Differentiating Trigeminal

Neuropathy From
Trigeminal Neuralgia
Does It Even Matter?
Justin Sandall, D.O.
Vanderbilt University Medical Center
Department of Anesthesiology, CA-2

Case Presentation

26 y/o female w/a history of chronic migraine HA, depression and

hypothyroidism presents for evaluation of L sided facial pain.
She relates a history of migraines since the age of 11; occurred
infrequently until beginning college in 2001 at which time they
increased in frequency to 2-3x/month.
~1 year ago she had her typical migraine which "didn't go away." She
now has a constant, throbbing/boring pain in her L periorbital/frontal
area with occ. radiation to the L maxilla.

She also has intermittent sharp, lancinating pains in those

same areas.

Her pain is worsened with anxiety, working out, loud noises, heat and
alleviated with application of cold, migraine medications and Lyrica.
Mother has noticed L sided facial swelling.
There is no association with brushing teeth, putting on makeup or
wind on the face. She denies changes in hearing, balance or
coordination. She also denies sensory changes, tearing, conjunctival
effusion and ataxia.
No h/o trauma or HSV.

Case Presentation

MEDICATIONS:
- Synthroid Oral Tablet 75 mcg 1 tablet by mouth daily
- Betaxolol 10mg PO twice daily
- Zoloft 150mg PO daily
- Migrelief 2 tabs PO
- Topamax 300mg OP daily
- Ondansetron tab PO PRN
- Indomethacin 25mg PO twice daily
- Zomig Zmt 5mg PO twice daily
- Lyrica 300mg
- Kariva BC
- Zyrtec 10mg

Case Presentation
Relevant Physical Exam

PERRL, CN II-XII intact b/l, NTTP along

trigeminal distribution w/o allodynia or
hyperesthesia, no sensory deficits, TMJ NTTP
b/l

Relevant Imaging

Previous work-up including CT and MRI

unrevealing

Trigeminal Neuralgia

Most common pain syndrome referable to a cranial nerve.1

Most common in adults > 50 y/o, women slightly more than men 2
Classically, pain is described as an electric shocklike, stabbing,
unilateral pain with abrupt onset and termination in distribution of
trigeminal nerve usually V2/3.2,3

Intervals between attacks are pain free

Minimal or no sensory loss in the region of pain

Precipitation from trigger areas or by certain daily activities, such as

eating, talking, washing the face, or cleaning the teeth3
Diagnosis is typically made by the history
Imaging is often pursued to r/o other causes of facial pain &/or to
evaluate for MS, vascular compression of the trigeminal nerve etc.
Typically, 80% of patients respond to medical therapy3

1st line therapy is carbamazepine2,3,5

Trigeminal Neuralgia

May target trigeminal nerve at various sites with nerve blocks if

unresponsive to medical therapy

Superficial V1/V2, gasserian ganglion

If responsive to local anesthetic block, may pursue trigeminal neurolysis

Most common target is the gasserian ganglion via the foramen ovale1
Studies have all used patients w/classic trigeminal neuralgia

Less premorbid depression/anxiety, more satisfied w/outcome, fewer side effect

complaints, more willing to repeat procedure1

Study by Taha and Tew in 1996 evaluated RF rhizotomy w/curved electrode,

RF rhizotomy, glycerol rhizotomy, balloon compression, and posterior fossa
exploration (microvascular decompression, partial trigeminal rhizotomy)4
Showed initial pain relief to be 91-98% with success of procedure in 85-98% and
pain recurrence in 15-54%

Glycerol rhizotomy had lowest initial pain relief, lowest procedure success and highest
pain recurrence

Complications of trigeminal neurolysis can be devastating and include

anesthesia dolorosa, loss of corneal sensation, keratitis, dysesthesia1

Trigeminal Neuropathy (included

atypical trigeminal neuralgia and
atypical facial pain)
Chronic or recurrent pain in the area of previous nerve injury,
numbness, dysesthesias, and chronic burning sensations.
Diagnostic evaluations rule out any other cause of pain.2

Doesnt meet White and Sweet criteria:2

The pain is paroxysmal.

The pain is confined to the trigeminal distribution.
The pain is unilateral.
The bedside clinical sensory examination is normal.
The pain may be provoked by light touch to the face (trigger zones)

Significant clinical challenge because the symptoms of PTN respond

poorly, if at all, to AED or surgical therapies commonly used in TN. 1,2

More likely to have sensory loss or allodynia5

Neurolytic treatment may actually worsen pain in this subgroup

More often associated with young, middle aged women and feelings
of depression
Motor cortex stimulation for trigeminal neuralgia seems promising
70% success rate compared to 50% for central pain5

Classic
trigeminal
neuralgia

Rare

Intraoral or
extraoral in
trigeminal
region

Each episode
of pain lasts
for seconds to
minutes;
refractory
periods, and
long periods
of no pain

Sharp,
shooting,
moderate to
very severe

Light touch
provoked
(e.g., eating,
washing,
talking)

Discrete
trigger zones

Atypical
trigeminal
neuralgia

Rare

Intraoral or
extraoral in
trigeminal
region

Sharp attacks
lasting
seconds to
minutes, more
continuoustype
background
pain, less
likely to have
complete pain
remission

Sharp,
shooting,
moderate to
severe but
also dull,
burning,
continuous
mild
background
pain

Light touch
provoked,
but
continuoustype pain not
so clearly
provoked

May have
small trigger
areas, variable
pattern

Trigeminal
neuropathy

Very
rare

Trigeminal
Continuous
area, but may
radiate beyond

Dull with
sharp
exacerbation

Areas of
allodynia,
light touch

Sensory loss,
subjectiveobjective,
progressive,
vasodilation
and swelling
may occur

Adapted from Essentials of physical medicine and rehabilitation: musculoskeletal disorders, pain, and rehabilitation/
[edited by] Walter R. Frontera, Julie K. Silver, Thomas D. Rizzo Jr.2nd ed. Chapter 90.

Case Resolution

26 y/o female with L sided facial pain in the setting of chronic migraine HA, h/o
depression and hypothyroidism. Given the nature of her pain, her history of
depression and migraine HA, her pain triggers or lack thereof and physical exam
findings, this most likely is atypical facial pain secondary to trigeminal neuropathic
pain in the V1/V2 distribution rather than classic trigeminal neuralgia. It is important
to make this distinction given that definitive treatment of trigeminal neuralgia (i.e.
neurolytic tx) can actually worsen the pain of trigeminal neuropathy. In addition, she
almost certainly has a component of transformed migraine HA that is contributory
thus one of our long-term goals will be to decrease the number of medicines she is
on.
1. Atypical facial pain
2. Trigeminal neuropathic pain in the V1V2 distribution
3. Transformed migraine headache
4. H/o depression
5. Hypothyroidism
Will schedule for superficial V1/V2 block and TPI and assess response. Needs to be
off indomethacin x7 days prior to procedure. May benefit from Gasserian ganglion
block and/or Stellate ganglion block down the road if not responsive to more
conservative measures. If responds well to the peripheral n. blocks, will use Botox for
long-term control. Meanwhile

References

Jackson T, Gaeta R: Neurolytic blocks revisited. Current

Pain and Headache Reports. 2008, 12:7-13.
Raj's practical management of pain/editors, Honorio T.
Benzon[et al.].4th ed. Chapter 25.
Essentials of physical medicine and rehabilitation:
musculoskeletal disorders, pain, and rehabilitation/
[edited by] Walter R. Frontera, Julie K. Silver, Thomas D.
Rizzo Jr.2nd ed. Chapter 90.
Taha JM, Tew JM: Comparison of surgical treatments for
trigeminal neuralgia: reevaluation of radiofrequency
rhizotomy. Neurosurgery 1996, 38:865-871
McMahon: Wall and Melzack's Textbook of Pain, 5th ed.
Chapter 37