版權所有，翻印必究
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。
<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。
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.
訂閱：
文章 (Atom)