Oral Med - trigeminal neuralgia Flashcards

1
Q

what nerves can be affected by neuralgia? (4)

A
  • Trigeminal – most common
  • Glossopharyngeal and Vagus (vagoglossopharyngeal neuralgia)
  • Nervus intermedius – branch of the facial nerve (geniculate neuralgia)
  • Occipital – less common
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2
Q

Whos most at risk of TG neuralgia? (2)

A

Usually elderly patient - predominantly in 60’s and above.
Females more than men

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3
Q

what are the causes of TGN? (4)

which is the most common?

A
  1. Idiopathic – no cause
  2. Classical = Vascular compression of the trigeminal nerve = most common cause
    - For it to be causative = must be evidence of compression/vascular trigeminal conflict – use MRI with contrast
    (not just a close relationship)
  3. Secondary
    Common causes:
    - Multiple sclerosis
    - Space-occupying intracranial tumours/lesion
  • Others/less common: skull-base bone deformity, connective tissue disease, arteriovenous malformation
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4
Q

Describe the cause of classical neuralgia.

how to we diagnose this?

A

Vascular compression of the trigeminal nerve

  • For it to be causative = must be evidence of compression/vascular trigeminal conflict

– use MRI with contrast

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5
Q

Describe the causes of secondary TGN. (2)

A
  • Multiple sclerosis
  • Space-occupying intracranial tumours/lesion
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6
Q

What are the two ways TGN can present?

what do patients complain of? (4)

A

2 different presentations:
* Purely paroxysmal (no pain/symptomless in between the attacks)
* concomitant continuous pain with superimposed stabbing attacks

  • One of the main characteristics:
    Unilateral maxillary or mandibular division pain
  • Stabbing pain (each attack, even if only a couple of seconds is a group of stabs)
  • stabbing lasts 5 - 10 seconds (can be up to a few mins)
  • pain Triggered by
  • Cutaneous = defined triggers on the skin/face
  • Wind, cold
  • Touch
  • Chewing/speaking/jaw movement
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7
Q

What characteristics would describe a non-typical TGN patient (red flags) (3)

A
  • Younger patient (>40yrs) – misdiagnosis or secondary cause
  • Sensory deficit in facial region = uncommon in TG more like trigeminal neuropathy
  • hearing loss = consider acoustic neuroma?
  • Other Cranial nerve lesions/deficits
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8
Q

How do we manage a non-typical TGN patient/red flag patient? (2)

A

ALWAYS test all the cranial nerves (identify sensory deficits and where)

ALL patients now get MRI

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9
Q

What is the first line management of TGN? (3 + 1)

A

Medications:
* Carbamazepine (antiepileptics)
if this drug is tolerated = most TG Should be responsive
* Oxcarbazepine (antiepileptics)
* Lamotrigine (slow onset of action)- if others cannot be tolerated

Can also be responsive to local anaesthesia (maxillary and mandibular branch)
- Use if there is an attack in the chair

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10
Q

Name the drugs used in second line management of TGN? (4)

A
  • Gabapentin
  • Pregabalin
  • Phenytoin
  • Baclofen
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11
Q

How do we manage TGN morning pain?

A

increase night time dose

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12
Q

List the side effects of carbamazepine. (5)

A
  • Blood dyscrasias
  • Thrombocytopenia
  • Neutropenia
  • Pancytopenia
  • Electrolyte imbalances (hyponatreamia)
  • Neurological deficits
  • Paraesthaesia
  • Vestibular problems
  • Liver toxicity
  • Skin reactions (including potentially life threatening)
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13
Q

What are the indications for surgical management of TGN? (2)

A

Not usually recommended if patient managing on medical therapy with moderate drug dose and no significant side effects

 Consider surgery when approaching maximum tolerable medical management even if pain controlled
 ‘Younger’ patients with significant drug use – will have many years of drug use

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14
Q

What causes painful trigeminal neuropathy? (3)

A
  • Herpes Zoster Virus (related to active varicella zoster virus infection, post-herpetic ‘neuralgia’)
  • Trauma (pain develops <6 months of traumatic event)
  • Idiopathic
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15
Q

What are the characteristics of PGN? (5)

A

presentation is usually a hybrid between this and TG neuralgia – consider them as a continuum/spectrum

  • pain is localized to the distribution(s) of the trigeminal nerve
  • commonly described as burning or squeezing or tingling or likened to pins-and-needles.
  • primary pain is usually continuous/nearly continuous and there can be a superimposed brief stabbing pain – however the stabs are not the predominant pain type, px complain of the background continuous burning pain
  • commonly accompanied by a clinically evident cutaneous allodynia
    where pain elicited on innocuous stimuli = touch
    (area which elicits pain in this case is much larger than the punctate trigger zones present in trigeminal neuralgia and is distributed all over the affected branch)
  • sensory deficits common (less common but not impossible in TG neuralgia)
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16
Q

What is the primary pain/complaint a patient with painful trigeminal neuralgia complains of?

A
  • primary pain is usually continuous/nearly continuous and there can be a superimposed brief stabbing pain – however the stabs are not the predominant pain type, px complain of the background continuous burning pain
17
Q

What are the characteristics of trigeminal autonomic cephalalgias?

A
  • Unilateral head pain - predominantly affects V1 (Ophthalmic branch of TG nerve)
  • Very severe / Excruciating/ worst pain ever
  • prominent cranial parasympathetic autonomic features (ipsilateral to the headache/pain)
  • Conjunctival injection / lacrimation
  • Nasal congestion / rhinorrhoea
  • Eyelid oedema
  • Ear fullness
  • Miosis and ptosis (Horner’s syndrome)
  • Attack frequency and duration differs
18
Q

Describe the onset of a cluster headache.

A

Onset = Rapid (max within 9 mins in 86%)

19
Q

Describe the duration of a cluster headache.

A

Duration = 15 mins to 3 hours (majority 45-90 mins)
Then Rapid cessation of pain

20
Q

What are the characteristics of cluster headaches? (9)

A
  • Excruciatingly severe (“suicide headache”)
  • Pain: mainly orbital and temporal
  • Attacks are strictly unilateral
  • Patients are restless and agitated during an attack
  • Prominent ipsilateral (other side from pain) autonomic symptoms
  • Migrainous symptoms often present
  • Premonitory symptoms: tiredness, yawning
  • Associated symptoms: nausea, vomiting, photophobia, phonophobia

Striking circadian periodicity
- attacks occur at the same time each day
- bouts occur at the same time each year

21
Q

What can trigger cluster headaches during a bout (but not in remission)?

A

alcohol

22
Q

Describe the onset of paroxysmal hemicrania.

A

rapid

23
Q

Describe the duration of paroxysmal hemicrania.

A

2-30 mins (shorter)
Then Rapid cessation of pain

24
Q

Describe the frequency of attacks in paroxysmal hemicrania.

A

2-40 attacks per day (no circadian rhythm aspect like Clusters)

25
Q

Describe the frequency of attacks in cluster headaches.

A

1-8 attacks per day (fewer than PH)

Follow a striking circadian periodicity

26
Q

What are the differences between cluster headaches and paroxysmal hemicrania? (3)

A

CH:
Striking circadian periodicity – key difference to Paradoxysmal hemicrania
- attacks occur at the same time each day
- bouts occur at the same time each year
PH = no circadian aspect

CH:
Longer duration of attack = 15-180 mins
PH:
Shorter attacks = 2-30 mins

CH:
Fewer attacks per day = 1-8
PH:
more attacks per day = 2-40

27
Q

What are the characteristics of paroxysmal hemicrania? (9)

A
  • Pain: mainly orbital and temporal
  • Attacks are strictly unilateral
  • Excruciatingly severe
  • 50% are restless and agitated during an attack
  • 10% attacks may be precipitated by bending or rotating the head
  • Background continuous pain can be present
  • 80% have chronic PH, 20% have episodic PH
  • Prominent ipsilateral autonomic symptoms
  • Migrainous symptoms may be present