Howard Jacobs, MD

Your 3:30 appointment is a 10-year-old boy, whom you’ve never met, with a chief complaint of “stomach pain.” You head to the exam room knowing this may be a 5-minute visit, but fearing that it may be a 45-minute visit.

Your patient is quietly sitting on the exam table in no distress playing a game console, and for a moment you think this may be easy. Then you get the history.

For the past 2 to 3 years, this young man has been plagued with repeated midline stomach pains, which (once he turns off his game) he describes as dull and achy. The pain is associated with nausea and usually vomiting. The vomitus is non-bloody, non-bilious. He denies diarrhea or other stool changes. He has a normal appetite between bouts, but has no appetite when he is in pain. He denies increased belching or sour brash. The pain is bad enough for him to miss school. His mother adds that he looks “drained” when he is ill.

He saw one of your partners several months ago who referred him to a gastroenterologist.

His workup has included CBC and differential, sedimentation rate, liver function tests, electrolytes, amylase and lipase, stool guaiac, urinalysis, a workup for celiac disease, and Mono and Hepatitis screens-all normal. He has had an upper GI with small-bowel follow through, a barium study, abdominal ultrasonography, endoscopy, and a colonoscopy-again all normal.

His mother is frustrated and sure it must be some kind of cancer.

This patient has abdominal migraines. But how do you make that diagnosis? Could you have made the diagnosis sooner?  

Between 9% and 15% of children complain of recurrent abdominal pain. Most cases are attributed to functional abdominal pain, defined as “chronic, idiopathic abdominal pain without anatomic, infectious, metabolic, or inflammatory cause.”

This broad category includes 4 distinct diagnoses

:
 •    Functional dyspepsia (functional abdominal pain or discomfort in the upper abdomen)
 •    Irritable bowel syndrome (functional abdominal pain associated with alteration in bowel movements

)
 •    Abdominal migraine (see below)
 •    Functional abdominal pain syndrome (functional abdominal pain without the characteristics of dyspepsia, irritable bowel syndrome, or abdominal migraine

Abdominal migraine is defined by the International Classification of Headache Disorders Version 2 or ICHD II

: 
 
 1.3.2 Abdominal Migraine
 An idiopathic recurrent disorder seen mainly in children and characterized by episodic midline abdominal pain manifesting in attacks lasting 1 to 72 hours with normality between episodes. The pain is of moderate to severe intensity and associated with vasomotor symptoms, nausea, and vomiting.

Diagnosis criteria:
 A.    At least 5 attacks fulfilling criteria B-D
 B.    Attacks of abdominal pain lasting 1 to72 hours (untreated or unsuccessfully treated)
 C.    Abdominal pain has all of the following characteristics:
     1.    midline location, periumbilical or poorly localized
     2.    dull or ‘just sore’ quality
     3.    moderate or severe intensity
 D.    During abdominal pain at least 2 of the following:
    1.    anorexia
    2.    nausea
    3.    vomiting
    4.    pallor
 E.    Not attributable to another disorder . . .

Most children with abdominal migraine will develop migraine headache in later life.

Let’s return to our patient. One key component of his history was missed . . . his family history. When asked, our patient’s mother states that she has had severe “menstrual headaches” for years. She describes photophobia and nausea with her headaches. At times, she takes Fioricet when she gets these headaches.

In any migraine disorder, the family history is vital. Migraines usually run in families. I tell my patients (only slightly tongue-in-cheek) that for every 100 patients I see with migraines, 80 tell me that someone on their mother’s side has headaches, 15 tell me that someone on their father’s side has headaches, and the other 5 are misinformed. In fact, 

 quoted above, includes the statement “. . . as well as a maternal history of migraine headaches” in its description of abdominal migraine.

On further questioning, you find that your patient often stays up to 1:00 AM playing video games and his abdominal pains are often associated with stressful events, such as school tests, family gatherings, or travel.

The usual patient with abdominal migraine is between 3 and 10 years old. Boys and girls are equally affected.

 Occasionally, patients will describe a prodrome or preceding aura; attacks can occur at regular intervals or they may be sporadic. Psychological stress, prolonged fasting, or lack of sleep may precipitate an attack. 

Abdominal migraine affects 1% to 4% of the pediatric population and represents 4% to 15% of patients with functional abdominal pain.

 Seventy percent of those affected go on to have migraine headaches.

 Unfortunately, abdominal migraine remains a diagnosis of exclusion, and it is not unusual for symptoms to go on for prolonged periods before the diagnosis is made.

There is limited evidence on therapy, but a few elements are clear. Lifestyle issues: poor sleep patterns, inconsistent eating habits, and stress need to be dealt with. Often, dealing with these issues alone will make a big difference in the patient’s life. Dietary measures can be explored, but are often difficult for the patient to comply with.

Migraine therapies such as sumatriptan may be helpful but formal trials are lacking. Prophylaxis should be reserved for only severely affected patients whose lives are significantly affected. Here again, controlled studies are lacking, but medicines used for migraine headache prophylaxis may be considered.

In our patient and in most cases, a clear explanation of the diagnosis and a lifestyle discussion will often go a long way toward easing the burden of the disease.
 
  
  


1. Carson L, Lewis D, Tsou M, et al. Abdominal migraine: an under-diagnosed cause of recurrent abdominal pain in children. 

 2011;51:707-712.
2. Di Lorenzi C. Chronic abdominal pain in children: a technical report of the American Academy of Pediatrics and the North American Society for Pediatric Gastroenterology, Hepatology and Nutrition: AAP Subcommittee and NASPGHAN Committee on Chronic Abdominal Pain. 

2005;40:249-261.
3. Kliegman R, Stanton B, Schor N, et al, eds. 

 19th ed. Philadelphia: Elsevier Saunders; 2011:1346-1349.
4. Headache Classification Committee. The international classification of headache disorders, cranial neuralgia and facial pain, 2nd ed. 

 2004;24(suppl 1):1-160.
5. Cuvellier J-C, Lepine A. Childhood pediatric syndromes.

2010;42:1-11.
6. Al-Twaijri WA, Shevell MI. Pediatric migraine equivalents: occurrence and clinical features in practice. 

Articles

Abdominal migraine affects up to 4% of the pediatric population and represents 4% to 15% of patients with functional abdominal pain. Most of those affected go on to have migraine headaches.

Abdominal Migraines in a 10-Year-Old Boy

There has long been a question about whether use of handheld cellular phones increases the risk of brain tumors. Are children and adolescents at higher risk because of their developing brain and smaller head size?

A quick search of my university’s reference database produced close to 100 separate titles on this subject since 2000.

Concern about the health risk of radiowaves and electronic radiation was heightened in May, 2011 when the World Health Organization’s International Agency for Research on Cancer published its findings that cell phones were possibly carcinogenic to humans.

 More precisely, the working group led by Jonathan Samet, MD, classified cell phones as a risk category 2B. 

“This category is used for agents for which there is 

in experimental animals. It may also be used when there is 

in experimental animals. In some instances, an agent for which there is 

 in humans and less than sufficient evidence of carcinogenicity in experimental animals together with supporting evidence from mechanistic and other relevant data may be placed in this group. An agent may be classified in this category solely on the basis of strong evidence from mechanistic and other relevant data.” (The italics are theirs.)

This does not read as hard evidence of a relationship. In fact, a review of available evidence does not support a significant increase in risk for the average user.  


There are a number of studies in animal models and in humans-both adult and children-that argue against a relationship between cell phone use and brain tumors. A 2001 animal model study showed that there was no “statistically significant evidence” that radiofrequency fields caused brain tumors.


In a human adult study in Denmark, using the national data base, comparing all citizens with mobile phone contracts to all those without contracts, there was no increased risk of brain tumors in the cell phone group.

The CEFALO study of children and adolescents in Denmark, Sweden, Norway, and Switzerland, also found no relationship.

Some studies do suggest a relationship and some suggest a potential increased risk only for the long-term or high-use cell phone subgroup.

 Even this association has been questioned, however.

There is no evidence that radiation from a handheld cell phone causes any DNA changes. Therefore, the biologic basis of any increased risk must be related to local heat production.

 If this is the case, should we be studying the increased risk of brain tumors associated with childhood fevers?

Most significantly, despite an exponential increase in the use of handheld mobile phones in the past 10 years in both the United States and Great Britain, there has been no corresponding increase in brain tumors.

One would assume that if there was such an association, that there would have been some corresponding increase in incidence of these malignancies.

All this information can make one comfortable that the likelihood of there being a relationship between cell phone use and brain cancer is quite small, and -if one exists- then it does so only for very heavy users.

Would it be prudent for heavy users to use a hands-free device? All one can say is, it certainly couldn’t hurt.

However, if we put all of this into perspective, we are left with 2 important questions:

1. Is this a moot issue? Are teenagers and young adults, in fact, even holding cell phones to their ears any more? An ever increasing proportion of communication is done by texting, and more and more of the remaining voice communication is done using a hands-free device, so the phone is nowhere near the head.

2. Are brain tumors the real risk? Even if the risk of brain cancer was shown to be increased with cellular phone use, the numbers would be small and would pale in comparison to the risk of injury and death caused by inattention while texting and voice cell phone use during driving.

References:
1. World Health Organization. International Agency on Research for Cancer classifies radiofrequency electromagnetic fields as possibly carcinogenic to humans. Press release 208. May 31, 2011. 

http://www.iarc.fr/en/media-centre/pr/2011/pdfs/pr208_E.pdf


2. Zook BC, Simmens SJ. The effects of 860 MHz radiofrequency radiation on the induction or promotion of brain tumors and other neoplasms in rats. 

2001;155:572-583.
3.  Frei P, Poulsen AH, Johansen C, et al. Use of mobile phones and risk of brain tumours: update of Danish cohort study. 


4. Aydin D, Feychting M, Schuz J, et al. Mobile phone use and brain tumors in children and adolescents: a multicenter case-controlled study. 

2011;103:1-13.
5.  Cardis E, Armstrong K, Bowman JD, et al. Risk of brain tumours in relation to the estimated RF dose from mobile phones: results from five Interphone countries. 

2011;68:631-640.
6. Khurana V, Teo C, Kundi M, et al. Cell phones and brain tumors: a review including the long-term epidemiologic data. 

2009;72:205-215.
7. Swerdlow A, Feychting M, Green A, et al.  Mobile phones, brain tumors, and the interphone study: where are we now? 

2011;119:1534-1538.
8. Ahlbom A, Green A, Kheifets L, et al. Epidemiology of health effects of radiofrequency exposure. 

 2004;112:1741-1754.
9. Inskip PD, Hoover RN, Devesa SS. Brain cancer incidence trends in relation to cellular telephone use in the United States. 

2010;12:1147-1151.
10. de Vocht F, Burstyn I, Cherrie JW. Time trends (1998-2007) in brain cancer incidence rates in relation to mobile phone use in England. 

Whether handheld phones increase the risk of brain tumors has long been controversial. Are children and adolescents at higher risk because of their developing brain and smaller head size?

Howard Jacobs, MD

Articles

Abdominal Migraines in a 10-Year-Old Boy

Cell Phones and Brain Tumors: Is There a Connection?