CMSD5280 Audition II PDF

CMSD5280 Audition II Auditory Cognition and Perception I: Neuroplasticity Dr. Olivier Valentin, Ph.D. OUTLINE 1. Overview of the human nervous system and function i. The peripheral nervous system ii. The central nervous system OUTLINE 1. Overview of...

CMSD5280 Audition II Auditory Cognition and Perception I: Neuroplasticity Dr. Olivier Valentin, Ph.D. OUTLINE 1. Overview of the human nervous system and function i. The peripheral nervous system ii. The central nervous system OUTLINE 1. Overview of the human nervous system and function i. The peripheral nervous system ii. The central nervous system 2. Neuroplasticity and its mechanisms i. Structural neuroplasticity ii. Functional neuroplasticity iii. Critical periods of plasticity OUTLINE 1. Overview of the human nervous system and function i. The peripheral nervous system ii. The central nervous system 2. Neuroplasticity and its mechanisms i. Structural neuroplasticity ii. Functional neuroplasticity iii. Critical periods of plasticity 3. Clinical implications of neuroplasticity i. Recovery mechanisms from neural injury ii. Disruptors of neural activity iii. Maladaptive plasticity Overview of the human nervous system and function 1- The peripheral nervous system  The human nervous system consists in two parts, the central nervous system and the peripheral nervous system. The peripheral nervous system is that part of the nervous system that lies outside the brain and spinal cord. It plays key role in both sending information from different areas of your body back to your brain, as well as carrying out commands from your brain to various parts of your body. Overview of the human nervous system and function 1- The peripheral nervous system 2- The central nervous system The central nervous system is a processing center that manages everything that our body does, from our thoughts and feelings to our movements. The central nervous system consists of the brain and the cord. Overview of the human nervous system and function Gray White matter matter 1- The peripheral nervous system 2- The central nervous system 2.1- The spinal cord  The spinal cord is a long, narrow, tube-like structure composed of nervous tissue, extending from the medulla oblongata in the lower brainstem down to the lumbar region of the vertebral column (backbone). In cross-section, the outer region of the spinal cord contains white matter tracts made up of sensory and motor axons. Beneath this outer region lies the grey matter, which consists of nerve cell bodies organized into three grey columns that give the area its butterfly-like shape. Overview of the human nervous system and function Cerebrum 1- The peripheral nervous system 2- The central nervous system 2.1- The spinal cord 2.2- The brain Brainstem Cerebellum  At a high level, the brain can be divided into the cerebrum, brainstem and cerebellum. Overview of the human nervous system and function 1- The peripheral nervous system 2- The central nervous system 2.1- The spinal cord 2.2- The brain 2.2.1- Cerebellum  The cerebellum, often referred to as the "little brain," is a fist-sized structure located at the back of the head, beneath the temporal and occipital lobes and above the brainstem. Similar to the cerebrum, it consists of two hemispheres. The outer region contains neurons, while the inner area facilitates communication with the cerebral cortex. Its primary functions include coordinating voluntary muscle movements and maintaining posture, balance, and equilibrium. Recent studies are investigating the cerebellum's potential roles in cognition, emotions, social behavior, and its involvement in conditions such as addiction, autism, and schizophrenia. Overview of the human nervous system and function 1- The peripheral nervous system 2- The central nervous system 2.1- The spinal cord 2.2- The brain 2.2.1- Cerebellum 2.2.2- Brainstem  The human brainstem is composed of the midbrain, the pons, and the medulla. The brainstem plays important functions in breathing, heart rate, arousal/consciousness, sleep/wake functions and attention/concentration. The brainstem contains several important relay stations for processing auditory information, including the cochlear nucleus, superior olivary complex, and inferior colliculus. Overview of the human nervous system and function 1- The peripheral nervous system 2- The central nervous system 2.1- The spinal cord 2.2- The brain 2.2.1- Cerebellum 2.2.2- Brainstem 2.2.3- Cerebrum  The cerebrum, the brain's largest component, is composed of two cerebral hemispheres, each with its cerebral cortex (the outer layers of grey matter) and underlying white matter regions. Its subcortical structures include the hippocampus, basal ganglia, and olfactory bulb. The cerebrum is made up of two C-shaped hemispheres, which are divided by a deep groove known as the longitudinal fissure. Popular psychology often makes broad generalizations about specific functions being lateralized to either the right or left side of the brain. However, these claims are typically inaccurate, as most brain functions are actually distributed across both hemispheres. However, some function have been well-established as lateralized, like for example the Broca's and Wernicke's Areas, which are primarily associated with language and are usually located in the left hemisphere. These areas often correspond with handedness, meaning they are typically found in the hemisphere opposite to the dominant hand. Overview of the human nervous system and function 1- The peripheral nervous system 2- The central nervous system 2.1- The spinal cord 2.2- The brain 2.2.1- Cerebellum 2.2.2- Brainstem 2.2.3- Cerebrum FRONTAL LOBE  The cerebrum is made up of the five main distinct regions of the human cerebral cortex, known as the lobes. The frontal lobe is positioned at the front of each cerebral hemisphere. It contains the prefrontal cortex, located in the most anterior section of the frontal lobe. This region is essential for working memory and executive control, which play a key role in organizing goals and managing complex tasks. Overview of the human nervous system and function Central sulcus 1- The peripheral nervous system 2- The central nervous system 2.1- The spinal cord 2.2- The brain 2.2.1- Cerebellum 2.2.2- Brainstem 2.2.3- Cerebrum PARIETAL LOBE  The parietal lobe is located above the occipital lobe and behind the frontal lobe and central sulcus. It plays a key role in integrating sensory information from various modalities, including spatial sense and navigation, touch via the somatosensory cortex, which is situated just posterior to the central sulcus in the postcentral gyrus, and the dorsal stream of the visual system. Major sensory inputs from the skin, such as touch, temperature, and pain, are relayed through the thalamus to the parietal lobe. Additionally, several areas within the parietal lobe contribute to language processing. Overview of the human nervous system and function 1- The peripheral nervous system 2- The central nervous system 2.1- The spinal cord 2.2- The brain 2.2.1- Cerebellum 2.2.2- Brainstem 2.2.3- Cerebrum OCCIPITAL LOBE  The occipital lobe is the primary visual processing center of the mammalian brain, containing the majority of the anatomical regions associated with the visual cortex. Overview of the human nervous system and function 1- The peripheral nervous system 2- The central nervous system 2.1- The spinal cord 2.2- The brain 2.2.1- Cerebellum 2.2.2- Brainstem 2.2.3- Cerebrum Lateral sulcus TEMPORAL LOBE  The temporal lobe is located beneath the lateral sulcus on both cerebral hemispheres of the mammalian brain. It plays a key role in processing sensory input and transforming it into meaningful information for the retention of visual memories, language comprehension, and emotion association. Overview of the human nervous system and function 1- The peripheral nervous system 2- The central nervous system INSULAR LOBE 2.1- The spinal cord 2.2- The brain 2.2.1- Cerebellum 2.2.2- Brainstem 2.2.3- Cerebrum  The insular lobe is a part of the cerebral cortex, folded deep within the lateral sulcus of each hemisphere. The insular lobes are thought to be involved in consciousness and contribute to various functions, many of which are linked to emotions or the regulation of the body's homeostasis. These functions include compassion, empathy, taste, perception, motor control, self-awareness, cognitive functioning, interpersonal relationships, and awareness of homeostatic emotions such as hunger, pain, and fatigue. Overview of the human nervous system and function 1- The peripheral nervous system 2- The central nervous system 2.1- The spinal cord 2.2- The brain 2.2.1- Cerebellum 2.2.2- Brainstem 2.2.3- Cerebrum 2.2.4- White vs grey matter Gray matter White matter  Grey matter consists of unmyelinated neurons and other cells in the central nervous system. It is found in the brain, brainstem, cerebellum, and extends throughout the spinal cord. White matter refers to regions of the central nervous system primarily composed of myelinated axons. Once considered passive tissue, white matter plays an active role in learning and brain functions by modulating the distribution of action potentials, serving as a relay, and coordinating communication between different brain areas. The term "white matter" is derived from its lighter appearance, which is due to the lipid content of myelin. Overview of the human nervous system and function 1- The peripheral nervous system 2- The central nervous system 2.1- The spinal cord 2.2- The brain 2.2.1- Cerebellum 2.2.2- Brainstem 2.2.3- Cerebrum 2.2.4- White vs grey matter 2.2.5- Neocortex  The neocortex, also known as the six-layered cortex, is a set of layers within the cerebral cortex that is involved in higher-order brain functions, including sensory perception, cognition, motor command generation, spatial reasoning, and language. It consists of grey matter, which includes neuronal cell bodies and unmyelinated fibers, surrounding deeper white matter made up of myelinated axons in the cerebrum. The neocortex is organized into six layers, labeled I to VI from the outermost to the innermost. Pyramidal neurons are essential in the neocortex: those in the upper layers II and III project their axons to other areas of the neocortex, while those in the deeper layers V and VI often send projections outside the cortex, such as to the thalamus, brainstem, and spinal cord. Overview of the human nervous system and function 1- The peripheral nervous system 2- The central nervous system 2.1- The spinal cord 2.2- The brain 2.2.1- Cerebellum 2.2.2- Brainstem 2.2.3- Cerebrum 2.2.4- White vs grey matter 2.2.5- Neocortex  A word about pyramidal neurons. Pyramidal neurons, the most abundant type in the brain’s cortex, differ from standard neurons by having two distinct sets of dendrites: apical dendrites and basal dendrites. One of the main structural features of the pyramidal neuron is the conic shaped cell body, after which the neuron is named. Overview of the human nervous system and function 1- The peripheral nervous system 2- The central nervous system 2.1- The spinal cord 2.2- The brain Sensory areas 2.2.1- Cerebellum 2.2.2- Brainstem 2.2.3- Cerebrum Motor areas 2.2.4- White vs grey matter 2.2.5- Neocortex 2.2.6- Cortical areas Association areas  The cortex is generally divided into three main regions: sensory, motor, and association areas. The primary sensory areas correspond to the primary cortical regions for each of the five sensory systems (taste, olfaction, vision, hearing, and touch). The motor areas are closely linked to the control of voluntary movements, particularly the fine, fragmented movements of the hand. The association areas, which are not part of the primary regions, are responsible for creating meaningful perceptual experiences, enabling effective interaction with the environment, and supporting abstract thinking and language. Overview of the human nervous system and function 1- The peripheral nervous system DORSAL 2- The central nervous system STREAM 2.1- The spinal cord 2.2- The brain 2.2.1- Cerebellum 2.2.2- Brainstem 2.2.3- Cerebrum 2.2.4- White vs grey matter 2.2.5- Neocortex 2.2.6- Cortical areas i. Sensory areas VENTRAL STREAM  The visual cortex, located in the occipital lobe, processes visual information. As visual input exits the occipital lobe, it follows two main pathways, or "streams," similar to how sound exits the phonological network. The ventral stream, also known as the "what pathway," leads to the temporal lobe and is involved in object and visual identification and recognition. The dorsal stream, or "where pathway," leads to the parietal lobe, which is responsible for processing an object's spatial location relative to the viewer and for speech repetition. Overview of the human nervous system and function 1- The peripheral nervous system 2- The central nervous system 2.1- The spinal cord 2.2- The brain 2.2.1- Cerebellum 2.2.2- Brainstem 2.2.3- Cerebrum 2.2.4- White vs grey matter 2.2.5- Neocortex 2.2.6- Cortical areas i. Sensory areas  The auditory cortex is the part of the temporal lobe. The primary auditory cortex is tonotopically organized, similar to the cochlea. It receives direct input from the medial geniculate nucleus of the thalamus, which is thought to help identify fundamental elements of sound, such as pitch and loudness. Surrounding the primary auditory cortex is the secondary auditory cortex, which is believed to refine auditory input further, organizing it into meaningful or potentially meaningful percepts. Overview of the human nervous system and function 1- The peripheral nervous system 2- The central nervous system 2.1- The spinal cord 2.2- The brain 2.2.1- Cerebellum 2.2.2- Brainstem 2.2.3- Cerebrum 2.2.4- White vs grey matter 2.2.5- Neocortex 2.2.6- Cortical areas i. Sensory areas  The primary somatosensory cortex is located in the postcentral gyrus of the brain's parietal lobe. Tactile representation in the primary somatosensory cortex is arranged in an inverted manner, with the toe at the top of the cerebral hemisphere and the mouth at the bottom. Each hemisphere of the primary somatosensory cortex only represents the contralateral (opposite) side of the body. The amount of cortex devoted to a body part is based on the density of cutaneous tactile receptors, not the absolute size of the body part. Areas with higher receptor density, such as the lips and hands, have a larger cortical representation, reflecting their greater sensitivity to tactile stimuli. The secondary somatosensory cortex plays a role in the high-level integration of somatosensory information, supporting the learning and memory of tactile and spatial environments. Overview of the human nervous system and function 1- The peripheral nervous system 2- The central nervous system 2.1- The spinal cord 2.2- The brain 2.2.1- Cerebellum 2.2.2- Brainstem 2.2.3- Cerebrum 2.2.4- White vs grey matter 2.2.5- Neocortex 2.2.6- Cortical areas i. Sensory areas ii. Motor areas  A few words about the motor areas: The right half of the motor area controls the left side of the body, and vice versa. Multiple areas contribute to motor control. The primary motor cortex is responsible for executing voluntary movements, while the supplementary motor areas and premotor cortex are involved in selecting these movements. Additionally, the sensory association area, premotor cortex, and supplementary motor cortex play roles in choosing the appropriate muscle programs for movement. Overview of the human nervous system and function 1- The peripheral nervous system 2- The central nervous system 2.1- The spinal cord 2.2- The brain 2.2.1- Cerebellum 2.2.2- Brainstem 2.2.3- Cerebrum 2.2.4- White vs grey matter 2.2.5- Neocortex 2.2.6- Cortical areas i. Sensory areas ii. Motor areas iii. Association areas  The association areas are regions of the cerebral cortex that do not belong to the primary sensory or motor areas. These areas responsible for the complex processing that goes on between the arrival of input in the primary sensory cortices and the generation of behavior. The parietal, temporal, and occipital lobes—located in the posterior part of the cortex—integrate sensory information with information stored in memory. The frontal lobe, or prefrontal association complex, is involved in planning actions and movement, as well as abstract thought. Overall, the association areas are organized as distributed networks across the brain. Neuroplasticity and its mechanisms WHAT IS NEUROPLASTICITY?  Neuroplasticity is the brain’s ability to adapt and change in response to environmental factors, stimuli, or experiences. Understanding this concept requires familiarity with the brain’s basic functioning. The brain consists of billions of neurons—specialized nerve cells that gather, process, and transmit information—connected through a complex network of electrical circuits. These connections enable neurons to communicate with each other and relay messages to other parts of the body via the nervous system. Neuroplasticity reflects the brain’s remarkable capacity to reshape and reorganize this intricate network of neural connections. Although no single comprehensive theory fully encompasses the various frameworks and mechanisms of neuroplasticity, the scientific community agrees that neuroplasticity can be categorized into two main types. Neuroplasticity and its mechanisms 1- Structural neuroplasticity  The first type is called structural plasticity, which refers to the brain's ability to modify its neuronal connections. During the span of life, new neurons are generated and integrated into the central nervous system. Structural plasticity involves anatomical changes in the brain, such as alterations in grey matter volume or synaptic strength, often driven by internal or external stimuli. These changes are frequently studied using imaging techniques like MRI to observe structural reorganization in the human brain. For example, when learning a new skill, such as playing a musical instrument, the repeated practice we do stimulates the growth of dendritic spines on neurons in motor-related brain regions. These spines form additional synaptic connections, physically altering neural circuits to reinforce and support the new skill. Neuroplasticity and its mechanisms 1- Structural neuroplasticity 2- Functional neuroplasticity Functional plasticity = 4 mechanisms 1- Homologous area adaptation 2- Map expansion 3- Cross-model reassignment 4- Compensatory masquerade  The second type is functional plasticity, which refers to the brain's ability to adapt the functional properties of its neural network. Functional plasticity can manifest in four distinct mechanisms: homologous area adaptation, map expansion, cross-model reassignment, and compensatory masquerade. Neuroplasticity and its mechanisms 1- Structural neuroplasticity 2- Functional neuroplasticity Occurs primarily during early critical 2.1- Homologous area adaptation periods of development, not in adulthood  Homologous area adaptation is the assumption of a particular cognitive process by a homologous region in the opposite hemisphere. It occurs during early critical periods of brain development, which means it is much more likely to happen in childhood or adolescence than in adulthood. Neuroplasticity and its mechanisms 1- Structural neuroplasticity 2- Functional neuroplasticity Occurs primarily during early critical 2.1- Homologous area adaptation periods of development, not in adulthood Involves compensating for damage by shifting cognitive function to the same region in the opposite hemisphere  Essentially, it involves the brain compensating for damage by shifting a cognitive function from one hemisphere to the opposite hemisphere, often to the same region in the other side of the brain. For instance, if a particular brain area is damaged in one hemisphere, the opposite hemisphere can take over its function. Neuroplasticity and its mechanisms 1- Structural neuroplasticity 2- Functional neuroplasticity Occurs primarily during early critical 2.1- Homologous area adaptation periods of development, not in adulthood Involves compensating for damage by shifting cognitive function to the same region in the opposite hemisphere Has limits (evidence from stroke recovery)  However, this adaptation has its limits. Research on stroke recovery shows that while some functions can be reassigned to the opposite hemisphere, this process is not always fully successful or complete. For example, Grafman et al. reported the of a patient who suffered a severe stroke destroying almost the entire left hemisphere, although he had some spared, functionally active islands in the left parietal and frontal cortices. Remarkably, this patient could read words but not nonwords. Word reading activated a broadly distributed network in the right hemisphere. Attempts to read nonwords activated widely scattered and punctate areas in the left hemisphere. This finding suggests that the right hemisphere could assume some functions of the left hemisphere after massive damage. It seems clear that the major reading pathways in the left hemisphere were destroyed, allowing the right hemisphere to assume its reading functions; however, phonological construction required for nonwords could not be transferred, highlighting some of the limitations of this form of functional neuroplasticity in adulthood. Neuroplasticity and its mechanisms 1- Structural neuroplasticity Occurs when cortical regions devoted to a 2- Functional neuroplasticity task extend into neighboring areas 2.1- Homologous area adaptation typically dedicated to other functions 2.2- Map expansion  Map expansion is the enlargement of a functional brain region on the basis of performance. It occurs when cortical regions that are responsible for a specific task begin to extend into neighboring areas that are typically dedicated to other functions. Neuroplasticity and its mechanisms 1- Structural neuroplasticity Occurs when cortical regions devoted to a 2- Functional neuroplasticity task extend into neighboring areas 2.1- Homologous area adaptation typically dedicated to other functions 2.2- Map expansion Involves the expansion of cortical regions due to frequent exposure to specific stimuli  Essentially, the brain reallocates space and resources to accommodate more processing power for a particular task as it is practiced more frequently. Neuroplasticity and its mechanisms 1- Structural neuroplasticity Occurs when cortical regions devoted to a 2- Functional neuroplasticity task extend into neighboring areas 2.1- Homologous area adaptation typically dedicated to other functions 2.2- Map expansion Involves the expansion of cortical regions due to frequent exposure to specific stimuli Results in structural brain changes (evidence from music practice)  A great example of map expansion can be seen with music training. Playing a musical instrument requires the brain to integrate multiple types of sensory and motor information simultaneously, along with feedback mechanisms to monitor and adjust performance. Research comparing professional musicians, amateur musicians, and non- musicians has found that musicians show significant increases in gray matter volume in areas such as the primary motor cortex, somatosensory cortex, premotor areas, anterior superior parietal regions, and the inferior temporal gyrus on both sides of the brain. In other words, extensive musical practice leads to the expansion of brain regions and the recruitment of additional neural resources to meet the demands of their daily tasks, Neuroplasticity and its mechanisms 1- Structural neuroplasticity Involves introducing new sensory inputs 2- Functional neuroplasticity into a brain region deprived of its original 2.1- Homologous area adaptation inputs 2.2- Map expansion 2.3- Cross-model reassignment  Cross-model reassignment involves the introduction of new inputs into a representational brain region that has been deprived of its main inputs. It occurs when a brain region, which has lost its original sensory input, starts to process new sensory information. Neuroplasticity and its mechanisms 1- Structural neuroplasticity Involves introducing new sensory inputs 2- Functional neuroplasticity into a brain region deprived of its original 2.1- Homologous area adaptation inputs 2.2- Map expansion 2.3- Cross-model reassignment Happens because sensory cortices share a similar six-layer processing structure  This can happen because the brain's sensory cortices, such as those for vision, hearing, or touch, share a similar six-layer processing structure. So, when one sensory input is lost, other regions can take over the job of processing different types of sensory input. Neuroplasticity and its mechanisms 1- Structural neuroplasticity Involves introducing new sensory inputs 2- Functional neuroplasticity into a brain region deprived of its original 2.1- Homologous area adaptation inputs 2.2- Map expansion 2.3- Cross-model reassignment Happens because sensory cortices share a similar six-layer processing structure Results in a functional reassignment of the affected brain region (evidence from brain compensating for vision loss)  For example, in individuals who experience vision loss, the brain can 'reassign' visual cortex areas to process auditory or tactile information instead. This process of functional reassignment helps compensate for the loss of vision by engaging other sensory modalities. MRI research shows that the visual cortex in blind individuals can become activated by sounds or touch, demonstrating how the brain can reorganize itself to adapt to new sensory demands. Neuroplasticity and its mechanisms Occurs after the loss of a brain function 1- Structural neuroplasticity following damage 2- Functional neuroplasticity 2.1- Homologous area adaptation 2.2- Map expansion 2.3- Cross-model reassignment 2.4- Compensatory masquerade  Compensatory masquerade, means that the novel use of an established, but intact, cognitive process to perform a task previously dependent upon an impaired cognitive process has occurred. It happens when a brain function is lost due to damage, but the brain finds alternative strategies to perform tasks that were previously handled by the damaged area. Neuroplasticity and its mechanisms Occurs after the loss of a brain function 1- Structural neuroplasticity following damage 2- Functional neuroplasticity 2.1- Homologous area adaptation Involves the brain finding alternative 2.2- Map expansion strategies to perform tasks when the 2.3- Cross-model reassignment original strategy is impaired 2.4- Compensatory masquerade  Instead of relying on the original neural pathways, the brain reorganizes itself and activates different areas to take over the lost function. Neuroplasticity and its mechanisms Occurs after the loss of a brain function 1- Structural neuroplasticity following damage 2- Functional neuroplasticity 2.1- Homologous area adaptation Involves the brain finding alternative 2.2- Map expansion strategies to perform tasks when the 2.3- Cross-model reassignment original strategy is impaired 2.4- Compensatory masquerade Leads to reorganization of pre-existing neuronal networks (evidence from compensatory mechanisms following brain trauma).  This type of plasticity is especially important for recovery after brain trauma. For example, after a stroke or injury, if a specific brain region responsible for motor control is damaged, other areas in the brain can sometimes step in to perform similar functions, even if they weren’t originally involved. This reorganization of existing neural networks helps compensate for the loss and allows individuals to continue carrying out everyday tasks, although the efficiency of the function may be reduced. Neuroplasticity and its mechanisms Periods in brain development when the nervous system is highly sensitive to specific stimuli and 1- Structural neuroplasticity more adaptable to changes 2- Functional neuroplasticity 2.1- Homologous area adaptation 2.2- Map expansion 2.3- Cross-model reassignment 2.4- Compensatory masquerade 3- Critical period of plasticity  A critical window refers to specific developmental periods when the brain is especially sensitive to stimuli and capable of significant synaptic, circuit, and behavioral changes. Neuroplasticity and its mechanisms Periods in brain development when the nervous system is highly sensitive to specific stimuli and 1- Structural neuroplasticity more adaptable to changes 2- Functional neuroplasticity Occurs mainly during prenatal development and 2.1- Homologous area adaptation childhood, with limited plasticity in adulthood 2.2- Map expansion 2.3- Cross-model reassignment 2.4- Compensatory masquerade 3- Critical period of plasticity  These periods begin in the prenatal brain and extend through childhood, becoming much more limited during adulthood. Neuroplasticity and its mechanisms Periods in brain development when the nervous system is highly sensitive to specific stimuli and 1- Structural neuroplasticity more adaptable to changes 2- Functional neuroplasticity Occurs mainly during prenatal development and 2.1- Homologous area adaptation childhood, with limited plasticity in adulthood Critical periods are influenced by cellular 2.2- Map expansion changes (molecular shifts) and sensory 2.3- Cross-model reassignment experiences (e.g., hearing, vision) 2.4- Compensatory masquerade 3- Critical period of plasticity  Two key factors influence the opening of critical periods: cellular changes (alterations in the molecular landscape) and sensory experiences (e.g., exposure to sound or visual input). Neuroplasticity and its mechanisms Periods in brain development when the nervous system is highly sensitive to specific stimuli and 1- Structural neuroplasticity more adaptable to changes 2- Functional neuroplasticity Occurs mainly during prenatal development and 2.1- Homologous area adaptation childhood, with limited plasticity in adulthood Critical periods are influenced by cellular 2.2- Map expansion changes (molecular shifts) and sensory 2.3- Cross-model reassignment experiences (e.g., hearing, vision) 2.4- Compensatory masquerade The maturation of inhibitory circuits and 3- Critical period of plasticity perineuronal nets helps close the critical period  The closure of critical periods is influenced by the maturation of inhibitory circuits, which are shaped by the formation of perineuronal nets around inhibitory neurons. Neuroplasticity and its mechanisms Periods in brain development when the nervous system is highly sensitive to specific stimuli and 1- Structural neuroplasticity more adaptable to changes 2- Functional neuroplasticity Occurs mainly during prenatal development and 2.1- Homologous area adaptation childhood, with limited plasticity in adulthood Critical periods are influenced by cellular 2.2- Map expansion changes (molecular shifts) and sensory 2.3- Cross-model reassignment experiences (e.g., hearing, vision) 2.4- Compensatory masquerade The maturation of inhibitory circuits and 3- Critical period of plasticity perineuronal nets helps close the critical period Myelin formation and its receptors contribute to closing critical periods by blocking axonal growth  Myelination also plays a crucial role in closing critical periods. Myelin and its associated receptors bind to axonal growth inhibitors, helping end the plasticity window. Neuroplasticity and its mechanisms Periods in brain development when the nervous system is highly sensitive to specific stimuli and 1- Structural neuroplasticity more adaptable to changes 2- Functional neuroplasticity Occurs mainly during prenatal development and 2.1- Homologous area adaptation childhood, with limited plasticity in adulthood Critical periods are influenced by cellular 2.2- Map expansion changes (molecular shifts) and sensory 2.3- Cross-model reassignment experiences (e.g., hearing, vision) 2.4- Compensatory masquerade The maturation of inhibitory circuits and 3- Critical period of plasticity perineuronal nets helps close the critical period Myelin formation and its receptors contribute to closing critical periods by blocking axonal growth Neuroscientists have long believed that once a given critical period is closed, it cannot be reopened  It was long believed that once a critical period closes, it cannot reopen. Neuroplasticity and its mechanisms 1- Structural neuroplasticity 2- Functional neuroplasticity 2.1- Homologous area adaptation 2.2- Map expansion 2.3- Cross-model reassignment 2.4- Compensatory masquerade 3- Critical period of plasticity  Critical period was first described by Konrad Lorenz who won the Nobel Prize for his discovery. Within 48 Hours of hatching if a little snow geese is exposed to its mother it forms a long lasting attachment to its mother but if its mother isn't available for some reason it'll make that attachment to any other moving object (in this case Dr. Lorenz, but it could be anything else like a model airplane). 48 hours later if you expose them to another moving or any other potential object that they could form an attachment to they won't form that attachment because the narrow critical period when the animals are extremely sensitive to and able to form these long-lasting memories is now closed. Neuroplasticity and its mechanisms 1- Structural neuroplasticity 2- Functional neuroplasticity 2.1- Homologous area adaptation 2.2- Map expansion 2.3- Cross-model reassignment 2.4- Compensatory masquerade 3- Critical period of plasticity  Let’s see how critical period of plasticity can impact development with another animal experiment. In their original work, Hubel and Wiesel found that the ocular dominance distribution across the cortical layers in primary visual cortex is roughly Gaussian in a normal adult. Neuroplasticity and its mechanisms 1- Structural neuroplasticity 2- Functional neuroplasticity 2.1- Homologous area adaptation 2.2- Map expansion 2.3- Cross-model reassignment 2.4- Compensatory masquerade 3- Critical period of plasticity  They also found that most cells were activated to some degree by both eyes, and about a quarter were more activated by either the contralateral or ipsilateral eye, as can be seen on this figure. Neuroplasticity and its mechanisms 1- Structural neuroplasticity 2- Functional neuroplasticity 2.1- Homologous area adaptation 2.2- Map expansion WAIT, 2.3- Cross-model reassignment WHAT IF… 2.4- Compensatory masquerade 3- Critical period of plasticity  Hubel and Wiesel then wonder whether this normal distribution of ocular dominance could be altered by visual experience. Neuroplasticity and its mechanisms 1- Structural neuroplasticity 2- Functional neuroplasticity 2.1- Homologous area adaptation 2.2- Map expansion 2.3- Cross-model reassignment 2.4- Compensatory masquerade 3- Critical period of plasticity  So they did this experience where they simply closed one eye of a kitten early in life and let the animal mature to adulthood (which takes about 6 months), and they found a remarkable change : Electrophysiological recordings now showed that very few cortical cells could be driven from the deprived eye; that is, the ocular dominance distribution had shifted such that nearly all cells were driven by the eye that had remained open. Thus, the absence of cortical cells that responded to stimulation of the closed eye was not a result of retinal degeneration or a loss of retinal connections to the thalamus. Rather, the deprived eye had been functionally disconnected from the visual cortex. Consequently, such animals are behaviorally blind in the deprived eye. Even if the formerly deprived eye is subsequently left open indefinitely, little or no recovery occurs. Neuroplasticity and its mechanisms 1- Structural neuroplasticity 2- Functional neuroplasticity 2.1- Homologous area adaptation 2.2- Map expansion 2.3- Cross-model reassignment 2.4- Compensatory masquerade 3- Critical period of plasticity  Okay but what if the same is done to an adult cat? Remarkably, the same manipulation—closing one eye—had no effect on the responses of cells in the visual cortex of an adult cat, as can be seen on the figure C:. If one eye of a mature cat was closed for a year or more, both the ocular dominance distribution measured across all cortical layers and the animal’s visual behavior were indistinguishable from normal when tested through the reopened eye. Thus, sometime between the time a kitten’s eyes open (about a week after birth) and a year of age, visual experience determines how the visual cortex is wired with respect to eye dominance. After this time, deprivation or manipulation has little or no permanent, detectable effect. Neuroplasticity and its mechanisms 1- Structural neuroplasticity 2- Functional neuroplasticity 2.1- Homologous area adaptation 2.2- Map expansion 2.3- Cross-model reassignment 2.4- Compensatory masquerade 3- Critical period of plasticity  In fact, further experiments showed that eye closure is effective only if the deprivation occurs during the first 3 months of life, which correspond to the critical period for the development of ocular dominance. During the height of the critical period (about 4 weeks of age in the cat), as little as 3 to 4 days of eye closure profoundly alters the ocular dominance profile of the striate cortex, as can be seen on this figure, Neuroplasticity and its mechanisms 1- Structural neuroplasticity 2- Functional neuroplasticity 2.1- Homologous area adaptation 2.2- Map expansion 2.3- Cross-model reassignment 2.4- Compensatory masquerade 3- Critical period of plasticity  The effect of strabismus, the misalignment of the two eyes, lead to a similar neural reorganisation. As we can see here, compared to normal cats, ocular dominance histograms from strabismic cats show that most cells in all layers are driven exclusively by one eye or the other. Contrary to normal vision, strabismus disrupt the alignment of the eyes, causing the primary visual cortex to receive conflicting visual information from each eye. This impairment makes it difficult to fuse the images from both eyes into a single cohesive view, while also hindering binocular interactions that are essential for depth perception. Neuroplasticity and its mechanisms Brain plasticity is highest during critical periods 1- Structural neuroplasticity in early development, when sensory experience 2- Functional neuroplasticity shapes cortical representations of the 2.1- Homologous area adaptation environment 2.2- Map expansion 2.3- Cross-model reassignment 2.4- Compensatory masquerade 3- Critical period of plasticity  Brain plasticity is maximal at specific time windows during early development, during which sensory experience is necessary to establish optimal cortical representations of the surrounding environment Neuroplasticity and its mechanisms Brain plasticity is highest during critical periods 1- Structural neuroplasticity in early development, when sensory experience 2- Functional neuroplasticity shapes cortical representations of the 2.1- Homologous area adaptation environment 2.2- Map expansion Once critical periods close, the brain becomes 2.3- Cross-model reassignment less “plastic”, and passive experiences have a 2.4- Compensatory masquerade reduced impact on plastic changes 3- Critical period of plasticity  After the closure of critical periods, a range of functional and structural elements prevent passive experience from eliciting significant plastic changes in the brain, which leads the adult brain to become far less plastic Neuroplasticity and its mechanisms Brain plasticity is highest during critical periods 1- Structural neuroplasticity in early development, when sensory experience 2- Functional neuroplasticity shapes cortical representations of the 2.1- Homologous area adaptation environment 2.2- Map expansion Once critical periods close, the brain becomes 2.3- Cross-model reassignment less “plastic”, and passive experiences have a 2.4- Compensatory masquerade reduced impact on plastic changes 3- Critical period of plasticity Recent findings suggest that under certain conditions, plasticity may be re-engaged  Recent research suggests that psychoactive substances (psychedelics) can be used to reopen plastic windows. A recent longitudinal study suggests that psilocybin, also known as magic mushrooms led to improvements in cognitive function, putatively stemming from increased plasticity. Neuroplasticity and its mechanisms Brain plasticity is highest during critical periods 1- Structural neuroplasticity in early development, when sensory experience 2- Functional neuroplasticity shapes cortical representations of the 2.1- Homologous area adaptation environment 2.2- Map expansion Once critical periods close, the brain becomes 2.3- Cross-model reassignment less “plastic”, and passive experiences have a 2.4- Compensatory masquerade reduced impact on plastic changes 3- Critical period of plasticity Recent findings suggest that under certain conditions, plasticity may be re-engaged This could potentially be used to repair damaged brain circuit  This is very interesting because this could lead to new therapeutic avenues. Several clinical trials have been initiated to investigate the potential of psychedelics as a treatment for mental health disorders. It is so promising that in 2018 and 2019, U.S. Food and Drug Administration granted the “breakthrough therapy” status for two psilocybin treatments developed to address treatment-resistant depression and major depressive disorder. Clinical implications of neuroplasticity 1- Recovery mechanisms from neural injury 1.1- Peripheral nervous system  When a peripheral nerve is injured, the part of the nerve that is cut off from its cell body undergoes a process called Wallerian degeneration. This means the part of the axon far from the injury site breaks down, and cells called macrophages clean up the debris. At the same time, Schwann cells, which normally surround and protect the axons, start to multiply and organize into rows along the nerve. These Schwann cells also produce special chemicals called neurotrophic factors that help encourage the regrowth of axons. They also provide a supportive surface that helps the axons grow back in the right direction. As a result, the damaged axons can grow back over long distances, sometimes even many centimeters, and reconnect with their original target cells. When the conditions are right, these regenerated axons can even form new connections with their target tissues, allowing the nerve to recover its function. Clinical implications of neuroplasticity 1- Recovery mechanisms from neural injury 1.1- Peripheral nervous system 1.2- Central nervous system  So, why does axonal damage in areas like the retina, spinal cord, or brain lead to permanent conditions like blindness or paralysis? The reason is that damage to axons in the adult central nervous system (CNS) causes a very different response compared to the peripheral nervous system. When CNS axons and their protective myelin sheaths break down after injury, the remains of the axons aren’t cleared away efficiently and can stay around for weeks, blocking regrowth. This problem is worsened by signals from glial cells and other cells at the injury site. For example, a protein called Nogo is released that directly blocks axon extension. Additionally, after CNS injury, astrocytes release more substances that prevent axons from growing, and inflammatory cells like microglia or macrophages also release signals that limit axon regeneration. As a result, even if a neuron tries to regenerate, it faces many obstacles that prevent it from regrowing and reconnecting with other neurons. Clinical implications of neuroplasticity WHEN YOU REALIZE FROGS CAN REGENERATE NEURONS… 1- Recovery mechanisms from neural injury 1.1- Peripheral nervous system 1.2- Central nervous system 1.3- Comparison with “lower” vertebrates BUT HUMANS CAN’T !  In the adult brains of fish and frogs, neuron replacement is gradual and likely related to ongoing low-level neurogenesis. However, the central nervous system of adult mammals, including humans, recovers only poorly from injury. By the late 1990s, researchers agreed that two regions in the mammalian brain—the hippocampus and the olfactory bulb—retain a limited capacity for adding new neurons even in adulthood. This process is gradual and highly localized, unlike the broader neurogenesis seen in fish and frogs. That said, whether this ability extends to the cerebral cortex in adults remains a topic of debate. Some studies in the mid-1990s suggested that new neurons might also be added to the cortex in adult mammals, including primates. If true, this would challenge our understanding of plasticity. However, many labs struggled to replicate these findings, leading to significant controversy in the field. Clinical implications of neuroplasticity 1- Recovery mechanisms from neural injury 1.1- Peripheral nervous system 1.2- Central nervous system 1.3- Comparison with “lower” vertebrates HOW TO SOLVE THIS CONTROVERSY? Clinical implications of neuroplasticity 1- Recovery mechanisms from neural injury 1.1- Peripheral nervous system 1.2- Central nervous system 1.3- Comparison with “lower” vertebrates NUCLEAR WEAPONS, BABY, YEAH !!  Swedish researchers had a clever idea: they used fluctuations in environmental exposure to the isotope carbon-14 (¹⁴C), caused by nuclear weapons testing, to determine whether cortical neurons are generated throughout an individual's lifetime. Normally, ¹⁴C levels in Earth's atmosphere are steady, but between the mid-1950s and early 1960s, nuclear testing caused a sharp increase. This provided a natural "birth- dating" tool. Researchers analyzed autopsy samples from the cerebral cortices of seven people born between 1933 and 1973. Their reasoning was simple: if adult neurogenesis occurred, individuals born before 1955 would show elevated ¹⁴C in their cortical neurons due to environmental exposure as adults. But if neurogenesis didn’t happen, only those born during or shortly after 1955–1963, when ¹⁴C levels spiked, would have labeled neurons. Clinical implications of neuroplasticity 1- Recovery mechanisms from neural injury 1.1- Peripheral nervous system 1.2- Central nervous system 1.3- Comparison with “lower” vertebrates  The results were clear: Individuals born before 1955 had no cortical neurons with elevated ¹⁴C levels; thus, no neurons had been generated in their adult cortices Clinical implications of neuroplasticity 1- Recovery mechanisms from neural injury 1.1- Peripheral nervous system 1.2- Central nervous system 1.3- Comparison with “lower” vertebrates  In contrast, those born after 1955, but before ¹⁴C levels returned to normal, had significant amounts of ¹⁴C-labeled neurons. The levels corresponded to atmospheric ¹⁴C at the time of their gestation and birth. Interestingly, non-neuronal cells in the brain had lower levels of ¹⁴C due to turnover—these cells are replaced over time, which dilutes their ¹⁴C content. Taken together, these results provide strong evidence against significant neurogenesis in the adult cerebral cortex, Clinical implications of neuroplasticity Neurodegenerative diseases (e.g., Alzheimer’s, Parkinson’s) 1- Recovery mechanisms from neural injury 1.1- Peripheral nervous system Autoimmune disease 1.2- Central nervous system (e.g., Multiple sclerosis) 1.3- Comparison with “lower” vertebrates Diseases of the central nervous system 2- Disruptors of neural activity (e.g., Epilepsy) Sensory deprivation (e.g., auditory cortex adaptation in deaf individuals)  The brain’s neural circuits rely on precise activity for healthy functioning, but a variety of conditions can disrupt this activity, often leading to significant challenges in daily life. For example, neurodegenerative diseases like Alzheimer’s and Parkinson’s involve the progressive loss of neurons, leading to memory problems, motor deficits, and other impairments. Autoimmune diseases like multiple sclerosis, on the other hand, involve the body’s immune system attacking the protective covering of nerve fibers, disrupting communication between the brain and body. Diseases of the central nervous system, such as epilepsy, are characterized by abnormal electrical activity in the brain, which can cause seizures and further impair neural function. Lastly, sensory deprivation, such as in deafness, can lead to the reorganization of the brain’s sensory areas—for instance, the auditory cortex adapting to process visual information instead of sound. Clinical implications of neuroplasticity 1- Recovery mechanisms from neural injury 1.1- Peripheral nervous system 1.2- Central nervous system 1.3- Comparison with “lower” vertebrates 2- Disruptors of neural activity 3- Maladaptive plasticity WTF IS THAT ?!  While neuroplasticity can be beneficial (i.e., restoring function), it can also be harmful. Maladaptive plasticity is when a connection that is made in the brain produces aberrant or negative symptoms. Clinical implications of neuroplasticity TINNITUS, AKA RINGING IN THE EARS 1- Recovery mechanisms from neural Very debilitating disorder that often follows hearing loss injury Constant low or high-pitched ringing 1.1- Peripheral nervous system in the ears 1.2- Central nervous system Psychological and emotional assault 1.3- Comparison with “lower” on the senses vertebrates Affect 43% of Canadians aged 16-79 2- Disruptors of neural activity 58 billion US dollars in healthcare 3- Maladaptive plasticity costs in North America 3.1- Tinnitus REMAINS INCURABLE Tinnitus, also known as ringing in the ears, is [click] a very debilitating disorder that often follows hearing loss. [click] It is characterized by a constant low or high-pitch that can be [click] psychologically and emotionally stressful. [click] Tinnitus affects 43% of Canadians aged between 16 and 79 yo and [click] costs 58 billion US dollars in North America. [click] Unfortunately, there is currently no known cure for tinnitus, which makes it a significant public health concern. Clinical implications of neuroplasticity TINNITUS, AKA RINGING IN THE EARS 1- Recovery mechanisms from neural injury 1.1- Peripheral nervous system 1.2- Central nervous system 1.3- Comparison with “lower” vertebrates 2- Disruptors of neural activity 3- Maladaptive plasticity 3.1- Tinnitus Normal Hearing Tinnitus + Hearing Loss Tinnitus stems from maladaptive brain plasticity following hearing loss. When the cochlea hair cells are damaged or missing, electrical signals aren’t transmitted as efficiently and hearing loss occurs. This sensory deprivation triggers a neural adaptation process that alters the neural gain to overcome the decrease in auditory sensitivity caused by the hearing loss. Such abnormally high neural gain leads to overamplification of the spontaneous neural firing rates that occurs in the absence of a physical sound source, which leads to aberrant auditory perceptions, called tinnitus. Clinical implications of neuroplasticity WHAT ABOUT… 1- Recovery mechanisms from neural injury 1.1- Peripheral nervous system 1.2- Central nervous system 1.3- Comparison with “lower” vertebrates 2- Disruptors of neural activity 3- Maladaptive plasticity 3.1- Tinnitus … RESEARCH?  I previously mention that psychedelics could be used to reopen critical windows of development. Research studies by Johns Hopkins and the Imperial College of London have shown that psilocybin can induce brain plasticity and treat mental and neurodegenerative disorders. In a recent work that is under review, we investigated whether and how psilocybin can promote auditory cortical plasticity using use state-of-the-art two-photon microscopy in mice to visualize and track the changes in the brain after receiving a combination of psilocybin and auditory stimulation. Clinical implications of neuroplasticity RESPONSIVE CELL CHANGE IN CELL SENSITIVITY COUNT 1- Recovery mechanisms from neural injury 1.1- Peripheral nervous system 1.2- Central nervous system 1.3- Comparison with “lower” vertebrates FIRING ACTIVITY 2- Disruptors of neural activity 3- Maladaptive plasticity 3.1- Tinnitus Note: unpublished results (under review) We found that administration of psilocybin acutely impairs stimulus specific adaptation in the primary auditory cortex in awake mice: Reduction in the number of auditory-responsive cells with repeated stimulation is inhibited by psilocybin ; [click] The drop in mean firing activity of auditory-responsive cells with repeated stimulation is reduced by psilocybin ; [click] With administration of psilocybin, auditory responsive cells retain sensitivity to lower sound intensities. Taken together, these results suggest that psilocybin alters inhibitory sensory gating and filtering of familiar stimuli in the primary auditory cortex, which supports models of psychedelic action in which bottom-up sensory inputs are disrupted. Maybe in the future, plasticity-inducing treatment will be shown to be effective for tinnitus. Clinical implications of neuroplasticity 1- Recovery mechanisms from neural injury 1.1- Peripheral nervous system 1.2- Central nervous system MALADAPTIVE PLASTICITY 1.3- Comparison with “lower” FOLLOWING HEARING vertebrates RESTORATION? 2- Disruptors of neural activity 3- Maladaptive plasticity 3.1- Tinnitus 3.2- CI & maladaptive plasticity  Numerous studies in cognitive sciences have highlighted that human rhythmic synchronization is more precise with auditory stimuli than with visual ones, even when the timing cues are identical. Deaf individuals have been shown to display a heightened proficiency in synchronizing their movements with visual timing cues, outperforming individuals with normal hearing. While cochlear implants are considered the most successful neural prosthesis, the signal transmitted to the auditory nerve remains severely degraded compared to natural hearing. Consequently, the ability to process and integrate information from different senses—known as multisensory integration—is impaired in cochlear implant users. Clinical implications of neuroplasticity 1. DO CI USERS POSSESS A PRE-IMPLANT 1- Recovery mechanisms from neural DEAFNESS VISUAL SYNCHRONIZATION injury 1.1- Peripheral nervous system ADVANTAGE WHILE MATCHING NH 1.2- Central nervous system AUDITORY SYNCHRONIZATION SKILLS? 1.3- Comparison with “lower” vertebrates 2- Disruptors of neural activity 2. DOES THE NEURAL REORGANIZATION 3- Maladaptive plasticity POST-IMPLANTATION NEGATE THE 3.1- Tinnitus VISUAL SYNCHRONIZATION ADVANTAGE 3.2- CI & maladaptive plasticity ACQUIRED BEFORE THE IMPLANT? This raises an important question: do cochlear implant users retain a visual synchronization advantage from their pre-implant deafness while maintaining auditory synchronization skills comparable to those of normal hearing individuals? [click] Alternatively, does the neural reorganization post-implantation negate the visual synchronization advantage acquired before implantation? Clinical implications of neuroplasticity 1- Recovery mechanisms from neural injury 1.1- Peripheral nervous system 1.2- Central nervous system 1.3- Comparison with “lower” vertebrates 2- Disruptors of neural activity 3- Maladaptive plasticity 3.1- Tinnitus 3.2- CI & maladaptive plasticity To answer these question, we assessed unimodal and multimodal auditory and visual abilities in cochlear implant users compared to normal hearing controls using a finger tapping synchrony task with four isochronous stimulus conditions: Audio only, Visual only, Audio Visual synchronous (in phase), Audio Visual asynchronous (out of phase) Clinical implications of neuroplasticity 1- Recovery mechanisms from neural injury 1.1- Peripheral nervous system CONSISTENCY 1.2- Central nervous system 1.3- Comparison with “lower” vertebrates 2- Disruptors of neural activity 3- Maladaptive plasticity 3.1- Tinnitus 3.2- CI & maladaptive plasticity Note: unpublished results (under review)  Consistency in the unisensory auditory condition did not differ significantly between the two groups; nor was there a difference between groups in the unisensory visual condition. However, both groups exhibited significantly better synchronization to auditory stimuli than to visual stimuli. A trend towards a greater advantage for auditory over visual synchronization was observed in normal hearing individuals compared to cochlear implant users Clinical implications of neuroplasticity 1- Recovery mechanisms from neural injury 1.1- Peripheral nervous system CONSISTENCY 1.2- Central nervous system 1.3- Comparison with “lower” vertebrates 2- Disruptors of neural activity 3- Maladaptive plasticity 3.1- Tinnitus 3.2- CI & maladaptive plasticity Note: unpublished results (under review) When the auditory timing was congruent with visual timing, normal hearing individuals demonstrated improved consistency compared to unisensory visual timing, while cochlear implant users did not show better consistency in this condition. This multisensory congruence effect was greater in normal hearing individuals than in cochlear implant users. In the asynchronous condition, the impact of incongruent auditory information was similar in both groups. Clinical implications of neuroplasticity BOTH POPULATIONS DEMONSTRATED SUPERIOR 1- Recovery mechanisms from neural CONSISTENCY IN AUDITORY SYNCHRONIZATION injury 1.1- Peripheral nervous system 1.2- Central nervous system 1.3- Comparison with “lower” vertebrates 2- Disruptors of neural activity 3- Maladaptive plasticity 3.1- Tinnitus 3.2- CI & maladaptive plasticity Note: unpublished results (under review) As anticipated, both cochlear implant users and normal hearing individuals demonstrated better consistency in auditory synchronization compared to visual synchronization. This result aligns with previous research reporting weaker consistency in synchronizing movement to visual flash-like stimuli. Clinical implications of neuroplasticity BOTH POPULATIONS DEMONSTRATED SUPERIOR 1- Recovery mechanisms from neural CONSISTENCY IN AUDITORY SYNCHRONIZATION injury 1.1- Peripheral nervous system CI USERS: NO VISUAL ADVANTAGE FROM PRE- 1.2- Central nervous system IMPLANT DEAFNESS 1.3- Comparison with “lower” vertebrates 2- Disruptors of neural activity 3- Maladaptive plasticity 3.1- Tinnitus 3.2- CI & maladaptive plasticity Note: unpublished results (under review) These results suggests that the visual synchronization advantage typically developed by deaf individuals due to their heavy reliance on the visual system is generally absent in the cochlear implant users of this study. Clinical implications of neuroplasticity BOTH POPULATIONS DEMONSTRATED SUPERIOR 1- Recovery mechanisms from neural CONSISTENCY IN AUDITORY SYNCHRONIZATION injury 1.1- Peripheral nervous system CI USERS: NO VISUAL ADVANTAGE FROM PRE- 1.2- Central nervous system IMPLANT DEAFNESS 1.3- Comparison with “lower” vertebrates CONGRUENT AV: NH > CI USERS, SUGGESTING 2- Disruptors of neural activity IMPEDED CROSS-MODAL INTEGRATION 3- Maladaptive plasticity 3.1- Tinnitus 3.2- CI & maladaptive plasticity Note: unpublished results (under review) Normal hearing individuals displayed improved consistency when presented with audio-visual synchronous stimuli, consistent with the idea that cross- modal timing congruence enhances sensory integration and temporal processing. In contrast, cochlear implant users did not exhibit a significant improvement in this condition. Previous research has shown that visual stimulations elicit activation in the auditory cortex of deaf individuals, a phenomenon also seen in cochlear implant users which suggests that the cortical reorganization caused by deafness is not fully reversed after implantation. Together with our results, this suggest that this incomplete reversal impedes the effective integration of temporal auditory stimulation from the implant and visual information, leading to a diminished cross-modal congruence advantage in cochlear implant users. Clinical implications of neuroplasticity BOTH POPULATIONS DEMONSTRATED SUPERIOR 1- Recovery mechanisms from neural CONSISTENCY IN AUDITORY SYNCHRONIZATION injury 1.1- Peripheral nervous system CI USERS: NO VISUAL ADVANTAGE FROM PRE- 1.2- Central nervous system IMPLANT DEAFNESS 1.3- Comparison with “lower” vertebrates CONGRUENT AV: NH > CI USERS, SUGGESTING 2- Disruptors of neural activity IMPEDED CROSS-MODAL INTEGRATION 3- Maladaptive plasticity 3.1- Tinnitus BOTH POPULATIONS ARE EQUALLY SUSCEPTIBLE 3.2- CI & maladaptive plasticity TO INCONGRUENT INFORMATION Note: unpublished results (under review) The similarity in interference from incongruent auditory information in the asynchronous condition suggests that both groups are similarly susceptible to cross-modal incongruence, which can disrupt the precision of synchronization. This indicates that post-implantation neural reorganization does not confer immunity to incongruent auditory information but instead affects the prioritization and integration of sensory cues. Overall, this research provides valuable insights into the impact of cochlear implants on audio-visual synchronization abilities, highlighting the need for further exploration into the neural mechanisms involved in post-implantation reorganization and its effects on sensory integration. Recap of Today’s Learnings Recap of Today's Learnings (1/4) Nervous system = peripheral + central NS Central NS = brain + spinal cord Brain = Cerebrum + Brainstem + Cerebellum Cerebrum = 2 hemispheres + 5 lobes White matter = myelinated axons Grey matter = unmyelinated neurons and other cells in the central nervous system Neocortex = 6 layers, involved in higher-order brain functions Layers II and III and V and VI are rich in pyramidal neurons Pyramidal neurons have two distinct sets of dendrites: apical dendrites and basal dendrites Recap of Today’s Learnings Recap of Today's Learnings (2/4) 3 main cortical areas: sensory, motor, and association areas Auditory cortex is the part of the temporal lobe Primary auditory cortex is tonotopically organized, similar to the cochlea Secondary auditory cortex is surrounding the primary cortex Multiple areas contribute to motor control Areas that are not primary sensory or motor areas = association areas Association areas are organized as distributed networks across the brain Recap of Today’s Learnings Recap of Today's Learnings (3/4) Association areas are responsible for generating a meaningful perceptual experience of the world, enabling effective interactions, and supporting abstract thinking and language Neuroplasticity is the brain’s ability to adapt and change in response to environmental factors, stimuli, or experiences Structural plasticity refers to the brain's ability to modify its neuronal connections Functional plasticity refers to the brain's ability to adapt the functional properties of its neural network Four distinct mechanisms for functional plasticity: homologous area adaptation, map expansion, cross- model reassignment, and compensatory masquerade Recap of Today’s Learnings Recap of Today's Learnings (4/4) Critical windows = specific developmental periods when the brain is especially sensitive to stimuli and capable of significant synaptic, circuit, and behavioral changes Brain plasticity is maximal at specific time windows during early development Peripheral NS can regenerated, central NS can't Tinnitus stems from maladaptive brain plasticity following hearing loss Post-implantation neural reorganization impact multisensory integration because of the incomplete reversal