The aim of this thesis was to investigate the input-specificity of sensory-induced plasticity in humans. This was achieved by varying the characteristics of sine gratings so that they selectively targeted distinct populations of neurons in the visual cortex. In Experiments 1-3, specificity was investigated with electroencephalography using horizontally- and vertically-oriented sine gratings (Experiment 1) or gratings of differing spatial frequency (Experiments 2 & 3). Increases in the N1b potential were observed only for sine gratings that were the same in orientation or spatial frequency as that used as the tetanus, suggesting that the potentiation is specific to the visual pathways stimulated during the induction of the tetanus. However, the increase in the amplitude of the N1b in Experiment 1 was not maintained when tested again at 50 minutes post-tetanus. This may have been due to depotentiation caused by the temporal frequency of stimulus presentation in the first post-tetanus block. To try to circumvent this potential confound, immediate and maintained (tested 30 minutes post-tetanus) spatial-frequency-specific potentiation were tested separately in Experiments 2 and 3, respectively. Experiment 3 demonstrated that the increased N1b was maintained for up to half an hour post-tetanus. In addition, the findings from Experiment 1, as well as the pattern of results from Experiments 2 and 3, indicate that the potentiation must be occurring in the visual cortex rather than further upstream at the lateral geniculate nucleus. In Experiment 4 functional magnetic resonance imaging was used to more accurately localise where these plastic changes were taking place using sine gratings of differing spatial frequency. A small, focal post-tetanic increase in the blood-oxygen-level-dependent (BOLD) response was observed for the tetanised grating in the right temporo-parieto-occipital junction. For the non-tetanised grating, decreases in BOLD were found in the primary visual cortex and bilaterally in the cuneus and pre-cuneus. These decreases may have been due to inhibitory interconnections between neurons tuned to different spatial frequencies. These data indicate that tetanic sensory stimulation selectively targets and potentiates specific populations of neurons in the visual cortex.

The aim of this thesis was to investigate the input-specificity of sensory-induced plasticity in humans. This was achieved by varying the characteristics of sine gratings so that they selectively targeted distinct populations of neurons in the visual cortex. In Experiments 1-3, specificity was investigated with electroencephalography using horizontally- and vertically-oriented sine gratings (Experiment 1) or gratings of differing spatial frequency (Experiments 2 & 3). Increases in the N1b potential were observed only for sine gratings that were the same in orientation or spatial frequency as that used as the tetanus, suggesting that the potentiation is specific to the visual pathways stimulated during the induction of the tetanus. However, the increase in the amplitude of the N1b in Experiment 1 was not maintained when tested again at 50 minutes post-tetanus. This may have been due to depotentiation caused by the temporal frequency of stimulus presentation in the first post-tetanus block. To try to circumvent this potential confound, immediate and maintained (tested 30 minutes post-tetanus) spatial-frequency-specific potentiation were tested separately in Experiments 2 and 3, respectively. Experiment 3 demonstrated that the increased N1b was maintained for up to half an hour post-tetanus. In addition, the findings from Experiment 1, as well as the pattern of results from Experiments 2 and 3, indicate that the potentiation must be occurring in the visual cortex rather than further upstream at the lateral geniculate nucleus. In Experiment 4 functional magnetic resonance imaging was used to more accurately localise where these plastic changes were taking place using sine gratings of differing spatial frequency. A small, focal post-tetanic increase in the blood-oxygen-level-dependent (BOLD) response was observed for the tetanised grating in the right temporo-parieto-occipital junction. For the non-tetanised grating, decreases in BOLD were found in the primary visual cortex and bilaterally in the cuneus and pre-cuneus. These decreases may have been due to inhibitory interconnections between neurons tuned to different spatial frequencies. These data indicate that tetanic sensory stimulation selectively targets and potentiates specific populations of neurons in the visual cortex.

The aim of this thesis was to investigate the input-specificity of sensory-induced plasticity in humans. This was achieved by varying the characteristics of sine gratings so that they selectively targeted distinct populations of neurons in the visual cortex. In Experiments 1-3, specificity was investigated with electroencephalography using horizontally- and vertically-oriented sine gratings (Experiment 1) or gratings of differing spatial frequency (Experiments 2 & 3). Increases in the N1b potential were observed only for sine gratings that were the same in orientation or spatial frequency as that used as the tetanus, suggesting that the potentiation is specific to the visual pathways stimulated during the induction of the tetanus. However, the increase in the amplitude of the N1b in Experiment 1 was not maintained when tested again at 50 minutes post-tetanus. This may have been due to depotentiation caused by the temporal frequency of stimulus presentation in the first post-tetanus block. To try to circumvent this potential confound, immediate and maintained (tested 30 minutes post-tetanus) spatial-frequency-specific potentiation were tested separately in Experiments 2 and 3, respectively. Experiment 3 demonstrated that the increased N1b was maintained for up to half an hour post-tetanus. In addition, the findings from Experiment 1, as well as the pattern of results from Experiments 2 and 3, indicate that the potentiation must be occurring in the visual cortex rather than further upstream at the lateral geniculate nucleus. In Experiment 4 functional magnetic resonance imaging was used to more accurately localise where these plastic changes were taking place using sine gratings of differing spatial frequency. A small, focal post-tetanic increase in the blood-oxygen-level-dependent (BOLD) response was observed for the tetanised grating in the right temporo-parieto-occipital junction. For the non-tetanised grating, decreases in BOLD were found in the primary visual cortex and bilaterally in the cuneus and pre-cuneus. These decreases may have been due to inhibitory interconnections between neurons tuned to different spatial frequencies. These data indicate that tetanic sensory stimulation selectively targets and potentiates specific populations of neurons in the visual cortex.

The aim of this thesis was to investigate the input-specificity of sensory-induced plasticity in humans. This was achieved by varying the characteristics of sine gratings so that they selectively targeted distinct populations of neurons in the visual cortex. In Experiments 1-3, specificity was investigated with electroencephalography using horizontally- and vertically-oriented sine gratings (Experiment 1) or gratings of differing spatial frequency (Experiments 2 & 3). Increases in the N1b potential were observed only for sine gratings that were the same in orientation or spatial frequency as that used as the tetanus, suggesting that the potentiation is specific to the visual pathways stimulated during the induction of the tetanus. However, the increase in the amplitude of the N1b in Experiment 1 was not maintained when tested again at 50 minutes post-tetanus. This may have been due to depotentiation caused by the temporal frequency of stimulus presentation in the first post-tetanus block. To try to circumvent this potential confound, immediate and maintained (tested 30 minutes post-tetanus) spatial-frequency-specific potentiation were tested separately in Experiments 2 and 3, respectively. Experiment 3 demonstrated that the increased N1b was maintained for up to half an hour post-tetanus. In addition, the findings from Experiment 1, as well as the pattern of results from Experiments 2 and 3, indicate that the potentiation must be occurring in the visual cortex rather than further upstream at the lateral geniculate nucleus. In Experiment 4 functional magnetic resonance imaging was used to more accurately localise where these plastic changes were taking place using sine gratings of differing spatial frequency. A small, focal post-tetanic increase in the blood-oxygen-level-dependent (BOLD) response was observed for the tetanised grating in the right temporo-parieto-occipital junction. For the non-tetanised grating, decreases in BOLD were found in the primary visual cortex and bilaterally in the cuneus and pre-cuneus. These decreases may have been due to inhibitory interconnections between neurons tuned to different spatial frequencies. These data indicate that tetanic sensory stimulation selectively targets and potentiates specific populations of neurons in the visual cortex.

Thesis (M.Sc.)--Memorial University of Newfoundland, Memorial University of Newfoundland, 1998. / Typescript. Bibliography: leaves 118-132.

The aim of this thesis was to investigate the input-specificity of sensory-induced plasticity in humans. This was achieved by varying the characteristics of sine gratings so that they selectively targeted distinct populations of neurons in the visual cortex. In Experiments 1-3, specificity was investigated with electroencephalography using horizontally- and vertically-oriented sine gratings (Experiment 1) or gratings of differing spatial frequency (Experiments 2 & 3). Increases in the N1b potential were observed only for sine gratings that were the same in orientation or spatial frequency as that used as the tetanus, suggesting that the potentiation is specific to the visual pathways stimulated during the induction of the tetanus. However, the increase in the amplitude of the N1b in Experiment 1 was not maintained when tested again at 50 minutes post-tetanus. This may have been due to depotentiation caused by the temporal frequency of stimulus presentation in the first post-tetanus block. To try to circumvent this potential confound, immediate and maintained (tested 30 minutes post-tetanus) spatial-frequency-specific potentiation were tested separately in Experiments 2 and 3, respectively. Experiment 3 demonstrated that the increased N1b was maintained for up to half an hour post-tetanus. In addition, the findings from Experiment 1, as well as the pattern of results from Experiments 2 and 3, indicate that the potentiation must be occurring in the visual cortex rather than further upstream at the lateral geniculate nucleus. In Experiment 4 functional magnetic resonance imaging was used to more accurately localise where these plastic changes were taking place using sine gratings of differing spatial frequency. A small, focal post-tetanic increase in the blood-oxygen-level-dependent (BOLD) response was observed for the tetanised grating in the right temporo-parieto-occipital junction. For the non-tetanised grating, decreases in BOLD were found in the primary visual cortex and bilaterally in the cuneus and pre-cuneus. These decreases may have been due to inhibitory interconnections between neurons tuned to different spatial frequencies. These data indicate that tetanic sensory stimulation selectively targets and potentiates specific populations of neurons in the visual cortex.

Este trabalho descreve o desenvolvimento de um equipamento de biofeedback para utilização por fisioterapeutas no tratamento de pacientes portadores de pé equino. Normalmente o pé equino está relacionado a uma das sequelas de um acidente vascular cerebral e é caracterizado pela dificuldade no controle motor do membro afetado, muitas vezes apresentando limitações relacionadas à sensibilidade e dificuldade em manter o calcanhar em contato com o solo durante a marcha. O equipamento foi construído com base no conceito de biofeedback, apresentando ao paciente, em tempo real, informações relacionadas à intensidade de força aplicada nos membros inferiores. O equipamento é composto de sensores de força flexíveis alojados em um par de sandálias, ligados a um circuito eletrônico microcontrolado. Todo o processamento é realizado por um MSP430, e a comunicação é feita por sinais de rádio através de um módulo CC1101. Os dados são apresentados em uma interface de software em um computador portátil a uma taxa de atualização de 20 Hz. O software possui diversas funcionalidades para atender tanto as necessidades dos fisioterapeutas quanto dos pacientes. Do ponto de vista do paciente, a interface apresenta um visual simples e objetivo, facilitando o entendimento das variações de força, apresentadas na forma de barras verticais. Foram utilizados também recursos visuais e sonoros para enfatizar aos pacientes quando os objetivos estipulados para seu tratamento foram atingidos. Outras funcionalidades foram desenvolvidas para que os fisioterapeutas tenham a opção de customizar a interface de biofeedback de acordo com a necessidade de cada paciente, além de possibilitar o armazenamento de todos os dados dos sensores para análises posteriores. O protótipo foi testado em 20 voluntários durante 10 sessões de fisioterapia, sendo 10 portadores da disfunção pé equino e outros 10 normais para compor um grupo de controle. O objetivo principal do protocolo fisioterapêutico foi melhorar a manutenção do contato como o solo no calcanhar afetado. Os valores de pressão no calcanhar afetado de todas as das sessões foram adquiridos a uma taxa de 20 Hz, armazenados e analisados segundo as seguintes métricas: média, máximos e somas acumuladas. Também foi realizada a avaliação de Berg para todos os voluntários. Os resultados demonstraram que, para as métricas analisadas e também para a avaliação de Berg, houve uma evolução em todos os pacientes. / This work describes the development of a biofeedback device to be used by physiotherapists during treatment of patients with equinus foot. Normally the equinus foot is related to one of the sequelae of a stroke and is characterized by difficulty in motor control of the affected limb, often resulting in limitations on sensitivity. The equipment was built on the concept of biofeedback, presenting to the patient, in real time, information related to the intensity of the forces applied to the lower limbs. The equipment consists of flexible force sensors accommodated in a pair of sandals, connected to a microcontrolled electronic circuit. The whole processing is performed by an MSP430, and the communication is done by radio signals through a CC1101 module. The data is presented in a software interface on a laptop computer at a refresh rate of 20 Hz. The software has many features to meet both the needs of physiotherapists as patients. From the point of view of patients, the interface was designed to be simple and objective, facilitating the understanding of force variations that change dynamically at the exact moment when the sensors are pressed. Visual signs and sound were also used to emphasize to patients when the goals established for their treatment has been reached. Other features were developed specifically for physicaltherapists, giving them the option to customize the biofeedback interface according to the needs of each patient, and also allowing the storage of all data transferred by the sensors for further analysis. A prototype was developed and tested on 20 volunteers over 10 sessions of physical therapy, 10 patients with equinus foot dysfunction, and 10 normal people to compose a control group. At the end of the treatment period, the data were analyzed by session, according to the average forces, the maximum values reached, the accumulated sums and Berg assessments. The results revealed an evolution in all patients, some of them in a greater degree and others in lower degree of progress.

Este trabalho descreve o desenvolvimento de um equipamento de biofeedback para utilização por fisioterapeutas no tratamento de pacientes portadores de pé equino. Normalmente o pé equino está relacionado a uma das sequelas de um acidente vascular cerebral e é caracterizado pela dificuldade no controle motor do membro afetado, muitas vezes apresentando limitações relacionadas à sensibilidade e dificuldade em manter o calcanhar em contato com o solo durante a marcha. O equipamento foi construído com base no conceito de biofeedback, apresentando ao paciente, em tempo real, informações relacionadas à intensidade de força aplicada nos membros inferiores. O equipamento é composto de sensores de força flexíveis alojados em um par de sandálias, ligados a um circuito eletrônico microcontrolado. Todo o processamento é realizado por um MSP430, e a comunicação é feita por sinais de rádio através de um módulo CC1101. Os dados são apresentados em uma interface de software em um computador portátil a uma taxa de atualização de 20 Hz. O software possui diversas funcionalidades para atender tanto as necessidades dos fisioterapeutas quanto dos pacientes. Do ponto de vista do paciente, a interface apresenta um visual simples e objetivo, facilitando o entendimento das variações de força, apresentadas na forma de barras verticais. Foram utilizados também recursos visuais e sonoros para enfatizar aos pacientes quando os objetivos estipulados para seu tratamento foram atingidos. Outras funcionalidades foram desenvolvidas para que os fisioterapeutas tenham a opção de customizar a interface de biofeedback de acordo com a necessidade de cada paciente, além de possibilitar o armazenamento de todos os dados dos sensores para análises posteriores. O protótipo foi testado em 20 voluntários durante 10 sessões de fisioterapia, sendo 10 portadores da disfunção pé equino e outros 10 normais para compor um grupo de controle. O objetivo principal do protocolo fisioterapêutico foi melhorar a manutenção do contato como o solo no calcanhar afetado. Os valores de pressão no calcanhar afetado de todas as das sessões foram adquiridos a uma taxa de 20 Hz, armazenados e analisados segundo as seguintes métricas: média, máximos e somas acumuladas. Também foi realizada a avaliação de Berg para todos os voluntários. Os resultados demonstraram que, para as métricas analisadas e também para a avaliação de Berg, houve uma evolução em todos os pacientes. / This work describes the development of a biofeedback device to be used by physiotherapists during treatment of patients with equinus foot. Normally the equinus foot is related to one of the sequelae of a stroke and is characterized by difficulty in motor control of the affected limb, often resulting in limitations on sensitivity. The equipment was built on the concept of biofeedback, presenting to the patient, in real time, information related to the intensity of the forces applied to the lower limbs. The equipment consists of flexible force sensors accommodated in a pair of sandals, connected to a microcontrolled electronic circuit. The whole processing is performed by an MSP430, and the communication is done by radio signals through a CC1101 module. The data is presented in a software interface on a laptop computer at a refresh rate of 20 Hz. The software has many features to meet both the needs of physiotherapists as patients. From the point of view of patients, the interface was designed to be simple and objective, facilitating the understanding of force variations that change dynamically at the exact moment when the sensors are pressed. Visual signs and sound were also used to emphasize to patients when the goals established for their treatment has been reached. Other features were developed specifically for physicaltherapists, giving them the option to customize the biofeedback interface according to the needs of each patient, and also allowing the storage of all data transferred by the sensors for further analysis. A prototype was developed and tested on 20 volunteers over 10 sessions of physical therapy, 10 patients with equinus foot dysfunction, and 10 normal people to compose a control group. At the end of the treatment period, the data were analyzed by session, according to the average forces, the maximum values reached, the accumulated sums and Berg assessments. The results revealed an evolution in all patients, some of them in a greater degree and others in lower degree of progress.

No description available.

The collection of sonnets Rings of a Thundering Tree (2000), by R.K. Belcher, is rich in metaphorical imagery; lending itself particularly well to textual analyses of imagined sensory perceptions. Although perspectives on or theories about metaphor can be deployed in such analyses, an imagined sense of sensory perception in itself theoretically frames the study of this poetic imagery. In this regard, the titles of the sonnets within this collection and their themes, as well as the title of the collection and the theme of ”South African decay” (with which this title is linked), are explored with an emphasis on imagined sensory experiences. / English Studies / M.A. (English)