Trigeminal Neuralgia Flashcards

1
Q

What is a neuralgia?

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the types of neuralgia?

A

Trigeminal

Glossopharyngeal and Vagus

Nervus intermedius (CN7)- geniculate

Occipital

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How common is trigeminal neuralgia?

A

Not common- 4.3 per 100,000
 Slight predilection for females
 Mostly 60+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the causes of trigeminal neuralgia?

A
  • 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 well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How does TN present?

A
  • 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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are some of the triggers for an attack of trigeminal neuralgia?

A
  • Cutaneous- defined point on skin of face
  • Cold/wind
  • Chewing
  • Speaking
  • Jaw movement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the difference between paroxysmal and continuous concomitant TN?

A

Paroxysmal- no pain between attacks

Concomitant- continuous pain with stabbing attacks superimposed

*Typically follows remission and relapsing course

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the features of the typical TN patient?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are examples of patients with suspected TN that would be considered atypical or a red flag?

A
  • 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the first line drug treatments for TN? (based on anti-epileptics)

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the second line drugs for TN?

A

Gabapentin
Pregabalin
Phenytoin
Baclofen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How is TN managed?

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the side effects of carbamazepine?

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What would be the gold standard way of monitoring patients taking carbamazepine?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the indications for surgical intervention in patients with TN?

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What surgical treatments are available for TN?

A

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

17
Q

What are some of the complications that could occur after surgery?

A

Death

Local effects – peripheral treatments (cryotherapy)

Sensory loss
-> Corneal reflex
-> General sensation
-> Hearing loss

Motor deficits

May reversible or irreversible

18
Q

What are the causes of painful trigeminal neuropathy?

A

Caused by HSV/VZV (post herpetic neuralgia- but is not typical of a neuralgia)

Trauma

Idiopathic

-> Can be hybrid of this and TN

19
Q

What are the features of trigeminal neuropathy?

A
  • 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
20
Q

What are the general features of trigeminal autonomic cephalalgias?

A
  • 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
21
Q

What are the parasympathetic autonomic features seen in TACs?

A

Cpnjunctival injection / lacrimation

Nasal congestion / rhinorrhoea

Eyelid oedema

Ear fullness

Miosis and ptosis (Horner’s syndrome)

22
Q

What are the different TACs and their frequency/duration?

A

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

23
Q

What are the presenting features of a cluster headache?

A
  • 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)
24
Q

Which migraine symptoms may be experienced during cluster headache?

A

Premonitory symptoms: tiredness, yawning

Associated symptoms: nausea, vomiting, photophobia, phonophobia

Aura

25
Q

How do bouts of cluster headaches occur?

A
  • 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
26
Q

What is a known trigger of cluster headache during a bout?

A

Alcohol

27
Q

What is a chronic cluster?

A

Bouts lasting 1 year without remission

Remission lasting less than a month

28
Q

What are the features of paroxysmal hemicrania?

A
  • 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
29
Q

How is paroxysmal hemicranial treated?

A

No abortive treatment

Responds prophylactically to indomethacin (NSAID- if these are contraindicated there is limited evidence to other treatments)

Alternatives – COX-II inhibitors, Topiramate

30
Q

What is the abortive treatment used in cluster headache attacks?

A

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

31
Q

What is the abortive treatment used in cluster headache bouts to increase remission period?

A

Occipital depomedrone/lidocaine injection

Tapering course of oral prednisone

32
Q

What are the preventive treatment for cluster headaches?

A

Verapamil- contraindicated in patients with conduction issues

Lithium- effective but can cause renal toxicity/diabetes
insipidus

Ergots- only in-patients

Methysergide

Topiramate

33
Q

What drug therapy may be used to treat cluster headaches if everything else has failed?

A

GRP monoclonal antibodies