| Indication |
For the acute treatment of migraine headaches with or without aura and the acute treatment of cluster headache episodes. |
| Pharmacodynamics |
Dihydroergotamine is indicated for the acute treatment of
migraine headaches with or without aura and the acute treatment of
cluster headache episodes. Dihydroergotamine binds with high affinity to
5-HT1Da and 5-HT1Db receptors. It also binds with high affinity to serotonin 5-HT1A, 5-HT2A, and 5-HT2C
receptors, noradrenaline a2A, a2B and a receptors, and dopamine D2L and
D3 receptors. The therapeutic activity of Dihydroergotamine in migraine
is generally attributed to the agonist effect at 5-HT1D receptors. |
| Mechanism of action |
Two theories have been proposed to explain the efficacy of 5-HT1D receptor agonists in migraine: 1) activation of 5-HT1D
receptors located on intracranial blood vessels, including those on
arterio-venous anastomoses, leads to vasoconstriction, which correlates
with the relief of migraine headache and 2) activation of 5-HT1D receptors on sensory nerve endings of the trigeminal system results in the inhibition of pro-inflammatory neuropeptide release. |
| Absorption |
Interpatient variable and may be dependent on the administration technique |
| Volume of distribution |
|
| Protein binding |
93% (to plasma proteins) |
| Metabolism |
Hepatic |
| Route of elimination |
The major excretory route of dihydroergotamine is via the bile in the feces.
Only 6%-7% of unchanged dihydroergotamine is excreted in the urine after intramuscular injection. |
| Half life |
9 hours |
| Clearance |
|
| Toxicity |
Side effects include abdominal pain, abnormal speech, coma,
confusion, convulsions, hallucinations, increase and/or decrease in
blood pressure, nausea, numbness, tingling, pain, and a bluish color of
your fingersand toes, slowed breathing, vomiting |
