Would Ray Charles and Stevie Wonder be as talented if they were not blind? There is a popular belief that blind people compensate with heightened sensitivity of other senses. Dr. Lofti Merabet studies sensory compensation and neuroplasticity in blind people and recently gave a talk on The Adaptive Brain of the Blind.
Merabet defines neuroplasticity as the ability of the brain to change its structural and functional organization in response to development, experience, the environment, or damage. Generally, there is greater adaption ability in response to changes that occur slowly and at young ages compared to sudden changes that occur later in life, and this has to do with brain development. Physiological evidence of an early critical period of visual development came from experiments in the 1960s and 1970s showing that the anatomy and functioning of the visual cortex is intrinsically linked to visual experiences in early life.
To demonstrate the phenomenal powers of neuroplasticity, Merabet tells of a man who had seemingly developed normally. As an adult, the man complained of persistent headaches, and an MRI showed that he had only a small portion of brain tissue. The man’s brain had gradually adapted to a point that the man seemed normal. On the other hand, neuroplasticity is not always positive. For example, in phantom limb pain, a person experiences pain in an amputated limb.
Neuroplasticity in blindness
What about sensory compensation? There is longstanding behavioral evidence that blind people’s other senses are keener than those of a sighted person, but the neuroscientific evidence for this has only started to emerge recently.
The visual cortex comprises 30-40% of the cortical surface, and Merabet studies what happens to it in people with ocular blindness. Functional neuroimaging shows an active visual cortex in a blind person reading Braille, thus demonstrating a non-visual function for the visual cortex. Other non-visual tasks, such as olfaction and localizing sound, also recruit the visual cortex. Conversely, when the visual cortex is damaged, such as in a stroke, a blind person may lose his ability to read Braille, even though the parts of the brain responsible for touch and language remain intact. This evidence supports the idea that the visual cortex is the seat of compensatory behaviors in people with ocular blindness.
Merabet puts compensatory abilities to the test in real life situations. He designed a computer game in which a building was mapped with audio cues (a knocking signified the presence of a door, e.g.). Blind children could play the game in one of two ways: exploratory, where they were free to explore the building on their own and which resulted in implicit learning of the building layout, or directed navigation, where they were shown around the building by a leader and which resulted in explicit learning. After learning the building’s layout through the game, the children went to the actual building where they performed navigational tasks. Merabet found that the implicit learners performed better overall, and he points out that this has important implications for rehabilitation treatment.
Cortical visual impairment
In cases of cortical visual impairment (CVI), the eyes are fully functional, but the visual cortex is destroyed. Ocular exams typically look normal in CVI patients even though there is significant visual impairment, such as problems with motion processing and even complete blindness.
Merabet points to the difficulty in relating brain structure, clinical presentation, and brain function in CVI patients. Although many CVI patients have enlarged ventricles easily visible on MRI, the size of the enlargement is not related to the extent of clinical dysfunction. Therefore, Merabet developed an imaging technique to better relate clinical presentation and brain structure.
CVI is a disorder of brain connectivity, not structure, so Merabet uses diffusion based imaging to map axonal connections in the visual cortex. A sighted person has three main connections from the visual cortex to other parts of the brain. Each connection is responsible for a different function: spatial processing, object processing, and attention processing. In CVI patients, the object processing pathway is intact, but the other two are missing. Interestingly, in ocular blindness, all three pathways remain intact, and show hyperconnectivity, perhaps accounting for compensatory behaviors.
Merabet emphasizes that optimal rehabilitation strategies for those with ocular blindness and with CVI will differ, but that CVI is not yet understood well enough to have specific treatments. Merabet is working toward creating CVI-specific treatments. He recently designed a simple tablet-based task to test CVI patients’ ability to detect motion. He is beginning to relate these results to imaging results with the ultimate goal of building a more complete diagnostic picture of CVI. In the future, he hopes to use this data to develop more effective rehabilitation strategies that take the differences between CVI and ocular blindness into account.
Merabet closes by saying that although he is excited about the data he is gathering, he is only beginning to understand how the information will be used in the clinical setting.
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