During an eye examination, a test such as cover testing or the Hirschberg test is used in the diagnosis and measurement of strabismus and its impact on vision. Retinal birefringence scanning can be used for screening of young children for eye misaligments.

Several classifications are made when diagnosing strabismus.

Strabismus may be classified as unilateral if the one eye consistently deviates, or alternating if either of the eyes can be seen to deviate. Alternation of the strabismus may occur spontaneously, with or without subjective awareness of the alternation. Alternation may also be triggered by various tests during an eye exam. Unilateral strabismus has been observed to result from a severe or traumatic injury to the affected eye.

A test called the Bielschowsky Darkening Wedge Test can be used to reveal and diagnose the presence of dissociated vertical deviation, although any (or no) amount of dissociative occlusion may also prompt it to occur.

The patient is asked to look at a light. One eye is covered and a filter is placed in front of the other eye. The density or opacity of this filter is gradually increased, and the behaviour of the eye under the cover is observed not of the eye beneath the filter. Initially, if DVD is present, the covered eye will have elevated, but as the filter opacity is increased the eye under the cover will gradually move downwards. This "Bielschowsky phenomenon" is present in over 50% of persons with prominent DVD, all the more if the DVD is asymmetric and amblyopia is present as well.

The Bielschowsky phenomenon is also present in the horizontal plane in patients with prominent DHD (dissociated horizontal deviation).

The cross-cover test, or alternating cover test is usually employed to detect heterophoria. One eye is covered, and then the cover is moved immediately over to the other eye. With heterophoria, when the cover is moved to the other eye, the eye that has just been uncovered can be seen to move from a deviated point. The difference between heterotropia and heterophoria can be easily understood as follows. With heterotropia, a correcting movement of the eye can be detected already by the simple cover test; with heterophoria, such correcting movement only takes place in the cross-cover test. People with heterophoria are able to create and maintain binocular fusion through vergence, and the cross-cover test purposely breaks this fusion, making the latent misaligment visible.

Whereas the cross-cover test allows a qualitative assessment to be done, a quantitative assessment of latent eye position disorders can be done using the Lancaster red-green test.

The prognosis for each patient with esotropia will depend upon the origin and classification of their condition. However, in general, management will take the following course:

1. Identify and treat any underlying systemic condition.

2. Prescribe any glasses required and allow the patient time to 'settle into' them.

3. Use occlusion to treat any amblyopia present and encourage alternation.

4. Where appropriate, orthoptic exercises can be used to attempt to restore binocularity.

5. Where appropriate, prismatic correction can be used, either temporarily or permanently, to relieve symptoms of double vision.

6. In specific cases, and primarily in adult patients, botulinum toxin can be used either as a permanent therapeutic approach, or as a temporary measure to prevent contracture of muscles prior to surgery

7. Where necessary, extra-ocular muscle surgery can be undertaken to improve cosmesis and, on occasion, restore binocularity.

DVD is often mistaken for over-action of the inferior oblique extra-ocular muscles. DVD can be revealed on ocular movement testing when one eye is occluded by the nose on lateral gaze. This eye will then elevate, simulating an inferior oblique over action. However, in a unilateral case, overaction of the superior rectus muscle in the unaffected dominant eye, can also be a causing factor as well as causing a V pattern exophoria.

"Congenital esotropia," or "infantile esotropia," is a specific sub-type of primary concomitant esotropia. It is a constant esotropia of large and consistent size with onset between birth and six months of age. It is not associated with hyperopia, so the exertion of accommodative effort will not significantly affect the angle of deviation. It is, however, associated with other ocular dysfunctions including oblique muscle over-actions, Dissociated Vertical Deviation (DVD,) Manifest Latent Nystagmus, and defective abduction, which develops as a consequence of the tendency of those with infantile esotropia to 'cross fixate.' Cross fixation involves the use of the right eye to look to the left and the left eye to look to the right; a visual pattern that will be 'natural' for the person with the large angle esotropia whose eye is already deviated towards the opposing side.

The origin of the condition is unknown, and its early onset means that the affected individual's potential for developing binocular vision is limited. The appropriate treatment approach remains a matter of some debate. Some ophthalmologists favour an early surgical approach as offering the best prospect of binocularity whilst others remain unconvinced that the prospects of achieving this result are good enough to justify the increased complexity and risk associated with operating on those under the age of one year.

In order to understand how heterophoria occurs, we must understand of how the eye can maintain proper fixation with non aligned visual axis. Heterophoria is actually the misalignment of the visual axis of both eyes. In other words, one or both eyes are not properly fixated to an object of interest. However, we must know that the eyes have a fusional vergence system which corrects this misalignment.

There is no definite treatment.

Because syphilis may be an underlying cause, it should be treated.

Treatment includes penicillin g benzathine 2.4mU IM as a single dose

Or Doxycycline (100 mg PO aid)for those being allergic to penicillin.

The eye findings of Parinaud's Syndrome generally improve slowly over months, especially with resolution of the causative factor; continued resolution after the first 3–6 months of onset is uncommon. However, rapid resolution after normalization of intracranial pressure following placement of a ventriculoperitoneal shunt has been reported.

Treatment is primarily directed towards etiology of the dorsal midbrain syndrome. A thorough workup, including neuroimaging is essential to rule out anatomic lesions or other causes of this syndrome. Visually significant upgaze palsy can be relieved with bilateral inferior rectus recessions. Retraction nystagmus and convergence movement are usually improved with this procedure as well.

Clinical exam may reveal sectoral paresis of the iris sphincter or vermiform iris movements. The tonic pupil may become smaller (miotic) over time which is referred to as "little old Adie's". Testing with low dose (1/8%) pilocarpine may constrict the tonic pupil due to cholinergic denervation supersensitivity. A normal pupil will not constrict with the dilute dose of pilocarpine. CT scans and MRI scans may be useful in the diagnostic testing of focal hypoactive reflexes.

Scanning techniques include EEG, SPECT, MRI, and CT brain scanning. These additional techniques are useful in determining what type of lesion the patient has, and allows physicians to determine more effective ways in treating the patient.

Neuropsychology is the study of neurobiology and psychology. Neuropsychological tests are utilized for the purpose of observing an individuals’ abilities in cognitive functioning, reasoning, and memories. The tests most commonly used for neuropsychological testing include WAIS-III, Stroop test, Bourdon Wiersma test, and the Rey-Osterrieth complex figure test. These tests allow physicians to evaluate the degree to which the bilateral lesions in the operculum have been affected, and allow for the determination of proper treatment.

A third cause of light-near dissociation is Parinaud syndrome, also called dorsal midbrain syndrome. This uncommon syndrome involves vertical gaze palsy associated with pupils that “accommodate but do not react." The causes of Parinaud syndrome include brain tumors (pinealomas), multiple sclerosis and brainstem infarction.

Due to the lack of detail in the older literature and the scarcity of AR pupils at the present time, it is not known whether syphilis can cause Parinaud syndrome. It is not known whether AR pupils are any different from the pupils seen in other dorsal midbrain lesions.

The condition is diagnosed clinically but physician

Adie's syndrome is not life-threatening or disabling. As such, there is no mortality rate relating to the condition; however, loss of deep tendon reflexes is permanent and may progress over time.

Macropsia is generally diagnosed once a patient complains of the characteristic symptoms, such as disproportionally large objects in their visual field. The Amsler Grid test can be used to diagnose macropsia, along with other visual maladies depending on the subjective disturbance reported by the patient after looking at the Amsler Grid. Outward bulging of the lines on an Amsler Grid is consistent with patients experiencing macropsisa. The New Aniseikonia Test (NAT) can quantify the degree of macropsia or micropsia independently in the vertical and horizontal meridians. The test consists of red and green semicircles on a black background with a white round fixation target. The size of the red semicircle is held constant while the green semicircle is varied in size in 1% increments. The patient wears a pair of red/green goggles so that one eye is tested at a time, and the patient attempts to determine when the semicircles are the same size. This is termed the reversal threshold and the size difference between the semicircles is reported as the degree of aniseikonia. A positive value indicates that the object was perceived bigger and thus corresponds to macropsia, and conversely a negative value indicates micropsia. The Aniseikonia Inspector contains an aniseikonia test based on the same principles as the NAT, but the test is run on a computer screen, it is based on a forced choice method, and it can measure the size difference as a function of the size of the objects. The functionality of being able to measure the size difference as function of the size (i.e. field dependent testing) is especially important when the macropsia (or micropsia) has a retinal origin.

Parinaud's syndrome, also known as dorsal midbrain syndrome, vertical gaze palsy, and Sunset Sign, is an inability to move the eyes up and down. It is caused by compression of the vertical gaze center at the rostral interstitial nucleus of medial longitudinal fasciculus (riMLF). The eyes lose the ability to move upward and down .

It is a group of abnormalities of eye movement and pupil dysfunction. It is caused by lesions of the upper brain stem and is named for Henri Parinaud (1844–1905), considered to be the father of French ophthalmology.

The most common way to treat forms of aniseikonia, including macropsia, is through the use of auxiliary optics to correct for the magnification properties of the eyes. This method includes changing the shape of spectacle lenses, changing the vertex distances with contact lenses, creating a weak telescope system with contact lenses and spectacles, and changing the power of one of the spectacle lenses. Computer software, such as the Aniseikonia Inspector, has been developed to determine the prescription needed to correct for a certain degree of aniseikonia. The problem with correction through optical means is that the optics do not vary with field angle and thus cannot compensate for non-uniform macropsia. Patients have reported significantly improved visual comfort associated with a correction of 5-10% of the aniseikonia.

With regard to drug-induced or virus-induced macropsia, once the underlying problem, either drug abuse or viral infection, is treated, the induced macropsia ceases.

Although qualitative and quantitative studies exist, there is little consensus on the proper method to assess for apraxia. The criticisms of past methods include failure to meet standard psychometric properties as well as research-specific designs that translate poorly to non-research use.

The Test to Measure Upper Limb Apraxia (TULIA) is one method of determining upper limb apraxia through the qualitative and quantitative assessment of gesture production. In contrast to previous publications on apraxic assessment, the reliability and validity of TULIA was thoroughly investigated. The TULIA consists of subtests for the imitation and pantomime of non-symbolic (“put your index finger on top of your nose”), intransitive (“wave goodbye”) and transitive (“show me how to use a hammer”) gestures. Discrimination (differentiating between well- and poorly performed tasks) and recognition (indicating which object corresponds to a pantomimed gesture) tasks are also often tested for a full apraxia evaluation.

However, there may not be a strong correlation between formal test results and actual performance in everyday functioning or activities of daily living (ADLs). A comprehensive assessment of apraxia should include formal testing, standardized measurements of ADLs, observation of daily routines, self-report questionnaires and targeted interviews with the patients and their relatives.

As stated above, apraxia should not be confused with aphasia; however, they frequently occur together. It has been stated that apraxia is so often accompanied by aphasia that many believe that if a person displays AOS; it should be assumed that the patient also has some level of aphasia.

There is no one definitive test for ideomotor apraxia; there are several that are used clinically to make an ideomotor apraxia diagnosis. The criteria for a diagnosis are not entirely conserved among clinicians, for apraxia in general or distinguishing subtypes. Almost all the tests laid out here that enable a diagnosis of ideomotor apraxia share a common feature: assessment of the ability to imitate gestures. A test developed by Georg Goldenberg uses imitation assessment of 10 gestures. The tester demonstrates the gesture to the patient and rates him on how whether the gesture was correctly imitated. If the first attempt to imitate the gesture was unsuccessful, the gesture is presented a second time; a higher score is given for correct imitation on the first trial, then for the second, and the lowest score is for not correctly imitating the gesture. The gestures used here are all meaningless, such as placing the hand flat on the top of the head or flat outward with the fingers towards the ear. This test is specifically designed for ideomotor apraxia. The main variation from this is in the type and number of gestures used. One test uses twenty-four movements with three trials for each and a trial-based scoring system similar to the Goldenberg protocol. The gestures here are also copied by the patient from the tester and are divided into finger movements, e.g. making a scissor movement with the forefinger and middle finger, and hand and arm movements, e.g. doing a salute. This protocol combines meaningful and meaningless gestures. Another test uses five meaningful gestures, such as waving goodbye or scratching your head and five meaningless gestures. Additional differences in this test are a verbal command to initiate the movement and it distinguishes between accurate performance and inaccurate but recognizable performance. One test utilizes tools, including a hammer and a key, with both a verbal command to use the tools and the patient copying the tester's demonstrated use of the tools. These tests have been shown to be individually unreliable, with considerable variability between the diagnoses delivered by each. If a battery of tests is used, however, the reliability and validity may be improved. It is also highly advisable to include assessments of how the patient performs activities in daily life. One of the newer tests that has been developed may provide greater reliability without relying on a multitude of tests. It combines three types of tool use with imitation of gestures. The tool use section includes having the patient pantomime use with no tool present, with visual contact with the tool, and finally with tactile contact with the tool. This test screens for ideational and ideomotor apraxia, with the second portion aimed specifically at ideomotor apraxia. One study showed great potential for this test, but further studies are needed to reproduce these results before this can be said with confidence. This disorder often occurs with other degenerative neurological disorders such as Parkinson's disease and Alzheimer's Disease. These comorbidities can make it difficult to pick out the specific features of ideomotor apraxia. The important point in distinguishing ideomotor apraxia is that basic motor control is intact; it is a high level dysfunction involving tool use and gesturing. Additionally, clinicians must be careful to exclude aphasia as a possible diagnosis, as, in the tests involving verbal command, an aphasic patient could fail to perform a task properly because they do not understand what the directions are.

Clinically, anosognosia is often assessed by giving patients an anosognosia questionnaire in order to assess their metacognitive knowledge of deficits. However, neither of the existing questionnaires applied in the clinics are designed thoroughly for evaluating the multidimensional nature of this clinical phenomenon; nor are the responses obtained via offline questionnaire capable of revealing the discrepancy of awareness observed from their online task performance. The discrepancy is noticed when patients showed no awareness of their deficits from the offline responses to the questionnaire but demonstrated reluctance or verbal circumlocution when asked to perform an online task. For example, patients with anosognosia for hemiplegia may find excuses not to perform a bimanual task even though they do not admit it is because of their paralyzed arms.

A similar situation can happen on patients with anosognosia for cognitive deficits after traumatic brain injury when monitoring their errors during the tasks regarding their memory and attention (online emergent awareness) and when predicting their performance right before the same tasks (online anticipatory awareness). It can also occur among patients with dementia and anosognosia for memory deficit when prompted with dementia-related words, showing possible pre-attentive processing and implicit knowledge of their memory problems. More interestingly, patients with anosognosia may overestimate their performance when asked in first-person formed questions but not from a third-person perspective when the questions referring to others.

When assessing the causes of anosognosia within stroke patients, CT scans have been used to assess where the greatest amount of damage is found within the various areas of the brain. Stroke patients with mild and severe levels of anosognosia (determined by response to an anosognosia questionnaire) have been linked to lesions within the temporoparietal and thalamic regions, when compared to those who experience moderate anosognosia, or none at all. In contrast, after a stroke, people with moderate anosognosia have a higher frequency of lesions involving the basal ganglia, compared to those with mild or severe anosognosia.

The prognosis for individuals with apraxia varies. With therapy, some patients improve significantly, while others may show very little improvement. Some individuals with apraxia may benefit from the use of a communication aid.

However, many people with apraxia are no longer able to be independent. Those with limb-kinetic and/or gait apraxia should avoid activities in which they might injure themselves or others.

Occupational therapy, physical therapy, and play therapy may be considered as other references to support patients with apraxia. These team members could work along with the SLP to provide the best therapy for people with apraxia. However, because people with limb apraxia may have trouble directing their motor movements, occupational therapy for stroke or other brain injury can be difficult.

No medication has been shown useful for treating apraxia.

Given the complexity of the medical problems facing ideomotor apraxia patients, as they are usually suffering from a multitude of other problems, it is difficult to ascertain the impact that it has on their ability to function independently. Deficits due to Parkinson's or Alzheimer's disease could very well be sufficient to mask or make irrelevant difficulties arising from the apraxia. Some studies have shown ideomotor apraxia to independently diminish the patient's ability to function on their own. The general consensus seems to be that ideomotor apraxia does have a negative impact on independence in that it can reduce an individual's ability to manipulate objects, as well as diminishing the capacity for mechanical problem solving, owing to the inability to access information about how familiar parts of the unfamiliar system function. A small subset of patients has been known to spontaneously recover from apraxia; this is rare, however. One possible hope is the phenomenon of hemispheric shift, where functions normally performed by one hemisphere can shift to the other in the event that the first is damaged. This seems to necessitate, however, that some portion of the function is associated with the other hemisphere to begin with. There is dispute over whether the right hemisphere of the cortex is involved at all in the praxis system, as some evidence from patients with severed corpus callosums indicates it may not be.

Although there is little that can be done to substantially reverse the effects of ideomotor apraxia, Occupational Therapy can be effective in helping patients regain some functional control. Sharing the same approach in treating ideational apraxia, this is achieved by breaking a daily task (e.g. combing hair) into separate components and teaching each distinct component individually. With ample repetition, proficiency in these movements can be acquired and should eventually be combined to create a single pattern of movement.

The nature of the alleged mental representations that underlie the act of pointing to target body parts have been a controversial issue. Originally, it was diagnosed as the effects of general mental deterioration or of aphasia on the task of pointing to body parts on verbal command. However, contemporary neuropsychological therapy seeks to establish the independence of autotopagnosia from other disorders. With such a general definition, a patient that presents with a dysfunction of or failure in accessing one of four mental representation systems suffers from autotopagnosia. Through observational testing, the type of mental misrepresentation of the body can be deduced: whether "semantic", "visuospatial", "somatosensory", or "motor misrepresentations". Neuropsychological tests can provide a proper diagnosis in regards to the specificity of patient’s agnosic condition.

1) Test 1: Body Part Localization: Free vision and no vision conditions

2) Test 2: On-line positioning of body vis-à-vis objects

3) Test 3: Localization of objects on the body surface

4) Test 4: Body part semantic knowledge

5) Test 5: Matching body parts: Effect of viewing angle

Some features are more or less likely to suggest PNES but they are not conclusive and should be considered within the broader clinical picture. Features that are common in PNES but rarer in epilepsy include: biting the tip of the tongue, seizures lasting more than 2 minutes (easiest factor to distinguish), seizures having a gradual onset, a fluctuating course of disease severity, the eyes being closed during a seizure, and side to side head movements. Features that are uncommon in PNES include automatisms (automatic complex movements during the seizure), severe tongue biting, biting the inside of the mouth, and incontinence.

If a patient with suspected PNES has an episode during a clinical examination, there are a number of signs that can be elicited to help support or refute the diagnosis of PNES. Compared to patients with epilepsy, patients with PNES will tend to resist having their eyes forced open (if they are closed during the seizure), will stop their hands from hitting their own face if the hand is dropped over the head, and will fixate their eyes in a way suggesting an absence of neurological interference. Mellers et al. warn that such tests are neither conclusive nor impossible for a determined patient with factitious disorder to "pass" through faking convincingly.