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2011年7月1日 星期五
認識低視力
一般到眼科醫生或視光師「驗眼」，所指「驗眼」，其實是以標準化的評估工具，量度成人或兒童的視覺敏銳度(Visual Acuity)，俗稱視力，是醫生或視光師屆定視覺能力的共同語言，概括而言，即兒童或成人眼睛看物件的清晰度。通常最常見的評估工具是「驗眼表」，而「驗眼表」的正式名稱是Snellen Chart（見下圖），Snellen Chart其實於1862年起源於歐洲荷蘭，由一位眼科醫生，名叫 Hermann Snellen所發明的，所以「驗眼表」亦以這位醫生的姓氏而命名。
我們若想知道兒童是否屬於視障，我們必需知道香港用來劃分完全失明(Total Blind)及低視能(Low Vision)的標準。
根據<香港復康計劃方案檢討05/07>，香港根據人類視覺功能而釐定的定義如下:
完全失明
i) 沒有視覺功能，即對光線沒有感覺。
低視能
i) 嚴重低視能 - 視覺敏銳度（指視力較佳的眼睛戴上矯正眼鏡後的視力）為6/120或更差，或視野縮窄，最闊的視野直徑對向20度或以下角弦（不論視覺敏銳度如何）；
ii) 中度低視能 - 視覺敏銳度為6/60或更差，但未達6/120；和
iii) 輕度低視能 - 視覺敏銳度為6/18或更差，但未達6/60。
本人有見大部份家長的提問，有以下兩點的補充：第一，在香港的法律定義中，兒童或成人視力較好的眼睛為準，視覺敏銳度是6/120或更差，已算是法定失明，可以向社會福利署申請Disability Allowance (DA)。第二，並非每個正常人的視力是6/6，以一個正常人而言，視覺敏銳度為6/6或更差，但未達6/18。所以如果子女的視覺敏銳度是6/12 或6/9.5 的話，那便屬於正常的視力範圍。
就以嚴重低視能為例，到底甚麼是6/120呢？（見下圖）6/120指正常人在120米距離看得清楚的字體，對於一個嚴重低視能的人仕而言，他需要在6米的距離才看見相同的字體。以科學方法計算，他的視力是一般人的5% 或 二十分之一。
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而視覺敏銳度亦有很多不同的寫法，如：6/120；3/60；20/400或是0.05，但所表達的意思卻是相同的。6是代表以「6米」作為驗眼時量度的距離單位；而3是代表以「3米」作為驗眼時量度的距離單位；20是代表以「20呎」作為驗眼時量度的距離單位；最後0.05是以小數作代表而且。所以則才所列出的數字（6/120；3/60；20/400或是0.05），所表達兒童或成人的視覺敏銳度（Visual Acuity）是完全相同的。
最後請注意一點：絕大部份家長一提及視覺敏銳度或視力，一定會提及所配戴眼鏡的近視，遠視或散光的度數，視覺敏銳度和近視遠視是兩種完全不相同的東西，請密切留意稍後「屈光不正」的文章。
我們若想知道兒童是否屬於視障，我們必需知道香港用來劃分完全失明(Total Blind)及低視能(Low Vision)的標準。
根據<香港復康計劃方案檢討05/07>，香港根據人類視覺功能而釐定的定義如下:
完全失明
i) 沒有視覺功能，即對光線沒有感覺。
低視能
i) 嚴重低視能 - 視覺敏銳度（指視力較佳的眼睛戴上矯正眼鏡後的視力）為6/120或更差，或視野縮窄，最闊的視野直徑對向20度或以下角弦（不論視覺敏銳度如何）；
ii) 中度低視能 - 視覺敏銳度為6/60或更差，但未達6/120；和
iii) 輕度低視能 - 視覺敏銳度為6/18或更差，但未達6/60。
本人有見大部份家長的提問，有以下兩點的補充：第一，在香港的法律定義中，兒童或成人視力較好的眼睛為準，視覺敏銳度是6/120或更差，已算是法定失明，可以向社會福利署申請Disability Allowance (DA)。第二，並非每個正常人的視力是6/6，以一個正常人而言，視覺敏銳度為6/6或更差，但未達6/18。所以如果子女的視覺敏銳度是6/12 或6/9.5 的話，那便屬於正常的視力範圍。
就以嚴重低視能為例，到底甚麼是6/120呢？（見下圖）6/120指正常人在120米距離看得清楚的字體，對於一個嚴重低視能的人仕而言，他需要在6米的距離才看見相同的字體。以科學方法計算，他的視力是一般人的5% 或 二十分之一。
<版權所有，翻印必究>
而視覺敏銳度亦有很多不同的寫法，如：6/120；3/60；20/400或是0.05，但所表達的意思卻是相同的。6是代表以「6米」作為驗眼時量度的距離單位；而3是代表以「3米」作為驗眼時量度的距離單位；20是代表以「20呎」作為驗眼時量度的距離單位；最後0.05是以小數作代表而且。所以則才所列出的數字（6/120；3/60；20/400或是0.05），所表達兒童或成人的視覺敏銳度（Visual Acuity）是完全相同的。
最後請注意一點：絕大部份家長一提及視覺敏銳度或視力，一定會提及所配戴眼鏡的近視，遠視或散光的度數，視覺敏銳度和近視遠視是兩種完全不相同的東西，請密切留意稍後「屈光不正」的文章。
Structure of Human Visual System and Visual Neurological Pathways
Structure of Human Visual System and Visual Neurological Pathways
The brain cortex has at least 30 specialized areas (Hyvarien, 2005) that handle specific parts of visual information. In our practice, we lack information about the specific exact lesion sites, but we do need to know the localized lesion areas that interfere with visual functions of CVI people. Human relies on vision for daily functioning, especially critical for young children who are in active developing stage of eye-hand functions. Human’s visual function highly depends on both ocular structures and neurological structures in our brain. These structures can be simply divided into Anterior Visual Pathway and Posterior Visual Pathway.
Geniculostriate Pathway
Visual images are received by Eyeballs and are converted into visual information in retina. The visual information is thus transmitted through Anterior Visual Pathway (Including Eyeball, Optic nerve, Optic Chiasm and Optic tract) to Lateral Geniculate Nucleus (LGN). Lateral Geniculate Nucleus, located in Thalamus, (Pitto & Kupers, 2005) is the landmark which differentiates Anterior Visual Pathway and Posterior Visual Pathway. The visual information is thus transferred through Optic Radiation to Primary Visual Cortex (striate cortex, V1) (Fig 2), located at the back of the brain, for primary visual processing.
Dorsal stream and Ventral stream
To serve higher visual functions (e.g. visually guided movement; integrating attention, recognition and route finding (Dutton, et al, 2003)), the Geniculostriate Pathway branches into the Dorsal stream and Ventral stream so as to associate with other lobes in the brain. The Dorsal stream connects between occipital lobes and parietal lobes to process the whole visual scene and carry out visually guided movement. (Dutton, et al, 2003) The Ventral stream connects between occipital lobes between occipital lobes and temporal lobe and process visual recognition (e.g. face recognition, line, angle and shape perception) and visual memory. (Dutton, et al, 2003; 2004)
Choose of element in visual scene (Dutton, et al, 2003)
“Choose of element” involves both dorsal and ventral stream. In daily life, to handle massive information surrounded us; our posterior parietal lobes are responsible for processing the overall visual scene and allow us to attend to the element of scene at one time. Posterior parietal lobes, together cooperate with temporal lobes (serve recognition) and the frontal lobes (serve attention to areas of interest and motor planning), human is able to integrate attention, visually guided movement (eye-hand coordinated movement), recognition and route finding. (Dutton, et al, 2003)
Tectal Pathway or Extrageniculate Pathway
There is another parallel visual pathway (Hyvarinen, 2005), which is called Tectal Pathway (Hyvarinen, 2005) or Extrageniculate Pathway (Ro & Rafal, 2006) serves for visual functions including perception of movement, visually guided movement, eye saccade (Hoyt, 2003; Ro & Rafal, 2006) and less effective color processing (Ro & Rafal, 2006). This pathway branches before Lateral Geniculate Nucleus (LGN) and brings visual information to Superior Colliculus (SC) (serves for rapid eye movements) and Pulvinar (PU).
Fig. 3 Tectal pathway (Hyvarinen, 2005)
Finally, visual information is transmitted to the cortical areas in parietal and occipital without the analysis of V1. (Hyvarienen, 2005; Ro & Rafal, 2006) (Fig. 3) As a result, people with cortical visual impairment still have good eye-hand co-ordination, detection of movement (Hoyt, 2003) and less effective color processing. (Hoyt, et al, 2003; Ro & Rafal, 2006) Although this parallel pathway together serves for visual function, CVI clients still have other significant deficits in visual recognitions including visual object agnosia, (Ogden, 1993) prosopagnosia (Ogden, 1993; Dutton, 2003) and Topographic agnosia. (Dutton, 2003) Since most of the lesion sites in CVI clients are Posterior Visual Pathway, neurological structures beyond LGN, (Watson, et al, 2007; Malkowicz, et al, 2006) Visual rehabilitation begins with the visual stimulation that promotes connections between synapse in human brain. (Powell, 1996) Neural-based stimulation that will eventually strengthen the neural pathway that are so critical for vision. (Powell, 1996) Therefore, training of these retinotectal and / or geniculoextrastriate pathways may be advantageous in restoration of visual function after primary visual cortex damage (Ro & Rafal, 2006).<Tang, W. (2008). Visual Rehabilitation for People with Cortical Visual Impairment. In Progress.>
References:
Dutton, G. N., Ballantyne, J., Boyd, G., Bradnam, M., Day, R., McCulloch, D., Mackie, R., Phillips, S., & Saunders, K. (1996). Cortical visual dysfunction in children: a clinical study. Eye, 10, 302-309.
Dutton, G. N. (2003). Cognitive vision, its disorders and differential diagnosis in adults and children: knowing where and what things are. Eye, 17, 289-304.
Dutton, G. N. (2003) Visual problem in children with damage to the brain. Visual Impairment Research. Visual Impairment Research, 4(2), 113-121.
Dutton, G. N., Saaed, A., Fahad, B., Fraser, R., Madaid, G., Mcdade, J., Mackintosh, A., Rane, T., & Spowart, K. (2004). Association of binocular lower visual field impairment, impaired simultaneous perception, disordered visually guided motion and inaccurate saccades in children with cerebral visual dysfunction – a retrospective observational study. Eye, 18, 27-34.
Dutton, G. N. (2008). Professionals CVI inventory version 2.
Ek, U. Fellenius, K. & Jacobson, L. (2003). Reading acquisition, cognitive and visual Jan, J. E. & Groenveld, M. (1993). Visual behaviors and adaptations associated with cortical and ocular impairment in children. Journal of Visual Impairment & Blindness, 4, 101-105.
Good, W. V., Jan, J. E., Burden, S. K., Skoczenski, A. & Candy, R. (2001). Recent advances in cortical visual impairment. Developmental Medicine & Child Neurology, 43, 56-60.
Groenveld, M., Jan, J. E. & Leader, P. (1990). Observations on the habilitation of children with cortical visual impairment. Journal of Visual Impairment & Blindness, 84, 11-15.
development, and self-esteem in four children with cerebral visual impairment. Journal of Visual Impairment & Blindness, 97, 741-754.
Hoyt, C.S. (2003). Visual function in the brain-damaged child. Eye, 17, 369-384.
Huo, R., Burden, S. K., Hoyt, C. S. & Good, W. V. (1999). Chronic cortical visual impairment in children: aetiology, prognosis, and associated neurological deficits. British Journal of Ophthalmology, 83(6), 670-675.
Hyvarinen, L. (2004). Understanding the behaviours of children with CVI. Retrieved Mar & Apr, 2004, from American Print House.
site: http://www.aph.org/cvi/articles/hyvarinen_1.html
Lueck, A. H., Dornbusch, H. & Hart, J. (1999). The effects of training on a young child with cortical visual impairment: an exploratory study. Journal of Visual Impairment & Blindness, 93, 778-793.
Morse, M. T. (1990). Cortical visual impairment in young children with multiple disabilities. Journal of Visual Impairment & Blindness, 84, 200-203.
Ogden, J. A. (1993). Visual object agnosia, prosopagnosia, achromatopsia, loss of visual imagery, and autobiographical amnesia flowing recovery from cortical blindness: case M. H. Neuroopsychologia, 31(6), 571-589.
Powell, S. A. (1996). Neural-based visual stimulation with infants with cortical impairment. Journal of Visual Impairment & Blindness, 90, 445-446.
Ro, T. & Rafal, R. (2006). Visual restoration in cortical blindness: insights from natural and TMS-induced blindsight. Neuropsychological Rehabilitation, 16(4), 377-396.
Roman-Lantzy, C. (2008). Cortical visual impairment: an approach to assessment and intervention. AFB Press.
Rosenberg, T., Flage, T. & Hansen, E. (1996). Incidence of registered visual impairment in the Nordic child population. British Journal of Ophthalmology, 80, 49-53.
Watson, T., Orel-Bixler, D. & Haegerstrom-Portnoy, G. (2007). Longitudinal quantitative assessment of vision function in children with cortical visual impairment. Optometry and Vision Science, 84(6), 471-480.
Widdig, W., Pleger, B., Rommel, O., Malin, J. & Tegenthoff, M. (2003). Repetitive visual stimulation: a neuropsychological approach to the treatment of cortical blindness, NeuroRehabilitation, 19, 227-237.
Zanelli, S. A., Naylor, M., Dobbins, N. (2008). Implementation of a “hypothermia for HIE” program: 2-year experience in a single NICU. Journal of Perinatology, 2(28), 171–175.
The brain cortex has at least 30 specialized areas (Hyvarien, 2005) that handle specific parts of visual information. In our practice, we lack information about the specific exact lesion sites, but we do need to know the localized lesion areas that interfere with visual functions of CVI people. Human relies on vision for daily functioning, especially critical for young children who are in active developing stage of eye-hand functions. Human’s visual function highly depends on both ocular structures and neurological structures in our brain. These structures can be simply divided into Anterior Visual Pathway and Posterior Visual Pathway.
Geniculostriate Pathway
Visual images are received by Eyeballs and are converted into visual information in retina. The visual information is thus transmitted through Anterior Visual Pathway (Including Eyeball, Optic nerve, Optic Chiasm and Optic tract) to Lateral Geniculate Nucleus (LGN). Lateral Geniculate Nucleus, located in Thalamus, (Pitto & Kupers, 2005) is the landmark which differentiates Anterior Visual Pathway and Posterior Visual Pathway. The visual information is thus transferred through Optic Radiation to Primary Visual Cortex (striate cortex, V1) (Fig 2), located at the back of the brain, for primary visual processing.
Dorsal stream and Ventral stream
To serve higher visual functions (e.g. visually guided movement; integrating attention, recognition and route finding (Dutton, et al, 2003)), the Geniculostriate Pathway branches into the Dorsal stream and Ventral stream so as to associate with other lobes in the brain. The Dorsal stream connects between occipital lobes and parietal lobes to process the whole visual scene and carry out visually guided movement. (Dutton, et al, 2003) The Ventral stream connects between occipital lobes between occipital lobes and temporal lobe and process visual recognition (e.g. face recognition, line, angle and shape perception) and visual memory. (Dutton, et al, 2003; 2004)
Choose of element in visual scene (Dutton, et al, 2003)
“Choose of element” involves both dorsal and ventral stream. In daily life, to handle massive information surrounded us; our posterior parietal lobes are responsible for processing the overall visual scene and allow us to attend to the element of scene at one time. Posterior parietal lobes, together cooperate with temporal lobes (serve recognition) and the frontal lobes (serve attention to areas of interest and motor planning), human is able to integrate attention, visually guided movement (eye-hand coordinated movement), recognition and route finding. (Dutton, et al, 2003)
Tectal Pathway or Extrageniculate Pathway
There is another parallel visual pathway (Hyvarinen, 2005), which is called Tectal Pathway (Hyvarinen, 2005) or Extrageniculate Pathway (Ro & Rafal, 2006) serves for visual functions including perception of movement, visually guided movement, eye saccade (Hoyt, 2003; Ro & Rafal, 2006) and less effective color processing (Ro & Rafal, 2006). This pathway branches before Lateral Geniculate Nucleus (LGN) and brings visual information to Superior Colliculus (SC) (serves for rapid eye movements) and Pulvinar (PU).
Fig. 3 Tectal pathway (Hyvarinen, 2005)Finally, visual information is transmitted to the cortical areas in parietal and occipital without the analysis of V1. (Hyvarienen, 2005; Ro & Rafal, 2006) (Fig. 3) As a result, people with cortical visual impairment still have good eye-hand co-ordination, detection of movement (Hoyt, 2003) and less effective color processing. (Hoyt, et al, 2003; Ro & Rafal, 2006) Although this parallel pathway together serves for visual function, CVI clients still have other significant deficits in visual recognitions including visual object agnosia, (Ogden, 1993) prosopagnosia (Ogden, 1993; Dutton, 2003) and Topographic agnosia. (Dutton, 2003) Since most of the lesion sites in CVI clients are Posterior Visual Pathway, neurological structures beyond LGN, (Watson, et al, 2007; Malkowicz, et al, 2006) Visual rehabilitation begins with the visual stimulation that promotes connections between synapse in human brain. (Powell, 1996) Neural-based stimulation that will eventually strengthen the neural pathway that are so critical for vision. (Powell, 1996) Therefore, training of these retinotectal and / or geniculoextrastriate pathways may be advantageous in restoration of visual function after primary visual cortex damage (Ro & Rafal, 2006).<Tang, W. (2008). Visual Rehabilitation for People with Cortical Visual Impairment. In Progress.>
References:
Dutton, G. N., Ballantyne, J., Boyd, G., Bradnam, M., Day, R., McCulloch, D., Mackie, R., Phillips, S., & Saunders, K. (1996). Cortical visual dysfunction in children: a clinical study. Eye, 10, 302-309.
Dutton, G. N. (2003). Cognitive vision, its disorders and differential diagnosis in adults and children: knowing where and what things are. Eye, 17, 289-304.
Dutton, G. N. (2003) Visual problem in children with damage to the brain. Visual Impairment Research. Visual Impairment Research, 4(2), 113-121.
Dutton, G. N., Saaed, A., Fahad, B., Fraser, R., Madaid, G., Mcdade, J., Mackintosh, A., Rane, T., & Spowart, K. (2004). Association of binocular lower visual field impairment, impaired simultaneous perception, disordered visually guided motion and inaccurate saccades in children with cerebral visual dysfunction – a retrospective observational study. Eye, 18, 27-34.
Dutton, G. N. (2008). Professionals CVI inventory version 2.
Ek, U. Fellenius, K. & Jacobson, L. (2003). Reading acquisition, cognitive and visual Jan, J. E. & Groenveld, M. (1993). Visual behaviors and adaptations associated with cortical and ocular impairment in children. Journal of Visual Impairment & Blindness, 4, 101-105.
Good, W. V., Jan, J. E., Burden, S. K., Skoczenski, A. & Candy, R. (2001). Recent advances in cortical visual impairment. Developmental Medicine & Child Neurology, 43, 56-60.
Groenveld, M., Jan, J. E. & Leader, P. (1990). Observations on the habilitation of children with cortical visual impairment. Journal of Visual Impairment & Blindness, 84, 11-15.
development, and self-esteem in four children with cerebral visual impairment. Journal of Visual Impairment & Blindness, 97, 741-754.
Hoyt, C.S. (2003). Visual function in the brain-damaged child. Eye, 17, 369-384.
Huo, R., Burden, S. K., Hoyt, C. S. & Good, W. V. (1999). Chronic cortical visual impairment in children: aetiology, prognosis, and associated neurological deficits. British Journal of Ophthalmology, 83(6), 670-675.
Hyvarinen, L. (2004). Understanding the behaviours of children with CVI. Retrieved Mar & Apr, 2004, from American Print House.
site: http://www.aph.org/cvi/articles/hyvarinen_1.html
Lueck, A. H., Dornbusch, H. & Hart, J. (1999). The effects of training on a young child with cortical visual impairment: an exploratory study. Journal of Visual Impairment & Blindness, 93, 778-793.
Morse, M. T. (1990). Cortical visual impairment in young children with multiple disabilities. Journal of Visual Impairment & Blindness, 84, 200-203.
Ogden, J. A. (1993). Visual object agnosia, prosopagnosia, achromatopsia, loss of visual imagery, and autobiographical amnesia flowing recovery from cortical blindness: case M. H. Neuroopsychologia, 31(6), 571-589.
Powell, S. A. (1996). Neural-based visual stimulation with infants with cortical impairment. Journal of Visual Impairment & Blindness, 90, 445-446.
Ro, T. & Rafal, R. (2006). Visual restoration in cortical blindness: insights from natural and TMS-induced blindsight. Neuropsychological Rehabilitation, 16(4), 377-396.
Roman-Lantzy, C. (2008). Cortical visual impairment: an approach to assessment and intervention. AFB Press.
Rosenberg, T., Flage, T. & Hansen, E. (1996). Incidence of registered visual impairment in the Nordic child population. British Journal of Ophthalmology, 80, 49-53.
Watson, T., Orel-Bixler, D. & Haegerstrom-Portnoy, G. (2007). Longitudinal quantitative assessment of vision function in children with cortical visual impairment. Optometry and Vision Science, 84(6), 471-480.
Widdig, W., Pleger, B., Rommel, O., Malin, J. & Tegenthoff, M. (2003). Repetitive visual stimulation: a neuropsychological approach to the treatment of cortical blindness, NeuroRehabilitation, 19, 227-237.
Zanelli, S. A., Naylor, M., Dobbins, N. (2008). Implementation of a “hypothermia for HIE” program: 2-year experience in a single NICU. Journal of Perinatology, 2(28), 171–175.
What is CVI?
What is CVI?
Cerebral Visual Impairment (CVI) is defined as bilateral visual impairment caused by damage to the posterior visual pathway, visual cortex or both. (Watson, et al, 2007; Malkowicz, et al, 2006; Hoyt, 2003; Jan & Groenveld 1993) (Fig. 1) There are many causes of CVI; the most common is Hypoxic-ischemic Encephalopathy (HIE). Other causes of CVI include infections, central nervous system malformations, neurological disorders, epilepsy, metabolic and neurodegenerative disorders, cerebral infarct or trauma. (Groenveld, et al, 1990; Jan & Groenveld, 1993; Morse, et al, 1990; Ek, et al, 2003; Malkowicz, et al, 2006)
Prevalence
CVI is clearly the most common cause of visual impairment in young children in developed countries. (Dutton et al, 1996; Hoyt, 2003; Jugnoo & Noriko, 2003; Rosenberg et al, 1996) In 1994 Chile, 2.1% children are diagnosed as CVI. In Huo’s 1999 study, 2.4% of 7,200 patients are examined as CVI in United Stated. In Hatton’s study published in eight years later, CVI dramatically increase to 24% of 1943 patients (quotated in National registry) examined in United Stated. In Northern Ireland, Belfast’s study revealed 45% of 76 patients are found to be CVI in the community. One of the reasons explaining the dramatic increase is the improvement in brain imaging techniques like Magnetic Resonance Imaging, MRI; Computed Tomography, CT Scan; Visual evoked potential, VEP & Electroencephalography (EEG), (Alexander, 1990; Good, et al, 2001; Widdig, et al, 2003; Watson, et al, 2007; Ro & Rafal, 2006) Second reason is the increased researches investigating this area were published in recent decade. These provoke the recognition of Medical officers in diagnosing CVI. Third reason is thanks to the advanced medical technologies like Hypothermia (Zanelli et al, 2008) in treating children with perinatal Hypoxic-ischemic Encephalopathy, HIE. The mortality rate was 16% in Canada from 1996 to 1997 while it was 10% in US in 2005 to 2006.
References:
Alexander, P. K. (1990) The effects of brain damage on visual functioning in children, Journal of Visual Impairment & Blindness, September, 372-376
Cohen-Maitre, S. A. & Haerich, P. (2005) Visual attention to movement and color in children with cortical visual impairment. Journal of Visual Impairment & Blindness, July, 389-402
Dutton, G. N. (2003) Cognitive vision, its disorders and differential diagnosis in adults and children: knowing where and what things are. Eye, 17, 289-304
Dutton, G., Ballantyne, J., Boyd, G., Bradnam, M., Day, R., McCulloch, D., Mackie, R., Phillips, S., & Saunders, K. (1996). Cortical visual dysfunction in children: A clinical study. Eye, 10, 302-309.
Dutton, G.N. (2003). Cognitive vision, its disorders and differential diagnosis in adults and children: Knowing where and what things are. Eye, 17, 289-304.
Dutton, G. N. (2003) Visual problem in children with damage to the brain. Visual Impairment Research, Visual Impairment Research, Vol.4, No.2, 113-121.
Dutton, G.N., Saaed, A., Fahad, B., Fraser, R., Madaid, G., Mcdade, J., Mackintosh, A., Rane, T., & Spowart, K. (2004). Association of binocular lower visual field impairment, impaired simultaneous perception, disordered visually guided motion and inaccurate saccades in children with cerebral visual dysfunction – A retrospective observational study. Eye, 18, 27-34.
Ek. U, Fellenius, K. & Jacobson, L. (2003) Reading acquisition, cognitive and visual development, and self-esteem in four children with cerebral visual impairment, Journal of Visual Impairment & Blindness, December, 741 – 754.
Good, W. V., Jan, J. E., Burden, S. K., Skoczenski, A. & Candy, R. (2001) Recent advances in cortical visual impairment. Developmental Medicine & Child Neurology, 43, 56-60
Groenveld, M., Jan, J. E. & Leader, P. (1990) Observations on the habilitation of children with cortical visual impairment. Journal of Visual Impairment & Blindness, 84, 11-15.
Hyvarien, L. (2005) CVI lecture series. Logan, UT: SKY-HI Institute, HOPE Inc
Hoyt, C.S. (2003). Visual function in the brain-damaged child. Eye, 17, 369-384.
Huo, R., Burden, S.K., Hoyt, C.S., & Good, W.V. (1999). Chronic cortical visual impairment in children: Aetiology, prognosis, and associated neurological deficits. British Journal of Ophthalmology, 83(6), 670-675.
Jan, J.E., & Groenveld, M. (1993). Visual behaviors and adaptations associated with cortical and ocular impairment in children. Journal of Visual Impairment & Blindness, April, 101-105.
Zanelli, S. A., Naylor, M., Dobbins, N. (2008) Implementation of a “hypothermia for HIE” program: 2-year experience in a single NICU. Journal of Perinatology, 2(28), 171–175.
Cerebral Visual Impairment (CVI) is defined as bilateral visual impairment caused by damage to the posterior visual pathway, visual cortex or both. (Watson, et al, 2007; Malkowicz, et al, 2006; Hoyt, 2003; Jan & Groenveld 1993) (Fig. 1) There are many causes of CVI; the most common is Hypoxic-ischemic Encephalopathy (HIE). Other causes of CVI include infections, central nervous system malformations, neurological disorders, epilepsy, metabolic and neurodegenerative disorders, cerebral infarct or trauma. (Groenveld, et al, 1990; Jan & Groenveld, 1993; Morse, et al, 1990; Ek, et al, 2003; Malkowicz, et al, 2006)
Prevalence
CVI is clearly the most common cause of visual impairment in young children in developed countries. (Dutton et al, 1996; Hoyt, 2003; Jugnoo & Noriko, 2003; Rosenberg et al, 1996) In 1994 Chile, 2.1% children are diagnosed as CVI. In Huo’s 1999 study, 2.4% of 7,200 patients are examined as CVI in United Stated. In Hatton’s study published in eight years later, CVI dramatically increase to 24% of 1943 patients (quotated in National registry) examined in United Stated. In Northern Ireland, Belfast’s study revealed 45% of 76 patients are found to be CVI in the community. One of the reasons explaining the dramatic increase is the improvement in brain imaging techniques like Magnetic Resonance Imaging, MRI; Computed Tomography, CT Scan; Visual evoked potential, VEP & Electroencephalography (EEG), (Alexander, 1990; Good, et al, 2001; Widdig, et al, 2003; Watson, et al, 2007; Ro & Rafal, 2006) Second reason is the increased researches investigating this area were published in recent decade. These provoke the recognition of Medical officers in diagnosing CVI. Third reason is thanks to the advanced medical technologies like Hypothermia (Zanelli et al, 2008) in treating children with perinatal Hypoxic-ischemic Encephalopathy, HIE. The mortality rate was 16% in Canada from 1996 to 1997 while it was 10% in US in 2005 to 2006.
References:
Alexander, P. K. (1990) The effects of brain damage on visual functioning in children, Journal of Visual Impairment & Blindness, September, 372-376
Cohen-Maitre, S. A. & Haerich, P. (2005) Visual attention to movement and color in children with cortical visual impairment. Journal of Visual Impairment & Blindness, July, 389-402
Dutton, G. N. (2003) Cognitive vision, its disorders and differential diagnosis in adults and children: knowing where and what things are. Eye, 17, 289-304
Dutton, G., Ballantyne, J., Boyd, G., Bradnam, M., Day, R., McCulloch, D., Mackie, R., Phillips, S., & Saunders, K. (1996). Cortical visual dysfunction in children: A clinical study. Eye, 10, 302-309.
Dutton, G.N. (2003). Cognitive vision, its disorders and differential diagnosis in adults and children: Knowing where and what things are. Eye, 17, 289-304.
Dutton, G. N. (2003) Visual problem in children with damage to the brain. Visual Impairment Research, Visual Impairment Research, Vol.4, No.2, 113-121.
Dutton, G.N., Saaed, A., Fahad, B., Fraser, R., Madaid, G., Mcdade, J., Mackintosh, A., Rane, T., & Spowart, K. (2004). Association of binocular lower visual field impairment, impaired simultaneous perception, disordered visually guided motion and inaccurate saccades in children with cerebral visual dysfunction – A retrospective observational study. Eye, 18, 27-34.
Ek. U, Fellenius, K. & Jacobson, L. (2003) Reading acquisition, cognitive and visual development, and self-esteem in four children with cerebral visual impairment, Journal of Visual Impairment & Blindness, December, 741 – 754.
Good, W. V., Jan, J. E., Burden, S. K., Skoczenski, A. & Candy, R. (2001) Recent advances in cortical visual impairment. Developmental Medicine & Child Neurology, 43, 56-60
Groenveld, M., Jan, J. E. & Leader, P. (1990) Observations on the habilitation of children with cortical visual impairment. Journal of Visual Impairment & Blindness, 84, 11-15.
Hyvarien, L. (2005) CVI lecture series. Logan, UT: SKY-HI Institute, HOPE Inc
Hoyt, C.S. (2003). Visual function in the brain-damaged child. Eye, 17, 369-384.
Huo, R., Burden, S.K., Hoyt, C.S., & Good, W.V. (1999). Chronic cortical visual impairment in children: Aetiology, prognosis, and associated neurological deficits. British Journal of Ophthalmology, 83(6), 670-675.
Jan, J.E., & Groenveld, M. (1993). Visual behaviors and adaptations associated with cortical and ocular impairment in children. Journal of Visual Impairment & Blindness, April, 101-105.
Zanelli, S. A., Naylor, M., Dobbins, N. (2008) Implementation of a “hypothermia for HIE” program: 2-year experience in a single NICU. Journal of Perinatology, 2(28), 171–175.
Visual Rehabilitation for People with Cortical Visual Impairment (CVI)
Visual Rehabilitation for People with Cortical Visual Impairment (CVI)
WILSON TANG, yu-fung,
甚麼是白化病? Albinism?
甚麼是白化病? Albinism?
白化病是一種天生的色素疾病，身體、頭髮、皮膚、眼睛及虹膜全部或部份缺乏色素。白化的原因是因為身體內的酵未能製造出黑色素(melanin)，身體出現咖啡色或白色現象。白化病是由父母的基因遺傳，出現double recessive狀況，故此就男性白化病者而言，父母均帶有隱性白化病的基因，絕大部份的白化病兒童均會建議輪候遺傳科，以DNA基因鑑定找出兒童及其父母的基因圖譜，繼而找出白化病的成因。
白化病視覺的影響
由於虹膜缺乏色素，白化病的兒童出現怕光情況(photophobia)，原因為虹膜阻隔光源進入眼睛內部的能力較弱。因此，大部份的白化病兒童視覺敏銳度因而大受影響，以本人的前線經驗而言，大部份兒童的視覺敏銳度均為中度至嚴重低視力。而他們在外出時候，較容易受到陽光的威脅，長期接觸陽光會影響眼球內部的結構及運作(如：視網膜(Chen, 2006))，長遠而言可引致失明。故白化病的兒童，外出時需要戴上太陽眼鏡，而家居及學校的室內燈光亦需要調配較暗，以減少光源直接進入眼球內部。
眼球震顫(Chen, 2006)亦是經常出現在白化病兒童眼睛的情況，白化病兒童眼球震顫的成因至今亦未明。但眼球震顫帶來的影響，令兒童出現重影(diplopia)，減低手眼協調性(eye-hand coordination)或頭暈(dizziness)等情況。部份兒童會出現側頭情況，此舉經常被老師或家長誤會為不專心，而事實上眼球震顫兒童側頭至某一點null point，眼球震顫的幅度是會減少。而每個兒童的null point位置亦不會相同，視乎眼球震顫的成因，及其眼球擺動的方向。
改善眼球震顫的方法
以往而言，眼球震顫最正接了當的方法就是動手術，拉緊貼著眼球上的六條肌肉。但本人臨床發現，只要透過感覺統合活動，加上正確的眼球肌肉活動訓練，能有效加強眼球肌肉控制(oculomotor control)，眼球震顫的情況是可以逐步減少。但若要完全根治眼球震顫，至今手術或訓練仍未有此成效。本人曾經訓練過一位十個月大的小朋友，訓練初期兒童仍需要以null point側頭視物，兒童不能夠進行橫向及縱向的視覺追蹤(visual tracking)，約半年後，null point已經消失，而眼球肌肉控制大為改善，能夠進行暢順的橫向及縱向視覺追蹤(smooth pursuit)。
Chen, H. (2006). Atlas of genetic diagnosis and counseling. Totowa, NJ: Humana Press.
白化病是一種天生的色素疾病，身體、頭髮、皮膚、眼睛及虹膜全部或部份缺乏色素。白化的原因是因為身體內的酵未能製造出黑色素(melanin)，身體出現咖啡色或白色現象。白化病是由父母的基因遺傳，出現double recessive狀況，故此就男性白化病者而言，父母均帶有隱性白化病的基因，絕大部份的白化病兒童均會建議輪候遺傳科，以DNA基因鑑定找出兒童及其父母的基因圖譜，繼而找出白化病的成因。
白化病視覺的影響
由於虹膜缺乏色素，白化病的兒童出現怕光情況(photophobia)，原因為虹膜阻隔光源進入眼睛內部的能力較弱。因此，大部份的白化病兒童視覺敏銳度因而大受影響，以本人的前線經驗而言，大部份兒童的視覺敏銳度均為中度至嚴重低視力。而他們在外出時候，較容易受到陽光的威脅，長期接觸陽光會影響眼球內部的結構及運作(如：視網膜(Chen, 2006))，長遠而言可引致失明。故白化病的兒童，外出時需要戴上太陽眼鏡，而家居及學校的室內燈光亦需要調配較暗，以減少光源直接進入眼球內部。
眼球震顫(Chen, 2006)亦是經常出現在白化病兒童眼睛的情況，白化病兒童眼球震顫的成因至今亦未明。但眼球震顫帶來的影響，令兒童出現重影(diplopia)，減低手眼協調性(eye-hand coordination)或頭暈(dizziness)等情況。部份兒童會出現側頭情況，此舉經常被老師或家長誤會為不專心，而事實上眼球震顫兒童側頭至某一點null point，眼球震顫的幅度是會減少。而每個兒童的null point位置亦不會相同，視乎眼球震顫的成因，及其眼球擺動的方向。
改善眼球震顫的方法
以往而言，眼球震顫最正接了當的方法就是動手術，拉緊貼著眼球上的六條肌肉。但本人臨床發現，只要透過感覺統合活動，加上正確的眼球肌肉活動訓練，能有效加強眼球肌肉控制(oculomotor control)，眼球震顫的情況是可以逐步減少。但若要完全根治眼球震顫，至今手術或訓練仍未有此成效。本人曾經訓練過一位十個月大的小朋友，訓練初期兒童仍需要以null point側頭視物，兒童不能夠進行橫向及縱向的視覺追蹤(visual tracking)，約半年後，null point已經消失，而眼球肌肉控制大為改善，能夠進行暢順的橫向及縱向視覺追蹤(smooth pursuit)。
Chen, H. (2006). Atlas of genetic diagnosis and counseling. Totowa, NJ: Humana Press.
甚麼是弱視?
甚麼是弱視? Amblyopia?
每當提及斜視的時候，家長往往接下來的提問必然是「咁係咪即係弱視呀?」我通常的回答是斜視和弱視是兩種完全不同的視障情況，但兩者卻互相有著關係。斜視是其中一個可以形成弱視的原因，大部份眼科醫生或視光師都會建議斜視的小朋友遮眼，第一個功效是加強斜視眼的眼肌活動訓練，以及加強該眼睛接收視覺訊息的能力。
弱視大多是基於其中一隻眼睛接收視覺訊息能力較弱，因而雙眼視物時出現偏差，腦部為求接收及分析較清楚的影像，因而拒絕接收較弱眼睛傳遞之視覺訊息，最後該眼睛出現看不見的情況，我們會稱之為弱視 (俗稱「懶眼」或lazy eye)。所以弱視是腦部發展的問題，而大多數主因並不在眼球。Amblyopia is a developmental problem in the brain, not an organic problem in the eye. (although organic problems can give rise to amblyopia which continue to exist after the organic problem has resolved) (McKee et al, 2003)
弱視可以復原嗎?
弱視一旦建立以後，一般是很難復原，但是可以有改善的空間。以往的概念是源於視覺發展黃金期為八歲，弱視眼在八歲前還可以嘗試訓練，但八歲以後就機會較微。但現時新的訓練概念已經相繼而出，基於腦神經可塑性，訓練和治療不單限制於兒童。外國曾做過年青人弱視的研究 (Holmes et al, 2006; Pediatric eye disease investigator group, 2005)，發現年青人，甚至乎成人，只要接受vision therapy和遮眼的訓練，弱視眼依然有改善的情況。但研究完了以後他們有否退步，甚至乎打回原形，卻是沒有提供任何跟進。孤勿論情況如何，只是帶如了我們一個新方向，弱視小朋友，青年人或是成年人，只要提供遮眼(eye patching)及vision therapy (視覺治療)，他們的視力可以有進步的空間。
References:
McKee, S. P., Levi, D. M. & Movshon, J. A. (2003). The pattern of visual deficits in amblyopia. Vision. 4 (5): 380 – 405.
Holmes, J. M., Repka, M. X., Kraker, R. T. & Clarke, M. P. (2006). The treatment of amblyopia. Strabismus 15 (1), 37 – 42.
Pediatric Eye Disease Investigator Group (2005). Randomized trial of treatment of amblyopia in children aged 7 to 17 years. Archives of Ophthalmology. 123 (4), 437 – 447.
每當提及斜視的時候，家長往往接下來的提問必然是「咁係咪即係弱視呀?」我通常的回答是斜視和弱視是兩種完全不同的視障情況，但兩者卻互相有著關係。斜視是其中一個可以形成弱視的原因，大部份眼科醫生或視光師都會建議斜視的小朋友遮眼，第一個功效是加強斜視眼的眼肌活動訓練，以及加強該眼睛接收視覺訊息的能力。
弱視大多是基於其中一隻眼睛接收視覺訊息能力較弱，因而雙眼視物時出現偏差，腦部為求接收及分析較清楚的影像，因而拒絕接收較弱眼睛傳遞之視覺訊息，最後該眼睛出現看不見的情況，我們會稱之為弱視 (俗稱「懶眼」或lazy eye)。所以弱視是腦部發展的問題，而大多數主因並不在眼球。Amblyopia is a developmental problem in the brain, not an organic problem in the eye. (although organic problems can give rise to amblyopia which continue to exist after the organic problem has resolved) (McKee et al, 2003)
弱視可以復原嗎?
弱視一旦建立以後，一般是很難復原，但是可以有改善的空間。以往的概念是源於視覺發展黃金期為八歲，弱視眼在八歲前還可以嘗試訓練，但八歲以後就機會較微。但現時新的訓練概念已經相繼而出，基於腦神經可塑性，訓練和治療不單限制於兒童。外國曾做過年青人弱視的研究 (Holmes et al, 2006; Pediatric eye disease investigator group, 2005)，發現年青人，甚至乎成人，只要接受vision therapy和遮眼的訓練，弱視眼依然有改善的情況。但研究完了以後他們有否退步，甚至乎打回原形，卻是沒有提供任何跟進。孤勿論情況如何，只是帶如了我們一個新方向，弱視小朋友，青年人或是成年人，只要提供遮眼(eye patching)及vision therapy (視覺治療)，他們的視力可以有進步的空間。
References:
McKee, S. P., Levi, D. M. & Movshon, J. A. (2003). The pattern of visual deficits in amblyopia. Vision. 4 (5): 380 – 405.
Holmes, J. M., Repka, M. X., Kraker, R. T. & Clarke, M. P. (2006). The treatment of amblyopia. Strabismus 15 (1), 37 – 42.
Pediatric Eye Disease Investigator Group (2005). Randomized trial of treatment of amblyopia in children aged 7 to 17 years. Archives of Ophthalmology. 123 (4), 437 – 447.
甚麼是斜視?
甚麼是斜視?
斜視是指雙眼的排列並非一致，而出現視軸上不平衡，雙眼未能同時專注於同一目標。Strabismus is a condition in which the eyes are not properly aligned with each other (American Optometric Association). 斜視簡單有以下幾種：i) 外斜視(exotropia); ii) 內斜視 (esotropia); iii) 上斜視 (hypertropia); iv) 下斜視 (hypotropia); v) 外隱斜 (exophoria) 及vi) 內隱斜 (esophoria)。(見下圖)
通常我們會作cover eye test測試，以得知雙眼的視軸是否出現不平衡。先讓小朋友注視一點目標(如:手指或筆尖等)，我們左右交替遮蓋他們的雙眼，如先遮蓋左眼，然後快速遮蓋右眼。正常的情況被遮蓋後再次看目標時眼睛沒有任何移動，但被遮蓋後再次看目標時，小朋友的眼睛向橫移動(tropia)或轉動(phoria)，則代表小朋友有斜視狀況。
斜視的成因有很多，最普遍的是家族性遺傳或是腦神經受創(CN III，CN IV或CN VI)，影響了眼球肌肉活動。每一隻眼睛均由六條肌肉所控制，當中包括i) medial rectus; ii) lateral rectus; iii) superior retus; iv) inferior retus; v) superior oblique & vi) inferior oblique。這六條肌肉可簡單分為三組antagonistic pair muscles，控制眼部的所有活動能力及方向，所以俗語經常說「眼仔look look」，其實是指這些肌肉的協調性。
斜視的影響
一般而言，斜視可影響兒童的深度感 (depth perception)，立體感(stereoscopic vision)，看物件是會出現重影(diplopia)，手眼協調(eye-hand coordination)，嚴重者會出現頭暈情況。簡單而言，他們看立體圖畫或立體電影時會出現困難。日常生活中，如上落樓梯，跑步及跳遠等，因為判斷距離高度出現困難，較容易出錯而跌倒。在學習上，如寫字，學習點、線、面及計算面積或體積的情況會吃力一點。我曾遇過一個個案，他和重影一起生活了十六年，看甚麼也是出現兩個影像，別人豎起手指給他數，他也會因會重影出現邢往往數錯數目。對他學習而言，最困難的莫過於數學畫圖表，特別是用格仔紙畫graph，對他而言，望著綠色的格仔紙，簡直是多生了一對複眼一樣，他往往需要以閉上一隻眼，才能夠完成畫graph這功課。
斜視的處理方法
1. 最常見亦最無傷害性的是「遮眼」，一定需要交由視光師或眼科醫生建議應該遮哪一隻眼及遮眼的時間。
2. 如持續遮眼而斜視沒有特別改善，眼科醫生一般建議手術，將偏離視軸的眼睛放回視軸上，以防止「弱視」的情況發生。而另外有情況是小朋友已經建立了「弱視」眼，醫生建議做手術是基於外觀上的考慮。
3. 感覺統合，本人的多年經驗，發覺以能覺統合當中的視覺及前庭刺激訓練，能有效提昇兒童的眼球肌肉控制，從而改善斜視情況。(欲知詳情可個別找我)
最後，由於0-8歲兒童腦部處於發展階段，腦部會自動拒絕接受由斜視眼傳至腦部的視覺信息，慢慢形成「弱視」，令斜視眼再看不到東西。所以當發現兒童出現斜視情況時，需及早尋求方法改善或醫治，
References:
American Optometric Association. Optometric Clinical Practice Guideline: Care of the patient with strabismus: esotropia and exotropia
斜視是指雙眼的排列並非一致，而出現視軸上不平衡，雙眼未能同時專注於同一目標。Strabismus is a condition in which the eyes are not properly aligned with each other (American Optometric Association). 斜視簡單有以下幾種：i) 外斜視(exotropia); ii) 內斜視 (esotropia); iii) 上斜視 (hypertropia); iv) 下斜視 (hypotropia); v) 外隱斜 (exophoria) 及vi) 內隱斜 (esophoria)。(見下圖)
通常我們會作cover eye test測試，以得知雙眼的視軸是否出現不平衡。先讓小朋友注視一點目標(如:手指或筆尖等)，我們左右交替遮蓋他們的雙眼，如先遮蓋左眼，然後快速遮蓋右眼。正常的情況被遮蓋後再次看目標時眼睛沒有任何移動，但被遮蓋後再次看目標時，小朋友的眼睛向橫移動(tropia)或轉動(phoria)，則代表小朋友有斜視狀況。
斜視的成因有很多，最普遍的是家族性遺傳或是腦神經受創(CN III，CN IV或CN VI)，影響了眼球肌肉活動。每一隻眼睛均由六條肌肉所控制，當中包括i) medial rectus; ii) lateral rectus; iii) superior retus; iv) inferior retus; v) superior oblique & vi) inferior oblique。這六條肌肉可簡單分為三組antagonistic pair muscles，控制眼部的所有活動能力及方向，所以俗語經常說「眼仔look look」，其實是指這些肌肉的協調性。
斜視的影響
一般而言，斜視可影響兒童的深度感 (depth perception)，立體感(stereoscopic vision)，看物件是會出現重影(diplopia)，手眼協調(eye-hand coordination)，嚴重者會出現頭暈情況。簡單而言，他們看立體圖畫或立體電影時會出現困難。日常生活中，如上落樓梯，跑步及跳遠等，因為判斷距離高度出現困難，較容易出錯而跌倒。在學習上，如寫字，學習點、線、面及計算面積或體積的情況會吃力一點。我曾遇過一個個案，他和重影一起生活了十六年，看甚麼也是出現兩個影像，別人豎起手指給他數，他也會因會重影出現邢往往數錯數目。對他學習而言，最困難的莫過於數學畫圖表，特別是用格仔紙畫graph，對他而言，望著綠色的格仔紙，簡直是多生了一對複眼一樣，他往往需要以閉上一隻眼，才能夠完成畫graph這功課。
斜視的處理方法
1. 最常見亦最無傷害性的是「遮眼」，一定需要交由視光師或眼科醫生建議應該遮哪一隻眼及遮眼的時間。
2. 如持續遮眼而斜視沒有特別改善，眼科醫生一般建議手術，將偏離視軸的眼睛放回視軸上，以防止「弱視」的情況發生。而另外有情況是小朋友已經建立了「弱視」眼，醫生建議做手術是基於外觀上的考慮。
3. 感覺統合，本人的多年經驗，發覺以能覺統合當中的視覺及前庭刺激訓練，能有效提昇兒童的眼球肌肉控制，從而改善斜視情況。(欲知詳情可個別找我)
最後，由於0-8歲兒童腦部處於發展階段，腦部會自動拒絕接受由斜視眼傳至腦部的視覺信息，慢慢形成「弱視」，令斜視眼再看不到東西。所以當發現兒童出現斜視情況時，需及早尋求方法改善或醫治，
References:
American Optometric Association. Optometric Clinical Practice Guideline: Care of the patient with strabismus: esotropia and exotropia
視覺與動作發展間的關係
視覺與動作發展間的關係
(摘錄自社團法人台北市視障者家長協會2008《親子互動20招》頁4-5)
原作者：Virginia Bishop 博士
翻譯註解：張千惠副教授 國立台灣師範大學特殊教育系
視覺不是一項可以完全獨立的功能，從生命早期，嬰兒就開始把看到的資訊和其他感官資訊聯結起來，以增強及促進知覺發展…
| 出生 | 眼睛角膜對觸摸有反射(動作)反應，瞳孔對光有反應但對強光會閉眼睛；初期發育未完全的凝視，約可注意看8-12吋(24公分-36公分)遠的臉孔。 |
| 1個月 | 開始會做水平的追視，但反應仍不靈光，可追視移動的東西至身體中線位置；會注視人的臉，因不對稱張力，頸部反射動作會注意到自己的手，出現保護性眨眼動作(未必每次都會出現)，可以明確的看到不同顏色(紅/黃/橙)，但對黑白色較有興趣。(不對稱張力於四個月大時會自動消失) |
| 2個月 | 開始用雙眼去注視、眼睛能夠固定，集中一點，對焦，可以垂直上下追視；較喜歡看人的臉勝於複雜的圖形，對黑白水平條紋較有興趣，目光可以注意看3吋和6吋近的距離、也可以看到約六英呎(約183公分)遠的東西；可注視較亮的光和紅色、橙色、黃色。(出現社會性的微笑，有預期週遭人事物的行為) |
| 3個月 | 眼睛的移動變的較靈活；可以轉移(換)目光注視之焦點，但有時仍會不協調，可以瞥見約一吋(3公分)遠的物體；媽媽可以利用一些視覺的刺激來告訴寶寶：該吃飯了，因為藉由這些視覺上的刺激，寶寶已經可以預期到母親要開始餵食了。會玩自己的手，看自己的手，可追視東西至80度角，但無法準確抓住晃動的物體，開始對黑白直線、橫條紋以及棋盤狀格子、鋸齒狀的線條有興趣，可以看到紅色、橙色、黃色 |
| 4個月 | 會注意看手，可以轉移目光注視之焦點(例：從甲處轉到乙處)，但經常會失去目標物；能夠辨認熟悉的面孔，會眼睛來探索新環境，可以追視東西過身體的中線；眼球可以做水平、垂直(上下)與環狀的運動，但有時仍會不協調，無法準確抓住晃動的物體，能夠注意到手中與放入口中的物體。(俯卧時能夠抬頭至90度) |
| 5個月 | 發展出手眼協調動作，共可成功地伸出摸到眼睛看到的東西；可以凝視靠近眼睛的東西，目光可以固定約3英呎(90公分)左右之處，並能立即轉移目光至較近處，會對鏡子微笑並拍打鏡中的影像，對黑白格、人的臉孔、對比鮮明的輪廓有興趣。 |
| 6個月 | 目光的移動較協調、靈活，可以容易地轉移目光注意力；會伸手趨近於熟悉的人或玩具，可以認得出約6英呎(約183公分)遠的臉孔；陌生人焦慮症於此時發生出來，開始時對東西的外型略可區辨，在目光注視下將東西由某一隻手換到另一隻手，大概可以預測東西掉落的位置；可以在3個或更多的物體之間來回轉移目光，可注視於某物消失之處，另外，不論光線的強弱，對光的反應較為持續一致。(俯卧姿態下可用雙臂撐起身體並保持頭部直立，頭部控制良好，玩弄並觀察自己的腳) |
| 7-8個月 | 視覺追視較順暢且可持久，但反應仍大多依自身對目標是否有興趣而定，會操弄物品，視力幾乎正常，辨識深度(立體感)的視覺能力正逐漸發展出來，會轉動手中的東西，並利用視覺探索該物。 |
| 9-10個月 | 會伸出食指探索新的東西，可看到近處約0.2-0.3公分大小的小東西，會觀察人臉的表情並試圖模仿；能夠自如的隨著大腦意念的控制，放下手中的東西，若大人將寶寶已看到的(面前)東西藏起來，寶寶會知道要去找尋該物，會注意到新的人物和場所，會使用眼睛來監控手和身體的移動。 |
| 1歲 | 會用食指、拇指合作揑取東西，近距離及遠距離的視力都不錯，雙眼並用的能力較強，能夠對焦並調整進入眼睛的光線，深度(立體感)的視知覺良好，可區辨不同的幾何形狀，自如的塗鴉，可用眼睛來監控身體在所處空間中的移動。 |
| 1歲_1歲半 | 發展垂直的方向(例如：行走、堆高積木)，配對相同的東西，指認書上的圖案，塗鴉時手有垂直、水平及畫圓弧的動作，指認形狀。 |
| 1歲-2歲 | 此時，寶寶可以僅依靠視覺能力來探索物體，模仿別人的動作，視覺記憶內容增多，所有相關視覺的技能更加熟練，能夠配對顏色和形狀。 |
| 3歲 | 能用塑膠拼板來配對簡單拼圖，可以大概畫出不規則圓形，可插長度約1吋(約3公分)的插捧入孔。 |
| 4歲 | 會分辨大小(配對)，有正確的深度立體感知覺概念，可區辨不同長度的線條，會仿畫『十』字形，可區辨大部份的形狀，有精確的手眼協調動作。 |
| 5歲 | 可精確自如地拿起及放下物品，會著色、使用剪刀和膠水，粗大動作的控制較佳，會畫基本幾何形狀，可用眼睛來判斷積木方塊之大小或形狀之差異，並依此視覺判斷來決定該如何排列或堆放，可觀察到圖案中的小細節。 |
視覺感知 (Visual Perception)
視覺感知 (Visual Perception) 是腦部接受眼睛的視覺訊息後，如何處理，分析及理解四周環境內的可見物象及光線。
“Visual perception is the ability to interpret information and surroundings from visible light reaching the eye”
視覺感知能力牽涉的範圍甚廣，由深度感，立體感至於動感亦涉及其中，對於視障幼兒而言，視覺感知能力(Visual Perception Skills)是學習文字及讀寫文字的所需具備的能力，而此能力的缺損，對幼兒成長影響較為深遠。根據TVPS, Test of Visual Perception Skills (non-motor)，視覺感知可分為七項，分別為I) 視覺辨別; II) 視覺記憶; III) 視覺空間關係 IV) 視覺形狀永恆 V) 視覺次序記憶 VI) 背景與主體及 VII) 部份與整體。就一般情況而言，這七項能力需要互相應用及統合，才能成為我們現有的視覺感知能力。
I) 視覺辨別: 利用視覺分辨物件的相同與不相同，以至進行配對活動或找不同。
II) 視覺記憶: 記憶眼睛所看見的東西。而記憶可簡單分為短期記憶(short-term memory)，工作記憶(working memory)及長期記憶(long-term memory)。
III) 視覺空間關係: 指物件在空間中的位置，亦是了解物件與物件之間的關係，即兒童是否認知物體與物體相應的位置。
IV) 視覺形狀永恆: 兒童從不同角度看見同一物件後，能否以辨別物件的相同與否
V) 視覺次序記憶: 運用視覺短暫記憶物件的排列或次序
VI) 背景與主體: 從簡單或複雜背景中找出所需要的物件
VII) 部份與整體: 看見物件的部份後，能否辨認出是哪一物件
而普遍的視障幼兒，不論是基於眼球受損，大腦受損或是斜視的問題，視覺感知能力較一般幼兒偏弱，或是深度感影響其判別物件之間的距離，判別物件之間的關係等，故較多時候視障幼兒認知文字，以視覺記憶文字或書寫文字的情況亦因視覺感知能力偏弱而有所影響。
“Visual perception is the ability to interpret information and surroundings from visible light reaching the eye”
視覺感知能力牽涉的範圍甚廣，由深度感，立體感至於動感亦涉及其中，對於視障幼兒而言，視覺感知能力(Visual Perception Skills)是學習文字及讀寫文字的所需具備的能力，而此能力的缺損，對幼兒成長影響較為深遠。根據TVPS, Test of Visual Perception Skills (non-motor)，視覺感知可分為七項，分別為I) 視覺辨別; II) 視覺記憶; III) 視覺空間關係 IV) 視覺形狀永恆 V) 視覺次序記憶 VI) 背景與主體及 VII) 部份與整體。就一般情況而言，這七項能力需要互相應用及統合，才能成為我們現有的視覺感知能力。
I) 視覺辨別: 利用視覺分辨物件的相同與不相同，以至進行配對活動或找不同。
II) 視覺記憶: 記憶眼睛所看見的東西。而記憶可簡單分為短期記憶(short-term memory)，工作記憶(working memory)及長期記憶(long-term memory)。
III) 視覺空間關係: 指物件在空間中的位置，亦是了解物件與物件之間的關係，即兒童是否認知物體與物體相應的位置。
IV) 視覺形狀永恆: 兒童從不同角度看見同一物件後，能否以辨別物件的相同與否
V) 視覺次序記憶: 運用視覺短暫記憶物件的排列或次序
VI) 背景與主體: 從簡單或複雜背景中找出所需要的物件
VII) 部份與整體: 看見物件的部份後，能否辨認出是哪一物件
而普遍的視障幼兒，不論是基於眼球受損，大腦受損或是斜視的問題，視覺感知能力較一般幼兒偏弱，或是深度感影響其判別物件之間的距離，判別物件之間的關係等，故較多時候視障幼兒認知文字，以視覺記憶文字或書寫文字的情況亦因視覺感知能力偏弱而有所影響。
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