trigeminal neuralgia and Trigeminal Autonomic Cephalalgias Flashcards
(31 cards)
neuralgia
definition
- 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)
nerves that can be involved in neuralgia pain
4
- Trigeminal (most common)
- Glossopharyngeal and Vagus
- Nervus intermedius (branch of facial nerve)
- Occipital
inicidence of trigeminal neuralgia
4.3:100000 population (USA)
* (5.9 female, 3.4 male)
Usually elderly patient - predominantly in 60’s and above.
* Younger pt = concern
causes of trigeminal neuralgia
3 main
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
presentation of trigeminal neuralgia
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
can trigeminal neuralgia present with otuher cranial nerve pain disorders?
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
typical TN pt
4
- Usually older patient
- ‘Mask-like’ face
- Appearance of excruciating pain (freeze from the pain)
- NO obvious precipitating pathology
trigeminal neuralgia pt - ‘red flags’
3
- 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
what to always do when suspect TN
ALWAYS test cranial nerves (identify sensory deficit) systematic examination
ALL patients now get MRI
TN drug therapy
first line
3
Carbamazepine - modified release
Oxcarbazepine
Lamotrigine (slow onset of action)
SIDE EFFECTS
TN drug therapy
second line
4
Gabapentin
Pregabalin
Phenytoin
Baclofen
management strategy of trigeminal neuralgia
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
carbamazepine side effects
wide range
key ones
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
GDP management of TN
if attack there and then – LA; otherwise liaise with GMP or oral med as outwith dental expertise to monitor bloods
TN surgery indications
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
TN surgery indications
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
surgical options for TN
4
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!)
possible complications of TN surgery
Local effects – peripheral treatments (cryotherapy)
Sensory loss
* Corneal reflex
* General sensation
* Hearing loss
Motor deficits
May reversible or irreversible
painful trigeminal neuropathy
causes
3
- Herpes Zoster Virus (related to active VZV infection, post-herpetic ‘neuralgia’)
- Trauma (pain develops <6 months of traumatic event)
- Idiopathic
characteristics of painful trigeminal neuropathy
4
- 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?
characteristics of painful trigeminal neuropathy
4
- 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?
trigeminal autonomic cephalagias
characteristic features
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
cluster headache
the attack
characteristics
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%
cluster headaches
the bout
characteristics
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
