Object. More than a quarter of spinal cord injured patients will develop an enlarging cystic cavity, or syrinx, within the spinal cord up to 30 years following the initial trauma. Enlarging syrinxes can cause progressive loss of function in patients who often already have a disability. Less than half the affected patients can be expected to improve following treatment. A lack of understanding of the pathophysiology of the disease is hampering attempts to improve on this poor prognosis. Investigation into the mechanisms of fluid flow and the role of ischaemia in this type of syringomyelia may help understand the causative mechanisms and lead to improved treatment outcomes. Materials and methods. Temporal and dose profiling of an animal model of post-traumatic syringomyelia was performed in Sprague Dawley rats. The cerebrospinal fluid tracer, horseradish peroxidase, was used for detailed analysis of the routes of fluid flow into the syrinx. The effects of variations in subarachnoid space compliance on syrinx formation and fluid flow were examined using shunt insertion, pseudomeningocele formation, and animals without subarachnoid adhesions. Local spinal cord blood flow was investigated with Doppler flowmetry, and the intracellular levels of ATP and adenosine phosphates were measured with a bioluminescence technique. Results. A reliable animal model that mimicked human syrinx pathology was refined. Excitotoxic injury selectively damaged neurones, and induced syrinx formation in a dose and time dependent fashion. Cerebrospinal fluid flows from the subarachnoid space along perivascular spaces into the cord and syrinx. Flow occurred along the perivascular spaces of the central branches of the anterior spinal artery, and was maximal at the level of the syrinx. Improving compliance by shunt insertion reduced syrinx size but preferential fluid movement into the syrinx was maintained. If arachnoid adhesions were absent, this preferential flow ceased and syrinxes were smaller. Pseudomeningocele formation proved technically difficult and was unhelpful in changing cord compliance. Spinal cord blood flow was decreased following syrinx formation. Early reductions occurred in ATP and ADP levels, and the intracellular ATP/ADP ratio remained below 0.2 at all time points following syrinx induction. Conclusions. CSF moves into the syrinx and spinal cord along perivascular spaces. Arachnoid adhesions may act to decrease localized subarachnoid space compliance and encourage fluid flow from the subarachnoid space along perivascular spaces and into the syrinx. Increasing distal subarachnoid space compliance does not prevent this preferential flow but may reduce the amount of flow. Fluid accumulation within the syrinx causes ischaemia through pressure effects on the surrounding spinal cord tissue, and may further syrinx enlargement by apoptosis. The results support and are consistent with a local arterial pulsation dependent pumping mechanism of cerebrospinal fluid flow.

Thesis (M.S.) -- University of Adelaide, Dept. of Surgery, 2000. / Bibliography: leaves 112-127.

Thesis (Ph. D.)--University of New South Wales, 2003. / Also available online.

Habilitationsschrift--Marburg. / Includes bibliographical footnotes.

Thesis (M.S.) -- University of Adelaide, Dept. of Neurosurgery, 2001. / Bibliography: leaves 155-180.

Bibliography: leaves 112-127. Study using an animal model (Sprague-Dawley rats) to elucidate the role of EAAs and spinal subarachnoid blockade in posttraumatic syringomelia. Results support the proposal that in posttraumatic spinal cord injury, primary injury and exitotoxic cell death, occuring secondary to elevated levels of EAAs, contribute to a pathologic process leading to the formation of spinal cavities, and a subarachnoid block by arachnoiditis is one of the pathogenic factors most responsible for initiating extension of the cavity.

Bibliography: leaves 155-180.

Introduction: Around a quarter of patients with spinal cord injury develop post traumatic syringomyelia (PTS), causing progressive neurological deficits. Current surgical treatment is unsatisfactory. Endogenous stem cell therapy, aiming at replacing lost tissue and repairing damaged ones by endogenous progenitors, may offer hope. Investigation into the reaction of endogenous progenitors in PTS may extend our knowledge about stem cell biology and help to develop a new treatment option for PTS. Endogenous stem cells were found to differentiate into astrocytes. Reactive astrocytes and gliosis are shown to have an important role in spinal cord injury, such as protecting neurons, limiting inflammation and regulating local environment to suit progenitors. We hypothesize that reactive astrocytes may play an important protective and potential therapeutic roles in PTS. The aim of this thesis is to study proliferation, differentition and location of endogenous progenitors and their roles in PTS. Materials and methods: Excitotoxic injury model of PTS was performed in adult Wistar rats. Proliferating cells were marked by either exogenous mitotic marker bromodeoxyuridine or endogenous mitotic marker Ki67.lmmunofluorescence techniques targeting mitotic markers were used to trace the proliferating cells. Immunofluorescent double staining techniques were used to phenotype the proliferating cells. Results: A large number of endogenous progenitors appear in PTS from 24 hours to at least 8 weeks post injury (PI). They proliferate much faster in PTS than in the control animals. Although less endogenous progenitors are observed after 4 weeks PI, their number is still much higher than that in the control animals. Immediately after injury, progenitors exist mainly in the white matter, but the majority of them shift their position closer to the lesion within 2 days. In the chronic stage, the majority of stem cells are located in and around the lesion site. Endogenous progenitors differentiate into astrocytes but not oligodendrocytes or neurons within 8 weeks. Astrocytes respond to injury by upgrading GFAP (1 day PI), becoming hypertrophic (7 days PI) and forming glial scar (2 weeks PI) in PTS. The development of a glial scar corresponds with the stage of cyst stability or reduction in size. Conclusions: Endogenous progenitors exist in PTS and they respond to injury by proliferating and shifting their position towards the lesion. These studies are important in understanding the endogenous stem cell response to PTS and lay the groundwork for future studies examining stem cell therapy for the condition. Endogenous progenitors in the PTS model differentiate into astrocytes, which help to form the glial scar lining the syrinx. Reactive gliosis may play an important role to seclude the injury site from healthy tissue, prevent a cascading wave of uncontrolled tissue damage and restrict the syrinx enlargement.

Thèse--Université de Paris. / "Index bibliographique": p. [73]-75.

Although headaches are a very common complaint, those accompanied by paresthesia and muscle wasting indicate an underlying neurological disorder. In this review, we present the case of a 58-year-old man with chronic headaches who developed tingling and numbness in his right limbs along with right-hand muscle atrophy.