Entoptic phenomena (from Greek ἐντός "within" and ὀπτικός "visual") are visual effects whose source is within the eye itself. (Occasionally, these are called entopic phenomena, which is probably a typographical mistake.)

In Helmholtz's words; "Under suitable conditions light falling on the eye may render visible certain objects within the eye itself. These perceptions are called "entoptical"."

Entoptic images have a physical basis in the image cast upon the retina. Hence, they are different from optical illusions, which are perceptual effects that arise from interpretations of the image by the brain. Because entoptic images are caused by phenomena within the observer's own eye, they share one feature with optical illusions and hallucinations: the observer cannot share a direct and specific view of the phenomenon with others.

Helmholtz comments on phenomena which could be seen easily by some observers, but could not be seen at all by others. This variance is not surprising because the specific aspects of the eye that produce these images are unique to each individual. Because of the variation between individuals, and the inability for two observers to share a nearly identical stimulus, these phenomena are unlike most visual sensations. They are also unlike most optical illusions which are produced by viewing a common stimulus. Yet, there is enough commonality between the main entoptic phenomena that their physical origin is now well understood.

Distortion of vision refers to straight lines not appearing straight, but instead bent, crooked, or wavy. Usually this is caused by distortion of the retina itself. This distortion can herald a loss of vision in macular degeneration, so anyone with distorted vision should seek medical attention by an ophthalmologist promptly. Other conditions leading to swelling of the retina can cause this distortion, such as macular edema and central serous chorioretinopathy.

An Amsler grid can be supplied by an ophthalmologist so that the vision can be monitored for distortion in people who may be predisposed to this problem.

Tunnel vision implies that the peripheral vision, or side vision, is lost, while the central vision remains. Thus, the vision is like looking through a tunnel, or through a paper towel roll. Some disorders that can cause this include:

Glaucoma - severe glaucoma can result in loss of nearly all of the peripheral vision, with a small island of central vision remaining. Sometimes even this island of vision can be lost as well.

Retinitis pigmentosa - This is usually a hereditary disorder which can be part of numerous syndromes. It is more common in males. The peripheral retina develops pigmentary deposits, and the peripheral vision gradually becomes worse and worse. The central vision can be affected eventually as well. People with this problem may have trouble getting around in the dark. Cataract can be a complication as well. There is no known treatment for this disorder, and supplements of Vitamin A have not been proven to help.

Punctate Inner Choroidopathy - This condition is where vessels gro (( material is missing ))

Stroke - a stroke involving both sides of the visual part of the brain may wipe out nearly all of the peripheral vision. Fortunately, this is a very rare occurrence

Distorted vision is a symptom with several different possible causes.

Closed-eye hallucinations and closed-eye visualizations (CEV) are a distinct class of hallucination. These types of hallucinations generally only occur when one's eyes are closed or when one is in a darkened room. They can be a form of phosphene. Some people report closed-eye hallucinations under the influence of psychedelics. These are reportedly of a different nature than the "open-eye" hallucinations of the same compounds.

There are five known levels of CEV perception which can be achieved either through chemical stimuli or through meditative relaxation techniques. Level 1 and 2 are very common and often happen every day. It is still normal to experience level 3, and even level 4, but only a small percentage of the population does this without psychedelic drugs, meditation or extensive visualization training.

DVD typically becomes apparent between 18 months and three years of age, however, the difficulties of achieving the prolonged occlusion required for accurate detection in the very young, make it possible that onset is generally earlier than these figures suggest.

Dissociation refers to the situation where the innervation of one eye causes it to move involuntarily and independently of the other eye. Usually both eyes work together as described by Hering's and Sherrington's laws of innervation. A DVD is a slow upward and sometimes temporal movement of one eye, with cortical suppression of the vision in that eye while it is deviated. On returning downward and possibly inward to take up fixation, the DVD slow movement will be reversed.

The dissociative movement seen 'objectively' should not be confused with the dissociation that occurs 'subjectively' - as when the brain begins to not visualise both images simultaneously (by ignoring or suppressing vision in that eye).

Coloboma of optic nerve, is a rare defect of the optic nerve that causes moderate to severe visual field defects.

Coloboma of the optic nerve is a congenital anomaly of the optic disc in which there is a defect of the inferior aspect of the optic nerve. The issue stems from incomplete closure of the embryonic fissure while in utero. A varying amount of glial tissue typically fills the defect, manifests as a white mass.

Vision in the affected eye is impaired, the degree of which depends on the size of the defect, and typically affects the visual field more than visual acuity. Additionally, there is an increased risk of serous retinal detachment, manifesting in 1/3 of patients. If retinal detachment does occur, it is usually not correctable and all sight is lost in the affected area of the eye, which may or may not involve the macula.

The cause is unclear. The underlying mechanism is believed to involve excessive excitability of neurons within the cortex of the brain.

Specifically the right lingual gyrus and left cerebellar anterior lobe of the brain.

Persisting visual snow can feature as a leading addition to a migraine complication called persistent aura without infarction, commonly referred to as persistent migraine aura (PMA). In other clinical sub-forms of migraine headache may be absent and the migraine aura may not take the typical form of the zigzagged fortification spectrum, but manifests with a large variety of focal neurological symptoms.

The role of hallucinogens in of visual snow is not clear. Hallucinogen persisting perception disorder (HPPD), a condition caused by hallucinogenic drug use, is sometimes linked to visual snow, but both the connection of visual snow to HPPD and the cause and prevalence of HPPD is disputed. Most of the evidence for both is generally anecdotal, and subject to spotlight fallacy.

Some neuro-ophthalmologists believe that visual snow is not a medical condition, but a poorly understood symptom. People report seeing "snow", much like the visual noise on a TV screen after transmission ends. These authors hypothesize that what the patients see as "snow" is their own intrinsic visual noise.

Many report more visual snow in low light conditions. This has a natural explanation. "The intrinsic dark noise of primate cones is equivalent to ~4000 absorbed photons per second at mean light levels below this the cone signals are dominated by intrinsic noise".

In addition to visual snow, many of those affected have other types of visual disturbances such as starbursts, increased afterimages, floaters, trails, and many others.

Palinopsia (Greek: "palin" for "again" and "opsia" for "seeing") is the persistent recurrence of a visual image after the stimulus has been removed. Palinopsia is not a diagnosis, it is a diverse group of pathological visual symptoms with a wide variety of causes. Visual perseveration is synonymous with palinopsia.

In 2014, Gersztenkorn and Lee comprehensively reviewed all cases of palinopsia in the literature and subdivided it into two clinically relevant groups: illusory palinopsia and hallucinatory palinopsia. Hallucinatory palinopsia, usually due to seizures or posterior cortical lesions, describes afterimages that are formed, long-lasting, and high resolution. Illusory palinopsia, usually due to migraines, head trauma, prescription drugs, or hallucinogen persisting perception disorder (HPPD), describes afterimages that are affected by ambient light and motion and are unformed, indistinct, or low resolution.

Riddoch syndrome (also known as the "Riddoch phenomenon") is an ocular affectation often caused by lesions in the occipital lobe which limit the sufferer's ability to distinguish objects. Only moving objects in a blind field are visible, static ones being invisible to the patient. The moving objects are not perceived to have color or detail. The subject may only have awareness of the movement without visual perception of it (gnosanopsia), or the general shape of a moving object may be perceivable as a shadow like outline.

At least one patient was able to use a rocking chair—putting non-moving surroundings in relative motion to her head—to improve her motion perception. She eventually was able to do the same with just voluntary movement of her head.

Posterior visual pathway cortical lesions (tumor, abscess, hemorrhage, infarction, arteriovenous malformation, cortical dysplasia, aneurysm) and various seizure causes (hyperglycemia, ion channel mutations, Creutzfeldt–Jakob disease, idiopathic seizures, etc.) cause focal cortical hyperactivity or hyperexcitability, resulting in inappropriate, persistent activation of a visual memory circuit.

Illusory palinopsia is a dysfunction of visual perception, resulting from diffuse, persistent alterations in neuronal excitability that affect physiological mechanisms of light or motion perception. Illusory palinopsia is caused by migraines, HPPD, prescription drugs, head trauma, or may be idiopathic. Trazodone, nefazodone, mirtazepine, topiramate, clomiphene, oral contraceptives, and risperidone have been reported to cause illusory palinopsia. A patient frequently has multiple types of illusory palinopsia, which represent dysfunctions in both light and motion perception. Light and motion are processed via different pathways, suggesting diffuse or global excitability alterations.

Inverse Marcus Gunn phenomenon is a rare condition that causes the eyelid to fall upon opening of the mouth. In this case, trigeminal innervation to the pterygoid muscles of the jaw is associated with an inhibition of the branch of the oculomotor nerve to the levator palpebrae superioris, as opposed to stimulation in Marcus Gunn jaw-winking.

Gestaltzerfall (German for "shape decomposition") refers to a type of visual agnosia and is a psychological phenomenon where delays in recognition are observed when a complex shape is stared at for a while as the shape seems to decompose into its constituting parts. With regards to kanji, a study has shown that delays are most significant when the characters are of the same size. When characters to recognize are of different sizes, delays are observed only when they are of different patterns.

The phenomenon was first described and named by C. Faust in 1947 as a symptom of the bilateral region of the parieto-occipital sulcus after a through and through bullet wound of this region. Afterwards, when the subject stared at a truck for a while the truck seemed to decompose into its motor, chassis, driver cab and the person could only focus on one of these parts until he briefly closed his eyes or looked away which reset the shape to the complete truck again.

The characteristic of orthographic satiation as opposed to semantic satiation is that meaning remains intact. It was suggested that this is different from semantic satiation and from the stimulus familiarization effect because orthographic satiation occurs after the perceivers have access to lexical meaning.

Aphantasia is the suggested name for a condition where one does not possess a functioning mind's eye and cannot visualize imagery. The phenomenon was first described by Francis Galton in 1880, but has remained largely unstudied since. Interest in the phenomenon renewed after the publication of a study conducted by a team led by Prof. Adam Zeman of the University of Exeter, which also coined the term "aphantasia". Research on the subject is still scarce, but further studies are planned.

Aphantasia is similar to invisible disabilities such as face blindness, word blindness, and tone deafness, though aphantasia itself has not been associated with any functional deficits.

Marcus Gunn phenomenon, also known as Marcus Gunn jaw-winking or trigemino-oculomotor synkinesis, is an autosomal dominant condition with incomplete penetrance, in which nursing infants will have rhythmic upward jerking of their upper eyelid. This condition is characterized as a synkinesis: when two or more muscles that are independently innervated have either simultaneous or coordinated movements.

Common physiologic examples of synkineses occur during sucking, chewing, or conjugate eye movements. There are also several abnormal cranial nerve synkineses, both acquired and congenital. Marcus Gunn jaw-winking is an example of a pathologic congenital synkinesis.

First described by the ophthalmologist Marcus Gunn in 1883, this condition presents in approximately 5% of neonates with congenital ptosis. This condition has been associated with amblyopia (in 54% of cases), anisometropia (26%), and strabismus (56%).

Tullio phenomenon, sound-induced vertigo, dizziness, nausea or eye movement (nystagmus) was first described in 1929 by the Italian biologist Prof. Pietro Tullio. (1881–1941) During his experiments on pigeons, Tullio discovered that by drilling tiny holes in the semicircular canals of his subjects, he could subsequently cause them balance problems when exposed to sound.

The cause is usually a fistula in the middle or inner ear, allowing abnormal sound-synchronized pressure changes in the balance organs. Such an opening may be caused by a barotrauma (e.g. incurred when diving or flying), or may be a side effect of fenestration surgery, syphilis or Lyme disease.

Patients with this disorder may also experience vertigo, imbalance and eye movement set off by changes in pressure, e.g. when nose-blowing, swallowing or when lifting heavy objects.

Tullio phenomenon is also one of the common symptoms of superior canal dehiscence syndrome (SCDS), first diagnosed in 1998 by Dr. Lloyd B. Minor, The Johns Hopkins University, Baltimore, United States.

Mees' lines or Aldrich–Mees' lines, also called leukonychia striata, are white lines of discoloration across the nails of the fingers and toes (leukonychia).

It must be emphasized that individuals without HPPD will sometimes notice visual abnormalities. These include floaters (material floating in the eye fluid that appears as black/dark objects floating in front of the eyes and are particularly visible when looking at the bright sky or on a white wall) and the white blood cells of the retinal blood vessels (seen as tiny, fast-moving and quickly disappearing white specks). Likewise, bright lights in an otherwise dark environment may generate trails and halos. Most people don't notice these effects, because they are so used to them. A person fearful of having acquired HPPD may be much more conscious about any visual disturbance, including those that are normal. In addition, visual problems can be caused by migraines, brain infections or lesions, epilepsy, and a number of mental disorders (e.g., delirium, dementia, schizophrenia, Parkinson's disease). For an individual to be diagnosed with HPPD, these other potential causes must be ruled out.

Mees' lines appear after an episode of poisoning with arsenic, thallium or other heavy metals, and can also appear if the subject is suffering from renal failure. They have been observed in chemotherapy patients.

The cause(s) of HPPD are not yet known. It has been theorized that HPPD is an anomaly in executive function brought on by the dis-inhibition of the COMT enzyme in the breakdown of catecholamines in the brain following hallucinogen use, resulting in sensory gating disruption.

In some cases, HPPD appears to have a sudden onset after a single drug experience, strongly suggesting the drug played a direct role in triggering symptoms. But in other cases, people report gradual worsening of symptoms with ongoing drug use. Drugs that have been associated with HPPD include CBD, LSD, 5-MeO-DiPT MDA, MDMA, psilocybin, diphenhydramine, PCP, synthetic cannabinoids, zolpidem, eszopiclone, and high doses of dextromethorphan, a high dose of the wakefulness enhancing agent modafinil combined with a CNS stimulant, namely, caffeine can also be a trigger. Additionally there are anecdotal reports of the atypical psychedelic "Salvia divinorum" causing persisting symptoms consistent with HPPD.