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This study examined the effects of prenatal exposure to methadone on clinical and neurobehavioural outcomes of infants between 40 and 42 weeks gestation. The aims of this study were: (a) to describe clinical and neurobehavioural outcomes of infants exposed to methadone during pregnancy, (b) to examine the effects of maternal methadone dose during pregnancy on infant clinical and neurobehavioural measures, and (c) to examine the extent to which associations between exposure to methadone during pregnancy and infant outcomes persisted after statistical control for a range of confounding variables. Two groups of study infants were recruited. These consisted of 51 consecutively recruited infants born to mothers maintained on methadone during their pregnancy and 42 randomly identified non-methadone exposed comparison infants. Prior to her child's birth, each pregnant woman completed a comprehensive maternal interview. At birth and during the infant's hospital stay a broad perinatal data-base was collected. At 42 weeks gestation infants underwent a neurobehavioural assessment including the NICU Network Neurobehavioural Scale (NNNS; Lester & Tronick, 2004) and infant cry analysis. Study results showed significant differences across several clinical and neurobehavioural measures. Infants exposed to methadone in utero were found to be significantly lighter, have smaller head circumferences, and spend longer in hospital. Neurobehaviourally, they were significantly less well regulated, less attentive, more easily aroused, more excitable, and more hypertonic. In addition, they exhibited less motor maturity, displayed more stress abstinence symptomatology, and required more support from the assessor in order to remain in an appropriate state. Concurrent analysis of infant cry characteristics revealed no significant differences between the fundamental frequencies or the melody contours of the two groups. However, infants prenatally exposed to methadone did display higher levels of frequency perturbation in their cries, as evidenced by analysis of their jitter factor and percentage of directional jitter. Analysis of the effects of maternal dose during pregnancy suggested that maternal dose levels above 60mg/day were general indicative of poorer infant outcomes than those below 60mg/day, with significant linear trends occurring across a number of measures. The extent to which associations between methadone exposure during pregnancy and infant outcomes reflected either a) the direct effects of methadone exposure and/or b) the effects of confounding factors correlated with maternal methadone use was examined using regression analysis. The results of this analysis for infant clinical outcomes showed confounding variables attenuated the effects of methadone exposure on infant birth length and, to some degree, infant head circumference. In contrast, associations between methadone exposure during pregnancy and most neurobehavioural outcomes remained significant, suggesting that maternal methadone use during pregnancy is an important, independent predictor of infant neurobehavioural functioning. These findings support the view that prenatal exposure to methadone has at least short term impacts on the infant's central nervous system (CNS) development. Important implications of possible vulnerabilities faced by these infants and their families are discussed.

This study examined the effects of prenatal exposure to methadone on clinical and neurobehavioural outcomes of infants between 40 and 42 weeks gestation. The aims of this study were: (a) to describe clinical and neurobehavioural outcomes of infants exposed to methadone during pregnancy, (b) to examine the effects of maternal methadone dose during pregnancy on infant clinical and neurobehavioural measures, and (c) to examine the extent to which associations between exposure to methadone during pregnancy and infant outcomes persisted after statistical control for a range of confounding variables. Two groups of study infants were recruited. These consisted of 51 consecutively recruited infants born to mothers maintained on methadone during their pregnancy and 42 randomly identified non-methadone exposed comparison infants. Prior to her child's birth, each pregnant woman completed a comprehensive maternal interview. At birth and during the infant's hospital stay a broad perinatal data-base was collected. At 42 weeks gestation infants underwent a neurobehavioural assessment including the NICU Network Neurobehavioural Scale (NNNS; Lester & Tronick, 2004) and infant cry analysis. Study results showed significant differences across several clinical and neurobehavioural measures. Infants exposed to methadone in utero were found to be significantly lighter, have smaller head circumferences, and spend longer in hospital. Neurobehaviourally, they were significantly less well regulated, less attentive, more easily aroused, more excitable, and more hypertonic. In addition, they exhibited less motor maturity, displayed more stress abstinence symptomatology, and required more support from the assessor in order to remain in an appropriate state. Concurrent analysis of infant cry characteristics revealed no significant differences between the fundamental frequencies or the melody contours of the two groups. However, infants prenatally exposed to methadone did display higher levels of frequency perturbation in their cries, as evidenced by analysis of their jitter factor and percentage of directional jitter. Analysis of the effects of maternal dose during pregnancy suggested that maternal dose levels above 60mg/day were general indicative of poorer infant outcomes than those below 60mg/day, with significant linear trends occurring across a number of measures. The extent to which associations between methadone exposure during pregnancy and infant outcomes reflected either a) the direct effects of methadone exposure and/or b) the effects of confounding factors correlated with maternal methadone use was examined using regression analysis. The results of this analysis for infant clinical outcomes showed confounding variables attenuated the effects of methadone exposure on infant birth length and, to some degree, infant head circumference. In contrast, associations between methadone exposure during pregnancy and most neurobehavioural outcomes remained significant, suggesting that maternal methadone use during pregnancy is an important, independent predictor of infant neurobehavioural functioning. These findings support the view that prenatal exposure to methadone has at least short term impacts on the infant's central nervous system (CNS) development. Important implications of possible vulnerabilities faced by these infants and their families are discussed.

Magister Scientiae - MSc / Background: Early postnatal radiation exposure from environmental, diagnostic or therapeutic sources is potentially deleterious to the developing nervous system resulting in oxidative stress, structural damage, altered neurochemistry, DNA damage, inflammatory stresses as well as correlating cognitive impairment during adult life. Numerous studies in literature have investigated the radioprotective effects of medicinal plants and beverages. However, only a few studies have focused on the radioprotective effects of rooibos, an indigenous South African herbal tea, well known for its many acclaimed health benefits. Aims: This study was done to investigate the diverse radioprotective potential of fermented Rooibos herbal tea (FRHT) consumed ad libitum by pregnant rats on the adult offspring rats exposed to a once-off 6 Gy dose of gamma irradiation on postnatal day 3. Methods: Twenty-four (24) adult female rats were equally divided into four groups (6 per group) as control (NS), radiation (X), tea (RT) and their combination. On PND 30, offspring rats were subjected to neurobehavioural assessment for open field and novel object recognition parameters and later sacrificed, the brain tissues removed and processed for histological, immunohistochemical and neurochemical analyses, using standard techniques. Results: Pre-treatment with FRHT showed overall protection against radiation-induced distortions in offspring rats by significantly improving exploratory activity, the frequency of central square entry, rearing episodes, cumulative freezing time and memory retention as indicated by a relatively higher recognition index. FRHT was also found to significantly improve the antioxidant defence mechanisms in the offspring rats by reversing lowered FRAP levels, increasing superoxide dismutase and catalase enzyme activities and reducing lipid peroxidation. Histological and immunohistochemical analyses showed that morphological alterations were generally attenuated in the RTX group and the high number of caspase-3 and Glial fibrillary acidic protein (GFAP)-positive cells was significantly reduced, indicating protective effects against apoptosis and gliosis. Conclusion: Taken together, our findings tend to suggest that the potential radioprotective effects of FRHT are multimodal, possibly executed through the anti-apoptotic, antioxidative, anti-gliosis and other mechanisms, as observed in this study, and this is often attributed to the high polyphenol content in Rooibos tea.

The aim of this study was to investigate the relationship between noncognitive symptoms and premorbid temperament in a group with Alzheimer’s disease. The relationship between premorbid temperament and noncognitive symptoms can be used to understand symptom susceptibility and risk, caregiver burdens, as well as providing insights into the neuroanatomical substrates of temperament and noncognitive behaviour. Sixty-three primary caregivers of Alzheimer’s patients fulfilled the eligibility criteria for this study. Information regarding the noncognitive symptoms and premorbid temperament was procured from the primary caregivers. In fifty-one cases, a secondary caregiver also provided information about the premorbid temperament of the Alzheimer’s patient. The latter was obtained to enhance the reliability of retrospective data. The Behaviour Rating Scale for Dementia, the Formal Characteristics of Behaviour-Temperament Inventory, and the Blessed Dementia scale were used to elicit data on noncognitive symptomatology, premorbid temperament, and current cognitive status, respectively. ii Noncognitive symptoms were grouped into two clusters namely neuropsychiatric and neurobehavioural disturbances. The neuropsychiatric cluster included mood and psychotic symptoms and the neurobehavioural cluster included vegetative and overall behavioural dysregulatory symptoms. Results showed that there is a wide spectrum of noncognitive symptom manifestation in patients’ profiles and that the neurobehavioural dysregulatory symptoms are more common than the neuropsychiatric symptoms in this Alzheimer’s cohort. With regard to symptom manifestation and cognitive status, a Pearson product moment correlational analysis showed that a lower level of cognitive functioning is significantly associated with aggressive episodes and a higher level of cognitive functioning with manifestations of depressive symptoms. In terms of interrater concordance on premorbid temperament ratings, intraclass correlations were significant for five of the six temperament domains, thus indicating a reliable estimate of premorbid disposition. Canonical correlational analysis yielded two significant variates. The first variate indicated that Alzheimer’s disease patients with a proclivity for aggressive behaviours and general behavioural deregulation but lower depressive profiles, were premorbidly more emotionally reactive, had low sensory thresholds (high sensitivity), and greater cognitive deficit. The second variate showed that patients with Alzheimer’s disease who tended to manifest with depressive and dysregulatory behaviour appear to have been premorbidly perseverative in temperament with a low sensory threshold (high sensitivity) and the tendency to maintain and attain a low level of activity (stimulation). Taken together, the significant variates revealed a dimensional relationship between depressive symptoms, aggressive symptoms, and behavioural dysregulation; and sensory sensitivity, emotional reactivity, perseverance, and activity, with cognitive status serving as a moderating variable. In conclusion, the study indicated a dimensional relationship between specific premorbid temperament traits and noncognitive symptoms, thereby highlighting the possible predictive influence of premorbid temperament on noncognitive manifestations in Alzheimer’s disease patients. / Thesis (PhD (Psychology))--University of Pretoria, 2005. / Psychology / unrestricted

Neuropsychological toxicology investigates the impact of chemical exposure on the structure and functioning of the nervous system and by implication the neuropsychological performance of affected individuals. As in mainstream neuropsychology, brain damage is assessed by measuring changes in the cognitive, psychomotor and emotional domains using diagnostic neuropsychological tests. The field of neuropsychological toxicology has undergone significant growth in the last 20 years, amongst growing concerns over people’s potential everyday exposure to approximately 70 000 chemicals. Growing awareness of the possible dangers associated with neurotoxic exposure has lead to the increased regulation of exposure levels especially in industrial settings. This in turn has lead to a gradual shift in neuropsychological toxicology from the assessment of severe neurotoxic damage to the evaluation of subclinical signs, which may develop into disabling damage over many years of exposure. The assessment of these subclinical signs has proven to be tricky as they cannot always be measured through diagnostic tests and may be mimicked or hidden by numerous confounding variables. The need for the effective assessment of these subclinical signs has created a need for more sensitive tests and improved research methodology. This paper uses evidence from cellular pathology and anatomical pathology (dynamic brain localisation theory) as a guide for the selection of neuropsychological tests. The purpose of the paper is to review the neuropsychological outcomes of toxic exposure, with an emphasis on test sensitivity (screening) and specificity (diagnostic) to carbon disulphide (solvent), manganese (metal) and organophosphate (pesticide) exposure. Findings from this review point to the possible advantages of the continued use of standardised neuropsychological batteries that enable the assessment of global functions in addition to tests that measure deficits associated with the toxicodynamics of the neurotoxin under investigation. Methodological recommendations include the use of simultaneous cross-sectional and longitudinal designs to control for numerous confounding variables and correlation designs to determine dose-response relationships. Future studies need to address the sensitivity and specificity criteria of various neuropsychological measures utilising the principle of neurotoxicodynamics. / Dissertation (MA (Research Psychology))--University of Pretoria, 2007. / Psychology / MA / unrestricted