Toradol (Ketorolac)
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CAUSES OF HEADACHES: NERVOUS TRANSMITTERS
There are three main types of substances acting as nervous transmitters: acetylcholine, catecholamines, and peptides.
Acetylcholine is the prime transmitter for the parasympathetic nervous system, which with the sympathetic system makes up the autonomic nervous system. Its effects are to some extent opposite to those of the sympathetic nerves: the heart is slowed, the gut becomes sluggish, the pupils become constricted. Physical exercise can make the effects of the parasympathetic more marked; this is the reason why an athlete often has a slow pulse rate, slow pumping of the heart being more efficient than rapid beating. Acetycholine also controls the muscles of the body, being released at nerve endings in muscle cells (the South American arrow poison, curare, works by blocking the effects of acetylcholine to produce paralysis).
Catecholamines: the sympathetic nervous system uses nor-adrenalin as a transmitter; this substance can be measured in the blood and its level is raised in situations such as stress or exercise when too much is released to be destroyed or taken up again. Tyramine, mentioned previously as a cause of migraine, has effects similar to those of noradrenalin. Another catecholamine, serotonin (5-hydroxytryptamine) has marked effects on the brain and is also present in the small blood cells (platelets) concerned in the first stages of blood clotting. Its relevance in the study of migraine is that it has a marked constrictive effect on blood vessels and its release from platelets can cause spasm in the related area.
Apart from their effects on blood vessels as nervous transmitters, amines also have local effects when coming into direct contact with the vessel wall. Cheese and red wine contain tyramine whereas chocolate contains phenylethylamine; once consumed these substances enter the blood stream and exert their effects on blood vessels. In those taking certain drugs for depression they may cause catastrophic rises in blood pressure. The chain reaction in patients on these drugs in no way resembles a migraine attack, however, and is more in keeping with the severe headache found with high blood pressure (hypertensive encephalopathy).
The finding that certain amines can cause vasomotor changes, raising the blood pressure and producing severe headaches, is of interest in the study of the causation of vascular headaches.
When small, measured quantities of the catecholamine transmitter tyramine are given, small, reproduceable rises in blood pressure are produced. Migraine patients need less tyramine than other people to achieve the same rise in blood pressure (there is a similar increased sensitivity to tyramine in depressed patients). The explanation may be that there is an increased sensitivity to tyramine in migraine subjects’, but it is uncertain whether this is secondary to the headaches or a sensitivity which is always present in migraine patients.
Tyramine raises blood pressure partly by stimulating the release of noradrenalin from nerve endings. These effects could spark off the changes discussed but the most obvious interpretation may not be the actual explanation. When migraine sufferers are given a tablet of tyramine, its metabolism and excretion resembles the results in similar experiments with depressed patients. It would be easy to deduce that migraine is linked to depression biochemically; but all that can be said at present is that certain people who have migraine and others who are depressed are similar in one particular biochemical measurement.
*31/152/5*
