There are suggestions that visual distortions, such as macropsia, can be associated with cocaine use. Episodes of temporary drug-induced macropsia subside as the chemicals leave the body.

Patients with both Epstein-Barr virus and infectious mononucleosis have cited an increase in the sizes of perceived objects, coinciding with other symptoms of Alice in Wonderland Syndrome. Additionally, it has been observed that Epstein-Barr patients who cite hallucinations display abnormal MRI scans. The MRI may show swelling of the cerebral cortex, transient T2 prolongation, and transient lesions. Unlike in MRI's, no abnormalities have been reported in CT scans. It is thus recommended that an Epstein-Barr patient who cites visual hallucinations have an MRI scan. Macropsia may appear either before the onset, or after the resolution, of all clinical symptoms associated with the illness. The duration of the disturbances have been shown to range between two weeks and seven months. Almost all patients with macropsia due to infectious mononucleiosis make full recoveries. Patients with Coxsackievirus B1 have reported numerous symptoms of Alice in Wonderland Syndrome, the most common of which being macropsia and micropsia.

Episodes of micropsia or macropsia occur in 9% of adolescents.

10-35% of migraine sufferers experience auras, with 88% of these patients experiencing both visual auras (which include micropsia) and neurological auras.

Micropsia seems to be slightly more common in boys than in girls among children who experience migraines.

Approximately 80% of temporal lobe seizures produce auras that may lead to micropsia or macropsia. They are a common feature of simple partial seizures and usually precede complex partial seizures of temporal lobe origin.

Central Serous Chorioretinopathy (CSCR) which can produce micropsia predominantly affects persons between the ages of 20 and 50. Women appear to be affected more than men by a factor of almost 3 to 1.

Micropsia can be caused by swelling of the cornea due to infection by the Epstein-Barr virus (EBV) and can therefore present as an initial symptom of EBV mononucleosis, a disease caused by Epstein-Barr virus infection.

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.

Of the published cases of palinopsia that are idiopathic or attributed to migraines, HPPD, prescription drugs, or head trauma, 94% described illusory palinopsia. Trazodone, nefazodone, mirtazapine, topiramate, clomiphene, oral contraceptives, and risperidone have been reported to cause illusory palinopsia. Clomiphene and oral contraceptives are the only prescription drugs reported to cause permanent symptoms. HPPD is most common after LSD ingestion, but can occur after any hallucinogen use. HPPD is commonly described in psychiatric literature and illusory palinopsia symptoms are sometimes not defined as palinopsia. It is not clear if there is a relationship between HPPD and the quantity and strength of hallucinogen doses taken.

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.

Illusory palinopsia (Greek: "palin" for "again" and "opsia" for "seeing") is a subtype of palinopsia, a visual disturbance defined as the persistence 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. Illusory palinopsia is likely due to sustained awareness of a stimulus and is similar to a visual illusion: the distorted perception of a real external stimulus.

Illusory palinopsia is caused by migraines, hallucinogen persisting perception disorder (HPPD), prescription drugs, and head trauma, but is also sometimes idiopathic. Illusory palinopsia consists of afterimages that are short-lived or unformed, occur at the same location in the visual field as the original stimulus, and are often exposed or exacerbated based on environmental parameters such as stimulus intensity, background contrast, fixation, and movement. Illusory palinopsia symptoms occur continuously or predictably, based on environmental conditions.

Whatever the cause, the bodily related distortions can recur several times a day and may take some time to abate. Understandably, the person can become alarmed, frightened, and panic-stricken throughout the course of the hallucinations—maybe even hurt themselves or others around them. The symptoms of the syndrome themselves are not harmful and are likely to disappear with time.

The average age of the start of Alice in Wonderland syndrome is six but it is very normal for some to experience the syndrome from childhood to their late 20s. It is also thought that this syndrome is hereditary because many parents that have AIWS report their children having it as well.

There is no good evidence for any preventive actions, since it appears this is a natural response to aging changes in the vitreous. Posterior vitreous detachment (PVD) has been estimated to occur in over 75 per cent of the population over age 65, that PVD is essentially a harmless condition (although with some disturbing symptoms), and that it does not normally threaten sight. However, since epiretinal membrane appears to be a protective response to PVD, where inflammation, exudative fluid, and scar tissue is formed, it is possible that NSAIDs may reduce the inflammation response. Usually there are flashing light experiences and the emergence of floaters in the eye that herald changes in the vitreous before the epiretinal membrane forms g

This ocular pathology was first described by Iwanoff in 1865, and it has been shown to occur in about 7% of the population. It can occur more frequently in the older population with postmortem studies showing it in 2% of those aged 50 years and 20% in those aged 75 years.

One study from as early as 1895 reported that approximately 10% of the population experiences hallucinations. A 1996-1999 survey of over 13,000 people reported a much higher figure, with almost 39% of people reporting hallucinatory experiences, 27% of which daytime hallucinations, mostly outside the context of illness or drug use. From this survey, olfactory (smell) and gustatory (taste) hallucinations seem the most common in the general population.

Anomalous experiences, such as so-called benign hallucinations, may occur in a person in a state of good mental and physical health, even in the apparent absence of a transient trigger factor such as fatigue, intoxication or sensory deprivation.

The evidence for this statement has been accumulating for more than a century. Studies of benign hallucinatory experiences go back to 1886 and the early work of the Society for Psychical Research, which suggested approximately 10% of the population had experienced at least one hallucinatory episode in the course of their life. More recent studies have validated these findings; the precise incidence found varies with the nature of the episode and the criteria of ‘hallucination’ adopted, but the basic finding is now well-supported.

Although the theory is controversial, there is a link between febrile seizures (seizures coinciding with episodes of fever in young children) and subsequent temporal lobe epilepsy, at least epidemiologically.

The causes of TLE include mesial temporal sclerosis, traumatic brain injury, brain infections, such as encephalitis and meningitis, hypoxic brain injury, stroke, cerebral tumours, and genetic syndromes. Temporal lobe epilepsy is not the result of psychiatric illness or fragility of the personality.

Men and women are diagnosed in equal numbers with depersonalization disorder. A 1991 study on a sample from Winnipeg, Manitoba estimated the prevalence of depersonalization disorder at 2.4% of the population. A 2008 review of several studies estimated the prevalence between 0.8% and 1.9%. This disorder is episodic in about one-third of individuals, with each episode lasting from hours to months at a time. Depersonalization can begin episodically, and later become continuous at constant or varying intensity.

Onset is typically during the teenage years or early 20s, although some report being depersonalized as long as they can remember, and others report a later onset. The onset can be acute or insidious. With acute onset, some individuals remember the exact time and place of their first experience of depersonalization. This may follow a prolonged period of severe stress, a traumatic event, an episode of another mental illness, or drug use. Insidious onset may reach back as far as can be remembered, or it may begin with smaller episodes of lesser severity that become gradually stronger. Patients with drug-induced depersonalization do not appear to be a clinically separate group from those with a non-drug precipitant.

Neither antidepressants nor antipsychotics have been found to be useful, Additionally antipsychotics can worsen symptoms of depersonalisation. To date, no clinical trials have studied the effectiveness of benzodiazepines. Tentative evidence supports naloxone and naltrexone.

A combination of an SSRI and a benzodiazepine has been proposed to be useful for DPD patients with anxiety.

Modafinil used alone has been reported to be effective in a subgroup of individuals with depersonalization disorder (those who have attentional impairments, under-arousal and hypersomnia). However, clinical trials have not been conducted.