trigeminal neuralgia and Trigeminal Autonomic Cephalalgias Flashcards

1
Q

neuralgia
definition

A
  • An intense stabbing pain
  • The pain is usually brief but may be severe.
  • Pain extends along the course of the affected nerve.
  • Usually caused by irritation of or damage to a nerve (but not exclusive)
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2
Q

nerves that can be involved in neuralgia pain

4

A
  • Trigeminal (most common)
  • Glossopharyngeal and Vagus
  • Nervus intermedius (branch of facial nerve)
  • Occipital
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3
Q

inicidence of trigeminal neuralgia

A

4.3:100000 population (USA)
* (5.9 female, 3.4 male)

Usually elderly patient - predominantly in 60’s and above.
* Younger pt = concern

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4
Q

causes of trigeminal neuralgia

3 main

A

Idiopathic

Classical
* Vascular compression of the trigeminal nerve (MRI needed)

Secondary
* Multiple sclerosis
* Space-occupying lesion

Others: skull-base bone deformity, connective tissue disease, arteriovenous malformation

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5
Q

presentation of trigeminal neuralgia

A

Unilateral maxillary or mandibular division pain > ophthalmic division

Stabbing pain
* 5 - 10 seconds duration (can feel like longer – cluster of attacks)

Triggers
* cutanoues
* Wind, cold
* touch
* chewing

Purely paroxysmal (symptom free) or with concomitant continuous pain (then superimposed stabbing attacks)

Remissions and relapses

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6
Q

can trigeminal neuralgia present with otuher cranial nerve pain disorders?

A

yes - on a continuum with other - present hybrid like

Acute spasms of ‘sharp, shooting pain’
* May be more than one division
* May be bilateral
* May have burning component
* May have vasomotor component

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7
Q

typical TN pt

4

A
  • Usually older patient
  • ‘Mask-like’ face
  • Appearance of excruciating pain (freeze from the pain)
  • NO obvious precipitating pathology
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8
Q

trigeminal neuralgia pt - ‘red flags’

3

A
  • Younger patient (>40yrs)
  • Sensory deficit in facial region* e.g. hearing loss – acoustic neuroma*
  • Other Cranial nerve lesions

ALWAYS test cranial nerves (identify sensory deficit) systematic examination
ALL patients now get MRI

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9
Q

what to always do when suspect TN

A

ALWAYS test cranial nerves (identify sensory deficit) systematic examination
ALL patients now get MRI

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10
Q

TN drug therapy
first line

3

A

Carbamazepine - modified release
Oxcarbazepine
Lamotrigine (slow onset of action)

SIDE EFFECTS

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11
Q

TN drug therapy
second line

4

A

Gabapentin
Pregabalin
Phenytoin
Baclofen

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12
Q

management strategy of trigeminal neuralgia

A

Should be responsive to Carbamazepine (if tolerated; almost diagnostic criteria)
* Maximise efficacy and minimise side effects
* inc tolerability is to prescribe prolonged release carbamazepine (tegratol)

Often difficult to control pain first thing in the morning
* Can inc night time dose

Pain diary is very helpful to identify modifications necessary to therapy

Can be responsive to local anaesthesia
* Maxillary and mandibular branch of trigeminal branch
* Useful if an attack when in dental chair

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13
Q

carbamazepine side effects

wide range
key ones

A

Blood dyscrasias
* Thrombocytopenia
* Neutropenia
* Pancytopenia

Electrolyte imbalances (hyponatreamia) – careful if pt on diuretic, PPI (omeprazole)

Neurological deficits
Paraesthaesia
Vestibular problems

Liver toxicity

Skin reactions (including potentially life threatening)

Blood monitoring on weekly basis for 1st month, then monthly – FBC, Us+Es, liver function test

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14
Q

GDP management of TN

A

if attack there and then – LA; otherwise liaise with GMP or oral med as outwith dental expertise to monitor bloods

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15
Q

TN surgery indications

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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15
Q

TN surgery indications

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

16
Q

surgical options for TN

4

A

Microvascular decompression (MVD) – classical trigeminal neuralgia
* Preferred surgical treatment where possible
* Requires a vessel impinging on the Trigeminal nerve root
(12 months) 1% mortality/10% morbidity

Destructive Central Procedures
* Radiofrequency thermocoagulation
* Retrogasserian glycerol injection
* Balloon compression
(9 months) 2% mortality

Stereotactic Radiosurgery
* Gamma knife – targeted radiation at the trigeminal ganglion to kill trigeminal nerve cells (only available in Sheffield)

Destructive Peripheral Neurectomies
* Only performed as a last resort after trial local anaesthesia
(6 months pain free without medication – can result in allodynia as well as TN!)

17
Q

possible complications of TN surgery

A

Local effects – peripheral treatments (cryotherapy)

Sensory loss
* Corneal reflex
* General sensation
* Hearing loss

Motor deficits

May reversible or irreversible

18
Q

painful trigeminal neuropathy
causes

3

A
  • Herpes Zoster Virus (related to active VZV infection, post-herpetic ‘neuralgia’)
  • Trauma (pain develops <6 months of traumatic event)
  • Idiopathic
19
Q

characteristics of painful trigeminal neuropathy

4

A
  • pain is localized to the distribution(s) of the trigeminal nerve
  • commonly described as burning or squeezing or likened to pins-and-needles.
  • primary pain is usually continuous or near-continuous. Superimposed brief pain paroxysms may occur, but not the predominant pain type.
  • more commonly accompanied by clinically evident cutaneous allodynia (pain stimulated from innocuous stimuli; much larger than the punctate trigger zones present in trigeminal neuralgia) and/or sensory deficits

PTN vs TN, on continuum of same spectrum?

19
Q

characteristics of painful trigeminal neuropathy

4

A
  • pain is localized to the distribution(s) of the trigeminal nerve
  • commonly described as burning or squeezing or likened to pins-and-needles.
  • primary pain is usually continuous or near-continuous. Superimposed brief pain paroxysms may occur, but not the predominant pain type.
  • more commonly accompanied by clinically evident cutaneous allodynia (pain stimulated from innocuous stimuli; much larger than the punctate trigger zones present in trigeminal neuralgia) and/or sensory deficits

PTN vs TN, on continuum of same spectrum?

20
Q

trigeminal autonomic cephalagias

characteristic features

A

Unilateral head pain
predominantly V1

Very severe / Excruciating

Usually prominent cranial parasympathetic autonomic features (ipsilateral to the headache)
* Conjunctival injection / lacrimation
* Nasal congestion / rhinorrhoea
* Eyelid oedema
* Ear fullness
* Miosis and ptosis (Horner’s syndrome)

Attack frequency and duration differs

21
Q

cluster headache

the attack

characteristics

A

Pain:
* mainly orbital and temporal
* Attacks are strictly unilateral
* Rapid onset (max within 9 mins in 86%)
* Duration: 15 mins to 3 hours (majority 45-90 mins)
* Rapid cessation of pain
* Excruciatingly severe (“suicide headache”)

**Patients are restless and agitated during an attack **(key difference from migraines (they have motion sensitivity))

Prominent ipsilateral autonomic symptoms

Migrainous symptoms often present
* Premonitory symptoms: tiredness, yawning
* Associated symptoms: nausea, vomiting, photophobia, phonophobia
* Aura in 14%

22
Q

cluster headaches

the bout

characteristics

A

Episodic in 80-90%
* Attacks “cluster” into bouts typically 1-3 months with remission lasting at least 1 month
* Attack frequency: 1 every other day to 8 per day
* May be continuous background pain between attacks
* Alcohol triggers attacks during a bout, but not in remission

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

10-20% chronic cluster
* Bouts last >1 year without remission or
* Remissions last <1 month

23
Q

paroxysmal hemicrania

characteristics

A

Pain:
* mainly orbital and temporal
* Attacks are strictly unilateral
* Rapid onset
* Duration: 2-30 mins
* Rapid cessation of pain
* **Frequency: 2-40 attacks per day (no circadian rhythm) **
* Excruciatingly severe
* 50% are restless and agitated during an attack

Prominent ipsilateral autonomic symptoms

Migrainous symptoms may be present

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

Absolute response to indomethacin dx criteria

24
Q

drug therapy for cluster headache TAC

A

Abortive (attack)
* Subcutaneous sumatriptan 6mg or nasal zolmatriptan 5mg
* 100% oxygen 7-12 l/min via a non-rebreathing mask (effective and safe) – no smokers in household allowed

Abortive (bout)
* Occipital depomedrone/lidocaine injection
* Or tapering course of oral prednisone

Preventative
* Verapamil (high doses may be required)
* Lithium
* Methysergide (retroperitoneal fibrosis)
* Topiramate
* CGRP monoclonal antibodies

25
Q

drug therapy for paroxysmal hemicrania

A
  • No abortive treatment
  • Prophylaxis with indomethacin
  • Alternatives – COX-II inhibitors, Topiramate
26
Q

cluster headache (TAC)

attack frequency
duration fo attack
pain quality
pain intesity
cicadian periodicity

A

attack frequency : 1-8
duration fo attack : 15-180mins
pain quality : sharp, throbbing
pain intesity : very severe
cicadian periodicity : 70%

suden onset and remission of pain
Patients are restless and agitated during an attack

27
Q

paroxysmal hemicrania (TAC)

attack frequency
duration fo attack
pain quality
pain intesity
cicadian periodicity

A

attack frequency : 1-40
duration fo attack : 2-30mins
pain quality : sharp, throbbing
pain intesity : very severe
cicadian periodicity : 45%

28
Q

TAC

A

trigeminal autonomic cepahlahias

29
Q

TN

A

trigeminal neuralgia