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Trigeminal Neuralgia
By, Meera Ramesh
TIC DOULOUREUX
FOTHERGILLS DISEASE
SUICIDE DISEASE
OCTOBER 7TH
INTRODUCTION
Disorder
characterized by
lancinating attacks
of severe facial
pain
Epidemiology and DemographicsEpidemiology and Demographics
- Incidence of approx 4 in
100,000
- Majority of cases occur
spontaneously
- Slight female
predominance
- Over age 50
Age of Onset
0
5
10
15
20
25
30
2nd 3rd 4th 5th 6th 7th 8th 9th
Decade
More than 70% of patients with TN are over 50
years of age at the time onset
- Pain typically consists of
lancinating paroxysms
- Mostly in Second &
Third trigeminal
divisions
- Right side most often
involved
- Pain attack is
stereotyped
- Symptom free between
attacks
- Lasts for several years if
left untreated.
Trigeminal Nerve Anatomy
Distribution of Pain by Division
32
17 17
15 14
4
0.4
0
5
10
15
20
25
30
35
Percent
V2,3 V2 V1,2,3 V3 V1,2 V1 V1,3
Trigeminal Division
The pain of TN……
- Paroxysmal attacks
- Electric shock like quality
- Sudden onset & severe in
intensity  facial grimace
- Duration btw 1 sec and 2 min
- Instantaneous electric shock
sensation that’s over in much
less than a sec – ‘lightning
bolt’
- Symptom free btw attacks.
Pain is commonly evoked by stimuli
including washing, shaving, smoking,
talking and/or brushing the teeth
(trigger factors) and frequently occurs
spontaneously. The pains usually remit
for variable periods.”
Trigger zones……
Etiology and Pathogenesis
• Dental pathosis
• Excessive traction
• Allergic
• Ischemia
• Mechanical trauma like aneurysms
• Compression distortion phenomenon
• Anomalies of superior cerebellar artery
• Secondary lesion
Clinical Presentation and
Physical Findings
Diagnosis of TN based on
distinctive signs &
symptoms.
Consists of 5 major clinical
features that define the
diagnosis of TN
ICHD Criteria for Classical TN (13.1.1)
A. Paroxysmal attacks of pain lasting from a fraction of a
second to 2 minutes, affecting one or more divisions of
the trigeminal nerve and fulfilling criteria B and C
B. Pain has at least one of the following characteristics:
1. intense, sharp, superficial or stabbing
2. precipitated from trigger areas or by trigger factors
C. Attacks are stereotyped in individual patient.
D. There is no clinically evident neurological deficit.
E. Not attribute to another disorder.
ICHD Criteria for Symptomatic TN (13.1.2)
A. Paroxysmal attacks of pain lasting from a fraction of a
second to 2 minutes, with or without persistence of aching
between paroxysms, affecting one or more divisions of
trigeminal nerve and fulfilling criteria B and C.
B. Pain has at least one of the following characteristics:
1. Intense, sharp, superficial or stabbing
2. Precipitated from trigger areas or by trigger factors.
C. Attacks are stereotyped in individual patient.
D. A causative lesion, other than vascular compression, has
been demonstrated by special investigations and/or
posterior fossa exploration.
Diagnosis of Trigeminal Neuralgia
ALL FACIAL PAIN IS NOT TRIGEMINAL NEURALGIA!
Diagnostic testingDiagnostic testing
Diagnostic brain imaging toDiagnostic brain imaging to
visualize anatomicvisualize anatomic
landmark around trigeminallandmark around trigeminal
ganglion and CPAganglion and CPA
CT, MRI – to rule out CPACT, MRI – to rule out CPA
lesions and to visualizelesions and to visualize
subtle vascular anomaliessubtle vascular anomalies
causing compressioncausing compression
Imaging in Trigeminal Neuralgia
In patients with types 1 and 2 trigeminal
neuralgia (TN1 and TN2) one can
identify:
– Presence of (NVC)
– Degree of NVC
– Nature
– Location
Findings can be confirmed during MVD
Right Trigeminal Nerve
Compressing vessel
Right Trigeminal Nerve
Compressing vessel
Pharmacological Treatment
AEDs
– Tegretol (carbamazepine)
gold standard
– Tripeptal (oxcarbazepine)
– Dilantin (phenytoin)
– Neurontin (gabapentin)
– Lyrica (pregabalin)
– Lamictal (lamotrigene)
– Topamax (topirimate)
– Gabatril (tiagabine)
– Keppra (levateracitam)
TCAs
– Elavil (amitriptyline)
– Pamelor (nortriptyline)
– Desipramine (norpramin)
Baclofen (lioresal)
Opioids
Adverse Effects of AEDs
Cognitive changes
Sedation
Nystagmus, ataxia, diplopia,
dizziness
Nausea, vomiting, headache
Allergic reaction
– Up to 7% with CBZ
– Some cross-reactivity between
CBZ and PHT
Surgical Treatment of TN
Microvascular decompression (MVD)
Percutaneous ablative procedures
– Radiofrequency thermal lesioning
– Glycerol injection
– Balloon compression
Stereotactic radiosurgery
– Gamma knife
– Linac-based
Peripheral ablative procedures (V1 and V2 pain)
– Peripheral branch neurectomy
– Alcohol neurolysis
Open destructive procedures
– Partial sensory rhizotomy
– Subtemporal ganglionectomy (Frazier-Spiller procedure)
Advantages of MVD
ONLY non-destructive
procedure.
Low risk of facial sensory
loss.
ONLY operation that
addresses vascular
compression
Disadvantages of MVD
Requires major surgery
MVD is generally associated
with more risks than
percutaneous procedures or
radiosurgery like CSF leak
More costly
Surgical Technique
Positioning
Skin Incision
Retromastoid craniectomy
T-shaped dural opening
Surgical Technique
Exposure of CPA
Visualization of trigeminal nerve
– Visualize the ENTIRE nerve from it’s
exit from the pons to it’s exit laterally
from the CPA
Decompression
– Mobilize and “pad” arteries
– Coagulate and divide veins
Operative Findings
Arterial compression
– Superior cerebellar artery
(SCA) – most common
– AICA
– PICA
– Vertebrobasilar artery
Venous compression
– More common with atypical
TN
Combined arterial and
venous compression
Operative Findings
Complications of MVD
Cerebellar injury <1%
Infectious complications
– Bacterial meningitis
– Aseptic meningitis
CSF leak 0-4%
Cranial nerve deficits
– Diplopia
– Sensory loss or dysesthesias 0.5-17%
– Facial weakness 0.5-15%
– Hearing loss <1 (0-19%)
Stroke
Mortality < 1%
Outcome Following Initial MVD
(N=1204 patients)
0
10
20
30
40
50
60
70
80
90
Initial 1 yr 10 yrs
Excellent Partial Failure
Barker F, Jannetta P, Bissonette D, et.al.: NEJM, 1996
Repeat MVD for Recurrent TN
All procedures used to initially treat TN
CAN be effective for recurrent TN
Less than 1/3 of patients undergo repeat
MVD
Lower success rates
Findings: New compressive vessel.
Higher incidence of perioperative
morbidity
– Increased risk of cranial nerve palsy
– Increased incidence of facial numbness (8%)
and/or facial dysesthesias
Percutaneous Procedures
Radiofrequency thermal lesioning
Glycerol injection
Balloon compression
Radiofrequency Lesioning
Glycerol Injection
Contrast in trigeminal cistern Contrast under temporal lobe
Balloon Compression
Radiosurgery for TN
Decision-Making in TN
When should surgery be considered?
– Success/failure of medical therapy
– Frequency of recurrences
– Duration of symptoms
Which operation should be done?
– Age and health of patient
– Willingness to except facial sensory
loss
– Previous procedures for TN
– Desires of patient
– Experience of surgeon
THANK YOU

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Trigeminal neuralgia By Meera R

  • 4.
  • 6. Epidemiology and DemographicsEpidemiology and Demographics - Incidence of approx 4 in 100,000 - Majority of cases occur spontaneously - Slight female predominance - Over age 50
  • 7. Age of Onset 0 5 10 15 20 25 30 2nd 3rd 4th 5th 6th 7th 8th 9th Decade More than 70% of patients with TN are over 50 years of age at the time onset
  • 8. - Pain typically consists of lancinating paroxysms - Mostly in Second & Third trigeminal divisions - Right side most often involved - Pain attack is stereotyped - Symptom free between attacks - Lasts for several years if left untreated.
  • 10. Distribution of Pain by Division 32 17 17 15 14 4 0.4 0 5 10 15 20 25 30 35 Percent V2,3 V2 V1,2,3 V3 V1,2 V1 V1,3 Trigeminal Division
  • 11. The pain of TN…… - Paroxysmal attacks - Electric shock like quality - Sudden onset & severe in intensity  facial grimace - Duration btw 1 sec and 2 min - Instantaneous electric shock sensation that’s over in much less than a sec – ‘lightning bolt’ - Symptom free btw attacks.
  • 12. Pain is commonly evoked by stimuli including washing, shaving, smoking, talking and/or brushing the teeth (trigger factors) and frequently occurs spontaneously. The pains usually remit for variable periods.”
  • 14. Etiology and Pathogenesis • Dental pathosis • Excessive traction • Allergic • Ischemia • Mechanical trauma like aneurysms • Compression distortion phenomenon • Anomalies of superior cerebellar artery • Secondary lesion
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  • 16. Clinical Presentation and Physical Findings Diagnosis of TN based on distinctive signs & symptoms. Consists of 5 major clinical features that define the diagnosis of TN
  • 17. ICHD Criteria for Classical TN (13.1.1) A. Paroxysmal attacks of pain lasting from a fraction of a second to 2 minutes, affecting one or more divisions of the trigeminal nerve and fulfilling criteria B and C B. Pain has at least one of the following characteristics: 1. intense, sharp, superficial or stabbing 2. precipitated from trigger areas or by trigger factors C. Attacks are stereotyped in individual patient. D. There is no clinically evident neurological deficit. E. Not attribute to another disorder.
  • 18. ICHD Criteria for Symptomatic TN (13.1.2) A. Paroxysmal attacks of pain lasting from a fraction of a second to 2 minutes, with or without persistence of aching between paroxysms, affecting one or more divisions of trigeminal nerve and fulfilling criteria B and C. B. Pain has at least one of the following characteristics: 1. Intense, sharp, superficial or stabbing 2. Precipitated from trigger areas or by trigger factors. C. Attacks are stereotyped in individual patient. D. A causative lesion, other than vascular compression, has been demonstrated by special investigations and/or posterior fossa exploration.
  • 19. Diagnosis of Trigeminal Neuralgia ALL FACIAL PAIN IS NOT TRIGEMINAL NEURALGIA!
  • 20. Diagnostic testingDiagnostic testing Diagnostic brain imaging toDiagnostic brain imaging to visualize anatomicvisualize anatomic landmark around trigeminallandmark around trigeminal ganglion and CPAganglion and CPA CT, MRI – to rule out CPACT, MRI – to rule out CPA lesions and to visualizelesions and to visualize subtle vascular anomaliessubtle vascular anomalies causing compressioncausing compression
  • 21. Imaging in Trigeminal Neuralgia In patients with types 1 and 2 trigeminal neuralgia (TN1 and TN2) one can identify: – Presence of (NVC) – Degree of NVC – Nature – Location Findings can be confirmed during MVD
  • 24. Pharmacological Treatment AEDs – Tegretol (carbamazepine) gold standard – Tripeptal (oxcarbazepine) – Dilantin (phenytoin) – Neurontin (gabapentin) – Lyrica (pregabalin) – Lamictal (lamotrigene) – Topamax (topirimate) – Gabatril (tiagabine) – Keppra (levateracitam) TCAs – Elavil (amitriptyline) – Pamelor (nortriptyline) – Desipramine (norpramin) Baclofen (lioresal) Opioids
  • 25. Adverse Effects of AEDs Cognitive changes Sedation Nystagmus, ataxia, diplopia, dizziness Nausea, vomiting, headache Allergic reaction – Up to 7% with CBZ – Some cross-reactivity between CBZ and PHT
  • 26. Surgical Treatment of TN Microvascular decompression (MVD) Percutaneous ablative procedures – Radiofrequency thermal lesioning – Glycerol injection – Balloon compression Stereotactic radiosurgery – Gamma knife – Linac-based Peripheral ablative procedures (V1 and V2 pain) – Peripheral branch neurectomy – Alcohol neurolysis Open destructive procedures – Partial sensory rhizotomy – Subtemporal ganglionectomy (Frazier-Spiller procedure)
  • 27. Advantages of MVD ONLY non-destructive procedure. Low risk of facial sensory loss. ONLY operation that addresses vascular compression
  • 28. Disadvantages of MVD Requires major surgery MVD is generally associated with more risks than percutaneous procedures or radiosurgery like CSF leak More costly
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  • 31. Surgical Technique Positioning Skin Incision Retromastoid craniectomy T-shaped dural opening
  • 32. Surgical Technique Exposure of CPA Visualization of trigeminal nerve – Visualize the ENTIRE nerve from it’s exit from the pons to it’s exit laterally from the CPA Decompression – Mobilize and “pad” arteries – Coagulate and divide veins
  • 33. Operative Findings Arterial compression – Superior cerebellar artery (SCA) – most common – AICA – PICA – Vertebrobasilar artery Venous compression – More common with atypical TN Combined arterial and venous compression
  • 35. Complications of MVD Cerebellar injury <1% Infectious complications – Bacterial meningitis – Aseptic meningitis CSF leak 0-4% Cranial nerve deficits – Diplopia – Sensory loss or dysesthesias 0.5-17% – Facial weakness 0.5-15% – Hearing loss <1 (0-19%) Stroke Mortality < 1%
  • 36. Outcome Following Initial MVD (N=1204 patients) 0 10 20 30 40 50 60 70 80 90 Initial 1 yr 10 yrs Excellent Partial Failure Barker F, Jannetta P, Bissonette D, et.al.: NEJM, 1996
  • 37. Repeat MVD for Recurrent TN All procedures used to initially treat TN CAN be effective for recurrent TN Less than 1/3 of patients undergo repeat MVD Lower success rates Findings: New compressive vessel. Higher incidence of perioperative morbidity – Increased risk of cranial nerve palsy – Increased incidence of facial numbness (8%) and/or facial dysesthesias
  • 38. Percutaneous Procedures Radiofrequency thermal lesioning Glycerol injection Balloon compression
  • 40. Glycerol Injection Contrast in trigeminal cistern Contrast under temporal lobe
  • 43. Decision-Making in TN When should surgery be considered? – Success/failure of medical therapy – Frequency of recurrences – Duration of symptoms Which operation should be done? – Age and health of patient – Willingness to except facial sensory loss – Previous procedures for TN – Desires of patient – Experience of surgeon