The dimensions of the cervical spinal canal (C3 – C7) of the South African black population were measured on skeletal remains of 179 individuals (90 males and 89 females divided into age categories of 30-45; 46-60 and 61-75 years), and compared to measurements taken from CT-scans of 55 individuals divided into the same categories. There was no significant difference between measurements taken on skeletal material and CT-scans. The spinal canal is larger in males (mean = 13.96mm) than in females (mean = 13.84mm) and the Pavlov ratio is larger for females (mean = 0.89) than males (mean = 0.81). The Pavlov ratio seems to overestimate the occurrence of spinal stenosis in this population group, as almost all individuals older than 46 years are classified as stenotic according to this ratio. The shape of the cervical spinal canal was determined morphometrically by processing digital images taken of vertebrae (C3 – C7) of 60 individuals with the tps-Series of software programs and was found to be significantly different between males and females. In males the canal is congenitally triangular, whereas in females the canal assumes a more “safe”, rounded shape. The low Pavlov ratio for this population group, especially in males, can possibly be explained by these shape differences. Even slight degenerative changes affecting the spinal canal, such as osteophytosis or ossification of the posterior longitudinal ligament (OPLL), will alter the triangular-shaped male canal in such a way that the spinal cord may become compromised. Cervical vertebrae of 107 individuals were inspected for occurrence of osteophytes within the spinal canal and the incidence of OPLL. Osteophyte occurrence within the cervical spinal canal is the same for males and females and OPLL occurs frequently within this population group, especially in the cephalic region (incidence: C3 = 64.5%; C4 = 47.7%; C5 = 21%; C6 = 12.2%; C7 = 7.5%). / Dissertation (MSc (Anatomy))--University of Pretoria, 2008. / Anatomy / unrestricted

Thesis (MAppSc in Physiotherapy)--University of South Australia, 1995

A mielopatia espondilótica cervical (MEC) é afecção relacionada diretamente com o estreitamento do canal vertebral cervical. O objetivo deste estudo foi avaliar variações morfométricas da coluna vertebral cervical em pacientes portadores de MEC por meio da ressonância magnética dinâmica nas posições neutra, em flexão e em extensão. Este é um estudo prospectivo de pacientes portadores de MEC secundária à doença degenerativa da coluna vertebral cervical. Os parâmetros morfométricos foram avaliados pelas sequências de ressonância magnética ponderadas em T2, no plano sagital em posições neutra, flexão e extensão. Os parâmetros estudados foram o comprimento anterior da medula espinhal (CAME), o comprimento posterior da medula espinhal (CPME), o diâmetro do canal vertebral (DCV) e o diâmetro da medula espinhal (DME). O CAME e o CPME foram mais longo em flexão do que nas posições em neutro e extensão, sendo encontrada diferença estatisticamente significativa entre a posição em flexão e extensão. O DCV e o DME foram maiores em flexão do que nas posições neutra e em extensão, no entanto não foi encontrada diferença estatisticamente significativa quando comparados nas posições em neutro, flexão e extensão. Desta forma, o exame de ressonância magnética dinâmica permite avaliar as variações morfométricas do canal vertebral cervical em pacientes portadores de mielopatia cervical espondilótica. / Cervical spondylotic myelopathy is a condition directly related to the narrowing of the cervical vertebral canal. The objective of this study was to evaluate morphometric variations of the cervical spine in patients with CSM using dynamic magnetic resonance imaging (MRI) in neutral, flexion and extension positions. This is a prospective study of patients with CSM secondary to degenerative disease of the cervical spine. The morphometric parameters were evaluated using T2-weighted MRI sequences in the sagittal plane with neutral, flexion and extension position of the neck. The parameters studied were the anterior length of the spinal cord (ALSC), the posterior length of the spinal cord (PLSC), the diameter of the vertebral canal (DVC) and the diameter of the spinal cord (DSC). The ALSC and PLSC were longer in flexion than extension and neutral position, with statistically significant difference between the flexion and extension position. The DVC and the DSC were greater in flexion than in extension and neutral position, however there was no statistically significant difference when comparing the positions in neutral, flexion and extension. Therefore, dynamic MRI allowed to evaluate morphometric variations in the cervical spinal canal in patients with cervical spondylotic myelopathy.

Thesis (MSc.(Anatomy)--Faculty of Health Sciences)-University of Pretoria, 2007. / Includes bibliographical references.

Low back pain (LBP) is the leading cause of disability globally and is most commonly associated with pathologies of the intervertebral disc (IVD), including spinal stenosis, disc herniation, and IVD degeneration. IVD cells within the local degenerative disc environment are known to produce abundant inflammatory cytokines and chemokines, leading to recruitment of immune cells, such as macrophages. The presence of both IVD cells and macrophages in the pro-inflammatory microenvironment further exacerbates the degenerative cascade, leading to production of additional inflammatory cytokines and catabolic enzymes that compromise the IVD ECM structural integrity. However, the individual contributions of IVD cells and macrophages on degeneration, as well as the impact of crosstalk between the cell types remains unknown. A systemic inflammatory response is also common in cases of chronic LBP, defined as lasting longer than 3 months. While systemic inflammation in the serum of patients with LBP has been widely observed in comparison to healthy controls, the impact of pain and disability severity on systemic inflammation has not been determined. Additionally, both the local and systemic inflammatory responses associated with IVD injury and LBP have been characterized independently; however, the connection between these responses and their role in the progression of pain has not been studied. This thesis addresses these questions through a variety of methodologies including characterization of clinical samples, in vivo injury modeling, and an in vitro co-culture system. First, transcriptomic analysis of whole blood from patients with chronic LBP and spine pathologies was performed to determine the signaling mechanisms contributing to pain and disability severity systemically. Circulating immune cell senescence, and decreased complement activation and Type I interferon signaling were shown to contribute to greater severity of disability in patients with LBP. Next, an inflammation-driven in vivo injury model utilizing intradiscal injection of the inflammatory stimulus, lipopolysaccharide (LPS), was developed to investigate the role of local inflammation in the progression of IVD degeneration. Intradiscal inflammatory stimulation increased degeneration, macrophage infiltration, and innervation, ultimately leading to a pain phenotype. RNA sequencing analysis of the AF and whole blood after injection was also performed to determine signaling mechanisms mediating the local and systemic inflammatory responses. Type I interferon signaling was commonly upregulated in both the AF and blood, indicating a direct connection between local and systemic inflammation. Additionally, an inverse relationship between the complement activation and neuronal signaling pathways provides an interesting parallel with the relationship observed between the complement system and disability severity clinically. An in vitro macrophage-IVD explant co-culture model was also created to gain understanding of the contributions of macrophages in the inflammatory microenvironment of the degenerating IVD. Using a transwell system limiting communication to paracrine signaling, pro-inflammatory M1 macrophages were shown to have detrimental effects increasing inflammation, while M2 macrophage were protective, decreasing production of inflammatory cytokines. Inflammatory-stimulated IVDs also polarized M0 macrophages towards an M1-like phenotype, further exacerbating inflammation and degradation. Taken together, this thesis indicates a key role for macrophages in the modulation of the local inflammatory environment. Local inflammation severity also directly regulates the systemic inflammatory response, contributing to a pain phenotype. Finally, in cases of chronic LBP clinically, systemic inflammation is dependent on pain and disability severity.

No description available.