The Insulin Tolerance Test and the Ovine Corticotrophin-Releasing Hormone Test in Episodic Cluster Headache

Leone, Massimo; Zappacosta, B.; Valentini, Sergio; Colangelo, Anna Maria; Bussone, Gennaro

doi:10.1046/j.1468-2982.1991.1106269.x

Cited by 23 publications

(24 citation statements)

References 20 publications

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“…Interleukin-1 alpha plasma levels are normal (16) in CH and cortisol levels are elevated (17)(18)(19) so that low mononuclear beta-endorphin levels are unlikely to be explained on this basis.…”

Section: Discussionmentioning

confidence: 99%

Beta-Endorphin Levels are Reduced in Peripheral Blood Mononuclear Cells of Cluster Headache Patients

Leone¹,

Sacerdote

D’Amico

et al. 1993

Cephalalgia

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Opioid system hypofunction has been postulated in cluster headache (CH) on the basis of reduced opioid levels found in the cerebrospinal fluid (CSF). In this study beta-endorphin levels were monitored in the peripheral blood mononuclear cells of 65 episodic CH patients (32 in remission and 33 in cluster period) and 50 healthy controls. Beta-endorphin levels were significantly lower than controls in CH patients experiencing both phases of the illness (ANOVA, p < 0.0001). The persistence of this abnormality during pain-free remission suggests a primary alteration in the regulation of beta-endorphin in peripheral blood mononuclear cells. We speculate that these findings reflect reduced CNS levels of beta-endorphin in CH.

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Section: Discussionmentioning

confidence: 99%

Beta-Endorphin Levels are Reduced in Peripheral Blood Mononuclear Cells of Cluster Headache Patients

Leone¹,

Sacerdote

D’Amico

et al. 1993

Cephalalgia

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“…Chazot et al [31] found that the normal morning peak in plasma cortisol was significantly phaseadvanced in patients with CH, although this finding has not been replicated by other investigators [32][33][34][35][36]. Multiple investigators have found that CH patients typically have elevations in baseline plasma cortisol levels [32][33][34][35][36], particularly during cluster periods, and that these elevations are independent of the presence of pain because they are not seen in patients with chronic low back pain [37]. Further elevations in plasma cortisol levels have been associated with specific CH attacks [34].…”

Section: Pathophysiologic Rationale For the Therapeutic Efficacy Of Cmentioning

confidence: 98%

“…Further elevations in plasma cortisol levels have been associated with specific CH attacks [34]. Dexamethasone suppression testing in CH patients has been found to be normal [38][39][40]; however, ovine corticotrophin-releasing hormone testing and insulin tolerance testing produced blunted plasma ACTH and cortisol elevations in patients with CH compared with control subjects [37,41]. Leone et al [37,41] have interpreted these collective findings as indicative of a primary dysfunction in the hypothalamic-pituitary-adrenal axis in CH.…”

Section: Pathophysiologic Rationale For the Therapeutic Efficacy Of Cmentioning

confidence: 99%

Corticosteroid treatment in cluster headache: Evidence, rationale, and practice

Shapiro

2005

Current Science Inc

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The use of corticosteroids in the treatment of cluster headache (CH) is commonplace and has been a mainstay of clinical practice for this indication for 50 years. The published evidence supporting this practice is weak, with no methodologically rigorous or large-scale controlled trials executed. Nonetheless, the clinical experiences of practitioners and the conclusion of investigators provide a clear signal of benefit from corticosteroid use in CH. The pathophysiologic explanation for this beneficial effect is unknown, but corticosteroid influences on inflammatory, hypothalamic-pituitary-adrenal, histaminergic, and opioid systems have been proposed. Best-practice parameters are unclear, but the professional consensus is that corticosteroids generally are effective for arresting CH attacks, only if administered in relatively high doses, and that safety concerns warrant courses of 4 weeks or less. Concomitant use of other prophylactic agents for CH in addition to corticosteroids usually is advisable because attacks often recur when the corticosteroid dose is tapered.

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“…Hypoglycemia also provokes release of the hypothalamic stimulators of ACTH secretion, corticotrophin-releasing hormone (CRH) and vasopressin, into the pituitary portal blood (15) and enhances their turnover in the median eminence (16). Based on this knowledge, insulin-induced hypo-glycemia together with the ovine-CRH (o-CRH) test was studied in cluster headache patients (17). There was a reduced response of the hypothalamic-pituitary-adrenal axis to both in the cluster period and during remission (17).…”

mentioning

confidence: 99%

“…Based on this knowledge, insulin-induced hypo-glycemia together with the ovine-CRH (o-CRH) test was studied in cluster headache patients (17). There was a reduced response of the hypothalamic-pituitary-adrenal axis to both in the cluster period and during remission (17). The question arose if this was secondary to pain or stress rather than indicating a primary hypothalamic dysfunction.…”

mentioning

confidence: 99%

The Insulin Tolerance Test and Ovine Corticotrophin-Releasing-Hormone Test in Episodic Cluster Headache II: Comparison With Low Back Pain Patients

Leone¹,

Maltempo²,

Gritti³

et al. 1994

Cephalalgia

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Hypothalamic involvement has been invoked to explain the periodicity of the cluster periods and rhythmicity of the pain attacks in cluster headache. To explore this hypothesis the ovine corticotrophin-releasing headaches sufferers during both cluster period and remission. A group of low back pain patients and healthy subjects comprised the control populations. For the o-CRH test, 7 healthy subjects, 7 low back pain patients, 6 cluster headache patients in remission, and 12 in cluster period were studied. Five healthy subjects, 7 low back pain patients, 6 cluster headache patients in remission, and 9 cluster period were administered the insulin tolerance test. Significantly increased basal cortisol levels were found in cluster headache patients in both illness phases (p < 0.0001), but not in low back pain patients. Significantly reduced cortisol response to the o-CRH test was observed in cluster headache patients in both phases compared to healthy controls (p < 0.02). A blunted ACTH and cortisol response (p < 0.0001 and p < 0.003 respectively) to the insulin tolerance test was present in cluster headache patients in both phases of the illness compared to healthy subjects and low back pain patients. On the contrary, the ACTH surge after insulin induced hypoglycemia was significantly increased in the low back pain patient group (p = 0.02). These results suggest that the altered hypothalamic-pituitary-adrenal axis responsiveness in cluster headache patients is not a consequence of the pain, and point to a central, probably hypothalamic derangement in this pathology.

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The Insulin Tolerance Test and the Ovine Corticotrophin-Releasing Hormone Test in Episodic Cluster Headache

Cited by 23 publications

References 20 publications

Beta-Endorphin Levels are Reduced in Peripheral Blood Mononuclear Cells of Cluster Headache Patients

Beta-Endorphin Levels are Reduced in Peripheral Blood Mononuclear Cells of Cluster Headache Patients

Corticosteroid treatment in cluster headache: Evidence, rationale, and practice

The Insulin Tolerance Test and Ovine Corticotrophin-Releasing-Hormone Test in Episodic Cluster Headache II: Comparison With Low Back Pain Patients

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