Cerebral polyopia

Last updated July 06, 2021

Cerebral diplopia or polyopia describes seeing two or more images arranged in ordered rows, columns, or diagonals after fixation on a stimulus.^[1]^[2] The polyopic images occur monocular bilaterally (one eye open on both sides) and binocularly (both eyes open), differentiating it from ocular diplopia or polyopia. The number of duplicated images can range from one to hundreds. Some patients report difficulty in distinguishing the replicated images from the real images, while others report that the false images differ in size, intensity, or color.^[1] Cerebral polyopia is sometimes confused with palinopsia (visual trailing), in which multiple images appear while watching an object.^[3] However, in cerebral polyopia, the duplicated images are of a stationary object which are perceived even after the object is removed from the visual field.^[3] Movement of the original object causes all of the duplicated images to move, or the polyopic images disappear during motion.^[4] In palinoptic polyopia, movement causes each polyopic image to leave an image in its wake, creating hundreds of persistent images (entomopia).^[4]^[5]

Infarctions, tumors, multiple sclerosis, trauma, encephalitis, migraines, and seizures have been reported to cause cerebral polyopia.^[1]^[6] Cerebral polyopia has been reported in extrastriate visual cortex lesions, which is important for detecting motion, orientation, and direction.^[1] Cerebral polyopia often occurs in homonymous field deficits,^[7] suggesting deafferentation hyperexcitability could be a possible mechanism, similar to visual release hallucinations (Charles Bonnet syndrome).

Presentation

Cerebral polyopia is most often associated with occipital or temporal lobe lesions, as well as occipital lobe epilepsy. This condition is relatively uncommon, thus further research regarding its causes and mechanism has not been performed. Polyopia can be experienced as partial second or multiple images to either side (or in any eccentricity) of an object at fixation.^[8] Polyopia occurs when both eyes are open, or when one eye is open, during fixation on a stimulus. Known cases of polyopia provide evidence that, in relation to the stimulus at fixation, multiple images can appear at a constant distance in any direction; gaps in portions of an object at fixation can exist; multiple images can be overlaid vertically, horizontally, or diagonally on top of the stimulus; and the multiple images can appear different sizes, alignments, and complexities.^[8] The complexity of the stimulus does not appear to affect the clarity of the multiple images.^[3] The physical distance of the stimulus from the patient (near or far) also does not seem to affect the presence of multiple images.^[7] However, if the stimulus is swung or moved, multiple images of that object can either be extinguished or transformed into different objects, depending on the severity of the condition.^[3]

The onset of polyopia is not immediate upon perception of visual stimuli; rather, it occurs within milliseconds to seconds of fixation upon a stimulus.^[8] Polyopia has been described by patients as images “suddenly multiplying.”^[8] These multiple images can drift, fade, and disappear, depending on the severity of the condition. These episodes of polyopia can last from seconds to hours. In one specific case, a patient described difficulties reading due to letters “run[ning] together” and momentarily disappearing.^[8]

Most cases of polyopia are accompanied by another neurological condition. Polyopia is often accompanied by visual field defects (such as the presence of a scotoma) or transient visual hallucinations.^[2] Polyopic images often form in the direction and position of such visual field defects.^[2] Current research shows that when stimuli are close to the patient’s scotoma, the latency of polyopic images is much shorter than if the stimuli was far from the scotoma, and there is a higher probability that polyopic images will result.^[2]

Causes

Though there is no clear cause of cerebral polyopia, many cases show associations with occipital or temporal lobe lesions.^[3] Most cases of polyopia occur when there are bilateral lesions to occipital or temporal cortex, however some cases are present with unilateral lesions.^[2] Thus, polyopia can result from any kind of infarction to the occipital or temporal lobes, though the exact mechanism remains unclear. Some cases have shown that polyopia is experienced when the infarctions were seen to be at the tips and outer surfaces of the occipital lobes.^[8] By contrast, some patients experience cerebral polyopia associated with headaches and migraines in the frontotemporal lobe.

The mechanism of infarction differs by patient, but polyopia is experienced most commonly in patients that suffer from epilepsy in the occipital cortex, or in patients who suffer from cerebral strokes.^[8] In cases of epilepsy, polyopia is often experienced alongside palinopsia as these two conditions share an epileptic mechanism.^[3]

Theories of Cerebral polyopia

The preliminary theory of cerebral polyopia proposed by Bender postulated that polyopia occurs as a result of instability of fixation due to occipital lobe disease.^[8] Under this explanation, small, involuntary eye movements that accompanied normal fixation were the cause of polyopic images. These involuntary eye movements lead to the development of new retinal and corresponding cortical regions that code for central vision called false maculae.^[2] Thus, polyopic images resulted from the stimulation of both the original and acquired maculae.

However, Bender’s theory does not account for recent studies in which fixation did not change and no eye movements were produced while polyopia was experienced, therefore polyopic images were not a result of involuntary eye movements.^[2] Instead, Cornblath offers a possible pathophysiological mechanism in which polyopia results from the recoding of visual receptive fields in primary visual cortex (Area V1).^[2] The report of polyopic images of complex objects at fixation suggests that the disorder is not limited to lower-order visual areas in occipital cortex (in which simple features such as borders and angles are encoded), but rather it involves the interaction between lower-order visual areas in the occipital lobe and higher-order visual areas in the temporal lobe that is postulated to code whole objects.^[2]

Another possible pathophysiological mechanism for this disorder is the reorganization of receptive fields of neurons close to the damaged area of visual cortex.^[2] This theory is supported by findings that parafoveal retinal lesions deprive a region of striate cortex of visual input, and as a result, the receptive fields of neurons near the boundary of the deprived cortical region enlarge and expand into nearby regions of the visual field.^[2] Thus, polyopia results from altered coding of contour information by neurons near the lesioned area.^[2] This mechanism offers that after a focal lesion of neurons in striate cortex, or following a retinal lesion depriving these neurons of visual input, the receptive fields of nearby healthy neurons converge to code information about contours of objects normally coded by the damaged neurons while still coding the same information about retinal location prior to the injury.^[2] This mechanism may explain why polyopia extending into a patient’s scotoma occurs following damage to primary visual cortex.^[2]

Treatment

Since this condition is usually coupled with other neurological disorders or deficits, there is no known cure for cerebral polyopia. However, measures can be taken to reduce the effects of associated disorders, which have proven to reduce the effects of polyopia. In a case of occipital lobe epilepsy, the patient experienced polyopia. Following administration of valproate sodium to reduce headaches, the patient’s polyopia was reduced to palinopsia. Further, after administering the anticonvulsant drug Gabapentin in addition to valproate sodium, the effects of palinopsia were decreased, as visual perseveration is suppressed by this anticonvulsant drug.^[3] Thus, in cases of epilepsy, anticonvulsant drugs may prove to reduce the effects of polyopia and palinopsia, a topic of which should be further studied.

In other cases of polyopia, it is necessary to determine all other present visual disturbances before attempting treatment. Neurological imaging can be performed to determine if there are present occipital or temporal lobe infarctions that may be causing the polyopia. CT scans are relatively insensitive to the presence of cerebral lesions, so other neurological imaging such as PET and MRI may be performed. The presence of seizures and epilepsy may also be assessed through EEG. In addition, motor visual function should be assessed through examination of pupillary reactions, ocular motility, optokinetic nystagmus, slit-lamp examination, visual field examination, visual acuity, stereo vision, bimicroscopic examination, and funduscopic examination.^[2]^[8] Once the performance of such functions have been assessed, a plan for treatment can follow accordingly. Further research should be conducted to determine if the treatment of associated neurological disturbances can reduce the effects of polyopia.

Related Research Articles

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The visual cortex of the brain is the area of the cerebral cortex that processes visual information. It is located in the occipital lobe. Sensory input originating from the eyes travels through the lateral geniculate nucleus in the thalamus and then reaches the visual cortex. The area of the visual cortex that receives the sensory input from the lateral geniculate nucleus is the primary visual cortex, also known as visual area 1 (V1), Brodmann area 17, or the striate cortex. The extrastriate areas consist of visual areas 2, 3, 4, and 5.

Micropsia is a condition affecting human visual perception in which objects are perceived to be smaller than they actually are. Micropsia can be caused by optical factors, by distortion of images in the eye, by changes in the brain, and from psychological factors. Dissociative phenomena are linked with micropsia, which may be the result of brain-lateralization disturbance.

The occipital lobe is one of the four major lobes of the cerebral cortex in the brain of mammals. The name derives from its position at the back of the head, from the Latin ob, behind, and caput, the head.

The visual field is the "spatial array of visual sensations available to observation in introspectionist psychological experiments". Or simply, visual field can be defined as the entire area that can be seen when an eye is fixed straight at a point.

Visual memory describes the relationship between perceptual processing and the encoding, storage and retrieval of the resulting neural representations. Visual memory occurs over a broad time range spanning from eye movements to years in order to visually navigate to a previously visited location. Visual memory is a form of memory which preserves some characteristics of our senses pertaining to visual experience. We are able to place in memory visual information which resembles objects, places, animals or people in a mental image. The experience of visual memory is also referred to as the mind's eye through which we can retrieve from our memory a mental image of original objects, places, animals or people. Visual memory is one of several cognitive systems, which are all interconnected parts that combine to form the human memory. Types of palinopsia, the persistence or recurrence of a visual image after the stimulus has been removed, is a dysfunction of visual memory.

Palinopsia is the persistent recurrence of a visual image after the stimulus has been removed. Palinopsia is not a diagnosis, it is a diverse group of pathological visual symptoms with a wide variety of causes. Visual perseveration is synonymous with palinopsia.

An aura is a perceptual disturbance experienced by some with epilepsy or migraine. An epileptic aura is in fact a seizure.

Cortical blindness is the total or partial loss of vision in a normal-appearing eye caused by damage to the brain's occipital cortex. Cortical blindness can be acquired or congenital, and may also be transient in certain instances. Acquired cortical blindness is most often caused by loss of blood flow to the occipital cortex from either unilateral or bilateral posterior cerebral artery blockage and by cardiac surgery. In most cases, the complete loss of vision is not permanent and the patient may recover some of their vision. Congenital cortical blindness is most often caused by perinatal ischemic stroke, encephalitis, and meningitis. Rarely, a patient with acquired cortical blindness may have little or no insight that they have lost vision, a phenomenon known as Anton–Babinski syndrome.

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Akinetopsia, also known as cerebral akinetopsia or motion blindness, is a rare neuropsychological disorder, affecting 1 to 2% of global population, in which a patient cannot perceive motion in their visual field, despite being able to see stationary objects without issue. There are varying degrees of akinetopsia: from seeing motion as frames of a cinema reel to an inability to discriminate any motion. There is currently no effective treatment or cure for akinetopsia.

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Homonymous hemianopsia Visual field loss on the left or right side of the vertical midline

Hemianopsia, or hemianopia, is a visual field loss on the left or right side of the vertical midline. It can affect one eye but usually affects both eyes.

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Hallucinatory palinopsia is a subtype of palinopsia, a visual disturbance defined as the persistent or recurrence of a visual image after the stimulus has been removed. Palinopsia is a broad term describing a group of symptoms which is divided into hallucinatory palinopsia and illusory palinopsia. Hallucinatory palinopsia refers to the projection of an already-encoded visual memory and is similar to a complex visual hallucination: the creation of a formed visual image where none exists.

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References

1 2 3 4 Jones, MR; Waggoner, R; Hoyt, WF (Mar 1999). "Cerebral polyopia with extrastriate quadrantanopia: report of a case with magnetic resonance documentation of V2/V3 cortical infarction". Journal of Neuro-Ophthalmology. 19 (1): 1–6. doi:10.1097/00041327-199903000-00001. PMID 10098539.
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 Cornblath, W. T.; Butter, C. M.; Barnes, L. L.; Hasselbach, M. M. (1998-12-01). "Spatial characteristics of cerebral polyopia: a case study". Vision Research. 38 (24): 3965–3978. doi: 10.1016/s0042-6989(97)00431-8 . ISSN 0042-6989. PMID 10211388.
1 2 3 4 5 6 7 Kataoka, Hiroshi; Ueno, Satoshi (2009-04-01). "Cerebral polyopia and palinopsia in a patient with occipital lobe epilepsy". Epilepsy & Behavior. 14 (4): 684–686. doi:10.1016/j.yebeh.2009.01.026. ISSN 1525-5069. PMID 19435573.
1 2 Gersztenkorn, D; Lee, AG (Jul 2, 2014). "Palinopsia revamped: A systematic review of the literature". Survey of Ophthalmology. 60: 1–35. doi:10.1016/j.survophthal.2014.06.003. PMID 25113609.
↑ Lopez, JR; Adornato, BT; Hoyt, WF (Oct 1993). "'Entomopia': a remarkable case of cerebral polyopia". Neurology. 43 (10): 2145–6. doi:10.1212/wnl.43.10.2145. PMID 8413985.
↑ Zakaria, A; Lalani, I; Belorgey, L; Jay Foreman, P (Dec 2006). "Focal occipital seizures with cerebral polyopia". Epileptic Disorders. 8 (4): 295–7. PMID 17150444.
↑ BENDER, MB; SOBIN, AJ (1963). "POLYOPIA AND PALINOPIA IN HOMONYMOUS FIELDS OF VISION". Transactions of the American Neurological Association. 88: 56–9. PMID 14272268.
1 2 3 4 5 6 7 8 9 Safran, A. B.; Kline, L. B.; Glaser, J. S.; Daroff, R. B. (1981-10-01). "Television-induced formed visual hallucinations and cerebral diplopia". British Journal of Ophthalmology. 65 (10): 707–711. doi:10.1136/bjo.65.10.707. ISSN 1468-2079. PMC 1039643 . PMID 7317323.

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[Jones-1] 1 2 3 4 Jones, MR; Waggoner, R; Hoyt, WF (Mar 1999). "Cerebral polyopia with extrastriate quadrantanopia: report of a case with magnetic resonance documentation of V2/V3 cortical infarction". Journal of Neuro-Ophthalmology. 19 (1): 1–6. doi:10.1097/00041327-199903000-00001. PMID 10098539.

[:0-2] 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 Cornblath, W. T.; Butter, C. M.; Barnes, L. L.; Hasselbach, M. M. (1998-12-01). "Spatial characteristics of cerebral polyopia: a case study". Vision Research. 38 (24): 3965–3978. doi: 10.1016/s0042-6989(97)00431-8 . ISSN 0042-6989. PMID 10211388.

[:1-3] 1 2 3 4 5 6 7 Kataoka, Hiroshi; Ueno, Satoshi (2009-04-01). "Cerebral polyopia and palinopsia in a patient with occipital lobe epilepsy". Epilepsy & Behavior. 14 (4): 684–686. doi:10.1016/j.yebeh.2009.01.026. ISSN 1525-5069. PMID 19435573.

[Gersztenkorn-4] 1 2 Gersztenkorn, D; Lee, AG (Jul 2, 2014). "Palinopsia revamped: A systematic review of the literature". Survey of Ophthalmology. 60: 1–35. doi:10.1016/j.survophthal.2014.06.003. PMID 25113609.

[5] Lopez, JR; Adornato, BT; Hoyt, WF (Oct 1993). "'Entomopia': a remarkable case of cerebral polyopia". Neurology. 43 (10): 2145–6. doi:10.1212/wnl.43.10.2145. PMID 8413985.

[6] Zakaria, A; Lalani, I; Belorgey, L; Jay Foreman, P (Dec 2006). "Focal occipital seizures with cerebral polyopia". Epileptic Disorders. 8 (4): 295–7. PMID 17150444.

[7] BENDER, MB; SOBIN, AJ (1963). "POLYOPIA AND PALINOPIA IN HOMONYMOUS FIELDS OF VISION". Transactions of the American Neurological Association. 88: 56–9. PMID 14272268.

[:2-8] 1 2 3 4 5 6 7 8 9 Safran, A. B.; Kline, L. B.; Glaser, J. S.; Daroff, R. B. (1981-10-01). "Television-induced formed visual hallucinations and cerebral diplopia". British Journal of Ophthalmology. 65 (10): 707–711. doi:10.1136/bjo.65.10.707. ISSN 1468-2079. PMC 1039643 . PMID 7317323.

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