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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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