[Are psychiatric diseases brain diseases?].
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Brain Diseases↗
Biomedical subjects
J Olesen
Publications and source records attributed to J Olesen.
[Familial occurrence of chronic tension headache].
Chronic tension-type headache occurs in 3% of the Danish population. the aetiology remains an enigma, even though it is one of the most frequent illnesses with chronic pain. A family study indicates the importance of genetic factors. Compared with the general population, first degree relatives (parents, siblings and children) of probands with chronic tension-type headache have a three-fold significantly increased risk of chronic tension-type headache, while spouses had no increased risk. Complex segregation analysis indicates multifactorial inheritance. Thus, a combination of genetic and environmental factors causes chronic tension-type headache.
Adult↗
Effect of inhibition of nitric oxide synthase on chronic tension-type headache: a randomised crossover trial.
BACKGROUND: Studies in animals have shown that nitric oxide plays an important part in central sensitisation and that inhibitors of nitric oxide synthase (NOS) decrease sensitisation in models of persistent pain. The efficacy of inhibitors of NOS has not been tested in patients with tension-type chronic headache. We aimed to show whether N(G)-monomethyl-L-arginine hydrochloride (L-NMMA), an inhibitor of NOS, is effective in relieving pain in such patients. METHODS: We undertook a randomised double-blind, crossover trial of 16 patients with chronic-tension-type headache. Patients were assigned intravenous infusion of 6 mg/kg L-NMMA or placebo on 2 days separated by at least 1 week in a randomised order. Headache intensity was measured on a 100 mm visual analogue scale, and on a verbal rating scale at baseline and at 30 min, 60 min, and 120 min after start of treatment. The primary endpoint was reduction of pain intensity on the visual analogue scale by the active treatment compared with placebo. FINDINGS: L-NMMA reduced pain intensity on the visual analogue scale significantly more than placebo: 120 min after start of treatment, the mean pain score was decreased from 49 to 33 with L-NMMA and from 44 to 40 with placebo (p=0.01). Pain intensity on the verbal rating scale was also significantly lower for treatment with L-NMMA than for treatment with placebo (p=0.02). INTERPRETATION: Inhibition of NOS had an analgesic effect in chronic tension-type headache. Further tests are required before clinical application.
Adult↗
Evidence of a genetic factor in migraine with aura: a population-based Danish twin study.
We studied the genetic influence on cause of migraine with aura (MA) by analyzing a twin population. The twin sample consisted of 2,026 monozygotic (MZ) twins and 3,334 same-sex dizygotic (DZ) twins, born from 1953 to 1960, from the population-based New Danish Twin Register. A validated questionnaire was used to screen for migraine, the response rate being 87%, and similar among MZ and DZ twins. All twin pairs with at least 1 twin with possible MA were interviewed by a physician experienced in headache diagnoses. The answers from the questionnaire as well as the zygosity of the twins were blinded for the interviewer. A total of 211 twin pairs were identified, of whom 77 pairs were MZ and 134 pairs were DZ. The lifetime prevalence of MA was 7% and with a male-to-female ratio of 1:1.1. The pairwise concordance rates were significantly higher in MZ (34%) than in DZ twin pairs (12%), emphasizing the importance of genetic factors in MA. However, environmental factors are also important, as the pairwise concordance rate was less than 100% in MZ twin pairs. The recurrence risk of MA was 50% in MZ and 21% in DZ twin pairs. In nontwin siblings, the recurrence risk of MA is 27%, which is similar to the recurrence risk in DZ twins. This indicates that MA is not developed due to specific environmental factors shared by the twins.
Adult↗
Muscle hardness in patients with chronic tension-type headache: relation to actual headache state.
It has recently been reported that the pericranial muscles in patients with chronic tension-type headache are harder, i.e. have a higher consistency, than in controls. The primary aim of the present study was to investigate whether muscle hardness is influenced by the presence or absence of actual headache and whether hardness is correlated to tenderness. The secondary aim was to compare muscle hardness between patients and healthy controls. Hardness of the trapezius muscle was measured with a hardness meter in 20 patients with chronic tension-type headache and in 20 healthy controls. The patients were examined on 2 days, 1 day with headache and 1 day without headache. Pericranial myofascial tenderness was recorded with manual palpation. In addition, muscle hardness was measured in another five patients out-side headache and in 30 healthy controls. The muscle hardness recorded in patients (n = 20) on days with headache, 98 +/- 26 kPa/cm, did not differ significantly from the muscle hardness recorded on days without headache, 100 +/- 21 kPa/cm, (P = 0.62). The muscle hardness was positively correlated to the local tenderness score recorded from the trapezius muscle both on days with headache (R = 0.52, P = 0.02) and on days without headache (R = 0.53, P = 0.02). The total tenderness score (TTS) recorded in patients on days with headache, 23 +/- 10, was significantly higher than the TTS recorded on days without headache, 15 +/- 11, (P = 0.0001). There was a significant difference between the TTS recorded in patients without headache, 15 +/- 11, and in controls, 4 +/- 4, (P = 0.002). The muscle hardness was significantly higher in patients on days without headache (n = 25), 97 +/- 20 kPa/cm, than in controls (n = 30), 87 +/- 16 kPa/cm (P = 0.03). On basis of previous and present results, we suggest that muscle hardness and muscle tenderness are permanently altered in chronic tension-type headache and not only a consequence of actual pain. In addition, the positive correlation between muscle hardness and tenderness supports the common clinical observation that tender muscles are harder than normal muscles.
Adult↗
[Familial hemiplegic migraine].
Familial hemiplegic migraine (FHM) is a rare subtype of migraine with aura. It is inherited as an autosomal dominant trait. A gene for FHM has been assigned to chromosome 19. This gene codes for a brain-specific calcium channel, and is responsible for FHM in 55% of the FHM families. Other FHM families have been linked to two different locations on chromosome 1. These locations contain possible candidate genes coding for calcium-and potassium channels. Thus FHM is a genetically heterogenous ion channel disorder, which is caused by at least three different genes. About 29% of the FHM families also have cerebellar ataxia, these families have all been linked to chromosome 19. The identification of the genes for FHM may be a key to the identification of the gene/genes for migraine with and without aura.
Chromosome Mapping↗
Soluble ICAM-1, demyelination, and inflammation in multiple sclerosis and acute optic neuritis.
We measured sICAM-1 in paired samples of serum and cerebrospinal fluid (CSF) from patients with an attack of multiple sclerosis (MS) (n = 50) and patients with acute monosymptomatic optic neuritis (ON) as a possible first attack of MS were also included (n = 25). Based on calculations of extended indices we found evidence of intrathecal synthesis of sICAM-1 both in patients with clinically definite MS and in patients with idiopathic ON compared to neurological control subjects. The amount of intrathecally synthesized sICAM-1 correlated significantly to the CSF leukocyte count and to the concentration of myelin basic protein in the CSF. The serum concentrations of sICAM-1 were not increased in patients with demyelinating disease compared to the neurological control subjects.
Acute Disease↗
[Spread and control of methicillin resistant Staphylococcus aureus in a department of dermatology].
Patients with skin diseases caused a spread of methicillin-resistant Staphylococcus aureus (MRSA) to 17 patients in our Department of Dermatology, because of their heavily scaly skin. Patients with severe dermatosis are regularly treated with dicloxacillin. The resistance of bacteria strain concerned suggests a selection because of the use of dicloxacillin in the Department. The strain is sensitive to gentamicin, which differentiates it from strains imported from abroad. Increased hygienic precautions, isolation of infected patients, staff and management efforts and a close contact with the microbiologists prevented MRSA from spreading to other hospital wards.
Aged↗
NF-kappa B p105 processing via the ubiquitin-proteasome pathway.
The p50 subunit of NF-kappa B is generated by proteolytic processing of a 105-kDa precursor (p105) in yeast and mammalian cells. Here we show that yeast mutants in the ubiquitin-proteasome pathway inhibit or abolish p105 processing. Specifically, p105 processing is inhibited by a mutation in a 20 S proteasome subunit (pre1-1), by mutations in the ATPases located in the 19 S regulatory complexes of the proteasome (yta1, yta2/sug1, yta5, cim5), and by a mutation in a proteasome-associated isopeptidase (doa4). A ubiquitinated intermediate of the p105 processing reaction accumulates in some of these mutants, strongly suggesting that ubiquitination is required for processing. However, none of the ubiquitin conjugating enzyme mutants tested (ubc1, -2, -3, -4/5, -6/7, -8, -9, -10, -11) had an effect on p105 processing, suggesting that more than one of these enzymes is sufficient for p105 processing. Interestingly, a mutant "N-end rule" ligase does not adversely affect p105 processing, showing that the N-end rule pathway is not involved in degrading the C-terminal region of p105. Unexpectedly, we found that a glycine-rich region of p105 that is required for p105 processing in mammalian cells is not required for processing in yeast. Thus, p105 processing in both yeast and mammalian cells requires the ubiquitin-proteasome pathway, but the mechanisms of processing, while similar, are not identical.
Adenosine Triphosphatases↗
Inheritance of chronic tension-type headache investigated by complex segregation analysis.
We investigated the mode of inheritance of chronic tension-type headache in 122 families. The probands were from the Copenhagen Headache Clinic, Denmark. The criteria of the International Headache Society were used. The patterns of segregation of chronic tension-type headache were assessed by complex segregation analysis performed with the computer program POINTER. Of the 122 probands with chronic tension-type headache, 56 had 71 first-degree relatives with chronic tension-type headache. The complex segregation analysis indicates that chronic tension-type headache has multifactorial inheritance.
Age Factors↗
Regional cerebral blood flow and oxygen metabolism during migraine with and without aura.
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Alcohol Drinking↗
Altered allelic distributions of the serotonin transporter gene in migraine without aura and migraine with aura.
Allelic variation of the human serotonin transporter gene (HSERT), a highly plausible candidate gene for susceptibility to migraine, was investigated in 266 individuals with migraine, including 173 having migraine without aura (MO), 94 having migraine with aura (MA), 18 with co-occurrence of MO and MA, plus 133 unaffected controls. The distribution of a polymorphism with different forms of a variable tandem number repeat (VNTR) in intron 2 were compared. The MO group had an over-representation of genotypes with two twelve repeat alleles (STin2.12) and a reduction of genotypes containing one ten repeat (STin2.10) compared to controls. The MA group showed a similar pattern, but also a trend towards an increase in genotypes containing the nine repeat allele of the VNTR (STin2.9). Genotypes containing this allele were found in 6.4% of the MA group compared to 2.3% of controls. The group with co-occurrence of MO and MA had a significantly different pattern of overall allele frequency distribution from controls, reflecting a reduction in genotypes containing the STin2.10 allele and a shift both to STin2.9 carriers and to STin2.12 homozygosity. These results support the view that susceptibility to MO and MA has a genetic component, that these disorders are distinct, and that genetic susceptibility may in some cases be associated with a locus at or near the serotonin transporter gene.
Adult↗
Nitric oxide synthase inhibition: a new principle in the treatment of migraine attacks.
Glyceryl trinitrate, an exogenous nitric oxide (NO) donor, and histamine, which causes NO formation in vascular endothelium, have been shown to trigger migraine attacks. However, it remains uncertain whether NO is involved in the subsequent phase of migraine attacks. To answer this question we studied the effect of L-NGmethylarginine hydrochloride (546C88), a NO-synthase inhibitor, on spontaneous migraine attacks. In a double-blind study design, 18 patients with migraine without aura randomly received 546C88 (6 mg/kg) or placebo (5% dextrose) i.v. given over 15 min for a single migraine attack (546C88:placebo, 15:3). Furthermore, 11 placebo-treated patients from previous double-blind trials with almost identical design were added to the placebo group in the statistical evaluation. Two hours after the infusion, 10 of 15 L-NGmethylarginine hydrochloride-treated patients experienced headache relief compared to 2 of 14 placebo-treated patients (p = 0.01). Symptoms such as phono- and photophobia were also significantly improved. A similar trend for nausea was not significant. We conclude that NO may be involved in the pain mechanisms throughout the course of spontaneous migraine attacks.
Adolescent↗
Measurement of muscle hardness: a methodological study.
The aim of the present study was to determine the intra- and interobserver variation during measurement of muscle hardness with a new instrument, a so-called hardness meter. In addition, we investigated the factors which may influence the recording of muscle hardness and whether the hardness differs within the same muscle. Hardness was measured at a standardized point on the trapezius muscle in 20 volunteers by 2 observers in random order and again by 1 of the observers after 30 min. Muscle hardness was then measured at 3 different locations on the trapezius muscle. In addition, the muscle hardness at the standard point was measured in 10 volunteers by both observers at 3 different speeds of the applied pressure. The intraobserver variation was 10% and the interobserver variation was 12% for recording of muscle hardness. There was no significant difference in hardness values from time to time within the same observer (p=0.12), while there was a significant difference in hardness measurements between observers (p=0.007). Muscle hardness differed significantly among the 3 anatomical locations (p=0.03). For both observers, there was a significant difference among hardness recordings obtained at 3 different speeds (p=0.01 and p=0.0001). In conclusion, we have shown that the hardness meter can measure muscle hardness reliably if the same observer is used throughout a study. The speed factor was a major source of variability In addition, we have demonstrated that muscle hardness differs within the same muscle. We suggest that the muscle hardness meter will be an important tool in future research of the mechanisms leading to myofascial pain.
Adult↗
Muscular factors are of importance in tension-type headache.
Recent studies have indicated that muscular disorders may be of importance for the development of increased pain sensitivity in patients with chronic tension-type headache. The objective of the present study was to investigate this hypothesis by examining the pain perception in tension-type headache with and without muscular disorders defined as increased tenderness. We examined 28 patients with episodic tension-type headache, 28 patients with chronic tension-type headache, and 30 healthy controls. Pericranial myofascial tenderness was recorded with manual palpation, and pressure pain detection and tolerances in cephalic and extracephalic locations with an electronic pressure algometer. In addition, thermal pain sensitivity and electromyographic activity were recorded. The main result was significantly lower pressure pain detection thresholds and tolerances in all the examined locations in patients with chronic tension-type headache with a muscular disorder compared to those without a muscular disorder. There were no such differences in any of the examined locations when the two subgroups of patients with episodic tension-type headache were compared. Thermal pain sensitivity did not differ between patients with and without a muscular disorder, while electromyographic activity levels were significantly higher in patients with chronic tension-type headache with than in those without a muscular disorder. Our results strongly indicate that prolonged nociceptive stimuli from the pericranial myofascial tissue sensitize the central nervous system and, thereby, lead to an increased general pain sensitivity. Muscular factors may, therefore, be of major importance for the conversion of episodic into chronic tension-type headache. The present study complements the understanding of the important interactions between peripheral and central factors in tension-type headache and may lead to a better prevention and treatment of the most prevalent type of headache.
Adult↗
No relation between cephalic venous dilatation and pain in migraine.
Evidence for the involvement of the cranial arterial system in migraine is plentiful, but it is unclear whether the cranial venous system may be involved in the mechanism of migraine pain. Venules are the preferentially involved vessels in the neurogenic inflammation animal model of migraine. The cranial and cerebral veins and sinuses are pain sensitive and receive sensory innervation from the trigeminal nerve. If the veins are involved in migraine pathogenesis, a venous dilatation would presumably be painful. The effect of a short lasting cranial venous dilatation, induced by applying pressure on the internal jugular veins (Queckenstedt's manoeuvre), was therefore compared with a placebo procedure, consisting of an equal pressure applied on to the lateral aspect of the neck. In each procedure pressure was applied for 10 seconds. The study used a single blind, randomised, cross over design, and 20 patients with an acute attack of migraine without aura participated. After each procedure, headache intensity was rated on a standardised five point scale. After Queckenstedt's manoeuvre 40% of the patients reported no change in headache intensity, 25% a worsening, and 35% an improvement of their headache. No significant difference between the headache intensity ratings during Queckenstedt's manoeuvre and the placebo manoeuvre was found (p=0.22). The findings make it unlikely that the cephalic venous system is of major importance in migraine pain mechanisms and, therefore, also less likely that neurogenic inflammation plays a significant part in humans during attacks of migraine without aura.
Adult↗
Double-blind, randomized, placebo-controlled study of oral, high-dose methylprednisolone in attacks of MS.
OBJECTIVE: There is only limited evidence from adequately controlled clinical trials to support high-dose methylprednisolone therapy for attacks of multiple sclerosis (MS) and none supporting oral administration. We assessed the effect of oral high-dose methylprednisolone therapy in attacks of MS. METHODS: Twenty-five patients with an attack of MS lasting less than 4 weeks were randomized to placebo treatment. Twenty-six patients received oral methylprednisolone (500 mg once a day for 5 days with a 10-day tapering period). The patients received scores on the Scripps Neurological Rating Scale (NRS) and Kurtzke Expanded Disability Status Scale. The symptoms were scored on a visual analog scale (VAS) before treatment and after 1, 3, and 8 weeks of treatment. Primary efficacy measures were NRS and VAS scores in the first 3 weeks and changes in NRS score and answers to an efficacy questionnaire administered after 8 weeks of treatment. RESULTS: Changes in NRS scores among methylprednisolone- and placebo-treated patients differed significantly in the first 3 weeks and after 8 weeks (p = 0.005 and p = 0.0007). VAS scores the first 3 weeks and treatment efficacy after 8 weeks also favored a beneficial effect of methylprednisolone treatment (p = 0.02 and p = 0.05). After 1, 3, and 8 weeks, 4%, 24%, and 32% in the placebo group and 31%, 54%, and 65% in the methylprednisolone group had improved one point on the Expanded Disability Status Scale score (all p < 0.05). No serious adverse events were seen. CONCLUSION: Oral high-dose methylprednisolone is recommended for managing attacks of MS.
Administration, Oral↗