Now you see me: Akinetopsia
- academicmemories
- Apr 1
- 7 min read
Magdalene Dochnal
The ability to perceive motion is essential in a myriad of everyday situations from knowing when it is safe to cross the street to making a cup of coffee. Part of the appeal of stop-motion films like Fantastic Mr. Fox (2009) is that they disrupt our visual system’s preference for smooth, fluid motion. But what if your perception of motion actually resembled such stop-motion cinematography? What if you were unable to perceive motion? This condition is called akinetopsia, or motion blindness (Kumar & Wroten, 2024). It falls under a category of conditions called visual agnosias: deficits in visual perception that arise not from any abnormalities in the eye like near- or farsightedness, but in the visual areas of the brain (Kumar & Wroten, 2024). Though exceptionally rare, akinetopsia’s effects can be debilitating, and understanding how the condition arises and exploring the lived experiences of those with akinetopsia can provide great insight into how the structure of the visual system informs its function.
Background
The visual system can be thought of as being organized into modules that each perform specialized computations which, when synthesized, provide us with a rich picture of what our environment looks like. The middle temporal visual area (area MT) in the extrastriate cortex is the module responsible for processing information about motion (Born & Bradley, 2005; Dubner & Zeki, 1971). This is partially accomplished via directional selectivity: neurons selectively firing for preferred directions of motion (Hotson et al., 1994; Zeki & Dunbar, 1971). This tuning can either be broad, meaning the neuron still fires at baseline levels when a stimulus is not moving in its preferred direction, or the directional tuning can be fine, meaning activity is inhibited when a stimulus is not moving in a neuron’s preferred direction (Born & Bradley, 2005). Neurons in area MT are also tuned for the speed of a stimulus, its size, its position on the retina, and binocular disparity, the difference in a stimulus’ position on the retina of each eye (Born & Bradley, 2005; Lagae et al., 1993; Liu & Newsome, 2005). Synthesizing data from each of these properties allows us to make important judgments, such as how fast a car is moving or in what direction a ball is being thrown.
Experiencing akinetopsia
Akinetopsia occurs as a result of damage to or downregulation of area MT cells. The kind of neuronal damage that causes akinetopsia can occur in many ways. Across 12 reported cases, common causes included: stroke (Blanke et al., 2003; Cooper et al., 2012; Heutink et al., 2019), epilepsy (Blanke et al., 2002; Maeda et al., 2019; Sakurai et al., 2013), Alzheimer’s disease (Cárdenas-Belaunzarán & Cerrillo-Avila, 2024; Pelak & Hoyt, 2005; Tsai & Mendez, 2009), Parkinson’s disease (Sasaki et al., 2022), traumatic brain injury (TBI; Pelak & Hoyt, 2005), and drug toxicity (Horton & Trobe, 1999). Other visual agnosias like achromatopsia (cortical color-blindness) or prosopagnosia (face blindness) arise from similar damage to cells in their function’s respective visual system modules (Kumar & Wroten, 2024).
The lived experiences of those with akinetopsia can vary greatly, and the factors that contribute to that variance are still largely unknown. In the most extreme cases of the condition, all objects are invisible to the viewer when they are moving, especially at high velocities or in environments with high degrees of visual noise (Blanke et al., 2002; Heutink et al., 2019; Rizzo et al., 1995; Zihl et al., 1983; Zihl & Heywood, 2015). A more common clinical presentation in case reports is cinematographic akinetopsia, where objects in motion are experienced in a series of freeze-frames or trailing images that collapse on each other as objects come to a stop (Horton & Trobe, 1999; Sakurai et al., 2013; Viscardi et al., 2024). Because area MT cells are selective for direction, some patients only experience motion blindness when an object is moving in a particular direction (Blanke et al., 2002). This presentation appears to be associated with patients whose area MT lesions are contained to only one hemisphere of the brain. For example, a patient with epileptic seizures stemming from the right amygdala and surrounding temporal and parietal areas displayed impaired motion direction discrimination for objects moving to her left along with smaller impairments to all objects moving in her left visual field (Blanke et al., 2002). Patients for whom motion direction discrimination is impaired regardless of direction typically have lesions across both hemispheres (Pelak & Hoyt, 2005; Rizzo et al., 1995; Zihl et al., 1983; Zihl & Heywood, 2015).
Some patients with akinetopsia do see their symptoms dissipate. In cases of patients with akinetopsia resulting from epilepsy, being administered the anticonvulsant carbamazepine resolved all visual symptoms (Maeda et al., 2019; Sakurai et al., 2013). For two patients who developed akinetopsia from the antidepressant nefazodone, symptoms resolved after discontinuing the drug or greatly lowering the dosage (Horton & Trobe, 1999). However, patients whose akinetopsia arises from TBI’s, strokes, or neurodegenerative disorders like Alzheimer’s and Parkinson’s are largely left with the condition for the rest of their lives (Kumar & Wroten, 2024).
Patients with more permanent area MT lesions often experience the most significant reductions in quality of life. One patient whose akinetopsia developed from a TBI was unable to engage in his favorite hobbies like hunting because his condition left him unable to distinguish fellow hunters (Pelak & Hoyt, 2005). Another patient whose akinetopsia developed from a bout with Alzheimer’s reported that they had to stop driving because they were unable to see other cars on the road or judge how fast they were driving (Pelak & Hoyt, 2005). Many patients with akinetopsia are not even aware of the full extent of their condition and thus do not end up seeing a neurologist or ophthalmologist for years. The previously mentioned patient with TBI-induced akinetopsia did not see a specialist until two years after the onset of his symptoms (Pelak & Hoyt, 2005). In extreme cases, some patients develop a pathological denial of their visual and neurological symptoms called anosognosia and may never seek treatment (Antoniello & Gottesman, 2020; Burns, 2004).
Significance
Treatment options for patients with akinetopsia arising from permanent brain lesions are few and far between. Therapeutic approaches to akinetopsia typically involve training patients to use perceptual cues from other sensory modalities to provide information about moving objects (Burns, 2004; Kumar & Wroten, 2024). For example, while patients often find it difficult to cross the street because they cannot see when cars are approaching, patients can use auditory information to determine whether cars are moving toward them or away from them before crossing the street. But even then, many patients with akinetopsia require consistent monitoring and close supervision to prevent injuries (Burns, 2004; Kumar & Wroten, 2024). The patients who experience the worst prognostic outcomes are those whose family or loved ones are unable to volunteer significant time to care for them or those who do not have access to at-home care.
42 years after the first reported case of akinetopsia, many questions remain incompletely answered regarding drivers of variety in clinical presentations, variance in prognostic outcomes, and case reports are still exceptionally rare. But since Zihl & colleagues’ account of Patient LM in 1983, knowledge of area MT and the field of motion perception has expanded greatly by investigating accounts of motion blindness. Research is still sorely needed to provide a more comprehensive account of this condition if more viable treatments are to be developed.
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