eMedicine Specialties > Ophthalmology > Neurologic Disorders

Trigeminal Neuralgia: Treatment & Medication

Author: Marc E Lenaerts, MD, FAHS, Staff Neurologist, Mercy Medical Group, Sacramento, CA; Associate Clinical Professor of Neurology, Department of Neurology, University of California at Davis, Sacramento
Contributor Information and Disclosures

Updated: Jan 29, 2010

Treatment

Medical Care

Treatment can be subdivided into pharmacologic therapy, percutaneous procedures, surgery, and radiation therapy. Adequate pharmacologic trials should always precede the contemplation of a more invasive approach. Most patients respond well to initial therapy, but some cases are resistant to any type of treatment.

Carbamazepine and oxcarbazepine are considered first-line therapy. Lamotrigine and baclofen are second-line therapy. Other treatments are third line and the evidence for their efficacy is scant.

Treatment for trigeminal neuralgia must be tailored individually, based on the patient's age and general condition. In the case of symptomatic trigeminal neuralgia, adequate treatment is that of its cause, the details of which are out of the scope of this article. Use of pharmacoprophylaxis or of surgical techniques used for the classic form can be tried, but no scientific evidence of efficacy has been produced.

  • Carbamazepine (Tegretol, Carbatrol) was introduced in the 1960s and has proven its efficacy in numerous studies. It remains the criterion standard of treatment for trigeminal neuralgia.8,9
  • Oxcarbazepine (Trileptal) has not been studied as extensively, but efficacy outcomes are similar. Better tolerability can be considered an advantage over carbamazepine.10
  • Lamotrigine (Lamictal) has been proven more effective than placebo. The dosage should be increased slowly for better tolerance (eg, 25-mg daily dose each week; up to 250 mg twice a day).11
  • Baclofen has demonstrated its efficacy but with a lower degree of evidence.12,13
Below are medications for which the evidence is scant; the author does not formally recommend them.
  • Gabapentin (Neurontin) seems to be effective, but no controlled studies are available.14
  • Phenytoin (Dilantin) is not recommended. Only anecdotal evidence exists. The dose varies greatly among patients.
  • Clonazepam (Klonopin) has moderate efficacy but is not recommended because of a low level of evidence and its adverse effects (eg, sedation) and dependence.
  • Amitriptyline (Elavil) can be tried, but the success rate is low.

Surgical Care

The timing for surgery is debatable, and no randomized study has addressed this question. However, the earlier a surgical technique is applied, it seems the better the outcome. At least 2 medication trials should be performed and carefully evaluated before more invasive techniques are instituted.15

The success rate varies according to the experience of the surgeon or the anesthesiologist, and, therefore, surgical correction should be performed only by experienced surgeons. Surgical therapy can be divided into procedures on the nerve or gasserian ganglion (external or percutaneous, usually performed by pain management specialists) and on the nerve root (open skull surgery called microvascular decompression and performed by neurosurgeons, and gamma-knife radiation performed by radiation therapists). Microvascular decompression has an overall better success rate, but it is more invasive. Percutaneous techniques may be more accessible to elderly patients who are at high surgical risk.

  • On the nerve root
    • Jannetta pioneered microvascular decompression. This procedure consists of opening a keyhole in the mastoid area and freeing the trigeminal nerve from the compression/pulsating artery; then, a piece of Teflon is placed between them. Large series have been published, and the initial efficacy is greater than 80%. Recurrence rates are among the lowest (20% at 1 y, 25% at 5 y) compared with other invasive treatments.16,17 Usually, it requires the demonstration of true contact and compression by the artery on the nerve, but series are published that show an almost equally effective result without any demonstrated abnormality on imaging or even frank compression shown preoperatively. Complications include chemical meningitis, ipsilateral hearing loss, and facial sensory loss or palsy. Mortality rates in experienced centers are less than 0.5%.A surgical image is below.

    • Microvascular decompression (Jannetta procedure) ...

      Microvascular decompression (Jannetta procedure) used to treat trigeminal neuralgia. The anteroinferior cerebellar artery and the trigeminal nerve are in direct contact. Courtesy of PT Dang, CH Luxembourg.

      Microvascular decompression (Jannetta procedure) ...

      Microvascular decompression (Jannetta procedure) used to treat trigeminal neuralgia. The anteroinferior cerebellar artery and the trigeminal nerve are in direct contact. Courtesy of PT Dang, CH Luxembourg.

    • Gamma-knife treatment consists of multiple rays (>200) of high-energy photons concentrated with high accuracy on the target (ie, trigeminal nerve root).18,19 This treatment destroys specific components of the nerve. Of those treated, 60% of patients are immediately free of pain, and more than 75% of patients have greater than 50% relief after 1.5 years. Recurrence rates are around 25 % between 1 and 3 years. This treatment can be used after a patient does not respond to any of the above-mentioned procedures, including this one. The device contains a stable source of radiation (60-Co) that frees this technique from requiring an external source of radioactivity (eg, cyclotron). See the clinical image below.

    • MRI with high resolution on the pons demonstratin...

      MRI with high resolution on the pons demonstrating the trigeminal nerve root. In this case, the patient with trigeminal neuralgia has undergone gamma-knife therapy, and the left-sided treated nerve (arrow) is enhanced by gadolinium.

      MRI with high resolution on the pons demonstratin...

      MRI with high resolution on the pons demonstrating the trigeminal nerve root. In this case, the patient with trigeminal neuralgia has undergone gamma-knife therapy, and the left-sided treated nerve (arrow) is enhanced by gadolinium.

  • On the gasserian ganglion 
    • Glycerol injection of the gasserian ganglion to selectively destroy the pain-transmitting fibers has been used for a long time. This injection has a higher efficacy rate and a lower recurrence rate than the alcohol injection. It is easy to perform, and anesthesia is not needed.
    • Pulsed radiofrequency on the trigeminal ganglion appears promising in reports.20,21 Likewise, linear-accelerated particle radiation appears to be a valid alternative.
  • On the peripheral nerve 
    • Percutaneous radiofrequency rhizotomy and percutaneous microcompression with balloon inflation are relatively inexpensive and accessible techniques, and they are less invasive than surgery, with a lower (long-term) efficacy-to-recurrence ratio. The result is highly dependent on the surgeon's skill. General anesthesia is required.
    • Alcohol or phenol injection of the trigeminus can be performed at various locations along the nerve, and the goal is to destroy selective pain fibers. Although it is an easy procedure, the success rate is low, in part because of a low selectivity of effect on the fiber type with this substance. Recurrence rates are around 50 % at 1 year.
  • Clinical guideline summaries

Consultations

Pain management specialists and/or a neurosurgeon should be consulted depending on the modality used to correct the trigeminal neuralgia.

Diet

No specific diet is recommended in trigeminal neuralgia.

Activity

Other than avoiding the triggers of trigeminal neuralgia, the activity of the patient should remain normal.

Medication

Treatment of trigeminal neuralgia is prophylactic. Indeed, no abortive therapy has been conceived for this very short-lived pain condition. Carbamazepine remains the criterion standard, but a number of other drugs have been used for a long time and with fair success. They should be considered successively in case of resistance. Rarely, combination therapy can be provided, but it should remain exceptional for tolerance reasons and because a synergistic effect rarely occurs.12 Duration of treatment depends on clinical evolution but usually is long-term, often lasting years. Topical analgesics have failed.24

Refer to Physician's Desk Reference (PDR) for details on medications mentioned.

Anticonvulsants

Reduce firing of nerve potentials in the trigeminal nerve.


Carbamazepine (Tegretol, Carbatrol)

Criterion standard in the medical management of trigeminal neuralgia, its efficacy has been demonstrated in multiple clinical trials. As of yet, a controlled trial has not occurred on oxcarbazepine (Trileptal), another carbamate close to carbamazepine. Slow-release forms now available allow a bid dosage. Titrating slowly improves tolerance.

Adult

200 mg PO tid (range 400-1600 mg/d, fractionated over the day); titrate slowly by 200 mg q3d

Pediatric

Not established

Serum levels may increase significantly within 30 d of danazol coadministration (avoid whenever possible); do not coadminister with MAOIs; cimetidine may increase toxicity, especially if taken in first 4 wk of therapy; may decrease primidone and phenobarbital levels (coadministration may increase carbamazepine levels)

Documented hypersensitivity; history of bone marrow depression; administration of MAOIs within last 14 d

Pregnancy

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

Precautions

Most frequent adverse effects are dizziness, ataxia, diplopia, hyponatremia, vertigo, and sedation. Life-threatening rashes can occur (rare and dose dependent); bone marrow suppression is rare but necessitates monitoring; monitor CBC count (bone marrow suppression) and sodium (hyponatremia) level monthly for at least 3 mo; monitor blood levels in case of toxicity or suspected noncompliance but not as routine; because of an autoinduction of its metabolism, carbamazepine levels tend to decrease after a few weeks of treatment, and dosage may need to be adjusted


Phenytoin (Dilantin)

Not as efficient as carbamazepine; use is based on same potential mechanisms.

Adult

300 mg PO qhs (range 100-400 mg/d qd/bid)

Pediatric

Not established

Amiodarone, benzodiazepines, chloramphenicol, cimetidine, fluconazole, isoniazid, metronidazole, miconazole, phenylbutazone, succinimides, sulfonamides, omeprazole, phenacemide, disulfiram, ethanol (acute ingestion), trimethoprim, and valproic acid may increase toxicity; effects may decrease when taken concurrently with barbiturates, diazoxide, ethanol (chronic ingestion), rifampin, antacids, charcoal, carbamazepine, theophylline, or sucralfate; may decrease effects of acetaminophen, corticosteroids, dicumarol, disopyramide, doxycycline, estrogens, haloperidol, amiodarone, carbamazepine, cardiac glycosides, quinidine, theophylline, methadone, metyrapone, mexiletine, oral contraceptives, and valproic acid

Pregnancy

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

Precautions

Monitor blood levels in case of potential toxicity but not as routine; adverse effects are dizziness, ataxia, somnolence, and diplopia (rare at usual therapeutic dosages)


Lamotrigine (Lamictal)

A few controlled studies document its efficacy. The adverse event to prevent is a rash, sometimes severe and life threatening, mostly if titration is too rapid.

Adult

25 mg PO qd initially, increase q2wk by 25 mg bid; increase until efficacy or adverse effects, not to exceed 250 mg PO bid

Pediatric

Not established

Acetaminophen increases renal clearance of lamotrigine, decreasing effects; similarly, phenobarbital and phenytoin increase lamotrigine metabolism, causing a decrease in lamotrigine levels; administration of valproic acid increases half-life

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

Monitor for rash and inform patient; other adverse effects are headache, anorexia, nausea, vomiting, and dizziness (infrequent)


Gabapentin (Neurontin)

Same mechanism of action is supposed to play a role. More expensive than the other drugs but has a very low adverse effect profile. No controlled study has been completed, but several open trials have reported an improvement on this drug. As for other indications, adequate dosage seems to vary greatly, and a trial should include raising the dose (eg, 3600 mg/d) as long as no efficacy is yet encountered, before stopping it. Given in 4 divided doses a day.

Adult

1200-3600 mg/d PO tid/qid
300 mg PO qd initially, then titrate 300 mg/d

Pediatric

Not established

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

Caution in impaired renal or hepatic function


Oxcarbazepine (Trileptal)

Close cousin of carbamazepine; presumably works on similar mechanisms. Offers a better tolerance and is easier to manage. Studies are limited, as opposed to the large body of high-level evidence with carbamazepine.

Adult

Average routine dose ranges 600-1800 mg/d; titration can be over a couple of weeks

Pediatric

Not established

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

Most frequent adverse effects are dizziness, ataxia, diplopia, hyponatremia, vertigo, and sedation; life-threatening rashes can occur (rare and dose dependent); bone marrow suppression is rare but can be monitored with CBC count (bone marrow suppression); monitoring of sodium (hyponatremia) levels not necessary; monitor blood levels for toxicity or suspected noncompliance but not as routine

GABA-agonists

GABA-agonist effect reduces the central projection of painful afferent impulses.


Baclofen (Lioresal)

Not as often efficient as carbamazepine. Has been demonstrated to be useful by well-conducted clinical studies.

Adult

10 mg PO tid, up to 30 mg PO tid, depending on response and tolerance
5 mg PO bid initially, gradually increase by 5 mg q2-3d

Pediatric

Not established

Opiate analgesics, benzodiazepines, alcohol, TCAs, guanabenz, MAOIs, clindamycin, and hypertensive agents may increase effects

Pregnancy

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

Precautions

Caution in patients with history of autonomic dysreflexia and when spasticity is used to obtain increased function; autonomic dysreflexia can result from withdrawal of this medication

Tricyclic antidepressants

A complex group of drugs that have central and peripheral anticholinergic effects, as well as sedative effects. They have central effects on pain transmission. They block the active re-uptake of norepinephrine and serotonin.


Amitriptyline (Elavil)

A minority of patients might respond to this drug. Anticholinergic adverse effects are the limitation.

Adult

25-75 mg/d PO qhs

Pediatric

Not established

Phenobarbital may decrease effects; coadministration with CYP2D6 enzyme system inhibitors (eg, cimetidine, quinidine) may increase levels; inhibits hypotensive effects of guanethidine; may interact with thyroid medications, alcohol, CNS depressants, barbiturates, and disulfiram

Documented hypersensitivity; MAOIs in past 14 d; history of seizures, cardiac arrhythmias, glaucoma, or urinary retention

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

Caution in cardiac conduction disturbances, history of hyperthyroidism, and renal or hepatic impairment; avoid using in elderly patients

Toxin

Recent experimental approach, mentioned to respond to patient inquiries. Not recommended because of scant evidence of efficacy. Appears to potentially decrease painful afferents, but mechanism of action remains unclear.25


Botulinum toxin (BOTOX®)

Subcutaneous injections have been beneficial in a pilot study, but these results await confirmation.

Adult

100 U in the zygomatic arch

Pediatric

Not established

Myasthenia; documented hypersensitivity

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

Excessive dosages can cause dysphagia or diplopia

More on Trigeminal Neuralgia

Overview: Trigeminal Neuralgia
Differential Diagnoses & Workup: Trigeminal Neuralgia
Treatment & Medication: Trigeminal Neuralgia
Follow-up: Trigeminal Neuralgia
Multimedia: Trigeminal Neuralgia
References

References

  1. Headache Classification Subcommittee of the International Headache Society. The International Classification of Headache Disorders: 2nd edition. Cephalalgia. 2004;24 Suppl 1:9-160. [Medline].

  2. Hess B, Oberndorfer S, Urbanits S, Lahrmann H, Horvath-Mechtler B, Grisold W. Trigeminal neuralgia in two patients with glioblastoma. Headache. Oct 2005;45(9):1267-70. [Medline].

  3. Al-Din AS, Mir R, Davey R, Lily O, Ghaus N. Trigeminal cephalgias and facial pain syndromes associated with autonomic dysfunction. Cephalalgia. Aug 2005;25(8):605-11. [Medline].

  4. Vincent M. SUNCT, lacrimation, and trigeminal neuralgia. Cephalalgia. Mar 1998;18(2):71. [Medline].

  5. Majoie CB, Hulsmans FJ, Castelijns JA, et al. Symptoms and signs related to the trigeminal nerve: diagnostic yield of MR imaging. Radiology. Nov 1998;209(2):557-62. [Medline].

  6. Tanaka T, Morimoto Y, Shiiba S, et al. Utility of magnetic resonance cisternography using three-dimensional fast asymmetric spin-echo sequences with multiplanar reconstruction: the evaluation of sites of neurovascular compression of the trigeminal nerve. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. Aug 2005;100(2):215-25. [Medline].

  7. Cruccu G, Biasiotta A, Galeotti F, Iannetti GD, Truini A, Gronseth G. Diagnostic accuracy of trigeminal reflex testing in trigeminal neuralgia. Neurology. Jan 10 2006;66(1):139-41. [Medline].

  8. Campbell FG, Graham JG, Zilkha KJ. Clinical trial of carbamazepine in trigeminal neuralgia. J Neurol Neurosurg Psychiatry. 1966;29:265-267.

  9. Rockliff BW, Davis EH. Controlled sequential trials of carbamazepine in trigeminal neuralgia. Arch Neurol. Aug 1966;15(2):129-36. [Medline].

  10. Beydoun A. Safety and efficacy of oxcarbazepine: results of randomized, double-blind trials. Pharmacotherapy. Aug 2000;20(8 Pt 2):152S-158S. [Medline].

  11. Zakrzewska JM, Chaudhry Z, Nurmikko TJ, Patton DW, Mullens EL. Lamotrigine (lamictal) in refractory trigeminal neuralgia: results from a double-blind placebo controlled crossover trial. Pain. Nov 1997;73(2):223-30. [Medline].

  12. Baker KA, Taylor JW, Lilly GE. Treatment of trigeminal neuralgia: use of baclofen in combination with carbamazepine. Clin Pharm. Jan-Feb 1985;4(1):93-6. [Medline].

  13. Fromm GH, Terrence CF, Chattha AS. Baclofen in the treatment of trigeminal neuralgia: double-blind study and long-term follow-up. Ann Neurol. Mar 1984;15(3):240-4. [Medline].

  14. Khan OA. Gabapentin relieves trigeminal neuralgia in multiple sclerosis patients. Neurology. Aug 1998;51(2):611-4. [Medline].

  15. Tatli M, Satici O, Kanpolat Y, Sindou M. Various surgical modalities for trigeminal neuralgia: literature study of respective long-term outcomes. Acta Neurochir (Wien). Mar 2008;150(3):243-55. [Medline].

  16. Olson S, Atkinson L, Weidmann M. Microvascular decompression for trigeminal neuralgia: recurrences and complications. J Clin Neurosci. Sep 2005;12(7):787-9. [Medline].

  17. Pollock BE, Ecker RD. A prospective cost-effectiveness study of trigeminal neuralgia surgery. Clin J Pain. Jul-Aug 2005;21(4):317-22. [Medline].

  18. Deinsberger R, Tidstrand J. Linac radiosurgery as a tool in neurosurgery. Neurosurg Rev. Apr 2005;28(2):79-88; discussion 89-90, 91. [Medline].

  19. Kondziolka D, Perez B, Flickinger JC, Habeck M, Lunsford LD. Gamma knife radiosurgery for trigeminal neuralgia: results and expectations. Arch Neurol. Dec 1998;55(12):1524-9. [Medline].

  20. Brabant S, Van Zundert J, Van Buyten JP. Proceedings of the World Pain Congress. In: Pulsed radiofrequency treatment of the gasserian ganglion in patients with essential trigeminus neuralgia: A retrospective study. San Francisco, CA: 2000.

  21. Browne L. Radiofrequency lesioning of the trigeminal ganglion for the treatment of trigeminal neuralgia. Ir Med J. Mar 1985;78(3):68-71. [Medline].

  22. [Guideline] International RadioSurgery Association. Stereotactic radiosurgery for patients with intractable typical trigeminal neuralgia who have failed medical management. National Guideline Clearinghouse. Jan 2009.

  23. [Guideline] Gronseth G, Cruccu G, Alksne J, et al. Practice parameter: the diagnostic evaluation and treatment of trigeminal neuralgia (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology and the European Federation of Neurological Societies. Neurology. Oct 7 2008;71(15):1183-90. [Medline].

  24. Kondziolka D, Lemley T, Kestle JR, Lunsford LD, Fromm GH, Jannetta PJ. The effect of single-application topical ophthalmic anesthesia in patients with trigeminal neuralgia. A randomized double-blind placebo-controlled trial. J Neurosurg. Jun 1994;80(6):993-7. [Medline].

  25. Türk U, Ilhan S, Alp R, Sur H. Botulinum toxin and intractable trigeminal neuralgia. Clin Neuropharmacol. Jul-Aug 2005;28(4):161-2. [Medline].

  26. [Best Evidence] Khedr EM, Kotb H, Kamel NF, Ahmed MA, Sadek R, Rothwell JC. Longlasting antalgic effects of daily sessions of repetitive transcranial magnetic stimulation in central and peripheral neuropathic pain. J Neurol Neurosurg Psychiatry. Jun 2005;76(6):833-8. [Medline].

  27. Blom S. Trigeminal neuralgia: Its treatment with a new anticonvulsant drug. Lancet. 1962;1:839-40.

  28. Dalessio DJ. Diagnosis and treatment of cranial neuralgias. Med Clin North Am. May 1991;75(3):605-15. [Medline].

  29. Dubner R, Sharav Y, Gracely RH, Price DD. Idiopathic trigeminal neuralgia: sensory features and pain mechanisms. Pain. Oct 1987;31(1):23-33. [Medline].

  30. Eide PK, Rabben T. Trigeminal neuropathic pain: pathophysiological mechanisms examined by quantitative assessment of abnormal pain and sensory perception. Neurosurgery. Nov 1998;43(5):1103-10. [Medline].

  31. Evans RW, Graff-Radford SB, Bassiur JP. Pretrigeminal neuralgia. Headache. Mar 2005;45(3):242-4. [Medline].

  32. Fromm GH. Pathophysiology of trigeminal neuralgia. In: Fromm G, Sessle B, eds. Trigeminal Neuralgia: Current Concepts Regarding Pathogenesis and Treatment. Butterworth: Woburn, MA; 1991:105-22.

  33. Kondziolka D. Functional radiosurgery. Neurosurgery. Jan 1999;44(1):12-20; discussion 20-2. [Medline].

  34. Rose FC. Trigeminal neuralgia. Arch Neurol. Sep 1999;56(9):1163-4. [Medline].

  35. Truini A, Galeotti F, Cruccu G. New insight into trigeminal neuralgia. J Headache Pain. Sep 2005;6(4):237-9. [Medline].

Further Reading

Keywords

trigeminal neuralgia, trigeminal nerve, headache, neuralgia, paroxysmal headache pain, tic douloureux, neuropathic pain, microvascular decompression, Jannetta procedure

Contributor Information and Disclosures

Author

Marc E Lenaerts, MD, FAHS, Staff Neurologist, Mercy Medical Group, Sacramento, CA; Associate Clinical Professor of Neurology, Department of Neurology, University of California at Davis, Sacramento
Marc E Lenaerts, MD, FAHS is a member of the following medical societies: American Academy of Neurology, American Headache Society, and International Headache Society
Disclosure: Nothing to disclose.

Medical Editor

Andrew W Lawton, MD, Medical Director of Neuro-Ophthalmology Service, Section of Ophthalmology, Baptist Eye Center, Baptist Health Medical Center
Andrew W Lawton, MD is a member of the following medical societies: American Academy of Ophthalmology, Arkansas Medical Society, and Southern Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Simon K Law, MD, PharmD, Assistant Professor of Ophthalmology, Jules Stein Eye Institute; Chief of Section of Ophthalmology Surgical Services, Department of Veterans Affairs Healthcare Center, West Los Angeles
Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Association for Research in Vision and Ophthalmology
Disclosure: Nothing to disclose.

Managing Editor

Brian R Younge, MD, Professor of Ophthalmology, Mayo Clinic School of Medicine
Brian R Younge, MD is a member of the following medical societies: American Medical Association, American Ophthalmological Society, and North American Neuro-Ophthalmology Society
Disclosure: Nothing to disclose.

CME Editor

Lance L Brown, OD, MD, Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri
Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy Sr, MD, Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences
Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology
Disclosure: Nothing to disclose.

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.