Cluster‐Like Headaches Associated With Internal Carotid Artery Dissection Responsive to Verapamil

Tobin, Joshua; Flitman, Stephen

doi:10.1111/j.1526-4610.2007.01047.x

Cited by 18 publications

(12 citation statements)

References 27 publications

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“…However, since this information is often missing, the number of CLH patients would be drastically reduced to 38 (12, 14, 16, 27: Among these 148 cases, we decided to exclude from further analysis of headache features those missing relevant information (n = 72) or those presenting with a clinical history and/or a physical examination immediately indicative of a secondary condition. To be more precise, in 13 cases the clinical case history and/or the physical examination upon first observation clearly pointed to a secondary cause ( [118][119][120]122). Criteria for screening the case reports according to the data reported in the articles, and the number of selected patients, are summarized in the flow chart in Fig.…”

Section: Methodsmentioning

confidence: 99%

Cluster-like headache. A comprehensive reappraisal

et al. 2009

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Among the primary headaches, cluster headache (CH) presents very particular features allowing a relatively easy diagnosis based on criteria listed in Chapter 3 of the International Classification of Headache Disorders (ICHD-II). However, as in all primary headaches, possible underlying causal conditions must be excluded to rule out a secondary cluster-like headache (CLH). The observation of some cases with clinical features mimicking primary CH, but of secondary origin, led us to perform an extended review of CLH reports in the literature. We identified 156 CLH cases published from 1975 to 2008. The more frequent pathologies in association with CLH were the vascular ones (38.5%, n = 57), followed by tumours (25.7%, n = 38) and inflammatory infectious diseases (13.5%, n = 20). Eighty were excluded from further analysis, because of inadequate information. The remaining 76 were divided into two groups: those that satisfied the ICHD-II diagnostic criteria for CH, 'fulfilling' group (F), n = 38; and those with a symptomatology in disagreement with one or more ICHD-II criteria, 'not fulfilling' group (NF), n = 38. Among the aims of this study was the possible identification of clinical features leading to the suspicion of a symptomatic origin. In the differential diagnosis with CH, red flags resulted both for F and NF, older age at onset; for NF, abnormal neurological/general examination (73.6%), duration (34.2%), frequency (15.8%) and localization (10.5%) of the attacks. We stress the fact that, on first observation, 50% of CLH presented as F cases, perfectly mimicking CH. Therefore, the importance of accurate, clinical evaluation and of neuroimaging cannot be overestimated.

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Section: Methodsmentioning

confidence: 99%

Cluster-like headache. A comprehensive reappraisal

et al. 2009

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“…In a recent review on secondary cluster headache, 11 out of 63 patients had a carotid/vertebral dissection [3]. A review in 2007 identified 6 patients with ICA dissection presenting with cluster-like features [10] and several more cases have been described [11,12,13,14,15]. In all these patients, headache attacks disappeared within 2 months.…”

Section: Discussionmentioning

confidence: 99%

Post-Operative Cluster Headache Following Carotid Endarterectomy

Dirkx

Koehler²

2017

Eur Neurol

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Background: Secondary cluster headache following carotid endarterectomy (CEA) is a rare condition and may help us understand the pathophysiology of primary cluster headache. Summary: We describe 2 patients diagnosed with cluster headache, fulfilling the ICHD-IIIB criteria, following CEA. Neither of the patients had headache prior to surgery. They both responded to treatment with oxygen and verapamil. Recent medical literature does not describe any definite cases of cluster headache following CEA. Cluster-like headache has been reported in several studies in the 1990s. Recent studies in primary cluster headache patients show evidence for a central origin of cluster headache in which no peripheral drive seems necessary. Key Messages: Our findings may provide more insight into the pathophysiology and show how a peripheral cause may lead to cluster headache. We hypothesize a role of the trigemino-autonomic reflex. Damage to the carotid artery may activate this reflex and trigger cluster headache. Injury to the internal carotid artery may unleash attacks in patients who are predisposed to develop cluster headache. Further study on the subject is needed to resolve this issue.

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“…Further reported warning signs suggesting symptomatic cluster headache include atypical pain quality or localization, attacks of longer duration than 3 hours, lack of pain-free interval, absence of diurnal periodicity, presence of tinnitus, or other neurologic deficits. 2,6 However, even clinically typical cluster headache without warning signs can be secondary, and therefore, in case of any doubt, MRI should be performed. 7 Ipsilateral headache is the most common symptom of ICAD, usually limited to the frontotemporal region and sometimes accompanied by anterolateral neck pain.…”

Section: Sectionmentioning

confidence: 99%

“…Successful prophylactic therapy was reported using verapamil or steroids also in symptomatic cluster headache. 6 Thus, the response to standard acute and prophylactic treatments does not allow any conclu-sions as to whether the "cluster headache" is idiopathic or secondary. …”

Section: Sectionmentioning

confidence: 99%

Clinical Reasoning: A 62-year-old migraineur with a new kind of headache attacks

Bertschi

Sturzenegger²,

Heß³

2012

Neurology

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A 62-year-old man presented with novel headache attacks with acute onset 4 weeks previously strictly confined to the right side. The attacks occurred almost daily, often after midnight, lasting 1 to 3 hours, occasionally longer. The pain was localized around and behind the right eye. The pain intensity was excruciating and the pain quality pulsatile. Ipsilateral lacrimation, conjunctival injection, and prominence of the temporal artery accompanied these attacks. During the attacks, the patient reported a sense of restlessness. Alcohol consumption and physical activity provoked attacks. No recent major trauma was identified.In his personal history, the patient had had tension-type headache and mainly left-sided migraine-like headache attacks for many years. The latter were of a hammering quality, irradiating from the occipital to the frontal region, and accompanied by nausea, photophobia, and phonophobia. In comparison, the new onset current attacks clearly differed from the previous attacks in terms of location, pain quality, intensity, frequency, duration, and attendant symptoms. Ancillary diagnoses included arterial hypertension, treated with amlodipine, and ␣-1 antitrypsin deficiency.Family history revealed a twin brother, who died of aneurysmal subarachnoid hemorrhage 6 years previously. Several relatives had migraine.On clinical examination, reduced width of the palpebral fissure on the right side compared to the left (ptosis), right miosis, and anhidrosis of the forehead (figure 1, A and B) were noticed. These findings persisted during the pain-free interval.

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Cluster‐Like Headaches Associated With Internal Carotid Artery Dissection Responsive to Verapamil

Cited by 18 publications

References 27 publications

Cluster-like headache. A comprehensive reappraisal

Cluster-like headache. A comprehensive reappraisal

Post-Operative Cluster Headache Following Carotid Endarterectomy

Clinical Reasoning: A 62-year-old migraineur with a new kind of headache attacks

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