Vascular Headache of Migraine Type Headache Classification Quickmenu Vascular Muscle-contraction Combined Nasal vasomotor reaction Delusional, hypochondriacal Nonmigrainous vascular Traction Cranial inflammation

1. Migraine with aura (Classic migraine)
2. Migraine without aura (Common) migraine
3. "Cluster" headache
4. "Hemiplegic" and "ophthalmoplegic" migraine
5. "Lower half" headache

Migraine with aura (Classic migraine)

Definition
Recurrent attacks of headache, widely varied in intensity, frequency and duration. Attacks are commonly unilateral in onset, associated with anorexia, and, sometimes, nausea and vomiting. Headaches are preceded by sharply defined transient visual and other sensory or motor prodromes or both.

Cause
Etiology unknown. Appears to be related to disordered brain physiology. Up to 70% of patients have a positive family history for headache. Frequently, the headache is an abnormal response to stress. The aura may be secondary to cerebral vasospasm; the head pain may be a result of activation of the trigeminovascular system.

Age of onset
usually starts during childhood or teenage years, up to 40 years of age.

Prodrome
Usually visual, but can be sensory, motor, speech or cognitive in nature.

Headache

description
usually unilateral, opposite the side of the prodrome.

frequency
one to two times a month

duration
v6-10 hours

quality
Throbbing, accompanied by nausea, vomiting, fatigue, sensitivity to light, noise, smells. In children, the headaches are more often bilateral and shorter in duration.

post headache phase May take 24 h to feel well\

Treatment


1. Symptomatic teatment
   1. Analgesic Medications
   2. Ergot preparations
   3. Sumatriptan
   4. Mechanism of action of sumatriptan and ergotamine.
   5. Drug treatment of migraine attacks

Prevention of Migraine

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1. Symptomatic teatment
   1. Analgesic Medications
      1. Aspirin, acetaminophen, propoxyphene, and codeine are all superior to placebo. Liquid formulations are more effective because they are absorbed more rapidly.

      2. Because gastric stasis often accompanies migraine, metoclopramide enhances the effectiveness of analgesic drugs. HOWEVER, metoclopramide can cause dystonia, and should be used sparingly in adults and should not be used in children or adolescents.

      3. When nausea and vomiting are present, suppository preparations of analgesics and antiemetics can be given. The most common antiemetics used are perphenazine, prochlorperazine, and chlorpromazine. These medications can cause tardive dyskinesia, which may be irreversible, and this risk should be discussed with the patient.

      4. COMBINED MEDICATIONS: Two types of combined medications are often used in these patients: isometheptene with acetaminophen and dichloralphenazone (Midrin), and aspirin with caffeine and butalbital (Fiorinal). Both combinations have addictive potential and can cause headache. In addition, there is no evidence that they are more effective than other analgesics. Fiorinal is approved only for treatment of tension headaches, Midrin is only "possibly effective" for migraine.

      5. Opioids should be used only for emergency treatment, in patients who have severe infrequent attacks that do not respond to other medications and/or in whom other medications are contraindicated. Meperidine is the most commonly administered opioid in this setting.

      6. NSAIDS are effective in treating migraine. There are no studies examining the relative efficacy of the various classes of NSAIDS for the treatment of migraine. These drugs may prevent neurogenically mediated inflammation in the trigeminovascular system through prostaglandin synthesis inhibition.

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   2. Ergot preparations
      1. In controlled trials, ergotamine has proved to be effective in no more that 50% of patients when given orally, sublingually, rectally, or nasally.

      2. The addition of caffeine to ergotamine enhances its absorption and possibly its vasoconstrictive activity.

      3. Ergotamine is best absorbed rectally. Metoclopramide may improve the absorption of ergotamine administered orally.

      4. Ergotamine has vasoconstrictor actions and can cause ischemia. It is therefore contraindicated in patients with coronary artery or peripheral vascular disease.

      5. Dihydroergotamine is available for parenteral use and is effective in treating migraine. Up to 90% of attacks stopped when the drug was given IV, but up to 26% of patients required more treatment secondary to recurrent HA. (In theses trials, phenothiazine was also given, which is effective alone)

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   3. Sumatriptan
      1. Sumatriptan is a serotonin (5-hydroxytryptamine (5-HT)) receptor agonist that is approved for the treatment of migraine.

      2. At the treatment dose of 6 mg SQ or 100 mg PO, peak plasma concentrations are achieved in 10 minutes and 1.5 hours, respectively.

      3. Bioavailability is >90% after SQ administration, but only 14% after PO administration. The drug is transformed into inactive metabolites in the liver, and excreted in the urine.

      4. Sumatriptan is effective in 70% patients within 60 minutes, and in 81% patients within 120 minutes after SQ administration. 12-20% pts will need additional analgesics, and 38-44% will have a recurrent HA within 24H, presumed to be a result of the short half life.

      5. When given orally, 75% patients will have relief within 4 hours, but recurrence rate is 44%. In patients with recurrence, 74% had relief with an additional treatment dose.

      6. The side effects are usually mild, and include reaction at the injection site, sensations of flushing, heat, and tingling, and neck pain with stiffness. 3-5% experience chest tightness, and rarely patients experience MI.

      7. The first dose should be given under medical supervision in patients who are likely to have unrecognized CAD (post menopausal females, men >40 years, patients with CAD risk factors). The drug is contradicted in patients with a history of MI, symptomatic IHD, prinzmetal's angina, or HTN. It should not be used with ergotamine preparations or vasoconstrictor drugs in general or when methysergide is being administered. In addition, it should not be given in patients receiving MAOIs or lithium.

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   4. Mechanism of action of sumatriptan and ergotamine.
      1. Four classes of 5-HT receptors are known: 5-HT1, 5-HT2, 5-HT3, and 5-HT4.

      2. Sumatriptan is a highly selective agonist of the D subtype of 5-HT1 receptors located on peripheral trigeminal nerve terminals that supply pain-sensitive vascular and meningeal structures, as well as the subtype of 5-HT1 receptors located on intracranial vessels, where it mediates contraction.

      3. Local release of peptides from sensory axons of the trigeminal nerve supply may cause sensitivity to pain (neurogenic inflammation) and promote local vasodilatation during a migraine attack. Calcitonin-gene-related peptide is released into jugular venous blood during a migraine, and this release is blocked by Sumatriptan. Acting presynaptically, Sumatriptan blocks the neuropeptide-mediated inflammatory response after trigeminal stimulation and may also block transmission in the trigeminal neurons.

      4. Ergotamine and dihydroergotamine have similar actions, and both have high affinity but less selectivity for 5-HT1 receptors. In addition, dihydroergotamine is a potent venoconstrictor, and it also has arterial vasoconstrictor effects, which may alleviate HA.

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Drug treatment of migraine attacks
drug	dose(mg)	peak plasma,hr	side effects
analgesic
ASA	500-650	1	dyspepsia, GI bld
acetaminophen	500	1	dyspepsia
propoxyphene	65	1	addiction
codeine	60	1	addiction, etc.
NSAID
naproxen	750-825	1-2	dyspepsia, GI bld
tolfenamic acid	200-400	1-2
flufenamic acid	250-400	1-2
mefenamic acid	500	1-2
flurbiprofen	300v	1-2
diclofenac sodium	50-100	1-2
ibuprofen	200-800	1-2
ketorolac	30-60 (IM)	0.5-1	NSAID + asthma
5-HT agonist
Ergotamine
oral	2-4	1-2	N/V, abd pain, diarrhea, muscle cramps, limb paresthesia, vasoconstriction
PR	2	0.5-2
SL	2-4	?
Dihydroergotamine
SQ	0.75-1	0.25-0.5	less severe than ergotamine
Sumatriptan
SQ	6	0.25	flushing, heat, tingling, neck pain, chest heaviness, pressure, pain
PO	100	1.5	as above
dopamine antagonist
metoclopramide,	IV 10	<0.25	dystonia
chlorpromazine,	IV 0.1mg/Kg	<0.25	tardive dyskinesia
Prochlorperazine,	IV 10	<0.25	tardive dyskinesia

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Prevention of Migraine

1. Consider only when attacks of migraine occur more than 2-3 times a month, the attacks are severe and limit normal activity, the patient is unable to cope with the attacks, symptomatic therapies have failed or had serious side effects, and attempts at nonpharmacologic prevention have failed. Some form of contraception (preferably barrier rather than oral contraception, since OCP can trigger HA) should be advised for females of childbearing age. Other medications, especially vasodilators, may trigger HA and should be discontinued.

2. Each medication should be given for an adequate time to judge its effectiveness, usually 2-3 months. Preventive medication is usually continued for 6 months or longer and gradually withdrawn after the frequency of HA diminishes.

3. Behavioral methods for stress reduction and management. Identification of triggering events, avoidance of or development of alternative coping skills for triggering events.




Drugs used to prevent migraines
Drug	daily PO dose (mg)	effectiveness	side effects
5-HT influencing
methysergide	2-8	++	muscle cramps, insomnia, tissue fibrosis
amitriptyline	10-150	++	wgt gain, drowsiness, dry mouth, blurred vision, cardiac arrhythmias, urinary retention
phenelzine	10-75	?	wgt gain, HTN
Adrenergic antagonist
propranolol	40-320	++	fatigue, nausea, bradycardia, hypotension, bronchospasm
metoprolol	200	++
atenolol	40-100	++
timolol	20	++
Nadolol	80-240	++
calcium-channel blocker
nifedipine	30	?-0	HA, tachycardia, depression
nimodipine	120	?	HA,tachy, wgt gain, constipation, depression
veapamil	280-300	?
NSAID
		?-++
misc.
valproic acid	800-1000	+	hair loss, wgt gain, hepatic dysfunction, neural-tube defect

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Migraine without aura (Common Migraine)

Definition
Vascular headache without striking prodromes and less often unilateral than classic migraine and cluster headache. Synonyms are: 'atypical migraine' or 'sick'' headache. Calling attention to certain relationships of this type headache to environmental, occupational, menstrual, or other variables are such terms as : 'summer', 'Monday', 'weekend', 'relaxation', 'premenstrual', and 'menstrual' headache. Sex ration same as in classic migraine: 3:1 in favor of women

Cause
same as classic migraine

Age of Onset
Begins at points of increasing life stress from childhood to age 40 years.

Prodrome
Not specific. Premonitory symptoms may be mood

Headache

description
Usually is unilateral, often shifting sides from one attack to another and occasionally bilateral. Location is temporal, parietal, or frontal, sometimes with a suboccipital component.

Frequency
varies widely. Commonly 2-6 events per month

Duration
8-10 hours but may last 2-4 days

Quality
Throbbing pain or constant ache if patient is lying still.

Post headache phase
Patient often feels exhausted, and feels well after 24 h.

Treatment
same as classic migraine

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Cluster headache

Definition
Vascular headache, predominantly unilateral, usually associated with flushing, sweating, rhinorhea, and increased lacrimation; brief in duration and usually occurring in closely packed groups separated by long remissions. Identical or closely allied are: erythroprosopalgia, ciliary or migrainous neuralgia, erythomelalgia of the head or histaminic cephalgia, and petrosal neuralgia. Sex ratio 4:1 in favor of men.

The facial characteristics are very typical: The patient generally has a leonine appearance with a thick-set jaw, accompanied by ipsilateral miosis, ptosis, conjuctival congestion, lacrimation, nasal stuffiness, or clear watery discharge. The autonomic symptoms disappear as the headache improves

Cause
Etiology unknown

Age of onset
May begin at age 8 to 10 years. More often, they begin during the late teen-age years or 20s.

Prodrome
Usually none

Headache

description
Headache starts as a pressure sensation over and around the eye or temple area. Within minutes, it reaches its peak, remaining at that level for 30-60 m. Then it dissipates quickly. Pain is generally unilateral and usually remains on the same side for the period of a given cluster.

frequency
Headaches occur in clusters, frequently several attacks in 24 h. Clusters may last 4-6 weeks, with long headache free intervals.

duration
30-60 min.

quality
constant boring and occasionally throbbing. Pain is located in and around the eye, over the temporal, maxillary, and frontal areas, and sometimes in the back of the neck in the suboccipital region. Pain is almost always severe to excruciating.

Treatment

1. Steroid therapy. Prednisone 40-60 mg daily for 3 days, then taper.

2. Lithium. lithium, 900 mg daily in divided doses. For chronic cluster headache, lithium may be continued for months to years.

3. Calcium-channel Blockers.

4. ergot preparations Ergotamine may be justified in some patients on a daily basis if other treatment is not effective.

5. Methysergide (Sansert), antiserotonin medication leading to vasoconstriction. Dose is 2-6 mg , Complications of long term use include pleuropulmonary fibrosis, retroperitoneal fibrosis, edema, valvular fibrosis. Most complications can be avoided if methysergide therapy is interrupted for 2 weeks after constant use for 3 months.

6. Cyproheptadine (Periactin), H1 blocker, antiserotonin, anti-cholinergic, depressant. Common side effect is weight gain.

Symptomatic treatment

1. Counter stimulation with hot or cold applications, vigorous exercise for 5-10 minutes, inhalation of 100% oxygen for 5-10 minutes.
2. ergotamine by inhalation, sublingually, orally, rectally, or injection.
3. Sumatriptan

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Hemiplegic migraine

Definition
Vascular headache featured by motor phenomena which persists during and after the headache. This headache occurs in patients with a history of classic or common migraine. The headache, when accompanied by hemiplegia, is usually more severe. Motor or sensory prodromes persist through the headache phase and may continue for several days afterward. This type of headache occurs in 0.3% of patients with migraine. The hemiplegia usually reverses after the attack, but it can become permanent after repeated attacks. It is more likely to occur in women receiving oral contraceptives or heavy users of ergotamine and/or tobacco. The mortality rate is 5%.

b>Cause
Etiology unknown. Associated with prolonged vasoconstriction and/or ischemia and hypercoagulable state, accompanied by increases platelet aggregability.

Age of onset
Most common in women 20-30 years of age.

Treatment

Prophylactic treatment

In patients who have had this type of headache previously,


1. papavering hydrochloride and aspirin, used either alone or in combination.
2. propranolol
3. calcium channel blockers
4. dipyridamole
5. avoid oral contraceptives and smoking

Symptomatic treatment


1. Aggressive treatment of headache. Rest, sedation and analgesic medication. Look for organic lesions.
2. Prednisone 15 mg Q 4h
3. AVOID ergot preparations. May make symptoms worse.
4. Calcium-channel blockers at the onset of attack.

D2. Ophthalmoplegic Migraine

Definition
Vascular headache featured by ocular phenomena which occur during and after the headache. It may lead to permanent neurologic deficit. Temporary paralysis of cranial nerve III is most common. Cranial nerves IV, VI, and V can be involved. Deficits usually begin during the headache and continue after the headache is over. The deficits may last days

Cause
Etiology unknown. Headache most likely results from mechanical compression of the affected nerve from dilated edematous adjacent arteries.

Age of onset
This disorder usually begins in childhood, sometimes as early as 2 to 3 years of age.

Prodrome
Visual prodromes develop together with the headache.

Headache
description Usually unilateral, throbbing

frequency
A few attacks per year.

duration
8-10h

quality
Usually severe

Treatment
MUST rule out organic causes, including leaking aneurysm of the internal carotid artery or posterior or anterior communicating arteries.

Treatment similar to classic or common migraines. In severe cases, corticosteroids may be helpful

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E. Lower half headache

Definition
Headache of possibly vascular mechanism, centered primarily in the lower face. In this group, there may be some instances of 'atypical facial' neuralgia, sphenopalatine ganglion neuralgia and vidian neuralgia. The is termed atypical to differentiate it from trigeminal or typical facial neuralgia. Headache predominantly occurs in women.

Cause
Headache is probably of vascular origin.

Age of onset
Disorder usually starts at age 20-30 years.

Prodrome
None

Headache

description
Usually unilateral but can be bilateral. At first the headache is episodic, often around menstrual periods. Later, the headaches are more frequent, last longer, and eventually become constant. Frequently, depression is present. Pain is located in the maxillary and periorbital areas, but it may involve the temple, ear, jaw and mandible.

frequency
As above

duration
8-10h, but can become constant

quality
Usually throbbing, but can be described as deep-seated aching, pulling or boring pain.

Treatment
Patient can be refractory to and mode of therapy. Treatment often involves treatment of depression. Ergot preparations may be helpful in patients with episodic headaches. Other medications used include tricyclic antidepressants, monamine oxidase inhibitors, methysergide, beta blockers, calcium-channel blockers. Surgery is rarely helpful, although patients frequently seek surgical cure.

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