Palinopsia Diagnosis Palinopsia Pictures Palinopsia Anxiety Palinopsia Test Palinopsia ICD 9 Palinopsia Cure Visual Snow Visual After Images
| Palinopsia | Afterimage | Glossary_of_psychiatry | Positive_visual_phenomena | Alexis_Kirke | Diplopia | List_of_neurological_conditions_and_disorders | Posterior_cerebral_artery | Flashback_(psychology) |
|This article needs additional citations for verification. (October 2008)|
Palinopsia (Greek: palin for "again" and opsia for "seeing") is a visual disturbance that causes images to persist to some extent even after their corresponding stimulus has left. These images are known as afterimages and occur in persons with normal vision. However, a person with palinopsia experiences them to a significantly greater degree, to the point where they become difficult or impossible to ignore. This often results in mild to severe anxiety and/or depression. Palinopsia sometimes appears on its own, but is more often accompanied by other visual disturbances such as visual snow, and can be attributed to a number of conditions affecting the brain including, but not limited to, medications, seizure disorders, tumors, occiptal lobe or visual pathway lesions, subcortical hemorrhage, and dural arteriovenous malformations.
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 can occur through several pathways, which makes teasing out the source of a patient's palinopsia difficult. 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.
In their 2007 article in the Journal of Neuro-Ophthalmology, ME Ritsema and MA Murphy advise that "palinopsia, or perseveration of a previously viewed image, may be caused by drug use or by posterior visual pathway lesions. Most cases of palinopsia due to visual pathway lesions have an associated homonymous hemianopic visual field defect. We report two patients with palinopsia caused by structural lesions of the posterior visual pathway in the absence of visual field defects. Patients with palinopsia should undergo neuroimaging even in the presence of normal visual fields."
In 2002, Hayashi et al. wrote of a "patient who exhibited transient palinopsia and visual hallucinations. Disturbances initially included an auditory component and increasingly were localized to the left visual field. These events occurred during recovery from a right subcortical hematoma with left homonymous hemianopia. Single-photon emission computed tomography (SPECT) demonstrated extensive perilesional hyperperfusion involving parts of the right parietal, temporal, and occipital cortex. Perilesional hyperperfusion disappeared as the visual abnormalities diminished. We believe that excitatory neuronal activation in perilesional cortex during recovery contributed importantly to the transient abnormal perceptions." 
In addition to subcortical hemorrhage and posterior pathway lesions being possible underlying conditions for this visual phenomenon, palinopsia also seems to occur in those with dural arterial defects which affect blood flow to the occipital regions of the brain. In their 1999 Neurology paper, Kupersmith et al. describe seven patients with visual disturbances, including palinopsia, which all have dural arteriovenous malformations (DAVMs). They describe that such malformations, if caught early, should be amenable to treatment before irreversible damage or visual field loss should occur through surgical intervention. In such patients, neurological and visual deficit can be correlated to venous hypertension, from incorrect occipital venous emptying.
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.
It is important for health care practitioners to be able to differentiate between the visual phenomenon of palinopsia and that described by those experiencing migraine aura. The aura described most often by migraineurs is a Scintillating scotoma, in which a zig-zag begins from a center of a field and moves outwards to encompass the visual field. Troost and Newton describe features of differentiating migraine headache from AVM (arteriovenous malformations) in a 1975 Journal of Ophthalmology article, to which there follow ups that include how to distinguish migraine visual aura from occipital epilepsy and other brain disorders.
Currently research into the causes and treatment of palinopsia is nearly 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, 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.
The treatment for palinopsia largely depends on the root cause for the disorder. If the disorder's root cause is epileptic in nature, anti-epileptic drugs will likely be prescribed. If the root cause of the disorder is due to brain damage, further evaluation by a neurologist is necessary to make informed decisions about treatment path for the patient in question. For those with dural defects, surgery may be required. Some 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.