Therapeutics – Migraine

advertisement
Migraine Definition - “Migraine is a familial disorder characterized by recurrent attacks of headache
widely variable in intensity, frequency and duration. Attacks are commonly unilateral and are usually
associated with anorexia, nausea and vomiting”
TRIGGERS OF MIGRAINE
 A migraine trigger is any environmental or physiological factor that leads to a headache in
individuals who are prone to develop headaches. Examples of triggers include:
 Sleep and migraine
 Fasting and migraine
 Bright lights and migraine
 Caffeine and migraine
 Chocolate, wine, tyramine, MSG, nitrites, aspartame and migraine
MIGRAINE – PATHOPHYSIOLOGY
Not completely understood. Some of the theories are:
1. VASCULAR THEORY
 Stress or some unknown factor triggers the release of certain protein fragments called peptides
(e.g., Substance P, calcitonin gene-related peptide, and others).
 These peptides dilate blood vessels and produce an inflammatory response that triggers overexcitation of the nerve cells in the trigeminal pathway. (This nerve pathway runs from the brain
stem to the head and face. These nerves spread to the meninges (the membrane covering of the
brain).
2. SEROTONIN THEORY
 Abnormal Calcium Channels. Some migraines may be due to abnormalities in the channels
within cells that transport the electrical ions calcium, magnesium, sodium, and potassium.
Calcium channels appear to play a particularly critical role in migraine patients:
 Calcium channels regulate the release of serotonin, an important neurotransmitter in
the migraine process. (A neurotransmitter is a chemical messenger that allows
communication between nerves in the brain.)
 Magnesium interacts with calcium channels and magnesium deficiencies have been
detected in the brains of migraine patients.
3. CENTRAL NERVOUS SYSTEM THEORY
 One theory of the cause of migraine is a central nervous system (CNS) disorder. The CNS consists
of the brain and spinal cord. In migraine, various stimuli may cause a series of neurologic and
biochemical events which affect the brain's vascular system.
4. CENTRAL NERVOUS SYSTEM SENSITIVITY THEORY
 Some research suggests that problem may result from a continuum of abnormalities in the
central nervous system .
 Such changes trigger a progression of symptoms starting with mild sensations, developing into
tension headache, and finally, progressing in some people to a migraine.
MIGRAINE CLASSIFICATION
According to Headache Classification Committee of the International Headache Society, Migraine has
been classified as:
 Migraine without aura (common migraine)
 Migraine with aura (classic migraine)
PHASES OF ACUTE MIGRAINE

Prodrome
 Vague premonitory symptoms that begin from 12 to 36 hours before the aura and
headache
 Symptoms include
 Yawning
 Excitation
 Depression
 Lethargy
 distaste for various foods
 Duration – 15 to 20 min

Aura
 Aura is a warning or signal before onset of headache
 Symptoms
 Flashing of lights
 Zigzag lines
 Difficulty in focusing
 Duration : 15-30 min

Headache
 Headache is generally unilateral and is associated with symptoms like:
 Anorexia
 Nausea
 Vomiting
 Photophobia
 Phonophobia
 Tinnitus

 Duration is 4-72 hrs
Postdrome
 Following headache, patient complains of




Fatigue
Depression
Severe exhaustion
Some patients feel unusually fresh
 Duration: Few hours or up to 2 days
SIGNS AND SYMPTOMS
The classic migraine headache is characterized by unilateral head pain preceded by various visual,
sensory, and motor symptoms, collectively known as an aura. Most commonly, the aura consists of
visual manifestations such as scotomas, photophobia, or visual scintillations (eg, bright zigzag lines)
Symptoms of migraine may include the following:






Headaches commonly occur when the person is awake, or they may have already started upon
awakening; less commonly, it may awaken the person at night
Throbbing or pulsatile headache, with moderate to severe pain that intensifies with movement
or physical activity
Unilateral and localized in the frontotemporal and ocular area
Pain typically builds up over a period of 1-2 hours, progressing posteriorly and becoming diffuse
Headache typically lasts 4-72 hours
Nausea (80%) and vomiting (50%), including anorexia and food intolerance, and lightheadedness
Postdromal symptoms may persist for 24 hours after the headache. They may include the following:




Feeling tired, “washed out,” or irritable
Feeling unusually refreshed or euphoric
Muscle weakness or myalgias
Anorexia or food cravings
Migraine variants include the following:







Childhood periodic syndromes
Late-life migrainous accompaniments
Vertebrobasilar migraine
Hemiplegic migraine
Status migrainosus
Ophthalmoplegic migraine
Retinal migraine
DIAGNOSIS
The clinical diagnosis of migraine headache is based on the patient’s history.
Examination for migraine headache may reveal the following:








Photophobia and/or phonophobia
Hemiparesis, aphasia, confusion, paresthesias/true numbness
Prodrome or aura
Cranial/cervical muscle tenderness
Horner syndrome (ie, relative miosis with 1-2 mm of ptosis on the same side as the headache)
Conjunctival injection
Tachycardia/bradycardia
Hypertension/hypotension
Physical examination findings suggesting a more serious cause of headache include systemic symptoms
(eg, myalgia, fever, malaise, weight loss, scalp tenderness, jaw claudication) and focal neurologic
abnormalities or confusion, seizures, or any impairment of level of consciousness. A migraine variant
may be suggested by focal neurologic findings that occur with the headache and persist temporarily
after the pain resolves, such as the following:



Unilateral paralysis or weakness: hemiplegic migraine
Aphasia, syncope, and balance problems: basilar migraines
Third nerve palsy, with ocular muscle paralysis and ptosis, including or sparing the pupillary
response: ophthalmoplegic migraine
Testing and imaging studies
Selection of laboratory and/or imaging studies for migraine headache is determined by the individual
presentation.
Neuroimaging (eg, CT scanning, MRI, MRA) is not necessary in patients with a history of recurrent
migraine headaches and a normal neurologic examination. However, perform neuroimaging for any of
the following features :










Onset of migraine after age 50 years
Change in the pattern of previous migraine
First or worst severe headache
New onset of headache in a patient with cancer or HIV infection
Headache with an abnormal neurologic examination
Headache with fever
Migraine and epilepsy
New daily persistent headache
Escalation of headache frequency/intensity in the absence of medication overuse headache
Posteriorly located headaches in children
Other tests
Neuroimaging should precede lumbar puncture to rule out a mass lesion and/or increased intracranial
pressure. The following are indications for lumbar puncture:




First or worst headache of a patient's life
Severe, rapid-onset, recurrent headache
Progressive headache
Atypical chronic intractable headache
MANAGEMENT
Acute/abortive medications
Acute treatment aims to stop or prevent the progression of a headache or reverse a headache that has
started, and it is most effective when given within 15 minutes of pain onset and when pain is mild.The
choice of migraine headache abortive medication is individualized, depending on the severity of the
attacks, associated symptoms such as nausea and vomiting, comorbid problems, and the patient's
treatment response.
Medications for migraine headache include the following:



Moderate headache: NSAIDs, isometheptene, ergotamine, naratriptan, rizatriptan, sumatriptan,
zolmitriptan, almotriptan, frovatriptan, eletriptan, dopamine antagonists
Severe headache: Naratriptan, rizatriptan, sumatriptan (SC,NS), zolmitriptan, almotriptan,
frovatriptan, eletriptan, DHE (NS/IM), ergotamine, dopamine antagonists
Extremely severe headache: DHE (IV), opioids, dopamine antagonists
A transdermal patch for migraine, sumatriptan iontophoretic transdermal system (Zecuity, NuPathe Inc),
was approved by the FDA in January 2013 for the acute treatment of migraine with or without aura in
adults. In addition to treating pain, the single-use patch treats migraine-related nausea, which may
affect up to half of the 16 million US adults diagnosed with and treated for migraine. FDA approval was
based on phase 3 trials involving 800 patients treated with more than 10,000 patches, in which the
patches safely and effectively relieved migraine pain, migraine-related nausea, sonophobia, and
photophobia within 2 hours of activation.
Preventive/prophylactic medications
Preventive treatment, which is given even in the absence of a headache, aims to reduce the frequency
and severity of the migraine attack, make acute attacks more responsive to abortive therapy, and
perhaps also improve the patient's quality of life.
The 3 principal classes of medications that are effective for migraine prevention are antiepileptics,
antidepressants, and antihypertensives. First-line agents for prevention of migraine headache include
the following:


High efficacy: Beta-blockers, tricyclic antidepressants, divalproex, topiramate
Low efficacy: Verapamil, NSAIDs, SSRIs
Second-line agents for prevention of migraine headache include the following:


High efficacy: Methysergide, flunarizine, MAOIs
Low efficacy: Cyproheptadine, gabapentin, lamotrigine
Use of botulinum toxin A has produced mixed results in patients with intractable migraine headaches
that fail to respond to at least 3 conventional preventive medications.
Nonpharmacologic management
Biofeedback, cognitive-behavioral therapy, and relaxation therapy are frequently effective and may be
used adjunctively with pharmacologic treatments. Occipital nerve stimulators may be helpful in patients
who are refractory to other forms of treatment.
Surgical deactivation of migraine headache trigger sites (eg, corrugator supercilii muscles,
zygomaticotemporal branch of the trigeminal nerve ) can help eliminate or significantly reduce migraine.
Download