Trigeminal neuralgia new classification and diagnostic grading for
- 1. TRIGEMINAL NEURALGIA: NEW CLASSIFICATION AND DIAGNOSTIC GRADING FOR PRACTICE AND RESEARCH American Academy of Neurology July, 2016 Dr.Sandra Mosses *Review article*
- 2. Neuropathic facial pain characterized by excruciating paroxysms of pain: lips gums cheek chin and rarely, in the distribution of the ophthalmic division of the fifth nerve
- 3. Why new diagnostic grading...?? existing criteria plagued by terminologic inconsistencies that compromise the communication among patients, physicians, and researchers latest version of the International Classification of Headache Disorders created difficulties by abandoning the term secondary TN, leaving a widely used designation for TN that is caused by a major neurologic disease hinder the triage of TN patients for therapy and clinical trials, and hamper the design of treatment guidelines
- 4. developed a new definition and diagnostic classification for TN that integrates an evaluation of diagnostic certainty based on criteria equivalent to those applied for neuropathic pain in general added assessment of diagnostic certainty will be helpful for treatment decisions help in the triage of TN patients for therapy and clinical trials
- 5. Definition TN is orofacial pain restricted to one or more divisions of the trigeminal nerve U/L (except in some cases asso with Multiple sclerosis) abrupt in onset and typically lasts only a few seconds (2 minutes at maximum) Arise spontaneously but these pain paroxysms can always be triggered by innocuous mechanical stimuli or movements If they report additional continuous pain, in the same distribution and in the same periods as the
- 6. Incidence 4-8/1,00,000 Middle aged and elderly ~60% in females
- 7. PATHOLOGY ectopic generation of action potentials in pain- sensitive afferent fibers of the fifth cranial nerve root just before it enters the lateral surface of the pons Compression --demyelination of large myelinated fibers that do not themselves carry pain sensation but become hyperexcitable and electrically coupled with smaller unmyelinated or poorly myelinated pain fibers in close proximity Thus tactile stimuli, conveyed via the large myelinated fibers, can stimulate paroxysms of pain
- 10. • posterior third of the scalp • back of the ear • angle of the mandible
- 11. Possible TN include notions of brief, sudden, stabbing, electric shock–like severe pain attacks paroxysms last up to few seconds --2 minutes Frequency of the pain attacks may range from 1 to over 50 a day periods of complete remission in up to 63% of patients may last from weeks to years
- 12. always unilateral the affected division of the trigeminal nerve and the side of the face may change over the course of the disease If the neuralgia involves 2 trigeminal divisions, they should be contiguous combination of the maxillary and mandibular divisions is most frequent TN in the ophthalmic division or the tongue --
- 14. Clinically established TN Stimulus-evoked pain is one of the most striking features of TN, with high diagnostic value (99%) pain is triggered by innocuous mechanical stimuli within the trigeminal territory, including the oral cavity Subtlety of the trigger maneuvers is another unique sign of TN. The stimulus may simply be
- 15. More complex maneuvers involve both tactile stimuli and facial movement, e.g., shaving, application of makeup, brushing teeth, eating, or drinking The location of the evoked pain may differ from the site of the stimulation and the pain can be felt as radiating
- 16. Allodynia • abnormal painful response to gentle stroking of the skin (in postherpetic neuralgia) • No trigger zones • No refractory period TN • TN is also often elicited by normally painless mechanical stimuli, or a combination of external stimuli and orofacial movements • Trigger zones and pain sensation may be dissociated (cross- excitation between somatosensory afferents) • refractory period of several seconds or minutes during which a second pain paroxysm cannot be provoked
- 17. Trigger zones central portion of the face around nose and mouth nasolabial fold lips tongue
- 19. Classical TN MRI demonstrates vascular compression with morphologic changes of the trigeminal nerve root Compression of the trigeminal nerve root by a blood vessel- superior cerebellar artery or on occasion a tortuous vein Because of its sensitivity to detect pathologic processes involving brainstem and cranial nerves running through the base of the skull, MRI is widely seen as the method of choice to examine the trigeminal nerve and root
- 21. In a recent meta-analysis of 9 high-quality blinded and controlled studies, neurovascular contact was found in 471 out of 531 symptomatic nerves (89%) and 244 of 681 asymptomatic nerves (36%), indicating high sensitivity but poor specificity Nerve dislocation or atrophy raised the specificity to 97% Compression of the trigeminal nerve root at its entry into the brainstem increased specificity and positive predictive value to 100% The degree of morphologic root changes is therapeutically relevant
- 22. However, it is important to acknowledge that all cited studies relied on a clinical diagnosis of TN before MRI MRI is a valuable diagnostic tool only if preceded by an evaluation of symptoms and signs that indicate probable TN. Only valuable if suspecting MS or assessing overlying vascular lesions to plan for decompression surgeries
- 23. • Visualise cisternal and cavernous nerve segments3D T2-weighted MRI • visualization of arteries3D timeof-flight magnetic resonance angiography • visualization of veins 3D T1-weighted MRI with gadolinium or phase-contrast MRI • detect abnormalities of the trigeminal nerve root that normalize following decompression or radiosurgery Diffusion tensor imaging (DTI)
- 24. Secondary TN (15%) • Benign-compress the root near its entry into the pons--focal demyelination and is thought to trigger paroxysmal ectopic discharges • Malignant-more likely to infiltrate the nerve and lead to axonal degeneration tumor at the cerebellopontine angle • TN in 2%–5% of patients with MS • MS is detected in 2%–14% of patients with TN • presence of demyelinating plaques in the pons • increased susceptibility of the trigeminal nerve root to neurovascular compression Multiple sclerosis
- 25. Clinical deficits of discriminatory sensory functions are highly suspicious of TN caused by a major underlying disease occurred in 25 out of 67 patients (37%) with TN secondary to tumors or MS Reverse conclusion is not true: absence of a sensory deficit does not rule out secondary TN
- 26. TN with continuous pain (Atypical TN) Pain between attacks It occurs in idiopathic, classical, or secondary TN dull, burning, or tingling distribution coincides with that of the paroxysmal pain, and fluctuations in intensity as well as periods of remission and recurrence
- 27. Drugs: o CARBAMAZEPINE 100mg OD (max1200mg) o OXCARBAZEPINE 300-1200mg BD o LAMOTRIGINE 400mg daily o PHENYTOIN 300-400mg daily o BACLOFEN 5-10mg TID Surgery: Microvascular decompression Gamma knife radiosurgery Radiofrequency thermal rhizotomy
- 28. Evaluation and treatment of TN regularly involve clinicians in diverse fields of medicine, including neurology, neuroradiology, neurosurgery, dentistry, maxillofacial surgery, and specialists in pain medicine A classification system for TN must account for common differential diagnoses in these disciplines Diagnostic requirements for idiopathic, classical, and secondary TN are based on a thorough review of clinical and etiologic features of TN
- 29. proposed new classification provides defined criteria that offer diagnostic accuracy with the added value of a grading system for neuropathic pain designed for intuitive implementation in diagnostic decisions and treatment guidelines will be reflected in the upcoming revision of the WHO’s ICD