Current neuropsychological models propose that the cognitive changes associated with healthy adult ageing are due to deterioration of the frontal lobes of the brain. Despite evidence that the frontal lobes are involved in age-associated cognitive decline, the behavioural and cognitive deficits demonstrated by older adults differ from the typical clinical picture presented by patients with frontal lobe damage. Furthermore, there are frontal lobe tests reported in the literature that are insensitive to the effects of healthy adult ageing despite being sensitive to the effects of frontal lobe dysfunction. These arguments speak against the current "frontal lobe hypothesis of ageing". Studies have demonstrated that the frontal lobes can be subdivided into at least two distinct areas: the dorsolateral and ventromedial prefrontal regions. Current neuropsychological models of ageing have failed to consider that age may differentially affect these regions and assume that there is uniform frontal decline. Autopsy and neuroimaging studies, however, suggest that the dorsolateral region deteriorates earlier and more rapidly than the ventromedial region. Therefore, the aim of this thesis was to outline and test a "dorsolateral" prefrontal theory of cognitive ageing where the dorsolateral functions deteriorate with age earlier and more rapidly than the ventromedial functions. In a series of experiments, age-associated declines in performance were found on all tasks sensitive to dorsolateral prefrontal dysfunction, but not on the majority of tasks sensitive to ventromedial prefrontal dysfunction. An attempt was also made to provide evidence for the specific localisation of the "dorsolateral" and "ventromedial" measures by assessing groups of patients with lesions to different areas of the frontal lobes. Whilst most of the tasks were sensitive to frontal lobe dysfunction, only two of the "dorsolateral" measures were found to be selectively sensitive to the dorsolateral prefrontal region. In conclusion, the profile of spared and impaired abilities in the older groups speaks against the traditional "frontal lobe" interpretation of cognitive ageing and is more supportive of a specific dorsolateral prefrontal theory of cognitive changes with age.

No description available.

<i>Objectives</i>- To investigate the relationship between neuropsychological symptoms, as measured by questionnaire, and formal measurements of neurological and psychological function.  To investigate the relationship between neuropsychological symptoms and solvent exposure estimates.  To test the hypothesis that neuropsychological disorder in solvent exposed workers is more likely to those with genetic predisposition. <i>Methods </i>- A nested case-control study was carried out in a cohort of former dockyard painters and community controls.  The 78 painters and 42 community controls had previously participated in a postal study that had shown an excess of neuropsychological symptoms amongst painters.  The 120 participants in the nested - case control study underwent detailed neuropsychological testing, colour vision testing, estimation of solvent exposure indices and genetic testing for GSTM1, GSTT1, NAT1 and NAT2 enzyme polymorphisms. <i>Results </i>-  A case-control analysis of 68 patients failed to demonstrate significant differences in neuropsychological function between symptomatic and asymptomatic painters as measured by the Q16.  Subsequent regression analyses of all 120 subjects showed a range of neuropsychological deficits with an exposure response relationship.  There was no convincing evidence of risk modification by any of the enzyme polymorphisms studied.  During the study a pattern of deficits was recognised, sufficient to constitute a syndrome of impaired colour vision, cognitive impairment impaired vibration perception and resting tremor. <i>Conclusions </i>- Exposure to mixed solvents is associated with neuropsychological impairment, the risk increasing with increasing intensity of exposure.  The risk of impairment was not altered in this study by the presence of different enzyme polymorphisms.

Thesis (Ph. D.)--University of Hawaii at Manoa, 1982. / Bibliography: leaves 129-153. / Microfiche. / vii, 153 leaves, bound 29 cm

Thesis--University of Wisconsin--Madison. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 71-77).

The purpose of this study was to investigate the effects of cerebral malaria on the neuropsychological functioning of non-immune Ghanaian children. Twenty hospital-referred children between ages 7 and 16 years who met the World Health Organization (W.H.O., 1986) research criteria for the diagnosis of cerebral malaria, and who had no known history of other neurological disease were recruited for this study. Twenty matched control healthy children without a history of malaria or other neurological disease were also assessed. Each subject was administered a battery of neuropsychological tests judged to be highly sensitive to brain injury and relatively impervious to linguistic or other cultural factors. These results (from comparisons using the general linear model) are the first to provide evidence of subacute neurobehavioural sequelae of cerebral malaria in children. Subjects demonstrated deficits in such functional domains as accuracy of visual scanning, immediate and delayed visual memory, bimanual tactile discrimination, perceptual abstraction and rule learning skills, right ear auditory information processing, and dominant hand motor speed. A strong negative association between coma duration and bimanual tactile discrimination performance was also found. Contrary to expectations, no evidence for emotional dysfunction resulting directly from cerebral malaria emerged from this study. Nonverbal reasoning, visuospatial processing, auditory attention and sequencing, verbal fluency, and fine motor dexterity were found to be intact. The pattern of neuropsychological test performance in this study was judged to be consistent with a small-vessel cerebrovasculitis secondary to infection with plasmodium falciparum. Implications and limitations of this investigation, as well as directions for future research were discussed in the context of malaria endemicity. / Graduate

Despite the fact that nightmares occur with regularity in the general population, most previous research has focused on clinical samples, and the genesis of idiopathic nightmares remains poorly understood. The aim of the present research was therefore to investigate the neuropsychological mechanisms of idiopathic bad dream and nightmare generation, with a particular focus on the limbic system. High versus low levels of limbic activation and its effect on the frequency of dream, bad dream, and nightmare recall, characteristics, and content were investigated using retrospective and prospective measures. Psychosocial stress – a phenomenon which increases activity in the limbic system – and its relationship to bad dreams and nightmares was also investigated, using questionnaires and a prospective dream diary study. Oral contraceptive use was included as a moderator variable as previous research has indicated that this may temper reactions to stress. The general hypothesis that greater activation of the limbic system results in a greater frequency of recall of bad dreams and nightmares, and also results in more negative dream content, was confirmed. It was also found that external factors which increase limbic activation such as psychosocial stress lead to a greater recall of bad dreams and nightmares. Although oral contraceptive use did not moderate the relationship between stress and bad dream and nightmare recall frequency, more generally positive dream content was found in users of oral contraceptives compared to non-users. Taken together, the results of the studies indicate that similar neuropsychological mechanisms may underlie the formation of idiopathic nightmares and nightmares in clinical conditions, and also that increased levels of limbic activation may result most commonly in negative dream content.

The content of dreams of children aged between three and five years old has been the topic of ongoing debate in past dream research. The bulk of this research was conducted by Foulkes (1982, 1999), who concluded that children of this age group experience impoverished dreams with little emotional content, an absence of active self-participation, and a lack of kinematic imagery (i.e., mental representations of movement, activities and interactions). These conclusions were based on the brief and mundane dream reports provided by children during his 1982 longitudinal laboratory study. However, Foulkes’ research did not test the children’s memory skills and ability to narrate an event, and did not compare these to the dream reports the children produced. The importance of memory skills and narrative ability as potential confounds when studying children’s dreams has been postulated in existing literature. In view of the findings of past studies on young children’s dreams and their cognitive capacity for dreaming, the present study re-examined the quantitative and qualitative features of dream reports of children aged three to five years old. The present study included parameters of testing memory skills and narrative ability to analyse whether these confound the dream report findings, and if so, whether one can draw any firm conclusions about dreams based on a dream report provided by the children.

ASD has an estimated prevalence of 1 in 68, making it one of the most common neurodevelopmental disorders in children. Furthermore, its prevalence is increasing; therefore, there is a rising demand for screening tools to help achieve beneficial early diagnosis and intervention outcomes. However, there is a lack of literature around ASD and ASD screening tool validity in South Africa. This thesis adapted and assessed the use of South African English, Afrikaans and IsiXhosa versions of the 23-item Modified Checklist for Autism in Toddlers (M-CHAT) screening tool, for a Western Cape state hospital. The M-CHAT was completed by parents (N=255) of children between the ages of 1.5 and 4.99 years, at the Red Cross Children's Hospital developmental clinic. The demographic variables of Child's Age or Sex, Income and Mothers Education did not significantly affect the M-CHAT scores. Furthermore, on qualitative inspection, neither Home language nor Ethnicity of the child appeared to affect the screening scores. Final M-CHAT scores and high internal consistencies were similar across the three M-CHAT language versions, likely indicating their equivalence in flagging ASD. Even the extended age range (4.01-4.99 years) included in this study, did not appear to affect the M-CHAT scores. The M-CHAT follow-up interview was important in determining the ASD risk outcome. Overall, 67% failed the M-CHAT initially, thus requiring follow-up questioning, and of those, 40% changed their outcome and subsequently passed. Interestingly, filling out the M-CHAT in a first or second language did not affect the percentage requiring the follow-up nor the proportions changing their outcome after follow-up. The items which were poor or good discriminators between those eventually passing or failing overall were investigated. The good discriminating items were not necessarily the same as the originally suggested critical items. Thus, new critical items and the possible removal of unnecessary items for this context may need further investigation. For phase 2, a small subgroup (n=38) filling in the English M-CHAT took part in formal ASD diagnostic assessments, using the Autism Diagnostic Observation Schedule (ADOS/ADOS-2). Preliminary investigations into the English M-CHAT's predictive abilities are promising. A cut-off of 3/23 items overall indicates high sensitivity (.84) and adequate specificity (.69). The adapted cut-off of 1/6 critical items results in good sensitivity (.76) and high specificity (.92). The promising results warrant further investigations into the predictive validity of all 3 language versions of the M-CHAT. This thesis takes the first steps in validating the use of the M-CHAT in this low SES context and indicates positive prospects for its future use in state clinics in the Western Cape, and ultimately South Africa.

Includes bibliographical references / Autism Spectrum Disorder (ASD) is a highly heritable prevalent pervasive developmental disorder. All cases have deficits in social communication and interaction and in restricted and repetitive behaviours and interests. The mechanisms underlying different clinical presentations remain elusive. Deficits in Theory of Mind (ToM), the ability to understand that others have mental states independent of one's own, have been suggested as a possibly underlying the socia l deficits in ASD. The serotonin transporter promoter length polymorphism (5 - HTTLPR) has been implicated in ASD, and as serotonin is implicated in social functioning more generally, it is possible that 5 - HTTLPR could underlie social functioning in ASD. As such, ToM and 5 - HTTLPR have been implicated in ASD, and specifically as underlying the social deficits typical of this disorder. This protocol assessed core ASD symptoms (i.e. deficits in social communication and interaction, and impairment in restricted and repetitive behaviours and interests) in 69 children with ASD between the ages of 7 and 14 years. The Autism Social Skills Profile, Social Communication Questionnaire, and Repetitive Behavior Scale - Revised assessed these symptoms. 5 - HTTLPR genotypes were established for 55 of these children. ToM was comprehensively assessed in 57 of the children using the University of Cape Town Autism Research Group's Theory of Mind Battery. This protocol is the first is a series of studies assessing the biological bases for social deficits in ASD. One of the main aims was to pilot the use of ASD scales in a local sample. The preliminary analyses assessed the performance of these scales. This data was also used to assess whether the new DSM - 5's merging of social communication and social interaction into a single domain was supported. Study One then assessed for possible relationships between 5 - HTTLPR and cores ASD symptoms, and hypothesised that the 5 - HTTLPR genotype with the most reduced serotonergic transmission woul d relate to increased deficits in social communication and interaction. Study Two explored possible relationships between core ASD symptoms and ToM, and between 5 - HTTLPR and ToM. It was expected that impairment in social communication and interaction would correlation with reduced ToM ability, and that ToM would be most impaired in children with the genotype with the most reduced serotonergic transmission. Preliminary analyses found the scales did not perform well in a local sample. This was likely due to cultural, socio - economic, and educational factors. The bluntness of the scales 13 and broad nature of ASD characteristics likely also contributed. The DSM - 5's diagnostic criteria were supported. Study One and Study Two found no relationships between core ASD symptoms, ToM, and 5 - HTTLPR. Core ASD symptoms were assessed very broadly and it was not possible to establish clear phenotypes for the participants, which likely undermined analyses. At most this protocol showed that broad assessment of core ASD symptoms is not specific enough to reveal relationships to underlying mechanisms, and that ToM and 5 - HTTLPR are not implicated when board measures are used. We emphasise the need for better measures in ASD. We also believe the serotonin system needs to be investigated beyond 5 - HTTLPR in ASD