Microvascular decompression surgery Dirk De Ridder www.brai²n.be 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 light flashes Rightsided trigeminal neuralgia Rightsided hemifacial spasm 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. 2. 3. 4. 5. 6. 7. 8. olfactory nerve: paroxysmal unilateral dysosmia ? optic nerve: paroxysmal light flashes leading to visual progressive deficit (Colapinto 1996) oculomotor nerve: oculomotor palsy (Nakagawa 1991) trochlear nerve: superior oblique myokimia (Scharwey 2000) trigeminal nerve: trigeminal neuralgia (Gardner 1959, Jannetta 1967) abducens nerve: abducens spasms (De Ridder 2007) facial nerve: hemifacial spasm (Gardner 1962, Jannetta 1970) 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vagal nerve: hypertension (Jannetta 1980), diabetes type 2 (Jannetta 2010) , atrial fibrillation ?, angina (De Ridder, unpublished data) 11.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 picture Unilateral 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 diagnosis Trigeminal autonomic headaches Autonomic features, alcohol, night Eagle syndrome MVD results 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) Alternative treatments Gamma knife vs MVD (Linskey 2008) MVD is superior in prospective nonrandomized 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 years MVD: 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 dysesthesia MVD: 96.5% & 0.3% RFR: 92.3% & 5.7% Long-term FU 50% recurrence rate > 2 years and 75% >4years after RFR 64% pain-free after 20 years Comparison of treatments for TN Treatment for TN 1. Medication: carbamazepine, gabapentin, baclofen 2. 3. Typical TN in healthy person 1. MVD 2. Pc RFR 3. SRS Atypical TN or comorbidity 1. Pc RFR 2. SRS Hemifacial spasm Clinical picture Unilateral 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 diagnosis Synkinesias: after facial palsy Treatment Carbamazepine, 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 picture Short 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 diagnosis Meniere’s Disease Aura, longer lasting, tinnitus together with vertigo Low frequency hearing loss No ABR MVD results 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’s Disease 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 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) MVD results MVD for tinnitus Outcome poor: combined results from all studies: 30% cured, 30% improved Study No cases Symptoms Tests Vessels found Results of MVD Okamura et al, 19 2000 HL 58% Tinnitus 95% ABR 100% 44% cured 47% improved 64% improved HL Ryu et al, 1999 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 40 MVD and Tinnitus Results depend on 1. 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) Pathophysiology of microvascular compression syndromes www.brai²n.be Pathophysiology MVC Ephaptic transmission (cross-talk) Chronic Ectopic excitation (in axon) Paroxysmal hyperactivity Focal demyelination Vascular compression Hypofunction Demyelination Moller 1999 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 Day 0 Congestion of nerve Bloodvessel Stasis of endothelial capillaries Secretion of protein-rich edema fluid in endoneurial space Fluid organizes Endoneurial fibrosis Nerve root Day 30 Extravasation (Evans blue albumine) Day 300 MVC of Vestibulocochlear nerve www.brai²n.be Anatomy of the Vestibulocochlear Nerve Complex Vestibular Nerve Superior Vestibular Nerve 18000 fibers (gray) 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 Facial Nerve 31000 fibers (white) 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 symptoms Facial nerve: cryptogenic or overt HFS Intermediate 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) peripheral REZ REZ central REZ REZ Peripheral Segment Nervous tissue PNS 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 tissue CNS nerve fiber = axon + oligodendrocyte Collected in bundle Travel more parallel No funicular plexus Supporting tissue No endoneurium No perineurium No epineurium Pia mater surrounds white matter bundle More susceptible to injury Less vascularized Anatomy of vestibulocochlear Nerve MVC has to be at REZ to be symptomatic (Jannetta 1979) CNS segment is sensitive to MVC, PNS segment less (Leclercq 1980, Moller Anti-oligo AL 1994, Ryu 1999, De Ridder 2002) 9 8 7 6 5 4 3 2 1 0 8 6 4 2 so ph ar yn ge al glo s fac ial ina l 0 n. VIII Ménière: 15/100,000 1/3=MVC ? incidence 10 ge m REZ 12 tri co ch lea ris distance to REZ Incidence is related to length of CNS segment (De Ridder 2002) Brainstem Evoked Auditory Potentials I Brainstem Auditory Evoked Potentials II III = 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 IV V VI Brainstem Evoked Auditory Potentials Vascular compression Criteria for MVC (M Moller 1990) II amplitude < 33% I II III Ipsi I-III IPL > 2.3 ms Contra III-V IPL > 2.2 ms Focal demyelination 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 Aβ Aα Aδ myelinated Unmyelinated C-fibers Tests in CVCS BAEP (Schwaber 1992) Wave I-III interval difference > 0,2 ms Wave I-III interval difference > 0,16 ms if low or absent wave II Wave II amplitude < 33 % contralateral side Contralateral wave III-V interval difference > 0,2 ms Contralateral wave III-V interval difference > 0,16 ms if low or absent wave II Ipsilateral wave I-III absolute interval > 2,3 ms Contralateral wave III-V absolute interval > 2,2 ms Audiogram (Schwaber 1992) High frequency hearing loss Mid frequency notch hearing loss Low frequency hearing loss Flat hearing loss 65 % 27 % 8% -- (12 %) (29 %) (11%) (50%) 66 % 57 % 30 % 24 % 2% MVC and preop BAEP changes Vascular compression First 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, Student T) df=21, p=0.013, 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 specific hearing 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 neurophysiology The 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 is related to dyssynchronized firing in n VIII And not to nerve damage and deafferentation Cfr TMS 2/15 only vs nl 50% 20,00 Pre/postop tinnitus intensity difference (dB) Tinnitus improvement correlates with postoperative peak II improvement Tinnitus improvement is not correlated to IPL I-III improvement 10,00 0,00 -10,00 -20,00 0,00 2,00 4,00 6,00 8,00 Pre/postop peak II ratio 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 at tinnitus frequency is result from nerve damage and not from dyssynchronized signal transmission 40,00 Pre/postop hearing loss difference (dB) Hearing loss improvement correlates with postoperative IPL I-III improvement Hearing loss improvement correlates not with peak II recurrence 30,00 20,00 10,00 0,00 -10,00 -20,00 -30,00 -0,05 0,00 0,05 0,10 0,15 0,20 0,25 Pre/postop IPL I-III difference (ms) 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 Microvascular compression Peak II amplitude decrease Dysfunction focal demyelination Tinnitus prolongation IPL I-IIIi Hearing loss at tinnitus frequency Ephaptic transmission Compensation Chronic ectopic excitation Reorganisation cochlear nucleus Colliculus inferior Verlenging IPL III-Vc Improved symmetrical signal transmission 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 Compensation in brainstem IPL I-III IPL I-III+ PEAK II IPL I-V IPL III-V M SD M SD M SD M SD Preoperative Ipsilateral Contralateral 2.58 2.11 .32 .11 3.58 3.03 .31 .27 4.44 4.36 .15 .34 1.80 2.05 .18 .14 Post-operative Ipsilateral Contralateral 2.47 2.11 .06 .13 3.13 3.35 .51 .34 4.39 4.07 .12 .09 1.91 1.90 .17 .09 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 Microvascular compression Peak II amplitude decrease Dysfunction focal demyelination Tinnitus prolongation IPL I-IIIi Hearing loss at tinnitus frequency Ephaptic transmission Compensation Chronic ectopic excitation Reorganisation cochlear nucleus Colliculus inferior Verlenging IPL III-Vc Improved symmetrical signal transmission De Ridder 2012 Summary De Ridder 2012 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 www.brai²n.org Importance of REZ ? Compression anywhere along cranial nerve, but especially anywhere along CNS segment 1. 2. 3. 4. Histological arguments Neurophysiological arguments Epidemiological arguments Clinical experience Importance of REZ ? 1. Histological arguments 1. 2. 3. 4. CNS segment has no endo-, peri- or epineurium Nerves do not divide nor branch, so they do not form a funicular plexus Nerves do not undulate, so have less elasticity 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 CVCS 1. 2. 3. IPL I-III increase (66%) not specific enough wave II disappearance (57%) second most frequent anomaly (Schwaber 1992) Rat experiments by Möller I II III Importance of REZ ? 3. Epidemiological argument 3 distance to REZ the longer the CNS segment the higher the incidence of MVC 5 4,5 4 3,5 3 2,5 2 2,5 2 1,5 1 1,5 1 0,5 incidence 3,5 0,5 0 0 trigeminal facial glossopharyngeal De Ridder 2002 Skinner 1931 Tarlov 1937 8 6 4 2 so ph ar yn ge al glo s fac ial ina l 0 * In some series upto 73% of CVCS had a preop diagnosis of Ménière (Ryu, 1998) incidence 10 ge m Ménière has an incidence of 15.3/100.000 i.e. 1/3 of Ménière’s disease might be CVCS* 12 tri 5-7/100.000 ? 9 8 7 6 5 4 3 2 1 0 co ch lea ris Expected incidence of CVCS ? distance to REZ Importance of REZ ? Importance of REZ ? At proximal segment 4. Clinical experience Decompression along CNS segment results in good outcome (not only at REZ) Sometimes even at peripheral segment REZ n. VIII At distal segment REZ n. VII MVC location & clinical picture www.brai²n.be MVC location and tinnitus type Vascular compression At CNS segment can result in nonpulsatile tinnitus (Moller 1993, De Ridder 2004) At PNS segment can result in pulsatile tinnitus (Nowe 2005, De Ridder 2005) or typewriter tinnitus (Levine 2006) Intrameatal loop 42 50 40 30 20 10 15 2 4 0 pulsatile tinnitus non-pulsatile tinnitus 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) Non-pulsatile tinnitus www.brai²n.be 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 distress Poor correlation between tinnitus matched sound intensity and tinnitus related distress (Moller 1994) Correlation between VAS and TQ is nonlinear (unpublished Vanneste) INTRAMEATAL VASCULAR COMPRESSION 1. Typewriter tinnitus www.brai²n.be INTRAMEATAL VASCULAR COMPRESSION 2. Pulsatile tinnitus www.brai²n.be 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 tinnitus Venous 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 tinnitus Intermittent Cause = 1. MVC ? (crowding posterior fossa) 2. brainstem traction ? BAEP changes in 75 % 100 % III-V prolongation 36 % I-III prolongation June 13-16, 2012 BRUGES http://www.brai2n.com/tri2012 Anatomy of Cranial Nerve Cranial nerve consists of two kinds of tissue Nervous tissue Supporting tissue different for central and peripheral segments Peripheral Segment Nervous tissue PNS 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 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 48 49 56 63 48 64 63 64 46 45 55 72 40 44 62 48 60 65 48 40 F M F M F F M M M F M M F F F M F F M F 15 3 9 2 2 4 4 3 14 7 2 11 2 5 4 5 2 3 1 11 VAS Preoperative 8 8 7 9 7 7 9 5 9 10 8 10 7 7 8 10 7 8 4 8 TQ Postoperative 8 7 10 8 7 4 9 6 7 10 3 10 1 5 7 10 7 4 4 6 Preoperative 29 63 52 46 71 73 29 33 63 59 77 77 44 37 49 Postoperative 36 54 73 59 58 69 70 35 25 57 55 63 11 63 54 66 63 16 De Ridder 2010 5% cured, 45% improved No improvement after 4 years ! Tinnitus intensity improves little Tinnitus distress not
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