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Biomedical subjects

Arne May

Publications and source records attributed to Arne May.

26 records · Page 2Linked to original sources
PubMed2003

Headaches with (ipsilateral) autonomic symptoms.

Primary short-lasting headaches broadly divide themselves into those associated with autonomic symptoms, so called trigemino-autonomic cephalgias (TACs), and those with little autonomic syndromes. The trigeminoautonomic cephalgias include cluster headache and paroxysmal hemicranias, in which head pain and cranial autonomic symptoms are prominent. The most striking feature of cluster headache is the circadian and circannual periodicity of the attacks. Inheritance may play a role in some families. The attacks are of extreme intensity, of short duration, occur unilaterally, and are accompanied by symptoms of autonomic dysfunction. Medical treatment includes both acute therapy aimed at aborting individual attacks and prophylactic therapy aimed at preventing recurrent attacks during the cluster period. Some types of trigemino-autonomic headaches, such as paroxysmal hemicrania and hemicrania continua have, unlike cluster headaches, a very robust response to indomethacin, leading to a consideration of indomethacin-sensitive headaches.

Autonomic Nervous System↗
PubMed2003

Headache: lessons learned from functional imaging.

Most idiopathic headache syndromes are still recognized as vascular headaches although the clinical picture points towards a central triggering cause. The early functional imaging work using PET shed light on the genesis of some syndromes, implying that the observed activation in migraine (brainstem) and in cluster headache (hypothalamic grey) is involved in the pain process in a permissive or triggering manner rather than simply as a response to first division nociception per se. Using the advanced method of voxel-based morphometry (VBM), it has been suggested that there is a correlation between the brain area activated particularly in acute cluster headache, the posterior hypothalamic grey matter, and some change in grey matter in the same region. Moreover, also in a PET study in cluster headache and experimental headache, a vasodilation of major basal vessels has been observed which is non-specific to the cause and most likely the effect of a trigemino-parasympathetic reflex. Taken together, functional neuroimaging in headache patients has revolutionised this area of study and provided unique insights into some of the commonest maladies in man, suggesting that migraine and cluster headache are primarily driven from the brain.

Animals↗
PubMed2003

Update on cluster headache.

PURPOSE OF REVIEW: Although cluster headache has traditionally been thought of as a vascular headache disorder, its periodicity suggests an involvement of central areas such as the hypothalamus. This review covers the past 3 years, which have seen remarkable progress in understanding the pathophysiology of circadian headache syndromes and have brought exciting news. RECENT FINDINGS: As more cluster headache patients are seen by headache specialists, new forms of this well-defined primary headache syndrome are being identified. In addition, we discuss recent findings with regard to abnormalities in the secretion of hormones, genetic influences, neuroimaging of cluster headache attacks, and the use of newer substances as preventive therapy in cluster headache. SUMMARY: We have entered a new diagnostic and therapeutic era in primary headache disorders. In recent reports, the use of deep brain stimulation of the hypothalamus has enabled intractable chronic cluster headache patients to be successfully operated upon. Further research in this field is urgently needed and the recent possibility of combining deep brain stimulation with positron emission tomography will certainly help to unravel the brain circuitry implicated in stimulation-produced analgesia. The time has come to use the evidence for a disorder of circadian rhythm in cluster headache to further the development of chronobiotics in the treatment of this disorder.

Cluster Headache↗
PubMed2002

Botulinum toxin A and the cutaneous nociception in humans: a prospective, double-blind, placebo-controlled, randomized study.

Aside from temporary chemodenervation of skeletal muscle and potential anti-inflammatory effects, a genuine peripheral antinociceptive effect of Botulinum Neurotoxin Type A (BoNT/A) has been suspected. To evaluate the effect of BoNT/A on cutaneous nociception in humans, 50 healthy volunteers received subcutaneous injections of 100 mouse units (MU) BoNT/A (Dysport) and placebo. Both forearms of each subject were treated in a double-blind fashion, one with verum, one with placebo. Heat and cold pain thresholds within the treated skin areas were measured with quantitative sensory testing (QST) and pain thresholds were evaluated with local electrical stimulation (ES). The tests were done before treatment, and after 4 and 8 weeks. No major side effects were noted. All participants completed the study. Heat and cold pain thresholds increased from baseline to week 4 by 1.4 degrees C for verum and by 1.1 degrees C for placebo. From baseline to week 8, the thresholds increased by 2.7 degrees C for verum and by 1.2 degrees C for placebo. Electrically induced pain thresholds shifted from baseline to week 4 by -0.07 mA for verum and by 0.01 mA for placebo. From baseline to week 8, the thresholds increased by 0.10 mA for verum and by 0.11 mA for placebo. None of these differences was statistically significant. The study shows that there is no direct peripheral antinociceptive effect of BoNT/A in humans. The efficacy of BoNT/A in various pain syndromes must be explained by other pathways such as chemodenervation or anti-inflammatory effects.

Administration, Cutaneous↗
PubMed2002

Observation on the integrity of the blood-brain barrier after microbubble destruction by diagnostic transcranial color-coded sonography.

OBJECTIVE: To investigate alteration of the blood-brain barrier from ultrasonic contrast agent destruction by diagnostic transcranial color-coded sonography using gadolinium-enhanced magnetic resonance imaging. METHODS: Healthy male volunteers received 10 mL (400 mg/dL) of Levovist (SH U 508A; Schering AG, Berlin, Germany; n = 6) or 3 mL of Optison (FS069; Mallinckrodt Inc, St Louis, MO; n = 4) followed by 0.3 mmol/kg magnetic resonance imaging contrast agent (Magnevist; Schering) intravenously. Then transcranial color-coded sonography was performed with a conventional color duplex sonographic system, which insonated the brain in a slightly angulated axial plane with temporal average intensity of less than 700 mW/cm2 or acoustic pressure amplitude of less than 2.69 MPa, attenuated by the temporal bone. Before, immediately after, and 2 hours after insonation, T1-weighted axial magnetic resonance imaging was performed. All magnetic resonance images were individually assessed, and T1 signal intensities were measured in 2 regions of interest in both hemispheres at the 3 time points. RESULTS: No focal contrast enhancement or damage to the brain and no significant difference between T1 signal intensities in the right and left brain regions could be detected during early or late phases when either ultrasonic contrast agent was used. CONCLUSIONS: This bioeffects study gives further evidence of the safety of ultrasonic destruction of Levovist and Optison microbubbles by diagnostic transcranial color-coded sonography. However, more subtle local effects may have been missed by gadolinium-enhanced magnetic resonance imaging. Studies on diagnostic contrast-enhanced transcranial color-coded sonography as well as microbubble-based drug delivery strategies should consider ultrasonic contrast agent microbubble characteristics and concentration as well as ultrasound transmission power levels.

Adult↗
PubMedDate not supplied

Cluster headache: pathogenesis, diagnosis, and management.

Cluster headache is a stereotyped primary pain syndrome characterised by strictly unilateral severe pain, localised in or around the eye and accompanied by ipsilateral autonomic features. The syndrome is characterised by the circadian rhythmicity of the short-lived attacks, and the regular recurrence of headache bouts, which are interspersed by periods of complete remission in most individuals. Headaches often start about 1-2 h after falling asleep or in the early morning, and show seasonal variation, suggesting that the hypothalamus has a role in the illness. Consequently, the vascular theory has been superseded by recognition that neurovascular factors are more important. The increased familial risk suggests that cluster headache has a genetic component in some families. Neuroimaging has broadened our pathophysiological view and has led to successful treatment by deep brain stimulation of the hypothalamus. Although most patients can be treated effectively, some do not respond to therapy. Fortunately, time to diagnosis of cluster headache has improved. This is probably the result of a better understanding of the pathophysiology in combination with efficient treatment strategies, leading to a broader acceptance of the syndrome by doctors.

Cluster Headache↗
PubMedDate not supplied

Transcranial color-coded duplex sonography of the carotid siphon: the coronal approach.

Transcranial color-coded sonography can assist in the assessment of the carotid siphon segments C1 and C5 employing two standardized coronal image planes. In 32 volunteers mean velocities in the C1 and C5 were 41+/-16 and 30+/-10 (cm/s+/-S.D.), pulsatility indices (PI) 0.92+/-0.22 and 0.93+/-0.27, and resistance indices (RI) 0.58+/-0.08 and 0.55+/-0.12, respectively. Concluding, this technique is useful in assessing the carotid siphon with the most robust parameters being PI and RI requiring further validation by the "gold standard" angiography.

Adolescent↗