Although the integrated relationship that exists between the lumbar spine and hip joints is frequently acknowledged in scientific journals and by medical professionals, specific functional and injury relationships, are speculative and have not been substantiated. Lumbar spine and hip dysfunctions are suspected to be associated with inhibition of the surrounding extensor musculature, particularly the gluteal muscles, and facilitation of the flexor musculature. This phenomenon has been observed in other joints following effusion and is often termed ‘arthrogenic inhibition’. Its apparent occurrence about the hip has never been validated. The primary objective of this thesis was to investigate whether arthrogenic inhibition occurred about the hip. If inhibition was found to exist, its relationship with volume vs pressure was investigated to determine if either of these factors were a more appropriate predictor of inhibition. Finally, compensatory motor patterns in response to apparent inhibition were of interest. Participants were allocated to the following groups: 1) Control 2) Intervention I (magnetic resonance arthrogram) or 3) Intervention II (therapeutic arthrogram). Electromyography was collected on the rectus abdominis, erector spinae, gluteus maximus and semimenbranosis bilaterally during hip rehabilitation exercises prior to and following the intervention. Intra-capsular pressure was measured during the intervention. The findings provided support for the presence of extensor-inhibition in the hip following infusion of intra-articular fluid with intra-capsular pressure being the most appropriate predictor of the magnitude of inhibition. Hip extensor inhibition appeared to be compensated for by lumbar spine extensors during the selected tasks. Arthrogenic inhibition should be considered in the clinical evaluation and management of patients with hip joint effusions and/or elevated intra-capsular pressure.

The ongoing electrical activity of the brain is known as the electroencephalograph (EEG). Event related potentials (ERPs) are voltage deviations in the EEG elicited in association with stimuli. Their elicitation require cognitive processes such as response to a recognised stimulus. ERPs therefore provide clinical information by allowing an insight into neurological processes. The amplitude of an event-related potential is typically several times less than the background EEG. The background EEG has the effect of obscuring the ERP and therefore appropriate signal processing is required for its recovery. Traditionally ERPs are estimated using the synchronised averaging of several single trials or sweeps. This inhibits investigation of any trial-to-trial variation, which can prove valuable in understanding cognitive processes. An aim of this study was to develop wavelet-based techniques for the recovery of single trial ERPs from background EEG. A novel wavelet-based adaptive digital filtering method for ERPs has been developed. The method provides the ability to effectively estimate or recover single ERPs. The effectiveness of the method has been quantitatively evaluated and compared with other methods of ERP estimation. The ability to recover single sweep ERPs allowed the investigation of characteristics that are not possible using the conventional averaged estimation. The development of features of a cognitive ERP known as the contingent negative variation over a number of trials was investigated. The trend in variation enabled the identification of schizophrenic subjects using artificial intelligence methods. A new technique to investigate the phase dynamics of ERPs was developed. This was successfully applied, along with other techniques, to the investigation of independent component analysis (ICA) component activations in a visual spatial attention task. Two components with scalp projections that suggested that they may be sources within the visual cortex were investigated. The study showed that the two components were visual field selective and that their activation was both amplitude and phase modulated.

Autism spectrum disorder (ASD) is a social, sensory and developmental condition that affects one in 59 children and specifically one in 42 boys. Despite the 15% increase in prevalence in the last two years, there is no specific etiology, objective diagnostic criteria, or drug treatment. However, up-regulation of inflammation in ASD patients has been demonstrated in blood samples. Increased peripheral inflammation could have devastating effects on the developing brain. Peripheral inflammation in the blood could cross the blood-brain-barrier to stimulate microglia in the brain to produce aberrant levels of cytokines that regulate neuroinflammation such as insulin-like growth factor one (IGF1) that could alter neuronal cell-surface expression and neurotransmission. Additionally, arginase serves as a marker of inflammation, produced and expressed during cellular remodeling during brain injury. A balance of neurotransmitters, glutamate and gamma-aminobutyric acid (GABA), is critical to facilitate inter-regional signaling in the brain. Alterations of inflammatory molecules and the effects on glutamatergic neurons ability to uptake GABA in certain brain areas is currently unknown in ASD. Pathological changes in brain areas associated with social behaviors have been identified in postmortem tissue from ASD donors when compared to typically developing (TD) age and gender matched control tissue, as well as, in imaging scans of living individuals with ASD. We hypothesize that expression of inflammatory related molecules are increased in the identified brain areas related to symptoms of ASD and can be associated with altered gene expression changes in neurons as shown by gamma-aminobutyric acid type A receptor alpha 1 subunit (GABRA1). Dysfunction of GABRA1 on glutamatergic neurons could disrupt the typical neuronal balance of glutamate and GABA signaling. Inflammatory markers, IGF1 and insulin-like growth factor one receptor (IGF1R), were evaluated using quantitative polymerase chain reaction (QPCR). Additionally, IGF1 and arginase were evaluated using immunohistochemistry in both white and gray matter from the anterior cingulate cortex (ACC). Laser capture microdissection (LCM) was used to obtain single cell captures of glutamatergic neurons. IGF1R and GABRA1 gene expression was measured using end point PCR. A significant increase in IGF1 expression was obtained in the white matter punch in comparison to typically developed age-matched subjects using QPCR during initial statistical significance, however, was ultimately not significant. Additionally, IGF1R expression was significantly increased in ASD neurons in comparison to TD subjects utilizing the LCM method. However, a decrease expression in GABRA1 trended significance indicating a possible alteration in the neuron’s ability to facilitate proper signaling. These findings are the foundation of future investigations of signaling pathways in ASD that may uncover cell-specific etiologies and drug therapies for a condition that is only projected to increase in prevalence.

The following dissertation analyses how users experience space with their different senses. And how we as designers can utilise this to improve rehabilitative designs’ responsiveness to cater to acute brain injury and post-operative neurological surgery patients. The medical field has shown a rapid increase in neurological development that changes the way doctors have been treating patients thus far. With the rapid growth in development, the associated disciplines need to react to the change in knowledge to provide a facility that accommodates new treatment methods that will always provide the patient with the best care. When dealing with specialised fields, the architectural design process is limited by the designers’ experience and knowledge, and when it comes to the medical field, it is almost always limited. The regulations and medical planning guidelines cater to the minimum requirements and systematic applications and not set to adapt to patient needs. Thus a multidisciplinary collaborative effort is needed to address the patient’s wellbeing properly. For the architectural profession to design responsive environments that help promote the patients’ passive recovery principles, we need to be able to identify the effect our spaces have on the brain. The research aims to broaden the philosophical approach to design to include rehabilitation principles to create more productive environments for patients. By studying the effect of the spaces on the brain, we know from the brain’s neuroplasticity that the constructive stimulation of the areas affected will increase its recovery rate. Once the principles have been identified, architectural drivers can be deduced from the data sets. If correctly implemented, the responsive design principles can help produce better rehabilitative methods that don’t have to rely solely on active rehabilitation applications. The end goal is to have this facility serve as a precedent for future projects with a multidisciplinary healthcare program that aims to incorporate responsible passive neurological treatments. / Mini Dissertation (MArch (Prof))--University of Pretoria, 2020. / Architecture / MArch (Prof) / Unrestricted

Autism spectrum disorder (ASD) is a neurodevelopmental disability affecting communication and social behaviors. Research is needed because the percentage of children affected by ASD is 1 in 59, and it is diagnosed in males at a rate of 1 in 42. Animal models must be used, because the neurological changes that lead to ASD occur during prenatal development. In this study, three mouse models were used to represent possible causes of ASD. The BTBR model is a genetically engineered model that displays social behavior deficits and has neuroanatomical findings similar to ASD. The other models include the Poly-IC and valproic acid injected mice which exposes the pregnant mother to a virus activating her immune system or a drug thought to affect brain development, respectively. In all three models the effects of brain-derived neurotrophic factor or BDNF, which is an important cytokine in the brain responsible for synaptic plasticity, maintenance and recognition, are being studied via expression levels of NTRK2. BDNF activates cell signaling cascades in glutamatergic neurons via the TrkB receptor which is encoded by the NTRK2 gene. It was previously found that NTRK2 expression was reduced in glutamatergic cells in people affected by ASD. The first outcome of the study is to determine gene expression differences in glutamatergic neurons captured from the cingulate cortex in all three models as well as in wild type control mice. Additionally, a second outcome of the study is to optimize a new protocol for single cell gene expression using a nested PCR method. This was done by comparing the previously used method for relative end-point PCR with the nested method to identify gene expression alterations. To prepare for the two PCR methods, samples were dehydrated and laser capture microdissection was performed on mouse brain tissue to obtain pyramidal neurons from the cingulate area. This area is highly connected to the limbic system and plays a role in personality and communication. All animal procedures were approved by the ETSU animal care committee. RNA isolation was performed on 1000 cells after which RNA was reverse transcribed into cDNA using the Superscript III cDNA synthesis system. Initial optimization experiments included using various amounts of starting cDNA and determining expression differences using relative end-point PCR and Agilent tape station. The same starting cDNA was used and initially 20 cycles of PCR were performed using Prime5 HotStart Master Mix followed by a quantitative PCR reaction using Powerup on the BioRad CFX96 RT detection system. Gene expression was performed using NTRK2 as the target gene and GAPDH as the reference gene for each method. Both methods will allow the detection of changes in the expression levels of NTRK2 and GAPDH when different sample concentrations are used. This data could help establish a link between maternal immune system activation or exposure to certain drugs during pregnancy with the occurrence of ASD.

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There is a higher prevalence of hearing loss in children with diagnosed neurological disorders than the general paediatric population. It is therefore essential that these children have their hearing assessed. Conventional behavioural audiometry requires participation from the child, and in a majority of this population with neurological pathology this is not always possible owing to their neurocompromised state. These children will have to undergo objective testing, such as the Auditory Brainstem Response (ABR) in order to obtain estimated hearing thresholds, as this requires no active involvement from the patient. This study therefore aims to describe the audiological ABR findings in order to determine hearing function in this group and to establish a relationship between audiological ABR findings to behavioural audiometry findings where these exist in a group of neurologically disordered children in a tertiary hospital in South Africa. Methods: A retrospective review was conducted on 40 ABR patient records of children between the ages of 5 months and 10 years diagnosed with a neurological disorder. Behavioural audiometry results were then sought for these children, where these existed. Hearing status was described for each child per ear for both objective and behavioural results, and descriptive statistics were conducted. Results: 56.25 % (n=45) of ears in this study presented with normal hearing on ABR testing. No behavioural audiometry results were obtained in 72.5 % (n=58) of ears in this study. Results correlated between ABR and behavioural testing for only 7.5% (n=8) of ears tested and in all eight of these ears the hearing result was within normal hearing limits. Twelve and a half percent (n=10) of ears were misdiagnosed on behavioural testing. More premature infants were able to be tested behaviourally when compared to other pathologies. Cerebral palsy, Down’s Syndrome, prematurity and RVD were the pathologies in which the most hearing losses were diagnosed. Conclusions: Behavioural audiometry appears a largely unreliable method of hearing testing in children diagnosed with neurological disorders as results were obtained in only 27.5 % of the study sample; however it remains the gold standard in paediatric hearing testing in order to evaluate the entire auditory system and provides information on how a child processes sound, unlike ABR testing which only provides hearing information up to the auditory brainstem. This study highlights the high prevalence of hearing problems in children with neurological disorders and therefore the importance of hearing testing in this population. Hearing thresholds should be established for subsequent remediation via objective testing. Conditioning should continue simultaneously for a behavioural audiological test battery with adaptations for the child’s developmental ability.