AN ABSTRACT OF THE THESIS OF Heather Hays, for the Master of Science degree in Behavior Analysis and Therapy, presented on June 30, 2016, at Southern Illinois University Carbondale. TITLE: USING PYRAMIDAL STAFF TRAINING TO DECREASE SOCIALLY UNACCEPTABLE SEXUAL BEHAVIORS AMONGST INDIVIDUALS WITH INTELLECTUAL DISABILITIES MAJOR PROFESSOR: Dr. Mark Dixon This current study expands the research of pyramidal training to the subject area of sex education. It utilizes the Behavioral Skills Training (BST) teaching package (instruction, model, role play and feedback) while applying the pyramidal training approach to teach appropriate boundaries to individuals with DD. Although this is not a complete sex education package, it will begin the research in this this subject area. With state hospitals closing their doors and more individuals with an ID entering the community, appropriate boundaries is an essential skill for both, individuals with an ID and the others in the community. Pyramidal training of the sexual education curriculum was introduced to the three participants in a consecutive manner. This study suggests that pyramidal training is an effective way to decrease spikes in target behaviors for individuals with intellectual disabilities at a day training facility. Future research should be conducted to look at more detailed sex education packages and teaching the curriculum in different environments.

The majority of corticospinal projections in primates and all corticospinal projections in other mammals exert their influence by integrating into spinal interneuronal circuits. Interneurons therefore represent an evolutionarily conserved target through which the corticospinal tract achieves motor and sensory control. Here I describe the postnatal maturation of the corticospinal tract. I show work aimed at fractionating cortical projections by combining recently developed retrograde viral tracing strategies with genetic access to distinct spinal interneuron populations. Using a 3-D reconstruction pipeline, I discuss the cortical origins of the corticospinal pathway in mice. I then demonstrate the differential distribution of corticospinal inputs to three interneuron populations with divergent functional roles. These studies suggest that primary motor cortex contacts functionally diverse spinal interneurons whilst premotor and somatosensory cortical regions are more restricted in their postsynaptic targeting.

Thesis (Ph. D.)--University of Washington, 2005. / Vita. Includes bibliographical references (leaves 108-122).

No description available.

More than half of all spinal cord injuries are anatomically incomplete, yet many of these result in complete loss of motor function below the level of injury. One approach to enhance functional recovery is to exploit spared CNS axons (that extend past the point of injury) to sprout and connect to potential targets. We have previously found that application of the neurotrophin; BDNF, to the sensory-motor cortex stimulates expression of regeneration associated genes such as GAP-43, and Tαl tubulin, and results in enhanced sprouting of injured corticospinal fibers rostral to the site of injury. Here, we investigated whether infusion of BDNF into the intact sensorimotor cortex induces sprouting of undamaged corticospinal fibers into denervated cervical spinal cord. We also studied the effect of this treatment using several behavioral tasks: gait analysis, forelimb inhibition during swimming, and food pellet reaching task. The results show that BDNF infusion into the intact sensorimotor cortex subsequent to a unilateral pyramidal lesion increases (3.2 fold) the sprouting of intact corticospinal fibers into the denervated, contralateral grey matter at the lumbar level of the spinal cord when compared with vehicle treated rats. This effect was not seen at the cervical level of the spinal cord. Functionally, unilateral pyramidal injury of corticospinal axons significantly increased toe spread of the contralateral denervated forelimb and hindlimb when compared to the uninjured side. BDNF treatment showed a recovery to presurgical levels. Testing of fine motor control with a food pellet reaching task demonstrated deficits in the impaired forelimb but did not show any improvement due to BDNF treatment.

More than half of all spinal cord injuries are anatomically incomplete, yet many of these result in complete loss of motor function below the level of injury. One approach to enhance functional recovery is to exploit spared CNS axons (that extend past the point of injury) to sprout and connect to potential targets. We have previously found that application of the neurotrophin; BDNF, to the sensory-motor cortex stimulates expression of regeneration associated genes such as GAP-43, and Tαl tubulin, and results in enhanced sprouting of injured corticospinal fibers rostral to the site of injury. Here, we investigated whether infusion of BDNF into the intact sensorimotor cortex induces sprouting of undamaged corticospinal fibers into denervated cervical spinal cord. We also studied the effect of this treatment using several behavioral tasks: gait analysis, forelimb inhibition during swimming, and food pellet reaching task. The results show that BDNF infusion into the intact sensorimotor cortex subsequent to a unilateral pyramidal lesion increases (3.2 fold) the sprouting of intact corticospinal fibers into the denervated, contralateral grey matter at the lumbar level of the spinal cord when compared with vehicle treated rats. This effect was not seen at the cervical level of the spinal cord. Functionally, unilateral pyramidal injury of corticospinal axons significantly increased toe spread of the contralateral denervated forelimb and hindlimb when compared to the uninjured side. BDNF treatment showed a recovery to presurgical levels. Testing of fine motor control with a food pellet reaching task demonstrated deficits in the impaired forelimb but did not show any improvement due to BDNF treatment.

The brain responds to injury during early development with alterations in behaviour and dendritic morphology of motor cortex neurons. Rats were exposed to damage either prenatally or after the first postnatal week, using different models of damage and motor cortex was examined. Prenatal injury resulted in a decrease in length, complexity and volume in layer II neurons, but no differences in layer V neurons or behavioural tasks. Postnatal damage produced increases in length of basilar dendrites, but no differences in spine density at 2 months of age, whereas at 6 months of age, an overall decrease in apical and basilar spine density was observed. Findings demonstrate the maturational status of the brain at the time of injury play a crucial role in response to injury.

The brain responds to injury during early development with alterations in behaviour and dendritic morphology of motor cortex neurons. Rats were exposed to damage either prenatally or after the first postnatal week, using different models of damage and motor cortex was examined. Prenatal injury resulted in a decrease in length, complexity and volume in layer II neurons, but no differences in layer V neurons or behavioural tasks. Postnatal damage produced increases in length of basilar dendrites, but no differences in spine density at 2 months of age, whereas at 6 months of age, an overall decrease in apical and basilar spine density was observed. Findings demonstrate the maturational status of the brain at the time of injury play a crucial role in response to injury.

Thesis (Ph.D.)--Auburn University, 2007. / Abstract. Includes bibliographic references (ℓ. 84-92)

More than half of all spinal cord injuries are anatomically incomplete, yet many of these result in complete loss of motor function below the level of injury. One approach to enhance functional recovery is to exploit spared CNS axons (that extend past the point of injury) to sprout and connect to potential targets. We have previously found that application of the neurotrophin; BDNF, to the sensory-motor cortex stimulates expression of regeneration associated genes such as GAP-43, and Tαl tubulin, and results in enhanced sprouting of injured corticospinal fibers rostral to the site of injury. Here, we investigated whether infusion of BDNF into the intact sensorimotor cortex induces sprouting of undamaged corticospinal fibers into denervated cervical spinal cord. We also studied the effect of this treatment using several behavioral tasks: gait analysis, forelimb inhibition during swimming, and food pellet reaching task. The results show that BDNF infusion into the intact sensorimotor cortex subsequent to a unilateral pyramidal lesion increases (3.2 fold) the sprouting of intact corticospinal fibers into the denervated, contralateral grey matter at the lumbar level of the spinal cord when compared with vehicle treated rats. This effect was not seen at the cervical level of the spinal cord. Functionally, unilateral pyramidal injury of corticospinal axons significantly increased toe spread of the contralateral denervated forelimb and hindlimb when compared to the uninjured side. BDNF treatment showed a recovery to presurgical levels. Testing of fine motor control with a food pellet reaching task demonstrated deficits in the impaired forelimb but did not show any improvement due to BDNF treatment. / Medicine, Faculty of / Graduate