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Disorders of sight

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Achromatopsia. Achromatopsia (ACHM) is a medical syndrome that exhibits symptoms relating to at least five separate individual conditions.

Achromatopsia

Although the term may refer to acquired conditions such as cerebral achromatopsia also known as color agnosia, it typically refers to an autosomal recessive congenital color vision condition, the inability to perceive color and to achieve satisfactory visual acuity at high light levels (typically exterior daylight). Akinetopsia. Akinetopsia (Greek: a for "without", kine for "to move" and opsia for "seeing"), also known as cerebral akinetopsia or motion blindness, is a neuropsychological disorder in which a patient cannot perceive motion in his or her visual field, despite being able to see stationary objects without issue.[1] There are varying degrees of akinetopsia: from seeing motion as a cinema reel to an inability to discriminate any motion.

Akinetopsia

There is currently no effective treatment or cure for akinetopsia. Signs and symptoms[edit] Apperceptive agnosia. Apperceptive agnosia is failure in recognition that is due to a failure of perception.

Apperceptive agnosia

In contrast, associative agnosia is a type of agnosia where perception occurs but recognition still does not occur.[1] When referring to apperceptive agnosia, visual and object agnosia are most commonly discussed; This occurs because apperceptive agnosia is most likely to present visual impairments. Associative visual agnosia. Inferior view of the brain, depicting the cerebral lobes.

Associative visual agnosia

Lesions on the occipito-temporal lobes are correlated with associative agnosia. Overview[edit] An agnosia that affects hearing, auditory sound agnosia, is broken into subdivisions based on level of processing impaired, and a semantic-associative form is investigated within the auditory agnosias.[2] Causes[edit] Associative visual agnosias are generally attributed to anterior left temporal lobe infarction,[8] caused by ischemic stroke, head injury, cardiac arrest, brain tumour, brain hemorrhage, or demyelination.[7][9] Environmental toxins and pathogens have also been implicated, such as, carbon monoxide poisoning or herpes encephalitis and infrequent developmental occurrences have been documented.[1][10] Asthenopia. Asthenopia (aesthenopia) from the Greek word "asthen-opia : ασθεν-ωπία" or eye strain is an ophthalmological condition that manifests itself through nonspecific symptoms such as fatigue, pain in or around the eyes, blurred vision, headache and occasional double vision.

Asthenopia

Symptoms often occur after reading, computer work, or other close activities that involve tedious visual tasks. When concentrating on a visually intense task, such as continuously focusing on a book or computer monitor, the ciliary muscle tightens. This can cause the eyes to get irritated and uncomfortable. Giving the eyes a chance to focus on a distant object at least once an hour usually alleviates the problem. Astigmatism (eye) For the more general class of optical aberrations, see Astigmatism.

Astigmatism (eye)

The refractive error of the astigmatic eye stems from a difference in degree of curvature refraction of the two different meridians (i.e., the eye has different focal points in different planes). For example, the image may be clearly focused on the retina in the horizontal plane, but not in the vertical plane. Astigmatism causes difficulties in seeing fine detail resulting in blurred vision.

Three options exist for the treatment of astigmatism: spectacles, contact lenses (either hard contact lenses or toric contact lenses), and refractive surgery. Blur from astigmatic lens at different distances Regular astigmatism – principal meridians are perpendicular. Color blindness. Prosopagnosia. Animation of the fusiform area, the area damaged in prosopagnosia.

Prosopagnosia

Prosopagnosia /ˌprɒsəpæɡˈnoʊʒə/ (Greek: "prosopon" = "face", "agnosia" = "not knowing"), also called face blindness,[1] is a cognitive disorder of face perception where the ability to recognize faces is impaired, while other aspects of visual processing (e.g., object discrimination) and intellectual functioning (e.g., decision making) remain intact. The term originally referred to a condition following acute brain damage (acquired prosopagnosia), but a congenital or developmental form of the disorder also exists, which may affect up to 2.5% of the population.[2] The specific brain area usually associated with prosopagnosia is the fusiform gyrus,[3] which activates specifically in response to faces.

The functionality of the fusiform gyrus allows most people to recognize faces in more detail than they do similarly complex inanimate objects. There are two types of prosopagnosia: acquired and congenital (developmental). Scotopic sensitivity syndrome. Scotopic sensitivity syndrome (SSS), also known as Visual Stress, Irlen Syndrome, and Asfedia, is a condition relating to the interaction of the central nervous system and the eyes at a physiological level with light.

Scotopic sensitivity syndrome

The effects of SSS are most noticeable during activities associated with reading, but an individual with the condition may notice the condition's effects in other activities. The exact cause of SSS is currently under debate within the scientific community. In addition, the scientific community has not reached a consensus on the most efficient method for treating the condition. However, in a joint statement, The American Academy of Ophthalmology, American Academy of Pediatrics, American Association for Pediatric Ophthalmology and Strabismus and American Association of Certified Orthoptists firmly repudiated the use of lenses for treating SSS, stating that there was no scientific evidence supporting their use. History[edit] Research[edit] Recovery from blindness. Recovery from blindness is the phenomenon of a blind person gaining the ability to see, usually as a result of medical treatment.

Recovery from blindness

As a thought experiment, the phenomenon is usually referred to as Molyneux's Problem. The first published human case was reported in 1728 by the Surgeon William Cheselden. Patients who experience dramatic recovery from blindness experience significant to total agnosia, having serious confusion with their visual perception. Visual agnosia.