There are a few cases of palinopsia with many of the same features as hallucinatory palinopsia (formed image perseveration) but with some important differences. The formed perseverated image may only last a couple seconds or may be black or translucent. These variants usually lack the realistic clarity of hallucinatory palinopsia, and the generation of the palinoptic images is affected by fixation time, motion, stimulus intensity, or contrast. These variants probably represent an overlap in hallucinatory and illusory palinopsia but are included in illusory palinopsia since they often co-exist with the other illusory symptoms.

Light streaking describes a comet-like tail which is seen due to motion between a person or a light. The streaking usually persists for several seconds before fading and often occurs with bright lights on a dark background. Patients commonly report of difficulty with night driving since the headlights of oncoming cars cause multiple streaks which obscure vision.

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.

Palinopsia is a pathological symptom and should be distinguished from physiological afterimages, a common and benign phenomenon. Physiological afterimages appear when viewing a bright stimulus and shifting visual focus. For example, after staring at a computer screen and looking away, a vague afterimage of the screen remains in the visual field. A stimulus consistently produces the same afterimage, which is dependent on the stimulus intensity and contrast, the time of fixation, and the retinal adaptation state. Physiological afterimages are usually the complementary color of the original stimulus (negative afterimage), while palinoptic afterimages are usually the same color as the original stimulus (positive afterimage). There is some ambiguity between illusory palinopsia and physiological afterimages since there are not concrete symptomatic criteria which determines if an afterimage is pathological.

Hallucinatory palinopsia consists of the following four symptom categories. A person often reports symptoms from multiple categories.

Hallucinatory palinopsia (Greek: "palin" for "again" and "opsia" for "seeing") is a subtype of palinopsia, a visual disturbance defined as the persistent or recurrence of a visual image after the stimulus has been removed. Palinopsia is a broad term describing a heterogeneous group of symptoms which is divided into hallucinatory palinopsia and illusory palinopsia. Hallucinatory palinopsia refers to the projection of an already-encoded visual memory and is similar to a complex visual hallucination: the creation of a formed visual image where none exists.

Hallucinatory palinopsia usually arises from posterior cortical lesions or seizures and can be the presenting symptom of a serious neurological disease. Hallucinatory palinopsia describes afterimages or scenes that are formed, long-lasting, high resolution, and isochromatic. The palinoptic images are not typically reliant on environmental parameters and often present with homonymous visual field deficits. Hallucinatory palinopsia occurs unpredictably and the persistent images can appear anywhere in the visual field, regardless of the location of the original stimulus. A patient will often have only a few episodes of hallucinatory palinopsia. Visual perseveration is synonymous with palinopsia.

Migraine and migraine with aura are common comorbidities. However, comorbid migraine worsens some of the additional visual symptoms and tinnitus seen in "visual snow" syndrome. This might bias research studies by patients with migraine being more likely to offer study participation than those without migraine due to having more severe symptoms. In contrast to migraine, comorbidity of typical migraine aura does not appear to worsen symptoms.

Patients with visual "snow" have normal equivalent input noise levels: Visual snow is a poorly understood symptom. Patients report seeing "snow", much like the visual noise on a TV screen after transmission ends. Some hypothesize that what the patients see as "snow" is their own intrinsic visual noise. Dennis Pelli and others' measurements assess whether visual-snow patients have increased levels of intrinsic visual noise.

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.

Inconspicuous akinetopsia is often described by seeing motion as a cinema reel or a multiple exposure photograph. This is the most common kind of akinetopsia and many patients consider the stroboscopic vision as a nuisance. The akinetopsia often occurs with visual trailing (palinopsia), with afterimages being left at each frame of the motion. It is caused by prescription drugs, hallucinogen persisting perception disorder (HPPD), and persistent aura without infarction. The pathophysiology of akinetopsia palinopsia is not known, but it has been hypothesized to be due to inappropriate activation of physiological motion suppression mechanisms which are normally used to maintain visual stability during eye movements (e.g. saccadic suppression).

Cerebral diplopia or polyopia describes seeing two or more images arranged in ordered rows, columns, or diagonals after fixation on a stimulus. The polyopic images occur monocular bilaterally (one eye open on both sides) and binocularly (both eyes open), differentiating it from ocular diplopia or polyopia. The number of duplicated images can range from one to hundreds. Some patients report difficulty in distinguishing the replicated images from the real images, while others report that the false images differ in size, intensity, or color. Cerebral polyopia is sometimes confused with palinopsia (visual trailing), in which multiple images appear while watching an object. However, in cerebral polyopia, the duplicated images are of a stationary object which are perceived even after the object is removed from the visual field. Movement of the original object causes all of the duplicated images to move, or the polyopic images disappear during motion. In palinoptic polyopia, movement causes each polyopic image to leave an image in its wake, creating hundreds of persistent images (entomopia).

Infarctions, tumors, multiple sclerosis, trauma, encephalitis, migraines, and seizures have been reported to cause cerebral polyopia. Cerebral polyopia has been reported in extrastriate visual cortex lesions, which is important for detecting motion, orientation, and direction. Cerebral polyopia often occurs in homonymous field deficits, suggesting deafferentation hyperexcitability could be a possible mechanism, similar to visual release hallucinations (Charles Bonnet syndrome).

Cerebral polyopia is most often associated with occipital or temporal lobe lesions, as well as occipital lobe epilepsy. This condition is relatively uncommon, thus further research regarding its causes and mechanism has not been performed. Polyopia can be experienced as partial second or multiple images to either side (or in any eccentricity) of an object at fixation. Polyopia occurs when both eyes are open, or when one eye is open, during fixation on a stimulus. Known cases of polyopia provide evidence that, in relation to the stimulus at fixation, multiple images can appear at a constant distance in any direction; gaps in portions of an object at fixation can exist; multiple images can be overlaid vertically, horizontally, or diagonally on top of the stimulus; and the multiple images can appear different sizes, alignments, and complexities. The complexity of the stimulus does not appear to affect the clarity of the multiple images. The physical distance of the stimulus from the patient (near or far) also does not seem to affect the presence of multiple images. However, if the stimulus is swung or moved, multiple images of that object can either be extinguished or transformed into different objects, depending on the severity of the condition.

The onset of polyopia is not immediate upon perception of visual stimuli; rather, it occurs within milliseconds to seconds of fixation upon a stimulus. Polyopia has been described by patients as images “suddenly multiplying.” These multiple images can drift, fade, and disappear, depending on the severity of the condition. These episodes of polyopia can last from seconds to hours. In one specific case, a patient described difficulties reading due to letters “run[ning] together” and momentarily disappearing.

Most cases of polyopia are accompanied by another neurological condition. Polyopia is often accompanied by visual field defects (such as the presence of a scotoma) or transient visual hallucinations. Polyopic images often form in the direction and position of such visual field defects. Current research shows that when stimuli are close to the patient’s scotoma, the latency of polyopic images is much shorter than if the stimuli was far from the scotoma, and there is a higher probability that polyopic images will result.

Akinetopsia can be separated into two categories based on symptom severity and the amount the akinetopsia affects the patient's quality of life.

There are a number of perceptual changes that can accompany HPPD. Typical symptoms of the disorder include: halos or auras surrounding objects, trails following objects in motion, difficulty distinguishing between colors, apparent shifts in the hue of a given item, the illusion of movement in a static setting, air assuming a grainy or textured quality (visual snow or static, by popular description, not to be confused with normal "blue field entoptic phenomenon"), distortions in the dimensions of a perceived object, and a heightened awareness of floaters. The visual alterations experienced by those with HPPD are not homogeneous and there appear to be individual differences in both the number and intensity of symptoms.

Visual aberrations can occur periodically in healthy individuals – e.g. afterimages after staring at a light, noticing floaters inside the eye, or seeing specks of light in a darkened room. However, in people with HPPD, symptoms are typically persistent enough that the individual cannot ignore them.

There is some uncertainty about to what degree visual snow constitutes a true HPPD symptom. There are many individuals who have never used a drug which could have caused the onset, but yet experience the same grainy vision reported by HPPD sufferers. There are a few potential reasons for this, the most obvious of which being the theory that the drug usage may exaggerate the intensity of visual snow. Another theory is that instead, there may be no change in the severity or magnitude of the visual snow, but perhaps the drug usage opens sensory pathways that result in the individual becoming more aware of any visual disturbances that may have simply not been noticed before the incidence of drug use. As for root cause of visual snow, some theories suggest that it is the result of thermal noise in the visual cortex or in the 'Optic Pathway' (encompassing photoreceptor cells on the retina, the optic nerve, and the optic chiasm), as eye tests for individuals who experience visual snow often reveal that physically, the eye is perfectly normal, and in many cases the individual still maintains 20/20 vision.

HPPD usually has a visual manifestation. Drugs affecting the auditory sense, like DiPT, may produce auditory disturbances, though there are few known cases. Some psychedelic drugs can produce temporary tinnitus-like symptoms as a side effect.

It also should be noted that the visuals do not constitute true hallucinations in the clinical sense of the word; people with HPPD recognize the visuals to be illusory, or pseudohallucinations, and thus maintain the ability to determine what is real (in contrast to some mental illnesses such as schizophrenia).

The visual problems of HPPD can occur along with other mental ailments. Of these, the most prominent are anxiety, panic attacks, depersonalization disorder, and depression.

While it is difficult, if not impossible, to establish a clear relationship between the visual and mental symptoms, those with HPPD often testify that a connection indeed exists. For example, some claim that anxiety can cause the visuals to become more prominent and vice versa.

One possible cause of increased anxiety and depression is the person reacting negatively to the visual disturbances.

Spatial disorientation, spatial unawareness is the inability of a person to correctly determine his/her body position in space. This phenomenon refers especially to aircraft pilots and underwater divers, but also can be induced in normal conditions—chemically or physically ("e.g.," by blindfolding). In aviation, the term means the inability to correctly interpret aircraft attitude, altitude or airspeed, in relation to the ground or point of reference, especially after a reference point ("e.g.," the horizon) has been lost. Spatial disorientation is a condition in which an aircraft pilot's perception of direction does not agree with reality. While it can be brought on by disturbances or disease within the vestibular system, it is more typically a temporary condition resulting from flight into poor weather conditions with low or no visibility. Under these conditions the pilot may be deprived of an external visual horizon, which is critical to maintaining a correct sense of up and down while flying.

A pilot who enters such conditions will quickly lose spatial orientation if there has been no training in flying with reference to instruments. Approximately 80% of the private pilots in the United States do not have an instrument rating, and therefore are prohibited from flying in conditions where instrument skills are required. Not all pilots abide by this rule and approximately 40% of the NTSB fatal general aviation accident reports list "continuation of flight into conditions for which the pilot was not qualified" as a cause.

Pathological nystagmus is characterized by "excessive drifts of stationary retinal images that degrades vision and may produce illusory motion of the seen world: oscillopsia (an exception is congenital nystagmus)".

When nystagmus occurs without fulfilling its normal function, it is pathologic (deviating from the healthy or normal condition). Pathological nystagmus is the result of damage to one or more components of the vestibular system, including the semicircular canals, otolith organs, and the vestibulocerebellum.

Pathological nystagmus generally causes a degree of vision impairment, although the severity of such impairment varies widely. Also, many blind people have nystagmus, which is one reason that some wear dark glasses.

Physiological nystagmus is a form of involuntary eye movement that is part of the vestibulo-ocular reflex (VOR), characterized by alternating smooth pursuit in one direction and saccadic movement in the other direction.

Reduplicative paramnesia is the delusional belief that a place or location has been duplicated, existing in two or more places simultaneously, or that it has been 'relocated' to another site. It is one of the delusional misidentification syndromes and, although rare, is most commonly associated with acquired brain injury, particularly simultaneous damage to the right cerebral hemisphere and to both frontal lobes.

Vertigo is a medically recognized term for the symptom of vestibular system disturbance. It may include a feeling of rotation or illusory sensations of motion or both. The general term dizziness is used by nonmedical people for those symptoms but often refers to a feeling of light-headedness, giddiness, drowsiness, or faintness, all of which must be differentiated from true vertigo, since the latter symptoms might have other causes.

Motion sickness occurs more frequently in migraine patients (30–50% more than in controls). Benign paroxysmal vertigo of childhood is an example of migraine-associated vertigo in which headache does not often occur. Basilar artery migraine (BAM) consists of two or more symptoms (vertigo, tinnitus, decreased hearing, ataxia, dysarthria, visual symptoms in both hemifields or both eyes, diplopia, bilateral paresthesias, paresis, decreased consciousness and/or loss of consciousness) followed by throbbing headache. Auditory symptoms are rare. However, a study showed a fluctuating low-tone sensorineural hearing loss in more than 50% of patients with BAM with a noticeable change in hearing just before the onset of a migraine headache. The attacks of vertigo are usually concurrent with the headache and the family history is usually positive. The diagnostician must rule out: TIAs, and paroxysmal vestibular disorder accompanied by headache.

There is also a familial vestibulopathy, familial benign recurrent vertigo (fBRV), where episodes of vertigo occur with or without migraine headache. Testing may show profound vestibular loss. The syndrome responds to acetazolamide. Familial hemiplegic migraine (FHM) has been linked to mutations in the calcium channel gene. (Ophoff et al. 1966 cf. Lempert et al.)

Anyone in an aircraft that is making a coordinated turn, no matter how steep, will have little or no sensation of being tilted in the air unless the horizon is visible. Similarly, it is possible to gradually climb or descend without a noticeable change in pressure against the seat. In some aircraft, it is possible to execute a loop without pulling negative G so that, without visual reference, the pilot could be upside down without being aware of it. This is because a gradual change in any direction of movement may not be strong enough to activate the fluid in the vestibular system, so the pilot may not realize that the aircraft is accelerating, decelerating, or banking.

Benign paroxysmal positional vertigo - Migraine is commonly associated with BPPV, the most common vestibular disorder in patients presenting with dizziness. The two may be linked by genetic factors or by vascular damage to the labyrinth.

Ménière's disease - There is an increased prevalence of migraine in patients with Ménière's disease and migraine leads to a greater susceptibility of developing Ménière’s disease. But they can be distinguished. Ménière's disease may go on for days or even years, while migraines typically do not last longer than 24 hours.

Motion sickness is more prevalent in patients with migraine.

Psychiatric syndromes Dizziness and spinning vertigo are the second most common symptom of panic attacks, and they can also present as a symptom of major depression. Migraine is a risk factor for developing major depression and panic disorder and vice versa.

Reduplicative paramnesia has been reported in the context of a number of neurological disorders, including stroke, intracerebral hemorrhage, tumor, dementia, encephalopathy and various psychiatric disorders.

Taken from the Benson and colleagues study, the following excerpt illustrates some of the core features of the delusion. The patient had suffered a head injury after a fall in his home. The impact had caused a fractured skull and frontal lobe damage to both sides (although more pronounced on the right) owing to the formation of intracerebral hematomas:

The illusory relocation to a familiar place, such as a home or town the patient knows well, is a common theme, although occasionally the patient believes they are resident in more fantastical or exotic locations (such as, in one case, Timbuktu).

The central symptom of sleep paralysis is being aware but being unable to move during awakening.

Imagined sounds such as humming, hissing, static, zapping and buzzing noises are reported during sleep paralysis. Other sounds such as voices, whispers and roars are also experienced. These symptoms are usually accompanied by intense emotions: such as fear, and panic. People also have sensations of being dragged out of bed or of flying, numbness, and feelings of electric tingles or vibrations running through their body.

Sleep paralysis may include hallucinations, such as a supernatural creature suffocating or terrifying the individual, accompanied by a feeling of pressure on one's chest and difficulty breathing. Another example of a hallucination involves a menacing shadowy figure entering one's room or lurking outside one's window, while the subject is paralyzed.

The body image distortion (affecting parietal regions and the temporoparietal junction) may result in the sleeper having bodily hallucinations, such as illusory limbs and out-of-body experiences. The content and interpretation of these hallucinations are driven by fear, somatic sensations, REM-induced sexual arousal, and REM mentation which are embedded in the sleeper's cultural narrative.

REM sleep physiology and somatic symptoms coupled with the awareness that one is paralyzed, can generate a variety of psychological symptoms during sleep paralysis, including fear and worry that are aggravated by catastrophic cognitions about the attack. This can activate a fight-flight reaction and panic-like arousal. Consequently, when the person attempts to escape the paralysis, somatic symptoms and arousal are exacerbated, as execution of motor programs in the absence of dampening proprioceptive feedback can lead to heightened sensations of bodily tightness and pressure, and even pain and spasms in limbs.

Sleep paralysis is when, during awakening or falling asleep, one is aware but unable to move. During an episode, one may hear, feel, or see things that are not there. It often results in fear. Episodes generally last less than a couple of minutes. It may occur as a single episode or be recurrent.

The condition may occur in those who are otherwise healthy, those with narcolepsy, or may run in families as a result of specific genetic changes. The condition can be triggered by sleep deprivation, psychological stress, or abnormal sleep cycles. The underlying mechanism is believed to involve a dysfunction in REM sleep. Diagnosis is based on a person's description. Other conditions that can present similarly include narcolepsy, atonic seizure, and hypokalemic periodic paralysis.

Treatment options for sleep paralysis have been poorly studied. People should generally be reassured that the condition is common and not serious. Other efforts that may be tried include sleep hygiene, cognitive behavioral therapy, and antidepressants.

Between 8% and 50% of people experience sleep paralysis at some time. About 5% of people have regular episodes. Males and females are affected equally. Sleep paralysis has been described throughout history. It is believed to have played a role in the creation of stories about alien abduction and other paranormal events.

Repressed memories are memories that have been unconsciously blocked due to the memory being associated with a high level of stress or trauma. The theory postulates that even though the individual cannot recall the memory, it may still be affecting them consciously, and that these memories can emerge later into the consciousness. Ideas on repressed memory hiding trauma from awareness were an important part of Sigmund Freud's early work on psychoanalysis. He later took a different view.

The existence of repressed memories is an extremely controversial topic in psychology; although some studies have concluded that it can occur in a varying but generally small percentage of victims of trauma, many other studies dispute its existence entirely. Some psychologists support the theory of repressed memories and claim that repressed memories can be recovered through therapy, but most psychologists argue that this is in fact rather a process through which false memories are created by blending actual memories and outside influences. One study concluded that repressed memories were a cultural symptom due to the lack of written proof of their existence before the nineteenth century, but its results were disputed by some psychologists, and the lack of written proof was eventually partially disproven.

According to the American Psychological Association, it is not possible to distinguish repressed memories from false ones without corroborating evidence. The term repressed memory is sometimes compared to the term dissociative amnesia, which is defined in the DSM-V as an “inability to recall autobiographical information. This amnesia may be localized (i.e., an event or period of time), selective (i.e., a specific aspect of an event), or generalized (i.e., identity and life history).”

According to the Mayo Clinic, amnesia refers to any instance in which memories stored in the long-term memory are completely or partially forgotten, usually due to brain injury.

According to proponents of the existence of repressed memories, such memories can be recovered years or decades after the event, most often spontaneously, triggered by a particular smell, taste, or other identifier related to the lost memory, or via suggestion during psychotherapy.