dirk de ridder - gp cme south/sat_room4_1100 mvd... · stacatto or typewriter sound very responsive...
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Dirk De Ridder
Microvascular decompression surgery
Microvascular Compression
Signs of microvascular compression (Jannetta, Moller)
Unilateral
Dysfunction of cranial nerve
Paroxysmal and intermittent
Typical evolution: more and longer
Triggers
Responsive to carbamazepine (sensory)
Average age > 50 years
atypical clinic : venous compression (women)
Examples: HFS, TN, DPV, GPN,…
Can be familial
Often bilateral (alternating, never simultaneous)
Multiple nerves
Diagnosis = Clinical picture + MRI
Typical clinical picture
+
Correlation between MRI and peroperative findings (Leal 2010, n=100)
Sensitivity = 96.7%
Specifity = 100%
MRI in MVC
Rightsided hemifacial spasm
Rightsided trigeminal neuralgia
Rightsided light flashes
MVC more common on right side (Hamlyn 1999)
MVC more in women (except Asia) (Hamlyn 1999)
MRI in MVC
Disabling positional vertigo + tinnitus
Cranial nerves
History
1934: Dandy - Trigeminal neuralgia is caused by MVC of trigeminal nerve
1959: Gardner – first MVDs for TN and HFS
1967: Jannetta popularizes MVD after introduction of use of microscope by Kurze in 1957
Microvascular compression syndromes
1. olfactory nerve: paroxysmal unilateral dysosmia ?
2. optic nerve: paroxysmal light flashes leading to visual progressive deficit (Colapinto 1996)
3. oculomotor nerve: oculomotor palsy (Nakagawa 1991)
4. trochlear nerve: superior oblique myokimia (Scharwey 2000)
5. trigeminal nerve: trigeminal neuralgia (Gardner 1959, Jannetta 1967)
6. abducens nerve: abducens spasms (De Ridder 2007)
7. facial nerve: hemifacial spasm (Gardner 1962, Jannetta 1970)
8. vestibulocochlear nerve: disabling positional vertigo, tinnitus, geniculate neuralgia (Jannetta 1980)
9. glossopharyngeal nerve: glossopharyngeal spasm (Jannetta 1980)
10. vagal nerve: hypertension (Jannetta 1980), diabetes type 2 (Jannetta 2010) , atrial fibrillation ?, angina (De Ridder, unpublished data)
11. accessory nerve: spasmodic torticollis (Freckmann 1981)
12. hypoglossal nerve: hemilingual spasm (De Ridder 2002, Osburn 2010)
Trigeminal neuralgia
Somatotopic organization of trigeminal nerve
Compression site determines pain location (Jannetta 1993)
V1: caudal compression
V2: medial or lateral compression
V3: rostral compression
Trigeminal neuralgia
Clinical pictureUnilateral
Very short knife-like stabbing pain paroxysms (less than second)
Triggered by cold, wind, food, drinks
Typical evolution: Paroxysms become more frequent and longer lasting
Start in 1 branch but can extend to other
Can develop hypoesthesia
Responsive to carbamazepine
Can become less typical
Ask for how it started
Differential diagnosisTrigeminal autonomic headaches
Autonomic features, alcohol, night
Eagle syndrome
Trigeminal neuralgia
Outcome :
70% pain-free after 10 years (n=1185, Barker 1996)
74% pain-free after 15 years (n=947, Sindou 2007, 2008, 2010)
Predictive factors
marked vascular compression at surgery >90% success rate at 15 years of FU (Sindou 2007)
vessel only in contact, only 60% cure rate at 15 years
Can be seen with MRI (Leal 2010)
Grade 1: contact Grade 2: indentation Grade 3: deviation
MVD results
Predictive factors TN (Sindou 2007)
Severity of compression (p = 0.001)
Amount of arachnoiditis (p = 0.002).
Preop TN duration doesn’t matter (p = 0.67)
Age doesn’t matter (p = 0.09)
Amount of atrophy doesn’t matter (p = 0.36)
MVD results
Alternative treatments
Gamma knife vs MVD (Linskey 2008)
MVD is superior in prospective non-randomized trial (n=80, 36 MVD)
γ-knife older (74 vs 54), longer (7.5 vs 2.6),
higher comorbidity (58.3 vs 2.8%)
Pain-free after 1, 2, 5 yearsMVD: 100, 88, 80%
γ-knife: 78, 50, 33%
Alternative treatments
Percutaneous rhizotomy vs MVD (Lee 1997, Tronnier
2001, Tatli 2008)
Pain-free postop and facial dysesthesiaMVD: 96.5% & 0.3%
RFR: 92.3% & 5.7%
Long-term FU50% recurrence rate > 2 years and 75% >4years after RFR
64% pain-free after 20 years
Comparison of treatments for TN
1. Medication: carbamazepine,
gabapentin, baclofen
2. Typical TN in healthy person
1. MVD
2. Pc RFR
3. SRS
3. Atypical TN or comorbidity1. Pc RFR
2. SRS
Treatment for TN
Hemifacial spasm
Clinical pictureUnilateral
Twitching of eye (typical, 98%) or orbicularis oris (atypical, 2%) muscles
Typical evolution: initially superior part of orbicularis oculi, later, inferior part, later orbicularis oris
Can lead to hemifacial palsy
Differential diagnosisSynkinesias: after facial palsy
TreatmentCarbamazepine, Botox, MVD
botox: 3 m,
Typical HFS (eye)
Inferior compression
Atypical HFS (mouth)
Superior compression
MVD results
Hemifacial spasm (Miller 2012)
N= 5685 meta-analysis
Outcome (3 year FU):
Complete resolution: 91.1%
Recurrence in 2.4% and 1.2% repeat MVD
Complications:
Transient complications:
facial palsy (9.5%),
hearing deficit (3.2%)
cerebrospinal fluid leak (1.4%)
Permanent complications:
hearing deficit (2.3%)
facial palsy (0.9%)
stroke (< 0.1%)
death (< 0.1%)
Disabling positional vertigo
Clinical pictureShort spells of vertigo (seconds)
Triggered by optokinetic stimuli
Typical evolution: more frequent and longer lasting
Associated other MVC symptoms of nVIII-VII
Tinnitus
Geniculate neuralgia
Hearing loss at tinnitus frequency
Hemifacial spasm (cryptogenic !)
ABR changes
Differential diagnosisMeniere’s Disease
Aura, longer lasting, tinnitus together with vertigo
Low frequency hearing loss
No ABR
Disabling positional vertigo (Jannetta 1996)
N=177
79% markedly improved or cured
11% recurred at 3 year FU
in one study (Ryu 1998) 73% of successful MVDs had preoperative diagnosis of Ménière’sDisease
MVD results
Glossopharyngeal neuralgia (Resnick, Ferroli
2009, Kandan 2010)
N= 92 (40,21,31)
Pain-free 79, 90, 90 %
Recurrence: 6% at 7.5 years
MVD results
Typewriter tinnitus
Typewriter tinnitus (Levine 2006, Nam
2009, Brantberg 2009)
Unilateral
Paroxysms
Intermittent
Trigger
Morse code, machine gun-like, stacatto or typewriter sound
Very responsive to carbamazepine
Due to intrameatal loop (Levine
2006) or nerve traction (Nam 2009)
Study No cases Symptoms Tests Vessels
found
Results of MVD
Okamura et al,
2000
19 HL 58%
Tinnitus 95%
ABR 100% 44% cured
47% improved
64% improved HL
Ryu et al,
1999
40 HL 77.5%
Tinnitus 100%
ABR 75% 45% cured
12% improved
Brookes, 1996 9 HL 71%
Tinnitus 100%
ABR, MRI 100% 33% cured
45% improved
Guevara et al,
2007
15 HL
Tinnitus 100%
ABR,MRI 100% 20% cured
33,3% improved
De Ridder et
al, 2009
22 HL
Tinnitus 100%
ABR, MRI 100% 5% cured
45% improved
Moller et al,
1993
72 HL 77%
Tinnitus 100%
ABR 100% 18% cured
33% improved
MVD results
MVD for tinnitusOutcome poor: combined results from
all studies: 30% cured, 30% improved
MVD and Tinnitus
Results depend on1. Tinnitus duration (Moller 1993, Brookes 1996, Jannetta 1997, Ryu 1998, De Ridder 2009)
If tinnitus < 3 year : outcome good
If tinnitus 3-5 year : outcome moderate
If tinnitus > 5 year : outcome poor
2. Hearing level (Ryu 1998)
If serviceable or normal hearing : outcome good
If severely impaired ( 60dB or more) : outcome poor
3. MRI demonstrates compression 78% good outcome (Brookes 1996, Ko 1997)
4. Gender If woman better outcome: 55 vs 29% (Moller 1993)
DECOMPRESS AS SOON AS POSSIBLE
MVD complications
Complications (Kalkanis 2003)
N= 277 surgeons
N= 1580 MVDs(1326 TN, 237 HFS, 27 GPN)
Mortality rate: 0.3%,
Discharge other than to home: 3.8%.
Neurological complications: 1.7%
Hematomas: 0.5%
Facial palsies: 0.6%
Ventriculostomy: 0.4%
Postoperative ventilation: 0.7%
Is it just the compression ?
Arguments against MVD (Monstad 2007)
1. MRA studies indicate that vascular contact with the trigeminal nerve is present in most healthy individuals (Peker 2009) and as common on the non affected side (Anderson
2006)
2. Treatment results of MVD in multiple sclerosis patients with TGN are almost as good (at least in the short term, they relapse more often) as in idiopathic cases (Broggi 2000, 2004)
3. MVD is reported to provide pain relief even in TGN patients without visible neurovascular contact (Revuelta-Gutierrez 2006)
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Pathophysiology of microvascular compression syndromes
Pathophysiology
MVC
Ephaptic transmission (cross-talk)
Ectopic excitation (in axon)
Paroxysmal hyperactivity
Focal demyelination
Hypofunction
Chronic
Vascular compression
Moller 1999
Demyelination
Only compression ?
DTI evaluates microstructure of nerve via FA, fractional anisotropy; RD, radial diffusivity; MD, mean diffusivity; AD, axial diffusivity.
Asymptomatic patients have normal microstructure, thus no demyelination, no axonal damage, no inflammation, no edema (Lin 2014)
Symptomatic TN have disturbed microstructure suggesting inflammation and edema not visible on gross imaging (DeSouza 2014)
And only on symptomatic side (Fujiwara 2011)
Histopathology
Endoneurial fibrosis
Chronic compression
Congestion of nerve
Stasis of endothelial capillaries
Secretion of protein-rich edema
fluid in endoneurial space
Fluid organizes
Endoneurial fibrosis
Nerve root
Extravasation
(Evans blue albumine)
Bloodvessel
Day 0
Day 30
Day 300
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MVC
of
Vestibulocochlear nerve
Anatomy of the Vestibulocochlear Nerve Complex
Vestibular Nerve 18000 fibers (gray)
Superior Vestibular Nerve 10500 fibers
Utricular Nerve 3500 fibers
Horizontal & Superior Ampullary N 3500 fibers each
Inferior Vestibular Nerve 7500 fibers
Saccular Nerve 3000 fibers
Posterior Ampullary Nerve 3500 fibers
Cochlear Nerve 31000 fibers (white)
Facial Nerve 7000 fibers
Intermediate Nerve 3000 fibers
Symptoms of MVC n VIII-VII
Symptoms associated with MVC n VIII – (VII)(Mollers and Jannetta)
Intermittent paroxysmal spells of unilateral typewriter tinnitus lasting only seconds
2. Associated ipsilateral symptomsFacial nerve: cryptogenic or overt HFSIntermediate nerve: otalgia with or without
deep prosopalgesia (geniculate neuralgia) or feeling of pressure in the ear
Vestibular nerve: vertiginous spells : short lasting, optokineticly induced
Cochlear nerve: frequency specific hearing loss
3. Typical evolution: spells more frequent, intermittent periods shorter, finally constant
Anatomy of the Vestibulocochlear Nerve
Functional Histology
Peripheral part : Schwann cells in myelin (wave I in BAEP)
REZ : at internal acoustic meatus
Vestibular more distal
Cochlear more proximal
Central part : oligodendroglia without epinerium but with pia mater (wave II in BAEP)
REZ
REZ
peripheral
central REZ
REZ
Peripheral Segment
Nervous tissuePNS nerve fiber = axon + Schwann cell
Each fiber undulates
Provides elasticity and protection from traction
form bundles = funiculi
divide and branch
Funicular plexus
Peripheral Segment
Supporting tissue
Endoneurium
Collagen rich connective tissue
Surrounds axon and Schwann cell
Fills funiculi = fasciculi
Perineurium
Thin sheath
Compartimentalizes funiculi
Imparts tensile strenghth
Epineurium
Loose areolar tissue
Surrounds funiculi
Forms nerve trunk
Central Segment
Nervous tissueCNS nerve fiber = axon + oligodendrocyte
Collected in bundle
Travel more parallel
No funicular plexus
Supporting tissueNo endoneurium
No perineurium
No epineurium
Pia mater surrounds white matter bundleMore susceptible to injury
Less vascularized
Anatomy of vestibulocochlear Nerve
MVC has to be at REZ to besymptomatic (Jannetta 1979)
CNS segment is sensitive to MVC, PNS segment less (Leclercq 1980, Moller
1994, Ryu 1999, De Ridder 2002)
Incidence is related to length of CNS segment (De Ridder 2002)
Anti-oligo AL
n. VIII
REZ
0123456789
coch
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trigem
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facial
glos
soph
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dis
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0
2
4
6
8
10
12
incid
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Ménière: 15/100,000
1/3=MVC ?
Brainstem Evoked Auditory Potentials
Brainstem Auditory Evoked Potentials = result of a synchronized firing pattern as a
reaction to an auditory stimulus (Moller 2000)
The more synchrony the higher the peak
Neural generators of BAEP (Moller)I : peripheral cochlear nerve
II : central cochlear nerve
III : cochlear nucleus
IV : superior olivary complex
V : lateral lemniscus
VI : inferior colliculus
I II III
IV V VI
Brainstem Evoked Auditory Potentials
Criteria for MVC (M Moller 1990)
Ipsi I-III IPL > 2.3 ms
Contra III-V IPL > 2.2 ms
I-III difference > 0.2 ms
III-V difference > 0.2 ms
I-III difference > 0.16 ms if low or absent II
III-V difference > 0.16 ms if low or absent II Aα
Aβ
Aδ
myelinated
Unmyelinated C-fibers
II amplitude < 33%
Vascular compression
Focal demyelination
I II III
Tests in CVCS
BAEP (Schwaber 1992)
Wave I-III interval difference > 0,2 ms 66 %
Wave I-III interval difference > 0,16 ms if low or absent wave II
Wave II amplitude < 33 % contralateral side 57 %
Contralateral wave III-V interval difference > 0,2 ms 30 %
Contralateral wave III-V interval difference > 0,16 ms if low or absent wave II
Ipsilateral wave I-III absolute interval > 2,3 ms 24 %
Contralateral wave III-V absolute interval > 2,2 ms 2 %
Audiogram (Schwaber 1992)
High frequency hearing loss 65 % (12 %)
Mid frequency notch hearing loss 27 % (29 %)
Low frequency hearing loss 8 % (11%)
Flat hearing loss -- (50%)
MVC and preop BAEP changes
Vascular compressionFirst two years no significant
BAEP changes (Pearson p=0.490)
After two years peak II decreases ipsilateral to the symptomatic compression (p=0.012, Chi Square)
Dyssynchronized firing
IPL I –III prolongs if peak II absent (definite: t=2.702, df=21, p=0.013, Student T)
Demyelination related slowing
The longer the compression the worse the damage (IPL I-III) (probable: n=16, r=0.501, Pearson P=0.048)
De Ridder, 2007
De Ridder 2007
MVC and Symptoms
Vascular compression
Induces frequency specifichearing loss (De Ridder 2005) due to the tonotopic structure of the auditory nerve (De Ridder 2004)
Low frequency hearing loss in hemifacial spasm (Moller 1985)
De Ridder 2005
MVC and Symptoms
Vascular compression symptoms…Induces frequency specific hearing
loss (De Ridder 2005)
The more hearing loss at tinnitus frequency the worse the tinnitus is perceived (TQ) (definite n=16, corr=0.750, p= 0.001)
… correlate with neurophysiologyThe longer the compression the more
damage (probable: n=16, r=0.501, Pearson P=0.048)
The more damage (IPL I-III) to the auditory nerve the worse the tinnitus (TQ) (probable: n=17, ρ=0.782, p<0.001; definite: n=9, ρ=0.811, p=0.008)
De Ridder 2007
MVC and Symptoms
The longer one has tinnitus associated with MVD the louder it is perceived (De Ridder 2010)
De Ridder 2010
Tinnitus and peak II
Tinnitus improvement correlates with postoperative peak II improvement
Tinnitus improvement is not correlated to IPL I-III improvement
Tinnitus is related to dyssynchronized firing in n VIII
And not to nerve damage and deafferentation
Cfr TMS 2/15 only vs nl 50%
8,006,004,002,000,00
Pre/postop peak II ratio
20,00
10,00
0,00
-10,00
-20,00
Pre
/po
sto
p t
inn
itu
s in
ten
sit
y d
iffe
ren
ce
(d
B)
Relation between pre/postop peak II ratio
and pre/postop tinnitus intensity difference (dB)
n=9; rs=-0.714; p=0.031 (Spearman)
De Ridder 2007
Hearing loss and IPL I-III
Hearing loss improvement correlates with postoperative IPL I-III improvement
Hearing loss improvement correlates not with peak II recurrence
Hearing loss at tinnitus frequency is result from nerve damage and not from dyssynchronized signal transmission
0,250,200,150,100,050,00-0,05
Pre/postop IPL I-III difference (ms)
40,00
30,00
20,00
10,00
0,00
-10,00
-20,00
-30,00
Pre
/po
sto
p h
eari
ng
lo
ss d
iffe
ren
ce (
dB
)
Relation between pre/postop IPL I-III difference
and pre/postop hearing loss difference (dB)
n=9; rs=0.857; p=0,003 (Spearman)
De Ridder 2007
Microvascular decompressions (De Ridder 2007)
MVC causes initial dyssynchronized firing resulting in tinnitus (peak II decreases)
Followed by nerve damage resulting in hearing loss at tinnitus frequency (IPL I-III prolongs)
The longer the compression lasts the more damage and the more hearing loss (at tinnitus frequency)
The more damage and hearing loss the worse the tinnitus is subjectively perceived
So in MVC the tinnitus initially is likely due to dyssynchronized firing pattern transmitted to auditory cortex
Later on it might due to deafferentation
Microvascularcompression
Ephaptic transmission
focaldemyelination
Dysfunction
Chronic ectopic excitation
Hearing loss at tinnitus frequency
prolongationIPL I-IIIi
Improved symmetrical signal
transmission
Colliculus inferior
Reorganisation cochlear nucleus
Tinnitus
Peak II amplitude decrease
VerlengingIPL III-Vc
Compensation
De Ridder 2007
What about contralateral IPL III-V ?
Hypothesis
Contralateral IPL III-V prolongation is compensation for slowing in ipsilateral I-III segment
Compensation cannot by slowing contralateral I-III (no cell bodies)
Could theoretically by speeding up ipsilateral III-V
Slow down
De Ridder 2012
Preoperative Post-operative
Ipsilateral Contralateral Ipsilateral Contralateral
IPL I-III M
SD
2.58
.32
2.11
.11
2.47
.06
2.11
.13
IPL I-III+ PEAK II M
SD
3.58
.31
3.03
.27
3.13
.51
3.35
.34
IPL I-V M
SD
4.44
.15
4.36
.34
4.39
.12
4.07
.09
IPL III-V M
SD
1.80
.18
2.05
.14
1.91
.17
1.90
.09
Compensation in brainstem
Preop ipsilateral peak II decreases and IPL I-III prolongs
Preop contralateral IPLIII-V longer (as a compensation ?)
Postop ipsilateral peak II and IPL I-III normalizes
Postop contralateral IPLIII-V normalizes
De Ridder 2012
Microvascular decompressions (De Ridder 2007)
MVC causes initial dyssynchronized firing resulting in tinnitus (peak II decreases)
Followed by nerve damage resulting in hearing loss at tinnitus frequency (IPL I-III prolongs)
The longer the compression lasts the more damage and the more hearing loss (at tinnitus frequency)
The more damage and hearing loss the worse the tinnitus is subjectively perceived
So in MVC the tinnitus initially might be due to dyssynchronized firing pattern transmitted to auditory cortex
Later on it is due to deafferentation
Compensation occurs in the brainstem, evidenced by reversible contralateral IPL III-V prolongation
Microvascularcompression
Ephaptic transmission
focaldemyelination
Dysfunction
Chronic ectopic excitation
Hearing loss at tinnitus frequency
prolongationIPL I-IIIi
Improved symmetrical signal
transmission
Colliculus inferior
Reorganisation cochlear nucleus
Tinnitus
Peak II amplitude decrease
VerlengingIPL III-Vc
Compensation
De Ridder 2012
Summary
De Ridder 2012
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Conclusion
MVC is clinical diagnosis (unilateral, paroxysmal, hyperactivity,
triggers, carbamazepine, more and longer, hypofunction)
likely exists for all cranial nerves
ABR & MRI for confirmation and delineation of nerve injury
Treatment results
For TN, HFS, GPN, DPV: ≥ 75% 10 year cure rate
For tinnitus worse:
Between 5 and 45% cured
Between 12 and 45% improved
Few worsened
Easy indication for TN, HFS, GPN, DPV, difficult indication for tinnitus
Importance of REZ ?
Compression anywhere along cranial nerve, but especially anywhere along CNS segment
1. Histological arguments
2. Neurophysiological arguments
3. Epidemiological arguments
4. Clinical experience
Importance of REZ ?
1. Histological arguments
1. CNS segment has no endo-, peri- or epineurium
2. Nerves do not divide nor branch, so they do not form a funicular plexus
3. Nerves do not undulate, so have less elasticity
4. Oligodendroglia form less lamellae than schwann cells ?
Importance of REZ ?
2. Neurophysiological arguments
1. BAEP monitoring
traction most dangerous for hearing loss(Raudzens 1982)
four patients lose all waves after Peak I
2. Möller’s criteria for CVCS1. IPL I-III increase (66%) not specific enough
2. wave II disappearance (57%) second mostfrequent anomaly (Schwaber 1992)
3. Rat experiments by Möller
I II III
Importance of REZ ?
3. Epidemiological argument
the longer the CNS segment
the higher the incidence of MVC
0
0,5
1
1,5
2
2,5
3
3,5
trigeminal facial glossopharyngeal
dis
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De Ridder 2002
Skinner 1931 Tarlov 1937
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Importance of REZ ?
Expected incidence of CVCS ?
5-7/100.000 ?
Ménière has an incidence of 15.3/100.000
i.e. 1/3 of Ménière’s disease might be CVCS*
* In some series upto 73% of CVCS had a preop diagnosis of Ménière (Ryu, 1998)
Importance of REZ ?
4. Clinical experience
Decompression along CNS segment results in good outcome (not only at REZ)
Sometimes even at peripheral segment
n. VII
At distal segment
n. VIII
REZ
REZ
At proximal segment
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MVC location & clinical picture
MVC location and tinnitus type
Vascular compression
At CNS segment can result in non-pulsatile tinnitus (Moller 1993, De Ridder
2004)
At PNS segment can result in pulsatile tinnitus (Nowe 2005, De Ridder 2005)
or typewriter tinnitus (Levine 2006)
15
2 4
42
0
10
20
30
40
50
pulsatile tinnitus non-pulsatile tinnitus
Intrameatal loop
intrameatal loop no loop
P < 0.00001, Fisher’s exact test
Typewriter tinnitus
Typewriter tinnitus (Levine 2006, Nam
2009, Brantberg 2009)
Unilateral
Paroxysms
Intermittent
Trigger
Morse code, machine gun-like, stacatto or typewriter sound
Very responsive to carbamazepine
Due to intrameatal loop (Levine
2006) or nerve traction (Nam 2009)
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Non-pulsatile tinnitus
Used classification
Classification Possible CVCS : initially intermittent
unilateral tinnitus spells without associated symptoms.
Probable CVCS : possible CVCS with associated symptoms (otalgia, vertigo or hemifacial spasms) or MRI demonstrating vascular compression of cochleovestibular nerve (using high resolution heavily T2 weighted CISS images) or abnormal ABR
Definite CVCS : probable CVCS with associated symptoms and/or abnormal ABR and/or abnormal MRI
Certain CVCS : definite CVCS which is surgically proven
De Ridder 2007
Why is this so ?
Tinnitus intensity and tinnitus distressPoor correlation between tinnitus matched sound intensity and tinnitus related distress (Moller 1994)
Correlation between VAS and TQ is nonlinear (unpublished Vanneste)
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INTRAMEATAL VASCULAR COMPRESSION
1. Typewriter tinnitus
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INTRAMEATAL VASCULAR COMPRESSION
2. Pulsatile tinnitus
Pulsatile tinnitus
15% unknown
Vascular loop in internal auditory canal ?
Hypothesis
Vascular loop induces turbulent flow in internal auditory canal
Transmitted to apex of cave where cochlea is located
Via bone conduction to cochlea
What about surgery ?
Surgical Results (De Ridder 2005)
4 patients operated
4 free of pulsations
2 recurrences
De Ridder 2005
If this is correct
Why do we not hear our carotids ?
Because of the pericarotid venous plexus
De Ridder 2005
Is that really so ?
Hyperdynamic flow in
Hypertension
Sports
Basilar artery hypoplasia / stenosis
Venous plexus dampens insufficiently
De Ridder 2005
Secundary cochleovestibular compression syndrome
1. Isolated compression
2. Induced compression
1. Overcrowding fossa posterior and/or Chiari (Sindou, De Ridder 2007)
2. Space occupying lesions (De Ridder 2008)
Tinnitus and Chiari (Wiggs 1996)
Pulsatile tinnitusVenous humm
Cause = ICP / Hydrocephalus
Worse on bending over
Disappears on ipsilateral jugular vene compression
Hearing improves on jugular vene compression (masking)
No BAEP changes
Non-Pulsatile tinnitusIntermittent
Cause = 1. MVC ? (crowding posterior fossa)
2. brainstem traction ?
BAEP changes in 75 %
100 % III-V prolongation
36 % I-III prolongation
June 13-16, 2012BRUGES
http://www.brai2n.com/tri2012
Anatomy of Cranial Nerve
Cranial nerve consists of two kinds of tissueNervous tissue
Supporting tissue
different for central and peripheral segments
Peripheral Segment
Nervous tissuePNS nerve fiber = axon +
Schwann cell
Each fiber undulates
Provides elasticity and protection from traction
form bundles = funiculi
divide and branch
Funicular plexus
perineurium
endoneurium
Surgical results
Patient Age Gender Tinnitus Duration
VAS TQ
Preoperative Postoperative Preoperative Postoperative1 48 F 15 8 8 29 362 49 M 3 8 7 63 543 56 F 9 7 10 52 734 63 M 2 9 8 46 595 48 F 2 7 7 586 64 F 4 7 4 71 697 63 M 4 9 9 73 708 64 M 3 5 6 29 359 46 M 14 9 7 33 25
10 45 F 7 10 10 63 5711 55 M 2 8 3 5512 72 M 11 10 10 59 6313 40 F 2 7 1 1114 44 F 5 7 5 6315 62 F 4 8 7 77 5416 48 M 5 10 10 77 6617 60 F 2 7 7 44 6318 65 F 3 8 4 3719 48 M 1 4 4 4920 40 F 11 8 6 16
5% cured, 45% improved
No improvement after 4 years !
Tinnitus intensity improves little
Tinnitus distress not
De Ridder 2010
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