Visual Allesthesia is a rare misperception consisting of the visualization of an object, briefly exposed to view, whose resulting image is seen in one hemifield of vision while a duplicated image is viewed simultaneously in the opposite visual hemifield. It is the result of diverse medical or surgical conditions that cause disruption of the ventral visual stream. Surgical procedures that cause damage of that area should be avoided.

Keywords: misperception, stroke, epilepsy, release phenomenon, visual processing

Visual perceptual abnormalities, better defined as positive spontaneous visual phenomena (PSVP),¹ are occasionally encountered in various fields of medicine and may be caused by a variety of pathological conditions. PSVP may be expressed as illusions,^2,3 which are the distortion of a visual stimulus that is present in the external environment, or as hallucinations where a stimulus is perceived when in reality none is present.⁴ Other types of PSVPs include palinopsia^1–5 which consist in the persistence of a visual sensation after its visual stimulus has ceased, and metamorphopsia, where the view of the objective´s size and/or form is altered. Another quite exceptional form of PSVP is Visual Allesthesia (VA), a condition that differs from illusions and hallucinations, in that a visual stimulus, present in the environment, is not distorted but its image is transposed from one homonymous visual field to the opposite one^2,6–13 resulting in the duplication of the viewed image, a duplication that is spatially reversed from the original one. In simple terms, it consists in seen the same half of an apple twice. VA, which at first could be interpreted as an ophthalmological refractive pathology, appears to be the result of damage to the occipito-temporal subcortical white matter^14,15 due to diverse medical conditions,¹⁶ the most common of which is a right-sided, posterior stroke. In the realm of neurosurgery, VA has been rarely reported in cases of intra or extra-axial tumors located in that vicinity^17,18 or, as an exceptional postoperative complication.¹⁹ Such a postoperative case¹⁹ prompted the writing of this review.

Published VA cases in the literature were collected and additional ones were found by perusing their references list and through Google searches. All the cases gathered were tabulated and analyzed in order to find their commonality and extract well founded conclusions (Table 1).

Review of this data supports the concept that VA´s pathological basis resides in damage to the temporo-occipital white matter with disruption of the ventral visual stream. It also confirms the marked prevalence of the pathology´s location in the non-dominant hemisphere. The ventral visual stream is a pathway through which visual information about the object´s color, size and form is transmitted from the striate cortex to the inferior temporal lobe (Brodman areas 20,37 and 38) for its processing.^20–23 Further analysis of the Table raises attention to the frequent association of VA with palinopsia (52%) and with seizure activity (78%), an association that suggests an ictal basis for VA, as its physio-pathogenic mechanism. This is further supported by the beneficial effect that anticonvulsive medications have over VA and the exacerbation of VA that results from the discontinuation or reduction in this therapy dosage. Further analysis showed that although visual field defects are frequently associated with VA, these are not an indispensable VA accompaniment. Another surprising finding of this review was the rarity of neglect syndrome associated with VA, an association which should be expected considering the mostly non-dominant temporo-occipital location of VA´s cases.²⁴ This low frequency is more likely due to a lack of appropriate testing for neglect in the reported cases, rather than to a real scarcity of neglect symptoms in patients with this condition.²⁵ Although the ultimate cause of misperceptions is in general, is nebulous, various theories have been advanced to explain VA, with varying degrees of acceptance. Among these, the interhemispheric hypotheses model, which seems plausible, is based on two postulates: 1) It sustains that sensory information does not only reach the hemisphere contralateral to the stimulation but it would also reach, in some degree, the ipsilateral one, and 2) It supports the notion that, in normal brain functioning, the hemispheric locus contralateral to the stimulus will inhibit the activity of the ipsilateral one, possibly through callosal interhemispheric transmission. Should this be the case, the presence of a unilateral brain lesion disrupting the ventral visual stream would cause an imbalance that could result in VA²⁶ by:

1. Eliciting epileptogenic activity in the related cortical area.
2. by the biochemical and molecular changes induced in the deafferented neurons, that result in their hyperexcitability.²⁷
3. by shutting-off an inhibitory circuitry, leading to a focal cortical excitation i.e., a release phenomenon.²⁷

These hypothetical mechanisms strengthen Jacob´s hypothesis⁶ that sustains that the irritated temporo-occipital cortex in the affected hemisphere, could hijack visual information from the normal contralateral homologous locus, attracting it, via callosal interhemispheric conduit,²⁸ and resulting in the duplicated image seen in VA.

In clinical practice, the type of PSVP encountered seems to depend on the particular cortical area affected by the pathological process.²² For instance, electrical stimulation of the striate cortex (area 17) results in simple visual forms such as phosphenes, while stimulation of areas 18 and 19 evokes intermediate, more organized types of visual perceptions.^20,21 From a neurosurgical perspective, intra or extra-axial expansive lesions involving the parieto-temporal area may lead not only to neurological deficits but also to SPVPs by local pressure or tissue destruction.^17,18 Moreover, similar deficits can also be induced by damage incurred during cerebral resections for uncontrollable epilepsy or other surgical interventions, depending on the technique and the surgical approach undertaken.^19,29,30

Considering the age of the patient, (because the outlook for recovery of function seems to be better in the younger age group),³¹ the extent and location of the cortical and/or subcortical areas affected, and their inherent plasticity³² these sequelae, VA among them, may be permanent or recover in a major or minor degree.

Ongoing research is focused on the detection and decoding of the mechanisms involved in generating and/or stimulating neural plasticity along the optic pathways,³³ possibly leading to newer and better rehabilitation methods that may eventually result in a better prognosis for these patients.³⁴

VA occurs infrequently in clinical practice and it results from damage to the ventral visual stream circuit within the parietal white matter. Its prognosis depends on the extent of the neural damage and on the inherent plasticity of the tissues affected. To avoid this postoperative deficit, transcortical interventions through this area should be avoided.

The author wants to thank Ms. Elizabeth Gonzalez and to Mr. Gabriel Zepeda for their bibliographical support and to Ms. Camila Berner and to Mr. Samuel Abogabir for their technical assistance.

This article highlights a neurological symptom (VA) rarely encountered in clinical practice and its possible physio-pathological basis. Further-more it emphasizes the significant neurological deficits incurred by surgical interventions that disrupt the parieto-occipital subcortical white matter, some of them currently still being employed as an approach to the lateral ventricle. Such interventions should only be performed with the intraoperative assistance of diffusion tensor imaging and a frameless navigation system.³⁰

The author declares no conflicts of Interest to report for this work.

This research did not receive any specific grant from funding agencies in the public, commercial or not-for-profit sectors.

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