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Abnormalities in cardiovascular parameters are a well-documented phenomenon in cluster headache. A 50-year-old man presented to the Marshfield Clinic with left-sided episodic cluster headache attacks associated with lightheadedness. He was taking lithium, which reduced the frequency and severity of attacks; however, he discontinued lithium therapy because of significant thyroid dysfunction. Before this admission, he had recurrent syncopal episodes during acute cluster attacks, where he would wake up on the floor.
On admission, the patient was in the midst of a cluster attack. Physical examination was remarkable for an elevated blood pressure of 200/170 mm Hg with a heart rate of 17 beats/min. He had no symptoms other than feeling lightheaded. Admission electrocardiogram (Figure A) showed severe bradycardia with junctional escape rhythm. His headache resolved with sumatriptan and oxygen therapy. All laboratory testing results, including cardiac enzymes and echocardiogram, were normal. Telemetry monitoring during cluster-free time showed a normal sinus rhythm at a mean heart rate of 70 beats/min. Sinus bradycardia, junctional escape rhythm, and multiple episodes of symptomatic sinus pauses associated with syncopal spells ranging from 2 to 8.56 seconds (Figure B) were observed during the midst of painful clusters. A cardiac angiogram showed normal coronary arteries.
Figure(A) Admission electrocardiogram shows severe sinus bradycardia with junctional escape rhythm. (B) Telemetry strip showing a sinus pause of 8.56 seconds associated with syncopal spell.
The occurrence of severe sympathovagal imbalance is characteristic of cluster headache. Conjunctival injection and nasal congestion are signs of parasympathetic hyperactivity, whereas frontal sweating, ptosis, and miosis reflect sympathetic hypofunction. Variations in heart rate, blood pressure, and electrocardiogram rhythm conduction disturbances have been reported during acute attacks.
we consistently found a progressive increase of both systolic and diastolic blood pressures from baseline to values of 200/100 mm Hg at the height of pain during each attack. At the cessation of cluster attack, our patient's heart rate and blood pressure rapidly returned to baseline levels. The pathogenesis of cluster headache remains incompletely understood. The most widely accepted theory is the central mechanism involving the hypothalamus.
reported a patient with cluster headache with an ocular prosthesis on the symptomatic side who nevertheless still exhibited bradycardia during acute cluster attacks.
Verapamil is widely regarded as the drug of choice for prophylaxis of cluster headache.
There is 1 case report in the literature in which methysergide used as prophylactic therapy eliminated the attacks and the accompanying asystole and syncopal spells
; however, methysergide is not currently marketed in the United States. Because of the significant medical consequences of the syncopal spells, with no suitable preventive therapy for the patient's cluster headache, a dual-chamber permanent pacemaker was implanted. The patient refused verapamil therapy and continued on sumatriptan and oxycodone. On follow-up visits, he reported no further syncopal spells but continued to have cluster attacks.
This case illustrates the need for careful monitoring of patients with cluster headache who present with dizziness and syncopal spells. Placement of a permanent pacemaker is a reasonable treatment option for patients who fail medical therapy or have significant side effects from the medications.
References
Russell D.
Storstein L.
Cluster headache: a computerized analysis of 24 h Holter ECG recordings and description of ECG rhythm disturbances.
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