Latent Dysautonomic Pupillary Lateralization in Cluster Headache. A Pupillometric Study

Fanciullacci, M; Pietrini, Umberto; Gatto, Gaetano; Boccuni, M; Sicuteri, F

doi:10.1046/j.1468-2982.1982.0203135.x

Cited by 74 publications

(77 citation statements)

References 16 publications

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“…a red, tearing eye, a small pupil and a stuffed nostril with rhinorrhea on the symptomatic side (Lance and Anthony, 1971;Sjaastad, 1992). There is some evidence indicating that dysfunction of the cephalic sympathetic nervous system may be primarily involved in the pathogenesis of CH (Fanciullacci et al, 1982;Salvesen et al, 1987a). However, these results which are preferentially based on studies of the pupillary response to various pharmacological agents, are somewhat conflicting.…”

Section: Introductionmentioning

confidence: 99%

Cephalic postganglionic sympathetic involvement in cluster headache–as evidenced by the pupillary responses to phenylephrine and tyramine

Havelius

Milos

Hindfelt

1997

Euro J of Neurology

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Twenty-six patients with episodic cluster headache were subjected to pupillometric examinations of the responses to bilateral conjunctival instillations of a single drop of a 1% phenylephrine and a 2% tyramine hydrochloride solution. Five patients had a Horner-like syndrome on the symptomatic side, where they exhibited an increased pupillary response to phenylepbrine and a decreased response to tyramine, i.e. a pattern compatible with postganglionic sympathetic dysfunction. It is suggested that these patients constitute a subgroup among the patients with cluster headache. The pupillary response to phenylephrine was frequently increased on the symptomatic side, while that to tyramine was reduced. This may indicate dysfunction of the sympathetic postganglionic fibers to the iris (and tentatively to the cephalic vasculature). Such an interpretation may be supported by the finding that a marked mydriatic response on the symptomatic side to tyramine was associated with an inactive cluster headache, frequently over many years.

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Section: Introductionmentioning

confidence: 99%

Cephalic postganglionic sympathetic involvement in cluster headache–as evidenced by the pupillary responses to phenylephrine and tyramine

Havelius

Milos

Hindfelt

1997

Euro J of Neurology

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“…While cranial vegetative symptoms of cluster headache seem to be related to an orthosympathetic hypofunction, often persisting during the silent period [9,10], our knowledge of the systemic vegetative system is still poor and results are often controversial. There are several reasons for this: (1) studies are carried out using different tests and in different periods (i.e., during attack, outside attack but within an active phase, outside the active period); (2) there is no standardised method as regards the study of the autonomic nervous system and it has been explored neurophysiologically, pharmacologically or by means of other techniques [7]; and (3) obtained values are often poorly comparable, as they are frequently influenced by internal and external factors (temperature, drugs, smoke, psychic conditions of the patient).…”

Section: Discussionmentioning

confidence: 99%

Systemic autonomic involvement in episodic cluster headache: a comparison between active and remission periods

et al. 2005

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IntroductionCranial autonomic involvement in episodic cluster headache (ECH) is known. Some vegetative symptoms are part of the diagnostic criteria for ECH and other trigemino-autonomic cephalalgias in the IHS classification [1]. Less is known about systemic autonomic impairment. Some authors [2][3][4][5][6][7] have described a derangement of cardiovascular responses during attacks of ECH. Moreover, a few authors have studied the differences between active and remission phase. We present a case-control study on systemic autonomic nervous activity, in particular its cardiovascular function, in ECH, during cluster periods and during remission phases. MethodsSeventeen ECH patients (14 males, 3 females, mean age 36.2 years, range 22-55) underwent a series of vegetative tests (Table 1), according to Ewing's protocol [8], to evaluate parasympathetic cardiovascular responses: lying to standing test (LST), Valsalva manoeuvre (VM) and deep breathing test (DBT); we also performed two tests, sympathetic skin response (SSR) and measurement of postural changes of blood pressure (PH), to assess vasoactive sympathetic pathway. Each patient was studied during either the active or silent period. We considered as active period when the last attack had occurred no more than 2 days before the study and silent period if the patient had been attack-free for the last 3 months and the following 2 months. Seventeen sex-and agematched healthy subjects were also evaluated as controls. During the active phase patients were drug-free; only symptomatic agents were allowed. The day of the study patients did not take coffee, tea or other foods containing sympathicomimetic amines. No patient suffered from diseases other than ECH; nobody was a smoker. Tables 2 and 3. SSR and PH showed no difference either between the active and the silent period or between ECH and normal controls. On the contrary, we found significant (p<0.01) differences in VM, LST and J Headache Pain (2005) 6:240-243 DOI 10.1007/s10194-005-0196-8 Systemic autonomic involvement in episodic cluster headache: a comparison between active and remission periods Values were then compared with normal controls. Our data show a parasympathetic, but not sympathetic, involvement. Moreover, this impairment seems to be "chronic", as it persists beyond the active period. Results Values are shown in

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“…With a battery of sympathetically acting eye drops, the pupillary impairment of sympathetic neuronal activity was demonstrated. Tyramine eye drops in CH patients induced an anisocoric pattern characterised by the pupil on the symptomatic side being smaller than the other pupil [9,10]. Asymmetric mydriatic response to the noradrenaline releaser tyra-mine was proposed as an objective diagnostic test for cluster patients.…”

Section: Horton's Headache Era At the Headache Center Of Florencementioning

confidence: 99%

When cluster headache was called histaminic cephalalgia (Horton’s headache)

Fanciullacci

2006

J Headache Pain

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At the end of the 1950s and the beginning of the 1960s, many desperate cluster headache (CH) patients came to the Headache Center of Florence, the only one in Europe at the time, to be examined. I was there… Horton's headache era More than 60 years ago Graham and Wolff [1, 2] proposed the vascular theory of migraine and related vascular headaches. At that time the clinical feature of the current CH syndrome was considered a migraine variant and therefore headache phase was attributed to painful dilatation and distension of the cephalic blood vessels. In 1939 Horton et al.[3] described cluster attack features, including increased temperature of the symptomatic side of the forehead and he reported the experience in treating this new vascular headache syndrome with histamine. But only in 1956, when Horton detailed the pain and its associated symptoms, did the syndrome become generally known [4]. However, Horton focused on the symptoms of episodes, omitting a description of the periodicity of occurrences. Therefore he considered this syndrome a vascular headache with chronic recurrent brief attacks similar to migraine. Horton used the term "histaminic cephalgia" [5] or "cephalalgia" [6], as he attributed this vascular painful syndrome to the potent vasodilator agent histamine. In many circles this form of headache has been called Horton's headache in his honour. Apart from acetylcholine, at that time histamine was the only known vasodilatative substance capable of explaining the vasodilatation phase of the so-called vascular headaches. Horton focused on the presumed role of histamine as an inducing factor of CH attacks as well as their prevention with histaminic desensitisation, and had J Headache Pain (2006) 7:231-234

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Latent Dysautonomic Pupillary Lateralization in Cluster Headache. A Pupillometric Study

Cited by 74 publications

References 16 publications

Cephalic postganglionic sympathetic involvement in cluster headache–as evidenced by the pupillary responses to phenylephrine and tyramine

Cephalic postganglionic sympathetic involvement in cluster headache–as evidenced by the pupillary responses to phenylephrine and tyramine

Systemic autonomic involvement in episodic cluster headache: a comparison between active and remission periods

When cluster headache was called histaminic cephalalgia (Horton’s headache)

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