Palinopsia necessitates a full ophthalmologic and neurologic history and physical exam. There are no clear guidelines on the work-up for illusory palinopsia, but it is not unreasonable to order automated visual field testing and neuroimaging since migraine aura can sometimes mimic seizures or cortical lesions. However, in a young patient without risk factors or other worrisome symptoms or signs (vasculopathy, history of cancer, etc.), neuroimaging for illusory palinopsia is low-yield but may grant the patient peace of mind.

The physical exam and work-up are usually non-contributory in illusory palinopsia. Diagnosing the etiology of illusory palinopsia is often based on the clinical history. Palinopsia is attributed to a prescription drug if symptoms begin after drug initiation or dose increase. Palinopsia is attributed to head trauma if symptoms begin shortly after the incident. Continuous illusory palinopsia in a migraineur is usually from persistent visual aura. HPPD can occur any time after hallucinogen ingestion and is a diagnosis of exclusion in patients with previous hallucinogen use. Migraines and HPPD are probably the most common causes of palinopsia. Idiopathic palinopsia may be analogous to the cerebral state in persistent visual aura with non-migraine headache or persistent visual aura without headache.

Due to the subjective nature of the symptoms and the lack of organic findings, clinicians may be dismissive of illusory palinopsia, sometimes causing the patient distress. There is considerable evidence in the literature confirming the symptom legitimacy, so validating the patient’s symptoms can help ease anxiety. Unidirectional visual trails or illusory symptoms confined to part of a visual field suggest cortical pathology and necessitate further work-up.

EEG testing can diagnose patients with medial temporal lobe epilepsy. Epileptiform abnormalities including spikes and sharp waves in the medial temporal lobe of the brain can diagnose this condition, which can in turn be the cause of an epileptic patient's micropsia.

The Amsler grid test can be used to diagnose macular degeneration. For this test, patients are asked to look at a grid, and distortions or blank spots in the patient's central field of vision can be detected. A positive diagnosis of macular degeneration may account for a patient's micropsia.

A controlled size comparison task can be employed to evaluate objectively whether a person is experiencing hemimicropsia. For each trial, a pair of horizontally aligned circles is presented on a computer screen, and the person being tested is asked to decide which circle is larger. After a set of trials, the overall pattern of responses should display a normal distance effect where the more similar the two circles, the higher the number of errors. This test is able to effectively diagnose micropsia and confirm which hemisphere is being distorted.

Due to the large range of causes that lead to micropsia, diagnosis varies among cases. Computed tomography (CT) and magnetic resonance imaging (MRI) may find lesions and hypodense areas in the temporal and occipital lobes. MRI and CT techniques are able to rule out lesions as the cause for micropsia, but are not sufficient to diagnose the most common causes.

There is limited data on treating the visual disturbances associated with HPPD, persistent visual aura, or post-head trauma visual disturbances, and pharmaceutical treatment is empirically-based. It is not clear if the etiology or type of illusory symptom influences treatment efficacy. Since the symptoms are usually benign, treatment is based on the patient’s zeal and willingness to try many different drugs. There are cases which report successful treatment with clonidine, clonazepam, lamotrigine, nimodipine, topiramate, verapamil, divalproex sodium, gabapentin, furosemide, and acetazolamide, as these drugs have mechanisms that decrease neuronal excitability. However, other patients report treatment failure from the same drugs. Based on the available evidence and side-effect profile, clonidine might be an attractive treatment option. Many patients report improvement from sunglasses. FL-41 tinted lenses may provide additional relief, as they have shown some efficacy in providing relief to visually-sensitive migraineurs.

Research needs to be performed on the efficacy of the various pharmaceuticals for treating illusory palinopsia. It is unclear if the symptoms' natural history and treatment are influenced by the cause. It is also not clear if there is treatment efficacy overlap for illusory palinopsia and the other co-existing diffuse persistent illusory phenomenon such as visual snow, oscillopsia, dysmetropsia, and halos.

Future advancements in fMRI could potentially further our understanding of hallucinatory palinopsia and visual memory. Increased accuracy in fMRI might also allow for the observation of subtle metabolic or perfusional changes in illusory palinopsia, without the use of ionizing radiation present in CT scans and radioactive isotopes. Studying the psychophysics of light and motion perception could advance our understanding of illusory palinopsia, and vice versa. For example, incorporating patients with visual trailing into motion perception studies could advance our understanding of the mechanisms of visual stability and motion suppression during eye movements (e.g. saccadic suppression).

There is no established treatment for visual snow. It is difficult to resolve visual snow with treatment, but it is possible to reduce symptoms and improve quality of life through treatment.

Medications that may be used include lamotrigine, acetazolamide, or verapamil. But these do not always result in benefits.

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.

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.

Treatment varies for micropsia due to the large number of different causes for the condition.

Treatments involving the occlusion of one eye and the use of a prism fitted over an eyeglass lens have both been shown to provide relief from micropsia.

Micropsia that is induced by macular degeneration can be treated in several ways. A study called AREDS (age-related eye disease study) determined that taking dietary supplements containing high-dose antioxidants and zinc produced significant benefits with regard to disease progression. This study was the first ever to prove that dietary supplements can alter the natural progression and complications of a disease state. Laser treatments also look promising but are still in clinical stages.

As yet, there is no cure available for HPPD. A study presented by Dr. Henry Abraham, at the Annual Meeting of the Biological Psychiatry Society in 2012, showed that two drugs, tolcapone and levocarb that are primarily used in the treatment of Parkinson's disease improved the symptoms of HPPD in one third of the 20 test subjects who had participated in the trial. As tolcapone, and levocarb, are not approved for use in HPPD, the principal treatments that are available seek to reduce distress without treating the underlying cause. Primarily benzodiazepines including clonazepam,

diazepam and alprazolam are prescribed with a fair amount of success. The anticonvulsant drug levetiracetam has been reported to diminish some of the visual symptoms, as well as reduce depersonalization and derealization symptoms, that can occur along with HPPD. The efficacy of levetiracetam in treating HPPD has been documented in a prospective study. Another anticonvulsant, lamotrigine, has also been used to successfully treat HPPD.

Some medications have been contraindicated on the basis of their effects on HPPD or the concurrent mental issues. The atypical antipsychotic risperidone is reported to worsen symptoms of HPPD during the drug's duration in some people.

Those with HPPD are often advised to discontinue all drug use, many of which are thought to increase visuals in the short-term. There are also less concrete factors that may be generally detrimental to those with HPPD. For example, sleep deprivation and stress are thought to increase HPPD 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.

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).

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