Migraine Edited

8/6/2019 Migraine Edited

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Migraine Headache Tension Headache Sinus Headache

Cluster headache SAH

Brain tumor/ mass lesion(Brain tumor.headache worsenswith body position change..vomiting in morning..neurologic s/s)

Pseudo tumor cerebri Temporomandibular joint dysfunction

Giant cell Arteritis Meningitis Right to Left Cardiac Shunt (PFO,ASD)**


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Age of onset

Frequency, intensity, and duration of attacks

Triggers (menstrual cycle), Associated symptoms (photophobia, N/V, )

Location and quality of pain (sharp, dull)

N

umber of headaches per month Family history of Migraines

Sleep and Diet hygiene (caffeine intake)

Use of pain meds (OTC, opioids)


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On general examination check b/p and pulse,

listen for bruits, palpate head and neck muscles,

and check temporal arterie

If neck stiffness or resistance to passive neck

flexion observed on exam consider meningitis

If papilledema observed on exam consider an

intracranial mass, meningitis or idiopathic

intracranial hypertension


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Migraine affects 12% of the united states populationincluding 18% of woman, 6% of men and 4% of children

Migraine typically begins affecting individuals inn therelate teens with peak prevalence occurring at approx age 40

Migraine is a major cause of disability in the workplaceleading to indirect costs to society greater than thirteenbillion dollars a year

More than 90% of patients with migraine have disabilitywith there attacksdespite the high level 60% of pts withmigraine have there headache diagnosed by a physician


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Recent research focusing on the physiologic causes of migraine hasrevealed a neurovascular etiology which includes neurochemicalimbalances, the trigeminal system and meningeal blood vessels

The large cerebral vessels, pia vessels, dura matter and large venoussinuses are innervated by sensory afferents that originate from thetrigeminal ganglion and upper cervical dorsal roots.

Stimulation of the trigeminal ganglion results in release of vasoactiveneuropeptides which lead to neurogenic inflammation. The two maincomponents of this inflammatory process are vasodilatation and plasma

protein extravasations Neurovascular theory proposes that migraine attacks are also generated in

the brain rather than just in the vasculature. The threshold for the initiationof cortical excitation is lowered because of neuronal hyper excitability


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Cortical spreading depression ofLeao (CSD) Self propagating wave of neuronal and glial depolarization that spreads across

the cerebral cortex.

Thought to activate trigeminal nerve afferents and alter blood brainmetalloproteinases (MMP) activation and up regulation.\

Thought to be the cause of auras

Serotonin Low serotonin state results in deficit in the serotonin descending pain

inhibitory system inducing trigeminovascular nociceptive pathways

Calcitonin gene related peptide (CGRP) Neuro peptide expressed in the trigeminal ganglia nerves. Functions as

neurogenic inflammatory agent and potent vasodilator of cerebral and duralvessels

potentiates trigeminovascular pain transmission from intracranial vessels to theCNS in addition to acting as mediator of neurogenic inflammation


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Stressful events

Change in sleep or meal schedules

Food (Monosodium glutamate, Nitrites, Tyramines,Phenylethylamine, Alcohol, Caffeine)

Enviornmental factors (Loud noise, odors, flickering lights)

Menses(Women suffer migraines three times more frequently than mendo; and, menstrual migraines affect 60 percent ofthese women.)


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Migraine w/o aura

Migraine with aura

Migraine variants (Menstrual migraine**, Retinal

migraine, Opthalmoplegic migraine, Familial

hemiplegic migraine, Hemiplegic migraine)


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Migraine aura is a group of neurological symptoms that canaccompany a migraine headache

Auras typically occur before the onset of migraine headache,

and the headache usually begins simultaneously with or justafter the end of aura phase

Aura presents as a progressive neurological deficit in theform of:

Visual disturbances (Flickering uncolored zigzag lines in visual field)

Sensory changes (numbness and tingling of lips, lower face and hands)

Motor weakness

Speech difficulties


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A) Aura has at least one of the following characteristicswithout motor weakness: Fully reversible visual symptoms including positive and/or

negative features Fully reversible sensory symptoms including positive

and/or negative symptoms

Fully reversible dysphasic speech disturbance

B) Aura has at least two of the following characteristicsHomonymous visual symptoms

At least one aura symptom develops gradually over greaterthan 5 minutes

Each symptom lasts between 5 and 60 minutes


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A)At least five headache attacks fulfill criteria B through D

B)Headache attacks lasting 4 to 72 hours (untreated or unsuccessfully treated

C)Headache has at least two of the following characteristic

Unilateral location

Pulsating quality

Moderate or severe pain intensity

Aggravation by, or causing avoidance of, routine physical activity ( e.g.walking or climbing stairs)

D) During headache, at least one of the following characteristics

Nausea and/ or vomiting

Photophobia and/or phonophobia

E) Headache cannot be attributed to another disorder If patient have the symptoms listed in the criteria, physicians are more comfortable that the pt truly has

that primary headache diagnosis and is less likely to have brain tumor or other gravecondition.neuroimaging is genaerally not necessary in adult patients presenting with typical migraine,normal findings on neurologic exam and no recent change in headache characteristicsonly 0.18% ofpt group show significant intraceranial pathologic lesion on neuro imaging

More than half of all pts meeting the international headache society criteria for migraine have migrainethat remain undiagnopsed


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Migraine that occurs within two days before throughthree days after migraine

Related to decreased estrogen levels that arise withmenstruation

Usually not associated with aura even in woman who

have migraine with aura at other times

Shown to be longer more severe and more resistantto treatment than other migraines.


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Migraine in children is generally shorter in duration thanmigraine in adults and often presents with less pronouncedassociated symptoms. Commonly presents as cyclicvomiting abdominal symptoms or paroxysmal vertigorather than head pain

Migraine is often mistaken for Sinus headache because theautonomic symptoms of migraine include nasal stuffinessor discharge which occur in 87% of patients with migraine

Migraine often confused with tension headache because75% of patients with migraine have neck pain during orimmediately before or after migraine and 10% havebilateral pain


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Functional brain imaging has identified abnormalitiesin the both the ascending and descending painpathways of patients with migraine both during and

between attacks. Alterations in blood flow to the dorsalpons, anterior cingulate cortex, visual cortex andauditory association cortex have been observed

Structural changes that have been noted to occur

including increased cortical thickness in motionprocessing visual areas increased density of theperiaqueduactal gray and dorsal lateral pons anddecreased gray matter in the anterior cingulate cortexand insula


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Do you have recurrent headaches that interfere with

work, family, or social functions?

Do your headaches last at least 4 hours?

Have you had new or different headaches in the past

6 months?

A migraine diagnosis is established id pt repliesyes to first 2 questions and no to 3rd


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Tension headache*

Cluster headache*

Sinus headache*

Medication overuse headache

SAH


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Most common type of headache in the generalpopulation.

Typically presents as bilateral non throbbing headache

of mild to moderate intensity in a

band likepatternw/o associated symptoms. Tension headaches differ from migraines in that they

commonly present bilaterally, lack of phono/photobiaand are not aggravated by physical activity.

Treatment options include oralN

SAIDs, combinationanalgesics containing caffeine, TCAs, Behavioraltherapy (i.e. stress reduction)

IHS classificationInfrequent episodic TTH with headache episodes less than one day a month


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A)At least 10 episodes fulfilling criteria B. through E. the number ofdays permonth with such headache determines the subtype

Less than 1 day a month: infrequent episodic TTH

1-14 days a month: frequent episodic TTH

Greater than 15 days a month: chronic TTH

B) Headache lasting from 30 min to 7 days for episodic TTH; headache lastshours or may be continuous for chronic TTH

C)At least twoofthe following pain characteristics:Pressing/non- pulsating quality Mild to moderate intensity (may inhibit but does not prohibit activities)

Bilateral location

No aggravation by walking up/down stairs or similar routine physical activityD) Both ofthe following:

No N/V

No Photo/Phonophobia

E) NotAttributed to another disorder


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Severe attacks of unilateral orbital or supra orbital accompanied by ipsilateralautonomic phenomenon (i.e. lacrimation, rhinnorrhea, nasal congestion , etc)lasting anywhere from 15min to 3hrs

Males predominantly affected 3:1

Episodic in nature followed by periods of remission

1st line treatment for acute episodes is inhaled oxygen and sub Q sumatriptan

Prophylaxis with verapamil

Preventative treatment is of utmost importance due to the frequency at which thesemay occur in a day ( up to 8x/day)KEY DISTIGUISHING FEATUREOF CLUSTE HEADACHE IS THAT PT REMAINS ACTIVECANT SIT STILL DUE TO PAINLidocaine and octreotide also promising for acute mngmntAlso effective is glucocorticoids, lithium and topiramate


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A) At least five headache attacks fulfilling criteria B through D

B)Severe unilateral orbital, supra orbital and/or temporal headache attacks, which lastuntreated for 15 minutes to 180 minutes. During part of the time course of thecluster headache, attacks may be less severe, less frequent, or of shorter or longer

durationC)The headache is accompanied by at least one of the following symptoms: Ipsilateral conjunctival injection or lacrimation

Ipsilateral nasal congestion and/or rhinorrhea

Ipsilateral eyelid edema

Ipsilateral forehead and facial swelling

Ipsilateral miosis and/or ptosis

A sense of restlessness and agitation

D)The attacks have a frequency from one every other day to eight per day

E)History and physical and neurological examination do not suggest any otherdisorder, and /or such a disorder is ruled out by appropriate investigations, orsuch disorder is ruled out by appropriate investigations, or such disorder is presetbut attacks do not occur for the first time in close temporal relation to thedisorder.


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Uncommon cause of recurrent headaches

True sinus headache occurs in conjunction with acutesinusitis, fever, and purulent discharge

Absence of these symptoms should point to migraine

as cause of headache


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Acute Treatment

Prophylactic Treatment

Alternative treatment


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Triptans (Sumatriptan, Zolmitriptan,Rizatriptan, Eletriptan) 5HT1b/1d agonists

inhibit the release of vasoactive peptides

promote vasoconstriction and block pain pathways to the brainstem

Ergotamine vasoconstrictive agent particularly affective if administered during prodrome

phase

Nausea often limits dose; poor bio availability

Dihydroergotamin Alpha adrenergic blocker acts as a potent venoconstrictor with minimal

peripheral arterial constriction Not associated with physical dependence or rebound headache

Typically administered with an anti emetic (i.e metaclopramide)Few trials comparing triptans most success found with riz and ele but that was

before sum.Pretreatment pain severity was strongest predictor of painrelef..also allodina study


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Anti depressants/ (Amitriptyline) Sedation, anticholinergicsymptoms

Anti Convulsants (Topiramate) Expensive

Residual benefit x 6months after d/c

Parasthesia, taste changes,weight loss

Betablockers (Propanalol, Timolol,) Reduces migraine freq and severity in 60-80% of pts

Long time to be effective

Poor side effect profile (erectile dysfunction, sedation)

CalciumChannel Blockers ( Verapamil, Nifedipine) 1st line for prophylaxis

tolerance

Ace Inhibitors/ARBs ( Lisinopril, Candesartan)\

NSAIDS (naproxen) Should be considered if pthaving at least 3 debilitating migrains per month Or to prevent neurologic damage in the presence of uncommon migraine conditions i.e

hemiplegic migraine


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More than four headaches a month

Last longer than 12 hrs

Failure of acute therapy

Pt Preference


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Botulinum toxin

Butterbur root

Coenzyme Q

Riboflavin

Acupuncture

Surgery (Closure of cardiac shunts)


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Bajwa, Zahid,M.D Sabhat,Ashraf, M.D Pathophysiology, ClinicalManifestations, and Diagnosis ofMigraine in AdultsUp to Date.com

Loretta L Muller D.O Diagnosing and managingMigraineHeadache:JAOA, Supplement 6,Vol 107,No11,November 2007

George RNissan, D.O, Merie L Diamond, M.D Advances in Migraine

Treatment JAOA , Supplement 2,Vol105,N04 April 2005 Andrew Charles M.D Advances in the Basic and Clinical Science of

MigraineNeurological Progress,Ann Neurol 2009;65:491-498 DynaMed [Internet]. Ipswich (MA): EBSCOPublishing. 1995 .[cited

2010 Aug 24]. Available fromhttp://www.ebscohost.com/dynamed/. Registration and login required.

Corey Foster,Nevile F. Mistry,Parvin F. Peddi, Shivak Sharma. TheWashington Manual ofMedical Therapeutics, 33rdEdition.

Anthony S. Fauci, Dennis S. Kasper, Dan L. Longo,Joseph Loscalzo,Eugene Braunwald, Stephen L. Hauser,J. Larry Jameson.HarrisonsPrinciples of InternalMedicine, 17thEdition.

Eugene C. Toy, Donald Briscoe, Bruce Britton, Bal Reddy. Case Files,Family Medicine, 2ndEdition.

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Migraine Edited