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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vagal nerve: hypertension (Jannetta 1980), diabetes type 2 (Jannetta 2010) , atrial fibrillation ?, angina (De Ridder, unpublished data)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

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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

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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