Palinopsia

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Palinopsia (Greek: palin for "again" and opsia for "seeing") is a visual disturbance defined as the persistent or recurrence of a visual image after the stimulus has been removed.[1] Palinopsia is not a diagnosis, but a broad term that describes a heterogeneous group of pathological visual symptoms with a wide variety of etiologies. Visual perseveration is synonymous with palinopsia.

In 2014, Gersztenkorn and Lee comprehensively reviewed all cases of palinopsia in the literature and subdivided it into two clinically relevant groups: illusory palinopsia and hallucinatory palinopsia.[2] Hallucinatory palinopsia, usually due to seizures or posterior cortical lesions, describes afterimages that are formed, long-lasting, and high resolution. Illusory palinopsia, usually due to migraines, head trauma, prescription drugs, or hallucinogen persisting perception disorder (HPPD), describes afterimages that are affected by ambient light and motion and are unformed, indistinct, or low resolution.

Differentiation from physiological afterimages[edit]

Palinopsia is a pathological symptom and should be distinguished from physiological afterimages, a common and benign phenomenon.[1][3][4] Physiological afterimages appear when viewing a bright stimulus and shifting visual focus. For example, after staring at a computer screen and looking away, a vague afterimage of the screen remains in the visual field. A stimulus consistently produces the same afterimage, which is dependent on the stimulus intensity and contrast, the time of fixation, and the retinal adaptation state. Physiological afterimages are usually the complementary color of the original stimulus (negative afterimage), while palinoptic afterimages are usually the same color as the original stimulus (positive afterimage). There is some ambiguity between illusory palinopsia and physiological afterimages since there are not concrete symptomatic criteria which determines if an afterimage is pathological.

Description[edit]

For more details on this topic, see Hallucinatory Palinopsia and Illusory Palinopsia.

Hallucinatory palinopsia is similar to a complex visual hallucination: the creation of a formed visual image where none exists. Hallucinatory palinopsia consists of formed, afterimages and scenes that are high-resolution, long-lasting, and occur unpredictably. These images or short scenes look realistic, with the same color, resolution, and clarity as the original stimulus. A common complaint is retaining the examiner’s fingers in the field of view, although palinopsia can occur with virtually any stimulus. The palinopsia usually lasts at least 15 seconds, but can persist for several hours or days. External parameters such as light, fixation, or motion do not typically affect the generation or appearance of hallucinatory palinopsia, implying that the objects, features, or scenes are already encoded in visual memory. Hallucinatory palinopsia can appear anywhere in the visual field regardless of the location of the original stimulus and often occurs in a visual field deficit.

Illusory palinopsia is likely due to sustained awareness of a stimulus and is similar to a visual illusion: the distorted perception of a real external stimulus. Illusory palinopsia consists of afterimages that are short-lived or unformed, occur in the same location in the visual field as the original stimulus, occur continuously or predictably, and are often exposed or exacerbated based on environmental parameters such as stimulus intensity, background contrast, fixation, and movement. Visual trailing is a common type of illusory palinopsia.

Associated symptoms[edit]

People with palinopsia frequently report other visual illusions and hallucinations such as photopsias, dysmetropsia (micropsia, macropsia, teleopsia, or pelopsia), Alice in Wonderland syndrome, visual snow, oscillopsia, entoptic phenomena, and cerebral polyopia.

Etiology and pathophysiology[edit]

For more details on this topic, see Hallucinatory Palinopsia and Illusory Palinopsia.

Posterior visual pathway cortical lesions (tumor,[1] abscess,[3] hemorrhage,[5] infarction,[1] arteriovenous malformation,[6] cortical dysplasia,[7] aneurysm[1]) and various seizure etiologies (hyperglycemia,[8] ion channel mutations,[9] Creutzfeldt-Jakob Disease,[10] idiopathic seizures,[11] etc.) cause focal cortical hyperactivity or hyperexcitability, resulting in inappropriate, persistent activation of a visual memory circuit. Of the cases of palinopsia from posterior cortical lesions or seizures, 93% described hallucinatory palinopsia.[2]

Illusory palinopsia is a dysfunction of visual perception, resulting from diffuse, persistent alterations in neuronal excitability that affect physiological mechanisms of light or motion perception. Of the cases of palinopsia that are idiopathic or attributed to migraines, HPPD, prescription drugs, or head trauma, 94% described illusory palinopsia.[2] Migraines and HPPD are probably the most common causes of palinopsia.[2] Trazodone,[12] nefazodone,[13] mirtazepine,[14] topiramate,[15] clomiphene,[16] oral contraceptives, and risperidone[17] have been reported to cause illusory palinopsia. A patient frequently has multiple types of illusory palinopsia, which represent dysfunctions in both light and motion perception. Light and motion are processed via different pathways, suggesting diffuse or global excitability alterations. Diffuse neuronal hyperexcitability could cause a pathological exaggeration of physiological light and motion perception mechanisms.

Clinical encounter[edit]

History[edit]

Palinopsia defines a heterogenous collection of symptoms and is not a diagnosis. Much prognostic information is provided by the clinical history. The examiner should determine if the symptom best describes hallucinatory palinopsia or illusory palinopsia, which involves inquiring about the content, length, and color of the persisting images or scenes, the time of day, the number of episodes, the location in the visual field of the original and perseverated images, and if light or motion exacerbates or exposes the palinopsia. It is important to take a careful neurological history as migraines, cerebrovascular accidents, visual seizures, and neoplasms can all cause palinopsia. The examiner should also ask about prescription drug use, head trauma, and hallucinogenic drug use.

Physical Exam[edit]

Palinopsia necessitates a proper ophthalmologic and neurologic physical exam to help alert the clinician to a possible serious etiology. However, the physical exam is often normal, especially with illusory palinopsia.

Work-up[edit]

Patients with palinopsia should have automated visual field testing. Homonymous field loss, unidirectional visual trails, or symptoms confined to part of a visual field suggests cortical pathology. Patients with hallucinatory palinopsia and patients with suspicious illusory symptoms (based on afterimage clarity, intensity, duration) should undergo neuroimaging. It is not unreasonable to order neuroimaging in regular illusory palinopsia, as migraine aura symptoms can occasionally mimic seizures or cortical lesions.[7] However, in a young patient without risk factors (vasculopathy, history of cancer, etc.) and no other worrisome symptoms or signs, neuroimaging for illusory palinopsia is low-yield but may grant the patient peace of mind. Due to the subjective nature of the symptoms and the lack of organic findings, clinicians may be dismissive of illusory palinopsia, sometimes causing the patient distress. There is considerable evidence in the literature confirming the symptom legitimacy, so validating the patient’s symptoms can help ease anxiety.[2]

Diagnosis and treatment[edit]

For more details on this topic, see Hallucinatory Palinopsia and Illusory Palinopsia.

It is generally easy to diagnose the underlying etiology of hallucinatory palinopsia. The medical history typically reveals concerning symptoms, and neuroimaging usually exposes cortical lesions. In patients with unremarkable neuroimaging, blood tests or clinical history often hints at the etiology, and visual seizures are at the top of the differential diagnosis. Hallucinatory palinopsia usually resolves after correcting the underlying disturbance. If no abnormalities are found, then the patient should receive further work-up or close follow-up.

In illusory palinopsia, the physical exam and work-up are almost always non-contributory and diagnosis is largely based on information from the clinical history. Palinopsia is attributed to a prescription drug if begin after drug initiation or dose increase. Palinopsia is attributed to head trauma if symptoms begin after the incident. Continuous illusory palinopsia in a migraineur is usually persistent visual aura. HPPD can occur any time after hallucinogen ingestion and is a diagnosis of exclusion in patients with a history of hallucinogen use. There is a lack of data on the treatment of the visual disturbances associated with HPPD, persistent visual aura, and head trauma, as well as idiopathic visual disturbances. Treatment is empirical and based on the patient’s distress and willingness to attempt different drugs. There are cases which report successful treatment with anti-epileptics and other drugs that reduce cortical excitability.[18][19] Sunglasses often improve symptoms, and FL-41 tinted lenses might provide additional relief.[20]

Overlap in hallucinatory and illusory palinopsia[edit]

There is some commonality in the two categories of palinopsia since the mechanisms of illusory palinopsia and hallucinatory palinopsia focus on a dysfunction of neuronal excitability and activity. The characteristics of each group are typical descriptions, not strict guidelines. For example, there is a report of a formed afterimage lasting 30–90 seconds but was more pronounced after fixation and with high contrast.[21] The clarity and duration of the perseverated images should be used as the predominant determining factors in determining the type of palinopsia. A small minority of cases also report illusory and hallucinatory palinopsia in a single patient.[2] The decision to order neuroimaging is the main clinical consideration when differentiating between illusory and hallucinatory palinopsia. Neuroimaging should be performed if there are any suspicious symptoms.

Future research[edit]

The mechanistic and symptomatic differences between hallucinatory palinopsia and illusory palinopsia could extrapolate to visual illusions and complex visual hallucinations, respectively. Hallucinatory palinopsia symptoms are usually transient and research is being directed to etiologies that cause the symptoms. There is hardly any data on treating illusory palinopsia, which is often continuous and distresses the patient. Research and funding is needed to study the efficacy of the various pharmaceuticals for treating illusory palinopsia. It is unclear if the symptoms' natural history and treatment are influenced by the etiology. It is also not clear if there is treatment efficacy overlap for illusory palinopsia and the other co-existing diffuse persistent illusory phenomenon such as visual snow, oscillopsia, dysmetropsia, and halos.[2]

Interestingly, the 10% of migraineurs with momentary, formed image perseveration report significantly fewer migraine headaches than migraineurs without these afterimages (4.3 vs. 14.4 attackers/year).[22] Studying these momentary, formed afterimages, in relation to alterations in cortical excitability, could advance our understanding of migraine pathogenesis and mechanisms associated with encoding visual memory.[2]

Future advancements in fMRI could potentially further our understanding of hallucinatory palinopsia and visual memory. Increased accuracy in fMRI might also allow for the observation of subtle metabolic or perfusional changes in illusory palinopsia, without using radiation in CT scans or radioactive isotopes. Studying the psychophysics of light and motion perception could advance our understanding of illusory palinopsia, and vice versa. For example, incorporating patients with visual trailing into motion perception studies could advance our understanding of the mechanisms of visual stability and motion suppression during eye movements (e.g. saccadic suppression).

References[edit]

  1. ^ a b c d e Bender, MB; Feldman, M; Sobin, AJ (Jun 1968). "Palinopsia.". Brain : a journal of neurology 91 (2): 321–38. PMID 5721933. 
  2. ^ a b c d e f g h Gersztenkorn, D; Lee, AG (Jul 2, 2014). "Palinopsia revamped: A systematic review of the literature.". Survey of ophthalmology. PMID 25113609. 
  3. ^ a b Arnold, RW; Janis, B; Wellman, S; Crouch, E; Rosen, C (Jan–Mar 1999). "Palinopsia with bacterial brain abscess and Noonan syndrome.". Alaska medicine 41 (1): 3–7. PMID 10224677. 
  4. ^ Stagno, SJ; Gates, TJ (1991). "Palinopsia: a review of the literature.". Behavioural neurology 4 (2): 67–74. PMID 24487436. 
  5. ^ Hayashi, R; Shimizu, S; Watanabe, R; Katsumata, Y; Mimura, M (Mar 2002). "Palinopsia and perilesional hyperperfusion following subcortical hemorrhage.". Acta neurologica Scandinavica 105 (3): 228–31. PMID 11886369. 
  6. ^ Kupersmith, MJ; Berenstein, A; Nelson, PK; ApSimon, HT; Setton, A (Jan 1, 1999). "Visual symptoms with dural arteriovenous malformations draining into occipital veins.". Neurology 52 (1): 156–62. PMID 9921864. 
  7. ^ a b Ogunyemi, A; Adams, D (May 1998). "Migraine-like symptoms triggered by occipital lobe seizures: response to sumatriptan.". The Canadian journal of neurological sciences. Le journal canadien des sciences neurologiques 25 (2): 151–3. PMID 9604138. 
  8. ^ Michel, EM; Troost, BT (Aug 1980). "Palinopsia: cerebral localization with computed tomography.". Neurology 30 (8): 887–9. PMID 7191073. 
  9. ^ Engelsen, BA; Tzoulis, C; Karlsen, B; Lillebø, A; Laegreid, LM; Aasly, J; Zeviani, M; Bindoff, LA (Mar 2008). "POLG1 mutations cause a syndromic epilepsy with occipital lobe predilection.". Brain : a journal of neurology 131 (Pt 3): 818–28. PMID 18238797. 
  10. ^ Purvin, V; Bonnin, J; Goodman, J (Dec 1989). "Palinopsia as a presenting manifestation of Creutzfeldt-Jakob disease.". Journal of clinical neuro-ophthalmology 9 (4): 242–6; discussion 247–8. PMID 2531161. 
  11. ^ Ossola, M; Romani, A; Tavazzi, E; Pichiecchio, A; Galimberti, CA (May 2010). "Epileptic mechanisms in Charles Bonnet syndrome.". Epilepsy & behavior : E&B 18 (1-2): 119–22. PMID 20471325. 
  12. ^ Hughes, MS; Lessell, S (Mar 1990). "Trazodone-induced palinopsia.". Archives of ophthalmology 108 (3): 399–400. PMID 2310343. 
  13. ^ Faber, RA; Benzick, JM (Apr 2000). "Nafazodone-induced palinopsia.". Journal of clinical psychopharmacology 20 (2): 275–6. PMID 10770476. 
  14. ^ Ihde-Scholl, T; Jefferson, JW (May 2001). "Mitrazapine-associated palinopsia.". The Journal of clinical psychiatry 62 (5): 373. PMID 11411821. 
  15. ^ Fontenelle, LF (Spring 2008). "Topiramate-induced palinopsia.". The Journal of neuropsychiatry and clinical neurosciences 20 (2): 249–50. PMID 18451209. 
  16. ^ Purvin, VA (Apr 1995). "Visual disturbance secondary to clomiphene citrate.". Archives of ophthalmology 113 (4): 482–4. PMID 7710399. 
  17. ^ Lauterbach, EC; Abdelhamid, A; Annandale, JB (Jan 2000). "Posthallucinogen-like visual illusions (palinopsia) with risperidone in a patient without previous hallucinogen exposure: possible relation to serotonin 5HT2a receptor blockade.". Pharmacopsychiatry 33 (1): 38–41. PMID 10721882. 
  18. ^ Wang, YF; Fuh, JL; Chen, WT; Wang, SJ (Dec 2008). "The visual aura rating scale as an outcome predictor for persistent visual aura without infarction.". Cephalalgia : an international journal of headache 28 (12): 1298–304. PMID 18727635. 
  19. ^ Evans, RW; Aurora, SK (Mar 2012). "Migraine with persistent visual aura.". Headache 52 (3): 494–501. PMID 22404709. 
  20. ^ Wilkins, AJ; Patel, R; Adjamian, P; Evans, BJ (Nov 2002). "Tinted spectacles and visually sensitive migraine.". Cephalalgia : an international journal of headache 22 (9): 711–9. PMID 12421156. 
  21. ^ Cummings, JL; Syndulko, K; Goldberg, Z; Treiman, DM (Apr 1982). "Palinopsia reconsidered.". Neurology 32 (4): 444–7. PMID 7199671. 
  22. ^ Belcastro, V; Cupini, LM; Corbelli, I; Pieroni, A; D'Amore, C; Caproni, S; Gorgone, G; Ferlazzo, E; Di Palma, F; Sarchielli, P; Calabresi, P (Jul 2011). "Palinopsia in patients with migraine: a case-control study.". Cephalalgia : an international journal of headache 31 (9): 999–1004. PMID 21628437.