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medicine.mc.vanderbilt.edu.doc

  1. 1. Tension Migraine M ig r a in e ( A u r a ) ClusterA n a l g e s i c R e b o u n d Vomiting Photophobia Sinusitis TMJ Trigeminal Neuralgia Ice Pick HA Dental Pain Migraine -not Tension HA Exertional HA -transient,benign Coital -benign Facial/Neck HA 5 Exertional HA 5 Throbbing Episodic Unilaterial Rhinorrhea, Flushing Pressure Persistent Bilateral Severity Common Familial
  2. 2. Tension Migraine M ig r a in e ( A u r a ) ClusterA n a l g e s i c R e b o u n d Vomiting Photophobia Sinusitis TMJ Trigeminal Neuralgia Ice Pick HA Dental Pain Migraine -not Tension HA Exertional HA -transient,benign Coital -benign Facial/Neck HA 5 Exertional HA 5 Throbbing Episodic Unilaterial Rhinorrhea, Flushing Pressure Persistent Bilateral Severity Common Familial
  3. 3. Subarachnoid Hemorrhage Subdural Hematoma Meningitis Tumor Malignant HTN Pseudotumor Cerebri Imminently Dangerous D x 's Abrupt stiff neck Severe MS changes Trauma HTN Seizure Anticoagulation Tx's Physical Exam HTN MS changes Fever focal neuro changes Papilledema meningismus Brudzinki's: involuntary flex of hips/knees Kernig's: ext of previous flexed knees Special Circumstances and/or Progressive D x 's Temp Art: Fever, arthalgins vision changes, jaw claudic, PMR symptoms Sinusitis : sinus tenderness Optic N : boring pain Glaucoma : elderly Cluster : Rhinorrhea H2V : rash Eye strain : overuse Tumor: hx of cancer, systemic symptoms, smoker, progressive, positional discrete HA Fever Sinusitis Meningitis Subdural Temporal Arteritis Glaucoma Tumor Sinusistis HIV Hx of Cancer Ocular Elderly
  4. 4. Subarachnoid Hemorrhage Subdural Hematoma Meningitis Tumor Malignant HTN Pseudotumor Cerebri Imminently Dangerous D x 's Abrupt stiff neck Severe MS changes Trauma HTN Seizure Anticoagulation Tx's Physical Exam HTN MS changes Fever focal neuro changes Papilledema meningismus Brudzinki's: involuntary flex of hips/knees Kernig's: ext of previous flexed knees Special Circumstances and/or Progressive D x 's Temp Art: Fever, arthalgins vision changes, jaw claudic, PMR symptoms Sinusitis : sinus tenderness Optic N : boring pain Glaucoma : elderly Cluster : Rhinorrhea H2V : rash Eye strain : overuse Tumor: hx of cancer, systemic symptoms, smoker, progressive, positional discrete HA Fever Sinusitis Meningitis Subdural Temporal Arteritis Glaucoma Tumor Sinusistis HIV Hx of Cancer Ocular Elderly
  5. 5. Imminently Dangerous S p e c ia l C ir c u m s t a n c e s a n d / o r P r o g r e s s iv e LP STAT CNS imaging CNS imaging Suspect acute SAH meningitis expectant observation CNS imaging Suspect subacute CNS infx ESR, biopsy, trial steroids MS Changes or focality on neuro exam Suspect Temp Art No evidence meningeal irritation Suspect tumor Imminently Dangerous S p e c ia l C ir c u m s t a n c e s a n d / o r P r o g r e s s iv e LP STAT CNS imaging CNS imaging Suspect acute SAH meningitis expectant observation CNS imaging Suspect subacute CNS infx ESR, biopsy, trial steroids MS Changes or focality on neuro exam Suspect Temp Art No evidence meningeal irritation Suspect tumor
  6. 6. Anderson Spickard, III, M.D., M.S. Headache in the Primary Care Setting Introduction 0* Headache is common. 1% of office and ER visits, 73% of adults in US have had a HA in last year, 5% seek medical help. 8-11 million Americans have migraines & 50% of these miss two or more days of work a month costing $5.6-7.2 billion annually to employers 1* Headache is troubling. Both physicians and patients need a healthy tolerance of the diagnostic and therapeutic uncertainty that exists in the evaluation of headache. In 1988, the International Classification of headaches was established to guide one through the often overlapping syndromes. We learn that while tension and migraine headaches are very similar, they are distinguished from the less common cluster headache and cranial neuralgias which are distinctively unilateral. We learn that medicines recommended for one type of headache may apply to other types of headache. In addition, concerns for whether the headache is truly benign and whether the patient is addicted to the offered treatments amplify uncertainty in the management of headache. Learning Objectives 2* to understand the salient features of the major causes of HA in the office setting 3* to develop an approach to HA that identifies the benign, common HA entities and distinguishes this group from the HA’s caused by serious disease 4* to understand the comprehensive approaches required to manage HA Outline Pages I. Approach to Headache History 2 Physical Exam 2 Distinguishing Features Amongst the Common, Benign HA’s 2 Worrisome Features of the Ominous Causes of Headache 3 When to Pursue Neuro-Imaging 3-4 II. Reference Information: Headache Syndromes and Treatments Migraine HA 5-9 Tension HA 10-11 Analgesic Rebound 11
  7. 7. Cluster HA 12 Worrisome HA 13 Facial/Neck Pain HA 13-14 Exertional HA 14
  8. 8. I. Approach to Headache History 5* onset, severity, pattern and location, describe from start to finish 6* previous HA’s and treatments, family history 7* associated symptoms: prodrome, aura, n/v, photo/phonophobia, rhinorrhea, tearing, sinus sx’s, blurr vision, jaw claudication 8* precipitants: trauma, exertion, stress, _ sleep, diet (chocolate, citrus fruit), drugs (analgesics, ergotamines, caffeine, etoh) Physical Exam 9* Blood pressure 10* HEENT: facial/scalp tenderness (Temporal Arteritis, Sinusitis) photophobia (Migraine, less common Tension) papilledema (Malignant HTN, Pseudotumor Cerebri) oropharyngeal disease (dental pain) neck (DJD) 11* Neuro: mental status, meningismus, focal deficits Distinguishing Features Amongst the Common, Benign HA’s Tension Migraine Migraine (aura) Cluster ¬ Common ¬ Familial, Female Severity → Vomiting, Photophobia → ¬ Pressure Throbbing → ¬ Persistent Episodic → ¬ Bilateral Unilateral → Rhinorrhea Flushing, Alcohol-Induced → Tension vs Migraine 12* Tension is less episodic, more daily and persistent, it is not worsened by exertion as is migraine, the patient can go on with his/her day. 13* Migraine patients are sicker with n/v/photophobia. Besides the aura, they can have premonitory (prodrome) sxs of hyper- or hypo-activity, depression, and food cravings hours to days before the next episode. Worrisome Features of the Ominous Causes of Headache A. New HA 8
  9. 9. 1. only 40% of new HA s are migraine or tension, 90% of chronic HA are migraine or tension B. Onset/Severity 1. abrupt HA 2. “worse ever” is the teaching but many benign HA’s are severe 3. if abrupt and severe, then worrisome C. Elderly 1. less tension and migraine HA in elderly 2. fever, joint aches, or vision changes → temporal arteritis periorbital → glaucoma trauma → subdural progressive, subtle, discrete location, positional → tumor smoker, systemic sxs, hx of cancer → tumor D. Fever 1. sinusitis, meningitis, subarachnoid hemorrhage E. Mental Status _s, Seizures, Papilledema, Meningismus, or Focal Neuro _s 1. these are obvious, don’t forget fundoscopic exam 2. Pseudotumor Cerebri, migraine, CVA, tumor, SAH, malignant HTN When to Pursue Neuro-Imaging A. New or Progressive Headache 1. Little epidemiological data, however, most authors advise diagnostic work-up (CT, MRI, LP, Sinusitis treatment, etc ... depending on the situation) if the above worrisome features are present in the patient with a new or progressive headache that is intractable to conventional therapy. B. With Normal Physical Exam 1. Studies 2,3 a. data from case series only, 9 prospective, 5 retrospective b. included “acute” and “chronic” HA, ER and outpatient settings, definitions widely variable c. chance of abnormality on CT or MRI 1.5% (tumor found in .9%, AVM in .1%, .2% aneurysm, .3% subdurals) d. even less prevalence if migraine features to HA e. recent estimates (Ontario group and others) of $75,000 to find one treatable vascular lesion in chronic HA pts with nl phy exams 2. American Academy of Neurology a. now discourages routine use in pts whose recurrent HA is dx’d 9
  10. 10. migraine 3. In favor of ordering the MRI or CT in chronic HA a. Diagnostic and therapeutic uncertainty Even without the above worrisome features, many would pursue head-imaging in any patient with chronic HA’s that are intractable to therapies despite compliance. Despite the small chance of finding disease, the risk is not zero. Diagnostic confusion and only modest treatment efficacy in chronic disabling HA often propel an investigation. Patients may need “ proof of health” before accepting the ongoing, comprehensive pharmacologic and non-pharmacologic approaches necessary for treatment. II. Headache Syndromes and Treatments Migraine Headache A. Epidemiology 1. familial in 70%, more common in women, young, lower SES 2. 1-4 disabling attacks a month in 25-40% of migraine pts 10
  11. 11. B. Pathophysiology 1. a type of vascular headache 2. simple: vasospasm causes the aura and dilation causes the headache 3. complex: aura due to spreading neuronal depression of cortex from ↓d metabolic demand rather than ischemia from vasospasm. Pain is due to dilation and d permeability of cranial vessels leading to exudate that incites a sterile inflammatory reaction. The inflamm activates nerve endings that ↓ the pain threshold of fibers projecting to the thalamus. C. Precipitants 1. pollution, hypoglycemia, oversleeping, fatigue, estrogen, nitrates, chocolate (phenlyethamine), cheeses (tyramine), diet soft drinks (aspartame),alcohol, menstruation, ETOH, missed meal, ↓ sleep, let down periods after stress (weekends, vacations), OCPs don’t trigger but may frequency and severity of attacks. D. Premonitory symptoms (not talking about an aura) 1. premonitory symptoms occur hours to several days prior to a migraine with or without aura and include hyper- or hypo-activity, depression, food cravings or repetitive yawning International Classification Definition in Bold E. Migraine Without Aura (Common Migraine) 80- 90% 14* lasts 4-72 hours 15* 2 of these: unilat pulsating by physical activity mod-severe 16* 1 of these: n/v, photo or phonophobia F. Migraine With Aura (Classic Migraine) 10% 0* 3 of these: 1) aura with focal cerebral cortical and /or brain stem dysfunction (visual scintillation, photophobia, dizziness, scotomas, tinnitus) 2) aura gradual over 4 or more minutes 3) aura doesn’t last more than 60 min 4) HA follows aura within 60 min and lasts 4-72 hrs G. Complicated Migraine rare 17* prodrome neurological manifestations last entire HA duration 18* may leave permanent residue Subtypes of Complicated Migraine: 1. Ophthalmoplegic M. : rare, third CN, young pt, some permanent damage from swelling of posterior cerebral arteries. 11
  12. 12. 2. Hemiplegic M. : HA plus motor and sens loss, unilateral, slower march of onset of sxs than CVA, recovery in days to weeks, 4-18% with family hx of these, worse from OCPs. 3. Basilar Artery M. : More common but still rare, young pt, vertigo, diplopia, mental status changes, tinnitus, ataxia. H. Reminders about Treatment of Migraine 19* strength of studies compromised by high placebo response (30-40%) & various definitions of HA and gradings of HA response 20* therapy individualized, for example, some pts have more problems with GI distress than head pain, therefore anti-emetic may be all they need I. Treatment of Acute Migraine 1. At Home a. ASA or Tylenol may work early in the HA b. NSAIDs: Naprosyn and Ibuprofen best studied 1) superiority to placebo and ergotamine in ridding HA and related sxs of n, light-headedness, photophobia, but may need metoclopramide to reduce vomiting adequately. (Of note, decreased gastric mobility occurs during acute attack and can limit absorption of analgesics) . 2) no head to head of NSAIDS 3) over-use of analgesics can cause rebound headache, see below 4) Naproxyn 550mg at onset and 1 hr later c. Anti-emetics (Compazine, Reglan, Phenergan) 1) no studies of home use though oral & rectal routes commonly employed, especially when GI distress a key symptom or need to augment absorption of analgesics 2) efficacy extracted from data of IV, IM, and rectal use in ER and clinic studies (see ER/Clinic section below) d. Midrin (isometheptene, a vasoconstrictor, and dichloralphenazone, a sedative, plus acetaminophen) 1) 2 capsules at onset, then 1 every hour, limit 5 per day, 15 per week e. Sumatriptan 1) 5 hydroxytryptamine agonist like serotonin causing vasoconstriction of intracranial vessels and modifies neuronal protein extravasation 12
  13. 13. 3) SQ well-studied, at least 4 trials early 90s a) 70% response vs 30% placebo, slightly earlier relief than DHE but more HA recurrence than DHE b) effective if given in full blown attack, no n/v c) problems 1) second dose ineffective if 1st dose didn’t work 2) 30-65% recurrence in 48 hr in sumatriptan group vs 20% placebo 3) $70 for two 6 mg doses at home 4) long term safety not established, isolated reports of MI, arrhythmias, and asthma, might give 1st dose in clinic if CV risk factors or asthma and don’t use w/in 24 hrs of ergotamine 4) Oral (25-100mg) with 80% response, also has out-performed ergotamine and Reglan+ASA f. Ergotamine Tartrate 1) alpha antagonist and serotonin agonist, used since 1930s 2) more effective in early attack (1mg q 30min up to 6 mg) 3) available as sublingual tablet alone (Ergostat) or in combination with caffeine in oral tablet (Cafergot) or rectal suppository (Wigraine) 4) problems with Ergotamine a) recently out-performed by NSAIDs and placebo, yet still advocated by Medical Letter, Reilly, and the Academy of Neurology 1,5,6 b) physical dependence manifested by rebound HA & tolerance if take more than 2 times a week (10mg/wk) c) exacerbates n/v in most trials d) vasoconstriction side effects are likely over- rated (data only from individual case reports) but generally contraindicated in pts with CAD, HTN, or pregnancy g. Fiorinal (ASA 325mg, Caffeine 40mg, Butalbital 50mg) used much with little data support, withdrawal HA if use more than 2 days a week like ergotamines h. Butorphanol (Stadol) spray, an opioid agonist-antagonist, better than placebo and IM methadone but drowsiness may limit use 2. In the hospital a.. Dihydroergotamine (DHE) 1) weaker vasoconstrictor than ergotamine tartrate 2) fewer side effects and practically no dependence 3) IV, IM, SQ, and intranasal 13
  14. 14. a) IV, IM as repeated doses in chronic intractable HA for 3-7d, induces nausea so premedication needed b) intranasal 2mg, 6 placebo trials, 3 parallel trials: relief up to 70% DHE group and 43% placebo group, efficacious in full blown attack as well c) no studies of outpatient use yet 3. Treatment of Acute Migraine in the Emergency Room or Clinic 21* most studies late 80s, early 90s and lack 24hr f/u to determine recurrences or how sleepy were patients when they got home a. better than placebo 1) IV or rectal Compazine (2 Ann Emerg Med studies) 2) IV Reglan 3) IV Thorazine 4) IV DHE b. head to head trials 1) IV Compazine > rectal Compazine 2) IV Thorazine > IV DHE 3) IV DHE > meperidine+hydroxyzine+butorphanol 4) Sumatriptan not compared yet to other meds c. uncontrolled trials 1) cohort studies of efficacy of IV Dexamethasone J. Prophylactic Treatment of Migraine (unknown mechanisms) 22* initiate when > 2-3 HA/ month or acute treatments are ineffective 23* not 100% effective, but will ↓ amt of analgesics needed 24* take 4-6 wk to work so continue analgesics and ergots 25* though remember daily analgesics, narcotics and ergots perpetuate HA on a rebound basis and are habit-forming 26* can wean slowly every 4-6 months to reassess need 1. Non-pharmacologic a) avoid ETOH, chocolate, cheese, sleep changes, missed meals, OCPs (controversial), caffeine (withdrawal HA if > 10 cups/d) & vasodilators (Hydralazine, Minoxidil, Prasozin) 2. Beta Blockers a) best studied (early 80s), inexpensive, & well-tolerated b) Propranolol 20 tid up to 80-320 mg/d or Inderal LA once/d c) ↓’s freq and severity in 60-80% of pts, unlike ca blk, doesn’t relieve aura d) Metoprolol, Nadolol used tho Propranolol &Timolol FDA approved 14
  15. 15. 3. Calcium Blockers a) also 60-80% of pts got relief but small samples, Nifedipine ’d HA in some studies, and much tolerance to Nifedipine and Verapamil b) therefore, though commonly used, not FDA approved 4. Anti-depressants a) Amitriptyline helped 50% of pts in late 70s studies, once day, helps sleep, 25-150mg/d b) Fluoxetine helpful in one 1992 study but small sample, > studies coming 5. Naprosyn a) only NSAID studied, use 550mg bid, not prn b) particular advantage in menstruation induced migraine taken several days before and during menstruation 6. Less commonly used a) old remedies (studies 1960s, 70s) 1) Ergotamine not effective prophylactically 2) Cyproheptidine (Periactin) 40% effective, $2 month but sedating 3) Methysergide (Sansert) 60-70%, $80 month, retroperitoneal, pulmonary, cardiac fibrosis so usually do not use 4) Depakote b) old remedies revisited 1) Valproic Acid: 400 mg bid, 86% of pts relieved double blind 1992, worked for just the severe not the mod or mild HA K. Conclusion of Treatment for Migraine 27* Start with an analgesic or anti-emetic, if unresponsive move to Ergotamine or Sumatriptan 28* Beta blockers best choice for prophylaxis 29* Oral Sumatriptan is new and DHE nasal spray is coming soon Tension Headache A. Epidemiology 1. aka muscle contraction HA 2. familial in just 3% 3. more association with depression and sleep disturbance B. Definition (formally muscle contraction HA) 15
  16. 16. International Classification Definition in Bold 30* lasts 30 min to 7 days 31* frequency: > 15 d/mo for > 6mo in chronic type (vs episodic type) 32* 2 of following: bilateral pressing, tightening not aggravated by activity mild-mod severity, can go on with day 33* no vomiting 34* no more than one of these: nausea, photophobia, phonophobia C. Relation to Migraine 1. Likely a continuum of migraine, often episodic migraine progresses to chronic daily HA with tension HA features, aka Transformed Migraine or Mixed Headache. 2. In general, migraine is more episodic and makes people more sick, tension is more of a constant pressure HA D. Relation to Analgesic Rebound Refractory tension HA is difficult to distinguish from analgesic rebound HA, both are headaches in the context of daily analgesic use. Sometimes discontinuation of analgesics is required to rule out a rebound effect (See Analgesic Rebound below). E. Treatment of Tension HA 1. Comprehensive approach: patience and insight, frequent visits, reassurance, naming emotional stressors, providing avenue for ventilation, head imaging may be needed to rule out organic ds as patients may not respond to chronic efforts of amelioration without this first 2. First line agents a. NSAIDs (Ibuprofen, Naprosyn) have out- performed ASA and Tylenol in at least three randomized trials b. Prophylaxis is used if more than 2 HA per week b. Non-sedating antidepressants: Fluoxetine (Prozac), Sertraline (Zoloft), Paroxetine (Paxil), Buproprion (Wellbutrin), Venlafaxine (Effexor), Nefazadone (Serzone), and Desipramine (Norpramin). c. Sedating antidepressants: Amitriptyline (Elavil), Doxepin (Sinequan, least anticholinergic effects of TCA’s), Imipramine (Tofranil), Trazodone (Desyrel), Nortriptyline (Pamelor, least sedating of TCA’s). d. These agents can be used in combo with BB or Ca+ Blk if migraine features. These prophylactic medications always work better if analgesics withdrawn. 3. Judicious use of habit forming medications: a. HA is daily and usually chronic, analgesics are necessary but 16
  17. 17. addicting meds (ergots, butalbital, narcotics, muscle relaxers, benzos) are to be avoided if possible. b. Recent recommendation of muscle relaxors: Chlorzoxazone (Parfon forte), Carisoprodol (Soma), and Metaxalone (Skelaxin) alone or in combo with aspirin, acetaminophen, caffeine, or all three. c. Benzodiazepine-butalbital combinations work well (Fiorinal, Fiorecet, Esgic, Phrenalin, Axotal) and have less abuse potential than narcotics.. 3. Refractory cases a. withdraw analgesic to rule out analgesic rebound b. IV DHE for 3-7 day effective in 90% 4. Non-pharmacological (adds only marginal improvement) a. if migraine features: same diet, exercise, and sleep issues as in migraine section b. heat, relaxation techniques, stretching exercises, physical therapy to strengthen neck muscles, correct posture, and improve mobility Analgesic Rebound Headache A. Definition 1. Cumbersome International Classification: “Chronic tension HA unassociated with disorder of pericranial muscles” 2. Defined in studies as pts with chronic HA taking meds 20 days per month B. Pathophysiology 1. Poorly understood: chronic analgesics may suppress serotonergic pathways making the patient more vulnerable to return of HA when med wears off C. Culprits 1. analgesics: tylenol, aspirin, NSAIDS, narcotics 2. headache medicines: caffeine, ergotamines C. Treatment of Analgesic Rebound 1. Stop daily analgesics ergots or sedative drugs 2. May then have to admit to hospital with IV DHE x 3-4 day as for any intractable HA: 90% will improve, half of these still improved in 6 mo 3. may be more common than think, alert MD will consider and tactfully ascertain use of daily prescription and nonprescription drugs Cluster Headache (RARE) International Classification Definition in Bold 35* unilateral orbital, supraorbital, and or temporal pain lasting 15-180 min 36* 1 of these on pain side: conjunctiva injection lacrimation 17
  18. 18. nasal congestion rhinorrhea forehead and facial sweating miosis ptosis eyelid edema 37* one every other day to eight per day A. Epidemiology 1. rare compared to migraine and tension HA 2. not familial 3. more in men (10:1), leonine appearance (alcoholic acromegaly): furrows forehead, folds in glabellar and nasolabial areas 4. strong relation to smoking 5. episodic (remissions of at least two weeks) or chronic (no remissions) B. Precipitants 1. etoh, high altitude, xs exercise, nitrates, change in sleep pattern C. Treatment of Acute Cluster 1. in principle abortive therapy not useful because no aura and attack is brief, yet ergotamine up to 4 mg/d is effective with less rebound than in migraines 2. Lidocaine nosedrops 2. Oxygen: 100% face mask X 15 min, 2 studies early 80s, 56% relief vs 7% placebo, works better if episodic cluster and pts < 50 yo. 3. Sumatriptan: 2 studies double blind, early 90s, 40% completely relieved vs 20% placebo D. Prophylaxis of Clusters 1. used at onset of HA, dc’d after exceed expected duration of HA episode 2. Prednisone 40 mg tapered over expected HA episode pattern, initially studied in 70s, still advocated in current reviews, e.g. 40mg q am x 1 wk, taper by 10 mg per week 3. Lithium 300 bid, old studies, used only in chronic clusters bc slow onset of action 4. Verapamil 80-240 tid in one study 5. Ergotamine 1mg qhs not proven but used, often in combo with Verapamil 1 m 6. Methylsergide (Sansert) effective in 75%, episodic use of 2-3 mos not long enough to develop complicating fibrosis Worrisome Headaches Obvious A. Intracranial Hemorrhage 1. obvious neuro findings on exam, trauma precedes subdural hemorrhage 18
  19. 19. B. Subarachnoid Hemorrhage (Ruptured Aneurysm) 1. violent, sudden, mean age 51 yo, occ precipitation by sex, cough, exercise 2. half will have Sentinel HA (from minor leak) with severe HA before ensuing neuro changes in next few minutes 3. most with focal neuro changes and/or depressed ms and/or meningismus 4. CT misses 20% of subarachnoid hemorrhages, do LP Not So Obvious C. Brain Tumor 1. tension type headache usually 2. worse with change in position (nonspecific), discrete location 3. progressive D. Temporal Arteritis 1. elderly, HA can be anywhere, < half located in temple area 2. scalp tenderness, jaw claudic, or diminished vision in 50+% 3. consider with new progressive HA in elderly E. Pseudotumor Cerebri 1. young women 2. obesity, OCPs, thyroid disease 3. n/v, blurred vision, papilledema Facial and Neck Pain Headaches A. Sinusitis 1. recent URI, tooth pain, purulent nasal discharge, poor response to decongestants 2. fever, facial tenderness, transillumination A. Temporomandibular Disorders 1. unilateral, lasts weeks to months, worse with eating 2. tenderness over joint and mastication muscles 3. limited jaw opening, but joint clicking, crepitus are common in individuals without headache 4. depressed and stressed pts without TMJ have same features B. Trigeminal Neuralgia 1. not headache as much as lancinating bursts of pain 2. elderly, occurs throughout day, worse with chewing, brushing teeth 3. normal films C. Chronic paroxysmal hemicrania 1. brief cluster like HA, 10-20/d, middle age women 2. indomethacin responsive 19
  20. 20. D. Ice Pick HA 1. associated with migraines 2. momentary unilateral sharp pain 3. indomethacin responsive C. Dental pain 1. pain around eye, temple, ear so don’t overlook oral-pharyngeal exam D. Cervical Spondylosis 1. elderly, neck pain, looks like tension HA 2. many people with asymptomatic abnormal neck films, thus films not diagnostic, to be sure, need unilateral neck or shoulder pain with radiculopathy and abnormal posture of neck Exertional Headaches A. Migraine HA 1. many headaches, esp migraine, transiently worsen with exertion, tension HA characteristically is not affected by exertion B. Exertional HA 1. this is transient de novo HA from strenuous exertion, is benign 2. Subarachnoid Hemorrhage begins similarly but is not transient C. Coital HA 1. transient during orgasm 2. not indicative of serious ds but is a variant of migraine 3. ergot before sex, indomethacin also good References 1. Abramowicz M, editor. Drugs for migraine. Medical Letter 1995;37:17-20. Brief review of status of the newer agents on the horizon for migraines. 2. Dumas MD, Pexman W, Kreeft JH. Computed tomography evaluation of patients with chronic headache. Can Med Assoc J 1994;151:1147-52. 1% of recurrent headaches lasting at least 6 months in patients with normal physical exams were found to have significant CT findings (tumor, aneurysm). It cost $75,000 to find one treatable lesion in these patients. 20
  21. 21. 3. Frishberg BM. The utility of neuro-imaging in the evaluation of headaches in patients with normal neurological exams. Neurol 1994;44:1191-7. Meta-analysis of 9 prospective and 5 retrospective studies of recurrent HA and CT and 5 prospective MRI studies. Findings: .9% tumor, .1% AVM, .2% aneurysm, .3% subdurals, (numbers less if HA had migraine picture vs unspecifie). Hypothesized treatable lesions found in .4% of migrainers, and 2.4% of unspecified HA. Nice discussion of limitations of studies (e.g. use of old CT scanners, variable definitions of HA) and how we need further cohort studies to determine true health outcomes of those with positive scans. 4. Headache Classification Committee of the International Headache Society: Classification and diagnostic criteria for headache disorders, cranial neuralgias, and facial pain. Cephalalgia 1988;8(suppl):279-284. This article summarizes the new classification of headaches but we don’t have this journal in the Vanderbilt library. 5. Kumar DL and Cooney TG. Headaches. Med Clin N Amer 1995;79:261-286. THE BEST REFERENCE for a comprehensive review of the definitions of migraine, tension, and cluster headaches and the studies that have directed our current treatment strategies. Does not emphasize the approach to headache. 6. Reilly BM. Headache. In Practical Strategies in Outpatient Medicine (pp.78-131). Philadelphia: W.B. Saunders Company, 1991. Too long to be a primary resource, appropriately used as a reference. Algorhythms outlining the approach to headache are a bit cumbersome and are simplified here. 7. Report of the Quality Standards Subcommittee of the American Academy of Neurology: Appropriate use of ergotamine tartrate and dihydroergotamine in the treatment of migraine and status migrainosus. Neurol 1995;45:585-7. Safety and efficacy of ergotamines confirmed by the panel. Counter-arguments include: 1) the evidence is based mainly on cohort studies and not randomized trials, 2) there are few comparisons of ergots with other HA medicines, and 3) ergots are highly addictive and should not be used more than twice a week. 21
  22. 22. 8. Solomon S. Migraine: current approaches to diagnosis and management. Hosp Pract 1991;April:95-114. Strengths: Quick read. Nice pictures to explain pathophysiology of migraines. Weaknesses: Really too simple and does not provide data to support use of older agents as he recommends. Newer agents not discussed. 9. Walker J, Parisi S, Olive D. Analgesic rebound headache. South Med J 1993;86:1202-5. Review of 100 cases of intractable chronic headache. 50% were due to analgesic rebound, defined as headache despite taking analgesics 20 days out of the month. Five days of inpatient IV DHE provided some relief in all patients. At 8 months, 95% still had a headache but most headache patterns were improved. F/u analgesic use unknown.

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