Frontotemporal dementia, or FTD, is a group of brain disorders resulting from the progressive deterioration of the frontal and temporal lobes. This damage leads to noticeable changes in personality, behavior, and the ability to use and understand language. While these symptoms are the most recognized hallmarks of the condition, FTD also manifests in distinct ways through a person’s eyes and vision. The neurodegeneration occurring deep within the brain can extend its reach to affect the physical structures of the eye, the intricate brain networks that control eye movement, and how the brain interprets visual signals.
Ocular Motor Abnormalities in FTD
The parts of the brain damaged by frontotemporal dementia are involved in supervising the complex muscle commands that direct eye movements. This disruption can lead to a range of ocular motor abnormalities, which are problems with the physical act of moving the eyes. These symptoms are often not isolated and can be particularly pronounced in specific disorders that overlap with FTD, namely Progressive Supranuclear Palsy (PSP) and Corticobasal Syndrome (CBS).
A common issue involves saccades, the quick, simultaneous movements of both eyes that allow us to rapidly shift our line of sight from one point to another. In a healthy individual, these movements are fast and precise, but in some forms of FTD, they can become impaired. Saccades may be noticeably slowed, or they may become inaccurate, consistently undershooting or overshooting the intended target. This can make activities that rely on quick visual scanning, such as reading or navigating a crowded room, more difficult.
Another function that can be compromised is smooth pursuit, which is the ability to track a moving object with stable and fluid eye movements. In FTD, particularly in related syndromes like PSP, this ability can degrade. This causes the person’s gaze to fall behind or catch up to the moving object with jerky, saccadic movements instead of a single, smooth motion.
Difficulties with voluntarily shifting gaze, known as gaze palsy, can also occur. This is often most apparent when a person tries to look up or, more commonly, down. This specific deficit is a classic feature of PSP. The impairment in downward gaze can create functional challenges, such as trouble seeing food on a plate or difficulty walking down stairs safely.
Visual Processing and Perception Deficits
Separate from the mechanics of eye movement, FTD can affect how the brain interprets the signals it receives from the eyes. In these cases, the eyes themselves may be perfectly healthy and able to move normally, but the brain’s processing centers are too damaged to make sense of the incoming visual information. This leads to deficits in perception, where a person can see an object but cannot understand what it is or what it means.
One example of this is visual agnosia, a condition where an individual loses the ability to recognize objects. A person with visual agnosia might be able to describe the features of an object, such as its color and shape, but be completely unable to name it or explain its use. The visual system is transmitting the data, but the temporal lobe damage associated with some forms of FTD prevents the brain from matching that data to stored knowledge.
A more specific and often distressing form of this is prosopagnosia, the inability to recognize familiar faces. Even the faces of close family members or a person’s own reflection in the mirror can become unrecognizable. While they may know they are looking at a face, the unique configuration of features that identifies a specific person is lost to them. This deficit is linked to degeneration in the right temporal lobe, a region affected in certain FTD variants.
Beyond recognizing objects and faces, FTD can impair a person’s sense of spatial awareness. This can manifest as difficulty judging distances, navigating familiar places, or understanding the layout of a room. This spatial disorientation arises from damage to brain networks that create our internal map of the world, making it challenging for the individual to move through their environment safely.
Structural Changes Within the Eye
The neurodegenerative processes of FTD are not confined to the brain; they can also cause measurable physical changes within the eye itself. The retina, a layer of light-sensitive tissue at the back of the eye, is an extension of the central nervous system. Because of this direct connection, the health of the brain can be reflected in the structure of the retina, which can be observed using non-invasive imaging techniques.
Research has revealed that FTD is associated with the thinning of specific layers within the retina. Unlike Alzheimer’s disease, which causes thinning in the inner retinal layers, FTD is more commonly linked to thinning of the outer retina. Studies have shown a reduction in the thickness of the outer nuclear layer (ONL) and the ellipsoid zone (EZ) in individuals with FTD. The ONL contains the cell bodies of the eye’s photoreceptors—the rods and cones that initially detect light.
This pattern of outer retinal thinning may be connected to the underlying tau pathology often seen in FTD. Tau is a protein that helps stabilize the internal skeleton of neurons and is important for the structure of retinal photoreceptors. When tau protein becomes abnormal in FTD, it can lead to the breakdown of these photoreceptors and the subsequent thinning of the outer retinal layers.
Using Eye Changes for Diagnosis and Differentiation
Observing and measuring FTD’s eye-related symptoms can provide objective evidence to support a diagnosis and help distinguish it from other neurodegenerative conditions with similar cognitive complaints, such as Alzheimer’s disease. This differentiation is important for predicting the course of the disease and managing symptoms.
Clinicians can use specialized tools to precisely measure the ocular abnormalities. Eye-tracking devices can record and analyze eye movements with high precision. These devices can quantify saccadic errors, assess the quality of smooth pursuit, and document limitations in gaze, providing objective data that can reveal patterns characteristic of FTD and its related disorders like PSP. Certain patterns, such as deficits in voluntarily suppressing reflexive eye movements, are more prominent in the behavioral variant of FTD.
In parallel, Optical Coherence Tomography (OCT) is a non-invasive imaging technique that uses light to create high-resolution, cross-sectional images of the retina. OCT allows neurologists and ophthalmologists to measure the thickness of individual retinal layers. This technology can detect the specific pattern of outer retinal thinning associated with FTD, which contrasts with the inner retinal thinning more typical of Alzheimer’s disease.
The combination of findings from eye-tracking and OCT scans can create a distinct visual signature for FTD. For example, a patient presenting with behavioral changes who also shows slowed vertical saccades and outer retinal thinning would be more likely to have an FTD-spectrum disorder than Alzheimer’s. These ocular biomarkers offer a more accessible and less invasive window into the brain’s health compared to lumbar punctures or expensive PET scans.