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Biomedical subjects

G Mathieson

Publications and source records attributed to G Mathieson.

16 recordsLinked to original sources
PubMed2001

Sarcoidosis presenting as an intramedullary spinal cord lesion.

OBJECTIVES: Sarcoidosis affects the spinal cord in only 0.43% of patients with sarcoidosis. Usually there is systemic involvement prior to the development of cord lesions. We present a case of sarcoid isolated to the intramedullary spinal cord, which was a diagnostic and therapeutic challenge. We review the case and then present a review of the literature with an emphasis on presentation, diagnosis and treatment. METHODS: We have reviewed a patient who presented with an isolated sarcoid granuloma affecting the cervical spinal cord. All pertinent history and physical information was extracted from the patient's chart and through patient interview. Laboratory, radiographic and pathological investigations are presented. RESULTS AND CONCLUSIONS: Fourteen patients have been reported with isolated intramedullary spinal cord sarcoidosis. Current practice supports the role of surgery for biopsy; mainstay of treatment is corticosteroids.

Adult↗
PubMed1986

Primary malignant tumours of the trigeminal nerve.

We report a case of primary malignant schwannoma of the trigeminal nerve, and review the 5 previously reported cases. Clinical presentation, along with radiological and pathological features are discussed.

Combined Modality Therapy↗
PubMed1984

Tissue reaction of morphine applied to the epidural space of dogs.

Epidural morphine has found increasing popularity in clinical trials for the relief of chronic and postoperative pain relief. This study was conducted to determine if there was any adverse tissue reaction when morphine was applied to the epidural space of dogs. Sixteen dogs were given 0.07 mg X kg-1 of morphine in a volume of 2 cc of normal saline into the epidural space. Gross and microscopic studies of the epidural space, dura, and spinal cord did not show any adverse tissue reaction.

Anesthesia, Epidural↗
PubMed1979

Opening of tight junctions in cerebral endothelium. I. Effect of hyperosmolar mannitol infused through the internal carotid artery.

Infusion of 1.8 M mannitol solution into the internal carotid artery of Wistar rats allows horseradish peroxidase (HRP) to cross cerebral vascular endothelium via intercellular pathways. This was made evident by density gradients of HRP observed in consecutive tight junctional compartments following in vivo administration, and by the passage of colloidal lanthanum through junctional membrane appositions of glutaraldehyde fixed cerebral endothelium. Three hours after mannitol infusion, small non-capillary vascular segments were still focally permeable to HRP. Twenty-four hours after the osmotic insult, the tracer was absent in the affected hemisphere. Water and electrolyte assays indicated absence of brain edema during the period of observation of blood-brain barrier opening.

Animals↗
PubMed1979

Opening of tight junctions in cerebral endothelium. II. Effect of pressure-pulse induced acute arterial hypertension.

Acute arterial hypertension was produced in male Wistar rats by pressure pulse through the right internal carotid artery. The pressure pulse was induced by infusion of physiological saline as a bolus, at a rate of 0.63 ml per second by syringe pump. Evans blue (Eb) was used to visualize the areas of blood-brain barrier opening. Intravenously injected horseradish peroxidase (HRP) was used to study the ultrastructural basis of permeability changes in cerebral endothelium. Eb outlined circumscribed areas of blood-brain barrier opening. HRP extravasation was found mainly around small arteries. The capillary network was affected to a much lesser extent. Electron microscopy showed that HRP crossed the endothelial cell layer by intercellular routes. Glutaraldehyde fixed brain samples permeated with colloidal lanthanum supported these observations.

Animals↗
PubMed1979

Blood-brain barrier opening to horseradish peroxidase in acute arterial hypertension.

Acute arterial hypertension was induced in male Wistar rats using two experimental techniques: (1) i.v. injection of Aramine and (2) infusion of physiological saline as a bolus via internal carotid artery. Horseradish peroxidase (HRP) was injected i.v. prior to both experimental procedures and subsequently localized in the brain by light and electron microscopy. In the saline infusion (pressure pulse) model, colloidal lanthanum was also applied as a diffusion tracer following fixation of the cerebral endothelium. In the Aramine model, extravsation of HRP correlated with abrupt elevation of blood pressure. In the pressure pulse model HRP extravasation was consistently visualized in the affected hemisphere. Electron microscopy showed consistent labeling of plasmalemmal vesicles by HRP in segments of cerebral endothelium. However, HRP was also clearly visualized in junctional pools suggesting focal opening of endothelial tight junctions as a pathway for extravasation of this tracer in both hypertensive models. Colloidal lanthanum not transported by plasmalemmal vesicles across endothelium after fixation of the brain also bypassed consecutive membrane appositions of endothelial tight junctions indicating existance of interendothelial pathways to macromolecules in acute arterial hypertension.

Acute Disease↗
PubMed1979

Periodic alternating gaze.

A 77-year-old man with autopsy-proven bilateral cerebral infarction had a periodic alternating conjugate horizontal ocular deviation for 2 days, which ceased shortly before death. There have been four previously reported patients with this disorder. The phenomenon suggests acute bilateral cerebral disease with a relatively intact brainstem.

Aged↗
PubMed1979

Dementia in Parkinson disease: a neuropathologic study.

Thirty-four autopsy cases conforming to the standard neuropathologic criteria of Parkinson disease were sex- and age-matched with controls who had died of infarct or trauma. All brains were reviewed for changes compatible with Alzheimer disease, and available clinical data were retrospectively reviewed. Nineteen (56 percent) of the Parkinson cases had shown some degree of dementia. The average parkinsonian brain weight was 1281 gm; it was 1365 gm for the controls (p less than 0.02). Plaques, neurofibrillary tangles, granulovacuolar degeneration, and cortical cell loss were present in all but one of the parkinsonian brains; these pathologic changes were present in fewer controls and to a lesser degree. The higher incidence of dementia in patients with Parkinson disease may be explained by the simultaneous presence of Alzheimer disease.

Aged↗