Three cases of symptomatic neuralgia of the trigeminal nerve due to an amyloidoma in the gasserian ganglion are described. The correct diagnosis was not made prior to histological examination of the surgical biopsy specimens. Medical history and clinical observation led to the diagnosis of a malignant process of the nasal cavities in the first patient; of an inflammatory dental focus in the second patient; and of multiple sclerosis in the third patient. CT findings were normal in cases 1 and 2; in case 3, a schwannoma was suspected from the CT appearances. In case 1, MRI had not been performed; in cases 2 and 3, MRI revealed a tumour mass which was also considered to be a schwannoma. Histologically, the tumours consisted of masses of amyloid deposits which had largely replaced the pre-existing ganglionic cells and satellite cells. Electron microscopy confirmed the fibrillar structure of the deposits. Immunohistochemistry and immunocytochemistry revealed the amyloid to belong to the AL-lambda subtype.
Results of treatment of acromegaly are often incomparable due to the different criteria which have been used for defining cure or control of disease. At the present time it is widely accepted, that the main criteria of cure must be normalization of IGF-1 and a GH in the OGTT < 2 ng/ml. In this retrospective study we investigated the endocrinological results of 56 patients, who were surgically treated because of a GH-producing pituitary adenoma, by different criteria. Twelve of our patients had had additional medical treatment after surgery, two received radiotherapy. At a mean follow-up of 34 months after surgery 66% of patients had a basal GH < 5 ng/ml, 64% had a GH in the OGTT < 2 ng/ml and 73% had normalization of IGF-1. The combined criteria of OGTT < 2 ng/ml and IGF-1 normalization have been fulfilled in 59% of patients. None of these latter patients developed a clinical recurrence during the follow-up period. An optimal result (endocrinological cure, no permanent surgical complications and intact pituitary function) was achieved in 43% of patients. Although surgery was responsible for 19 new pituitary axis deficiencies (7 corticotropic axis, 8 thyrotropic axis and gonadotropic axis), 22 partial deficiencies improved to normalization after surgery (respectively 6, 3, and 13). Pre-operatively 55% of patients had no pituitary deficiency, after surgery this was 61%, leaving a net positive result of 6% less pituitary deficiencies. The authors conclude that normalization of IGF-1 combined with an OGTT < 2 ng/ml are adequate criteria for the definition of cure of acromegaly. However, the authors propose to include post-treatment hypopituitarism as an additional criterion by which treatment of acromegaly should be evaluated.
Summary24 hours after a circumscribed cold injury of the cortex dog brains were perfused from the lateral ventricle and the frontal subaraehnoidal space to the eisterna magna with an artificial CSF containing trace amounts of 35S-labelled thiosulphate. Simultaneously the extraeellular tracer was administered intravenously.Extracellular fluid volume was estimated and found to be increased from 10 to 15% in the oedematous cortex and from 10 to 27% in the oedematous white matter. The actual size of ECS in oedematous white matter, however, must be larger as indicated by the relative alterations of thiosulphate distribution, tissue water, sodimn and chloride. Apparently a small part of the fluid accumulation affects the cellular compartment in oedematous white matter. It may be concluded from the close spatial correspondence of the spreading of 1181 albumin mad Evans blue, the increase in water and sodium content, and the enlargement of the TSS that the dilated extraeellular channels are filled with a plasma like oedema fluid, derived from blood.The oedema resulting from a local cold injury to the cortex produces all experimental model bearing similarities to the oedema following traumatic brain injury. This model has often been used to study the disturbance of blood-brain barrier to various compounds 3, G, 11, 13, 14 as well as the morphological 3, 4, 5, 15, 22 and chemical changes 3, 6, 16 that occur in oedematous tissue. In contrast, the sequence of events oeeuring during the formation of oedema and the physiochemieal forces (in terms of diffusior~ and driving forces) involved in the formation and resolution of brain oedema are not adequately kaowm Of
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