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35 Cards in this Set
- Front
- Back
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pertinent HA history
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Prior history of HA
Multiple HA types Age of onset Location and radiation Pain quality and severity HA frequency, duration Mode of onset and termination, sleep onset Precipitating, exacerbating and alleviating factors Associated symptoms Medication and general medical history History of head trauma Family history of HA |
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physical examination in HA
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Inspection, palpation and percussion of the skull
Assessment of the ears Evaluation of the temporomandibular joints Palpation of glandular and lymphatic tissue Inspection of the teeth and oropharynx Assessment of the nose and paranasal sinuses Examination of the eyes - fundi Assessment of extracranial vessels - STA Palpation of head and neck muscles, neck mobility |
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Clues to serious disease presenting with HA
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Sudden “first or worst” HA
Simultaneous/subsequent neurologic deficit Focal signs, increased ICP Fever or meningeal signs Side locked HA Onset after age 50 Vomiting days to weeks before HA Altered consciousness Behavioral changes Paroxysmal hypertension Endocrine changes Onset after Valsalva Onset with head move-ment, change in position Change in pattern or response to therapy Not a standard syndrome Also Hx of trauma and progressive inc in severity Higher likelihood of secondary HA if immunosuppressed. |
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Diagnostic testing for HA
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imaging- CT, MR: tumor, hydrocephalus, hemorrhage, sinovenous thrombosis, vascular malformations, sinusitis
LP: SAH, encephalitis/meningitis, BIH, low pressure HA Angiography: aneurysmal SAH, vasculitis STA biopsy, ESR, CRP: GCA Polysomnography: OSA EEG, skull films: no indication |
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HA with acute onset
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SAH, sentinel HA
Thunderclap HA Intracranial hemorrhage Sinovenous thrombosis Arterial dissection Meningitis/encephalitis Acute sinusitis Neoplasm Migraine Acute glaucoma Acute hydrocephalus Trigeminal neuralgia Hypertensive urgency, pheochromocytoma Systemic illness |
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subarachnoid hemorrhage
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Clinical pattern – sudden & severe HA, initial unconsciousness, photophobia, nausea, stiff neck
Pain is usually occipital or generalized Etiologies - aneurysm, AVM, trauma, bleeding diathesis, angiitis, vasculopathies Lateralized HA is usually ipsilateral to aneurysm Focal signs from ICH or pressure from aneurysm 25-50% 30 day mortality, 10% before admission Complications – rebleeding, ischemic deficits 2º to vasospasm 25+% are misdiagnosed due to failure to recognize the spectrum of symptoms, failure to recognize limitations of CT or failure to do LP/interpret CSF findings. Delay in dx may increase mortality - rebleeding can occur early. Inc suspicion if onset exertional, vomiting or szs at onset |
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CSF pigments in SAH
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Temporal profile of pigment changes in CSF after SAH. RBC count maximal at 24 hrs and subsides over 7-10 days. Hb appears in 1st 4-10 hrs and peaks at 2 days. Bilirubin appears at 9-15 hrs and remains elevated for 10-14 days. Xanthochromia may not be present until 12 hrs.
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xanthochromia
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Xanthochromia is not reliably found before 12 hrs
RBC lysis -> oxyhemoglobin (pink/orange) -> bilirubin (yellow) OxyHb is produced in vivo or in vitro; bilirubin is produced only in vivo Bbilirubin may be detected by spectrophotometry CSF may also appear yellow from high protein, jaundice, rifampin or carotenoids |
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LP SAH vs. Traumatic
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SAH
Pressure: normal to increased RBC count: same Supernatant: xanthochromic WBC: proportional to RBC or increased later Clotting: absent Higher level: similar Traumatic Pressure: normal RBC count: clearing Supernatant: clear WBC: proportional to RBC Clotting: rarely present Higher level: usually clear |
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SAH warning leaks
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In retrospective studies, 28-60% of patients with aneurysmal SAH experience “warning leaks” days to weeks prior to the index bleed
The warning leak may be misinterpreted as migraine, tension-type HA, cervical strain, sinusitis, viral syndrome Failure to recognize prior leak may affect clinical grade and outcome |
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thunderclap HA
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Severe, self limited HA with sudden onset suggesting SAH, normal imaging and clear CSF
Associated with unruptured aneurysm (Day & Raskin, 1986) or segmental vasoconstriction Mechanisms - mural hemorrhage, expansion of aneurysm, vasculitis, migraine variant Does the incidence of aneurysms in thunderclap HA exceed that in the general population? Is angiography or MRA indicated? |
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HA and Tumor
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HA occurs in 60% of patients with brain tumors but tumor is a rare cause of HA
No features are pathognomonic but the typical pattern is intermittent, worse in AM, aggravated by bending, Valsalva or exertion and associated with nausea or vomiting HA is usually ipsilateral to the tumor HA occurs earlier if the tumor is infratentorial Occipital or neck pain with supratentorial tumors usually indicates increased ICP |
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CNS infection and HA
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Retro-orbital pain, pain with eye movement
Bacterial meningitis - fever, HA, meningismus, cognitive changes, and leukocytosis is readily recognized. Do not delay LP Viral infection differentiated by CSF formula - repeat LP may be necessary if done early Aseptic meningitis may mimic SAH Suspect Herpes if febrile illness with focal signs, szs and CSF blood |
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cervicocephalic dissection
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HA in up to 90%, neck pain in » 20%
ICA dissection - HA is usually unilateral, orbital or frontal ® ear or jaw Vertebral dissection - occipitonuchal pain Associated features - oculosympathetic paresis (58%), bruit (30-40%), focal neuro sxs (67%) Risk factors - trauma, FMD, Ehlers-Danlos, OCPs Treatment – anticoagulants, stenting Prognosis is generally good |
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Cranial arteritis
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(GCA)
A widespread giant cell arteritis affecting medium and large elastic arteries Rare prior to age 55 Clinical syndromes - HA, visual loss (ION), jaw claudication, PMR, constitutional symptoms ESR, CRP are variably elevated Definitive diagnosis by STA biopsy - skip lesions Rapid response to corticosteroids |
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HA of rhinosinusitis
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Frontal pain with facial, ear or dental pain
Clinical, endoscopic, CT/MRI and/or lab evidence of acute or acute on chronic rhinosinusitis HA or facial pain develops simultaneous with an acute exacerbation of rhinosinusitis and resolves within days of remission or successful treatment Chronic sinusitis is not validated as a cause of HA Previously referred to as sinus HA Clinical evidence is nasal purulence, hypo- or anosmia, nasal obstruction and/or fever. |
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trigeminal neuralgia
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High intensity, brief, jabbing or lancinating pain in the distribution of V, usually V1 or V2
Cutaneous trigger zones or triggering activities Suspect multiple sclerosis if bilateral May be associated with glossopharyngeal neuralgia or hemifacial spasm Vascular cross compression syndrome Therapy - anticonvulsants, baclofen, blocks, decompressive or ablative procedures, gamma knife |
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Dx of Migraine
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Untreated or unsuccessfully treated duration of 4-72 hours
At least two of the following - unilateral, pulsatile, moderate to severe intensity, aggravated by routine activity At least one of the following - nausea or vomiting, phono- and photophobia No other explanation Five or more attacks fulfilling the above criteria The dx is made historically. If typical history and normal exam, further investigation is usually unnecessary. Familial disorder with variable frequency and intensity. Migraineurs frequently have more than one kind of HA Major differential with rebound HA or SAH vs. thunderclap HA Typical auras are homonymous hemianopia, sensory or motor deficit deficits, aphasia. Aura tends to build up gradually, sxs may occur in succession, they last < I hr and HA follows w/in 1 hr. Other typical features of sensory aura include a march and cheiro-oral distribution. May occur with or without aura – typical aura is reversible visual, sensory or language disturbance developing gradually over < 1 hr with positive or negative symptoms Aura may occur without headache Persistent aura may occur with or without radiographic evidence of infarction Chronic migraine occurs > 15 days/month over 3 mos without a history of medication overuse |
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DX of tension-type HA
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Duration 30 minutes to 7 days
At least two - bilateral, pressing or tight, mild to moderate, not aggravated by routine exertion Photo- or phonophobia (not both), no nausea or vomiting No underlying disease May be associated with pericranial tenderness Episodic if frequency < 15 d/mos; chronic if greater Tension-type HA is ubiquitous - prevalence is 90% in women and 65% in men. Infrequent episodic if < 1/mos; frequent if > 1/mos and < 15/mos |
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Chronic daily HA
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2% of the population; much higher in HA clinics
Most common cause is transformed migraine Medication overuse and psychological factors are frequently present Consecutive days with long medication free intervals is much less likely to cause chronic daily HA than regular use several days each wk 10% are refractory - poor response to prophylaxis during medication overuse |
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medication overuse HA
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HA present 15 days/month
Two of the following – bilateral, pressing or tightening, mild to moderate intensity for analgesics and ergotamine; migrainous for triptans Use of simple analgesic 15 days/mos or use of opioids, combination analgesics, triptans, or ergotamine 10 days/mos over 3 mos HA has developed or markedly worsened during medication overuse HA resolves or reverts to previous pattern within 2 mos of discontinuation of medication |
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pathogenesis of migraine
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Unmyelinated trigeminovasc C fibers which innervate blood vessels. They contain glutamate + substance P (SP), neurokin A (NKA), and calcitonin gene related peptide (CGRP).
These neurons have antidromic and orthodromic functions. Orthodromic conduction transmits nocioception to CNS via nucleus caudalis of the trigeminal nerve in the medulla. Antidromic (neurosecretory) effect - release of SP, NKA, CGRP from peripheral terminals. SP, in turn, activates mast cells to release histamine and bradykinin) and causes platelets to release 5-HT. These vasoactive peptides cause extravasation of plasma proteins from dural vessels, which leads to ‘neurogenic inflammation, ” which is a proposed mechanism of pain. Axon-axon reflex - orthodromic transmission stimulates antidromic conduction from branch points and produces a reverberating mechanism enabling a single nerve to supply several blood vessels. Trigger of trigeminovascular activity is unknown. 5HT1 agonists (triptans, ergotamine, DHE) work by activating inhibitory prejunctional 5HT1B,D receptors, which inhibits neurogenic inflammation and slows central transmission of pain impulses, or a possible direct action on 5HT1B,D receptors in TNC or vascular 5HT1B receptors. Neurogenic inflammation is also blocked by NSAIDs (and chronic administration of methysergide). NSAIDs act directly on the vessel;. 5-HT1D agonists block neurotransmitter release but can not prevent substance P or neurokinin induced inflammation. Activation of inferior frontal lobe, locus coeruleus in pons (central noradrenergic center) and dorsal raphe in the midbrain (serotoninergic center) in PET studies during migraine w/o aura. Activation of locus coeruleus can decrease blood flow and dorsal raphe may increase it. Is this the migraine pacemaker? DHE binds dorsal raphe |
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migraine abortive agents
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Non-narcotic analgesics - ASA, acetaminophen, NSAIDs, isometheptane/dichloralphenazone, butalbital ± caffeine combinations
5HT1 agonists – ergotamine, DHE, triptans Dopamine antagonists – metoclopramide, phenothiazines IV lidocaine/diphenhydramine, IN lidocaine Corticosteroids IV Na valproate Ketorolac, narcotic analgesics |
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therapeutic considerations in abortive agents for migraine
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Migraine type, severity, frequency, mode of onset
Previous medication experience - treatment failure, headache recurrence Potential for drug dependence, rebound headache Comorbid medical conditions Preferred route of administration Cost Remember nausea and slowing of gastric absorption during attack |
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Triptans
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Triptans are specific 5HT1B/1D agonists
Not analgesics - prevent neurogenic inflammation Reduce HA, nausea and photophobia in migraine with or without aura Triptans differ in pharmacology and delivery systems - fast onset, high potency vs slow onset, low potency, duration of action More effective early in the headache - may not prevent HA if given during the aura Cost effective as part of a stratified approach |
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allodynia and triptan response
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Sensitization of central trigeminovascular neurons cutaneous allodynia
71 HAs in 31 patients treated at 1 or 4 hrs Rx with SC sumatriptan, rizatriptan or zolmitriptan Complete pain relief by 2 hrs in 93% without allodynia and 15% with Attacks without allodynia respond equally to triptans regardless of time of dose |
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safety of triptans
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Class specific risk of vasoconstriction – exceptional reports of MI, stroke and death
Oral and nasal triptans better tolerated than SC Minimal clinical risk with appropriate patient selection – avoid use in uncontrolled HTN, CAD or variant angina, basilar/hemiplegic migraine, stroke/TIA Be certain of the dx - avoid in atypical HA Evaluate patients at high risk for CAD before use Interactions - methysergide, MAOIs, SSRIs, propranolol (rizatriptan), macrolides (eletriptan), other 5HT1 agonists Use with caution in hepatic dysfunction Do not use in pregnant or lactating women Safety is unaffected by duration of treatment, frequency of administration or number of doses per attack within recommended guidelines Relatively low risk of rebound HA |
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IV DHE for intractable HA
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Reduce dose for nausea or vomiting
Delay or hold for SBP > 150 or DBP > 95 mm Hg Give metoclopramide for first six doses - preferable to prochlorperazine for repeated administrations Avoid narcotics for pain Treat diarrhea with diphenoxylate/atropine (Lomotil) Treat dystonic reactions with diphenhydramine Continue q 8-12 hours for 2-4 doses once HA free |
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IV NA valproate
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Open label, prospective study of 66 attacks in 61 patients with IHS migraine
300 mg valproate in 100 cc NS over a mean of 10 minutes Significant improvement of HA in 73% - associated symptoms also improved Recurrence in 22% with mild or no pain No serious adverse effects |
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general principles of migraine prophylaxis
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When to treat?- frequent HA (3-4/mos), when abortive therapy is ineffective or poorly tolerated, when HA is incapacitating or associated with focal neurological deficit
Monotherapy - begin one agent with the greatest potential efficacy and least side effects and allow an adequate trial Combination therapy if single agent doesn’t work Episodic prophylaxis in exercise or menstrual HA Avoid excessive use of abortive agents |
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migraine prophylaxis agents
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b-adrenergic blockers
Calcium channel blockers Antidepressants - tricyclics, SSRIs, MAOIs Anti5-HTergics - methysergide, cyproheptadine Prostaglandin inhibitors - ASA, NSAIDs AEDS - valproic acid, gabapentin, topiramate, levetiracetam, zonisamide Other - clonidine, montelukast, Li, DA blockers, ACE Is, ARBs, B2, feverfew, coQ, Botox Behavioral therapies, avoidance of precipitants |
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beta adrenergic blockers and migraine
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Propranolol is the prototype
Partial agonists are ineffective Greater effect on frequency than severity/duration Central adrenergic mechanisms or 5-HT1A receptor binding; D-propranolol has no b blocking activity but is still effective Rapidly effective, qd administration Adverse effects - fatigue, hypotension, brady-cardia, depression, wheezing Patients may respond to one beta blocker but not another. Pindolol has strongest 5-HT activity but poor prophylactic agent; atenolol is effective but has very weak if any 5-HT activity. Usually effective w/in 3-4 wks but may take up to 3 months at maximum dose to assess efficacy. Typical doses 120-320 mg/day. Taper if discontinuing it. |
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antidepressants and migraine
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Effectiveness of TCAs is independant of antidepressant effect – amitriptyline is the best studies in migraine
Amitriptyline may be superior to propranolol for mixed migraine and TTH Little evidence for an effect of SSRIs except improvement of comorbid depression Downregulate amine receptors, 5-HT2 antagonists Consider MAOIs in selected, refractory patients Amitriptyline, doxepine and fluoxetine have been studied in clinical trials. Newer SSRI may be preferable due to fewer side effects. May want to avoid trazodone due to priapism in men and its metabolite, mCPP (m-chlorophenyl piperazine), which may precipitate HA. Response to antidepressants may be fairly rapid - 7-10 days MAO inhibitors can be use with or without a cyclic - diet and medication interactions. If using MAOI/TCA combination start TCA first. |
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calcium channel blockers and migraine
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Flunarizine and verapamil are most effective – nimodipine and nifedipine are probably ineffective
Greater effect on frequency than severity of HA 4-6 week delay to onset of therapeutic effect Mechanism of action - 5-HT2 blockade, ¯ 5-HT release, suppression of spreading depression Adverse effects - constipation, hypotension, heart block, flushing 5-HT release is Ca dependent. May hav etheoretic advantage for patients with neurologic accompaniments. Better tolerated than beta blockers. |
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AEDs and migraine
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Mechanisms in migraine – GABAergic or glutaminergic mediated neurotransmission, inhibition of Na or Ca channels
Best data for VPA and topiramate – FDA approval Gabapentin has also been shown effective in blinded clinical trials Lamotrigine decreases frequency of auras May be cost effective |
