Optometry - Journal of the American Optometric Association
Volume 81, Issue 8 , Pages 394-404, August 2010

Palinopsia

  • Brian Abert, O.D.

      Affiliations

    • Vista Eye Care, Thornton, Colorado
    • Corresponding Author InformationCorresponding author: Brian Abert, O.D., Vista Eye Care, 4243 E. 136th St., Suite #342, Thornton, Colorado 80602.
    • ,
  • Pauline F. Ilsen, O.D.

      Affiliations

    • Department of Veterans Affairs Optometry, Los Angeles, California

Article Outline

Abstract 

Background

Palinopsia is a visual phenomenon that has been associated with brain neoplasia, epilepsy, trauma, systemic disease, psychiatric illness, and illicit as well as prescribed drug use. Despite some resemblance to diplopia, polyopia, and physiologic afterimage formation, palinopsia is actually a distinct entity often suggestive of disease through its distinct signs and symptoms. Careful patient history, visual field testing, and neuroimaging are among the tools used to diagnose palinopsia.

Case Reports

Four case reports of patients with palinopsia are presented. With the first patient, the palinopsia was associated with extensive lysergic acid diethylamide (LSD) use. The second patient's palinopsia was determined to be secondary to head trauma from a motor vehicle accident. The third patient began to experience palinopsia after he had been prescribed trazodone for insomnia. The fourth patient was found to have multiple potential etiologies. These 4 unique patients highlight the causes and management of palinopsia.

Conclusions

Optometrists should be aware of the symptoms of palinopsia to enable them to recognize this phenomenon and minimize the chance of misdiagnosis. Learning the physiologic mechanisms behind this uncommon disorder can help the clinician correctly identify its cause. Although palinopsia itself is not a disease, it is indicative of a disease, and the symptoms of palinopsia may be a manifestation of a serious underlying systemic dysfunction that could warrant treatment. In addition, identifying the symptoms of palinopsia can put patients at ease with regard to the often disturbing visual symptoms.

Keywords: Palinopsia, Visual perseveration, Visual hallucinations, After-images, Perceptual disorder, Polyopia

 

Palinopsia is a reoccurrence of visual perception after the stimulating object has been removed.1, 2, 3, 4, 5, 6, 7, 8, 9, 10 The term palinopsia, from the Greek word meaning again, was coined by Critchley in 1951.1, 11 Among the more common descriptions of the phenomenon are those of rapidly moving objects leaving visual echoes or cometlike trails or images following the viewer's direction of gaze12, 13, 14, 15, 16 as well as the symptom of “stroboscopic vision.”10 Palinoptic images may be of well-remembered objects or objects with some emotional significance to the patient, although any object has the potential to be visually recalled through this phenomenon.1 The term flashbulb memory, however, is not related to palinopsia and instead refers to the recollection of specific events assumed to be significant for the individual experiencing it.17

The strange nature of palinopsia is responsible for its being difficult to accurately diagnose. In 1968, Bender et al.2 stated that palinoptic images usually do not originate from objects viewed in the past; however, more recent literature has indicated the contrary. In fact, weeks may pass between the original visual stimulus and its reperception, and because the patient may not remember having seen the original stimulus, the phenomenon may be regarded incorrectly as a visual hallucination.6, 7 Bender et al.2 thought that palinopsia may be considered a type of visual hallucination or optical illusion, and Critchley1 also suggested that palinopsia might be hallucinatory in nature. Strictly speaking, however, palinopsia is not a hallucination because a hallucination is the “perception of an external stimulus without a source in the external world.”18 Palinopsia is more consistent with real visual impressions than it is with visual hallucinations.19 Kinsbourne and Warrington12 believed palinopsia to be an “enhancement” of normal afterimage formation, although this is generally not the accepted modern theory on palinoptic origination.

The terminology used to describe palinopsia has been somewhat contested in the literature, in no small part because of the variety of disciplines that are involved in the diagnosis and management of palinoptic patients. The term visual perseveration is common in the literature and was recognized by Bender et al.2 as an alternate term for palinopsia. This report describes both “palinopsia” and “visual perseveration” as the same phenomenon.

Four case reports of patients with palinopsia are presented. In the first case, the palinopsia is associated with a history of extensive lysergic acid diethylamide (LSD) use. The second patient's palinopsia was determined to be secondary to head trauma sustained in a motor vehicle accident. The third patient began to experience palinopsia after he had been prescribed trazodone for insomnia; the symptom abated when he stopped taking the drug. The fourth had multiple potential etiologies, as he had a history of LSD use, head trauma, and trazodone use. These 4 unique patients highlight the causes and management of palinopsia.

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Case reports 

Case 1 

A 53-year-old black man was referred by his primary care provider for a comprehensive eye examination to evaluate “progressive, insidious blurry vision…not acute.” The patient denied any history of ocular injury or surgery. He initially denied flashes of light and floaters but then articulated that he did get “flashes” of light in his vision, which he believed to be a consequence of past chronic lysergic acid diethylamide (LSD) abuse. He described the “flashes” of light as “a reel of film in slow motion” and stated that he perceived things moving “frame by frame” (see Figure 1). He reported that the phenomenon was infrequent, having experienced it twice in the preceding 6 months.

Medical history was significant for a stab wound to the chest 21 years prior resulting in a collapsed lung. When the patient was 29 years old, he was hit on the temple with a crowbar. No visual changes occurred after either of these incidents. The patient reported occasional headaches that were reduced with over-the-counter pain medications. No visual auras were associated with these headaches. In addition to the LSD use, the patient had a history of cocaine and alcohol abuse, though he reported being free from drugs and alcohol for 29 years. He also smoked 1 pack of cigarettes per day since he was 18 years old. Other medical problems included hypertension, which was poorly controlled because of noncompliance with his medication regimen. His medications included atenolol, felodipine, and terazosin.

The patient's visual acuity was corrected to 20/20 in each eye through a subjective refraction of -0.25-0.75 × 165 in the right eye and -0.25-1.00 × 010 in the left. He required a +2.00 diopters (D) add for near work. He had normal pupillary responses, no movement on cover testing, full versions, and no misses on finger counting confrontation visual field testing. Slit lamp biomicroscopy found mild blepharitis, corneal arcus, 1+ nuclear sclerotic cataracts, and 1+ cortical cataracts in both eyes (OU). Intraocular pressures were measured at 10 mmHg in the right eye (O.D.) and 11 mmHg in the left eye (O.S.) by Goldmann applanation tonometry (GAT). Dilated fundus examination found chorioretinal scars nasally and inferior-temporally O.S. and inferior-nasally O.D., with no choroidal rupture or macular disease noted in either eye. The patient also had white without pressure nasally O.D., a posterior vitreous detachment O.S., and cup-to-disc ratios of 0.3 O.D. and 0.25 O.S.

At the conclusion of his examination, spectacles were ordered, warm compresses were prescribed for lid hygiene, and retinal detachment precautions were explained with regard to the white without pressure. In reference to choroidal scarring, angiotensin-converting enzyme (ACE), rapid plasma reagin (RPR), and purified protein derivative (PPD) skin testing were obtained to rule out sarcoid, syphilis, and tuberculosis, respectively. No neuroimaging was ordered.

No further follow-up was possible with the patient: 3 months after his eye examination, he had metastatic colon cancer diagnosed. He underwent surgery to stop internal bleeding and lived the last month of his life in a coma.

Case 2 

A 28-year-old white man presented with a history of visual disturbances after a motor vehicle accident 4 years prior and a chief complaint of difficulty seeing up close for extended periods. Ocular history was also significant for an airbag inflation accident that had occurred several years earlier, when the patient was in the Marine Corps, resulting in a left eye hyphema. There was no history of ocular surgery.

The patient blamed his involvement in the motor vehicle accident on a history of blacking out while driving. He noticed “vision changes right after the accident” and previously had never experienced visual disturbances. The patient denied ever having had magnetic resonance imaging (MRI) before or after the accident.

The patient had a medical history of methamphetamine, marijuana, and alcohol abuse, though he denied ever having used LSD. He had been treated with several medications for his anxiety, depression (dating back to his teen years), symptoms related to post-traumatic stress disorder (PTSD), and a suicide attempt 4 years prior. Two years before his eye examination, he had been prescribed citalopram and fluoxetine. Use of these were discontinued less than 6 months after initiation, and he was then prescribed venlafaxine. At the time of his visit to our clinic, the patient denied taking any medications and claimed that he was not drinking or using illicit drugs.

At the examination, his entering uncorrected visual acuities were 20/20 O.D. and O.S. His subjective refraction was +1.00 dioptric sphere (DS) O.D. and O.S. He had normal pupillary responses, no movement on cover testing, full versions, no misses with confrontation visual field testing, and no misses on a reliable Humphrey FDT C-20-1 screening field. He showed a normal optokinetic nystagmus (OKN) reflex. The Farnsworth-Munsell D-15 color vision test was normal for each eye. Slit lamp biomicroscopy found no ptosis, clear corneas, and clear crystalline lenses OU. Corneal sensitivity appeared to be normal and symmetrical with cotton wisp testing based on observation of a blink reflex. Intraocular pressures were measured at 13 mmHg O.D. and O.S. (GAT). Dilated fundus examination found normal, healthy fundi O.D. and O.S., with cup-to-disc ratios of 0.35 O.D., O.S.

The patient was asked to elaborate on the visual phenomenon. He referred to the anomaly as “streamers” and found them particularly bothersome when driving at night or in the early morning (see Figure 2). He described these streamers as brightly colored opaque bands. The bands tended to form when the patient was near bright lights. The streamers typically had sharp edges and appeared in multiple copies. He described the light as “going and going and doubling back on itself.” The streamers were bright and usually the same color as the stimulus that triggered them.

The patient reported that he had to significantly alter his lifestyle to cope with the visual phenomenon. The patient moved himself and his family away from the city in an attempt to get away from bright city lights. He was advised to discontinue driving. The patient stated that he had given up driving because he did not feel safe behind the wheel with the visual phenomenon interfering with his perception of the road in the early morning, twilight, or at night. At the time of his eye examination, the patient reported that he still perceived the streamers and that he had not blacked out in several months.

The patient said that he was once scheduled for an MRI but never went to his appointment. The patient was unconcerned about the visual phenomenon, explaining that he had “gotten used to” it as part of his life. An MRI of the brain was recommended, but the patient declined. He was advised to return on an annual basis for a comprehensive eye examination or as needed if a new problem arose.

Case 3 

A 59-year-old white man presented with a history of palinopsia secondary to trazodone use with no visual complaints. His ocular history was significant for strabismus surgery at age 28. He reported that his “eyes turned outward” only when he was tired, and brief episodes of diplopia would resolve with blinking. His previous ocular history was significant for cataracts and stable macular drusen O.D. and O.S.

The patient had a medical history of hypertension, hyperlipidemia, trauma from a bicycle accident 21 years prior that resulted in an injury to his left shoulder, and a neck and shoulder injury after falling off a truck 9 years earlier. The patient had no history of seizures, although he had migraine headaches diagnosed when he was in his 20s. These migraines were found to be triggered by food sensitivities, and after learning to avoid certain packaged foods, the migraines resolved.

Ten years before his eye examination, the patient was prescribed trazodone, 100 mg for his insomnia, and paroxetine to improve his mood. Approximately 6 months after starting trazodone, the patient reported to his primary care physician that for 5 minutes he had perceived the same image “over and over again.” He noted that he had a slight headache in his right temporal region when the visual phenomenon began to occur. The patient explained that he was experiencing a great deal of pressure in his personal life at the time. Three days later, the patient reported to his physician that both of his eyes perceived “stop-action motion pictures,” and were leaving visual “trails” (see Figure 3). The patient had no headache or nausea and had migraine-equivalent visual aura diagnosed. A neurologist subsequently saw the patient to evaluate this symptom. Although the visual phenomenon did not bother the patient, he remained concerned about discovering the cause. MRI results were normal, finding “no evidence of cortical infarct and no evidence of microvascular ischemic disease. The occipital lobes are normal in appearance bilaterally.” The patient's trazodone was tapered down to 50 mg/day over 1 week and then discontinued in an attempt to establish it as the cause of his palinopsia. The symptom quickly resolved, and the patient was started on zolpidem for his insomnia. After several months taking zolpidem, the patient found that he preferred trazodone in spite of the visual symptoms because it afforded him better sleep than did zolpidem.

At the time of his most recent ocular evaluation, the patient was taking losartan, hydrochlorothiazide, amlodipine, atenolol, atorvastatin, allopurinol, omeprazole, magnesium chloride, potassium citrate, paroxetine, and trazodone 100 mg. He denied that he had ever used LSD, smoked cigarettes, consumed alcohol, or used illicit drugs.

Upon examination, he was found to have 20/20 best-corrected vision O.D. and O.S. through a subjective refraction of O.D.: -0.75-0.50 × 070, O.S.: -2.50-0.25 × 100. He had normal pupillary responses and full confrontation visual field testing. Cover test found an 8–prism diopter intermittent exotropia. Versions were full. Farnsworth-Munsell D-15 color vision testing found no abnormality. The OKN response was normal with the drum rotating in both directions. Biomicroscopy found clear corneas, nuclear sclerotic cataracts, and trace cortical spoking OU and no lid ptosis. Intraocular pressures were 12 mmHg O.D. and 14 mmHg O.S. (GAT). Dilated fundus examination found cup-to-disc ratios of 0.35 O.D. and O.S. and was otherwise unremarkable.

The patient was asked to elaborate further on the visual phenomenon. The episodes tended to last for about half an hour each morning. The phenomenon was stable, occurring daily upon exposure to bright light. The patient described seeing “translucent shades of gray,” which never contained color. To perceive them, relative movement needed to occur between him and an object. He often saw multiple, distinct copies of an image at the same time, which he described as resembling a slow-motion “strobe-type movie.” The patient found the symptom to be a curious occurrence and considered them an interesting and nonthreatening side effect of his medication.

He had palinopsia diagnosed secondary to trazodone use. No further investigation was warranted because the association with trazodone treatment was “challenged” by discontinuation and resumption of the medication, neuroimaging was normal, and the neurological evaluation was otherwise negative. Annual comprehensive eye examinations were advised.

Case 4 

A 57-year-old white man presented with a chief concern of distance blur. His ocular history was negative for injury, surgery, or disease. He also mentioned a 40-year history of perceiving “trailing images.”

The patient had a medical history significant for hypertension, depression, suicide attempts, and panic disorder, as well as polysubstance abuse. His history also included multiple head traumas; in his 20s, he had been involved in numerous fist fights, resulting in bilateral trauma to the temporal regions and in being “knocked unconscious” several times. Additionally, he received a left temporal injury during an ice skating accident. In another incident during his 20s, he was thrown from a horse, suffering an unspecified head injury. In his 30s, the patient was involved in an automobile accident and received an unspecified head injury. The patient explained that he had experienced painful nonthrobbing headaches for the last 15 years. No visual auras were associated with the headaches. There was no history of stroke or epilepsy. He had a recent history of alcohol, tobacco, and marijuana abuse. Crack cocaine, amphetamine, heroin, and LSD use were reported to all be in sustained remission. Medications included allopurinol, loratadine, trazodone 100 mg, hydrocodone/acetaminophen, lisinopril, mirtazapine, and amlodipine. Trazodone allowed him to get to sleep at night, although he reported nightmares secondary to its use.

Upon examination, the best-corrected visual acuity was determined to be 20/20 in each eye through a subjective refraction of O.D.: -0.50-0.50 × 105, OS: -0.75 DS. He had normal pupillary responses and no misses on a reliable Humphrey FDT C-20-1 screening field. Cover test found no heterotropia or phoria. Versions were noted to be full, and the OKN reflex was normal. No color deficiency was revealed with D-15 testing. Slit lamp biomicroscopy found no ptosis, clear corneas, and 1+ nuclear sclerotic cataracts OU. Corneal sensitivity was observed to be normal as tested with a cotton wisp. Intraocular pressures of 12 mmHg OU were measured by Goldmann applanation tonometry. Dilated fundoscopy found cup-to-disc ratios of 0.4 round O.D. and 0.45 obliquely inserted O.S. and was otherwise unremarkable.

Further history was obtained from the patient regarding his visual symptom. The patient first experienced what he referred to as “tracers” shortly after using LSD in his teens. The tracers occurred at all waking hours and in all fields of gaze. The tracers were seen when an object moved relative to its background. The result was full-color, translucent, cometlike trails that often produced a row of multiple distinct images of a brightness and intensity comparable with the original object. Occasionally, the tracers resembled a “movie, but slowed down.” The patient also described “beams of light” coming down from light bulbs and lamps, looking like haloes, and that when viewing parallel lines (a doorway, for instance) the 2 parallel walls comprising the doorway would change size in a teeter-totter fashion (see Figure 4). Because he had experienced the phenomenon constantly for 40 years, the patient indicated that his attitude toward the visual phenomenon was that of nonthreatened neutrality.

The report of an enhanced MRI of the brain that had been performed 3 years ago was reviewed. The MRI found a “small old lacunar infarct in the belly of the pons” and was otherwise normal.

The patient had palinopsia diagnosed. Because the symptom was longstanding and because the MRI was negative for neoplastic disease, no further investigation was pursued. It was concluded that the palinopsia was primarily related to the LSD use, because its onset preceded the head traumas and trazodone therapy but may have been exacerbated by the head traumas and trazodone. Annual eye examinations were recommended.

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Discussion 

Palinopsia is a symptom experienced by a variety of patients. Because its cause may be a life-threatening condition, discovering its source is of paramount importance. Understanding the accompanying signs and potential etiologies of palinopsia can greatly assist in diagnosis and efficient treatment of patients.

Characteristics of palinopsia 

Kinsbourne and Warrington12 reported a palinoptic patient who was irritated by bright light and glare from car headlights or sunshine as well as visual objects superimposed on actual objects. Jacome20 reported on a patient with objects appearing in the visual fields after viewing them and irritating flashes of light seen at night. Purvin21 reported that palinopsia may be exaggerated by moving from light to dark environments. Cummings et al.22 reported on a patient whose palinopsia was most likely to occur if the stimulus was brightly colored. Motion may be a factor in the formation of palinoptic images,2 and head shaking has been reported to aid in its termination.20

Michel and Troost8 suggested that palinopsia is always accompanied by a visual deficit, although symptoms of palinopsia have been reported with normal visual fields.1, 23, 24 More recent literature incorporating illicit and prescribed drug etiologies of palinopsia report that visual field defects are not seen in many drug-induced cases.3, 4, 21 Pomeranz and Lessel16 suggested that without accompanying cerebral disease, no visual field defects accompany palinopsia. Transient field defects in palinopsia were reported by Ardila et al.25 Homonymous field defects were found in 43 of 60 of Bynke's palinoptic patients,19 although that study group notably did not include patients experiencing palinopsia secondary to drug use. Johnson and Loge26 similarly found nearly all palinopsia cases to be associated with a homonymous field defect, though again, no cases of drug-included palinopsia were included in their analysis.

Interestingly, Michel and Troost8 described a palinoptic patient with normal standard perimetry (“normal” perimetry technique not specified) although with a subtle left homonymous field defect found using confrontation testing and a decreased optokinetic response. Occipital cortex hallucinations usually project to the contralateral visual field that is often the blind one, and lesions of the occipital cortex are known to produce visual phenomena.27

Palinopsia is frequently accompanied by similar reoccurring perceptual phenomenon. Recurrent somatosensory perceptions include perceiving a rough texture on a patient's arm hours after having actually touched a rough surface.22 Metamorphopsia, the alteration in the shape or form of an object as it is perceived, occasionally accompanies palinopsia.23

Palinopsia typically is transient, resolving in several days to several months28 but rarely more that a year.29 However, it is important to recognize that resolution of palinopsia is dependant on its root cause.

Differentiation of palinopsia from other visual phenomena 

To correctly understand its nature, palinopsia must be differentiated from benign physiologic afterimages with which it may initially be similar to in description. Classic, everyday afterimages are experienced when an intense stimulus results in an image being perceived during the first several seconds after the removal of the stimulus.12 Physiologic afterimages are a normal occurrence and are always present unless the subject is blind as a result of retinal or visual pathway disease.2 The intensity of physiologic afterimages increases during the first few seconds after removal of the stimulus and then gradually fades away and passes through a series of color changes.12 Pomeranz and Lessel16 concluded that because their patient experienced an extended duration of palinoptic images that did not gradually fade, a distinction between palinopsia and physiologic afterimages was made. Providing additional evidence, physiologic afterimages typically are negative, whereas palinoptic images are usually the same colors as the initial stimulus.2 Although palinopsia may resemble physiologic afterimages, they occur more readily and are of longer duration.12 Physiologic afterimages occur when a retinal stimulus bleaches photochemical pigments in the retina.30

In cases in which the delay between the initial stimulus and the palinoptic image amounts to long periods of time, it is unlikely that palinopsia is caused by physiologic afterimages, even though the 2 phenomena share some of the same features.6 If palinopsia is indeed related to physiologic afterimages, some pathology is responsible for lowering the threshold for afterimage formation,12 and accepting that palinopsia originates from physiologic afterimages does not help to explain its underlying mechanisms.19 Afterimages can be associated with activation of a distinct neural network,31 and localizing the cause of any visual phenomenon is thus the goal in the management of palinoptic patients.

Etiologies of palinopsia 

It is important to recognize that palinopsia is merely a symptom, and although usually not an isolated sign,2, 19 it can indeed occur in otherwise healthy patients.16 A great variety of etiologies has been associated with palinopsia (see Table 1). Palinopsia is strongly suggestive of toxic, metabolic, or neurologic pathway disease28 and Blythe et al.32 suggested that it is most accurate to recognize palinopsia as a symptom resulting specifically from neuronal mechanisms.32

Table 1. Etiologies of palinopsia
Systemic diseasePrescribed medicationsIllicit drugs

•Charles Bonnet syndrome22

•Cotard's syndrome55

•Creutzfeldt-Jakob disease10

•Depression53

•Head trauma12

•Human immunodeficiency virus53

•Huntington's chorea53

•Kartagener's syndrome37

•Leber's hereditary optic neuropathy16

•Leukemia39

•Mania53

•Migraine53

•Multiple sclerosis20

•Narcolepsy53

•Nonketotic hyperglycemia26

•Occipital lobe glioblastoma49

•Perilesional hyperperfusion51

•Picks disease53

•Post-traumatic stress disorder53

•Schizophrenia2, 53

•Sleep deprivation53


•Beta Blockers53

•Clomiphen citrate21

•Interleukin 2 therapy56

•Maprotiline61

•Mirtazapine15

•Nefazodone14

•Paroxetine withdrawal60

•Risperidone59

•Topiramate13, 57

•Trazodone4

•Zosuquidar58


•MDMA “ecstasy”63

•LSD53

•Marijuana53

•Phencyclidine53

Palinopsia secondary to brain lesions 

In many cases, palinopsia is a symptom of systemic disease,26 brain lesions,5, 6, 7, 8, 9, 33, 34, 35, 36, 37, 38 abscess,39 granulomata, or encephalitis2 that can be caused by a localized lesion, vascular disease, trauma,2, 11 or surgery.19 The occurrence of palinopsia in the absence of drug use or psychosis is almost always found to be secondary to a cerebral lesion.40

Killer and Buettner41 speculated that the majority of pseudohallucinosis might be explained by subtle brainstem lesions. Palinopsia is not known to result from lesions of the anterior half of the brain, retina, optic nerve, or the chiasm.2 Brain lesions responsible for palinoptic symptoms may be right sided, left sided, or bilateral.1 Because palinopsia is a visual occurrence, Michel and Troost8 assumed it to be generally caused by defective visual information processing in the occipital lobe, and it is known that right-sided lesions often result in visual disturbances, including difficulties with facial perception.42 Evans43 considered palinopsia to usually localize to the nondominant occipito-temporal cortex. Because of the constant visual input it receives, the occipital lobe is among the most active sites in the brain, making it especially vulnerable to injury by various lesions.44

Jacobs et al.45 reported that 12 of 14 palinoptic patients had lesions on the right side of their brains. Bender et al.2 found that 10 of their 12 patients had right-sided lesions, although there are many case reports of left-sided lesions in the literature as well. Palinopsia has been associated with lesions of the left occipital lobe,8, 28, 36, 37 right occipital lobe,7, 8, 9, 25, 34, 38 medial occipital lobe,46 right temporo-parieto-occipital region,6, 47 right occipito-temporal region,5 right temporal lobe,5, 24 right parieto-occipital,49 right parietal,11, 23, 48 and right temporal occipital lobes.49 Meadows and Munro5 agreed with Bender et al. in that palinoptic lesions are often right occipito-temporal in nature.

Methods of localizing lesions suspected of inducing palinopsia include computerized tomography (CT) and magnetic resonance imaging (MRI). However, palinopsia can occur in the presence of normal imaging.47 Normal imaging may be obtained even when the palinopsia presents with field loss.11 By cross-correlating a functional MRI time series with hallucination events, hallucinatory cerebral activity can be mapped into areas of increased activity, with affected areas defining the type of hallucinatory experience reported.50

Palinopsia associated with epileptic phenomena 

Palinopsia and metamorphopsia can occur as manifestations of epilepsy.23 Epilepsy is well known to be associated with palinopsia, and it is possible that seizures of the visual processing and memory centers of the brain might be the underlying cause of palinopsia. However, palinopsia can occur even at times when the patient is not having seizures.2 Correlating patient data is critical because epilepsy-induced palinopsia can also present with normal visual fields.24 Swash24 regarded vision abnormalities to be characteristic of temporal lobe epilepsy.

In addition to imaging methods, electroencephalography (EEG) has provided evidence of a posterior temporal lesion associated with palinopsia and epilepsy.24 Lefèbre and Kölmel6 reported that based on EEG findings, their patient's palinopsia was representative of temporo-parietal epileptic phenomena. In a study of epileptic patients, Engelsen et al.44 reported that 18 of 19 patients had EEG changes involving the occipital lobes, but only 11 of 17 patients had occipital changes that were visible with MRI. Critchley1 suggested that 2 of his reported cases appeared to be epilepsy related. When seizures are abated with anticonvulsant medication, all episodes of palinopsia also subside.45 Carbamazepine, traditionally used in anticonvulsive therapy, has also been found to reduce palinopsia in symptomatic patients.32, 47 Kupersmith et al.46 concluded that because carbamazepine was found to reduce palinopsia, seizure activity was responsible for the palinopsia. In addition, phenytoin has also been found to reduce palinopsia in symptomatic patients.9

Palinopsia may be a symptom of epilepsy, which itself is often a symptom of brain lesions. Kondziella and Maetzel49 reported a case in which a patient experienced palinopsia associated with epileptic seizures caused by an occipital lobe glioblastoma. Systemic disease can result in epilepsy, as seen in a patient with palinoptic symptoms, and seizures brought on by nonketotic hyperglycemia with measured glycosylated hemoglobin of 15.3%.26 Clearly, systemic disease must be considered when treating palinoptic patients.

Palinopsia associated with systemic disease 

Palinopsia has been reported to occur alongside a wide range of diseases. Diseases associated with palinopsia include Leber's hereditary optic neuropathy,16 perilesional hyperperfusion,51 loss of vision,16 nonketotic hyperglycemia,26 Kartagener's syndrome,37 Charles Bonnet syndrome,52 multiple sclerosis,20 and leukemia.39 In addition, visual hallucinations may occur in Alzheimer's disease, Picks disease, human immunodeficiency virus, Huntington's chorea, narcolepsy, and in patients who are sleep deprived.53

Interestingly, palinopsia was seen alongside the triad of spongiform change, neuronal loss, and astrocytosis characteristic of Creutzfeldt-Jakob disease (CJD).10 CJD is a rare neurodegenerative disease that belongs to the group of human spongiform encephalopathies, usually affecting elderly people.54

Palinopsia has been reported in association with head trauma. Kinsbourne and Warrington12 reported a palinoptic patient who had suffered a blow to his right forehead.

Migraine is the most common single cause of visual hallucinations and illusions,53 and palinopsia can be present either before or after a migraine attack.40 Distinguishing palinopsia from migrainous auras is challenging, although migraine patients often have a family history of headaches, and their aural hallucination may occur only several times weekly or monthly with accompanying headaches lasting hours to days.53

Palinopsia with psychiatric conditions 

Psychiatric conditions associated with palinopsia include mania, depression, and substance dependence.53 Psychiatric palinopsia is typically of a severe nature, and it is unlikely that palinoptic images are psychogenic.35

Palinoptic experiences may occur in schizophrenia.2, 53 Marneros and Korner29 reported a case of palinopsia in schizophrenia that was elicited most often when the patient was exhausted, thus linking palinopsia with the patient's specific mental state. Major depression, especially in the elderly, can present with hallucinations.53 Patients with PTSD can have illusions or hallucinations as well as delusional thoughts.53 Whether depression or PTSD makes a patient more susceptible to palinopsia is not known.

Cotard's syndrome is a psychiatric condition in which delusional patients believe themselves to be dead.55 Bilateral dysfunction of the intersections of the parietal, temporal and occipital lobes could be responsible for Cotard's syndrome as well as palinopsia.55

Prescribed drug use and palinopsia 

Commonly used ophthalmic medications are not known to specifically cause palinopsia, although topical eye medications, including atropinics and beta blockers, have the potential to cause visual hallucinations, particularly in the elderly.53

Palinopsia has been found to be brought on by a variety of prescribed medications. Interleukin 2 therapy has been associated with palinopsia.56 Topiramate, used in the treatment of migraine headaches, has a dose-related association with the elicitation of palinopsia.13, 57 Zosuquidar, an anticancer medication, has been found to result in occasional palinopsia.58 Nefazodone,14 mirtazapine,15 and trazodone4 have all been reported to cause palinopsia. Clomiphen citrate resulted in palinopsia that persisted for years after use of the drug.21

Palinopsia was reported to be associated with risperidone therapy, although this conclusion was drawn in a report of palinoptic symptoms occurring while the patient was simultaneously taking trazodone.59 Paroxetine withdrawal was found to induce palinopsia in one patient.60 Maprotiline has been reported in association with palinopsia, although those palinoptic symptoms may be an aura associated with the epilepsy that is already established as a side effect of maprotiline.61

Illicit drug use and palinopsia 

Patients with substance dependence often have perceptual abnormalities, and this is especially common in users of stimulants, cocaine, and hallucinogenics such as LSD, phencyclidine (PCP), and marijuana.53 In addition, visual hallucinations have been reported after cessation of cannabis use.62 3,4-Methylenedioxymethamphetamine (MDMA or “ecstasy”) caused palinopsia that persisted for 2 years but eventually resolved with fluoxetine treatment in a case reported by McGuire et al.63 Sunness suggested that in her young palinoptic patient an additive effect from several illicit drugs was the cause of palinopsia.64

The most common natural hallucinogens are psilocybin mushrooms and mescaline, and the most commonly abused synthetic hallucinogen is LSD.3 Approximately one fourth to one third of LSD users will experience some form of flashback phenomena.65 In a study of 123 prior LSD users, 44.3% experienced trailing phenomena.66 LSD exerts an inhibitory effect on the level of synaptic transmission in the brain.67 Patients often describe a “trailing phenomenon” or “motion picture frames” that remain frozen in space long enough to be perceived individually.66 Gaillard and Borruat62 concluded that LSD flashback phenomena rarely occur long after the last intake of LSD, although when it does occur, precipitating factors such as ethanol or medication use are often present. Among other precipitating factors, Kawasaki and Purvin3 found LSD flashbacks associated with anesthetized tooth extraction and prolonged hot bathing.

Trazodone and LSD both inhibit serotonin reuptake and interfere with the homeostasis of serotonin levels in the brain, although how the serotonin reuptake inhibitors are related to visual illusion has not been addressed.7

Potential physiologic mechanisms of palinopsia 

Palinopsia may be caused by damaged neural connections or drug stimulation that prevents inhibition of signals to the cerebral neural system.12 It may also be the result of disconnection between dedicated areas of visual association and visual memory.68

Medications that result in palinopsia provide valuable insight into the physiologic mechanism of the phenomenon. Nefazodone-induced palinopsia may owe its effects to serotonergic interaction.14 Animal experiments have found that trazodone inhibits the neuronal uptake of serotonin,4 although Fournier and Zackon11 claimed that a chemical mechanism for palinopsia related to serotonin reuptake inhibitors has not been demonstrated. Perhaps acting by an alternate method, topiramate is known to enhance gamma-aminobutyric acid responses and suppress high-frequency action potential firing.57

Curiously, Purvin21 believed clomiphene-induced palinopsia originated from retinal toxicity because of her patient's associated palinoptic precipitated by moving from dark to light environments. By contrast, Abraham66 interprets the dark to light environment emergence phenomenon to be related to a failure of an inhibitory system in the visual pathway.

Diagnostic investigation and management 

Although Critchley1 considered palinopsia to generally be rare, Bynke19 suggested that the phenomenon is more common than generally believed and pointed out that palinopsia is often mistakenly diagnosed as migraine. Ogunyemi and Adams38 reported on 2 patients experiencing palinopsia secondary to sumatriptan use that was incorrectly diagnosed as migraine with visual aura. Fournier and Zackon11 presented a patient who experienced palinopsia after a motor vehicle accident. This patient was initially considered to be malingering, although objective findings later indicated parietal lobe dysfunction. It is quite probable that if all cases of visual hallucinations were analyzed more carefully, palinopsia would be diagnosed more routinely.2

Smith47 suggested that palinopsia is probably underdiagnosed and that his patient might have had confusion rather than a localized neurologic disease. In fact, the symptom of palinopsia has been known for years, with its first mention in print by 19th-century French author Guy de Maupassant, who was thought to have personally experienced the phenomenon.69 Another reason that palinopsia may not be widely reported also stems from confusing terminology such as psychiatry's referring to palinoptic symptoms as afterimagery or visual flashbacks.3 Palinopsia is an unusual symptom with which many clinicians outside neurology may be unfamiliar.39 Treating palinoptic patients is challenging and often requires interaction from multiple disciplines including neurology, eye care, and psychiatry.41, 53

There is a relative lack of exposure among neurologists and eye care professionals to the long-term care of substance abusers, and these patients may be reluctant to seek out non–mental health professionals with regard to symptoms that are related to illegal drugs.3 Vaphiades et al.33 observed that patients with phosphenes, photopsia, and formed visual hallucinations often did not report their occurrence until specifically questioned and reassured about the normality of the phenomena in the setting of a disease state.33 Several of Lance's34 patients experienced fear of insanity when dealing with their palinoptic images. Patterson et al.39 described a patient who was reluctant to disclose his palinoptic symptoms fearing mental illness. It is thus important to recognize the signs and causative factors for palinopsia, and then to carefully elicit symptoms from the patients because they may be apprehensive, embarrassed, or confused about their symptoms.

Palinopsia is regarded by some as a “pseudohallucination,” and because the hallucinatory character of the phenomenon is evident to the patient, it therefore typically is not frightening.41 If not properly diagnosed, severe paranoia or anxiety may develop in a patient with no other significant psychiatric abnormalities.28 If an explanation is provided to the patient, the paranoia, agitation, and psychotic depression often will resolve.28 Critchley1 reported on a patient who presented with a small hemorrhage and raised blood pressure during a routine eye examination. Visual symptoms, including palinopsia, were later reported, and the patient eventually died from a right fronto-parietal hemorrhage and posterior parieto-occipital infarction.1 The strong association between palinopsia and neurologic drug effects, visual field loss, and brain lesions makes it a fascinating but nonetheless crucial symptom that necessitates investigation and management. Johnson and Loge's report26 of palinopsia secondary to high glycosylated hemoglobin dramatically illustrates how palinopsia can draw attention to dangerous systemic conditions.

Palinopsia is usually reported by patients with psychiatric or neurologic disorders or by current or former drug users,16 although it can be challenging to diagnose because it is associated with a great variety of factors. The key to accurate diagnosis lies in having a knowledgeable clinician elicit a comprehensive case history from the patient.

To begin with, a thorough inventory of medications, prescribed and illicit, is needed for any patient who is apparently experiencing hallucinations.53 Clinicians should ask specifically about LSD use in all patients with suspected palinopsia to prevent anxiety and excessive diagnostic testing.3, 64 Having the patient completely describe the actual experience in great detail may also assist in localization, differential diagnosis, and treatment.70 Because use of clomiphen citrate, an infertility drug, can rarely cause palinopsia, it is important to inquire specifically about a female palinoptic patient's use of infertility medications.21

Patients experiencing palinopsia may also describe their symptoms as double vision. It is important to consider a list of the differentials for double vision, which include vergence insufficiencies, supranuclear abnormalities, brainstem lesions, dysfunction of ocular motor nerves, neuromuscular junction problems, thyroid eye disease, displacement of the eye or eye muscle, and breakdown of a pre-existing strabismus.71 The examining clinician must recognize that a patient's reported symptom of palinopsia could be misinterpreted as monocular diplopia.5

Other differential diagnoses should include occipital lobe epilepsy, visual deprivation hallucinations, basilar migraine, psychotropic substances abuse, and various psychiatric conditions.49 In such patients, the use of simple tests such as bilateral simultaneous presentation of the examiner's hands or colored targets may detect more subtle deficits than are found by routine perimetry.8

Further investigation with CT, MRI, or EEG, and consultation with neurology or psychiatry would depend on the suspected associated condition.

There is some limited experience with treating symptoms of palinopsia with medications. A nonepileptic patient experienced reduced symptoms of palinopsia 48 hours after carbamazepine was initiated at 400 mg/day.72 Kupersmith et al.46 found that although carbamazepine reduced the intensity of palinopsia, the phenomenon was still brought on by exercising. Benzodiazepine and phenothiazine have been used with a high success rate to treat post-LSD flashbacks,66 and fluoxetine has been used to treat palinopsia caused by ecstasy use.63 Generally, antiepileptic drugs have shown the most promise in the treatment of palinopsia, and Silva et al.72 speculated that the antipalinoptic effect seen with anticonvulsive medications is probably similar in mechanism to its antiepileptic effect.

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Conclusions 

Palinopsia is an interesting occurrence, although its presence is hardly a triviality. Palinopsia is always indicative of some systemic dysfunction. It is important for the clinician to be aware of the benign causes of palinopsia seen in patients with certain drug histories or in patients taking certain prescribed medications. Occasionally, palinopsia is a symptom of undiagnosed neurologic disease, and thus knowing how to identify it as such can literally save a patient's life. Besides the more dramatic outcomes from the disease processes that are associated with palinopsia, those experiencing the symptom may be nervous about their condition and deserve to be reassured that what they experience is a documented, well-researched phenomenon.

In the setting of an optometric practice, it is always beneficial to be aware of disorders such as palinopsia so that they can be identified and managed. Palinopsia is rare, but there are indications that it is much more common than currently known. Those experiencing palinopsia often are reluctant to bring their rather disturbing symptoms to the attention of the person examining them, thus placing the charge on the clinician to recognize associated factors and to ask the correct questions of the patient.

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PII: S1529-1839(10)00257-5

doi:10.1016/j.optm.2009.12.010

Optometry - Journal of the American Optometric Association
Volume 81, Issue 8 , Pages 394-404, August 2010

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