Term
| what is the most common cause of chronic pain? |
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Definition
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Term
| what are the pain sensitive structures in the head? |
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Definition
| the intracranial arteries (particularly around the meninges), dura, scalp vessels, skin, muscle, and cranial nerves. beyond these and parts of the thalamus, the brain is largely pain insensitive. |
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Term
| what are the classifications of h/a? |
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Definition
| migraine, tension-type h/a, cluster h/a, misc. h/a unassociated w/structural lesion, h/a associated w/head trauma, h/a associated w/a vascular disorder (ischemic attacks, TIA), h/a associated w/nonvascular intracranial disorders, h/a associated w/drugs or drug withdrawal (vasodilating nitrates), h/a associated w/systemic infection (very common), h/a due to metabolic disorders, h/a due to disorders of the cranium/neck/teeth/sinuses/eyes, and cranial neuralgias. |
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Term
| what is the classic migraine? |
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Definition
| migraine w/aura. a h/a preceded by or accompanied by a transient neurologic or visual phenomenon (aura). |
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Term
| what is the common migraine? |
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Definition
| h/a w/o neurologic disturbance or aura. |
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Term
| what is the complicated migraine? |
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Definition
| florid or persistent neurologic deficits (profound and distressing - stroke-like w/a speech difficulty etc.) |
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Term
| are migraines more common in pts who have asthma and DM combined? |
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Definition
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Term
| what are other common misdiagnoses for migraines? |
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Definition
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Term
| what disability class is severe migraine ranked in? |
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Definition
| the highest class (along w/psychosis or dementia) |
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Term
| how many migraine pts have a fam hx? |
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Definition
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Term
| when is the most common age for migraine onset? |
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Definition
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Term
| what are the prodromal symptoms of a migraine (~day before h/a)? |
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Definition
| mental/mood changes, depression and euphoria. sluggishness, fatigue, anorexia, and food cravings. |
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Term
| what is the migraine aura? |
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Definition
| *scintillating scotoma - which typically starts as a little flashing dot in the corner of the visual field may gradually expand to obliterate a good portion of the visual field (typically unilateral w/in the same h/a). also: *fortification spectra, *paresthesias (marching numbness up limb), and *vertigo. |
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Term
| what characterizes the migraine attack? |
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Definition
| 60% are unilateral, they may be variable between dull/steady and pulsatile, pts experience photophobia/phonophobia/osmophobia, n/v, and lightheadedness - all of which is aggravated by any physical activity. *cephalic allodynia: heightened sensitivity to normal cutaneous stimuli (like w/sunburn) of the scalp may also occur - and if it does this is an indication the pt may become more refractory to tx. |
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Term
| a migraine is a an episodic h/a lasting 4-72 hrs with_________? |
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Definition
| *any 2 of: unilateral, throbbing, worsened by movement, moderate/severe. and *any 1 of: n/v or photophobia and phonophobia. |
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Term
| what are the rapid screening questions for migraine pts? |
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Definition
| 1) do you get nauseated or sick to your stomach?. 2) does light bother you w/the h/a? 3) did your h/a limit you from working, studying or getting what you needed to done in the past 3 mos? -> sensitivity – 81%, specificity – 75% |
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Term
| what characterizes the basilar migraine variant? |
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Definition
| vertigo, tinnitus, diplopia, and ataxia |
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Term
| what characterizes the ophthalmoplegic migraine variant? |
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Definition
| CN III paralysis, more common in *children - (common w/unruptured aneurysm) |
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Term
| what characterizes the hemiplegic migraine variant? |
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Definition
| autosomal dominant inheritance |
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Term
| what are the more common migraine triggers? |
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Definition
| stress/worry, menstruation (associated with estrogen withdrawal), glare/dazzle (high contrast situations, pattern sensitivity), physical exertion/fatigue, sleep excess/deprivation, hunger, head trauma, foods, barometric changes, and pungent odors. |
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Term
| what are the less common migraine triggers? |
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Definition
| high altitude exposure, high humidity, excessive vit A, anemia (common in women), drugs (NTG/nifedipine), OCPs (more common w/high estrogen pills, women with auras have an increased risk of stroke while on OCPs), reading/refractive errors, and allergies. |
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Term
| what % of women w/migraines w/aura have a patent foramen ovale? |
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Definition
| 50%. closing it may help w/the migraines. |
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Term
| what foods commonly trigger migraines? |
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Definition
| aged cheeses, alcohol (beer+red wine), caffeine, chocolate, dairy products, fermented/pickled foods, citrus fruits, figs, raisins, nitrates, monosodium glutamate (MSG), artificial sweeteners (aspartame/saccharin), sulfites, nuts, legumes, pea pods, and yeast products |
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Term
| why are migraines so commonly misdiagnosed as involving the sinus? |
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Definition
| almost 50% of patients have accompanied autonomic symptoms: runny nose, watery eyes or a combination of both. |
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Term
| is the vascular theory for migraines still regarded? |
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Definition
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Term
| is the spreading (cortical) depression theory for migraines still regarded? |
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Definition
| no - but it does correlate with the observation of spreading oligemia (decreased CBF occurring across the cortex) |
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Term
| what is the serotonergic transmission migraine theory? |
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Definition
| platelet serotonin falls during migraine attacks (unstable serotonergic transmission -> increased activity of raphe cells -> spreading of oligemia [from PCA -> MCA]). most migraine drugs have an effect on the migraine system. |
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Term
| what is the currently accepted theory for migraine pathophysiology? |
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Definition
| the neurogenic theory - migraines are caused by a *primary disturbance of brain function. disturbances in serotonergic transmission produce changes in cerebral blood flow (not necessary for pain however), sterile inflammation then occurs in the walls of meningeal vessels which are innervated by the trigeminal nerve and consequently most head pain is referred to CN V1. the trigeminal nucleus also extends several segments downward and thus could come in contact to nucleus supplying upper cervical nerve roots - causing headaches in the neck/occipital region. the trigeminal nucleus is also very close to the superior salivatory nucleus and perhaps this explains lacrimal gland stimulation. |
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Term
| what is step therapy for migraines? |
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Definition
| start w/weak drugs and build up to stronger drugs until some effect is reached. "recipe for failure" |
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Term
| what is stratified therapy for migraines? |
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Definition
| determine pts level of need and prescribe the drug w/the correct potency |
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Term
| is acetaminophen or ASA generally considered to be more effective for migraines? |
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Definition
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Term
| what are the rapid acting triptans? |
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Definition
| sumatriptan, rizatriptan, zolmitriptan, almotriptan, and eletriptan. |
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Term
| what are the delayed acting triptans? |
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Definition
| naratriptan and frovatriptan |
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Term
| what characterizes the best administration of triptans? |
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Definition
| start w/the highest dose and work downward if pt is getting ADRs. start tx early (treat early: use less medication than if delay treatment). triptans shouldn't be used more than 2x weekly. |
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Term
| what is the MOA for the triptans? |
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Definition
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Term
| what are relative contraindications for the triptans? |
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Definition
| pts w/CAD, PVD or uncontrolled HTN. |
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Term
| when might opioids be used in migraine tx? |
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Definition
| as a rescue agent if triptan isn't working |
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Term
| when is it important to tx a migraine? |
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Definition
| before the mild phase of the h/a progresses, which is usually when cephalic allodynia occurs. past this point, the medication will be less likely to help. triptans can also cause nausea if they are taken once the h/a has become severe. |
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Term
| what characterizes prophylactic migraine tx? |
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Definition
| prophylactic tx should be considered if pts need for triptans exceeds 2x/wk. |
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Term
| what drugs can be used for prophylactic migraine tx? |
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Definition
| beta blockers (younger people tend to tolerate them poorly - cause a lot of problems with exercise intolerance, fatigue and occasionally depression), Ca++ channel blockers (not as good for migraine, better for cluster), TCAs (very effective, given at night), SSRIs (not generally effective unless mood involvement), anticonvulsants (valproic acid - very effective, but ADRs), gabapentin (wt gain), and topiramate (wt loss, memory difficulty, cognitive deficits). |
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Term
| how can botulinum toxin be used to tx migraines? |
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Definition
| injected in a pattern over the forehead, temporalis, trapezius, occipitalis and cervical paraspinals. |
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Term
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Definition
| an almost daily h/a resultant from overuse of medications in excessive and too frequent doses (transformed migraine) or emotions. they may exhibit features of both migraine and tension-type h/a's which are refractory to tx. drugs which may cause this: caffeine and triptans. abstinence from medications will usually produce a positive change w/in 3-4 days. |
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Term
| how are tension-type h/a's classified? |
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Definition
| 2 of these 3: pressing/tightening, bilateral, and not aggravated by routine physical activity. both no n/v and no photo/phonophobia. no evidence of organic dx (very important to r/o brain tumor w/imaging). |
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Term
| what is an episodic TT h/a? |
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Definition
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Term
| what is an chronic TT h/a? |
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Definition
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Term
| what is the pathophysiology of tension h/a's? |
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Definition
| no increase in scalp muscle EMG activity compared to migraine (named based on characteristics of pain), similar pt profile to migraine (women) and tension/migraine h/a co-exist in many pts. |
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Term
| what is tx for tension h/a? |
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Definition
| pharmacotherapy: similar to migraine (avoid daily analgesic use - avoid rebound h/a). physical therapy: OMT, massage, and biofeedback. psychological: only if emotional factor is majorly involved. |
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Term
| what are common h/a triggers for the h/a-prone pt? |
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Definition
| drugs, stress, alcohol (red wine), sleep disturbance, hunger, hormonal changes, etc |
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Term
| are tension and migraine h/a's possibly the same thing? |
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Definition
| yes - tension h/a may be lower intensity migraine. both are responsive to the same drugs. |
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Term
| what is the migraine spectrum? |
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Definition
| (prominent vomiting, lateralized h/a, focal neurologic symptoms) classic migraine -> common migraine -> tension/vascular h/a -> tension h/a (nondescript pain, rare vomiting, holocephalgia) |
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Term
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Definition
| a benign recurring h/a syndrome affecting *9 males to every female featuring boring, excruciating, throbbing, unilateral pain (frequently periorbital or retro-orbital). often associated w/horner's syndrome, rhinorrhea and nasal congestion. *extreme restlessness (physical activity seems to help) occurs during the attack and it is triggered by alcohol. |
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Term
| what is the cluster cycle? |
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Definition
| 1-6 attacks/day (frequently at night) for 30-90 min. these attacks "cluster" for weeks - months then remit. the suprachiasmatic nucleus is thought to be the locus of the problem, thus explaining the relation to the circadian rhythm. |
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Term
| what is tx for cluster h/a's? |
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Definition
| symptomatic: ergotamine, *injectable sumatriptan, and *100% O2. prophylactic: prednisone (h/a's may return if pt's stop meds), valproate, methysergide, lithium and verapamil. |
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Term
| what characterizes giant cell arteritis? |
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Definition
| a connective tissue disorder which involves *unilateral, intense, boring pain in a tender, non-pulsatile temporal artery. 2F:1M. 50% of these pts also have polymyalgia rheumatic and >90% have an ESR. jaw claudication is highly specific to this disease (ischemia to masseter muscles from decrease blood flow through inflamed arteries). this is less severe but more continuous than a cluster h/a. fever/wt loss: common. |
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Term
| what is the 50-50 rule for giant cell arteritis? |
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Definition
| consider if h/a w/both age and sed rate > 50. need 3 of these 5: age > 50, sed rate > 50, new onset localized h/a, non-pulsatile/tender artery, and positive bx. |
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Term
| what is the main concern w/giant cell arteritis? |
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Definition
| 1/3-1/2 of patients will develop blindness if not treated |
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Term
| how does giant cell arteritis appear pathologically? |
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Definition
| inflammation of medium sized arteries |
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Term
| what is tx for giant cell arteritis? |
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Definition
| prednisone 60-80 mg/day and temporal artery bx. if GCA suspected and ESR, begin prednisone while awaiting bx. |
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Term
| what are signs of subarachnoid hemorrhage (SAH)? |
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Definition
| *sudden onset of severe (*worst*) h/a and *nuchal rigidity. may or may not have focal findings such as CN III. |
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Term
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Definition
| CT w/o contrast (look for blood in cisterns), lumbar puncture (look for blood) then centrifuge CSF (blood will form pellet of unlysed RBCs if recent, will form yellow supernatant [xanthochromia] along w/pellet if less recent). |
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Term
| what is pseudotumor cerebri? |
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Definition
| pts w/a normal neuro exam except signs related to ICP along: papilledema (funduscopic/blind spot), h/a, and rarely: CN6 palsy (false visual sign - nerve itself is ok, just pressed by ICP) |
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Term
| how is pseudotumor cerebri diagnosed? |
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Definition
| normal CT (no mass) and lumbar puncture w/elevated opening pressure (> 18-20 cm) |
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Term
| what etiologies are associated with pseudotumor cerebri? |
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Definition
| drugs: tetracycline, vit A, steroid withdrawal. endocrine abnormalities: most common in young women w/menstrual abnormalities. |
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