A. Overview
- Very common presenting symptom to primary care and emergency room physicians
- Major focus is on ruling out serious (potentially life threatening) causes of HA
- In addition, HA as a component of systemic disease should be considered
- The history with careful attention to details is very helpful in focusing further evaluation
- The physical exam is also very helpful for ruling out serious causes
- If the assessment of the doctor and the patient differ considerably after the initial evaluations, referral to a HA specialist or radiographic imaging may be beneficial
- Types of Headaches considered here
- Serious Causes of HA
- Common Headache
- Migraine Headache
- Cluster Headache
SERIOUS CAUSES OF HEADACHE |
A. Introduction- Usually anatomic or Inflammatory in nature
- Compare with "common" HA, which is usually vascular
- Must be ruled out in all patients with "new" HA
- Overview of Serious Causes of HA
- Subarachnoid Hemorrhage
- Cerebral Vein Thrombosis (cerebral venous sinus thrombosis)
- Cavernous Sinus Thrombosis
- Cerebral Parenchymal Hemorrhage
- Increased Intracranial Pressure
- Meningitis / Encephalitis
- Vasculitis / Temporal Arteritis
- Pseudotumor Cerebri
- Cerebral artery dissections
- Acute angle closure glaucoma
- Hypertensive Emergency
- Suggestive of Serious Causes of HA (Box 1, Ref [1])
- Fundamental change or progression in HA pattern
- First and/or worst HA
- Abrupt onset attacks, including those awakening
- Abnormal physical examination results
- Neurological symptoms lasting >1 hour
- New HA in individuals <5 years or >50 years
- New HA in patients with cancer, immunosuppression, pregnancy
- HA associated with alteration in or loss of consciousness
- HA triggered by exertion, sexual activity, or Valsalva maneuver
- Suggestive of Migraine Versus "Serious" HA Cause [28]
- Pulsating
- Duration 4-72 hours
- Unilateral
- Nausea
- Disabling
- Presence of 4 of these 5 gives likelihood ratio (LR) for migraine of 24
- Presence of 3 of these 5 gives LR for migraine of 3.5
- Presence of 1 or 2 of these 5 gives LR of 0.4
- Neuroimaging Recommended for [28]:
- Cluster-type headache: LR ~11
- Abnormal neurological examination: LR ~5
- Undefined HA: LR ~4
- HA with aura: LR ~3
B. Subarachnoid Hemorrhage (SAH) [2]
- About 1-2% of headaches in an emergency department are due to SAH
- Etiology
- Most (~80%) caused by rupture of aneurysm
- Usually due to berry aneurysm in Circle of Willis
- May lead to vasospasm which can cause cerebral infarction
- Increased intracranial pressure (ICP, due to obstruction) and attendant symptoms
- Non-aneurysmal SAH occurs in ~20% of cases and has better prognosis
- Non-aneurysmal SAH includes isolated perimesencephalic SAH
- Symptoms
- Sudden onset HA; worst HA of life (~25% of these patients have SAH)
- May be preceded by "warning" HA (~35% of SAH patients)
- This "sentinal bleed" may herald second and usually more serious bleed
- Nausea, vomiting, fatigue, weakness leading to obtundation
- May have spontaneous resolution of symptoms if bleed stops
- Cerebral venous sinus thrombosis may also cause worst HA of life [4]
- Evaluation
[Figure] "Circle of Willis"
- Major concern is increased intracranial pressure (ICP)
- Rapid Neurologic Examination including fundoscopy
- Radiography: CT or MRI
- Lumbar Puncture (LP) - in any patient with posisble SAH and negative CT
- Misdiagnosis occurs in 25-50% of cases; these cases have poorer prognosis
- Computerized Tomography (CT)
- ~95% sensitive for SAH
- If CT is negative and suspicion continues to be high, then do lumbar puncture
- MRI may also be used and better distinguishes clot from bleed [4]
- Lumbar Pucture (LP)
- Blood in CSF from SAH
- Lumbar puncture should be done to rule out the10-15% of CT negative SAH
- If progression occurs, angiogram and emergent surgery may be required
- Treatment
- Neurosurgical Evacuation of bleed
- Nimodipine (Nimotop®) may help prevent vasospasm
- Lower blood pressure
- Reverse antiplatelet agents (with transfusion)
- Correct coagulopathies
- Treatment of ICP
C. Increased Intracranial Pressure (ICP)
- Usually slower onset than SAH
- Causes of Increased ICP
[Figure] "Intracranial Pressure"
- Mass effect (tumor, abscess)
- Hydrocephalus
- Malignant Hypertension
- Types of Hydrocephalus
- Elevated pressure - increased CSF production and/or decreased removal
- "Normal" pressure - slow onset headache, mental status chages, ataxia, incontinance
- Pseudotumor cerebri
- Supraduchal
- Arnold-Chiari Malformation
- Cerebral sinus thrombosis [5]
- Symptoms include papilledema and Cranial Nerve VI palsy
- CT essential; consider MRI
- LP, if indicated and safe, should include both opening and closing pressures
- Treatment aimed at decreasing cerebral blood flow, lowering pressures
- Normalize blood pressures
- Reduce seizure risk
- Reduce vasospasm
- Early invasive intervention for ruptured aneurysms associated with improved outcomes
- Microvacular neurosurgical clipping - slightly reduced risk of bleeing
- Endovascular coiling - associated with better outcomes, reduced seizures overall
D. Meningitis
- Infectious agents (viral, bacterial, fungal, protozoan)
- Encephalitis - particularly viral
- Blood (irritation)
- Carcinomatous meningitis
- Inflammatory reaction to metastatic cancer
- Usually occurs with breast, lung, renal cancers
- Medications - NSAIDs, some antibiotics, intravenous globulin (aseptic meningitis)
- Lumbar Puncture is essential for diagnosis and to guide therapy
E. Vasculitis
- Giant Cell (Temporal) Arteritis usually occurs in patients >50-60 yrs old
- Headache (or scalp pain) is usually unilateral and may occur with jaw claudication
- Commonly associated with Polymyalgia Rheumatica (~30% of cases)
- Temporal artery tenderness often present
- Leukocytosis and high ESR are common
- If suspected, must treat immediately with oral steroids (eg prednisone 60mg po)
- Failure to treat may result in blindness
- Biopsy of Temporal artery is definitive diagnostic method (80-90% sensitive)
- Other Systemic Vasculitides
- Polyarteritis Nodosa
- Systemic Lupus with CNS Involvement
- Behcet's Syndrome
- Isolated Vasculitis of the Central Nervous System
- Small to medium vessel vasculitis
- Headache, meningitis, encephalitis
- Abnormal LP and MRI
F. Pseudotumor Cerebri [7]
- Introduction
- Disorder of intracranial pressure (ICP) regulation
- Also called Benign Intracranial Hypertension
- CSF pressures increase with normal studies: no mass lesion or hydrocephalus
- Major threat is to patients vision
- Reported association with use of sulfa antibiotics (TMP/SMX)
- No known cause
- Symptoms
- Due only to increased ICP
- Headache ~95%
- Dizziness ~25%
- Nausea ~30%
- Visual Changes ~50%
- Diplopia ~30%
- Change in Mental Status ~10%
- Signs
- Papilledema 100%
- CN VI Palsey 20%
- Blind Spot increased 90%
- Visual Acuity decreased 10%
- Studies
- Computed Tomography should always be done to rule out mass lesion, hydrocephalus
- Lumbar Puncture: Pressure >20cm required for diagnosis; all other CSF studies normal
- Contributing Factors
- Young > Elderly (peak mid 30s)
- Obesity (~75%)
- F>M ~3:1
- Probably NOT related to abnormal regulation of estrogen itself
- May be related to increased estrones, which are produced by adipocytes
- No association with infection, endocrine disease, medications
- Abnormally low CSF resorption most likely plays a role
- Normal CSF production is ~0.35mL/min (21mL/hr)
- Lumbar puncture (LP) removes ~30mL but this is replaced in ~1.5hrs
- However, LP relieves symptoms in >90% of patients
- Treatment
- Repeated LPs as needed
- Each LP should decrease ICP to <18cm
- Prednisone 40-60mg po qd x 2 weeks then taper
- Glucocorticoids only for resistant symptoms, visual changes, LP failure, patient refusal
- Acetazolamide (Diamox®) - 1gm of long acting form qd will reduce ICP
- Shunt - very unusual for patients to require shunts
- Prognosis
- ~30% completely resolve with single LP
- Multiple LP's will cure most other patients
- All symptoms usually resolve over 6-12 months, many within 2 weeks
G. Cerebral Veinous Sinus Thrombosis (CVT) [4,8]
- Also called cerebral vein thrombosis
- Most often affects young adults (75% women) and children
- Highly variable symptoms and clinical course
- Incidence 3-4 cases per 1 million population annually
- >80% have good neurologic outcome; mortality <20%
- Mechanisms
- Thrombosis of central veins - local effects caused by venous obstruction
- Thrombosis of major sinuses which cause intracranial hypertension
- Presentation
- Wide range of symptoms, nearly always including very severe (global) headache
- Focal motor or sensory deficits
- Dysphasia
- Seizures - may cause post-ictal hemiparesis ("Todd's paresis")
- Impaired consciousness
- Intracranial mass appearance on CT or MRI
- D-dimers are elevated >500ng/mL in most patients with acute CVT [9]
- Risk Factors [10]
- Oral Contraceptives
- Factor V Leiden (activated protein C resistance)
- Prothrombin G20210A mutation
- Anticlotting factor (proteins C or S, antithrombin) deficiency
- Malignancy
- Trauma
- Autoimmune Disease
- Cerebral infection
- Pregnancy
- Prothrombotic risk found in ~85% of cases
- Head inury, direct sinus or jugular vein injury, and neurosurgical procedures also causes
- Otitis and mastoiditis may be complicated by CVT
- Treatment [4]
- Heparin acutely - overall reduces poor outcome/death ~50%
- Overlap with warfarin and maintain for ~6 months for standard risk patients
- Endovascular thrombolysis is experimental
- Oral acetazolamide (500-1000mg daily) for intracranial hypertension
- Lumbar puncture to relieve tension only after evaluation for space-occupying process
- Surgical evacuation of clot
- Treat underlying disorder
- Recurrent sinus thrombosis occurs in 2-4% of cases
H. Cavernous Sinus Thrombosis
- Usually secondary to oculonasal infections
- Syndrome
- Orbital edema with eye pain, tenderness on palpation
- Chemosis, cyanosis of upper face present
- Venous congestion
- Palsy of CN III, IV, V(3), and VI
- Patient appears acutely ill
- High fever
- Headache
- Nausea and vomiting
- Additional Ophthalmic Symptoms
- Ophthalmoplegia
- Pupillary changes
- Retinal hemorrhages
- Papilledema
- Sensory changes in ophthalmic division (3) of CN V
- CSF usually normal unless associated meningitis or subdural empyema
- Differentiate from mucormycetes infection, usually in diabetics or immunosuppressed
- Treatment with potent anti-staphylococcal and anti-anaerobic antibiotics
- Anticoagulation usually of minimal benefit
A. Types- Tension
- Cluster
- Migraine
- Neuropsychiatric
- Tic doloreux
- Cranial Neuralgia
- Depression
- Fibromyalgia
- Carotidynia
- Pain of face, neck, ear and head
- Due to distention or dilatation of one or both extracranial arteries
- Newly Defined HA Types
- Drug rebound HA - common with ergotamines, butalbital, NSAID and Tylenol® overuse
- Hypnic HA: throbbing pain, age >65, <1 hour, no systemic symptoms; responds to lithium
- Paroxysmal hemicrania: F>M, severe, sharp, periorbital pain; responds to indomethacin
- Transformed migraine: increased severity and frequency over decades
- Posttraumatic HA: may be due to axonal swelling, usually with head and neck pain
- Chronic Daily HA: HA >15 days per month for >3 months (new category; see below)
B. Tension HA [12]
- Most common type of headache, usually intermittant [13]
- Episodic tension HA occurs in 30-80% of persons in North America
- Slight female predominance
- Increased incidence with increasing education levels
- Chronic tension-type HA is very uncommon
- Probably due to abnormal vascular tone within pericranial muscles
- Types of Tension Headaches
- Generalized
- Bilateral
- Steady and Dull
- Diagnostic Criteria
- HA pain accompanied by at least 2 of the following 3:
- Pressing/tightening (nonpulsatile quality), bilateral, no effect of physical activity
- Required: no nausea or vomiting
- Photophobia or phonophobia absent, or only one present
- Greater than 15 days per month with HA
- No evidence of organic disease
- Classification
- Episodic tension type HA associated with disorder of pericranial muscles
- Chronic tension type HA associated with disorder of pericranial muscles
- HA of tension type not fulfilling criteria above
- Treatment
- Aspirin or Acetaminophen - 1000mg po as needed
- Other NSAIDs - Naproxen (375-500mg po) appears to very effective
- Treat as if typical vascular (such as migraine) HA
- Fiorcet® / Fiorinal® - always last line; may be habit forming
- Severe headaches may require hospitalization
- Spinal manipulation does not improve episodic tension-type HA [14]
- Nitric oxide synthetase (NOS) inhibition is effective in early studies [15]
- Prophylaxis
- Non-pharmacologic: behavioral modification, exercise, biofeedback
- Tricyclic antidepressant (see below) - minor improvements [16,17]
- Serotonin reuptake inhibitor such as fluoxetine [17]
- Anti-epileptics - carbamazepine, gabapentin, others
- Consider muscle relaxant such as tizanidine 6-18mg in more severe cases
- Combined stress management therapy and tricyclics more effective than either alone [16]
C. Carotidynia
- Pain anywhere above shoulders due to extracranial artery abnormalities
- Extensive differential
- Neuralgias - facial, cluster HA's, disc disease and cervical OA
- Musculoskeletal - myofascial pain, muscle strain, TMJ syndrome, bruxism
- Infection and/or inflammation - temporal arteritis (GCA) main concern, infections
- Classic carotidynia
- Rule out other causes as described above
- Etiology is migrainous (vasodilation/spasm) or arteriosclerosis (insufficiency)
- Therapy based on cause and/or classification
D. Intracranial Hypotension [18,19]
- Orthostatic headaches
- ~5 per 100,000 per year
- Peak age ~40 years
- More common in women
- Diverse Causes
- Due to reduced cerebrospinal fluid (CSF) pressure OR
- Reduced CSF volume (or both)
- Caused by single or multiple CSF leaks
- Thought to be related to leakage of CSF from spinal meningeal diverticuli
- Diagnosis [20]
- Lumbar puncture and measurement of CSF pressure is standard
- MRI shows subdural fluid collections, enhancement of pachymeninges, engorgement of venous structures, pituitary hyperemia, sagging of brain (mnemonic: SEEPS)
- Color doppler imaging of superior ophthalmic vein may be as effective, non-invasive
- Myelography required to idenitfy spinal CSF leadk
- Treatment
- Bed rest
- Epidural blood patching
- Percutaneous placement of fibrin sealant
- Surgical CSF leak repair
E. Common Daily HA [3]
- HA >15 days per month for >3 months
- Category includes many primary and secondary HA types
- Transformed migraine
- Medication overuse HA
- Other types
- Risk Factors
- Obesity
- History of frequent HA
- Caffeine consumption
- Overuse of acute HA medications (>10 days/month)
- Transformed Migraine
- Head pain >15 dyas per month for >1 month
- Average HA lasting >4 hours / day if untreated
- History of any form of episodic migraine or HA with migrainous components
- Medication Overuse HA
- HA present >15 days per month with development or marked worsening of pain during medication overuse and resolution of pain within 2 months of discontinuation of medicine
- Overuse: HA medicastion >3 months
- Use of ergotamine, triptans, opioids or combinations >10 days/month
- Use of simple analgesics at least 15 days per month
- Total use of HA medications at least 15 days per month
- Prevention of Transformed Migraine or Medication Overuse HA
- Limit or eliminate caffeine consumption
- Regular exercise
- Regular mealtimes and sleep schedules
- Treat coexistant anxiety and/or depression
- Pharmacologic agents similar to that for migraine prevention
- Initiate pharmacologic therapy and adjust dose to tolerability or >50% HA reduction
- Pharmacologic Prevention of Common Daily HA
- Tricyclic antidepressant such as amitriptyline 10mg po qhs initially, up to 100mg qhs
- SSRI such as fluoxetine or paroxetine, initiate 10mg po qd, up to 60mg daily
- Gabapentin target dose 300-1200mg tid
- Topiramate target dose 50-200mg qd divided
- Divalproex target dose 500-2000mg per day, divided
- Tizanidine target dose 8-20mg
- Botulinum toxin type A: 25-260U q3 months
A. Types- Migraine without aura (common migraine)
- Attacks lasting 4-72 hours (untreated)
- At least 2 of: unilateral, pulsating, moderate to severe, aggrevated by movement
- At least 1 of: nausea or vomiting, photophobia, phonophobia
- Migraine with aura (classic migraine)
- One or more transient focal neurological aura symptoms
- Gradual development of aura symptom over >4 minutes, or several symptoms in a row
- Aura symptoms last 4-60 minutes (untreated)
- Headache follows or accompanies aura within 60 minutes
- Ophthalmoplegic migraine
- Retinal migraine
- Childhood periodic syndromes
- Complicated migraine
B. Causes
- Trigger foods
- Tobacco Smoke
- Estrogens
- Fumes and Vapors
- Dehydration
- High Altitudes
- Genetic Causes
- Currently unclear what percentage of migraine suffers have genetic cause
C. Symptoms
- Throbbing HA
- Nausea / vomiting - due to decreased grastric motility
- Photophobia
- Feeling of doom occurs more in "Classic Migraine" as an "aura"
- In common migraine, there is usually not an aura
- Most commonly affects 20-40 year old females; rarely new onset >45 years old
- If new onset "migraine" occurs in patient >40 years old, strongly consider CT scan
E. Therapeutic Intervention
- Control Pain Acutely
- NSAIDS are useful for mild migraines
- Serotonin receptor (5-HT1B/D) blockers are first line for moderate to severe migraines
- Nausea and vomiting usually reponds to prochlorpromazine or metaclopramide
- Opiates may be useful for resistant migraines and for patients intolerant of other drugs
- More dangerous causes of HA must be ruled out (see above)
- Prevention of Migraines
- Initially, try elimination diet: eliminate all implicated foods and add back singly
- Discontinue vasoconstrictor (usually sympathomimetic) medications
- Add prophylactic agents (see below)
F. Treatment of Acute Exacerbations [23]
- Non-Steroidal Anti-Inflammatory Drugs (NSAID)
- Mainly for mild to moderate HA
- Generally poorer control of concurrent migraine symptoms than other agents
- GI distress and bleeding is a concern
- Renal dysfunction can occur, particularly with concomitant use of other nephrotoxins
- Serotonin Receptor Type 1B/1D Agonists [24,25]
- First line agents for control of moderate to severe migraines
- "Triptans": Sumatriptan (Imitrex®), Zolmitriptan (Zomig®), others
- Eletriptan 80mg, rizatriptan 10mg, almotriptan 12.5mg provide highest success rates overall [24]
- Side effects include chest pain, vasocontstriction, wheezing, flushing
- Contraindications: coronary artery disease, previous reaction, ECG changes
- Should not be used with other serotonergic agents, or within 2 weeks of MAO inhibitor
- Specific agents discussed under migraine
- Dihydroergotamine (DHE)
- Derivative of ergotamine with less vasoconstriction and adverse effects
- Can be given sc, im, iv, and newer intranasal therapy
- ~70% of patients will have relief within 2 hours of injection
- DHE Nasal Spray (Migranal®) - one spray (0.5mg)/nostril x 1, repeat in 15 minutes
- Nasal form may be safer, more effective
- May cause hypertension or cardiac valvular lesions
- Other ergot derivatives are third line therapy
- Dopamine Antagonists
- Primarily improve nausea and vomiting
- Metoclopramide (Reglan®) - also improves gastric emptying; 10mg iv usually given
- Prochlorperazine (Compazine®) 10mg iv or per rectum
- Chlorpromazine 25mg iv
- Often given with diphenhydramine (Benadryl®) or hydroxyzine 25mg iv or im
- Side effects of dopamine antagonists: dystonia, tardive dyskinesia
- Opiates - for severe migraines are used for third line therapy
- Fiorinal®: Caffeine + ASA + Butalbital (not recommended)
G. Prophylaxis [6,25]
- Usually for >3 months migraine or migraines >1 / week
- ß-adrenergic blockers first line
- Amitriptyline or verapamil usually second line
- Topiramate (preferred), gabapentin (Neurontin®) are reasonable second line alternatives [26]
- Divalproex (valproate) usually third line
- Candesartan (an angiotensin II receptor blocker) - particularly in hypertensive persons
- Methysergide only for recurrent, refractory migraines
- Each specific agent for prophylaxis should be used for at least 1 month before switching
- For details
A. Characteristics- Men ~90%, usually older age of onset (~30 years)
- Prevalence <1%, much less common than migraine
- Excruciating unilateral pain, centered over eye
- Duration 15-180 minutes and occurs 1-8 per 24 hour period
- Recur daily for 3-12 weeks then stop for 3-12 months
- Hence the name "cluster"
- Associated unilateral autonomic symptoms
- Conjunctival injection or lacrimation
- Nasal congestion or rhinorrhea
- Forehead and facial sweating
- Miosis
- Ptosis or Eyelid edema
- Nausea and vomiting are very uncommon
- Patients generally cannot remain still
- ~85% of patients are cigarette smokers
B. Pathophysiology
- Inheritability
- Familial occurrance in 7% of first degree relatives; 14X increased risk
- ~2X increased risk in second degree relatives
- Newer theories of pathophysiology
- Now believed to be neurovascular
- Severe unilateral pain mediated by first (ophthalmic) division of trigeminal nerve (CN V)
- Autonomic symptoms, including lacrimation, due to activation of parasympathetic outflow from cranial nerve (CN) VII
- Activation of blood flow in hypothalamus during attacks has been described [27]
- Abnormal hypothalamic grey matter function may play a major role in cluster headaches
- Sympathetic Paralysis
- Miosis and ptosis due to neuropraxic injury of postganglionic fibers in most patients
- This dysfunction may originate centrally in the hypothalamus as above
- Autonomic symptoms may also be secondary to trigeminal discharge
- Nitroglycerin, a vasodilator, can trigger cluster HA in susceptible individuals
- Many experts now regard cluster HA as a hypothalamic syndrome
C. Differential Diagnosis
- Trigeminal neuralgia
- Migraine
- Pheochromocytoma
- Temporal arteritis
- Tolosa-Hunt syndrome
- Raeder's Syndrome
- Brain Tumor
- Intracranial Vascular Malformation (AVM, Hemangioma, others)
- Post-traumatic headache
- Conversion Disorder
D. Acute Therapy
- Oxygen 7-10 L/min x 10-60 minutes with non-rebreathing facial mask
- Treat for 20 minutes
- Sitting, upright position
- No contraindications for use of oxygen
- ~60% response rate within 30 minutes
- Lidocaine, 4% intranasal - effective in minority of patients, but very safe
- Serotinin 5HT1B/D Agonists (Triptans)
- Sumatriptan (Imitrex®) 6mg sc or 50-100mg po
- ~75% efficacy of sc injected sumatriptan within 20 minutes
- Contraindications include cardiovascular and cerebrovascular disease
- Zolmitriptan (Zomig®) 5mg nasal spray also effective [11]
- No benefit of oral sumatriptan 100mg po tid for prevention of cluster HA
- Ergotamines (nasal 3 puffs or injection 0.5-1mg, sc, im or iv, or po/per rectum)
- Caffeine / ergotamine combination agents (Cafergot®, Ercaf®, Wigraine®)
- Narcotics
- Standard: meperidine (Demerol®) im
- Butorphanol (Stadol®) nasal spray or
E. Prophylaxis
- Efficacy of prophylaxis for cluster HA is controversial
- Verapamil
- Mainstay of prophylactic therapy
- Dose 120mg tid clearly reduced attack frequency and use of abortive agents [21]
- Dose is 120-480mg po qd usually divided; full effect in 2-3 weeks
- Overall, very safe agent
- Main side effects are bradycardia and constipation
- Synergistic with lithium
- Lithium: 300-1200mg per day (monitor serum levels)
- Prednisone
- Usual starting dose is 30-60mg po qd 1-2 weeks
- Then tapered over 1-3 weeks
- General precautions for glucocorticoid use
- Valproex Sodium
- 750-1500mg/day in divided doses
- Monitor for side effects carefully
- Hepatic dysfunction, pancreatitis and bone marrow suppression are possible
- Ergotamine: 1mg po qhs or bid
- Methysergide (Sansert®)
- Maximum of 4-6 month use with 1 month drug holidays
- Dose is 2-8mg divided in 3 doses each day
- Retroperitoneal fibrosis is major side effect - cumulative dose and time related
- Peripheral ischemia, CNS with halucinatory symptoms are rare
- May suppress cluster HA, then discontinue
- Occipital Nerve Stimulation [29]
- Suboccipital region electrodes for nerve stimulation for refrectory cluster HA
- Of 8 patients, 2 had >90%, 3 moderate (~40%), 1 mild (25%) improvement
References
- Kaniecki R. 2003. JAMA. 289(11):1430

- Suarez JI, Tarr RW, Selman WR. 2006. NEJM. 354(4):387

- Dodick DW. 2006. NEJM. 354(2):159
- Ciccone A, Citterio A, Santilli I, Sterzi R. 2000. Lancet. 356(9244):1818 (Case Report)

- Stam J. 2005. NEJM. 352(17):1791

- Silberstein SD. 2004. Lancet. 363(9406):381

- Friedman DI. 2004. Neruol Clin. 22(1):99

- Thaler DE and Frosch MP. 2002. NEJM. 346(21):1651 (Case Record)

- Tardy B, Tardy-Poncet B, Viallon A, et al. 2002. Am J Med. 113(3):238

- Martinelli I, Sacchi E, Landi G, et al. 1998. NEJM. 338(25):1793

- May A. 2005. Lancet. 366(9488):843

- Welch KMA. 2001. JAMA. 286(8):960

- Schwartz BS, Stewart WF, Simon D, Lipton RB. 1998. JAMA. 279(5):381

- Bove G and Nilsson N. 1998. JAMA. 280(18):1576

- Ashina M, Lassen LH, Bendtsen L, et al. 1999. Lancet. 353(9149):287

- Holroyd KA, O'Donnell FJ, Stensland M, et al. 2001. JAMA. 285(17):2208

- Tomkins GE, Jackson JL, O'Malley PG, et al. 2001. Am J Med. 111(1):54

- Schievink WI. 2006. JAMA. 295(19):2286

- Mokri B, Piepgras DG, Miller GM. 1997. Mayo Clin Proc. 72:400

- Chen CC, Luo CL, Wang SJ, et al. 1999. Lancet. 354(9181):826

- Leone M, D'Amico D, Frediani F, et al. 2000. Neurology. 54:1382

- Goadsby PJ, Lipton RB, Ferrari MD. 2002. NEJM. 346(4):257

- Drugs for Migraine. 1998. Med Let. 40(1037):97

- Ferrari MD, Roon KI, Lipton RB, Goadsby PJ. 2001. Lancet. 358(9294):1668

- Snow V, Weiss K, Wall EM, et al. 2002. Ann Intern Med. 137(10):840

- Gabapentin for Chronic Pain. 2004. Med Let. 46(1180):29

- May A, Bahra A, Buchel C, et al. 1998. Lancet. 352(9124):275

- Detsky ME, McDonald DR, Baerlocher MO, et al. 2006. JAMA. 296(10):1274

- Burns B, Watkins L, Goadsby PJ. 2007. Lancet. 369(9567):1099
