There are two kinds of afterimages. The first kind is of a relatively short duration and is positive, meaning that the color of the afterimage is the same as that of the original image. The other type is a negative afterimage, meaning that the colors of the original image are inverted, which tends to last comparatively longer. The duration of the positive afterimage generally does not depend upon the length of exposure to the original image, while the intensity and duration of the negative afterimage depend on that of the original image. In other words, viewing an image for a longer period of time, or being exposed to a brighter image, can lead to either a longer or more vivid afterimage, or both.
Both positive and negative afterimages are experienced by those with normal vision. For example, a very fast-moving object will often be perceived as having a trail, as might a point of light, such as a moving hand-held flashlight, in an otherwise unlit room. These are both examples of positive afterimages, or "trails." Lasting negative afterimages can occur after prolonged exposure to an unchanging visual stimulus, due to the "tiring" of cone cells. The canonical example of this uses the color-inverted American flag (see the article on afterimages).
For palinopsia sufferers, the effects are largely the same, however the intensity and length of stimulus required to produce a noticeable afterimage is much less. This can apply to both positive and negative afterimages; for example, virtually any moving object will often be accompanied by trails, and negative afterimages can be formed after viewing an object for seconds or less. Furthermore, the afterimages can accumulate if the time between stimuli is shorter than the time it takes for an afterimage to fade.
Palinopsia is thus a condition which mimics normal phenomena, but with far greater intensity. The degree to which the afterimages are amplified can vary over time, in different circumstances (e.g. different amounts of ambient light, levels of stress, amount of sleep, or influence of substances), and from person to person.
The pathology which leads to palinopsia is unknown. Though normal negative afterimages are generally understood to be a retinal phenomenon, palinopsia is thought to be a brain-related disorder, and not an eye-related disorder. This is likely because palinopsia is most commonly encountered in connection with diseases, drugs or injuries which affect the brain. Palinopsia is a common symptom of hallucinogen persisting perception disorder (HPPD), and can be the only symptom. It can also be caused by vascular disease, certain prescription medications or head trauma.
Although palinopsia refers to a specific type of visual symptom, there are other conditions, such as visual snow, which often accompany it. Many of these disorders can be loosely described as "overactive vision." As such, the predominate hypothesis states that these and certain other visual disorders may be the result of a lack of inhibitory neural signals in all or part of the visual center of the brain (in particular, the lateral geniculate nucleus, which is the primary processor of information received from the retina). Due to lack of inhibition, the neurons continue to fire when they otherwise would be suppressed, which results in increased perception of visual activity. In 2001 Dr. Henry David Abraham demonstrated increased brain activity in HPPD sufferers (in this case equivalent to palinopsia) following a visual stimulus, supporting this hypothesis. However, further details are unknown.
Some people suffering from ocular migraine or, rarely, occipital lobe epilepsy, can also have bouts of palinopsia, or persistent palinopsia. A rare condition known as persistent migraine aura without infarction, in which one experiences a migraine aura constantly, can be accompanied by or described by palinopsia.
Currently research into the causes and treatment of palinopsia is all but nonexistent. Research articles concerning palinopsia, which are relatively rare, most often only document its occurrence, typically as either a reversible or irreversible effect of a prescribed medication or injury. Due to the comparatively few sufferers of the disorder, awareness is largely restricted to those affected and their confidants. As such, funding is difficult to come by.
From a practical point of view, studying the causes and treatment of palinopsia presents many challenges to the researcher. Since the condition does not produce effects apparent to an outside observer, animal testing, an invaluable tool for the study of many diseases, is impossible unless more is known about the pathology. If, as is likely, the problem stems from differences at the neuronal level, cell culture experiments or animal model experiments could lead to an understanding of how to induce, and possibly correct, the malfunction. However, characterizing that pathology would be a difficult process, as the option of isolating known dysfunctional neurons from a sufferer would be very difficult, as palinopsia is not fatal (by way of contrast, much of our early knowledge of the pathology in Alzheimer's Disease was learned by examining the brains of recently deceased Alzheimer's sufferers). Future research, such as advances in MRI technology, or immunofluorescence experiments, might allow insight into the physiological differences between the visual systems of persons with normal vision and those with palinopsia, without requiring invasive procedures. In addition, advances in knowledge of the brain, particularly in how the brain recycles visual stimuli, might provide an explanation for palinopsia.
As the neurological basis for palinopsia is unknown, treatments which target the condition itself are as yet non-existent. Most treatments involve benzodiazepines, which are prescribed primarily for their anxiety-reducing effects, although as they promote uptake of GABA, an inhibitory neurotransmitter, they might reduce the overstimulation which has been shown to occur in palinopsia sufferers. However, few if any patients treated with benzodiazapenes report any noticeable, let alone complete, reversal of visual symptoms, and thus treatments for the underlying condition remain unknown.
In some instances, cases resolve themselves after a period of time, though the length of time varies considerably and can be lifelong; in fact what little evidence there is suggests that the condition is lifelong more often than not. Most sufferers seek to adapt to their condition by accepting it as part of normal experience. However, this adaptation is not as easy as it might seem and can take many years.