Coexistence of Pupillary and Heart Sympathergic Asymmetries in Cluster Headache

Boccuni, M; Morace, G; Pietrini, Umberto; Porciani, Maria Cristiana; Fanciullacci, M; Sicuteri, F

doi:10.1046/j.1468-2982.1984.0401009.x

Cited by 15 publications

(7 citation statements)

References 38 publications

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“…In fact, pretreatment with clonidine augmented the degree of anisocoria induced by tyramine instillation, increasing the mydriatic response only on the pain-free side in CH patients. This finding has been corroborated by Salvesen et al (15) and by Boccuni et al (16). The latter authors have also demonstrated that hyperventilation-provoked sympathergic stimulation produces electrocardiographic changes consistent with asynchronous repolarization due to impaired central sympathetic activity.…”

Section: Discussionsupporting

confidence: 61%

Efficacy of Transdermal Clonidine in Short-Term Treatment of Cluster Headache: A Pilot Study

D’Andrea¹,

Perini²,

Granella³

et al. 1995

Cephalalgia

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Some clinical as well as pharmacological indications seem to suggest that a reduction of the noradrenergic tone occurs in cluster headache (CH), during both the active and remission periods. But sharp fluctuations of the sympathetic system may trigger the attacks. Clonidine, an alpha-2-adrenergic presynaptic agonist, regulates the sympathetic tone in the central nervous system. Therefore, a continuous administration of low-dose clonidine could be potentially beneficial in the active phase of CH by antagonizing the variations in noradrenergic tone. After a run-in week, we administered transdermal clonidine (5 - 7.5 mg) for one week to 13 patients suffering from CH, either episodic (8 cases) or chronic (5 cases). During clonidine treatment, the mean weekly frequency of attacks dropped from 17.7 +/- 7.0 to 8.7 +/- 6.6 (p = 0.0005), the pain intensity of attacks measured on the visual analogue scale from 98.0 +/- 7.2 to 41.1 +/- 36.1 mm (p = 0.001), and the duration from 59.3 +/- 21.9 to 34.3 +/- 24.6 min (p = 0.02). This open pilot study strongly suggests that transdermal clonidine may be an effective drug in the preventive treatment of CH. Its efficacy is possibly due to its central sympatho-inhibition, which reduces or prevents the occurrence of fluctuations of noradrenaline release that may induce the attacks.

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Section: Discussionsupporting

confidence: 61%

Efficacy of Transdermal Clonidine in Short-Term Treatment of Cluster Headache: A Pilot Study

D’Andrea¹,

Perini²,

Granella³

et al. 1995

Cephalalgia

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“…1,2 Many researches have been carried out to understand the actual relationship between painful crises and autonomic features, which tend to play a prominent role in headache pathophysiology. 8,9,10,11,12 Some evidence, however, points out a more complex autonomic defect, since most of these symptoms involve both a sympathetic and a parasympathetic activation, such as salivation, nasal secretion and tea ring . An asymmetric sympathetic regulation of the pupillary reactivity, nasal glands secretion, and forehead sweating support the idea of defective sympathetic function on the symptomatic side.…”

Section: Introductionmentioning

confidence: 99%

Impaired Cardiovascular Reflexes in Cluster Headache and Migraine Patients: Evidence for an Autonomic Dysfunction

Boiardi¹,

Munari²,

Milanesi

et al. 1988

Headache

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SYNOPSIS To investigate autonomic nervous system involvement in cluster headache (CH) and migraine, we compared the cardiovascular reflex responses of common migraine and CH subjects to a group of controls. A battery of 5 well‐codified autonomic tests was applied: (1) deep breathing test (DB); (2) lying to standing test (LS); (3) Valsalva manoeuvre (VAL); (4) postural hypotension test (PH); (5) blood pressure response to sustained handgrip (SHG). Our data confirm an autonomic dysfunction in CH, mainly affecting the parasympathetic system. Evidence for an impairment of sympathetic cardiovascular reflex regulation was obtained in the common migraine group.

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“…Does this also affect autonomic control of the heart, which contains distinct right and left innervations? Changes in the T‐wave configuration as well as an increase in QT c which could be caused by differential sympathetic activity in the right and left stellate ganglion would seem to confirm this . The proposed mechanism involves differences in the length of action potentials in different parts of the heart leading to asynchronous repolarization producing the increased QT c .…”

Section: Resultsmentioning

confidence: 84%