[Sumatriptan (Imigran) and migraine with aura--is the price too high?].
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Denmark↗
Biomedical subjects
T S Olsen
Publications and source records attributed to T S Olsen.
The distal nephron is preferentially infiltrated by inflammatory cells in acute interstitial nephritis.
In acute interstitial nephritis (AIN), mononuclear cells invade the tubules (tubulitis). The segmental localization of tubulitis is not precisely known. To clarify this question, formalin-fixed kidney biopsy specimens from 13 patients with AIN were studied stereologically by identifying cortical tubules with segment-specific markers. The periodic acid-Schiff reaction, peanut lectin, and antibodies against Tamm-Horsfall protein and epidermal cytokeratins all applied to the same section were used to identify the proximal tubules (PTs), distal convoluted tubules, distal straight tubules, and the cortical collecting system (connecting tubules and cortical collecting ducts), respectively. Morphometrically, an estimate of the relative volume of the inflammatory cell infiltrates within each category of tubular segments was obtained. Inflammatory cells were infrequently found in PTs (1.2%) but were frequently localized in distal tubules and the cortical collecting system (7.6%). There was no difference in the amount of the inflammatory cell infiltrate within these segments. Re-examination of an electron microscopic study of AIN carried out in this laboratory revealed that mononuclear cells were rarely seen in convoluted PTs but were frequently observed in straight PTs and all segments distal to them. The observations indicate that it is the distal nephron which is primarily affected by inflammatory cell infiltration in AIN.
Acute Disease↗
Early time course of N-acetylaspartate, creatine and phosphocreatine, and compounds containing choline in the brain after acute stroke. A proton magnetic resonance spectroscopy study.
BACKGROUND AND PURPOSE: The early time course after acute stroke of cerebral N-acetylaspartate, creatine and phosphocreatine, and compounds containing choline was studied in vivo by means of localized water-suppressed proton magnetic resonance spectroscopy. METHODS: Eight patients with acute stroke were studied serially in the acute phase, 1 week after, and 2-4 weeks after the onset of clinical symptoms. Ten healthy volunteers served as controls. A stimulated echo (STEAM) sequence was used for measurement of the brain metabolites in a volume of interest located within the infarcted area as visualized by magnetic resonance imaging. For quantification, the unsaturated water signal was used as the internal standard. Regional cerebral blood flow in the infarcted area was measured relative to a symmetrically located unaffected area by means of single-photon emission computed tomographic scanning, using 99mTc-labeled d,l-hexamethylenepropyleneamine oxime as the flow tracer. RESULTS: Relative regional cerebral blood flow was considerably reduced in the infarcted area in the acute phase. After 1 week, hyperemia was seen in all but one patient. The N-acetylaspartate content was significantly reduced, with the loss appearing to occur between 6 and 24 hours after the stroke incident. The reduction in N-acetylaspartate content was greater in the central part than in the peripheral part of the infarcted area. Creatine and phosphocreatine were also reduced in the infarcted area, whereas no significant change was seen in the choline content. CONCLUSIONS: Assuming that N-acetylaspartate content reflects neuronal survival or loss, our results may suggest that treatment procedures with restoration of blood flow to severely ischemic areas should be initiated within the first 6 hours after stroke onset.
Acute Disease↗
Hemolytic uremic syndrome in a patient with systemic sclerosis treated with cyclosporin A.
The case is presented of a 48-year-old female suffering from diffuse cutaneous systemic sclerosis (diffuse scleroderma) since 8 years, who went into renal failure as part of hemolytic uremic syndrome following 3 weeks' treatment with 3.8 mg/kg cyclosporin A. Hemolytic uremic syndrome has previously been described in transplant patients receiving cyclosporin A. There are also four cases reported in the literature of renal failure developing in middle aged females with diffuse cutaneous systemic sclerosis after short-term use of low dosage cyclosporin A treatment. It is suggested, that it may be wise not to use cyclosporin A to this category of patients, in which it can not be ruled out, that even a low dose therapy may trigger the rapid onset of scleroderma renal crisis or as in our case provoke hemolytic uremic syndrome.
Acute Disease↗
Postcapillary venule-like transformation of peritubular capillaries in acute renal allograft rejection. An ultrastructural study.
To describe ultrastructural changes in renal peritubular capillaries during acute allograft rejection, biopsy specimens from five allografts with acute rejection were studied electron microscopically and compared with control specimens. The thickness, cross-sectional area, and luminal circumference of capillary endothelium were estimated morphometrically. Thickening of endothelial cells, loss of fenestration, increase in endothelial cell organelles, increased adherence and passage of lymphocytes and monocytes, and defects in the endothelial lining were demonstrated. The luminal circumference representing the size of the capillary was not changed. A balloonlike fragmentation of endothelial cells was sometimes observed around lymphocytes, suggesting cytotoxic injury to capillaries. The observations indicate that during rejection-induced endothelial activation, peritubular capillaries exhibit postcapillary venule-like transformation that enhances the influx of inflammatory cells into the kidney allograft.
Adult↗
[Rehabilitation of patients with apoplexy. Possibilities, duration and effect].
A close relationship exists between the severity of a stroke and the functional level that can be obtained after rehabilitation. The goal of rehabilitation, therefore, should be based on the severity of the stroke. Remission mainly takes place (more than 80%) within the first three months post stroke. Remission after six months is very rare. Age and side of hemiparesis do not seem to influence the effect of rehabilitation significantly. It is not elucidated whether the severity of the stroke influence the effect of rehabilitation. Most of the controlled and the randomized studies indicate that rehabilitation of stroke patients, especially in rehabilitation units, accelerate remission, reduces length of stay and gives rise to a lasting improvement of function.
Adult↗
Migraine-related stroke in childhood.
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Cerebrovascular Circulation↗
Cerebrovascular instability in a subset of patients with stroke and transient ischemic attack.
In six patients, we observed remarkably unsteady blood flow and indications of vasospasms on the arteriolar level in connection with episodes of focal cerebral ischemia. The patients originated from a prospective consecutive study of 53 patients with stroke and transient ischemic attack who had been examined by cerebral angiography and rapidly repeated regional cerebral blood flow measurements using the intracarotid xenon 133 method. In 47 patients, regional cerebral blood flow values, flow patterns, and clinical condition were stable during the repeated regional cerebral blood flow measurements. In six patients, pronounced regional hypoperfusion and hyperperfusion developed during the course of examination. In the hypoperfused regions, flow was transiently reduced to values consistent with ischemia, and in four of these patients this was accompanied by transient neurological deficits. The arteriogram and isotope angiograms ruled out spasms of large arteries or thromboembolism. A condition of cerebrovascular instability on the arteriolar level probably was induced by the examination procedure. These patients were hypersensitive to the provoking stimuli either habitually or as a consequence of previous ischemic accidents. It is suggested that in some patients with focal cerebral ischemia, the primary cause might be spasms of the smallest resistance vessels rather than thromboembolism.
Aged↗
Immunohistochemical identification of tubular segments in percutaneous renal biopsies.
To identify the renal cortical tubular segments involved in tubulo-interstitial disease in formalin-fixed, paraffin-embedded percutaneous kidney biopsies, we developed multiple immunolabeling protocols using segment-specific tubular markers. The present study of biopsies from patients with minimal change or thin basement membrane nephropathy provides a baseline for interpretation of histopathology. Proximal tubules were stained either by the PAS reaction or by the biotinylated Phaseolus vulgaris erythroagglutinin (PHA-E)-streptavidin-gold-silver system (brush borders black). The anti-Tamm-Horsfall (THP) antibody-immunoperoxidase (aminoethylcarbazole, AEC-IPO), and anti-epidermal cytokeratins (ECK) antibodies-immunoalkaline-Fast Blue BB methods marked the distal straight tubules and the cortical collecting system red-brown and blue, respectively. When these immunolabelings were combined, the coapplication of AEC-PO-labeled peanut agglutinin (PNA) or anti-epithelial membrane antigen antibody-AEC-IPO technique (both are markers for distal nephron) visualized the apical membranes of distal convoluted tubules. In the protocol PHA-E + PNA + THP + ECK, the tubular basement membranes were outlined by the anti-laminin antibody-AEC-IPO staining, carried out simultaneously. The protocol PNA + THP + ECK + PAS was found to be quite appropriate multiple immunolabeling method for the tubules, and is recommended for use as a tool in the study of tubulo-interstitial diseases.
Adolescent↗
Outcome following occlusion of the middle cerebral artery.
Outcome was studied prospectively in 28 consecutive patients with occlusion of the middle cerebral artery (MCA). They comprise a subgroup of 101 consecutive patients with TIA or stroke less than or equal to 75 years of age, admitted within 72 h after the stroke. Cerebral angiography and CT-scan were performed within 1-2 days of admission. CT-scan was repeated 6 months later. Functional status on admission, 3 and 6 months after the stroke was evaluated using the Rankin disability scale (score 1-2: independent of others care, score 3-5: dependent on others care). The degree of hemiparesis was measured using the Medical Research Council's score. Thirteen had infarcts with a diameter less than or equal to 3 cm (mean 2.5 +/- 0.9 cm); 15 had infarcts greater than 3 cm (mean 6.3 +/- 1.4 cm); 10 had trunk occlusions; 18 had branch occlusions. MCA occlusions with large infarcts and severe hemiparesis on admission carried a poor outcome. Eleven (85%) of 13 patients with the case in only 1 (7%) of the 15 with infarcts greater than 3 cm, the remaining 14 (93%) had either died (40%) or were dependent (53%) (p less than 0.00005). Eleven (85%) of 13 patients with mild hemiparesis on admission were independent, while 13 (87%) of 15 with moderate or severe hemiparesis on admission had either died (40%) or were dependent on others' care (47%) 6 months after the stroke (p less than 0.0004). Type of occlusion (branch trunk) was a poor predictor of outcome.
Cerebral Arterial Diseases↗
[Rehabilitation of stroke patients. Possibilities, duration and effect].
A close relationship exists between the severity of a stroke and the functional level that can be obtained after rehabilitation. The goal of rehabilitation, therefore, should be based on the severity of the stroke. Remission mainly takes place (more than 80 per cent) within the first three months post stroke. Remission after six months is very rare. Age and side of hemiparesis do not seem to influence the effect of rehabilitation significantly. It is not elucidated whether the severity of the stroke influence the effect of rehabilitation. Most of the controlled and the randomized studies indicate that rehabilitation of stroke patients, especially in rehabilitation units, accelerate remission, reduces length of stay and gives rise to a lasting improvement of function.
Activities of Daily Living↗
Portal hypertension without liver cirrhosis in renal transplant recipients.
A rare syndrome of portal hypertension with esophageal varices but without evidence of cirrhosis in the liver biopsy was seen in 3 patients in a series of 1000 renal allotransplant recipients immunosuppressed with azathioprine and prednisone. The liver disease began 3-6 years after transplantation with abnormal liver function tests and esophageal varices with bleeding episodes. One patient had also ascites. Liver biopsy at the beginning of liver disease showed in one patient normal structure which eventually developed to slight diffuse fibrosis and nodular hyperplasia. One patient had diffuse fibrosis, and the third patient had strong sinusoidal engorgement with nodular hyperplasia, later on developing to cirrhosis. One patient is still alive and well, the two others died from liver insufficiency. 39 cases of non-cirrhotic portal hypertension in renal transplant recipients and histologic evidence of peliosis, sinusoidal dilatation, nodular hyperplasia or hepatic veno-occlusive disease have been identified in the literature. The cause of this disease is presumably azathioprine, but its rarity shows that it must depend also on other factors.
Adult↗
Radiologic manifestations of focal cerebral hyperemia in acute stroke.
In 16 acute stroke patients with focal cerebral hyperemia angiography and regional cerebral blood flow (rCBF) were studied 1 to 4 days post stroke. CT was performed twice with and without contrast enhancement 3 +/- 1 days and 16 +/- 4 days post stroke. Angiographic evidence of focal cerebral hyperemia was seen in 8 patients in the form of early filling veins. In 5 of these the hyperemic areas were located within infarcted areas and in 3 patients in areas which appeared normal on CT. In the remaining 8 patients the hyperemias were located perifocally around ischemic infarcts. Early filling veins were not seen in this type of hyperemia. The blood flow was higher and the transit time of the contrast medium was faster in the former type of hyperemia probably because of arteriovenous shunting. Contrast enhancement was not observed on the early CT but was typically seen in the infarcts on the late CT at a time when the hyperemic state is known to have vanished. It is concluded that focal cerebral hyperemia is not responsible for contrast enhancement on CT.
Acute Disease↗
[Migraine aura--vascular or neuronal disease?].
During the migraine-aura cerebral blood flow (CBF) is reduced in areas corresponding to the neurological deficits and symptoms. Whether this CBF reduction is the primary cause of the neurological deficits (the vascular theory) or a secondary result of primary neuronal dysfunction in particular "spreading depression" (SD) (the neurogenic theory) is still under discussion. The latter theory is supported by CBF investigations performed during attacks of migraine with aura (MA). The CBF reduction was found to be modest (20-35%) and not sufficient to cause ischemia which usually demands reduction of CBF by more than 50%. In addition the low-flow area appeared to "spreading" in the same manner as that seen in SD in the rat ("spreading oligemia"). Recent studies indicate, however, that the CBF reduction in most cases, after all, is sufficient to cause ischemia and that "spreading oligemia" might be an artifact caused by "scattered radiation". Persistent neurological deficits, EEG abnormalities and infarcts on CT-scans are seen after MA, thus further supporting the theory of vascular dysfunction (vasospasm) and ischemia as the cause of the migraine-aura.
Cerebrovascular Circulation↗
[Migraine aura as the cause of apoplexy in young adults].
In the five year period 1972-1977, 27 patients aged 15-45 years were admitted to a neurological department in the Copenhagen area because of acute focal neurological deficits, lasting more than 24 hours and of presumably vascular origin i.e. stroke. In seven cases, the neurological deficits were of thromboembolic origin and in further seven cases the deficits occurred in relation to migraine with aura. Two cases were classified as migraine-equivalents. In the remaining eleven cases it was not possible to decide whether the persisting neurological deficits were of migrainous or thromboembolic origin. Nine of these 11 patients were women. Nine had headache and six had nausea/vomiting or photo/phonofobia. Cerebral angiography was performed in five of these 11 patients and in all the angiograms were normal. Migraine-aura was most probably the cause of the persisting deficits in some of these 11 patients. It is concluded, that migraine-aura is relatively often the cause of stroke in young adults.
Adolescent↗
[Migraine with aura (classical migraine) in patients examined for cerebrovascular disease].
Four patients were investigated for cerebrovascular origin of focal neurologic deficits. Three of the patients had persistent deficits. However, during cerebral angiography and subsequent regional cerebral blood flow (rCBF) investigation all patients developed attacks of migraine with aura. During the rCBF study focal reduction of the blood flow, typical for migraine with aura, developed in the posterior brain regions. It is concluded that vasospasm of migrainous origin might be the cause of the neurological deficits in the four patients.
Adult↗
Timing and topography of cerebral blood flow, aura, and headache during migraine attacks.
Ten years of study has resulted in considerable but fragmented knowledge about regional cerebral blood flow in migraine with aura (classic migraine). In the present study, the number of repeatedly studied patients (n = 63) was large enough to determine statistically significant sequences of events and statistically significant spatial relations. The first observable event was a decrease of regional cerebral blood flow posteriorly in one cerebral hemisphere. Further development of this pathological process was accompanied by the aura symptoms. Thereafter headache occurred while regional cerebral blood flow remained decreased. During the headache phase, regional cerebral blood flow gradually changed from abnormally low to abnormally high without apparent change in headache. In some patients headache disappeared while regional cerebral blood flow remained increased. Although regional cerebral blood flow reduction and aura symptoms in the great majority of patients were unilateral, one-third had bilateral headache. Unilateral headache usually localized to the side on which regional cerebral blood flow was reduced and from which the aura symptoms originated (i.e., aura symptoms were perceived to occur contralaterally but presumably originated in the hypoperfused hemisphere). Our results suggest a simple model for migraine attacks: A pathological disturbance in one cerebral hemisphere causes the aura symptoms and after a time delay, it also causes the headache by stimulating local vascular nociceptors. Bilateral headache caused by a unilateral cerebral disturbance may be explained by recent neuroanatomical and neurophysiological findings.
Adolescent↗
Severe non-occlusive ischemic stroke in young heroin addicts.
Two heroin addicts, aged 30 and 35 years, developed severe ischemic stroke shortly after intravenous injection of heroin. Arteriograms, CT-scans, and Technesium-99 scintigrams demonstrated non-occlusive extensive infarctions in the carotid territory. Cerebral blood flow investigation in one showed severe hyperemia of the entire left carotid artery territory, including areas, where infarction did not develop. Stroke was not due to arterial occlusion. It was more likely due to generalized hypoxia combined with decreased perfusion pressure in the carotid territory on one site because of external compression of the carotid artery during the intoxicated comatose state.
Adult↗