Skrevet av Emne: Ice cream headache  (Lest 5404 ganger)


  • Juniormedlem
  • **
  • Innlegg: 15
    • Vis profil
Ice cream headache
« på: 12.03.2010, 16:%i:1268407045 »
Her er en artig artikkel med et meget interessent tilsvar, som jeg kom over for en tid tilbake.
Er det bare min oppfatning eller er det forsket mer på iskremhodepine enn på klasehodepine ?

Det kan godt være at klase-hodene kan lære noen triks i fra iskrem-hodene...

Ice cream headache

No need for abstinence
All sorts of things can cause headache. For migraineurs, attacks can be provoked by chocolate, cheese, cured meats, or non-food such as stress or changes in sleep habits. Headaches can herald serious neurological disease. Some people have a benign type of headache provoked by coughing or, rarely, by coitus. Many people feel that headaches are caused by eye strain or chronic sinus problems, although probably they are not.

The most common cause of head pain is ice cream, occurring in one third of a randomly selected population.1 It occurs regardless of whether someone suffers from other types of headache. Children know all about ice cream headache, although I have found that they know it best by the descriptive term "brain freeze."

The pain begins a few seconds after the rapid ingestion of cold foods or beverages and peaks in 30-60 seconds. The pain is usually located in the midfrontal area, but can be unilateral in the temporal, frontal, or retro-orbital region. It is a stabbing or aching type of pain that recedes 10-20 seconds after its onset. Rarely, it persists for two to five minutes.2 Studies have been conflicting as to whether ice cream headache is more common in people who experience migraine. Raskin and Knittle found this to be the case, with ice cream headache occurring in 93% of migraine sufferers and in only 31% of controls.3 However, a subsequent study found ice cream headache to be more common in people without migraine.2 These inconsistencies may be due to differences in subject selection?the subjects of the first study were drawn from a hospital population, whereas the controls in the second were student volunteers. While ice cream headaches are usually benign and brief, migraines are occasionally triggered by the cold stimulus.2

Ice cream headache has been studied as an example of referred pain.4 5 Experimenting on himself, Smith characterised the features of the headache.5 Applying crushed ice to the palate, he found that ipsilateral temporal and orbital pain developed 20-30 seconds later. Bilateral pain occurred when the stimulus was applied in the midline. The headache could be elicited only in hot weather; attempts to reproduce the pain during the winter were unsuccessful, even with use of a cold stimulus of the same temperature. Bird et al found a similar relation with respect to site of application of the cold substance and ipsilateral occurrence of the resultant pain.2 Some of their subjects also experienced an associated toothache.

The vascular mechanisms invoked to explain the features of migraine were also applied to ice cream headache. Wolf and Hardy characterised cold induced pain in the hand, showing that pulsation in the digital artery diminished in proportion to the intensity of pain and that injection of vasopressin increased the intensity of pain.6 Smith observed that the blanching and subsequent redness of the fingers associated with cold induced pain pointed to vascular mechanisms, with pain occurring when the fingers showed erythema and increased blood flow.5 A similar progression from constriction to dilatation has been invoked as the mechanism underlying the aura and pulsatile pain phases of migraine. Primary neural mechanisms are now thought to underlie these vascular features.

Raskin has suggested that ice cream headache may represent a model of migraine, in that both encompass disordered thresholds to sensory stimuli.1 It would be of interest to determine whether antimigraine drugs that modulate serotonergic pathways have any effect on ice cream headache.

No treatment is usually required, and sufferers rarely seek medical attention. Since the posterior aspect of the palate is most likely to produce the referred pain of ice cream headache, avoiding contact of the cold food with this area can effectively eliminate the symptoms. Most people arrive at such preventive measures without the advice of doctors. Ice cream abstinence is not indicated.

Joseph Hulihan, Assistant professor a

a Department of Neurology, Temple University Health Sciences Center, 3401 N Broad Street, Philadelphia, PA 19140, USA

  • Raskin NH. Headache. 2nd ed. London: Churchill Livingstone, 1988.
  • Bird N, MacGregor A, Wilkinson MIP. Ice cream headache?site, duration, and relationship to migraine. Headache 1992;32:35-8. [Medline]
  • Raskin NH, Knittle SC. Ice cream headache and orthostatic symptoms in patients with migraine. Headache 1976;16:222-5.
  • Wolff HG, ed. Headache and other head pain. 2nd ed. Oxford: Oxford University Press, 1963.
  • Smith RO. Ice cream headache. In: Vinken PJ, Bruyn GW, eds. Handbook of clinical neurology. Vol 5. Chichester: John Wiley, 1968:188-91.
  • Wolf S, Hardy JD. Studies on pain?observations on pain due to local cooling and on factors involved in the "cold pressor" effect. J Clin Invest 1941;20:521-33.


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.
  • 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.
  • 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.
  • Poole JW, Sammartano RJ, Boley SJ Hemodynamic basis of the pain of chronic mesenteric ischemia. Am J Surg. 1987 Feb;153(2):171-6.
  • 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.
  • Fiddian-Green RG. Provocative test for chronic mesenteric ischemia. Am J Gastroenterol. 1992 Apr;87(4):543
  • Joseph Hulihan Ice cream headache BMJ 1997; 314: 1364
  • 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
  • Herbert JM, Savi P. P2Y12, a new platelet ADP receptor, target of clopidogrel. Semin Vasc Med. 2003 May;3(2):113-22.
  • 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.
  • 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.
  • David Taggart About impaired minds and closed hearts BMJ 2002; 325: 1255-1256
  • Stephen Wolfram. A New Kind of Science. Wolfram Media, Inc., 2002.