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E Waldenlind

Publications and source records attributed to E Waldenlind.

At least 19 recordsLinked to original sources
PubMed2006

beta-Receptor response to noradrenaline in cluster headache. A study of adipose tissue lipolysis.

We have previously shown decreased lipolysis in both phases of cluster headache (CH), as an indication of a sympathetic dysregulation. Reduced lipolysis could be a result of diminished beta-receptor sensitivity in adipose tissue. The aim of this study was to measure the lipolytic response to noradrenaline in 10 CH patients in remission and in 10 healthy subjects, to estimate beta-receptor function. Microdialysis technique was used to measure the increase of glycerol, the end-product of lipolysis, during infusion of noradrenaline into the adipose tissue. Noradrenaline infusion resulted in a distinct elevation of glycerol. The average glycerol increase was significantly higher in CH patients (121% +/- 48) than in healthy subjects (77% +/- 41) (P < 0.05), which indicates increased beta-receptor response to noradrenaline in CH patients in remission. This may be due to up-regulated beta-receptor sensitivity, secondary to reduced sympathetic outflow and a primary autonomic disturbance in CH.

Adipose Tissue↗
PubMed2005

Lipolysis in smokers during tobacco withdrawal: a pilot study.

OBJECTIVE: Nicotine has an influence on several metabolic events, such as lipid metabolism. Habitual smoking increases plasma levels of glycerol as well as noradrenaline, which is the main stimulating hormone of adipose tissue lipolysis. However, the long-term effect of smoking on lipolysis is unclear. We compared nocturnal lipolysis in habitual smokers during short-term tobacco withdrawal with a control group of non-smokers. MATERIAL AND METHODS: Sixteen healthy subjects (9 heavy smokers and 7 non-smokers) were recruited in the study. The smokers were not permitted to smoke for at least 7 h before the test. The microdialysis technique was used to measure glycerol levels, the end-product of lipolysis, in subcutaneous adipose tissue. Variations in adipose tissue blood flow were measured using the ethanol technique. Glycerol, lactate and glucose concentrations as well as ethanol outflow/inflow ratio were measured between 2400 and 0600 h. RESULTS: There were no significant differences in subcutaneous glycerol or glucose concentrations between smokers and non-smokers. Between 0300 and 0600 h, lactate levels in smokers were lower than those in non-smokers. Adipose tissue blood flow did not differ between the groups. CONCLUSIONS: Despite potent acute and direct effects of smoking on lipolysis, we could not find any significant differences in basal lipolysis rate between smokers during short-term tobacco withdrawal and non-smokers.

Blood Glucose↗
PubMed2005

Familial cluster headache. Is atypical cluster headache in family members part of the clinical spectrum?

Familial cluster headache (CH) was analysed in 21 Swedish families. Diagnosis was made according to The International Classification of Headache Disorders 2004. We identified 55 affected, of whom 42 had episodic or chronic CH, one had probable CH and 12 had atypical symptoms. The atypical cases did not fulfil the diagnostic criteria for CH, but had clinical symptoms with more resemblance to CH than to migraine or other trigeminal autonomic cephalgia syndromes. The overall male : female ratio was 1.8:1. The overall mean age at onset was significantly lower in the second/third generation than in the first generation (mean age at onset 22 vs. 31 years, SD +/- 7 vs. 13 years; P < 0.01). This may be anticipation or selection bias, since individuals with late age at onset from the second/third generation may not yet have symptoms. The prevalence of migraine was 24% (13/55), i.e. similar to the prevalence in the general population. The high incidence of atypical CH cases in the Swedish families with other members affected with CH may suggest that the spectrum of CH is broader than previously thought. We suggest that atypical CH in CH families may represent an expanded spectrum of the disease with a common aetiology, i.e. a common genetic background.

Adult↗
PubMed2004

Periods of cluster headache induced by nitrate therapy and spontaneous remission of angina pectoris during active clusters.

Glyceryl trinitrate (GTN) is known to induce single extra attacks of cluster headache (CH) during active cluster periods, most probably via actions of nitric oxide (NO). Induction of whole periods of CH by organic nitrates has, however, attracted little attention in the literature. We report on eight patients with episodic CH and coexistent effort-induced angina pectoris. Cases 1-6 had been free of their headaches for many years but got recurrence of CH within a few weeks after the administration of long-acting organic nitrates (isosorbide-dinitrate, isosorbide-5-mononitrate or slow-release GTN) aimed at treating their chest pains. These nitrate-induced headache periods were more severe and had a longer duration than the previous spontaneous ones. Furthermore, one of the subjects and two additional cases experienced a marked reduction of their anginal attacks during successive CH periods. Exercise time to effort-induced angina was increased in all three patients and one of them revealed a markedly elevated threshold for eliciting ischaemic cardiac symptoms by standardized physical exercise on a cycle ergometer. We hypothesize whether extra CH periods elicited by sustained nitrate therapy and remission of angina pectoris during active clusters are caused by central mechanisms involving inhibition of sympathetic tone and effects on both cranial vessels and cardiac functions.

Adolescent↗
PubMed2003

A note on cluster headache in a population-based twin register.

Evidence of a familial risk factor in cluster headache is accumulating and studies of twin concordance may resolve family resemblance into genetic and environmental influences. The past literature on cluster headache in twins comprises a few case reports of concordant monozygotic pairs. Swedish twin pairs with a diagnosis of cluster headache were selected through a cross-match of national registers of twin births and hospitalizations. Seventeen discordant twin pairs were found, in which it was possible to verify cluster headache status in 11 complete pairs (two monozygotic, four dizygotic, and five unlike-sexed pairs). In both members of a female monozygotic pair, migraine without aura developed after birth of the first child and remitted by menopause, whereas post-menopausal development of chronic cluster headache occurred in only one of them. The importance of individual specific factors for cluster headache was demonstrated. However, to explain familial aggregation a larger sample of affected twin pairs is necessary.

Adult↗
PubMed2002

Age at onset and sex ratio in cluster headache: observations over three decades.

Five hundred and fifty-four patients with episodic cluster headache (ECH) and chronic cluster headache (CCH) were examined between 1963 and 1997. Mean age at onset was significantly higher in women with CCH compared with women with ECH and in men with ECH or CCH. In women with CCH age at onset was evenly distributed from 10 to 69 years, whereas in men with CCH and in both sexes with ECH, there was a peak when they were in their 20s. In women with ECH a second peak of onset occurred in their 50s. Although not statistically significant, primary CCH started later in women (mean 50.8 years) than secondary CCH (mean 35.5 years). There was a significant variation in the male : female ratio with respect to age at onset, being largest between 30 and 49 years of age (ECH 7.2 : 1; CCH 11.0 : 1) and lowest after 50 (ECH 2.3 : 1; CCH 0.6 : 1). During the observation period of more than 30 years there was a trend towards a decreasing male preponderance; the male : female ratio was significantly higher among patients with onset before rather than after 1970. The proportion of episodic vs. chronic CH did not change during the study period. The nature of the sex- and age-related pattern of cluster headache onset remains to be elucidated but mechanisms associated with sex hormone regulation, perhaps of hypothalamic origin, may be involved, as well as environmental factors related to lifestyle.

Adolescent↗
PubMed2002

Hyperbaric oxygen treatment of active cluster headache: a double-blind placebo-controlled cross-over study.

Sixteen patients, 12 with episodic and four with chronic cluster headache (CH) according to the International Headache Society criteria (1), participated in the study. They were randomly selected to start with one out of two different hyperbaric treatments in a double-blind, placebo-controlled, cross-over study design. Both gases were administered by mask inside a multiplace hyperbaric chamber for 70 min at 250 kPa (2.5 ATA) in two sessions 24 h apart. Active treatment was 100% oxygen (HBO treatment), while placebo treatment was 10% oxygen in nitrogen (hyperbaric normoxic placebo = sham treatment) corresponding to breathing air at sea level. All patients were decompressed on air. The patients documented the number of headache attacks and their degree of severity according to a modified VAS scale (level 0-4, where level 0 = no headache and level 4 = very severe headache). A headache index (HI = sum of (number of attacks times degree of severity)) was calculated for the run-in week prior to and the week after each separate treatment. A treatment was regarded as effective if it reduced the HI by>50%. Blood samples were taken from the external jugular vein before and during hyperbaric treatment (after 30 and 70 min), 1 day and 1 week after each treatment for analyses of calcitonin gene-related peptide (CGRP), vasoactive intestinal peptide (VIP) and neuropeptide Y (NPY) and in a few patients also endotheline and nitrate. No difference between HBO and sham treatment on the HI or the prophylactic effect was observed in our study. However, 83% of the episodic CH patients and 25% of the chronic ones responded to either of the two treatments with at least 50% reduction of HI or remission for shorter or longer periods. This response rate exceeds an expected high placebo response due to the study procedure. Two episodic CH patients still experienced remission on follow-up 1 year after sham treatment. Five patients reported mild or moderate CH attacks during the sham treatment, and none during the HBO treatment. Changes in neuropeptides, endotheline and nitrate levels did not differ systematically when comparing the two different hyperbaric treatments or with respect to responders and non-responders. We conclude that two HBO sessions were not more effective than two sham treatments in reducing the HI and interrupting the CH period when given in a well-established cluster period or in chronic CH. The hyperbaric condition itself seems effective in reducing the HI, at least in patients with episodic CH, although a powerful placebo response can not be ruled out.

Adult↗
PubMed2002

Analysis of nitric oxide synthase genes in cluster headache.

The aetiology of cluster headache is still not yet completely understood, but the potential relevance of genetic factors has been recognized during recent years. Nitric oxide (NO) plays a critical role in the regulation of vasodilation, neurotransmission, inflammation and many other events throughout the body. NO also appears to be an important mediator of vascular headache pathophysiology. In this study we have performed an association analysis of five polymorphic microsatellite markers in the three different NO synthase (NOS) genes; nNOS (NOS1), iNOS (NOS2A) and eNOS (NOS3). Ninety-one cluster headache patients diagnosed according to International Headache Society criteria and 111 matched controls were studied. Phenotype and allele frequencies were similarly distributed in patients and controls except for an iNOS (NOS2A) pentanucleotide repeat allele which was significantly more common in controls. We observed a higher phenotype frequency of this allele in our control group compared with rates in control groups of other studies, whereas the frequency in our patients was similar to that in controls from previous reports. Thus, we conclude that it is unlikely that genetic variations within the NOS genes contribute greatly to cluster headache susceptibility.

Adult↗
PubMed2001

CACNA1A gene polymorphisms in cluster headache.

Cluster headache (CH) is a primary headache disorder where the aetiological and pathophysiological mechanisms still are largely unknown. An increased risk of CH in first- and second-degree relatives suggests the importance of genetic factors. Mutations of the P/Q type calcium channel alpha 1 subunit (CACNA1A) gene on chromosome 19p13 have been shown to cause several neurological disorders with a wide clinical spectrum, mainly episodic diseases. Missense mutations of the gene cause familial hemiplegic migraine (FHM) and it is also likely to be involved in the more common forms of migraine. The CACNA1A gene is thus a promising candidate gene for CH. In this study we performed an association analysis of an intragenic polymorphic (CA)n-repeat with marker D19S1150 and a (CAG)n-repeat in the 3'UTR region, in 75 patients with CH according to IHS criteria and 108 matched controls. Genotypes and allele frequencies were similarly distributed in patients and controls. Linkage disequilibrium between the two markers was similar in patients and controls. We conclude that an importance of the CACNA1A gene in sporadic CH is unlikely.

Adult↗
PubMed2000

Cluster headache is not associated with signs of a systemic inflammation.

OBJECTIVE: To investigate whether there is clinical or biochemical evidence for a transient systemic inflammation during active periods of cluster headache. METHODS: Twenty-seven male and female consecutively selected patients with episodic cluster headache filled in questionnaires aiming at detecting any concurrent systemic vasculitic or rheumatoid disease. They were physically examined by both a neurologist and a rheumatologist independent of each other. Blood and urine samples were taken one to three times during an active cluster period and once in remission. The following analyses were performed: hemoglobin, erythrocyte sedimentation rate, C-reactive protein, complete blood counts including differential counts, creatinine, albumin, creatine kinase, electrophoreses of serum (with haptoglobin, orosomucoid, IgG, IgM), von Willebrand's factor, antinuclear antibodies, rheumatoid factor, cytoplasmic antineutrophil cytoplasmic autoantibodies, perinuclear antineutrophil cytoplasmic autoantibodies, and routine urinary tests. An age- and sex-matched control group of 99 consecutive patients attending the Outpatient Department of Neurology for symptoms/diseases other than severe headache completed the same questionnaire as the patient group. RESULTS: Only one patient with cluster headache showed clinical signs (livedo reticularis) that could have been due to an ongoing systemic vasculitis. Most symptoms were equally or even more prevalent in the control group than among the patients with cluster headache. However, cold feet were about twice as prevalent among female patients with cluster headache than in the control group. This was considered due to their smoking habits. Laboratory tests showed no statistically significant differences between the active cluster periods and remission. There were some slightly abnormal values in single laboratory tests, some of which were probably due to concurrent upper respiratory infections. The findings of laboratory tests for one patient could have been due to nephritis. All patients were negative for cytoplasmic antineutrophil cytoplasmic autoantibodies and perinuclear antineutrophil cytoplasmic autoantibodies. CONCLUSIONS: These results were taken as evidence that no systemic inflammation is present during the active cluster headache period. However, whether a local retro-orbital inflammation underlies the pathophysiology of cluster headache remains obscure.

Adolescent↗
PubMed2000

A follow-up study of 60 patients after an assumed first period of cluster headache.

During 1981-96 a series of 60 consecutive out-patients was examined in relation to an assumed first period of cluster headache (CH). On follow up in 1998 we found that six were deceased at a mean age of 56.5 years (range 45-74 years), of whom one had a definitive CH diagnosis and five had one documented headache period only. Six patients were lost to follow up because they could not be reached. In the final group for evaluation (n = 49) it was found that 13 (26.5%) patients had had one cluster period only during a mean observation time of 8.9 years. Out of 36 patients with a definitive CH diagnosis according to International Headache Society (IHS) criteria, 31 patients had episodic CH, four patients had primary chronic CH and one patient had secondary chronic CH. Of the patients with a definitive CH diagnosis, 83% on follow up had had a recurrence of a second period of CH within 3 years or continuous attacks (chronic/semichronic CH) from the onset. Evidently some patients may suffer from one cluster period only. In our patient material only 17% had a second cluster period after 3 years.

Adult↗
PubMed1997

Sympathetic vasoconstrictor outflow to extremity muscles in cluster headache. Recordings during spontaneous and nitroglycerin-induced attacks.

To search for evidence of sympathetic dysregulation during cluster headache attacks, microneurographic recordings of muscle nerve sympathetic activity (MSA) were obtained from the peroneal nerve. In three recordings commenced after the onset of spontaneous attacks, MSA was about twice as high during the attack as afterwards. In four nitroglycerin-induced attacks, MSA showed a rise paralleling the pain, preceded by an initial peak. The latter accompanied hypotension, whereas the rise coinciding with cluster headache was associated with rising blood pressure. The normal baroreflex-governed pulse synchrony of MSA was preserved both during spontaneous and provoked attacks. In seven cluster headache patients in whom nitroglycerin did not cause an attack, only an initial peak in MSA occurred. Nor was any late nitroglycerin-induced rise in MSA observed in nine healthy subjects; the initial peak in MSA and heart rate was followed by a rapid return to normal despite a falling blood pressure. It is concluded that cluster headache attacks are associated with an increase in MSA that elevates blood pressure by causing vasoconstriction, and that this increase, rather than indicating sympathetic dysregulation, is a normal pain-evoked secondary phenomenon. The findings in healthy subjects support the notion that nitroglycerin has a central sympatho-inhibitory effect.

Adult↗
PubMed1994

Lowered circannual urinary melatonin concentrations in episodic cluster headache.

The circannual secretion of melatonin in 14 Swedish and 15 Italian patients suffering from episodic cluster headache was compared with 14 Swedish and 15 Italian healthy controls matched for sex and age. Overnight samples of urine were collected once a month from 8 to 14 months and kept at -20 degrees C until analysed with RIA. The melatonin concentrations in nocturnal urine were permanently low in cluster headache and there was no consistent change of the melatonin concentration in relation to cluster periods occurring during the study. There was no definitive circannual or infraannual rhythmicity of melatonin in patients or controls. Multiple analysis of variance with repeated measurements showed a significant effect of disease (p < 0.05), but not of time. Sex, geographical location, age, and smoking also had significant effects (p < 0.001) on the melatonin concentrations. Lower melatonin levels in cluster headache patients than in controls may in part be related to a larger number of smokers in the patient group. The relation between tobacco use and melatonin should be further studied.

Adult↗
PubMed1993

MR-angiography during spontaneous attacks of cluster headache: a case report.

Magnetic resonance (MR) angiography was performed during and between two spontaneous and untreated attacks in a 24-year old male patient with episodic cluster headache. The ipsilateral ophthalmic artery was observed to be markedly dilated during both attacks. No changes were seen in the internal carotid artery or any of the main arterial branches on either side. A repeat MR-angiography two weeks later when the patient was in clinical remission showed no abnormalities. Our present case report suggests that the MR technique provides a useful method for non-invasive angiography during spontaneous attacks of cluster headache.

Adult↗
PubMed1992

Cytochrome-P450-dependent hydroxylation in cluster headache.

Two isozymes of the cytochrome-P450-dependent drug oxidizing system exhibit polymorphism. Five to 10% of a Caucasian population are deficient in debrisoquine-hydroxylase activity and about 3% in mephenytoin-hydroxylase activity (poor metabolizers). We tested the hypothesis of a possible over-representation of poor metabolizers among patients with cluster headache. The individual metabolic capacity was determined in 30 cluster headache patients after administration of a test dose of 10 mg of debrisoquine and 100 mg of mephenytoin. Two patients (6.7%) were poor metabolizers of debrisoquine and one (3.3%) a poor metabolizer of mephenytoin. This was no different from the rate of poor metabolizers, 7.1% and 3.3% respectively, in a reference panel of healthy Swedish volunteers.

Adult↗
PubMed1992

Sumatriptan in chronic cluster headache: results of continuous treatment for eleven months.

A 32-year-old man received a total of 480 injections of subcutaneous sumatriptan 6 mg for the treatment of acute attacks of chronic cluster headache over an eleven-month period. Over 90% of the attacks resolved within 10 min of treatment (average 6.8 +/- 3.4). As a comparison, the average duration of 61 attacks occurring over the same period, but not treated with sumatriptan, was 56.1 +/- 20.8 min. This difference was highly significant. There was no clinical evidence of tachyphylaxis, and there were no adverse effects. This is the first report of a long-term treatment of cluster headache with sumatriptan. It is concluded that sumatriptan in this case was an effective and well-tolerated treatment for cluster headache.

Adult↗