most apt to notice the after-images if he
awakened in the middle of the night, when fatigued, after
having several alcoholic drinks, and on emerging into the

light from a movie theater. A neurologic examination and
cranial MRI gave normal results. An EEG showed left
temporal high-voltage theta activity during sleep deprivation and a generalized high-voltage burst during stage-two
sleep. This activity was interpreted as insignificant. His
medical history was notable for two episodes of depression
more than a decade earlier, which was treated successfully
with tricyclic antidepressants. He also had sleep apnea. Otherwise there was no history of neurologic or ophthalmologic
disease. The patient denied any prior abuse of any drugs.
Examination at age 43 showed that his visual acuities
were 20/15 in both eyes with normal color vision (Ishihara), fundi, and visual fields. When reevaluated 10
months later, the findings on examination were unchanged. His visual symptoms had persisted despite a
course of Clonazepam and carbamazepine therapy, and he
had developed a symptom in which sounds would sometimes briefly reverberate.
Patient 9. A 20-year-old previously healthy woman incurred brief loss of consciousness and a nondisplaced right
orbital fracture in a bicycle collision. No other clinical or
radiologic abnormalities were discovered at the time, and
she did not require surgery. Recovery was complete without evident residua. Her psychiatric, ophthalmologic, and
neurologic histories were otherwise negative. She denied
using illicit drugs currently or previously. Her only medication was a birth control pill. There was no pertinent
family history. At age 29 she developed new symptoms. At
night, illuminated areas appeared to have a purple hue.
She also noticed that after looking at a bright image she

Figure 2. Patient 8. Patient’s computerassisted drawing of a palinoptic image.
February (2 of 2) 2000

NEUROLOGY 54

857

would continue to see it for as long as at least 1 minute
after looking away. The duration of the after-image was
independent of the duration of gaze but was related to its
brightness. The after-image did not appear to change size
with the distance to the surface against which it was projected. Seven months later she noted additional symptoms.
Moving objects appeared to leave a trail or smear and she
would see repetitive images that she referred to as “echoes” of some moving objects. These symptoms were most
apt to intrude in the morning, and wearing sunglasses
reduced the frequency of the symptoms. Cranial MRI and
neurologic examination revealed no abnormalities.
Neuro-ophthalmologic examination 8 months after onset showed that her uncorrected visual acuities were 20/15
in each eye with normal color vision (Ishihara) and full
visual fields to the I4e on the Goldmann perimeter. Her
anterior segments, pupils, lids, eye movements, and fundi
were unremarkable. The patient refused trials of medications and no follow-up information is available.

Discussion. The following lists the circumstances
in which palinopsia and related positive visual phenomena have been encountered:
Causes and associations of palinopsia
Drugs
• Marijuana1,2
• Mescaline3
• Lysergic acid diethylamide1-3
• 3,4-Methylenedioxymethamphetamine4
• Interleukin 25
• Trazodone6
• Clomiphene citrate7
• Nefazodone8,9
Seizures
• Temporal10
• Occipital11,12
• Periodic lateralized epileptiform discharges13
Focal cerebral lesions
• Trauma14,15
• Parasite16
• Abscess17,18
• Stroke19,20
• Tumor19,21
• Arteriovenous malformation22,23
Creutzfeldt–Jakob disease24
MS25
Carbon monoxide poisoning26
Nonketotic hyperglycemia27
Migraine28
Psychiatric disease
• Schizophrenia29,30
• Psychotic depression31
• Charles Bonnet syndrome32
The assignment of patients among the various categories is somewhat arbitrary because there is overlap. For example, seizures undoubtedly are the
mechanism for the palinopsia in some of the cases of
focal cerebral lesions, and some of the patients with
858 NEUROLOGY 54

February (2 of 2) 2000

ictal palinopsia have a focal cerebral lesion. The patients whose histories form the basis of the current
report do not fit into any of these categories. To the
best of our knowledge palinopsia and related positive
visual phenomena have not been reported in healthy
persons or in patients with disease confined to the
eye or optic nerve. Bender et al.21 provide a very
limited description of a case in which a hypertensive
patient blind in one eye from an unspecified cause,
and with hypertensive retinopathy, developed palinopsia. The information that was provided about
that patient is insufficient to determine whether cerebral lesions might also have been present.
Three of our patients had subnormal visual acuities; two of them developed their symptoms shortly
after vision became impaired. Visual hallucinations
may be released when visual function is disrupted
(the Charles Bonnet syndrome), but only rarely do
those patients report palinopsia.32 None of the three
patients with impaired vision reported the imagery
that is characteristic of the Charles Bonnet syndrome;
namely, images unrelated to what the individual has
seen recently. Nevertheless, the symptoms might
have been precipitated by the loss of vision, especially because in two of them the symptoms developed when the vision was lost. Because the
remaining patients had normal visual function at the
time of their symptoms, some other mechanism
would have to be invoked.
None of our patients had evidence of lesions of the
cerebral hemispheres at the time of their symptoms.
One had the visual auras of migraine, but his symptoms did not occur with his migraines. Another patient had vascular headaches at the time her
palinopsia first appeared, but her symptoms persisted after her headaches resolved. One patient experienced palinopsia as she recovered from an attack
of optic neuritis, which was, in retrospect, the sentinel manifestation of MS. However, she had neither
clinical nor MRI evidence of cerebral involvement
then or later. MS tends not to cause symptoms of
higher visual dysfunction even when it ravages the
brain, but we are aware of the report of an MS patient with palinopsia.25 In that patient the symptoms
might have been residua of a prior bilateral optic
neuritis, but MRI results were not reported in that
patient. Our patient with “repetitive images” after
laser treatment of diabetic retinopathy later developed a stroke, and it is possible that there was cerebral ischemia that went undetected at the time that
she experienced her visual symptoms.
Although in one published case of palinopsia a
patient could read an unfamiliar eye chart at which
he had merely glanced when its image reappeared to
him after he had looked away, the symptom generally cannot be verified.14 Therefore it remains possible, but in our opinion unlikely, that our patients
fabricated their symptoms. Two of the patients were
or had been depressed, and another had found his
first attack of palinopsia a source of considerable
anxiety, but the symptoms presented in the others at

a time when they were healthy emotionally. In none
of the patients was secondary gain evident. There
have been several reports of palinopsia and related
positive visual phenomena developing or persisting
in individuals who abused drugs even after the drug
abuse had ceased.1,2 Although our patients denied
having abused drugs, we recognize that it would not
be unusual for patients to misrepresent their drug
history.
It is also possible that our patients noticed and
became fixated on physiologic after-images. However, in each patient the characteristics of the palinoptic images differed in some respect from
physiologic after-images. These differences included
multiple images on eye movement (Patient 5), multiple adjacent images (Patient 6), an interval between
the original stimulus and the appearance of the
after-image (Patient 7), trailing of the after-image
(Patients 4, 8, and 9), isochromatic images (Patients
1, 2, and 4), constancy of image size regardless of the
background (Patient 4), long duration (Patients 2
and 9), and seeing the images only with one eye
(Patient 3).
Palinopsia is a symptom about which physicians
are not apt to inquire and about which patients
might not complain, especially if the patient is neurologically healthy, not on drugs, and feeling well.
Patients with palinopsia might readily assume that
their after-images are physiologic, and there is indeed evidence that the characteristics of the “retinal”
after-image and those of palinoptic images overlap.13
In any case, it is likely that palinopsia and related
positive visual phenomena are more prevalent, both
in the healthy as a normal visual phenomenon as
well as in the ill, than would be inferred from the
paucity of reported patients. In light of our experience, it is clear that positive visual phenomena are
not necessarily a symptom of brain disease or drug
toxicity, or need have immediate or long-term consequences. However, the mechanism underlying the
symptoms in these patients remains obscure.
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Palinopsia and polyopia in the absence of drugs or cerebral disease
Howard D. Pomeranz and Simmons Lessell
Neurology 2000;54;855-859
DOI 10.1212/WNL.54.4.855
This information is current as of February 22, 2000
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