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Biomedical subjects

M Lauritzen

Publications and source records attributed to M Lauritzen.

At least 73 records · Page 4Linked to original sources
PubMed1988

Quisqualate, kainate and NMDA can initiate spreading depression in the turtle cerebellum.

This study evaluated the role of excitatory amino acid (EAA) receptor activation in spreading depression (SD), using the in vitro turtle cerebellum as a model system. SD was triggered by electrical stimulation or by elevated K+ after the cerebellum had been conditioned for at least 30 min with physiological saline in which most of the chloride had been replaced by propionate. SD was recognized as a transient (1-3 min) negative shift of extracellular potential accompanied by depression of evoked potentials (15-30 min) and an increase of extracellular K+ up to 60 mM, which spread across the cerebellum at rates of 1-7 mm/min. SD usually commenced in the granular layer, which apparently contains the 3 major EAA receptor subtypes, quisqualate, kainate and N-methyl-D-aspartate (NMDA), then subsequently spread to the molecular layer, which is largely free of NMDA receptors. Glutamate, aspartate, NMDA, kainate and quisqualate all triggered SD. Kynurenic acid and 2-aminophosphonovaleric acid (APV) inhibited SD under certain conditions further suggesting involvement of EAA receptors. The initiation of SD was blocked by high Mg2+ and facilitated in low extracellular Mg2+, which also eliminated the delay in molecular layer SD onset. Our data suggest that no one EAA receptor subtype is singly responsible for SD.

2-Amino-5-phosphonovalerate↗
PubMed1988

Magnetic field associated with spreading depression: a model for the detection of migraine.

Slow variations of the magnetic field were recorded in real time during spreading depression (SD) in the isolated turtle cerebellum. The magnetic signal lasted for 2-10 min with the largest amplitude in the first minute. The field strength was of sufficient magnitude to be measured unaveraged at 2-4 cm from the tissue. The directions and time course of the magnetic signal indicated that cerebellar SD is accompanied by current normal to the cerebellar surface. The observations reported here are of clinical interest due to the potential involvement of SD in various neurological disorders, notably head trauma and migraine.

Animals↗
PubMed1988

Prevalence of microalbuminuria, arterial hypertension, retinopathy and neuropathy in patients with insulin dependent diabetes.

Diabetic nephropathy is the main cause of the increased morbidity and mortality in patients with insulin dependent diabetes. The prevalence of microalbuminuria was determined in adults with insulin dependent diabetes of five or more years' duration that had started before the age of 41. All eligible patients (n = 982) attending a diabetes clinic were asked to collect a 24 hour urine sample for analysis of albumin excretion by radioimmunoassay; 957 patients complied. Normoalbuminuria was defined as urinary albumin excretion of less than or equal to 30 mg/24 h (n = 562), microalbuminuria as 31-299 mg/24 h (n = 215), and macroalbuminuria as greater than or equal to 300 mg/24 h (n = 180). The prevalence of microalbuminuria and macroalbuminuria was significantly higher in patients whose diabetes had developed before rather than after the age of 20. The prevalence of arterial hypertension increased with increased albuminuria, being 19%, 30%, and 65% in patients with normoalbuminuria, microalbuminuria, and macroalbuminuria respectively. The prevalence of proliferative retinopathy and blindness rose with increasing albuminuria, being 12% and 1.4%, respectively, in patients with normoalbuminuria, 28% and 5.6% in those with microalbuminuria and 58% and 10.6% in those with macroalbuminuria. An abnormal vibratory perception threshold was more common in patients with microalbuminuria (31%) and macroalbuminuria (50%) than in those with normoalbuminuria (21%). This study found a high prevalence (22%) of microalbuminuria, which is predictive of the later development of diabetic nephropathy. Microalbuminuria is also characterised by an increased prevalence of arterial hypertension, proliferative retinopathy, blindness, and peripheral neuropathy. Thus, urinary excretion of albumin should be monitored routinely in patients with insulin dependent diabetes.

Adult↗
PubMed1987

Magnetic field associated with neural activities in an isolated cerebellum.

A superconducting sensor was used to measure the magnetic field evoked from the isolated cerebellum of the turtle by brief electrical stimulations of the dorsal surface. The field was generated by neuronal activities, since its amplitude was reduced when Mn2+ was applied and completely abolished with tetrodotoxin. In normal bathing medium, the field amplitude at a distance of 17 mm was as much as 1 pT, demonstrating that the magnetic technique can be used to remotely monitor neural activities in regions of 10 mm3 or even less.

Animals↗
PubMed1987

Change of cerebrovascular reactivity after cortical spreading depression in cats and rats.

The purpose of the present study was to examine the pial arteriolar diameter and evoked vascular responses after single episodes of cortical spreading depression (CSD) in rats and cats in order to elucidate the mechanisms of the persistent change of cortical perfusion which succeeds CSD. This problem is of potential clinical interest also since CSD may be involved in migraine pathophysiology. Using an open cranial window technique, pial arteriolar diameters were measured with an image splitting method. Vascular reactivity was tested by local perivascular microapplication of mock cerebrospinal fluid (CSF) containing high and low levels of K+, high and low pH, adenosine and bradykinin before and after CSD which was triggered by intracortical injection of KCl. During CSD a monophasic vasodilatation of 26.0 +/- 3.7% (mean +/- S.E.M.; cat) or 64.6 +/- 3.9% (rat) was observed. Following CSD, the cat developed persistent vasodilatation (16.7 +/- 1.9%) while the rat exhibited vasoconstriction (12.1 +/- 1.8%). Both species displayed a severely impaired responsiveness to constrictor and dilating stimuli as compared to pre-CSD values. The responses were reduced by 28-84%, dependent on the substance tested. It is concluded that vascular reactivity is severely impaired after CSD (15-75 min) and that this might explain the impaired coupling between flow and metabolism after CSD.

Adenosine↗
PubMed1987

MEG source models and physiology.

We report in vitro experiments on the source(s) of the magnetic fields produced by the brain. Theoretical arguments suggest that the dominant sources should be dipolar and oriented parallel to the scalp. Using an isolated turtle cerebellum as a model, we find that the fields produced following dorsal stimulation are attributable to current flow perpendicular to the cerebellum surface, suggesting Purkinje cell sources. We also discuss observations of longer lasting fields associated with spreading depression induced in the cerebellum.

Brain↗
PubMed1987

Regional cerebral blood flow during cortical spreading depression in rat brain: increased reactive hyperperfusion in low-flow states.

The purpose of the present study was to characterize the initial vascular events accompanying cortical spreading depression (CSD) of the rat brain. Regional cerebral blood flow (rCBF) was measured during the first 1-2 min of CSD using 14C-iodoantipyrine autoradiography. The material included a reference group, and 4 groups where rCBF was altered by indomethacin treatment, hypo- or hypercapnia, or one previous episode of CSD. rCBF did not change prior to, or during the onset of CSD. Thirty seconds later, rCBF increased depending on the pre-existing level of blood flow, i.e. the rise of rCBF was pronounced at depressed flow levels, but small or absent at normal or high flow levels. The prevalent view that CSD is intimately associated with vasodilatation was accordingly not supported. The activated rCBF in normocapnic rats ranged between 93 and 175 ml/100g/min, supranormal values were the exception rather than the rule. The rCBF rise, when present, probably succeeds a period of brain hypoxia, and should be classified as a reactive hyperfusion. The results together with earlier clinical and experimental findings, support that CSD may serve as experimental migraine model.

Anesthesia, General↗
PubMed1987

Viscosity of plasma in patients with rheumatoid arthritis.

The viscosity of plasma (PV) was investigated in 27 outpatients with classical or definite rheumatoid arthritis (RA) according to the American Rheumatism Association (ARA) criteria. The measurements showed a significantly raised PV in patients with RA (p less than 10(-5)) compared with a control group. There was a positive correlation between the PV and the blood erythrocyte sedimentation rate (B-ESR), and the increase in the PV is largely explained by increased concentrations of the plasma proteins, fibrinogen, and IgG.

Adult↗
PubMed1987

Cerebral blood flow in migraine and cortical spreading depression.

Migraine is a common disease which expresses itself by paroxysmal headache, commonly accompanied by transient neurological symptoms. There are at the moment two important theories concerning the cerebral mechanisms of migraine: The vascular theory which attributes migraine to spasm of a cerebral artery causing local hypoxia and transient focal symptoms followed by neurogenically mediated extra- and/or intracranial vasodilation causing headache, i.e. migraine is understood in terms of a primary perturbation of blood vessel function. Another, but neglected viewpoint relates migraine to a paroxysmal, transient depolarization of primarily cortical neurones causing transient focal symptoms and headache, i.e. migraine is understood in terms of a primary perturbance of neuronal function. This review summarizes clinical and experimental studies concerning these two theories with special emphasis on classic migraine, i.e. paroxysmal headache accompanied by focal symptoms of short duration. At begin of the classic migraine attack regional cerebral blood flow (rCBF) declines in the posterior part of the brain. Subsequently the hypoperfused region expands anteriorly, independent of the territories of supply of the large cerebral arteries. This observation speaks clearly against reduced perfusion as consequence of arterial spasm. The rate of spread of the reduced perfusion is about 2 mm/min and the changes of perfusion appear to follow the cortex corresponding to the convexities. Tests of regulation of rCBF show normal blood pressure autoregulation, but reduced responsiveness to change of arterial carbon dioxide tension and in response to mental activation. These observations are consistent with arteriolar vasoconstriction as cause of reduced perfusion. Vascular tone at the arteriolar level is, however, mainly determined by local factors, and change of local neuronal function could therefore be the basis of increased arteriolar tone and reduced rCBF. Analysis of the time course of perfusion reduction and symptoms reveals that perfusion frequently declines before the patient experiences any focal symptoms. The focal symptoms frequently start after spread of the hypoperfusion has begun, but usually ceases altogether within another 30 minutes, while the reduced perfusion persists for a couple of hours, when the patient suffers from headache. This temporal relationship between symptoms and rCBF changes precludes that the focal symptoms are secondary to reduced rCBF. Furthermore, migraine headache is not related to increased rCBF. On this background the acute migraine attack can hardly be explained by a primary arterial vasospasm.(ABSTRACT TRUNCATED AT 400 WORDS)

Acute Disease↗
PubMed1986

Uncoupling of cerebral blood flow and metabolism after single episode of cortical spreading depression in the rat brain.

The present study was undertaken to evaluate whether the persistent hypoperfusion following cortical spreading depression (CSD) in rat brain was accompanied by alterations of regional cortical glucose consumption (rCGU). rCGU was measured using 2-deoxy-[14C]glucose and autoradiography at 15-60 min after single CSD episodes. rCGU did not differ in cortical regions invaded by CSD as compared to the contralateral side and to sham-treated rats. The results suggested impairment of the metabolism-flow couple after CSD.

Animals↗
PubMed1986

Classic migraine. A prospective recording of symptoms.

Systematic prospective records of aura symptoms were obtained from 50 patients, who filled in report forms during the aura phase of two attacks. The pattern of the various aura symptoms was remarkably constant during two attacks. Visual aura was recorded by 94% of the patients, somato-sensory aura symptoms by 40%, motor disturbances by 18% and speech difficulties by 20%. Visual aura was unilateral in 55%, somato-sensory aura symptoms were unilateral in 80% and motor aura was unilateral in 100%. Surprisingly, headache was absent in 20% of the aura attacks. When unilateral headache and unilateral aura symptoms occurred in the same attack, headache was most often contralateral to the somato-sensory and motor aura symptoms. Our observations are in accordance with the hypothesis that the pathophysiological process responsible for the aura symptoms in classic migraine starts at the visual cortex.

Adolescent↗
PubMed1985

Clinical trial of nimodipine for single attacks of classic migraine.

In a randomized, double-blind cross-over study, 43 patients with classic migraine received 40 mg Nimodipine and placebo as sublingual capsules. There was no significant effect on patients' preference, development of headache, need for escape medicine, duration of headache, severity of headache or headache index. Considerable methodological problems were encountered. Only 54% of the 79 patients selected for the trial could be evaluated. Suggestions for future trials are made.

Clinical Trials as Topic↗
PubMed1985

rCBF after TIA and during migraine attacks.

TIA is usually caused by embolism from a carotid stenosis. The stenosis has no hemodynamic significance, but recent studies of regional cerebral blood flow have indicated that this occurs in a few cases. Traditionally, TIA are not considered to cause cerebral damage, but CT-studies have revealed a number of silent infarcts and rCBF measurements have shown even more persistent abnormalities of blood flow. In classic migraine, alterations of rCBF are completely different, indicating a mechanism progressing in the cerebral cortex, probably the spreading depression of Leao. Similar blood flow changes are not seen in common migraine, where tomographic rCBF determinations have been normal.

Cerebrovascular Circulation↗
PubMed1985

On the possible relation of spreading cortical depression to classical migraine.

During the first 1 to 2 h of the classical migraine attack a hypoperfusion develops which starts in the posterior part of the brain and progresses anteriorly at a rate of 2-3 mm/min. The hypoperfusion stops at primary sulci outlining major cortical macro- and microstructural changes, but seems not to be inhibited by other changes of the cortical architecture. The low flow regions are cortical and the low flow persists for 4-6 h, until the attack abates. Regions of hyperperfusion are either minor or non-existent. A similar behavior characterizes the velocity and mode of evolution of a cortical spreading depression, a transient perturbation of cortical neuronal function which has profound and long-lasting influence on the cortical blood flow. This paper briefly summarizes the arguments which have been put forward in recent years suggesting that spreading depression is a pathogenetic mechanism of migraine.

Animals↗
PubMed1984

Long-lasting reduction of cortical blood flow of the brain after spreading depression with preserved autoregulation and impaired CO2 response.

The purpose of the present study was to examine the cerebral perfusion after spreading depression with special emphasis on its relation to the perfusion changes in migraine. The cerebrovascular reactivity to changes of arterial PCO2 tension in the range of 24-70 mm Hg and to changes of MABP in the range of 55-150 mm Hg was studied in the rat brain after one episode of cortical spreading depression. Regional CBF (rCBF) was measured in the frontal, parietal, and occipital cortex, the basal ganglia, and the cerebellum of both hemispheres after the intravenous bolus injection of [14C]iodoantipyrine. rCBF decreased in the cortical regions to 69-73% of control values for 1 h after spreading depression in every single rat, but remained unchanged in the basal ganglia and cerebellum. CBF changed with alterations of arterial carbon dioxide tension in all brain regions. In control regions, CBF changed by 2.8-3.9% per mm Hg PaCO2 change, whereas in the spreading depression cortex, CBF changed by only 1.3-1.5%. The difference between control and spreading depression cortex was significant at p less than 0.001, indicating a reduced CO2 sensitivity of the cortical regions invaded by spreading depression. rCBF remained unchanged in all brain regions in the MABP range of 80-150 mm Hg, reflecting the intact autoregulatory function of the two sides, and at a MABP of less than 80 mm Hg, rCBF decreased in parallel in symmetrical regions. It is concluded that the hypoperfusion after spreading depression is due to a vasoconstrictor stimulus overriding the vasodilatory effect of acid pH.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Regional cerebral blood flow during migraine attacks by Xenon-133 inhalation and emission tomography.

Regional cerebral blood flow (rCBF) was measured by single photon emission tomography, using Xenon-133 inhalation during migraine attacks. The method yields images of three brain slices, depicting rCBF with a spatial resolution of 1.7 cm. Twelve patients with common migraine showed a normal cerebral blood flow pattern during an attack. Of 11 patients with classical migraine, 8 displayed a unilateral region of hypoperfusion, while 3 had a normal flow pattern. The focal decrease of blood flow average 17 per cent as compared with the symmetrical contralateral region. The localization of the blood flow reduction corresponded to the tomographic representation of the lateral aspect of the cortex in 8 patients, while in one patient the mesial aspect also appeared to be involved. The low-flow regions were always on the side opposite to the focal neurological symptoms. The hypoperfusion remained through the headache period for four to six hours. Regions of relative or absolute hyperaemia were not observed during headache of either form of migraine. Between attacks, rCBF was normal except in one patient who had a minor low-flow region in the insula. The cortical distribution of the vasomotor changes in classical migraine appeared unrelated to the distribution of major cerebral arteries and may represent a manifestation of disturbed cerebral metabolism, possibly the spreading depression of Leão. Since classical migraine in most cases was associated with intracranial blood flow changes while common migraine was not, the study was taken to support that these two forms of migraine may differ, not only on a clinical basis, but also on pathophysiological grounds.

Adolescent↗