Scotoma

Abstract

A scotoma is an area of lost or depressed vision within the visual field, surrounded by relatively preserved sight. It can arise anywhere along the visual system — from the retina, through the optic nerve, to the visual cortex — so its shape and location map the site of the damage that produced it. Its most instructive feature is that people are usually unaware of a scotoma, because the brain fills the missing region with the colour and texture of its surroundings, a completion process that reveals how vision is actively constructed rather than passively received. The transient scintillating scotoma of migraine aura, expanding across the field as a shimmering arc, gave nineteenth-century observers the first window onto a wave travelling across the visual cortex. Scotomas thus sit at the meeting point of clinical measurement and the psychology of perception.

Keywords: scotoma, perceptual filling-in, visual field, perimetry

A scotoma is not darkness so much as absence. Where the visual field has a scotoma, the corresponding part of the world is simply not delivered to awareness — and, crucially, the gap is rarely experienced as a black hole. Instead the brain completes the region seamlessly from its surroundings, so a person may drive, read, and recognise faces for years with a substantial blind area they have never noticed (Gerrits & Timmerman, 1969). That everyday invisibility is exactly what makes the scotoma valuable to cognitive psychology: it exposes the machinery of perceptual filling-in, the process by which the visual system infers what must be present in a region it cannot actually see.

The account below moves from what a scotoma is, through the kinds clinicians distinguish, to the filling-in that hides it from its owner, then to the dramatic transient scotoma of migraine that first revealed cortical travelling waves, and finally to how scotomas are measured and lived with. The recurring theme is that a hole in the visual field is never just a hole: what surrounds it, and how the brain treats it, is a map of how sight is built.

Figure 1

A Visual Field With a Central Scotoma and the Physiological Blind Spot

What a Scotoma Is

A scotoma is a region of the visual field in which vision is absent or depressed, bordered by an area of normal or better sight. The word is Greek for darkness, but the term is defined by location within the field rather than by any subjective blackness: a scotoma is a hole in the map of what the eye can see, and it is characterised by where that hole falls, how large it is, and how complete the loss within it is (Phu, Khuu, Yapp, Assaad, Hennessy, & Kalloniatis, 2017). An absolute scotoma is a region where no stimulus, however bright, is detected; a relative scotoma is one where vision is merely dimmed or degraded, so that a bright target is seen but a faint one is missed.

Because the visual field is a topographic projection of the world onto the retina and onward onto the brain, the position and shape of a scotoma point to the site of the damage that caused it. A lesion of the macula — the central retina — produces a central scotoma that destroys the fine, high-acuity vision used for reading and face recognition; damage along the nerve-fibre bundles of the retina produces the curved arcuate scotoma characteristic of glaucoma; and a lesion of the visual cortex produces a field defect whose edge respects the vertical midline. The scotoma is thus a diagnostic signature, its geometry encoding the anatomy of the fault.

Everyone already carries one scotoma without knowing it. The physiological blind spot is the small region of each eye's field, about 15° to the temporal side of fixation, that corresponds to the optic disc, where the optic nerve leaves the eye and the retina has no photoreceptors. It is a genuine absolute scotoma present in every healthy eye, yet no one perceives a gap there in ordinary vision — the first and most familiar demonstration that the visual system does not simply report the retinal image but actively completes it (Ramachandran & Gregory, 1991).

Kinds of Scotoma

Clinicians distinguish scotomas along two orthogonal dimensions: how much vision is lost within the region, and where the region falls in the field. On the first dimension, an absolute scotoma admits no vision at all, while a relative scotoma spares the detection of large or bright targets but not small or dim ones — a distinction that matters because a relative scotoma can be missed unless the test uses sufficiently faint stimuli (Phu et al., 2017). On the second dimension, the position and shape of the loss carry most of the clinical information, because they follow the anatomy of the visual pathway.

Two cautions keep this taxonomy honest. First, the categories are descriptions of where and how much, not of cause: the same pattern can have more than one origin, and the mapping to a lesion is a strong lead, not a diagnosis. Second, one pattern — the scintillating scotoma — is set apart from the rest by being transient and positive: it announces itself with shimmering light rather than hiding as a silent gap, and it resolves within an hour. The demonstration below places each static pattern on a schematic field and shows how its geometry maps to the region of vision it removes.

Perceptual Filling-In

The most psychologically remarkable fact about scotomas is that their owners generally cannot find them. A person with a stable retinal scotoma reports no black patch, no missing region, nothing at all — the field looks whole. Gerrits and Timmerman documented this directly in patients with retinal scotomata, showing that the region of lost vision was actively filled in with the brightness and colour of its surround rather than being perceived as a defect (Gerrits & Timmerman, 1969). Filling-in is not a failure to notice; it is a positive perceptual construction, the visual system supplying a best guess for a region from which it receives no signal.

Ramachandran and Gregory made the process controllable by inducing artificial scotomas in healthy observers. When a small region of a flickering textured display is held on a fixed retinal location while the observer maintains fixation, that region fades within seconds and is replaced by the surrounding texture — the observer sees continuous texture where a blank patch objectively remains (Ramachandran & Gregory, 1991). The completion takes measurable time to build, depends on the properties of the surround, and can even fill in with a texture that never existed at the location, which shows it to be an inference rather than a copy.

The neural basis of this inference was pinned down by De Weerd and colleagues, who recorded from cells in the visual cortex of monkeys viewing an artificial scotoma. Neurons whose receptive fields lay inside the scotoma, initially silent because nothing stimulated them, gradually began to respond as though the surrounding texture extended into their region — and the time course of that climbing response matched the perceptual time course of filling-in (De Weerd et al., 1995). Computational work then showed that such completion can be understood as the visual system solving an interpolation problem, propagating surface information inward from the borders of the missing region (Zur & Ullman, 2003). Reviewing the accumulated evidence, Komatsu argued that filling-in is a general operating principle of visual cortex, in which the represented surface is reconstructed from edges and context rather than transmitted point for point (Komatsu, 2006).

The Scintillating Scotoma of Migraine

Not every scotoma is a silent, stable gap. The scintillating scotoma of migraine aura is a transient, positive phenomenon: a small shimmering spot near fixation that, over ten to thirty minutes, expands into a crescent of jagged, flickering light — often a zig-zag or castellated border known as a fortification spectrum — drifting toward the periphery and leaving a temporary blind area in its wake before clearing completely. Hubert Airy, who experienced the phenomenon himself, published the first careful drawings of this expanding fortified arc in 1870, giving science its first detailed record of a scotoma in motion (Airy, 1870).

The moving arc turned out to be a window onto the cortex. Karl Lashley, mapping his own recurrent scintillating scotomas onto the visual field and then, using the geometry of the cortical map, onto the surface of the primary visual cortex, inferred that the phenomenon reflected a wave of intense activity followed by suppression sweeping across the cortex at roughly three millimetres per minute (Lashley, 1941). Lashley made this deduction decades before the underlying event could be observed, purely from the timing and shape of what he saw. His inferred wave corresponds to what is now called cortical spreading depression, a slowly propagating wave of neuronal depolarisation and subsequent silencing that is the accepted physiological substrate of the aura (Charles, 2018).

Functional imaging closed the loop between Lashley's inference and the living brain. Hadjikhani and colleagues recorded the visual cortex during a spontaneous migraine aura and captured a wave of altered blood-oxygen signal that began near the cortical representation of fixation and marched forward across the retinotopic map, at a speed and direction matching the perceived scotoma — a direct human observation of the spreading event Lashley had reconstructed from perception alone (Hadjikhani et al., 2001). The scintillating scotoma is thus a rare case in which a subjective visual experience can be read as a legible trace of a specific neural event travelling across the cortex.

Assessment and Measurement

A scotoma is mapped by perimetry, in which the patient fixates a central point while small targets of varying brightness are presented across the field and their detection is recorded, yielding a chart of where vision is present, depressed, or absent. The method's central limitation follows from its logic: because it depends on the patient reporting what they detect while holding steady fixation, an unstable or eccentric fixation can smear or displace a scotoma on the chart, and a relative scotoma is registered only if the target is faint enough to fall below the depressed threshold (Phu et al., 2017). Choosing which perimetric strategy fits which condition is itself a considered decision, since different diseases produce characteristic patterns that some test grids are better placed to reveal (Hepworth & Rowe, 2018).

When a central scotoma destroys the fovea, the visual system adapts by adopting a new anchor for looking. Patients with macular disease spontaneously develop a preferred retinal locus (PRL), an off-centre patch of surviving retina that takes over the fixational role the fovea can no longer perform, so that they direct this new locus, rather than the dead centre, at whatever they wish to inspect (Fletcher & Schuchard, 1997). Reaching a consensus on how the PRL should be defined and measured took considerable work, because a single patient may use more than one locus depending on the task (Crossland et al., 2011).

The PRL is a striking case of large-scale plasticity in the adult visual system, and it raises a question that bears directly on rehabilitation: when a retinal region falls silent, does the corresponding cortex reorganise, and can that reorganisation be harnessed? Reviews of adult cortical plasticity after visual field loss argued that the reorganisation seen after a scotoma has real implications for diagnosis and for training patients to use their residual vision efficiently (Safran & Landis, 1996). Studies of central vision loss have gone on to document both the functional strategies patients adopt and the cortical adaptations that accompany them, tying the behavioural PRL to changes in how the cortex represents the surviving field (Cheung & Legge, 2005).

Worked Example

Consider how Lashley reasoned from a scintillating scotoma to a speed on the cortex — a calculation that turns a private visual experience into a physical measurement. Suppose the shimmering leading edge of an aura takes 20 minutes to travel from the point of fixation out to about 20° of eccentricity in the visual field. The question is how fast the underlying disturbance is moving across the primary visual cortex.

The step that makes this possible is cortical magnification: the visual field is mapped onto V1 unevenly, with the central few degrees allotted a disproportionately large share of cortex. A standard estimate of the human map (used here as textbook background, not a new empirical claim) gives the cortical distance from the representation of fixation to eccentricity E as d(E) = 17.3 × ln(1 + E / 0.75) millimetres.

d(20°) = 17.3 × ln(1 + 20 ÷ 0.75) = 17.3 × ln(27.67) = 17.3 × 3.32 ≈ 57 mm

So the edge that swept from fixation to 20° in the field travelled about 57 mm across the cortex. Dividing that cortical distance by the time taken gives the propagation speed.

speed = 57 mm ÷ 20 min ≈ 2.9 mm/min

The result, roughly three millimetres per minute, is exactly the figure Lashley reported from his own auras (Lashley, 1941), and it falls squarely within the 2–3 mm/min range now accepted for cortical spreading depression (Charles, 2018). The example makes Lashley's insight concrete: the perceived speed of the scotoma across the field is not the speed of anything in the world, but once the field is re-expressed in cortical millimetres it becomes the speed of a real wave crossing the brain — the same wave later imaged directly during aura (Hadjikhani et al., 2001). The uneven cortical map is what converts a shape drawn on the visual field into a measurement on tissue.

Discussion

The scotoma has earned a place in cognitive psychology well beyond its clinical importance, because it makes visible a principle that ordinary, gap-free vision hides: the percept is a construction, not a transcription. The clearest proof is that a stable scotoma is usually invisible to the person who has it. If seeing were simply the delivery of the retinal image to awareness, a region with no input would appear as a void; instead it is filled with the surround, and the filling is an active, time-consuming, context-dependent inference that can be watched forming in an artificial scotoma and traced to climbing activity in visual cortex (Ramachandran & Gregory, 1991; De Weerd et al., 1995). What the scotoma removes, the brain silently rebuilds, and the rebuilding is the phenomenon of interest.

The transient scotoma of migraine adds a second lesson, about the relation between experience and neural events. Lashley's reconstruction of a cortical wave from the drifting geometry of his own aura, later confirmed by imaging, is a rare demonstration that a subjective visual experience can be quantitatively decoded as the trace of a specific, physically characterised process in the cortex (Lashley, 1941; Hadjikhani et al., 2001). Few phenomena let the psychology of perception and the physiology of the cortex be lined up so precisely against each other.

For theory, the enduring point is that the visual field is a representation the brain maintains, not a passive readout of the eye. It can be locally deleted by damage anywhere along the pathway; it can be locally reconstructed by filling-in; it can be reorganised, as when a preferred retinal locus takes over from a destroyed fovea; and it can be transiently overwritten by a cortical wave. Each of these is a manipulation of the same underlying map, and studying how the map behaves when it is torn, patched, or overrun is one of the most direct routes into how normal sight is assembled (Komatsu, 2006).

Current Directions

Much current work is methodological, aimed at measuring scotomas more sensitively and matching the test to the disease. Because standard perimetry depends on stable fixation and can miss a shallow relative scotoma, effort has gone into selecting and standardising perimetric strategies for particular neurological and ophthalmic conditions, so that the pattern of loss is captured rather than blurred (Hepworth & Rowe, 2018). In parallel, the rise of high-resolution retinal imaging has reframed the visual field test not as a stand-alone verdict but as one measurement to be read alongside structural imaging, since a functional scotoma and a structural lesion each constrain the interpretation of the other (Phu et al., 2017).

A second, applied front concerns living with a central scotoma. Building on the discovery that patients spontaneously adopt a preferred retinal locus, research has turned to whether that adaptation can be trained — whether a patient can be taught to place a more advantageous locus on the target, and whether the visual cortex supports such relearning (Crossland et al., 2011). The link between the behavioural strategy and its cortical substrate, first drawn in studies of central vision loss, remains the pivot on which rehabilitation turns: if the cortex representing the lost field can be recruited to serve the surviving retina, the practical gains for people with macular disease are substantial (Cheung & Legge, 2005).

Common Misconceptions

“A scotoma looks like a black spot in the visual field.”

Usually the opposite. A stable scotoma is generally not seen as black or as anything at all, because the brain fills the region in with its surroundings, so the field appears whole and the loss goes unnoticed until it is tested (Ramachandran & Gregory, 1991).

“Everyone would notice a large blind area in their field.”

People routinely do not. Patients with substantial retinal scotomata can be unaware of them entirely, precisely because filling-in conceals the gap — which is why scotomas must be found by perimetry rather than by asking the patient (Gerrits & Timmerman, 1969).

“The migraine's shimmering scotoma is a problem in the eye.”

It is cortical, not ocular. The scintillating scotoma reflects a wave of activity crossing the visual cortex; it appears in the field of both eyes together and its spread matches the cortical map, not the retina (Hadjikhani et al., 2001).

“A scotoma always means the visual cortex is damaged.”

Not so. A scotoma can arise anywhere along the visual system; its shape locates the fault, and many scotomas are retinal or optic-nerve in origin, such as the arcuate loss of glaucoma or the central loss of macular disease (Phu et al., 2017).

Commonly Confused With

Scotoma vs. Cortical Blindness

Both are losses of vision, but they differ in extent and in where the fault lies. A scotoma is a localised region of loss within an otherwise seeing field, and it can originate anywhere along the visual pathway — retina, optic nerve, or cortex. Cortical blindness is the whole-field or hemifield loss produced specifically by destruction of the primary visual cortex, with intact eyes and pupils. Ask two questions: is the loss a patch inside a working field (scotoma) or the loss of a whole half-field or more (cortical blindness); and is the lesion necessarily cortical (cortical blindness) or possibly retinal (scotoma). A dense homonymous hemianopia is, in effect, a very large cortical scotoma.

Scotoma vs. Charles Bonnet Syndrome

These are opposite responses of the brain to missing visual input, and the filling-in of a scotoma is exactly what invites the confusion. When a scotoma is filled in, the brain supplies the surrounding colour and texture, so the region looks continuous with its neighbourhood and nothing is added that is not already there. In Charles Bonnet syndrome the brain, deprived of input by eye disease, generates formed hallucinations — faces, figures, patterns — that the person knows are not real. Ask whether the brain is quietly completing a gap with its surround (scotoma filling-in) or actively inventing detailed images that do not match the surround (Charles Bonnet); the first hides a loss, the second populates it.

Glossary

Absolute scotoma.

A region of the visual field in which no stimulus is detected, however bright; the most complete form of localised visual loss.

Arcuate scotoma.

A curved band of visual loss arching out from the region of the blind spot, following the course of the retinal nerve-fibre bundles; characteristic of glaucoma.

Central scotoma.

A scotoma over the point of fixation that destroys high-acuity vision for reading and face recognition; typically caused by disease of the macula.

Cortical magnification.

The uneven mapping of the visual field onto the visual cortex, in which the central field is allotted a disproportionately large area of cortex.

Fortification spectrum.

The jagged, zig-zag or castellated luminous border of a migraine scintillating scotoma, so named for its resemblance to the plan of a fortified town.

Perceptual filling-in.

The active construction by which the visual system completes a region receiving no input, using the colour, brightness, and texture of the surround.

Perimetry.

The clinical mapping of the visual field by presenting small targets at many locations while the patient fixates centrally and reports what they detect.

Physiological blind spot.

The normal absolute scotoma in every eye corresponding to the optic disc, where the optic nerve leaves the retina and no photoreceptors are present.

Preferred retinal locus (PRL).

An off-centre patch of surviving retina that a patient with a central scotoma adopts as a substitute fovea for fixation and inspection.

Primary visual cortex (V1).

The first cortical stage of vision, in the occipital lobe; its retinotopic map is what lets a scotoma's field geometry be re-expressed as a cortical distance.

Relative scotoma.

A region of the visual field in which vision is depressed but not absent, so that bright or large targets are seen while faint or small ones are missed.

Scintillating scotoma.

A transient, expanding, shimmering visual disturbance of migraine aura, leaving a temporary blind area in its wake and reflecting a wave crossing the visual cortex.

Scotoma.

An area of absent or depressed vision within the visual field, bordered by an area of normal or better sight.

Visual field.

The total extent of space seen by an eye or eyes while fixation is held steady; the map on which a scotoma is a localised gap.

Key Researchers

Hubert Airy

(deceased, 1838–1903). English physician who, drawing his own migraine auras, published in 1870 the first detailed depiction of the expanding fortified arc of the scintillating scotoma — the founding visual record of a scotoma in motion (Airy, 1870). Wikipedia

Hidehiko Komatsu

(living). Visual neuroscientist, emeritus at Japan's National Institute for Physiological Sciences, whose review of perceptual filling-in synthesised the psychophysics and physiology into the view that visual cortex reconstructs surfaces rather than transmitting them point for point (Komatsu, 2006). Faculty page

Karl Spencer Lashley

(deceased, 1890–1958). American psychologist at Harvard University who mapped his own scintillating scotomas and inferred, decades before it could be observed, a wave of activity and suppression crossing the visual cortex at about three millimetres per minute (Lashley, 1941). Wikipedia

Gordon E. Legge

(living, b. 1948). Vision scientist at the University of Minnesota whose work on low vision, reading with central scotomas, and the definition of the preferred retinal locus tied the behaviour of patients to the cortical adaptations that accompany central vision loss (Cheung & Legge, 2005; Crossland, Engel, & Legge, 2011). ORCID

Vilayanur S. Ramachandran

(living). Neuroscientist at the University of California, San Diego who, with Richard Gregory, made perceptual filling-in experimentally tractable by inducing artificial scotomas in healthy observers and timing their completion (Ramachandran & Gregory, 1991). Faculty page

Peter De Weerd

(living). Cognitive neuroscientist at Maastricht University whose recordings from monkey visual cortex during an artificial scotoma showed neurons inside the scotoma coming to respond to the surrounding texture, giving filling-in a neural correlate (De Weerd, Gattass, Desimone, & Ungerleider, 1995). ORCID

Frequently Asked Questions

What is a scotoma?

A scotoma is an area of absent or reduced vision within the visual field, surrounded by an area of normal sight. It can be caused by damage anywhere along the visual system — the retina, the optic nerve, or the visual cortex — and its shape and position help locate where the damage lies.

Why can't people usually see their own scotoma?

Because the brain fills the missing region in with the colour and texture of its surroundings, a process called perceptual filling-in. The field appears continuous and whole, so a stable scotoma often goes completely unnoticed until it is revealed by a visual field test.

What is the difference between an absolute and a relative scotoma?

In an absolute scotoma no stimulus is seen at all, however bright. In a relative scotoma vision is only depressed: a bright or large target is detected, but a faint or small one is missed. A relative scotoma can be overlooked unless the test uses sufficiently faint targets.

What is a scintillating scotoma?

It is the transient visual disturbance of migraine aura: a shimmering, often zig-zag arc of light that expands across the field over ten to thirty minutes, leaving a temporary blind area behind it before clearing. It reflects a wave of activity crossing the visual cortex, not a problem in the eye.

Is the physiological blind spot a scotoma?

Yes. The blind spot is a genuine absolute scotoma present in every healthy eye, corresponding to the optic disc where the optic nerve leaves the retina and there are no photoreceptors. It goes unnoticed in everyday vision because the brain fills it in.

How is a scotoma measured?

By perimetry, in which the patient fixates a central point while small targets are shown at many field locations and their detection is recorded. The result is a map of where vision is present, depressed, or absent, though it depends on the patient holding steady fixation.

Can a person adapt to a central scotoma?

Yes. People who lose central vision spontaneously develop a preferred retinal locus, an off-centre area of surviving retina that takes over the role of the fovea for fixation and inspection. Rehabilitation research studies how to make this adaptation more effective.

Does a scotoma mean the brain is damaged?

Not necessarily. Many scotomas are retinal or optic-nerve in origin, such as the central loss of macular disease or the arcuate loss of glaucoma. A scotoma indicates a fault somewhere along the visual pathway, and its geometry points to where.

References