eMedicine Specialties > Neurology > Headache and Pain

Chronic Paroxysmal Hemicrania: Treatment & Medication

Author: Manish K Singh, MD, Assistant Professor, Department of Neurology, Teaching Faculty for Pain Management and Neurology Residency Program, Hahnemann University Hospital, Drexel College of Medicine; Medical Director, Neurology and Pain Management, Jersey Institute of Neuroscience
Coauthor(s): Jashvant Patel, MD, Medical Director, Department of Pain Medicine and Comprehensive Rehabilitation, Medical College of Pennsylvania Hahnemann University
Contributor Information and Disclosures

Updated: Sep 3, 2009

Treatment

Medical Care

  • The treatment of choice for CPH is indomethacin, which has an absolute effect on the symptoms. Both episodic CH and CPH respond well to indomethacin.
  • Other medications that may provide relief include salicylates (aspirin), naproxen, prednisone, celecoxib, piroxicam, acetazolamide, and ergotamine. One prospective open trial conducted with 10 patients experiencing CPH suggests that acetylsalicylic acid (and probably naproxen and diclofenac) and verapamil (for prophylaxis) are the most effective second-line drugs. In another report, two teenaged girls who demonstrated dramatic, yet incomplete, improvement with indomethacin had nearly complete relief with verapamil monotherapy.13
  • The efficacy of sumatriptan in CPH is still controversial.14,15,16
  • Oxygen, lithium, carbamazepine, and other anticonvulsants are ineffective in patients with CPH.
  • Anesthetic blockade of the occipital nerves and supraorbital nerve have not provided significant relief. Occipital nerve blockade helps in distinguishing CPH and HC from cervicogenic headache. Supraorbital nerve blockade may help in distinguishing HC and supraorbital nerve neuralgia (in which nerve block is markedly effective).
  • Reliable evidence of efficacy of chiropractic manipulation, acupuncture, or surgical management in the treatment of CPH does not exist.

Consultations

Ophthalmologist - To evaluate ocular pathology such as glaucoma or orbital pseudotumor

Medication

Drug of choice in the treatment of CPH is indomethacin. When a patient experiences frequent unilateral headaches (ie, >4 attacks in 24 h), a drug trial with indomethacin should be considered. The dose of indomethacin should be increased to at least 150 mg/d for 3-4 d. Beneficial effect is seen usually within 48 h, but may take as long as 5 d. In one study, indomethacin effect was complete within 24 h in most patients, and frequently the effect was seen within 8 h. Maintenance dosage is usually 25-100 mg/d but may range from 12.5-300 mg/d. After discontinuation of medication, symptoms usually reappear within 12 h to a few days. However, long remission periods lasting years have been described.

About 10% of patients may experience adverse effects of indomethacin, including dyspepsia, nausea, vomiting, vertigo, gastric bleeding, purpura, and other conditions. To prevent gastric adverse effects, antacids, misoprostol, or an H2 antagonist or proton pump inhibitor may be coadministered when indomethacin is being used for longer periods. An indomethacin suppository is another option for gastric intolerance or when a higher dose (eg, 300 mg/d) is needed.

A recent article suggests that topiramate could be helpful as a preventive agent.

Nonsteroidal anti-inflammatory drugs (NSAIDs)

These agents have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known, but they may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms may exist as well, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell-membrane functions.


Indomethacin (Indocin)

Has absolute effect on symptoms of CPH. Available as immediate-release preparation, sustained-release preparation, suppository, and oral suspension. Ninety capsules of branded immediate-release indomethacin costs $61.38 and generic costs $25.93. Thirty capsules of sustained-release indomethacin costs $64.57 and generic costs $42.46. Recently, in one pharmacy review, cost for 30 days treatment with generic indomethacin 50 mg bid was estimated to be $5.58.

Adult

Immediate release: 25-50 mg PO tid
Sustained release: 75 mg PO qd/bid
Suppository: 50 mg PR

Pediatric

<14 years: Not recommended except for neonates with patent ductus arteriosus
>14 years: Administer as in adults

Concomitant use with other NSAIDs not advisable because of increased possibility of GI toxicity; diflunisal associated with serious GI hemorrhage; may reduce renal function, use caution when using medications that are excreted by kidneys; may decrease tubular secretion of methotrexate and potentiate its toxicity; like other NSAIDs, may blunt natriuretic effect of furosemide by inhibiting prostaglandin synthesis; can reduce diuretic, natriuretic, and antihypertensive effects of various other diuretic medications; probenecid may increase plasma levels; may increase serum concentration and prolong half-life of digoxin

Documented hypersensitivity; syndrome of nasal polyps; angioedema or bronchospastic reaction to aspirin and other NSAIDs; pulmonary hemorrhage; active GI bleeding, or history of recurrent GI lesions; simultaneous use of lithium (may result in lithium toxicity)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studies in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in patients with renal insufficiency (ie, serum creatinine > 2 mg/dL), hepatic dysfunction, bleeding disorders (ie, platelets <75,000/mm3), parkinsonism, depression, epilepsy, psychiatric disturbances (may cause worsening of symptoms); can mask usual signs and symptoms of infection; fluid retention and peripheral edema have been reported in a few patients


Naproxen sodium (Aleve, Anaprox, Naprelan, Naprosyn)

For relief of mild to moderately severe pain; inhibits inflammatory reactions and pain by decreasing activity of cyclooxygenase, which results in decrease of prostaglandin synthesis.

Adult

275 mg PO tid or 550 mg bid (proper dose guidelines for CPH not established)

Pediatric

<12 years: Not recommended
>12 years: Administer as in adults

Probenecid may increase toxicity; may decrease effects of loop diuretics; may increase serum lithium levels; anticoagulants may prolong PT

Documented hypersensitivity; peptic ulcer disease; renal or hepatic impairment; concomitant or recent use of anticoagulants; hemorrhagic conditions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Long-term use enhances potential for adverse effects, particularly gastropathy or nephropathy


Ibuprofen (Motrin, Ibuprin)

DOC for patients with mild to moderately severe pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.

Adult

400-800 mg PO q8h, not to exceed 3200 mg/d (proper dose guidelines for CPH not established)

Pediatric

<12 years: Not recommended
>12 years: Administer as in adults

Probenecid may increase toxicity; may decrease effects of loop diuretics; may increase serum lithium levels; anticoagulants may prolong PT

Documented hypersensitivity; peptic ulcer disease; renal or hepatic impairment; concomitant or recent use of anticoagulants; hemorrhagic conditions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Long-term use enhances potential for adverse effects, particularly gastropathy or nephropathy


Aspirin (Anacin, Ascriptin, Bayer Aspirin)

Treats mild to moderately severe pain. Inhibits prostaglandin synthesis, which prevents formation of platelet-aggregating thromboxane A2.

Adult

Initial dose: 900-1000 mg PO; may be repeated after 2 h if necessary (proper dose guidelines for CPH not established)

Pediatric

<12 years: Not recommended
>12 years: Administer as in adults

Probenecid may increase toxicity; may decrease effects of loop diuretics; may increase serum lithium levels; anticoagulants may prolong PT

Documented hypersensitivity; peptic ulcer disease; renal or hepatic impairment; concomitant or recent use of anticoagulants; hemorrhagic conditions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Long-term use enhances potential for adverse effects, particularly gastropathy or nephropathy

Calcium channel blockers

These agents inhibit calcium ions from entering slow channels, select voltage-sensitive areas, or vascular smooth muscle. Verapamil may be an effective calcium channel blocker for prophylaxis of CPH.


Verapamil (Calan, Verelan, Covera-HS)

During depolarization, inhibits calcium ion from entering slow channels or voltage-sensitive areas of vascular smooth muscle.

Adult

Sustained release: 120 mg/d PO qd; not to exceed 480 mg/d
Immediate release: 40 mg PO tid; not to exceed 480 mg/d

Pediatric

Not established

Carbamazepine, phenobarbital, hydantoins, vitamin D, sulfinpyrazone, and rifampin may decrease serum concentrations by increasing hepatic metabolism; amiodarone may increase toxicity; beta-blockers may increase cardiac depressant effect; cimetidine may increase serum levels; may increase serum levels of cyclosporine, theophylline, carbamazepine, and digoxin

Documented hypersensitivity; sinus bradycardia; cardiogenic shock; second- and third-degree heart block; sick-sinus syndrome; ventricular tachycardia; congestive heart failure; atrial fibrillation or flutter associated with accessory conduction pathways

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Use caution in severe left ventricular dysfunction, hepatic or renal impairment, or hypertrophic cardiomyopathy; patients may report headache (which improves after weeks of treatment), hypotension, and dizziness

Corticosteroids

These agents may be effective in treatment of CPH. Pain relief may occur via inhibition of prostaglandin synthesis.


Prednisone (Sterapred)

May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity. High dose prescribed for first few days, followed by gradual taper.

Adult

40-60 mg/d PO in divided doses for 5 d, followed by slow taper over 2 wk (proper dose guidelines for CPH not established); long-term use not recommended

Pediatric

Not established

May increase digitalis toxicity secondary to hypokalemia; monitor for hypokalemia when coadministered with diuretics; phenobarbital, phenytoin, or rifampin may increase metabolism of corticosteroids, which decreases their effects; estrogens may decrease clearance; may decrease effects of salicylates

Documented hypersensitivity; viral infection; peptic ulcer disease; hepatic dysfunction; connective tissue infections, fungal or tubercular skin infections; systemic fungal infections or serious infections except septic shock or tuberculous meningitis

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Long-term use may predispose patients to hyperglycemia, manifestations of latent diabetes mellitus, nonketotic hyperosmolar state, osteoporosis, avascular necrosis of hip, cataracts, steroid myopathy, cushingoid appearance, weight gain, suppression of pituitary-hypothalamic axis, peptic ulcer disease, suppression of growth (children), unmasking of latent infections (eg, tuberculosis, herpes zoster), increased predisposition to fungal and parasitic infections
Suppression of pituitary-hypothalamic axis may cause patients to require higher doses at times of stress
Water retention resulting from therapy may precipitate congestive heart failure; hypertension and hypokalemia may occur

Anticonvulsants

Agents with state-dependent sodium channel–blocking action and inhibitory activity of neurotransmitter GABA may have prophylactic effects on CPH.


Topiramate (Topamax)

Sulfamate-substituted monosaccharide with broad spectrum of antiepileptic activity that may have state-dependent sodium channel–blocking action, potentiates inhibitory activity of neurotransmitter GABA. In addition, may block glutamate activity. Not necessary to monitor plasma concentrations to optimize therapy.

Adult

25 mg PO hs; increase to 50 mg PO hs at 1 wk interval and increase further as necessary; patients with migraine will respond to 50 mg to 100 mg hs

Pediatric

Not established

Phenytoin, carbamazepine and valproic acid can significantly decrease topiramate levels; topiramate reduces digoxin and norethindrone levels, when administered concomitantly; concomitant use with carbonic anhydrase inhibitors may increase risk of renal stone formation and should be avoided; use topiramate with extreme caution when administering concurrently with CNS depressants since may have an additive effect in CNS depression, as well as other cognitive or neuropsychiatric adverse events

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Risk of developing a kidney stone formation is increased 2-4 times that of untreated population; risk may be reduced by increasing fluid intake; caution in renal or hepatic impairment; patients taking topiramate should seek immediate medical attention if they experience blurred vision or periorbital pain; continued usage after symptoms develop, can lead to glaucoma; primary treatment is discontinuation of topiramate; if left untreated, serious sequelae, including permanent vision loss, may occur; oligohidrosis and hyperthermia has been reported predominantly in children during vigorous exercise or exposure to warm environmental temperatures (ensure proper hydration prior and during activity and warm temperatures); may cause hyperchloremic, non-anion gap metabolic acidosis acute or chronic metabolic acidosis resulting in hyperventilation, and nonspecific symptoms, such as fatigue and anorexia, or more severe adverse effects including cardiac arrhythmias or stupor; chronic, untreated metabolic acidosis may increase nephrolithiasis or nephrocalcinosis risk, osteomalacia (ie, rickets in pediatric patients), or osteoporosis with an increased risk for bone fractures; chronic metabolic acidosis in pediatric patients may also reduce growth rates; measure baseline and periodic serum bicarbonate; sprinkle capsules should be swallowed whole or carefully open capsule and sprinkle contents on soft food immediately before ingestion, do not chew or crush

More on Chronic Paroxysmal Hemicrania

Overview: Chronic Paroxysmal Hemicrania
Differential Diagnoses & Workup: Chronic Paroxysmal Hemicrania
Treatment & Medication: Chronic Paroxysmal Hemicrania
Follow-up: Chronic Paroxysmal Hemicrania
References
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Further Reading

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Keywords

Sjaastad syndrome, IHS code: 3.2 chronic paroxysmal hemicrania, ICD-9 code: 346.9 hemicrania, CPH, headache, indomethacin, chronic paroxysmal hemicrania, unilateral headache, headaches with autonomic activation, headaches without autonomic activation, chronic and episodic paroxysmal hemicrania, short-lasting unilateral neuralgiform headache with conjunctival injection and tearing, SUNCT syndrome

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Contributor Information and Disclosures

Author

Manish K Singh, MD, Assistant Professor, Department of Neurology, Teaching Faculty for Pain Management and Neurology Residency Program, Hahnemann University Hospital, Drexel College of Medicine; Medical Director, Neurology and Pain Management, Jersey Institute of Neuroscience
Manish K Singh, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Pain Medicine, American Association of Physicians of Indian Origin, American Headache Society, American Medical Association, and American Society of Regional Anesthesia and Pain Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Jashvant Patel, MD, Medical Director, Department of Pain Medicine and Comprehensive Rehabilitation, Medical College of Pennsylvania Hahnemann University
Jashvant Patel, MD is a member of the following medical societies: Alberta Medical Association, American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, American Medical Association, American Society of Regional Anesthesia and Pain Medicine, and Medical Society of the State of New York
Disclosure: Nothing to disclose.

Medical Editor

Jorge E Mendizabal, MD, Consulting Staff, Corpus Christi Neurology
Jorge E Mendizabal, MD is a member of the following medical societies: American Academy of Neurology, American Headache Society, National Stroke Association, and Stroke Council of the American Heart Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

James H Halsey, MD, Professor, Department of Neurology, University of Alabama Medical Center
James H Halsey, MD is a member of the following medical societies: American Academy of Neurology, American Heart Association, American Medical Association, American Neurological Association, American Society of Neuroimaging, Medical Association of the State of Alabama, New York Academy of Sciences, Pan American Medical Association, Sigma Xi, Society for Neuroscience, and Southern Medical Association
Disclosure: Nothing to disclose.

CME Editor

Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital
Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association
Disclosure: Nothing to disclose.

Chief Editor

Howard A Crystal, MD, Professor, Departments of Neurology and Pathology, State University of New York Downstate; Consulting Staff, Department of Neurology, University Hospital and Kings County Hospital Center
Howard A Crystal, MD is a member of the following medical societies: American Academy of Neurology and American Neurological Association
Disclosure: Medivations Honoraria Consulting

 
 
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