Trigeminal Neuralgia Flashcards
What is a neuralgia?
- Intense stabbing pain- tends to be brief but severe
- Goes along course of affected cranial nerve
- Can be caused by irritation or damage (not always)
- Classified based on aetiology
What are the types of neuralgia?
Trigeminal
Glossopharyngeal and Vagus
Nervus intermedius (CN7)- geniculate
Occipital
How common is trigeminal neuralgia?
Not common- 4.3 per 100,000
Slight predilection for females
Mostly 60+
What are the causes of trigeminal neuralgia?
- Idiopathic
- Vascular compression of CN5 (classical)- vessel near trigeminal nerve is not always causative (for it to be causative there must be evidence of compression- vascular trigeminal conflict)
-> High res MRI - Secondary- MS, Intra-cranial lesions like tumours (b/m), deformity of skull base, connective tissue disease, arterial-venous malformations
How does TN present?
- Tends to affect maxillary and mandibular division
- Sharp, shooting burning Stabbing pain lasting 5-10 secs (can be multiple or clusters)
- Longer attacks last a few minutes- if longer TN is unlikely
- Can be bilateral
- Have burning component
- May have vasomotor component (TAC)
What are some of the triggers for an attack of trigeminal neuralgia?
- Cutaneous- defined point on skin of face
- Cold/wind
- Chewing
- Speaking
- Jaw movement
What is the difference between paroxysmal and continuous concomitant TN?
Paroxysmal- no pain between attacks
Concomitant- continuous pain with stabbing attacks superimposed
*Typically follows remission and relapsing course
What are the features of the typical TN patient?
Older
Mask like face- lack of expression (fear of making facial movement that may trigger attack)
Excruciating pain- freeze during attack, can’t talk or do anything
No obvious precipitating pathology
What are examples of patients with suspected TN that would be considered atypical or a red flag?
- Young patients <40- misdiagnosis, or secondary cause of TN (refer for imaging urgently)
- Sensory deficit- hearing loss (suspect acoustic neuroma)
- Other cranial nerve lesions
-> Carry out systematic CN investigations
What are the first line drug treatments for TN? (based on anti-epileptics)
- Carbamazepine- can be short- or long-term release (long term minimises side effects as it avoids fluctuation in serum concentration)
- Oxcarbazepine
- Lamotrigine- if other 2 not tolerated
What are the second line drugs for TN?
Gabapentin
Pregabalin
Phenytoin
Baclofen
How is TN managed?
- Mostly responsive to carbamazepine if tolerated
- Aim to maximise efficacy and minimise side effects (prolonged release- Tegretol?)
- Increase night dose to control pain in morning
- Pain diary- help with history and can help you adapt regimen of patient
- Responsive to LA- most useful thing you can do for patient in dental setting
What are the side effects of carbamazepine?
Blood dyscrasias
-> Thrombocytopenia
-> Neutropenia
-> Pancytopenia
Electrolyte imbalances (hyponatreamia)
-> careful with combining with diuretics and PPIs
Neurological deficits
-> Paraesthaesia
-> Vestibular problems
Liver toxicity
Skin reactions (including potentially life threatening)
What would be the gold standard way of monitoring patients taking carbamazepine?
Weekly blood monitoring (FBC, UE, LFT) if patient on carbamazepine
- Monthly after initial trial
- May be considered out with the scope of GDP to monitor toxicity (are facilities available?)- Liaise with GMP
What are the indications for surgical intervention in patients with TN?
- If maximum medication doses are being taken
- Patients in their 50s using significant amount of drugs as treatment
- if patient managing on moderate drug therapy with no intolerable side effects, surgery is not recommended
What surgical treatments are available for TN?
Microvascular decompression- if vessel impinging on nerve root
Stereotactic Gamma knife radiosurgery
-> targeted radiation at the trigeminal ganglion to kill trigeminal nerve cells
Destructive Central Procedures
-> Radiofrequency thermocoagulation
-> Retrogasserian glycerol injection
-> Balloon compression
Destructive Peripheral Neurectomies
-> Only performed as a last resort after trial local anaesthesia
What are some of the complications that could occur after surgery?
Death
Local effects – peripheral treatments (cryotherapy)
Sensory loss
-> Corneal reflex
-> General sensation
-> Hearing loss
Motor deficits
May reversible or irreversible
What are the causes of painful trigeminal neuropathy?
Caused by HSV/VZV (post herpetic neuralgia- but is not typical of a neuralgia)
Trauma
Idiopathic
-> Can be hybrid of this and TN
What are the features of trigeminal neuropathy?
- Pain is localised to one or more distributions of CN5
- Tingling, burning, squeezing, pins and needles sensations
- Continuous background pain (there may be stabbing superimposed)- main complaint of patient
- Accompanied by cutaneous allodynia- pain elicited by touch (larger than trigger points of TN, is usually distributed over all branches of CN5)
- Sensory deficits are more common in neuropathy than TN
What are the general features of trigeminal autonomic cephalalgias?
- Unilateral
- Affects ophthalmic branch
- Severe/excruciating pain (worst of the worst)
- Suicide headache
- Accompanied by prominent parasympathetic autonomic features (ipsilateral to pain)
- Differing attack frequencies and duration amongst different types
What are the parasympathetic autonomic features seen in TACs?
Cpnjunctival injection / lacrimation
Nasal congestion / rhinorrhoea
Eyelid oedema
Ear fullness
Miosis and ptosis (Horner’s syndrome)
What are the different TACs and their frequency/duration?
Cluster headache
-> 1-8 daily, lasts 15-180mins
Paroxysmal Hemicrania
-> 1-40 daily, lasts 2-30 mins
SUNCT
-> 3-200 daily, lasts 5-240 secs
What are the presenting features of a cluster headache?
- Unilateral- strictly
- Rapid onset with rapid cessation
- Can last up to 3 hours
- Patients are restlessness and agitated during attack (different from migraines where they suffer motion sensitivity)
- Prominent ipsilateral autonomic symptoms
- Migraine symptoms can present alongside (challenging for non-specialist to differentiate)
Which migraine symptoms may be experienced during cluster headache?
Premonitory symptoms: tiredness, yawning
Associated symptoms: nausea, vomiting, photophobia, phonophobia
Aura
How do bouts of cluster headaches occur?
- Clusters of headache occur over period of 1-3 months usually with 1 month remission (may get multiple in one day)
- There may be background pain between attacks
- Circadian periodicity- same time of day or year
What is a known trigger of cluster headache during a bout?
Alcohol
What is a chronic cluster?
Bouts lasting 1 year without remission
Remission lasting less than a month
What are the features of paroxysmal hemicrania?
- Shorter duration (up to 30 mins)
- Rapid onset an cessation
- More frequent (2-40 attacks per day)
- Does not follow circadian rhythm
- 50 % restless and agitated during attack
- May be caused by bending or rotating of the head
- More likely to become chronic rather than episodic
How is paroxysmal hemicranial treated?
No abortive treatment
Responds prophylactically to indomethacin (NSAID- if these are contraindicated there is limited evidence to other treatments)
Alternatives – COX-II inhibitors, Topiramate
What is the abortive treatment used in cluster headache attacks?
Subcutaneous sumatriptan 6mg or nasal zolmatriptan 5mg
100% oxygen 7-12 l/min via a non-rebreathing mask (effective and safe)
-> no smokers in house
What is the abortive treatment used in cluster headache bouts to increase remission period?
Occipital depomedrone/lidocaine injection
Tapering course of oral prednisone
What are the preventive treatment for cluster headaches?
Verapamil- contraindicated in patients with conduction issues
Lithium- effective but can cause renal toxicity/diabetes
insipidus
Ergots- only in-patients
Methysergide
Topiramate
What drug therapy may be used to treat cluster headaches if everything else has failed?
GRP monoclonal antibodies
