While technically not a hallucination but rather a distortion of an otherwise real image, metamorphopsia is a particular type of visual disturbance characterized by wavy or warped vision. It is tested using an Amsler grid, during which patients are asked if a grid with straight lines appears wavy or distorted. Metamorphopsia most commonly localizes to the macula (e.g., age-related macular degeneration, central serous chorioretinopathy, epiretinal membrane) but can also occur transiently in migraine.
Scheerer’s phenomenon is experienced as small bright dots arcing across the visual field, often temporally to nasally. They are most often experienced when looking against a light background, for instance a clear blue sky, and are thought to represent leukocytes traveling through the retinal circulation. Purkinje figures are generated by the retinal vasculature casting a shadow on the photoreceptor layer of the retina in response to bright light. Flick and pressure phosphenes are brief flashes of light that arise due to mechanical stimulation of the outer retina, either by eye movement or manual pressure on the globes, respectively.
Pathologic photopsias commonly occur in vitreoretinal disease due to mechanical irritation or inflammation of the outer retina, which causes signals to be transmitted to the optic nerve in the absence of direct stimulation by light. As such, a sudden increase in flashes or floaters, especially if monocular, is concerning for retinal detachment and should always be evaluated with dilated fundus examination. When severe eye pain is present, acute angle-closure glaucoma should also be considered and is also an ophthalmic emergency; it may be precipitated by medications commonly prescribed by neurologists, such as topiramate. Acute idiopathic blind spot enlargement comprises a group of autoimmune retinopathies characterized by enlargement of the physiologic blind spot, which may be accompanied by mild optic disc edema. It is distinguished from optic neuritis and other optic neuropathies by prominent symptoms of photopsias out of proportion to vision loss.
Release hallucinations refer to visual hallucinations that occur in the context of vision loss, due to either ocular, pregeniculate, or retrogeniculate visual pathway lesions. While the genesis of hallucinations is complex and incompletely understood, one hypothesis is that they represent an imbalance between internal and external visual stimuli. Under normal conditions, the brain relies on external visual stimulation to suppress internal (cortically generated) visual percepts. When vision loss occurs, external stimulation is decreased, and internal visual stimuli fill in those areas in which vision is lacking. Charles Bonnet syndrome refers to visual hallucinations occurring in older individuals with ophthalmic disease, often age-related macular degeneration. They are classically thought to have normal cognition and insight into the unreal nature of their hallucinations, though some of these traditional diagnostic criteria have been questioned.
Peduncular hallucinosis occurs due to midbrain lesions, often ischemic and with associated ocular motor abnormalities. The patient typically experiences vivid, complex imagery and may or may not have insight into their unreal nature. The mechanism of peduncular hallucinosis is unclear but is thought to represent abnormal regulation of rapid eye movement (REM) sleep centers in the reticular activating system—essentially, dream-like imagery from REM sleep intruding into wakefulness. Cognitive and sleep disturbances may also be present.
Palinopsia refers to the persistence of a visual percept after its object is no longer present. Examples include continuing to see a person even though he or she has already left the room, seeing a string of objects behind an object that is moving, and superimposing part of one image (e.g., a man’s beard) onto other images (e.g., the face of a person who has no beard). Central polyopia is the multiplication of objects within an image. It is the rare cause of monocular diplopia due to neurologic disease. Both occur in the setting of parietooccipital lesions or hallucinogenic drug exposure and likely exist on a similar spectrum.
The content of formed visual hallucinations in neuropsychiatric disease does not readily distinguish between specific etiologies, but the presence of accompanying symptoms and signs is of great diagnostic value. For example, parkinsonism or cognitive impairment would suggest an underlying neurodegenerative disorder such as Lewy body disease or Alzheimer disease, whereas delusions and disordered thought would be more consistent with a primary psychotic disorder. Note that in Parkinson disease and Lewy body disease, visual hallucinations may initially occur in the relative absence of overt cognitive impairment and with preserved insight; they may also be triggered or exacerbated by dopaminergic therapy such as dopamine agonists. Visual hallucinations in narcolepsy typically occur as the patient is falling asleep (hypnagogic hallucinations) or awakening from sleep (hypnapompic hallucinations); there may also be a history of sleep paralysis or cataplexy. Multiple drugs may precipitate visual hallucinations, particularly illicit drugs such as LSD, psilocybin, and mescaline; hallucinations are also seen with drug and alcohol withdrawal.
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