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

Formed image perseveration refers to a single, stationary object that remains fixed in one’s visual field. These pathological afterimages look realistic and have the same color and clarity as the original stimulus. The palinopsia lasts at least 15 seconds, but may persist for hours or days. For example, a patient sees a cat, and an identical copy of the cat remains fixed in the field of view for 30 minutes. A patient commonly complains of the perseverated fingers of an examiner. These afterimages often occur in visual field deficits but may occur anywhere in the visual field, regardless of the location of the original stimulus. The generation of the afterimages is not affected by external conditions such as the length of fixation, stimulus intensity, contrast, or motion. The palinoptic image can appear immediately after seeing the original image or may be delayed in time.

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.

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.

People with palinopsia frequently report other visual illusions and hallucinations such as photopsias, dysmetropsia i.e. Alice in Wonderland syndrome (micropsia, macropsia, teleopsia, and pelopsia), visual snow, oscillopsia, entoptic phenomena, and cerebral polyopia.

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.

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).

The occurrence of MES has been suggested to be very high among the hearing impaired through acquired deafness or the ear condition known as tinnitus. Though exact causation is uncertain, it has been theorized that the "release phenomenon" is taken into effect. The "release phenomenon" says that individuals with acquired deafness may experience musical hallucinations because the lack of stimulation, which can give room for the brain to interpret internal sounds as being external.

Sufferers typically hear music or singing and the condition is more common in women. The hallucinatory experiences differ from that commonly experienced in psychotic disorders although there may be some overlap. The most important distinction is the realization that the hallucinations are not real. Delusional beliefs associated with the hallucinations may occur, but some degree of insight should be preserved. There should not be any other psychotic symptoms present, especially hallucinations in other modalities.

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

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).

Musical ear syndrome (MES) describes a condition seen in people who have hearing loss and subsequently develop auditory hallucinations. "MES" has also been associated with musical hallucinations, which is a complex form of auditory hallucinations where an individual may experience music or sounds that are heard without an external source. It is comparable to Charles Bonnet syndrome (visual hallucinations in visually impaired people) and some have suggested this phenomenon could be included under this diagnosis.

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.

Tactile hallucination is the false perception of tactile sensory input that creates a hallucinatory sensation of physical contact with an imaginary object. It is caused by the faulty integration of the tactile sensory neural signals generated in the spinal cord and the thalamus and sent to the primary somatosensory cortex (SI) and secondary somatosensory cortex (SII). Tactile hallucinations are recurrent symptoms of neurological diseases such as schizophrenia, Parkinson's disease, Ekbom's syndrome and delerium tremens. Patients who experience phantom limb pains also experience a type of tactile hallucination. Tactile hallucinations are also caused by drugs such as cocaine and alcohol.

Focal aware seizures are seizures which affect only a small region of the brain, often the temporal lobes or structures found there such as the hippocampi. People who have focal aware seizures remain conscious. Focal aware seizures often precede larger focal impaired awareness seizures, where the abnormal electrical activity spreads to a larger area of the brain. This can result in a tonic-clonic seizure.

- Presentation

Focal onset aware seizures are a very subjective experience, and the symptoms vary greatly between people. This is due to the varying locations of the brain the seizures originate in e.g.: Rolandic. A focal aware seizure may go unnoticed by others or shrugged off by the sufferer as merely a "funny turn." Focal aware seizures usually start suddenly and are very brief, typically lasting 60 to 120 seconds.

Some common symptoms of a focal onset aware seizure, when the person is awake, are:

- preserved consciousness

- sudden and inexplicable feelings of fear, anger, sadness, happiness or nausea

- sensations of falling or movement

- experiencing of unusual feelings or sensations

- altered sense of hearing, smelling, tasting, seeing, and tactile perception (sensory illusions or hallucinations), or feeling as though the environment is not real (derealization) or dissociation from the environment or self (depersonalization)

- a sense of spatial distortion—things close by may appear to be at a distance

- déjà vu (familiarity) or jamais vu (unfamiliarity)

- laboured speech or inability to speak at all

- usually the event is remembered in detail

When the seizure occurs during sleep, the person will often become semi-conscious and act out a dream they were having while engaging with the real environment as normal. Objects and people usually appear normal or only slightly distorted to them, and will be able to communicate with them on an otherwise normal level.

However, since the person is still acting in the dream-like state from which they woke, they will assimilate any hallucinations or delusions into their communication, often speaking to a hallucinatory person or speaking of events or thoughts normally pertaining to the dream they were having or other hallucination.

While asleep symptoms include:

- onset usually in REM sleep

- dream like state

- appearance of full consciousness

- hallucinations or delusions

- behavior or visions typical in dreams

- ability to engage with the environment and other people as in full consciousness, though often behaving abnormally, erratically, or failing to be coherent

- complete amnesia or assimilating the memory as though it was a normal dream on regaining full consciousness

Although hallucinations may occur during focal aware seizures they are differentiated from psychotic symptoms by the fact that the person is usually aware that the hallucinations are not real.

- Jacksonian march

Jacksonian march or Jacksonian seizure is a phenomenon where a focal aware seizure spreads from the distal part of the limb toward the face (on same side of body). They involve a progression of the location of the seizure in the brain, which leads to a "march" of the motor presentation of symptoms.

Jacksonian seizures are initiated with abnormal electrical activity within the primary motor cortex. They are unique in that they travel through the primary motor cortex in succession, affecting the corresponding muscles, often beginning with the fingers. This is felt as a tingling sensation, or a feeling of waves through the fingers when touched together. It then affects the hand and moves on to more proximal areas on the same side of body. Symptoms often associated with a Jacksonian seizure are sudden head and eye movements, tingling, numbness, smacking of the lips, and sudden muscle contractions. Most of the time any one of these actions can be seen as normal movements, without being associated with the seizure occurring. They occur at no particular moment and last only briefly. They may result in secondary generalized seizure involving both hemispheres. They can also start at the feet, manifesting as tingling or pins and needles, and there are painful cramps in the foot muscles, due to the signals from the brain. Because it is a partial seizure, the postictal state is of normal consciousness .

A focal impaired awareness seizure is a seizure that is associated with unilateral cerebral hemisphere involvement and causes impairment of awareness or responsiveness, i.e. alteration of consciousness.

- Presentation

Focal impaired awareness seizures are often preceded by an aura. The seizure aura is a focal aware seizure. The aura may manifest itself as a feeling of déjà vu, jamais vu, fear, euphoria or depersonalization. The aura might also occur as a visual disturbance, such as tunnel vision or a change in the perceived size of objects. Once consciousness is impaired, the person may display automatisms such as lip smacking, chewing or swallowing. There may also be loss of memory (amnesia) surrounding the seizural event. The person may still be able to perform routine tasks such as walking, although such movements are not purposeful or planned. Witnesses may not recognize that anything is wrong.

Focal impaired awareness seizures might arise from any lobe of the brain. They most commonly arise from the temporal lobe, particularly the amygdala, hippocampus, and neocortical regions. A common associated brain abnormality is mesial temporal sclerosis. Mesial temporal sclerosis is a specific pattern of hippocampal neuronal loss accompanied by hippocampal gliosis and atrophy. Focal onset impaired awareness seizures occur when excessive and synchronous electrical brain activity causes the impaired awareness and responsiveness. The abnormal electrical activity might spread to the rest of the brain and cause a "focal to bilateral seizure" or a generalized tonic–clonic seizure. The newer classification of 2017 groups only focal and generalized seizures, and generalised seizures are those that involve both sides of the brain from the onset.

About 7% of individuals with Parkinson's disease also experience mild or severe types of tactile hallucinations. Most of these hallucinations are based on the sensation of a particular kind of animal. Several case studies were conducted by Fénelon and his colleagues on parkinson's patients that had tactile hallucinations. One of his patients described that he sensed "spiders and cockroaches chewing on his lower limb" which was rather painful. Several other patients felt that there was a parasitic infestation of their skin which caused lesions on their skins due to the obsessive need of itching. Fénelon also analyzed the particular types of tactile hallucinations experienced, the timing of such experience and certain drugs that could eliminate such experience. It was concluded that patients with both Parkinson's disease and tactile hallucinations not only experienced sensations elicited by insects under their skin but also by vivid tactile sensations of people. These hallucinations were aggravated during evening times due to altered arousal states and were alleviated by dopaminergic treatment such as the intake of clozapine. The study also explains that the pathophysiology of tactile hallucinations is uncertain, however, such hallucinations can be attributed to narcoleptic rapid eye movement sleep disorders due to its concordance with visual hallucinations. Moreover, it emphasizes that individuals who have had Parkinson's for a longer period of time have a more severe form of tactile hallucinations than with individuals who have succumbed to this disease for just a short period of time.

Clinical drugs used as an antiparkinsonian agent such as Trihexyphenidyl are known to create tactile hallucinations in parkinson patients.

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.

Visual hallucinations due to focal seizures differ depending on the region of the brain where the seizure occurs. For example, visual hallucinations during occipital lobe seizures are typically visions of brightly colored, geometric shapes that may move across the visual field, multiply, or form concentric rings and generally persist from a few seconds to a few minutes. They are usually unilateral and localized to one part of the visual field on the contralateral side of the seizure focus, typically the temporal field. However, unilateral visions moving horizontally across the visual field begin on the contralateral side and move toward the ipsilateral side.

Temporal lobe seizures, on the other hand, can produce complex visual hallucinations of people, scenes, animals, and more as well as distortions of visual perception. Complex hallucinations may appear to be real or unreal, may or may not be distorted with respect to size, and may seem disturbing or affable, among other variables. One rare but notable type of hallucination is heautoscopy, a hallucination of a mirror image of one's self. These "other selves" may be perfectly still or performing complex tasks, may be an image of a younger self or the present self, and tend to be only briefly present. Complex hallucinations are a relatively uncommon finding in temporal lobe epilepsy patients. Rarely, they may occur during occipital focal seizures or in parietal lobe seizures.

Distortions in visual perception during a temporal lobe seizure may include size distortion (micropsia or macropsia), distorted perception of movement (where moving objects may appear to be moving very slowly or to be perfectly still), a sense that surfaces such as ceilings and even entire horizons are moving farther away in a fashion similar to the dolly zoom effect, and other illusions. Even when consciousness is impaired, insight into the hallucination or illusion is typically preserved.

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.

Charles Bonnet syndrome is the name given to visual hallucinations experienced by a partially or severely sight impaired person. The hallucinations can occur at any time and can distress people of any age, as they may not initially be aware that they are hallucinating, they may fear initially for their own mental health which may delay them sharing with carers what is happening until they start to understand it themselves. The hallucinations can frighten and disconcert as to what is real and what is not and carers need to learn how to support sufferers. The hallucinations can sometimes be dispersed by eye movements, or perhaps just reasoned logic such as, "I can see fire but there is no smoke and there is no heat from it" or perhaps "We have an infestation of rats but they have pink ribbons with a bell tied on their necks." Over elapsed months and years the manifestation of the hallucinations may change, becoming more or less frequent with changes in ability to see. The length of time that the sight impaired person can suffer from these hallucinations varies according to the underlying speed of eye deterioration. A differential diagnosis are ophthalmopathic hallucinations.

Oneirophenia and schizophrenia are often confused although there are distinct differences between the conditions. Oneirophrenia has some of the characteristics of simple schizophrenia, such as a confusional state and clouding of consciousness, but without presenting the dissociative symptoms which are typical of that disorder. Oneiophrenia often begins with the inability to focus on things while schizophrenia frequently starts with a traumatic event. Persons affected by oneirophrenia have a feeling of dream-like derealization which, in its extreme form, may progress to delusions and hallucinations. Therefore, it is considered a schizophrenia-like acute form of psychosis which remits in about 60% of cases within a period of two years. It is estimated that 50% or more of schizophrenic patients present oneirophrenia at least once.

Oneirophrenia (from the Greek words "" ("oneiros", "dream") and "" ("phrenos", "mind")) is a hallucinatory, dream-like state caused by several conditions such as prolonged sleep deprivation, sensory deprivation, or drugs (such as ibogaine). Oneirophrenia is often confused with an acute case of schizophrenia due to the onset of hallucinations. The severity of this condition can range from derealization to complete hallucinations and delusions. Oneirophrenia was described for the first time in the 1950s but was studied more in the 1960s. Although it is still cited in diagnostic manuals of psychiatry, such as DSM-IV and in the International Statistical Classification of Diseases and Related Health Problems (ICD), oneirophrenia as a separate entity is out of fashion nowadays.

Chronic hallucinatory psychosis is a psychosis subtype, classified under "Other nonorganic psychosis" by the . Other abnormal mental symptoms in the early stages are, as a rule, absent. The patient is most usually quiet and orderly, with a good memory.

It has often been a matter of the greatest difficulty to decide under which heading of the recognized classifications individual members of this group should be placed. As the hallucinations give rise to slight depression, some might possibly be included under melancholia. In others, paranoia may develop. Others, again, might be swept into the widespread net of dementia praecox. This state of affairs cannot be regarded as satisfactory, for they are not truly cases of melancholia, paranoia, dementia praecox or any other described affection.

This disease, as its name suggests, is a hallucinatory case, for it is its main feature. These may be of all senses, but auditory hallucinations are the most prominent. At the beginning, the patient may realize that the hallucination is a morbid phenomenon and unaccountable. They may claim to hear a "voice" speaking, though there is no one in the flesh actually doing so. Such a state of affairs may last for years and possibly, though rarely, for life, and the subject would not be deemed insane in the ordinary sense of the word.

It's probable, however, that this condition forms the first stage of the illness, which eventually develops on definite lines. What usually happens is the patient seeks an explanation for the hallucinations. As none is forthcoming he/she tries to account for their presence and the result is a delusion, and, most frequently, a delusion of persecution. Also, it needs to be noted that the delusion is a comparatively late arrival and is the logical result of the hallucinations.

In one of the few reported cases, the subject presented with muscle weakness and fatigue, muscle twitching, excessive sweating and salivation, small joint pain, itching and weight loss. The subject also developed confusional episodes with spatial and temporal disorientation, visual and auditory hallucinations, complex behavior during sleep and progressive nocturnal insomnia associated with diurnal drowsiness. There was also severe constipation, urinary incontinence, and excessive lacrimation. When left alone, the subject would slowly lapse into a stuporous state with dreamlike episodes characterized by complex and quasi-purposeful gestures and movements (enacted dreams). Marked hyperhidrosis and excessive salivation were evident. Neurological examination disclosed diffuse muscle twitching and spontaneous and reflex myoclonus, slight muscle atrophy in the limbs, absence of tendon reflexes in the lower limbs and diffuse erythema especially on the trunk with scratching lesions of the skin.

Compulsive behaviours, stereotypies and reduplicative paramnesias can be part of the CNS spectrum.

In all of the reported cases, the need for sleep was severely reduced and in some cases not necessary. The duration of sleep in one case decreased to about 2–4 hours per 24-hour period. Clinical features pertaining to insomnia include daytime drowsiness associated with a loss of ability to sleep, intermingled with confusional oneiric status, and the emergence of atypical REM sleep from wakefulness. The Polysomnogram (PSG) picture of this disease is characterized by an inability to generate physiological sleep (key features are the suppression of the hallmarks of stage 2 non-REM sleep: spindles and K complexes) and by the emergence of REM sleep without atonia. The involvement of the thalamus and connected limbic structures in the pathology indicate the prominent role that the limbic thalamus plays in the pathophysiology of sleep. In a case documented in 1974, PSG findings documented the sustained absence of all sleep rhythms for up to a period of 4 months.

Electroencephalography (EEG) in one case was dominated by "wakefulness" and “subwakefulness” states alternating or intermingled with short (< 1 min) atypical REM sleep phases, characterized by a loss of muscle atonia. The “subwakefulness” state was characterized by 4–6 Hz theta activity intermingled with fast activity and desynchronized lower voltage theta activity, behaviourally associated with sleep-like somatic and autonomic behavior. The subject was said to suffer from “agrypnia excitata”, which consists of severe total insomnia of long duration associated with decreased vigilance, mental confusion, hallucinations, motor agitation, and complex motor behavior mimicking dreams, and autonomic activation. CNS and autonomic symptoms were caused by impaired corticolimbic control of the subcortical structures regulating the sleep-wake and autonomic functions.