Electrocardiographic changes during migraine attacks.

OBJECTIVES: To clarify whether electrocardiographic (ECG) changes can be identified during a migraine attack and to determine whether there are ECG differences between periods with and without headache. BACKGROUND: The clinical signs and symptoms of migraine point to involvement of the autonomic nervous system, and especially to disrupted regulation of the circulatory system and autonomic balance. This disruption may be more marked during a migraine attack. During a migraine attack, autonomic imbalance within the heart and its vessels conceivably may result in ECG abnormalities. METHODS: In 30 patients with migraine, the ECG variables of heart rate, abnormalities of rhythm, PR interval, QRS duration, corrected QT interval, T inversion, and ST-segment changes were recorded during migraine attacks and pain-free periods. RESULTS: Of the 30 patients studied during a migraine attack, 9 (30%) had one or more abnormalities of rhythm (including sinus arrhythmia, atrial premature contraction, and ventricular premature contraction), 20% had PR intervals greater than 0.20 seconds, 40% had corrected QT intervals greater than 0.44 seconds, 66% had T inversion, and 40% had ST-segment abnormalities. No patient had arrhythmia, PR intervals greater than 0.20 seconds, or corrected QT intervals greater than 0.44 seconds during a pain-free period. No differences were noted for ST-segment changes, T inversion, and total ECG changes between periods with and without headache, but both PR and corrected QT intervals were significantly longer during migraine attacks than during pain-free periods. CONCLUSIONS: We conclude that ECG abnormalities often are present during a migraine attack, and for most of these, particularly PR and corrected QT interval lengthening, these abnormalities will be absent or less prominent during pain-free intervals.

Basic toxicological approach has been effective in two poisoned patients with amitraz ingestion: case reports.

Amitraz, a formamidine insecticide and acaricide used in veterinary practice, presents side effects in humans related to its pharmacological activity on alpha 2-adrenergic receptors. There is little information available in the literature about the toxicology of the product in man and the treatment of this poisoning. In this report, the clinical and laboratory features of amitraz poisoning in two patients by a veterinary formulation also containing xylene are presented. The major clinical findings were unconsciousness, drowsiness, respiratory failure requiring mechanical ventilation, miosis, hypothermia and bradycardia. The laboratory findings were hyperglycemia, hypertransaminasemia and increased urinary output. Supportive management of this poisoning in humans is suggested in only a few articles and there is no specific antidote for the subsequent possible pharmacological effects of amitraz. In our two cases, we performed supportive treatment such as mechanical ventilation, atropine, gastric lavage, active carbon, oxygen and fluid administration. We concluded that the basic approach to the patient with amitraz poisoning, including initial stabilization to correct immediate life-threatening problems, treatment to reduce absorption and measures to improve elimination of the toxin, is effective.