Primary Exertion Headache

Triggers and Signs of Migraine and Headache

Primary Exertion Headache | Johns Hopkins Medicine

Tension Headaches, Cluster Headaches, and Migraines

There are a few types of headaches. Is yours the dull pain that comes from a tension headache, or is it the forceful pounding, throbbing, and nausea from a migraine? Getting good headache treatment starts with identifying which type of headache you have.

Types of Headache
There are three main types of headaches: tension-type, cluster, and migraine.

Many structures surrounding the brain sense pain, particularly tension in muscles, and changes in your blood vessels. However, the brain itself has no pain sensing nerves, and you probably have a headache as the surrounding tissues report their discomfort.

Tension headaches often result from straining muscles that cover your skull, or your face or neck muscles. They can also occur when the blood vessels that circulates in your head, face, and neck open. Stress, exercise, and medication are just some things that can make your blood vessels open and give you a short-term tension headache.

Headache pain from tension headaches usually comes on gradually, and then clears up in a few hours. If your tension headaches are severe or occur regularly, you should see your doctor. However, most headaches are just a part of life and no cause for concern.

If you experience a cluster headache, the sharp pain will occur suddenly, and concentrate behind one eye. Headache experts attribute these sudden headaches to certain medications, smoking, heavy alcohol use, and problems with a section of your brain called the hypothalamus.

Migraine Headaches: Symptoms
More than 60 million American adults report experiencing a migraine, and they affect women at a rate 3 times higher than men.1 Most people with migraines experience their first migraine as an adult, but children and teenagers can fall victim to them, too.

A pounding, throbbing, pulsating or deeply aching headache, nausea, and immobilizing pain are the main symptoms of migraine headaches. Other common symptoms may include:

  • one-sided blind spots and blurred vision
  • sensitivity to light, noise, or odors
  • fatigue and confusion
  • feeling cold or sweaty
  • a stiff or tender neck
  • light-headedness

About 20%  of people with migraines experience an aura lasting 15 to 20 minutes prior to the onset of the actual migraine.1,2 The most common aura is visual where people experience blind spots, flashing lights, and glowing zigzagging forms. Auras also involve other senses, such as numbness or a tingling feeling. They may even affect speech and confuse the migraine victim.

Learn more about migraine and headache symptoms.

Migraine Causes
Medical experts are not sure what causes migraines. Shifting levels of serotonin and other chemicals in the brain may provoke migraines, but neurologists and brain scientists admit that we have a lot to learn before we understand the cause completely.

The list below covers a selection of migraine causes; learn more about what causes migraines in our detailed migraine and headache causes article.

There are a number of migraine triggers. Food can often trigger migraines, so you should consider avoiding:

  • alcoholic beverages
  • caffeine
  • legumes, pea pods, lentils, beans, nuts, and peanut butter
  • pickled and fermented foods such as soy sauce, pickles, sauerkraut, and olives
  • bologna, ham, herring, hot dogs, pepperoni, sausage, and other aged or cured meat
  • meat tenderizer, seasoned salt, bouillon cubes, and monosodium glutamate (MSG)
  • buttermilk, sour cream, and other cultured dairy
  • aged cheese
  • the artificial sweetener aspartame
  • avocados
  • onions
  • passion fruit and papaya
  • coffee cake, donuts, sourdough bread, and other items containing fresh or brewer's yeast
  • chocolate, cocoa, and carob
  • figs, red plumbs, and raisins

Other common migraine triggers include:

  • fumes and strong odors
  • stress
  • bright lights
  • loud noises
  • fatigue
  • depression
  • weather changes
  • poor sleep
  • interruptions in your diet such as missing a meal
  • certain medications
  • hormonal changes
  • smoking
  • exercise, sex, and other intense activities

If you live with migraine headaches, avoiding triggers may help you drastically reduce the number of episodes you have to endure.

Updated on: 04/09/18

Migraine and Headache Causes

Source: https://www.practicalpainmanagement.com/patient/conditions/headache/triggers-signs-migraine-headache

Johns Hopkins Gazette | April 10, 2006

Primary Exertion Headache | Johns Hopkins Medicine
Johns Hopkins researchers have discovered a previously unrecognized role played by the gene HIF-1 as it helps cells survive when a lack of oxygen decreases production of an energy-rich molecule called ATP and increases production of toxic molecules.

ATP supplies energy the cell needs to perform each of its many chemical reactions and tasks, and in this way acts as the “currency” for the cell's energy economy.

A report on the work, done with mouse cells genetically altered to lack the HIF-1 gene, appears in the March 8 issue of Cell Metabolism.

A cell's energy demands are met by two major types of sugar (glucose) using machines similar to the two types of engines in a hybrid car. One machine, the mitochondrion, is an organelle that breaks down the glucose-using oxygen and produces ATP; the other does the same thing�albeit less efficiently�without using oxygen, in a process called glycolysis.

the hybrid car, cells use oxygen and the internal combustion engine at higher speeds and rely on an electric engine without need for oxygen consumption at lower speeds. Cells consume glucose through its main energyproducing machine, the mitochondrion, when oxygen is ample. But the internal combustion engine, this process generates pollutants or toxic oxygen molecules.

At lower oxygen levels, when cells are starved for oxygen�as during exertion or trauma�the genetic switch that the Johns Hopkins researchers found deliberately shuts off the cell's mitochondrial combustion engine, which scientists had long�and erroneously�believed ran down on its own due to lack of oxygen.

“The unexpected discovery is that this genetic switch actively shuts off the mitochondrion under low oxygen conditions, apparently to protect cells from mitochondrial toxic oxygen pollutants,” said Chi Van Dang, professor of medicine, cell biology, oncology and pathology, and vice dean for research at the School of Medicine.

Dang says the switch may be a target for cancer drugs because a cancer cell's survival depends on it to convert glucose to lactic acid through glycolysis even in the presence of ample oxygen. Disruption of the switch by a drug may cause cancer cells to pollute themselves with toxic oxygen molecules and undergo apoptosis or cell death.

The new finding, made by graduate student Jung-whan Kim and the team led by Dang, showed that during oxygen deprivation, or hypoxia, the HIF-1 gene cuts the link between two ATP-making biochemical pathways: glycolysis, which makes modest amounts of ATP by breaking down the glucose without using oxygen; and the TCA cycle in the mitochondrion, which normally uses oxygen to produce large amounts of ATP by processing a by-product of glycolysis.

The disruption of this link blocks the tendency of the mitochondrion to make toxic molecules as it struggles to produce ATP during hypoxia. These toxic molecules, called reactive oxygen species, or ROS, damage molecules in the cell and even cause the cell to undergo apoptosis.

The target of HIF-1 is the conversion of pyruvate�the by-product of glycolysis�into another molecule called acetyl co-enzyme A, according to Dang. When oxygen levels are normal, the cell produces acetyl CoA and feeds it into the TCA cycle within the mitochondrion. The mitochondrion then processes acetyl CoA using oxygen to obtain large amounts of ATP.

It was already known that during hypoxia HIF-1 accelerates the output of ATP by glycolysis, Dang noted. But until now, he said, researchers thought that HIF-1 simply turned up glycolysis and let the mitochondrion slow down on its own and produce less ATP.

Because the mitochondrion runs on oxygen, it doesn't work properly in hypoxic conditions, Dang said. Instead, glycolysis is left to shoulder the burden of making ATP by being prodded into overdrive by HIF-1. And left to itself during hypoxia, the mitochondrion produces reactive oxygen species that threaten the life of the cell.

“But our discovery clearly shows that hypoxia doesn't simply trigger a passive shutdown of the mitochondrion,” Dang said. “Instead, HIF- 1 acts as a genetic switch to actively shut down mitochondrial function and prevent the production of reactive oxygen species.”

The Johns Hopkins team demonstrated that HIF-1 shuts down the TCA cycle by preventing an enzyme called PDH from converting pyruvate made by glycolysis into acetyl CoA.

Specifically, HIF-1 blocks the ability of PDH to make this conversion. HIF-1 does this by activating a protein called PDK, which binds to PDH and prevents it from performing this critical task.

This starves the TCA cycle of acetyl CoA and shuts it down.

The Hopkins researchers made their discovery using mouse embryo fibroblast cells that were genetically altered to lack HIF-1. When the investigators exposed these socalled HIF-1 null MEFs to hypoxic conditions, the cells were unable to activate PDK to block mitochondrial function. This showed that HIF-1 is required to activate PDK.

The team then genetically engineered HIF-1 null MEFs and forced PDK to work� even in the absence of the HIF-1 gene.

The hypoxic cells once again accelerated glycolysis and produced increased amounts of ATP; and with the PDK forced to work, the cells were also able to shut down the TCA cycle.

This showed that PDK is the protein activated by HIF-1 to prevent the mitochondrion from producing ROS.

The other authors of this paper are Kim, Irina Tchernyshyov and Gregg L. Semenza, who discovered HIF-1 a decade ago.

This work was supported in part by the National Institutes of Health, National Cancer Institute and National Heart, Lung and Blood Institute. Kim is a Howard Hughes Medical Institute Predoctoral Fellow; Dang is the Johns Hopkins Family Professor in Oncology Research.

Source: https://pages.jh.edu/~gazette/2006/10apr06/10switch.html