Trigeminal neuralgia Diagnosis investigations.pptx

Trigeminal neuralgia diagnosis

1. Trigeminal neuralgia a dilemma for General Dentist Dr Riaz (PGR omfs ) DR. Minahil Naeem (House officer)

2. Learning Objectives Identify the etiology and epidemiology of trigeminal neuralgia. Outline the appropriate history, physical, and evaluation of trigeminal neuralgia. Review the treatment and management options available for trigeminal neuralgia. Describe interprofessional team strategies for improving care coordination and communication to improve outcomes in patients with trigeminal neuralgia.

3. Scenario A 51-year-old female presented with a main complaint of severe, sharp, intermittent electrical s hock like pain on the left side of her face. Triggered by talking, washing her face, eating and brushing of her teeth

4. Scenario No significant Extraoral and Intraoral Findings TMJ examination: Symmetrical opening. Bilateral Clicking on opening. Medical History: No comorbidities or significant medical history

5. Trigeminal Neuralgia A highly disabling disorder characterised by very sudden,severe brief stabbing, electric shock like recurrent episodes of pain. Involving one or more distribution of Trigeminal(V)Nerve Also known as tic douloureux which means "painful tic." – Nicholaus Andre Fothergill’s Disease –John Fothergill

6. Epidemiology L ifetime prevalence of TN is estimated to be 0.16%–0.3% Annual incidence is 4–29 per 100 000 person-years M ore prevalent in women than in men (F:M ratio 3:2) Mean age of onset of 53–57 years and range of 24–93 years in adult series

7. Anatomy of Trigeminal nerve Fifth cranial nerve. Largest cranial nerve Mixed nerve Both sensory and motor function Sensory supply: facial skin, mucous membranes and sinuses of the face Motor(mandibular branch): supplies the muscles of mastication

8. Anatomy of Trigeminal nerve: Origin Three  sensory nuclei and one  motor nucleus At the level of the  pons , the sensory nuclei merge to form a sensory root The motor nucleus continues to form a motor root.

9. Anatomy of Trigeminal nerve: Ganglia I n the  middle cranial fossa , the sensory root expands into the trigeminal ganglion Located lateral to cavernous sinus in a depression in temporal bone know as trigeminal cave

10. Anatomy of trigeminal nerve: Branches Trigeminal ganglion gives rise to 3 divisions:  ophthalmic  (V1),  maxillary  (V2) and  mandibular  (V3). M otor root passes inferiorly to the sensory root, along the floor of the trigeminal cave. Its fibers are only distributed to the  mandibular division

11. Pathophysiology TN pain precipitated by: Proximal compression of the trigeminal sensory root near the brainstem by a blood vessel (artery or vein) which is a vulnerable area to demyelination. (Classical) Abnormal expression of voltage-gated sodium channels (Classical and Idiopathic)

12. Pathophysiology   a compressing loop of an artery (most commonly the superior cerebellar artery) or vein ( most commonly the transverse pontine vein) compressing the cisternal portion of the trigeminal nerve . Although rare, posterior fossa tumors can be another cause Multiple sclerosis may also cause trigeminal neuralgia(Higher incidence)

13. Findings in History(The Term Bank) Laterality and site of pain Frequency and duration of attacks Triggers and trigger zones Refractory period Associated cranial autonomic symptoms

14. Laterality and Site of Pain Right side is more affected (60%).(with mandibular nerve commonly involved) Greater incidence of right-sided facial symptoms is due to the foramen rotundum and foramen ovale being narrower on the right side of the cranium Bilateral simultaneous pain is rare (1.7%–5%); side-alternating unilateral pain paroxysms Maxillary and Mandibular division more commonly affected.

15. Frequency and Duration of Attacks Frequency and Duration of TN attacks: highly variable Pain usually lasts from less than a second up to 2 min in the majority (74%) Number of attacks in approximately 40% of patients report more than 10 attacks daily. Relapsing–remitting pattern in approximately two-thirds of patients but has a chronic pattern in the remaining one-third.

16. Triggers and Trigger zones(Hallmark) Triggered by innocuous mechanical stimulation of the face and intraoral mucosa ipsilateral to the side of the pain 91%–99 patients report triggered attacks Light tactile is most potent trigger conversely, painful and thermal stimulation seems ineffective Common triggers include light touch, talking, chewing, brushing teeth, washing or drying, drinking and shaving

17. Triggers and Trigger zones Most common trigger zones Nasolabial fold, Upper lip(18.7%), Lateral part of the lower lip, Ala of the nose Lateral brow Preauricular area (9.3%) Chin, Cheek and The alveolar gingiva

18. Refractory Period Attacks followed by a period of seconds or minutes during which further attacks cannot be provoked. This is a diagnostic point of differentiating Trigeminal neuralgia from trigeminal autonomic cephalalgia, SUNHA (Short-Lasting Unilateral Neuralgiform Headache Attacks)

19. Associated cranial autonomic symptoms This potentially poses a challenge differentiating TN from trigeminal autonomic cephalalgias and SUNHA Rasmussen described 98 out of the 229 (43%) with such symptoms associated with pain. These symptoms include: lacrimation (31%), rhinorrhoea (9%), hypersalivation (7%) facial swelling/flushing (5%)

20. Quality of life of TN patient inability to speak or eat constant fear of pain that may return at any time even between attacks In 34% of patients with TN, even employment was impacted. serious impairment of their individual daily function and their quality of life. Reduced measures of daily functioning, quality of life, well-being, sleep, mood, and overall health status Depression

21. Examination The physical and neurological examinations are generally normal Approximately 30% of cases can have sensory changes including mild hypoaesthesia During very severe attacks, the pain can evoke ipsilateral facial muscle contraction (tic douloureux) Dentist must carry out examination of all cranial nerves Diagnosis mostly rely on a Good History of the patient

22. Examination with respect to general dentist Extraoral-presence/absence of Maxillary sinusitis Temporomandibular disorder Intraoral Dental caries Pulpitis Dental sensitivity Periodontal disorders Pericoronitis Cracked tooth Alveolar osteitis

23. Examination with respect to general dentist When such condition are not present The patient should be referred to oral and maxillofacial surgeon for further evaluation. When diagnosis is not clear: Extraction of tooth or teeth should not be performed. REFERENCE TO EXTRACTIONS IN TRIGEMINAL

24. White and Sweet criteria for idiopathic cases The criteria emphasize 5 major clinical features including 1. Paroxysmal pain, 2. Presence of trigger zone, 3. Unilateral presentation 4. Pain confined to trigeminal distribution and 5. Normal sensory examination

25. Diagnostic Criteria kk Headache Classification Subcommittee of The International Headache Society. The International classification of headache disorders . . 3rd edn . Cephalalgia, 2018: 38. 1–211. k

26. Diagnosis Corneal reflex :fine tip of a cotton swab, touching but not dragging the wisp of cotton over the cornea Both the upper and lower cornea are tested; the upper half of the cornea is innervated by V1, the lower by V2.(palpebral reflex) Sensory Examination: conducted with light touch (cotton wool), pinprick, vibration, and hot/cold sensation, ending with deep pressure on forehead,cheek and jaw Motor Function: ask the patient to clench his teeth.Both Masseters shoulf feel firm and strong with contracting temporalis Jaw jerk reflex(masseter reflex): mandible is tapped with a tendon hammer at a downward angle just below the lips at the chin while the mouth is held slightly open. In response, the  masseter muscles  will jerk the mandible upwards

27. Sensory Examination and Corneal Reflex Jaw Jerk Reflex

28. Differential Diagnosis As dentist try to rule out dental cause first

29. Differential Diagnosis

30. Differential Diagnosis

31. Differential Diagnosis

32. Management Plan Prognostic Factors Investigation Treatment strategies: Pharmacological preventive treatments Neuromodulation techniques Surgical treatment/ procedures

33. Prognostic Factors Intact preoperative facial sensation correct diagnosis Patients with first division trigeminal pain only may have symptomatic TN (STN) (that is, due to multiple sclerosis or tumor)12, which is more difficult to treat Neurovascular Conflict(NVC) seen in MRI; More on symptomatic site (majorly due to arteries) Anticonvulsant responsiveness(pre-operative to radiosurgery) Neurovascular contact with morphological changes

34. Investigations MRI of the brain is the gold-standard investigation to exclude secondary causes of TN. If MRI is contraindicated than: CT scan of the head CT cerebral angiogram PET scan trigeminal-evoked potentials and/or neurophysiological recordings of trigeminal reflexes

35. Pharmacological P reventive T reatments Carbamazepine and oxcarbazepine (First line) Lamotrigine ( Intolerence to carbamazepine and oxcarbazepine ) Gabapentin and pregabalin Baclofen(TN in people with multiple sclerosis who may be using the drug for spasticity) Botulinum toxin type A Other drugs may Include : phenytoin, tizanidine , levetiracetam , misoprostol (especially in patients with multiple sclerosis), topiramate , pimozide , duloxetine and eslicarbazepine . A novel sodium channel blocker, vixotrigine,(needs cardiac monitoring )

36. Neuromodulation Techniques(The Novelty) electrical Gasserian (trigeminal) ganglion stimulation, peripheral nerve stimulation, invasive motor cortex stimulation non-invasive cortex stimulation Repetitive transcranial magnetic stimulation ( rTMS ) self-conducted motor cortex transcranial direct-current stimulation ( tDCS )

37. Injection Therapy Percutaneous retrogasserian Glycerol rhizotomy : Injected into cistern(from 0.2 ml to 0.4 ml) Damages TN and block the pain signals a later recurrence of pain in some cases many experience facial numbness or tingling.

38. Treatment of Acute Attacks Use of local anesthetic trigeminal division nerve blocks typically with a long-acting local anesthetic (bupivacaine). Occasionally, the application of a topical amide local anesthetic preparation ( lidocaine 2%–5%) may be effective

39. Surgical treatment/ procedures T hree types of surgical intervention available: (1) invasive, non-ablative ( microvascular decompression) Surgery of First Choice in classical TN pain-free rate of 62%–89% after 3–10 years of follow-up annual risk of recurrence is less than 2% 5years after the operation

40. A B C Fig A: nerve is compressed by the main trunk of the SCA (A) and its branches (B and C) Fig B: Implanting pieces of Teflon between the offending artery and Trigeminal Nerve. Fig C:   The vessel is mobilized and generously padded away from the nerve to prevent any contact with neural tissue. Fibrin glue may be used to reinforce this construct

41. (2) invasive, ablative Controlled lesioning of the trigeminal ganglion or root by: Mechanical (balloon compression), Thermal (radiofrequency thermocoagulation ) Themical means (glycerol rhizolysis )

42. Surgical treatment/ procedures (3)non- invasive,ablative (stereotactic radiosurgery which focuses radiation at the trigeminal root entry zone) Least invasive

43. Conclusion Trigeminal neuralgia (TN) is characterized by recurrent, unilateral, brief (<1s–2min), very painful, electric shock like pain episodes in the trigeminal distribution that are abrupt in onset and termination Currently classified into three subgroups: idiopathic, classical and secondary, based on imaging findings; MR brain imaging Diagnosis is crucial for deciding the correct treatment Pharmacological Treatment Neromodulatory Treatment Surgical Treatments

44. References Tanweer Hussain Bangash 1. Trigeminal neuralgia: frequency of occurrence in different nerve branches. Fall 2011;1(2):70-2. doi : 10.5812/kowsar.22287523.2164. Epub 2011 Sep 26.Available from: Trigeminal neuralgia: frequency of occurrence in different nerve branches - PubMed (nih.gov) Humberto Santo Neto *, Jose´ Angelo Camilli, Maria Julia Marques. Trigeminal neuralgia is caused by maxillary and mandibular nerve entrapment: Greater incidence of right-sided facial symptoms is due to the foramen rotundum and foramen ovale being narrower on the right side of the cranium. Departamento de Anatomia , Instituto de Biologia , Universidade Estadual de Campinas (UNICAMP), CP 6109, Campinas 13084-971, SP, Brazil. 6 June 2005