headache analyzer

Here you'll find information and free articles on:

• Chronic Headache and the Cycle of Pain
• Who Gets Better?
• Are Botox Injections Effective?
• Migraine and Neurotransmitters

Chronic Headache and the Cycle of Pain.  Free article.

Learn about the causes and treatments for chronic headache. Read our Free Clinical Monograph, "Managing Tension Headahces."
This monograph will explain the causes of tension headaches, types of pain including the "cycle of pain" and how this cycle must  be broken in order to achieve relief.
To view Free monograph "Managing Tension Headaches"   click here. It is in PDF format.

Who Gets Better? Free article.

Read this free article about the "sticking points" that interfere with headache patients getting better as viewed through the eyes of a headache specialist.  It is in PDF format.

Are Botox Injections Effective?

Botox (boutulinum toxin A) is known to induce muscle relaxation.

A University of Toronto study (randomized double blind/placebo based design) with 26 patients who were classified as chronic daily headache sufferers was conducted. Half the population received botox injections while the other half were given a saline placebo.

Measurements included a subjective headpain and range of neck motion outcomes. At the end of 2 weeks and 4 weeks measurements of improvement were made. Those receiving botox injections had "significant improvemnt in pain reduction and range of motion." The placebo group showed no statistically significant change. In another study of migraine sufferers at the University of California 51% of a test population reported complete response to botox injections while 38% reported partial response.

The evidence shows that botox "inhibits the release of neurotransmitters" and thereore possesses an "analgesic effect."

Migraine and Neurotransmitters 

What follows is a simplified version of how migraine is generated creating pain in the blood vessels of the head and the role neurotransmitters play in this process.First we'll start with some background material on neuron cells themselves. There are three types of neurons.
Sensory neurons, whose role is to receive initial stimuli from sense organs, such as eyes, ears or nose ... plus impulses coming from within the body. 
Inter-neurons,  also called connector neurons, whose job is to read impulses received from sensory neurons.
Motor neurons, with a role of stimulating muscular contraction or regulate certain glands.

Nerve impulses are passed from one neuron to the next neuron by a series of chemical events. An impulse travels through a neuron in roughly 7 milliseconds.

Neurons have three parts: a cell body, dendrites and an axon.

Each neuron in the central nervous system contains a nerve cell body with dendrites branching off, acting as a receiver that gathers signals from other cells. At the opposite end of the nerve cell lies the axon, a thin fiber that sends signals.

The nerve impulse is received by a dendrite and moves along through the nerve cell body to the axon. At the end of the axon the nerve impulse is transmitted to the dendrite in the next nerve cell.

Where the impulse is finally transmitted to depends upon what type of neuron is involved.
Neurons do not touch each other. There is a gap between two neurons, called a synapse.
The nerve impulse must cover the gap between neuron cells to continue on its path. Either electrical conduction or chemical process can be the driver in carrying the nerve impulse across the synapse.

At the end of the axon of the transmitting neuron a calcium ion (ion = negative charge) enters the signaling cell. The plasma membrane surrounding a cell is the point at which certain substances move from the extra-cellular fluid (fluid outside the cell membrane) to the inside of the cell, and vice versa.

Proteins in the plasma membrane form openings or channels in the membrane where substances such as ions are allowed to pass.

Neurotransmitters.  When calcium moves into the axon of the sending or transmitting neuron cell (through an opening or channel) a chemical called a neurotransmitter is released into the synapse.Neurotransmitters are made in the cell body of the neuron and then transported down the axon to the axon terminal.

Molecules of neurotransmitters are stored in small "packages" called vesicles. Neurotransmitters are released from the axon terminal when their vesicles "fuse" with the membrane of the axon terminal, spilling the neurotransmitter into the synaptic gap.

The chemical that makes up the neurotransmitter moves across the synapse and binds to proteins on the membrane of the neuron that is about to receive the impulse. Protein acts as a receptor for different neurotransmitters.

Whether the receiving neuron cell is excited or inhibited depends upon the chemical that acts as the transmitter. After doing its work the neurotransmitter chemical, whether it is one that excites the receiving neuron or inhibits it, is released by the receiving neuron and goes back into the synapse.

Neuron re-uptake.For normal synaptic functioning, the neurotransmitter must be removed from the synapse. Frequently, it is moved back into the neuron that released it (a process called "re-uptake").

Enzymes acting as a catalyst break up the neurotransmitter into smaller molecules. 
These smaller molecules are recycled by the membrane of the sending neuron cell so another round of neurotransmission can occur. This is the way that the action of the neurotransmitter serotonin is stopped. If the neurotransmitter was allowed to stay in the synapse it would alter the reaction in the receiving "neuron, muscle fiber or gland cell indefinitely". An example is the effect of cocaine.

Cocaine intake yields euphoria because it blocks transporters from up-taking the neurotransmitter dopamine.

Dopamine then stays in the synaptic gap longer than it normally would, and produces "excessive stimulation of certain brain regions."
Common Neurotransmitters.Among the more common neurotransmitters are:

• Acetylcholine which either stimulates or inhibits muscle contraction
• Dopamine, the lack of which in the brain results in behaviors seen in Parkinson's disease
• Epinephrine (adrenalin) which can produce either stimulatory or inhibitory behavior
• Norepinephrine (noradrenalin) which increases blood pressure
• Serotonin which is associated with mood, learning, memory and tension

Migraine and Serotonin.The evidence for migraine implicates:

• the neurotransmitter serotonin
• changes in blood vessel size
• the activity of nerve fibers that relay sensory signals.

The first substantial lead came in the early 1960s. Studies of migraine sufferers' urine revealed serotonin abnormalities. Additional research suggested that boosting serotonin levels could decrease migraine symptoms.

When the drug methysergide was administered it seemed to ward off migraines by blocking serotonin activity.

This puzzled researchers.  Why, if increased serotonin decreased migraine symptoms and methysergide blocked serotonin, did methysergide reduce migraine symptoms?

The answer was found when it was discovered that there are different families and subtypes of serotonin receptors, or receiving areas on cells where serotonin works to produce different actions.

It is now known that "methysergide blocks the activity of serotonin at one type of receptor while mimicking the effect of serotonin at another type of receptor."

This mimicking effect makes extended blood vessels tighten and migraine symptoms diminish.

Unlike methysergide, the drug sumatriptan bypasses the blocking action and activates only the desired receptors.

Trigeminal Nerve System.  Further research has led to the belief that the trigeminal nerve system is involved in migraine.

The trigeminal nerve system carries information from "blood vessels in the head, from the membranes that surround the brain, and from the spinal cord to the brain stem. "

The trigeminovascular system connects the brain to the cranial blood vessels. One end of the double-ended axon of the trigeminal nerve is connected to the pain sensitive cranial vessels and the other connects to the brain stem.

While the trigger and sequence of events are still unclear, many scientists believe that the migraine attack effects serotonin based activities. During a migraine attack, the blood vessels dilate.

This "stretching" of the blood vessel walls produce migraine symptoms. One hypothesis is that during a migraine attack, the activation of the trigeminal nerve causes the release of peptides, which are protein fragments and this release results in inflammation of the blood vessels and increased migraine pain.

Antimigraine Drugs. Many researchers believe that sumatriptan and other related antimigraine drugs neutralize one or both of these migraine contributors (serotonin or peptides) through their actions on specific serotonin receptors.

In effect, the drug sumatriptan targets serotonin receptors located on the trigeminal nerve and the blood vessels that effect the head as well as other parts of the body such as the heart.

Sources for this article:  "Principle of Anatomy and Physiology,"Tortora and Grabowski; "Critical Decisions in Headache Management," Giammarco, Edmeads and Dodick; "Headache in Clinical Practice," Silberstein, Lipton and Goadsby; "Biology for Dummies," Siegfried;"Brain Reviews," Society for Neuroscience.