Carotid dissection mimicking a new attack of cluster headache

Elisa Candeloro,Isabella Canavero,Natascia Ghiotto,Anna Cavallini,Giuseppe Micieli,Paolo Vitali,Maurizia Maurelli

doi:10.1186/1129-2377-14-84

Abstract

BackgroundSymptomatic cluster headache (CH) secondary to internal carotid artery dissection (ICAD) has been frequently reported, however, as far as we know, the coexistence of episodic CH and acute symptomatic CH secondary to ICAD has not.Case reportA 39 year-old man, affected by episodic CH since the age of 19, presented an atypical headache associated with his usual autonomic symptoms. After a series of negative tests, MRA eventually revealed dissection of the right distal internal carotid artery.Discussion and conclusionsThe coexistence of episodic CH and acute CH symptomatic of ICAD in our patient suggests that, at least in some cases, CH and ICAD may be different expressions of a common underlying cause: hidden vessel wall damage. When risk factors and the change - though partial - of clinical features suggest symptomatic cases, CH patients have to be strictly monitored over time. Given the lack of a gold standard investigation for dynamic diseases such as dissections, these patients require multimodal diagnostic investigation over time, even in cases where exams are normal at onset.

Highlights

Symptomatic cluster headache (CH) secondary to internal carotid artery dissection (ICAD) has been frequently reported, as far as we know, the coexistence of episodic CH and acute symptomatic CH secondary to ICAD has not.Case report: A 39 year-old man, affected by episodic CH since the age of 19, presented an atypical headache associated with his usual autonomic symptoms
To our knowledge, the occurrence of acute symptomatic CH secondary to ICAD in a patient affected by episodic CH has never been reported
On the 5th day Duplex sonography was performed and disclosed a steno-occlusive distal process: the investigation disclosed the complete filling of the lumen with Pulse Repetition Frequency (Figure 2B) and a waveform with a very low amplitude, high-resistance and no diastolic flow (Figure 2D); the increased pulsatility and notable reduction in blood flow amplitude and velocity were consistent with the development of a stenosis downstream and suggested a possible worsening of carotid dissection

Summary

Discussion and conclusions

The coexistence of episodic CH and acute CH symptomatic of ICAD in our patient suggests that, at least in some cases, CH and ICAD may be different expressions of a common underlying cause: hidden vessel wall damage. When risk factors and the change - though partial - of clinical features suggest symptomatic cases, CH patients have to be strictly monitored over time. Given the lack of a gold standard investigation for dynamic diseases such as dissections, these patients require multimodal diagnostic investigation over time, even in cases where exams are normal at onset

Background

Discussion

Conclusions