Headaches

What causes the pain?

The nerve tissue of the brain is not pain sensitive; however the connective tissues lining the brain, known as the meninges, are dense with pain sensing nerve endings. When there is pressure, inflammation, infection, chemical imbalance or stretch in these tissues, the nerves fire signals to the pain-interpreting centre in the brain, and we experience the phenomenon we all call “pain”.

From a primary care point of view, head pain can be sorted into three categories according to urgency of care required:

Immediate medical attention required – Osteopaths are well trained to identify these circumstances and manage prompt onward referral.

Further investigation required – You need to be seen by your GP in the near future for pharmaceutical control or onward referral for imaging or blood tests.

Safe to treat  – The majority of headache presentations are safe to treat and osteopathy can be very helpful.

Osteopathic Treatment

Liem (2001) states that Osteopathic treatment to the neck and Cranial Osteopathy can aid in the relief of Migraines. With an Osteopathic consultation, a better understanding of your condition will be achieved.

Tension Type headaches

It stands to reason that avoiding the triggers for TTHs would be a good way of managing them. The common triggers listed in academic writing about TTHs are stress, eye strain, sleep deprivation, hunger and posture. It sounds like a holiday would cure most of that! The notable exception is posture.

When anatomists discovered that the muscle tissues of the upper neck are continuous with the meninges of the brain stem, this provided a good theoretical basis for the observed link between neck muscle tension and headaches. In recent years, this type of headache has become known as Cervicogenic, which translates as “coming from the neck”.

Treatment – As most people know, Osteopaths are well equipped to relax muscle tension, and this would explain our success rate at treating Cervicogenic headaches. I also believe that relieving muscle and other tissue tension has a positive influence on stress levels and sleeping.

Migraines

Migraines are defined as one sided pulsing pain present in the head that is present from 4 up to 72 hours. Additional symptoms include nausea, vomiting, photophobia (sensitivity to light) and phonophobia (increased sensitivity to sound). Females are three times more likely to suffer from headaches, than males.

Stages:

  1. The prodrome, which occurs hours or days before the headache in up to 60% of cases. Symptoms vary between person to person – altered mood, fatigue, yawn, food craving, dizziness, stiff musculature (mainly neck), increase/decrease urination and visceral symptoms.
  2. The aura, which immediately precedes the headache – there are 4 types: multicolored lights (photopsia) zig zag lines (scintillating scotoma), blurred or shimmering or cloudy vision, and hemianopsia. There may be pins and needles in face and/or arms and hands.
  3. The pain/headache phase – mostly unilateral and aggrevated by physical exertion. Nausea in 90% of cases, possible vertigo and cold extremities.
  4. The postdrome – soreness over the headache area, general fatigue and ‘hungover’ feeling.

Theories behind cause:

The cause behind migraines aren’t fully understood. There are, however, several theories.

Triggers:

Can be stress, hunger, types of food and fatigue. Migraines are more likely to occur around menstruation. Other hormonal influences, such as menarche, oral contraceptive use, pregnancy, perimenopause, and menopause, also play a role.

Depolarization:

Also known as cortical spreading depression, which is associated with the aura of migraine. In cortical spreading depression, neurological activity is initially activated, then depressed over an area of the cerebral cortex. Releases inflammatorymediators leading to irritation of cranial nerve roots, most particularly the trigeminal nerve, which conveys the sensory information for the face and much of the head.

Vascular:

Studies have shown aura coincides with constriction of blood vessels in the brain. This may start in the occipital lobe, in the back of the brain, as arteries spasm. The reduced flow of blood from the occipital lobe triggers the aura. When the constriction stops and the aura subsides, the blood vessels of the scalp dilate. The walls of these blood vessels become permeable and some fluid leaks out. This leakage is recognized by pain receptors in the blood vessels of surrounding tissue. In response, the body supplies the area with chemicals which cause inflammation.

Serotonin:

Low serotonin levels in the brain may lead to a process of constriction and dilation of the blood vessels which trigger a migraine. Serotonergic agonists, such as triptans, activate serotonin receptors to stop a migraine attack.

Melanopsin receptor:

A melanopsin-based receptor has been linked to the association between light sensitivity and migraine pain, but this is currently speculation.

Neural:

When certain nerves or an area in the brain stem become irritated, a migraine begins. In response to the irritation, the body releases chemicals which cause inflammation of the blood vessels. These chemicals cause further irritation of the nerves and blood vessels and results in pain. Substance P is one of the substances released with first irritation. Pain then increases because substance P aids in sending pain signals to the brain.

Unifying theory:

Both vascular and neural influences cause migraines.

  1. Stress triggers changes in the brain
  2. These changes cause serotonin and/or histamine to be released
  3. Blood vessels constrict and dilate.
  4. Chemicals, including substance P, irritate nerves and blood vessels, causing neurogenic inflammation and pain.