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    Cortical Visual Impairment and Blindness: by Komal Sharma

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    Ophthalmology Discussion
    Cortical visual impairment (CVI) is blindness or visual impairment caused by damage to the occipital cortex. It can be congenital, due to conditions like hypoxic ischemic encephalopathy in term infants or periventricular leukomalacia in preterm infants. It can also be acquired later in life due to events like traumatic brain injury, stroke, or meningitis. Common signs of congenital CVI include variable vision, better peripheral than central vision, photophobia, preserved color vision, poor depth perception, and better vision with movement. Management involves vision therapy and use of assistive devices. Acquired CVI is typically diagnosed via brain imaging and can cause hemianopsia or complete blindness

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    Cortical Visual Impairment and Blindness: by Komal Sharma

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    Ophthalmology Discussion
    51 views15 pages
    Cortical visual impairment (CVI) is blindness or visual impairment caused by damage to the occipital cortex. It can be congenital, due to conditions like hypoxic ischemic encephalopathy in term infants or periventricular leukomalacia in preterm infants. It can also be acquired later in life due to events like traumatic brain injury, stroke, or meningitis. Common signs of congenital CVI include variable vision, better peripheral than central vision, photophobia, preserved color vision, poor depth perception, and better vision with movement. Management involves vision therapy and use of assistive devices. Acquired CVI is typically diagnosed via brain imaging and can cause hemianopsia or complete blindness

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    Cortical visual impairment (CVI) is blindness or visual impairment caused by damage to the occipital cortex. It can be congenital, due to conditions like hypoxic ischemic encephalopathy in term infants or periventricular leukomalacia in preterm infants. It can also be acquired later in life due to events like traumatic brain injury, stroke, or meningitis. Common signs of congenital CVI include variable vision, better peripheral than central vision, photophobia, preserved color vision, poor depth perception, and better vision with movement. Management involves vision therapy and use of assistive devices. Acquired CVI is typically diagnosed via brain imaging and can cause hemianopsia or complete blindness

    Copyright:

    © All Rights Reserved
    Download as PPT, PDF, TXT or read online from Scribd
    Download as ppt, pdf, or txt
    51 views15 pages

    Cortical Visual Impairment and Blindness: by Komal Sharma

    Uploaded by

    Ophthalmology Discussion
    Cortical visual impairment (CVI) is blindness or visual impairment caused by damage to the occipital cortex. It can be congenital, due to conditions like hypoxic ischemic encephalopathy in term infants or periventricular leukomalacia in preterm infants. It can also be acquired later in life due to events like traumatic brain injury, stroke, or meningitis. Common signs of congenital CVI include variable vision, better peripheral than central vision, photophobia, preserved color vision, poor depth perception, and better vision with movement. Management involves vision therapy and use of assistive devices. Acquired CVI is typically diagnosed via brain imaging and can cause hemianopsia or complete blindness

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    Cortical Visual Impairment and

    Blindness

    By komal sharma
    Definition of Cortical Blindness and Visual
    Impairment Congenital and
    Acquired
    • Blindness or Visual Impairment (CVI) due to
    bilateral damage to the occipital cortex (Hoyt,
    2003).
    • The absence or reduction of vision in either
    eye while still maintaining a normal pupillary
    response to light and a normal ocular
    examination.
    • It can occur both congenitally and it can be
    acquired, with many fewer cases acquired.
    Congenital CVI Diagnosis and
    Evaluation

    • Diagnosis of exclusion and based on history


    information.
    • Perinatal hypoxia/ischemia, Traumatic Brain
    Injury (TBI), encephalitis and meningitis.
    • About 75% have accompanying neurological
    deficits in a recent study.
    Common Causes
    of CVI in Children

    • Hypoxic Ischemic Encephalopathy (HIE) term


    infant
    • Periventricular Leukomalacia (PVL) pre-term
    infant
    • TBI– shaken baby, accidental head injuries,
    meningitis, shunt failure, severe seizures,
    cardiac arrest, CNS developmental delays
    Congenital CVI
    Common Signs and Symptoms
    • Vision appears variable, even hour to hour
    • Children with CVI may be able to use their peripheral
    vision more efficiently than their central vision.
    • One third are photophobic, others are light gazers.
    • Color vision is generally preserved.
    • The vision of children with CVI has been described as
    “looking through a piece of Swiss cheese”.
    • May exhibit poor depth perception, influencing their
    ability to reach for a target.
    • Vision may be better when either the visual target or
    the child is moving.
    Congenital CVI
    Common Signs and Symptoms

    • Blunted or avoidant social gaze


    • Brief fixations, intermittent following
    • Reduced visual acuity
    • Visual field loss - generalized constriction,
    inferior altitudinal, hemianopic defect
    • Reduced responses to visual stimuli when
    music, voices, and other sounds are present,
    and often, when the child is touched
    Congenital CVI Management and
    Intervention
    • Case Example
    – CS 12 year old Caucasian male
    • 28 week premature, birth weight 1 lb, 15 oz.
    • Central apnea, ototoxicity (Gentamicin) with hearing
    loss
    • Cochlear implants at age 3
    • Currently in good health, wheelchair bound with head
    rest (cannot sustain erect head posture)
    • Inclusion sixth grade, resource and lifeskills, OT, PT and
    ST at school. TVI and O and M
    • Uses a Dynavox for communication, Smart board
    Assessment

    • Cardiff Cards (preferential viewing) were utilized for


    visual acuity with contact lens correction:
    OD, OS 20/40
    (Previous exams spanning 7 years started with VA of OD
    20/130, OS 20/130 with gradual improvement)
    • 30^ Alternating Exotropia
    • Vertical gaze palsy with more restriction in downgaze
    than upgaze, horizontal eye movements are intact
    • Full visual fields in each eye
    Assessment

    • Normal color vision with Pease Allen preferential


    viewing plates
    • Intact contrast with Hiding Heidi cards 1.25%
    • Normal accommodative response (MEM
    retinoscopy)
    • Refractive error :
    Right eye: +1.75 – 1.25 x 170
    Left eye: +0.75 -0.50 x 170
    • Ocular health evaluation demonstrated intact
    structures internal and external
    Acquired CVI
    Diagnosis and Evaluation

    • MRI/CAT scan would indicate location of


    damage which would lead to diagnosis of CVI
    • Varied levels of improvement of visual field
    and visual acuity after sometimes total loss of
    vision with CVA or TBI
    Acquired CVI
    Common Symptoms
    • Most common vision loss is hemianopsia
    • Less common is bilateral occipital loss with
    near or total blindness
    • Usually no strabismus or other ocular disorder
    • Anton Syndrome – the patient may deny the
    vision loss entirely, may be aware of color
    • Patients may be able to navigate the
    environment despite serious vision loss
    “Blindsight”
    Blindsight

    • Existence of 2 extrastriate pathways for objects and spatial


    vision
    – Ventral stream projecting to the inferior temporal lobe – the
    “what” pathway
    – Dorsal stream projecting to the parietal lobe – the “where”
    pathway
    • Recent studies of patients with lesions in V1 provide some
    evidence for existence of connections (remaining
    perception of motion) or the Riddoch phenomenon
    • Cat study demonstrated transient deficit with recovery in a
    matter of days, probable relocation to similar structures.
    Rushmore RJ, Bertram P, Valero-Cabre A Recovery of function following
    unilateral damage to visuospatial cortex Exp Brain Res (2010) 203: 693-
    700

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