Motion blindness (Akinetopsia) is a higher-order visual processing disorder in which the ability to visually perceive moving objects is selectively impaired. It is caused by lesions in the extrastriate cortex, particularly the V5/MT area (middle temporal area), and is characterized by preserved perception of stationary objects, color vision, and form perception.
The term originates from Greek a (negation) + kine (move) + opsia (see), meaning “motion blindness.” In 1911, Potzl & Redlich first reported similar symptoms in a patient with bilateral occipital lobe damage, and in 1991, Zeki named it “akinetopsia”1)2).
The most extensively studied case is patient L.M. (Zihl et al., 1983). Selective impairment of motion perception due to bilateral V5 area damage led her to report, “People suddenly appear here or there, but I don’t see them moving”3).
Epidemiology: Only 25 clinical cases have been reported in the literature. Over the past 40 years, the reporting frequency is about one case every 2.5 years, making it an extremely rare disease1). Age of onset ranges from 19 to 73 years (mean ~50 years), with 56% male and 44% female1). However, due to low disease awareness, many cases may remain undiagnosed.
The dorsal visual stream (dorsal stream) is the “where” pathway involved in spatial relationships and motion vision, with the V5 area playing a central role.
Only 25 clinical cases have been reported in the literature, with an average frequency of one case every 2.5 years over the past 40 years1). Due to low disease awareness, many undiagnosed cases may exist, and the actual incidence and prevalence are unknown.
The main complaint of akinetopsia is impaired perception of moving objects. Two forms of expression are known.
Freeze-frame type
Stroboscopic experience: Moving objects appear as a series of still images, like a slideshow.
Patient descriptions: “It feels like watching individual frames of a movie reel,” “stop-motion animation,” “like being inside a strobe light” 2)
Frequency: This is a major phenotype observed in the majority of clinical cases.
Object disappearance type
Disappearance experience: When an object moves, it disappears from the visual field and becomes invisible.
Patient description: When a person moves, they disappear and then suddenly reappear in a different location.
Characteristics: The faster an object moves, the more likely it is to disappear.
This significantly impacts daily life, making basic actions such as pouring water into a container, driving, or walking difficult 2). Perception of motion information through hearing and touch remains intact.
There are two main types. In the “freeze-frame type,” moving objects appear as if in stop-motion, and in the “object disappearance type,” objects disappear when moving2). In both cases, the faster the motion, the more pronounced the impairment. Perception of stationary objects is preserved.
The breakdown of causes of motion blindness (analysis of 25 clinical cases) is shown below1)2).
| Cause | Percentage | Notes |
|---|---|---|
| Stroke | 28% (7 cases) | Infarction of the occipitoparietal V5 area. Bilateral posterior cerebral artery infarction is common. |
| Neurodegenerative disease | 16% (4 cases) | Alzheimer’s disease (posterior cortical atrophy) is the main cause. |
| Traumatic brain injury | 12% (3 cases) | Head trauma |
| Epilepsy | 12% (3 cases) | Focal epilepsy of the right temporoparietal cortex |
| Drug-induced | 8% (2 cases) | Nefazodone (SSRI antidepressant) |
Cerebrovascular disease is the most common cause, and occipital lobe damage is most often due to posterior cerebral artery infarction. In temporal lobe disorders, tumors or infections may also be causes. Other reported causes include subcortical hemorrhage, Creutzfeldt-Jakob disease, brain metastasis (first reported by Viscardi et al., 2024), and hallucinogen persisting perception disorder (HPPD)2).
There is a report of motion blindness (freeze-frame and visual trails) caused by toxicity of the antidepressant nefazodone (an SSRI)2). It was reversible upon discontinuation of the drug. Inquiring about current medications is important for diagnosis.
There are no definitive diagnostic tests or specific examination findings. Eliciting highly specific subjective symptoms (e.g., freeze-frame, strobe-like visual experiences) is the first step in diagnosis. Since complaints in higher-order visual dysfunction are often vague, it is important to consider symptoms predicted by the lesion location and perform specific tests.
Afferent and efferent pathways are usually normal. Motion perception tests include ball-catching tasks, ocular tracking, motion direction discrimination, contrast sensitivity (moving grating patterns), random dot patterns, and motion speed discrimination 1).
Treatment of the underlying disease is fundamental, and there are currently no approved drugs for motion blindness itself.
Motion blindness due to organic lesions is often irreversible. No change in the deficit was observed during follow-up of patient L.M.2). Recovery of visual field defects after cerebral infarction is poor in elderly patients, but may occur in younger patients.
Vestibular rehabilitation and visual rehabilitation may be considered, but there is no strong evidence. The following compensatory strategies have been reported1).
Prognosis varies greatly depending on the cause. In epileptic or drug-induced cases, reversible recovery can be expected by addressing the cause2). On the other hand, in cases due to organic lesions such as cerebral infarction or neurodegenerative disease, it is often irreversible, and rehabilitation with compensatory strategies is the mainstay.
Visual information is transmitted from the retina through the optic nerve to the lateral geniculate nucleus (LGN), then to V1 (primary visual cortex), and subsequently to V2 through V5. The V5/MT area (middle temporal area) specializes in evaluating speed and direction and is located bilaterally at the temporoparieto-occipital junction.
The visual pathway is broadly divided into two processing streams.
Dorsal Stream
Function: The “where” pathway. Processes spatial relationships and motion.
Core region: V5/MT area. Specializes in evaluating speed and direction.
When impaired: Motion blindness (akinetopsia).
Ventral stream
Function: “what” pathway. Processes form, color, and object recognition.
Core area: V4. Specializes in form and color processing.
When damaged: Prosopagnosia, color agnosia, etc.
fMRI-based classification of visual areas has identified 10 regions: V1 (V1v/V1d), V2 (V2v/V2d), V3 (V3v/V3d), V4v, V8, V3A, V3B, V7, MT+, and LO. Area V5 is involved not only in motion perception but also in form perception, semantic processing, and attention2).
Different cortical pathways exist for slow (<6°/s) and fast (>22°/s) motion. The V5 area is important for processing fast motion, while at slow speeds, direction-selective neurons in V1/V2 (about 10% of the total) can compensate 1). This explains the clinical picture where faster-moving objects are harder to see.
Area V5 specializes in processing fast motion, so damage to V5 impairs perception of fast-moving objects. On the other hand, slow motion can be compensated by direction-selective neurons in V1/V2, so perception is relatively preserved (dynamic parallel processing theory) 1).
Browne et al. (2025) conducted a systematic review of 25 clinical cases and 27 experimental cases, showing that motion blindness is more heterogeneous phenomenologically, pathophysiologically, and etiologically than previously thought 1).
Viscardi et al. (2024) reported the first case of motion blindness due to brain metastasis, demonstrating that this condition can also arise from secondary brain lesions 4).
Neuroplasticity and congenital lesions: In children with congenital V1 damage, unconscious visual motion perception was preserved in the damaged hemifield, but not in children with acquired damage (Tinelli et al., 2013). This finding highlights the importance of neuroplasticity 5).
Future challenges and prospects have been pointed out as follows1).
