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Keywords:

  • migraine;
  • child;
  • asystole;
  • vomiting;
  • autonomic nervous system

Abstract

  1. Top of page
  2. Abstract
  3. CASE HISTORY
  4. COMMENTS
  5. REFERENCES

A variety of symptoms that accompany migraine in the child and adult are mediated by the autonomic nervous system. Significant effects on cardiac rhythm are uncommon, but can be life threatening. We describe a 3-year-old girl in whom migraine-associated vomiting precipitated cardiac asystole which was effectively treated with a cardiac pacemaker.

Abbreviation:
ANS

autonomic nervous system

Symptoms resulting from activation of the autonomic nervous system (ANS) frequently accompany migraine. In children, symptoms such as pallor, diaphoresis, and pupillary dilation may surpass head pain as the predominant features.1-3 Similarly, gastrointestinal (GI) complaints such as nausea, vomiting, and diarrhea can exist without headache.4 Recurrent “cyclic” vomiting in which the GI symptoms predominate may be due to primary GI, endocrine metabolic, or infectious etiologies.5 However, it is likely that a majority of cases are “migraine variants” (ie, abdominal migraine based upon clinical symptoms, family history, response to medication and quantitative electroencephalographic [EEG] changes).6,7

In this report, we describe a child who experienced recurrent episodes of prolonged asystole, which were likely secondary to the vomiting component of migraine.

CASE HISTORY

  1. Top of page
  2. Abstract
  3. CASE HISTORY
  4. COMMENTS
  5. REFERENCES

The patient was the product of a normal full-term pregnancy, labor, and spontaneous vaginal delivery. Other than several episodes of otitis media and a rash with penicillin, a review of systems was unremarkable.

The patient had her first headache at 31 months of age during the evening. Several hours later, she awoke, vomited, “collapsed, appeared gray and limp with teeth clamped down tight” for less than 60 seconds, and then “all of a sudden came to,” according to her mother. By the time the paramedics arrived, she returned to her normal state. However, prior to getting into the ambulance, she vomited again and lost consciousness for less than 10 seconds. Within 1 minute, she had another episode of vomiting followed by loss of consciousness for 10 seconds. She was transported to the emergency department where physical examination and electrocardiogram (ECG) were normal.

Subsequently, the patient experienced several episodes of nausea, vomiting, and diarrhea not associated with fever and during which she had a “spacey look.” On one occasion, she was so unresponsive that she was taken to the emergency department. These events prompted magnetic resonance imaging (MRI) of the head and EEG, both of which were normal.

At 41 months, the patient vomited, appeared “spacey,” and slept for 45 minutes. Later in the day, she vomited, “collapsed,” and had tonic stiffening of all extremities. The paramedics were called and witnessed an episode of vomiting, stiffening, facial twitching, and rolling of the eyes. Several more events occurred in the local emergency department during which a 16-second period of asystole was documented. She was then transferred to our facility for further evaluation. Neurologic examination was entirely normal. The family history was remarkable for her mother who has intermittent frontal and temporal throbbing headache associated with nausea, photophobia, and phonophobia.

A chest x-ray and transthoracic cardiac ultrasound were normal. Cardiac telemetry revealed frequent sinus pauses in an otherwise normal rhythm. To reproduce the symptoms associated with vomiting, ipecac was administered in the cardiac electrophysiology laboratory. This resulted in 15 seconds of asystole similar to the event recorded in the referring hospital. The duration of the event was sufficiently brief that she did not lose consciousness. A transvenous pacemaker system was implanted and demonstrated to function appropriately when vomiting and bradycardia were induced with ipecac. An EEG performed the next day was normal other than induction of bradycardia (and pacemaker function) on the ECG following right, then left ocular compression (Figure 1). No typical clinical events were recorded during the EEG. She was discharged from the hospital on no medications.

image

Figure 1—. Electroencephalogram demonstrating bradycardia and cardiac pacer activation. “Press” indicates application of ocular pressure to the right globe. Note the onset of bradycardia after 6 seconds, followed by the pacemaker artifact. Calibration is 10 microvolts and 1 second.

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By 44 months of age, she began to have bifrontal, throbbing headaches associated with pallor, nausea, and, rarely, vomiting which were usually relieved by acetaminophen and sleep. The headaches increased in frequency to one to four per week, until she was started on nortriptyline 25 mg at night at 54 months of age. Following a dose increase to 50 mg at night, she became headache-free within 6 months and self-discontinued the medication 18 months later. She did well for 4 months when she had a severe headache associated with 10 minutes of complete confusion regarding her location, telephone number, and situation. She returned to normal after sleep. Since that time, the patient has had intermittent headaches (one to four per month), which have not caused any school loss and are effectively treated with acetaminophen. Due to episodes of inattention, impulsivity, and disruptive behavior in school, she was started on methylphenidate for attention deficit hyperactivity disorder at 8 years of age.

COMMENTS

  1. Top of page
  2. Abstract
  3. CASE HISTORY
  4. COMMENTS
  5. REFERENCES

This patient experienced several different variations of headache phenomena including migraine without aura, and confusional and abdominal migraine. It was in the context of the “cyclic vomiting” that she experienced several episodes of syncope, some associated with hypoxia induced tonic seizures. Subsequent evaluation established that these episodes were due to vomiting-induced bradycardia and asystole. The first headache at 31 months was not otherwise described due to the child's limited expressive abilities. By 44 months, she was better able to characterize the location and quality of the pain. As not all of the headaches had a duration of 2 hours or more and were not clearly unilateral in location, the International Headache Society (IHS) criteria for pediatric migraine without aura (IHS 1.1) were not strictly met. However, a set of revised criteria has been proposed which recognizes that the manifestations of migraine differ in young children.8

Irregularities in central nervous system9 and ANS10-12 activity can result in arrhythmias. For instance, sinus bradycardia can result from excessive vagal or decreased sympathetic tone.12 Sinus bradycardia is also associated with a variety of states ranging from meningitis, sepsis, hypoxia, vomiting, and vasovagal syncope. Activities such as diving, nasopharyngeal stimulation, and ocular pressure are also known to produce a reflex bradycardia.13 The oculocardiac reflex is mediated primarily by the vagus nerve and modulated by sympathetic tone.

A variety of measures have been used to evaluate ANS function in migraine that have included pupillometry and the cold pressor test14; pulse rate variation with normal and deep breathing, Valsalva maneuver, blood pressure response to tilt table15; spectral analysis of heart rate instability16; plasma norepinephrine levels, response to norepinephrine infusion, ocular instillation of epinephrine17; and quantitative measures of sympathetic and parasympathetic function.18 Autonomic nervous system function in the headache-free state has revealed evidence of increased sympathetic fluctuation,16 sympathetic hypofunction,14,17 or no differences from controls.14

Relatively few reports have documented the occurrence of arrhythmias during migraine.19 An adult has been reported who developed three episodes of atrial fibrillation during attacks of basilar artery migraine.20 Another report described a 27-year-old woman who was noted to have a persistent arrhythmia (ventricular premature beats, prolonged QT and inverted T waves) following presentation with basilar migraine.21 It is not clear from the report if the dysrhythmia was precipitated by migraine or was simply detected in the context of a headache that resulted in transient loss of consciousness. A 24-hour Holter study of 20 migraineurs reported “bouts of sinus tachycardia alternating with sinus bradycardia, nonphasic sinus arrhythmia, ST changes, T inversion, and ventricular premature beats” between headaches.22 It is not stated which, if any of these findings occurred coincident with a migraine. The authors suggested that the sinoatrial node of migraineurs has enhanced sensitivity to sympathetic and vagal tone. Another Holter study of five patients with paroxysmal hemicrania documented sinoatrial block in one patient and atrial fibrillation in another during their headaches.23

The relationship of vomiting and arrhythmias has not been systematically studied in children. An adult has been reported who had complete atrioventricular block precipitated by spontaneous and ipecac-induced vomiting.24 It can be hypothesized that due to enhanced vagal tone, vomiting may result in significant bradycardia. This is due to transient decrease of inward depolarizing currents, which are the basis for normal cardiac automaticity. However, an escape rhythm usually occurs during vomiting, which prevents prolonged asystole.25

Although the ANS is frequently involved in the symptomatology of migraine, the paucity of reports in the literature suggests that it is rarely life threatening. In the case presented in this report, the critical stimulus was the migraine-triggered vomiting which resulted in asystole either by providing excessive stimulation to a hypersensitive sinoatrial node or by an excess of vagal outflow.

To the best of our knowledge, this is the first reported case of a migraine-associated vomiting that induced a malignant cardiac rhythm in a child.

REFERENCES

  1. Top of page
  2. Abstract
  3. CASE HISTORY
  4. COMMENTS
  5. REFERENCES
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