I have gotten ice cream backaches my whole life and never understood the concept of a "brain freeze."

I got a lot of goofy looks when I wold wiggle and squirm to try to get rid of the backache I'll tell you, and as a kid that has something happen to them that happens to no one else, you can guess that it was a source of ridicule.

I'm not the only one I know that gets backaches, but the other two are my mother and sister, and at that, my sister alternates between a headache and a backache.

My brother gets headaches, though. Maybe it's a latent trait of some variety. If it were simply a vaso-constriction in the brain or cold traveling through your blood stream, the response would be 100%. However, it wasn't 100% even in the migraine group. My thought, based on my experience with my immediate family having the problem, is that there is a chromosome that triggers the effect of the Ice Cream Headache, and another to show where it is.

Competing interests: None declared

i find that when ice cream comes into contact with the roof of the mouth and the back of the throat a temporary brain freze results that, if endured, will end in a few seconds. However, I also find that anything you ingest warmer than the ice cream quickly reverses the problem.

Competing interests: None declared

This is an intriguing problem. Two observations come to mind. The first was a man in his forties with hypertension who had a coeliac axis stenosis and who developed abdominal pain whenever he drank cold water (1). His pain was accompanied by a gastric intramucosal acidosis, which would appear in my current thinking to be caused by the rate of energy release by ATP hydrolysis that exceeds the rate at which ATP is resynthesised by oxidative phosphorylation. Revascularisation eliminated the the intramucosal acidosis and like the other patients studied appeared to eliminate his symptoms but these patients are notoriously difficult to evaluate. Food of course is the usual stimulus. Another investigator has comfirmed our provocative findings (2).

One mechanism by which intragastric stimuli might cause abdominal pain is by causing vascular or smooth muscle muscle spasm. Another mechanism is by causing a steal of blood flow from a midgut supplied by stenotic mesenteric arteries (3,4,5). Neither of these would seem to account for an ice cream headache (6). A haematogenous or neural/humoral reflex needs to be invoked.

A decrease in temperature causes a rise in pH by a purely physical effect (7). If high enough it will inhibit oxidative phosphorylation by eliminating the protonmotive force driving ATP resynthesis by oxidative phosphorylation. In so doing it might increase the [ADP] and induce a haemotological changes such as activation of the ADP receptors on platlets (8). Cold is known to cause cryoprecipitation of blood products in some patients.

As the supply of oxygen is not inhibited in these circumstances the stage may be set for free radical release upon rewarming. In which case a bolus of free radicals might be released not only into portal venous blood but also into gastric lymphatics and have direct access to the brain by draining into the thoracic duct. Perhaps this caused the ice cream headache.

The release of free radicals upon reperfusion has been implicated in the causation of pain (9). Furthermore the free radical release induced by reperfusion after a transient fall in gastic intramucosal pH has been implicated in multiple organ dysfunction (10). Neurological ddysfunction appears to be the most sensitive symptomatic measure of multiple organ dysfunction in awake patients(11).

Sir Thomas Lewis brought the scientific method to the investigation of human disease at the bedside when he was at Univeisty College. In 1927 he described the triple response to a cutaneous njury, flush(redline), flare(red zone) & weal(edema), and the classic five signs - rubor(redness), tumor(swelling), calor(Heat), dolor (pain) and loss of function of inflammation are well known. It starts with dilatation of blood vessels(vasodilatation) to bring more blood (Hyperemia) and along with it the mediators of defence & healing. Blood vessels become leaky allowing escape of fluids(transudation), proteins & cells (exudation) into tissue space causing edema. The WBC crawl out of capillary(emigration) towards site of injury attracted by chemicals(Chemotaxis) and engulf debris (phagocytosis). Antibodies and other chemical mediators of inflammation serve to neutralise the injurious agents such as microbes.

If one thinks about cutaneous injury, which contrary to visceral injury is painful, it occurs in an hyperoxia, hypocarbic environment. This should inhibit oxidative phosphorylation by elevating the pH and thereby presumably prevent the generation of free radicals until reperfusion when it could be excessive. If blood flow is compromised at first from vasocontriction and platelet plugging coling should also occur compounding thelevation in pH in increasing the need for an exothermic metabolic response, one that iappears to occur with anaerobic glycolysis. The lumen of the gut is, in contrast, microaerophilic. It has a very low pO2, relative to air, and a pCO2 the same as that in arterial blood or a little higher on occasions. These are not circumstances in which free radicals should be produced in anything like the amount presumabky seen after, for example, removal of a colonic polyp. The difference might account in part for the difference in pain experienced.

The release of free radicals upon reperfusion might be responsible for the initial pain experienced in the triple and for an ice cream headache, the latter being a systemic and the former a local manifestation. The pain associated with the later inflammatory response might be a regional manifestation.

If in the evolution of man avoiding the toxic effects of oxygen has been a crucial property then, thinking in terms of a simple cellular automata or Wolfram rule(12), pain is a likely derivative. It is not a response that would have included a nervous system until evolution was far advanced.

1. Fiddian-Green RG, Stanley JC, Nostrant T, Phillips D. Chronic gastric ischemia. A cause of abdominal pain or bleeding identified from the presence of gastric mucosal acidosis. J Cardiovasc Surg (Torino). 1989 Sep-Oct;30(5):852-9.

2. Faries PL, Narula A, Veith FJ, Pomposelli FB Jr, Marsan BU, LoGerfo FW The use of gastric tonometry in the assessment of celiac artery compression syndrome. Ann Vasc Surg. 2000 Jan;14(1):20-3.

3. Poole JW, Sammartano RJ, Boley SJ Hemodynamic basis of the pain of chronic mesenteric ischemia. Am J Surg. 1987 Feb;153(2):171-6.

4. Boley SJ, Brandt LJ, Veith FJ, Kosches D, Sales C A new provocative test for chronic mesenteric ischemia. Am J Gastroenterol. 1991 Jul;86(7):888-91.

5. Fiddian-Green RG. Provocative test for chronic mesenteric ischemia. Am J Gastroenterol. 1992 Apr;87(4):543

6. Joseph Hulihan Ice cream headache BMJ 1997; 314: 1364

7. JOHN W. SEVERINGHAUS, POUL ASTRUP, and JOHN F. MURRAY Blood Gas Analysis and Critical Care Medicine. Am. J. Respir. Crit. Care Med., Volume 157, Number 4, April 1998, S114-S122

8. Herbert JM, Savi P. P2Y12, a new platelet ADP receptor, target of clopidogrel. Semin Vasc Med. 2003 May;3(2):113-22.

9. Xanthos D, Francis L, Bennett G, Coderre T. Animal Models of Chronic Pain: Chronic post-ischemia pain: A novel animal model of Complex Regional Pain Syndrome Type I produced by prolonged hindpaw ischemia and reperfusion in the rat. J Pain. 2004 Apr;5(3 Suppl 2):S1.

10. Nielsen VG, Tan S, Baird MS, McCammon AT, Parks DA Gastric intramucosal pH and multiple organ injury: impact of ischemia-reperfusion and xanthine oxidase. Crit Care Med. 1996 Aug;24(8):1339-44.

11. David Taggart About impaired minds and closed hearts BMJ 2002; 325: 1255-1256

12. Stephen Wolfram. A New Kind of Science. Wolfram Media, Inc., 2002.

Competing interests: None declared

Competing interests: None declared