| 1. |
- Agardh, Carl-David, et al.
(författare)
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Improvement of peripheral nerve function after institution of insulin treatment in diabetes mellitus. A case-control study
- 1983
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Ingår i: Acta Medica Scandinavica. - 0001-6101. ; 213:4, s. 283-287
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Tidskriftsartikel (refereegranskat)abstract
- The influence of improved diabetic control on peripheral nerve function was studied before and 3-4 months after institution of insulin treatment in 22 diabetics unsatisfactorily controlled by oral hypoglycemic agents. After institution of insulin treatment, diabetic control was improved as demonstrated by decreasing levels of HbA1. There was an overall tendency towards improvement of motor and sensory conduction velocities, however significant only in the upper extremities. There was a tendency towards improved temperature sensitivity in the legs, while no changes occurred in the hands and face. The sensation for vibration did not change. It is concluded that improved diabetic control, even in elderly patients with long-standing diabetes, is followed by neurophysiological signs of improved peripheral nerve function.
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| 2. |
- Abdul-Rahman, A, et al.
(författare)
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Local cerebral blood flow in the rat during severe hypoglycemia, and in the recovery period following glucose injection
- 1980
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Ingår i: Acta Physiologica Scandinavica. - 0001-6772. ; 109:3, s. 307-314
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Tidskriftsartikel (refereegranskat)abstract
- In order to assess the influence of severe hypoglycemia on local cerebral blood flow (1-CBF) artificially ventilated rats, maintained on 70% N2O, were injected with insulin to provide either an EEG pattern of slow-wave polyspikes, or cessation of spontaneous EEG activity for 5, 15 or 30 min ("coma"). In other animals, glucose was injected at the end of a 30 min period of "coma" and 1-CBF was measured after recovery periods of 5, 30, 90, or 180 min. Local CBF was measured autoradiographically with 14C-iodoantipyrine as the diffusible tracer. In the slow-wave polyspike period 1-CBF was increased in most of the structures studied, and reached values that were 1.4 to 3.2 times greater than control. In many structures, cessation of EEG activity was accompanied by a further increase in 1-CBF, with some structures (thalamus, hypothalamus, pontine gray, and cerebellar cortex) showing flow rates of 400--500% of control. The increase in 1-CBF was unrelated to arterial hypertension, hypercapnia, or hypoxia. 5 min after glucose injection the hyperemia persisted in only some of the structures studied; in others, the 1-CBF were close to, or below, control values. During the subsequent recovery period 1-CBF was markedly reduced with some structures (cerebral cortical areas, hippocampus, and caudate-putamen) showing flow rates of only 20--35% of control. In others, notably pontine gray and cerebellar cortex, secondary hypoperfusion was never observed. The hypoperfusion was unrelated to arterial hypertension, hypocapnia, or increase in intracranial pressure. It is concluded that, like hypoxia and ischemia, substrate deficiency due to hypoglycemia is accompanied by vasodilatation in the brain. Furthermore, like long-lasting ischemia, severe hypoglycemia is followed by a delayed hypoperfusion syndrome that, by restricting oxygen supply, may well contribute to the final cell damage incurred.
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| 3. |
- Agardh, Carl-David, et al.
(författare)
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Persistent vegetative state with high cerebral blood flow following profound hypoglycemia
- 1983
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Ingår i: Annals of Neurology. - : Wiley. - 1531-8249 .- 0364-5134. ; 14:4, s. 482-486
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Tidskriftsartikel (refereegranskat)abstract
- A persistent vegetative state (severe dementia) developed in a 30-year-old man following hypoglycemic coma. Despite the poor clinical outcome, sensory evoked response recovered between 6 and 34 months after the insult. The cerebral blood flow level at rest after 34 months was slightly above the normal range. This finding contrasts with the low cerebral blood flow regularly reported in patients who are comatose or stuporous following severe brain hypoxia-ischemia.
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| 4. |
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| 5. |
- Nilsson, B, et al.
(författare)
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Cerebrovascular response during and following severe insulin-induced hypoglycemia: CO2-sensitivity, autoregulation, and influence of prostaglandin synthesis inhibition
- 1981
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Ingår i: Acta Physiologica Scandinavica. - 0001-6772. ; 111:4, s. 455-463
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Tidskriftsartikel (refereegranskat)abstract
- The objective of the present experiments was to study mechanisms governing cerebrovascular responses during severe hypoglycemia, and in the posthypoglycemic recovery period. To that end, lightly anesthetized (70% N2O) and artificially ventilated rats were injected with insulin so as to abolish spontaneous EEG activity for 15 or 30 min ("coma"). In separate animals, recovery was induced by glucose administration. Previous experiments have shown that in normo- or moderately hypertensive animals hypoglycemic coma is accompanied by a relatively marked increase in cerebral blood flow (CBF), and that a delayed hypoperfusion develops in the recovery period. The present results demonstrate that oxygen supply is in excess of the demands during coma, and falls below control during recovery. During hypoglycemic coma, the CO2 response of the circulation was retained but autoregulation was lost. In the recovery period, both CO2 response and autoregulation were lost. Pretreatment with indomethacin was introduced in order to evaluate the possible influence of fatty acid cyclo-oxygenase products on the pattern of CBF changes. Measurements of local cerebral blood flow (1-CBF) showed that, in the majority of structures analysed, indomethacin failed to modulate the changes in CBF. It is concluded that alterations in cerebrovascular tone and loss of autoregulation induce flow changes that may influence substrate and oxygen availability during hypoglycemia. The pronounced decrease in CBF and the loss of autoregulation and CO2-response in the post-hypoglycemic period may influence functional, metabolic and morphological recovery. The 1-CBF findings indicate that neither the increase in CBF during hypoglycemia nor the reduction in flow in the posthypoglycemic period are mediated by mechanisms related to prostaglandin metabolism.
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| 6. |
- Danielsen, N, et al.
(författare)
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Axonal growth in mesothelial chambers. The role of the distal nerve segment
- 1983
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Ingår i: Scandinavian Journal of Plastic and Reconstructive Surgery. - 0036-5556. ; 17:2, s. 25-119
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Tidskriftsartikel (refereegranskat)abstract
- An experimental model is presented for studying nerve regeneration over gaps of various lengths between the both ends of a severed nerve. After transferring left and right sciatic nerves of rat to the back, the gap between the two nerve ends could be bridged by a preformed, tube-shaped mesothelial chamber of a desired length. When the gap length was 10 mm or less, a well developed nerve structure was generated in the chamber between the nerve ends, and axons from the left sciatic nerve reinnervated muscles in the right limb via the right sciatic nerve. When the gap length was extended to 15 mm or more no such regeneration occurred. When no distal nerve end was introduced into the chamber, there was a limited growth into this chamber over only 5-6 mm. This "limited growth phenomenon" is discussed with respect to a lack of "trophic" or cellular support from a distal nerve segment. It is also proposed that the termination of growth, seen under these circumstances, may suggest a new principle for avoiding the development of neuromas after nerve transections.
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| 7. |
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| 8. |
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| 9. |
- Frisén, Lars, 1939, et al.
(författare)
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Episodic astigmatism heralding generalized myopathy: report of a case managed with a new type of soft contact lens.
- 1984
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Ingår i: Ophthalmology. - 0161-6420. ; 91:2, s. 179-82
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Tidskriftsartikel (refereegranskat)abstract
- A 29-year-old woman presented with marked variations in refraction. A few minutes of physical exertion or reading at a close distance induced up to 2D of myopia and 2D of myopic astigmatism, which regressed upon resting with closed eyes. Cycloplegic agents did not affect the refractive changes, which were shown to be due to variations in corneal curvatures. The eyes were otherwise clinically normal. A few months later the patient developed signs of a progressive, generalized myopathy of unknown origin. The muscular disease was resistant to treatment. The refractive changes were effectively controlled by means of a new type of soft contact lens, with a semi-rigid center.
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| 10. |
- Frisén, Lars, 1939
(författare)
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Fundus changes in acute malnutritional optic neuropathy.
- 1983
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Ingår i: Archives of ophthalmology (Chicago, Ill. : 1960). - 0003-9950. ; 101:4, s. 577-9
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Tidskriftsartikel (refereegranskat)abstract
- A peculiar dilation and tortuosity of small retinal vessels within the arcuate areas of the retinal nerve fiber layer occurred in a series of patients with acute malnutritional optic neuropathy ("tobacco-alcohol amblyopia"). These evanescent vascular abnormalities may be caused by arteriovenous shunting. They seem to be specific indicators of the early phase of this disease.
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