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R Gibb

Publications and source records attributed to R Gibb.

30 records · Page 2Linked to original sources

Orofacial artefactual disease.

Self-induced lesions of the face and mouth may occasionally be encountered in dental practice. In general the deliberate creation of orofacial lesions is an indication of underlying psychiatric disease of various types that usually involve a personal gain by the patient from having such lesions. We present three cases of deliberately self-induced lesions and discuss the problem of diagnosis and management of these cases.

Adult↗

Possible anatomical basis of recovery of function after neonatal frontal lesions in rats.

Rats given medial frontal lesions on Postnatal Day 1 or Day 10 were trained on the Morris water task on Days 19-21 or Days 56-58. The operated groups were equally impaired at the water task on Days 19-21, but the Day 10 rats had recovered by 56 days. Dendritic arborization and spine density were analyzed in parietal layer II-III pyramidal cells. At Day 60, but not at Day 22, the Day 10 animals had more dendritic spines per unit dendritic length than did the controls or Day 1 rats. Thus, there was functional recovery rather than sparing after frontal lesions at 10 days, and the recovery was correlated with an increase in dendritic spines.

Age Factors↗

Cortical and striatal structure and connectivity are altered by neonatal hemidecortication in rats.

The cortical cytoarchitecture, cortical thickness, corticostriatal connections, cortical dendritic arborization, and striatal patch-matrix compartmentalization were compared in rats with neonatal (1 day of age) or adult hemidecortication. Neonatal hemidecortication produced few changes in cytoarchitecture of the remaining hemisphere and did not preclude the development of a patch-matrix compartmentalization in either striatum. There was a significant modification of contralateral cortical-striatal connections, however, as there were extensive crossed connections from layer II/III of the prefrontal cortex in the neonatal hemidecorticates, which contrasts with connections from layer V in the normal brain. Adult hemidecorticates had no crossed corticostriatal connections. Neonatal hemidecortication also led to an increase in cortical thickness relative to adult operates or controls and the neonatal hemidecorticates, and led to an increase in dendritic arborization in layer II/III pyramidal cells of the somatosensory and motor cortex but not in the visual or temporal cortex. The results suggest that the behavioral sparing of sensorimotor and some prefrontal functions after neonatal hemidecortication could be supported, in part, by the anatomical changes in the prefrontal and sensorimotor connectivity and dendritic arborization.

Animals↗

Sparing of function after neonatal frontal lesions correlates with increased cortical dendritic branching: a possible mechanism for the Kennard effect.

This study examined the possibility that the presence or absence of behavioral sparing following neonatal frontal lesions might be correlated with changes in the complexity of dendritic branching. Rats were given bilateral frontal lesions in either adulthood, the day of birth, or on day 10. Ninety days later the animals were trained in a spatial navigation task. The animals' brains were then processed for Golgi-Cox staining and the dendritic branching of the pyramidal cells in the parietal cortex was analyzed. Frontal cortical lesions in newborn rats produced a severe behavioral deficit in the water task whereas frontal removal at 10 days of age allowed sparing of function relative to adult operates (that is, the Kennard effect). Analysis of dendritic arbor in sensorimotor cortex revealed that the day-10 animals exhibited a dramatic proliferation of dendritic arbor relative to control rats. In contrast, the day-1 animals had slightly less dendritic branching than control animals. Rats with frontal lesions in adulthood showed a small, but significant, increase in dendritic branching. The correlation between behavioral sparing and the increase in dendritic arborization following neonatal lesions may be illustrative of a general mechanism underlying the Kennard effect.

Animals↗

Environmental enrichment and cortical injury: behavioral and anatomical consequences of frontal cortex lesions.

Rats with large unilateral or bilateral frontal cortical lesions were placed in either isolated or enriched housing conditions for 90 d and then were compared behaviorally and neuroanatomically to control rats. The frontal lesions reduced chronic body weight, produced impairments in claw cutting, food hoarding, tongue extension, and spatial navigation in the Morris water task, and increased running wheel activity. Enriched rearing attenuated many of the behavioral changes, but with the exception of tongue extension and spatial navigation, it had similar effects in both normal and brain-injured animals. Analysis of the brains showed that enrichment increased brain weight and dendritic branching in visual cortex similarly in normal and brain-injured rats. In contrast, however, enrichment affected parietal neurons in normal but not in brain-damaged animals. Instead, the frontal operates showed an increase in parietal branching irrespective of the rearing condition, which implies that the lesion itself may have led to some form of reactive synaptogenesis that subsequently precluded environmental effects.

Animals↗