Acute Intracranial Haemorrhage: Pathophysiological and Magnetic Resonance Studies

Jenkins, Alistair (1989) Acute Intracranial Haemorrhage: Pathophysiological and Magnetic Resonance Studies. MD thesis, University of Glasgow.

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Previous studies have shown an extensive area of ischaemia around an acute intracerebral haematoma, and that this ischaemia contributes to patients' clinical condition and outcome. The relative contribution of tissue pressure and chemical vasoconstriction in the production of ischaemia is uncertain. If vasoconstrictors present in blood were found to play a significant role, and if ischaemia could be detected early, it might prove possible to improve blood flow by pharmacological manipulation of the vasoconstrictor effect. The studies reported here used the new technique of Magnetic Resonance Imaging (MRI) to investigate intracerebral and subarachnoid haemorrhage, and associated changes in the brain parenchyma. Ischaemic change was assayed in an experimental animal model using different intracerebral space-occupying lesions, and local effects of a haematoma were observed at stages up to three months. The first part of the study was concerned with assessing the sensitivity and specificity of MRI in acute and subacute intracranial haemorrhage (ICH). The diagnostic yield of MRI is determined by the choice of radiofrequency (RF) pulse sequences appropriate to the condition. A system was developed which used computer analysis of in vitro relaxation time measurements of brain, blood and cerebrospinal fluid (CSF) to predict optimum pulse sequences for imaging patients with ICH. T1 and T2 of fresh human post-mortem grey matter and white matter, and of CSF from patients undergoing myelography, were measured in vitro using a MR spectrometer. Relaxation times of blood from volunteers, and of CSF samples after the addition of blood to simulate different degrees of subarachnoid haemorrhage (SAH), were also measured daily for 15 days. T1 and T2 of blood fell sharply over the first 48 hours and gradually over the rest of the period. There was an insignificant fall in the values for bloodstained CSF. On day one, there were substantial differences between the relaxation times of all the tissues, but the fall in the relaxation times of blood led to overlap with the values for brain tissue. A simple computer program used these measurements to calculate values for image signal intensity for all the tissues. Signal intensity values were obtained for all the pulse sequence combinations available on the Picker 0.15T imager. From these results, sequences were chosen which produced the greatest separation of the signal intensities, and hence the image contrast, of normal and haemorrhagic tissues. A Spin-echo (SE) 2200/80 sequence was chosen for clinical imaging studies as it combined good tissue contrast with good definition and a short imaging time (9.2 mins). Clinical studies were then undertaken on patients with subarachnoid haemorrhage, intracerebral haematoma and head injury. Conclusions 1. Intracranial haemorrhage from a variety of causes was well demonstrated by Magnetic Resonance Imaging in both acute and subacute situations in three series of selected patients. To diagnose haemorrhage conclusively, care must be exercised in the selection of radiofrequency pulse sequences. Computer modelling of MRI using data from in vitro tissue studies proved to be a useful method of selecting appropriate sequences. 2. MRI showed extensive tissue change around small and large haematomas at an early stage, while the signal intensity of haematomas seen on MR images was lower compared to that of uninvolved brain than had been predicted by in vitro studies. It was thought possible that these two findings might be in part explained by early transudation of fluid from the haematoma, but it was not possible to prove this in patients or to produce an appropriate animal model for MR and tissue analysis. 3. Small animal studies showed an immediate and profound effect on the vasculature in the region of an intracerebral haematoma and at more distant sites which could not be explained solely by its space- occupying effect, as similar-sized lesions of inert fluids did not cause changes of equal extent. It is therefore possible that substances diffusing or tracking from the clot might contribute to ischaemia, but this could not be proven experimentally, although blood was seen to track along the perivascular spaces for some distance from the clot. In the experimental situation widespread ischaemia was transient; local ischaemic change increased to a peak by 48 hours, and reduced progressively thereafter with concomitant phagocytosis and absorption of the clot to leave a small glial scar. (Abstract shortened by ProQuest.).

Item Type: Thesis (MD)
Qualification Level: Doctoral
Keywords: Medicine, Neurosciences
Date of Award: 1989
Depositing User: Enlighten Team
Unique ID: glathesis:1989-77850
Copyright: Copyright of this thesis is held by the author.
Date Deposited: 14 Jan 2020 11:53
Last Modified: 14 Jan 2020 11:53

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