Thanks to our Aussie colleague Steve Leslie who commented on A Stroke of Genius, noting that this experience of rotated vision came up in a post on their Australian list recently, and relating an illuminating article about it: Reversal of Vision Metamorphopsia Clinical and Anatomical Characteristics. It is quite a remarkable article, meriting its own post, so let’s begin with the title of the paper itself.
The authors use “reversal of vision” to categorize any perceived visual rotation of an object (or more commonly the entire scene) through 1 to 180 degrees of space. You’ll recall from Part 1 that Christine Hung-Oak Lee, reported a 90 degree rotation of the visual scene, though several of the case reports in this article note the world turned upside down – strikingly an inverted cup of tea, the fluid improbably content to remain in its porcelain boundaries.
And what about the term “metamorphopsia”? We associate this with perceived distortion, usually associated with macular disease such as AMD that disturbs the retinal elements. But a good etymologist would break it down as: opsia = vision; morph = form; and meta = beyond, and that’s the way the authors intend it here. There is a reversal of visual form that occurs beyond the normal perception of things. So we know that it’s a central mechanism beyond the retinal level, whereas the more common metamorphopsias are the opsias in which objects change size (mic or macropsias) or are distorted. These visual changes are long-lasting, in contrast with the short duration visual inversions of form due to central visual disturbances at a level beyond the eyeballs (usually cortical), as depicted here:
The asymmetrical letters R in the right visual field and L in the left visual field are used to demonstrate the reversal of vision phenomenon. A, Reversal of vision in patient 1. Note the counterclockwise tilting of the left visual field and complete 180° reversal of vision of the right visual field. B, Reversal of vision in patient 4. Complete reversal of vision was interrupted by oblique clockwise vision metamorphopsia. C, Complete reversal of vision in the coronary plane in patients 2, 3, 5, and 6. D, Complete reversal of vision in the sagittal plane. E, Complete reversal of vision in the horizontal plane.
The six cases in the article that Steve Leslie shared, from the Neurology Department at Haddasah Hospital in Jerusalem, are summarized in their paper as follows:
Conjectures about the mechanisms of RVM through the literature review in this article are fascinating. Here is what the authors propose:
“The spatial representation of visual stimuli in the central nervous system is formed by combining information from various modalities, both retinal and extraretinal. To create a valid representation of space, a series of coordinate frame transformations is performed. Retinal inflow is combined with ocular position information to produce head-centered representation. To represent body-centered coordinates, the 7a parietal cortex and the intraparietal area have neurons that respond to the eye position as well as the head position. The relationship between the relevant representation of visual stimuli and RVM is based on world-centered coordinates (allocentric). Information about the position of the head derives from otolith and vestibular inputs together with proprioceptive information from neck muscles. These signals, when combined with eye and retinal position information, can encode locations in world-based coordinates. Experiments in rats typified “direction tuned” cells, the activity of which were modulated by the orientation of the whole body. These cells in the posterior parietal region are multimodal cells. They are activated by both visual and integral vestibular signals to form the representation of space. We know that this orientation system is widely distributed in the central nervous system. This might explain the various locations of insults causing RVM. It is clear that both retinal and extraretinal disturbances can bring about a mismatch of information that would lead to RVM. Any transient inconsistent correspondence of vestibular information or lack of information due to a brainstem lesion would potentially lead to RVM. In particular, a disturbance of the central otolith pathway that would deprive higher brain centers of necessary information about the head position in the roll plane, which is the plane relevant to the phenomenon of RVM in most patients. Distinct areas in the brainstem that mediate vestibular tone in the horizontal, vertical, and roll planes have recently been discovered. Dysfunction of these specific regions in the brainstem might lead to vestibular tone imbalance, and that in turn would induce RVM along 1 or more of the principal orthogonals.
In conclusion, failure to perceive space in an allocentric coordinate frame, particularly in the coronal roll plane, is potentially the critical event underlying RVM. Reversal of vision is always a transient visual illusion caused by either brainstem or parieto-occipital lesions. It is a pure disorder of far space perception that should be clearly differentiated from certain body scheme disorders and other types of visual metamorphopsia. The polymodal nature of the neuronal network that governs the perception of allocentric coordinates and their widespread distribution in the central nervous system might allow for a rapid recovery from RVM when correct and new information is processed.”