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Biomedical subjects

M Juhler

Publications and source records attributed to M Juhler.

At least 37 records · Page 2Linked to original sources
PubMed1997

Lower urinary tract symptoms in lumbar root compression syndromes: a prospective survey.

STUDY DESIGN: A prospective, observational survey. OBJECTIVES: To describe lower urinary tract symptoms in uncomplicated lumbar root compression syndromes with special reference to prevalence, nature, and severity, and to analyze whether the occurrence of lower urinary tract symptoms correlates with age, pain, analgesic intake, or the type and level of compression. SUMMARY OF BACKGROUND DATA: Lower urinary tract symptoms with lumbar root compression are well known in the classic but rather rare cauda equina syndrome. However, micturition difficulties seem to be far more frequent in lumbar root compression syndromes. METHODS: One hundred eight male patients admitted for surgery for lumbar disc herniation or spinal stenosis were investigated with an extensive questionnaire about their micturition. RESULTS: Fifty-five percent had significant lower urinary tract symptoms. Eighty percent of the patients with spinal stenosis had symptoms. Thirty-three patients had irritative symptoms, 36 had obstructive symptoms, and 23 had retention symptoms. Twenty-four had severe symptoms. Median compression resulted in more symptoms than paramedian compression. There was no correlation between age, level of compression, drug intake, or pain score and lower urinary tract symptoms. CONCLUSIONS: Lower urinary tract symptoms of mixed type occur with a high prevalence in male patients with lumbar root compression syndromes referred for neurosurgical evaluation and treatment.

Adult↗
PubMed1997

Frontal brain and leptomeningeal biopsy specimens correlated with cerebrospinal fluid outflow resistance and B-wave activity in patients suspected of normal-pressure hydrocephalus.

OBJECTIVE: Normal-pressure hydrocephalus (NPH) is a potentially treatable syndrome with abnormal cerebrospinal fluid dynamics. Meningeal fibrosis and/or obliteration of the subarachnoid space has been suggested as the pathoanatomic basis. The purpose of the present study was to investigate whether meningeal fibrosis causes increased resistance to cerebrospinal fluid outflow (R(out)) and/or increased B-wave activity and whether pathological changes in the brain parenchyma after brain compliance, causing increased B-wave activity. METHODS: The study involved a group of 38 consecutively studied patients with clinical and radiological evidence of idiopathic NPH, for whom a frontal brain biopsy was obtained. For 29 patients, hydrodynamic criteria of NPH were fulfilled and a ventriculoperitoneal shunt was performed. RESULTS: Meningeal fibrosis was found in 12 of 25 biopsies containing arachnoid tissue, but no correlation with R(out) or B-waves was found. Pathological parenchymal changes, most often Alzheimer's disease (10 cases) or vascular changes (10 cases), were found in 21 biopsies, but no correlation with B-waves or R(out) was found. CONCLUSION: The results suggest that leptomeningeal fibrosis is not the only pathoanatomic basis of increased R(out) and/or B-wave activity in patients with NPH and that various degenerative changes in the parenchyma may be responsible for the altered cerebrospinal fluid dynamics characteristic of NPH.

Adult↗
PubMed1997

Effects of morphine and naloxone on cerebral blood flow and metabolism in experimental subarachnoid hemorrhage.

OBJECTIVE: Naloxone is reported to improve the clinical condition of patients with subarachnoid hemorrhage (SAH). If this effect is vascular determined is unknown, wherefore the influence of morphine and naloxone on cerebral blood flow (CBF) and metabolic rate of oxygen (CMRO2) after SAH was evaluated. MATERIAL AND METHODS: Two groups of 8 rats each with SAH and 2 corresponding groups of controls were investigated. CBF was calculated by the intracarotid 133Xenon method and CMRO2 as the product of CBF and the difference between systemic arterial and cerebral venous oxygen content. RESULTS: In controls morphine, 1 mg/kg administered intravenously, decreased CBF by 25% (P < 0.001) without changing the CBF/CMRO2 ratio. In animals with SAH CBF was decreased by 32% (P < 0.001) and CBF/CMRO2 ratio by 38% (P < 0.01). Naloxone, 40 micrograms/kg administered intravenously neither influenced CBF nor the CBF/CMRO2 ratio in the 2 groups. CONCLUSION: The reported clinical effect of naloxone after SAH can, according to our results, not be explained by changing the relationship between CBF and metabolism.

Analgesics, Opioid↗
PubMed1996

Reduction of cerebral cortical [3H]ouabain binding site (Na+,K(+)-ATPase) density in dementia as evaluated in fresh human cerebral cortical biopsies.

Na+,K(+)-ATPase density in human cerebral cortex was for the first time studied by vanadate facilitated [3H]ouabain binding to intact samples. Fresh human cerebral cortical biopsies were obtained as a result of diagnostic frontal lobe biopsy from patients with normal pressure hydrocephalus (NPH) syndrome and associated dementia. For control measurements post-mortem samples were obtained from patients without clinically observed dementia. [3H]ouabain binding kinetics were evaluated: when incubating samples in 1 microM [3H]ouabain binding equilibrium was obtained after 6 h of incubation, non-specific uptake and retention amounted to only 2.3% of total uptake and retention of [3H]ouabain and release of specifically bound [3H]ouabain during washout in the cold occurred only slowly (T1/2 = 37 h). Evaluation of receptor affinity for ouabain was in agreement with a heterogeneous population of [3H]ouabain binding sites. [3H]Ouabain binding was significantly reduced after frozen storage of samples before measurements. Post-mortem degradation of cerebral [3H]ouabain binding sites occurred only slowly (T1/2 = 75 h). No significant variation in [3H]ouabain binding site density was observed between the cerebral lobes with occipital, parietal and temporal values (means +/- S.E.M., n = 5) amounting to 10281 +/- 649, 11267 +/- 1011 and 9263 +/- 615 pmol/g wet wt., respectively. [3H]Ouabain binding measured in frontal cortical samples gave values of (means +/- S.E.M., n = 5) 4274 +/- 1020 and 11397 +/- 976 pmol/g wet wt. delta % = 62; P < 0.05) in patients with dementia and controls, respectively. Human cerebral cortical capacity for active K+ uptake was around 37- and 16-fold greater than in skeletal muscular and myocardial tissue, respectively.

Aged↗
PubMed1995

The effect of nimodipine on autoregulation of cerebral blood flow after subarachnoid haemorrhage in rat.

Disturbance of the autoregulation of the cerebral blood flow (CBF) is frequently seen following subarachnoid haemorrhage (SAH) and is possibly partly caused by cerebral ischaemia. It is well-known, that the calcium channel blocker nimodipine reduces the incidence of cerebral infarction and ischaemic dysfunction after SAH. The aim of the present study was to investigate the effect of nimodipine on autoregulation of CBF in an experimental model of SAH. The autoregulation was investigated in 10 control rats with SAH and in 10 nimodipine treated rats with SAH by serial measurements of CBF using a 133Xenon intracarotid injection method during controlled blood pressure manipulations. In the control rats the autoregulation was severely disturbed, no plateau was found where CBF was independent of changes in the arterial blood pressure (MABP). In rats treated with intravenous nimodipine (0.03 mg/kg body weight/h), CBF was 33.0% higher and MABP 5.3% higher compared with the controls. CBF was found constant in the MABP interval between 60 and 100 mmHg which indicates, that nimodipine improves the autoregulation of CBF after SAH.

Animals↗
PubMed1995

Heterogeneous cerebral glucose metabolism in normal pressure hydrocephalus.

The regional cerebral metabolic rate for glucose (rCMRglu) has never been investigated in large consecutive groups of patients with normal pressure hydrocephalus (NPH), a potentially treatable form of dementia with an unpredictable outcome after shunt surgery. Using PET and 18F-2-fluorodeoxyglucose, rCMRglu was studied in 18 patients who fulfilled hydrodynamic criteria for NPH and in whom a biopsy of the frontal cortex was obtained. When compared with an age matched group of 11 healthy subjects, the patients with NPH showed a significant rCMRglu reduction in all cortical and subcortical regions of interest. Individual metabolic patterns, however, disclosed a large topographical heterogeneity. Furthermore, histopathological examination identified Alzheimer's disease or cerebrovascular disease in six cases, and no parenchymal disease or non-specific degenerative processes in the remaining 12. After separating the patients according to the histological diagnosis, the rCMRglu patterns were still heterogeneous, the abnormalities ranging from focal to diffuse in both subgroups. After shunt operation, 11 patients did not improve or worsened clinically. Six patients improved; of those, two had Alzheimer changes and two cerebrovascular changes in their biopsy. The metabolic pattern of these six patients did not differ from the rest of the NPH group. The results indicate that the NPH syndrome may be non-specifically associated with different degenerative disorders. The metabolic heterogeneity, together with the heterogeneous histopathological findings, indicate the necessity of reevaluating the pathogenesis of the NPH syndrome, and may account for the high variability in the success rate of shunt surgery series.

Aged↗
PubMed1994

Cerebral blood flow autoregulation in acute intracranial hypertension.

The present series of experiments was carried out to investigate CBF autoregulation during fixed levels of acute increased intracranial pressure (ICP). Three groups of six rats each, one with normal ICP (8 mmHg), one with moderately increased ICP (30 mmHg), and one with severely increased ICP (50 mmHg), were investigated. ICP was maintained by continuous infusion of lactated Ringer solution into the cisterna magna. Cerebral perfusion pressure (CPP), calculated as mean arterial blood pressure--ICP, was increased by intravenously infused norepinephrine and decreased by controlled bleeding. In all groups the corresponding autoregulation curve included a plateau where CBF was independent of changes in CPP, demonstrating intact autoregulation. However, a significant shift of the lower limit of autoregulation (LL) toward lower CPP levels during severe intracranial hypertension was observed (p < 0.006). In the controls the LL was found at CPP = 73 +/- 6 mmHg, in moderately increased ICP the LL was 59 +/- 4 mmHg, and in severely increased ICP the LL was 51 +/- 4 mmHg. These results indicate that an acute elevation of ICP activates a reserve capacity of cerebral resistance vessels that dilate further below the normal physiological LL to maintain CBF at low levels of CPP.

Animals↗
PubMed1993

Cerebral blood flow autoregulation after experimental subarachnoid hemorrhage during hyperventilation in rats.

The purpose of the current study was to investigate whether impaired cerebral blood flow (CBF) autoregulation after experimental subarachnoid hemorrhage (SAH) could be restored by hyperventilation. SAH was induced in rats by injection of autologous blood into the cisterna magna. CBF was measured using intracarotid injection of 133Xe. Autoregulation was studied in four groups of animals: normoventilated controls, hyperventilated controls, normoventilated animals with SAH, and hyperventilated SAH animals. PaCO2 in the normocapnic groups was 38-42 mm Hg and 25-30 mm Hg in the hypocapnic groups. CO2 reactivity after SAH was intact as hyperventilation decreased CBF by 38% in controls and by 46% in animals with SAH. Mean arterial pressure (MAP) was unaffected in both groups. In the controls, hypocapnia caused a shift of the autoregulation curve toward lower CBF levels without changing the lower limit of autoregulation. In the SAH group in the normocapnic state, autoregulation was absent as the obtained curve was a straight line, such that CBF increased with increasing MAP. However, during hypocapnia CBF was constant in the MAP interval between 60-150 mm Hg showing reestablishment of autoregulation by hyperventilation.

Animals↗
PubMed1992

Cerebral blood flow autoregulation in experimental subarachnoid haemorrhage in rat.

Haemodynamic instability is of great importance in clinical management of patients with subarachnoid haemorrhage (SAH). The significance of angiographically demonstrable vasospasm for disturbances of cerebral blood flow (CBF) and cerebral autoregulation has not yet been clarified. The present study was designed to describe disturbances of cerebral autoregulation during the timecourse of experimental SAH (eSAH) in rats. A second aim of the study was to relate the results to a reported timecourse of angiographic vasospasm in the same animal model. Previous studies have shown that the timecourse of angiographically visible vasospasm in eSAH is biphasic with maximal spasm at 10 min and 2 days after induction of eSAH. At 5 days, the vasospasms have resolved. CBF was measured using a 133-Xenon intracarotid injection method which allowed serial measurements of mean hemispheric CBF during controlled manipulations of arterial blood pressure. In this way, an autoregulation curve could be constructed. The present study shows that autoregulation is severely disturbed or even totally absent at 2 and 5 days after eSAH. Thus there seems to be no direct correlation between presence of angiographic vasospasm and impairment of autoregulation, or that the impairment of autoregulation is more protracted than the presence of cerebral vasospasm, presuming a correlation exist.

Acid-Base Equilibrium↗
PubMed1992

Hyponatraemia in acute brain disease.

Hyponatraemia (HN) can result from a wide range of mechanisms, and therapy must be individualized. Two theories of the origin of HN in acute brain disease have prevailed. The first is the cerebral salt wasting syndrome (CSWS), where excessive natriuresis caused by some unknown cerebral natriuretic factor lowers the total sodium pool of the body and hence the plasma concentration. The second theory is the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), where an increase in total body water is caused by unphysiological secretion of ADH, lowering the concentration of sodium in the plasma. A third possibility is 'sodium shift', i.e. a displacement of sodium from the extracellular to the intracellular space with a simultaneous movement of potassium in the opposite direction. The morbidity and mortality associated with HN only arise in cases where the rate of development of HN was 0.5 mmol h-1 or more. Symptoms respond promptly when the HN is quickly corrected with furosemide and 3% sodium chloride.

Acute Disease↗
PubMed1989

Hemodilution increases cerebral blood flow in acute ischemic stroke.

We measured cerebral blood flow in 10 consecutive, but selected, patients with acute ischemic stroke (less than 48 hours after onset) before and after hemodilution. Cerebral blood flow was measured by xenon-133 inhalation and emission tomography, and only patients with focal hypoperfusion in clinically relevant areas were included. Hemodilution was done according to the hematocrit level: for a hematocrit greater than or equal to 42%, 500 ml whole blood was drawn and replaced by the same volume of dextran 40; for a hematocrit between 37% and 42%, only 250 ml whole blood was drawn and replaced by 500 cc of dextran 40. Mean hematocrit was reduced by 16%, from 46 +/- 5% (SD) to 39 +/- 5% (SD) (p less than 0.001). Cerebral blood flow increased in both hemispheres by an average of 20.9% (p less than 0.001). Regional cerebral blood flow increased in the ischemic areas in all cases, on an average of 21.4 +/- 12.0% (SD) (p less than 0.001). In three patients, a significant redistribution of flow in favor of the hypoperfused areas was observed, and in six patients, the fractional cerebral blood flow increase in the hypoperfused areas was of the same magnitude as in the remainder of the brain. In the last patient, cerebral blood flow increased relatively less in the ischemic areas. Our findings show that cerebral blood flow increases in the ischemic areas after hemodilution therapy in stroke patients. The marked regional cerebral blood flow increase seen in some patients could imply an improved oxygen delivery to the ischemic tissue.

Acute Disease↗
PubMed1988

Pathophysiological aspects of acute experimental allergic encephalomyelitis.

Traditionally, research in experimental allergic encephalomyelitis (EAE) has focussed on immunological and histopathological aspects. The present review introduces a physiological approach to EAE. As EAE is characterized by many small, focal lesions in the central nervous system (CNS), methods with a high spatial resolution should be used to conduct studies on regional pathophysiology in the condition. Quantitative autoradiography seems an ideal method as it offers, 1) high regional resolution (approximately 50 um), 2) precise quantitation and, 3) a direct correlation between regional histopathology and pathophysiology. By the use of this method, the author has performed studies on 1) regional blood-brain barrier (BBB) permeability, and 2) regional metabolism of energy substrate and related subjects, (i.e. regional cerebral blood flow, regional cerebral glucose metabolic rate and regional pH). Corresponding to the EAE lesions (lymphocytic accumulations), there is a considerable increase in BBB permeability. Metabolism of energy substrate at the lesion sites is severely deranged, which is expressed in a CBF/CMR ratio of 3 ml/mumol compared to the normal 1.5 ml/mumol. No changes in regional pH are seen in the lesions. Unrelated to the lesion sites there is a 50% decrease in blood flow in cerebral cortex. This observation probably reflects a functional decrease in cortical flow due to sensory motor impairment.

Animals↗
PubMed1988

Danish very-low-dose aspirin after carotid endarterectomy trial.

The effect of very-low-dose aspirin as an antithrombotic agent was evaluated blindly in 301 patients who had recently undergone carotid endarterectomy. After randomization, 150 patients received aspirin and 151 received placebo. The two groups were comparable with regard to age, sex, blood pressure, previous cerebrovascular events, and smoking habits. The effect of the study medication on platelet aggregation was measured twice in each patient during the first 2 months and at each follow-up visit; the dose was individually adjusted. In 76% of the patients receiving aspirin, 50 mg/day gave satisfactory platelet inhibition, 13% needed 60 mg/day, 8% needed 70 mg/day, and 3% needed 100 mg/day. Platelet aggregation was found to be inhibited in only 1.2% of the measurements in the patients receiving placebo. Observation during treatment averaged 21 months; total intention-to-treat follow-up averaged 25 months. For the combined outcome events of transient ischemic attack, stroke, acute myocardial infarction, and vascular death, aspirin reduced risk by 11% (95% confidence limits: -38% to 48%, p greater than 0.1). Thus, there was no significant effect of very-low-dose aspirin in our trial.

Aspirin↗
PubMed1988

The course of transient ischemic attacks.

Seventy-eight patients admitted with their first cerebrovascular episode of presumed ischemic origin were evaluated during the first 24 hours to decide whether the differential diagnosis of stroke versus transient ischemic attacks (TIAs) could be made earlier than after 24 hours, if the initial degree of neurologic deficit and the persistence of symptoms beyond a certain limit of time were taken into account. Within 1 hour, 50% of TIA cases had recovered, and 90% had recovered within 4 hours. Neurologic deficit graded by a score at onset was significantly less in TIA patients than in stroke patients. We concluded that persistence of symptoms beyond a few hours and to a lesser extent the severity of symptoms at onset or at admission give a reliable indication of the diagnosis.

Arterial Occlusive Diseases↗
PubMed1987

Cation permeability of the blood-brain barrier in streptozotocin-diabetic rats.

Decreased sodium permeability across the blood-brain barrier occurs in streptozotocin-treated rats after 2 weeks of diabetes. To establish whether this is a phenomenon specific for cations, the blood-brain barrier permeability for sodium, potassium and calcium was studied with an arterial integral uptake technique. Experiments were performed in control rats and, after two weeks after diabetes induction, in untreated streptozotocin-diabetic rats and in insulin-treated streptozotocin rats. In untreated diabetes, the neocortical blood-brain barrier permeability for sodium decreased by 35% (5.2 +/- 1.7 vs 3.4 +/- 1.1 10(-5).cm3.s-1.g-1) and potassium permeability by 39% (19.8 +/- 5.7 vs 12.1 +/- 3.9 10(-5).cm3.s-1.g-1), whereas no differences in calcium permeability occurred. Insulin treatment was associated with an increase in the blood-brain barrier permeability to sodium (4.8 +/- 1.0 10(-5).cm3.s-1.g-1) as compared to untreated diabetes (3.4 +/- 1.1 10(-5).cm3.s-1.g-1). It is concluded that the observed changes in sodium and potassium permeability cannot be caused by electrostatic membrane changes. More specific abnormalities of the transport of sodium and potassium across the blood-brain barrier are likely to occur; disturbances in the sodium-potassium-pump activity could account for such alterations.

Animals↗
PubMed1987

A method for 14C and 3H double-label autoradiography.

The present study describes and validates a 3H/14C double-label autoradiographic method in which separation of the labels was obtained by sequential film exposures to film types sensitive to 14C only and to both 3H and 14C, respectively. The error in assuming a pure 14C image on the first film was 2-3%. A linear subtraction equation was developed for calculation of the 3H activity expressed in 14C equivalents as the difference in tissue activity between the second and the first film exposure. The actual 3H activity in the tissue could be obtained by multiplying the result by 25 (14C to 3H conversion factor). The subtraction procedure was validated for absolute 14C and 3H activities of 100-1,300 nCi/g and 600-11,000 nCi/g, respectively, and for relative 3H/14C activities between 5 and 10. Self-absorption of 3H in white matter was corrected for by multiplication by 1.61 (self-absorption coefficient). This factor was close to unity for 14C.

Animals↗
PubMed1987

Simultaneous determination of regional cerebral blood flow, glucose metabolism, and pH in acute experimental allergic encephalomyelitis.

Regional cerebral blood flow (rCBF), regional cerebral glucose metabolic rate (rCMR), and regional pH (r-pH) were measured simultaneously in fulminant acute experimental allergic encephalomyelitis (EAE) by the use of triple-label autoradiography. No changes were found in the absence of lesions (lymphocytic accumulations). In the lesions, rCBF was 79% increased and rCRM was 13% increased, whereas r-pH was unaltered compared to normal values. The reported changes result in a CBF/CMR ratio of almost 3 in the lesions compared to the normal value of 1.5. The changes may be interpreted as primary disturbances in glucose metabolism, resulting in a secondary increase in CBF. This theory is supported by quoted observations on abnormal morphology and abnormal enzyme content in brain mitochondria in EAE.

Acute Disease↗