Is the Root Entry/Exit Zone Important in Microvascular Compression Syndromes?

Ridder, Dirk De; Møller, Aage R.; Verlooy, Jan; Cornelissen, Maria; Ridder, Leo De

doi:10.1097/00006123-200208000-00023

Cited by 135 publications

(106 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…This corresponds to the first 15 mm after the nerve exit [21]. Potential causes for nerve injury are focal irritation by a blood vessel [2,3,5,12,16,23,32,39], tumor or cyst [1,24] compression, demyelination, trauma and unidentified causes.…”

Section: Pathophysiology and Etiologymentioning

confidence: 99%

“…This concept was further evaluated -mainly by neurosurgeons -in terms of the pathophysiology, area of compression and treatment by decompression of the eighth nerve [2,12,16,23,32]. In 1984 it was called "disabling positional vertigo" by Jannetta and colleagues [18], from a clinical point of view a heterogeneous syndrome of vertigo with symptoms of various durations (from seconds to days), various characteristic features (spinning vertigo, light-headedness or gait instability without vertigo), and varying accompanying symptoms.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Vestibular paroxysmia: Diagnostic criteria

Strupp¹,

Lopez-Escamez

Kim

et al. 2017

VES

166

105

View full text Add to dashboard Cite

Abstract. This paper describes the diagnostic criteria for vestibular paroxysmia (VP) as defined by the Classification Committee of the Bárány Society. The diagnosis of VP is mainly based on the patient history and requires: A) at least ten attacks of spontaneous spinning or non-spinning vertigo; B) duration less than 1 minute; C) stereotyped phenomenology in a particular patient; D) response to a treatment with carbamazepine/oxcarbazepine; and F) not better accounted for by another diagnosis. Probable VP is defined as follows: A) at least five attacks of spinning or non-spinning vertigo; B) duration less than 5 minutes; C) spontaneous occurrence or provoked by certain head-movements; D) stereotyped phenomenology in a particular patient; E) not better accounted for by another diagnosis.Ephaptic discharges in the proximal part of the 8th cranial nerve, which is covered by oligodendrocytes, are the assumed mechanism. Important differential diagnoses are Menière's disease, vestibular migraine, benign paroxysmal positional vertigo, epileptic vestibular aura, paroxysmal brainstem attacks (in multiple sclerosis or after brainstem stroke), superior canal dehiscence syndrome, perilymph fistula, transient ischemic attacks and panic attacks. Current areas of uncertainty in the diagnosis of VP are: a) MRI findings of vascular compression which are not diagnostic of the disease or predictive for the affected side because they are also observed in about 30% of healthy asymptomatic subjects; and b) response to treatment with carbamazepine/oxcarbazepine supports the diagnosis but there are so far no randomized controlled trials for treatment of VP.

show abstract

Section: Pathophysiology and Etiologymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Vestibular paroxysmia: Diagnostic criteria

Strupp¹,

Lopez-Escamez

Kim

et al. 2017

VES

166

105

View full text Add to dashboard Cite

show abstract

“…Wuertenberger i saradnici [19] zaključuju da vertigo može biti uzrokovan venskom mikrovaskularnom kompresijom na n. VIII u unutrašnjem slušnom hodniku i da može biti tretirana mikrovaskularnom dekompresijom. De Ridder i saradnici [20] tvrde da vaskularni kompresivni sindrom započinje pri vaskularnom kontaktu duž CNS segmenta kranijalnog nerva, dok su periferni segmenti više rezistentni na kompresiju, što potvrđuje i Reisser [21] u svojim radovima. Potvrđeno je i da tranzitorni region nerva, Obersteiner-Redlich-ova zona, prelaz iz perifernog u dio CNS segment, kao i mijelinska ovojnica proksimalnog centralnog dijela u odnosu na ovojnicu perifernog dijela vrlo osjetljiva zona na vaskularnu kompresiju [10], da adherencija krvnih sudova za akson u ovoj zoni mogu uzrokovati demijelinizaciju neuroleme, i prateće lezije nerva [15].…”

Section: Diskusijaunclassified

Morfološka i topografska analiza krvnih sudova cisternalnog segmenta vestibulokohlearnog nerva

Bućma

Krivokuća

Sladojević

et al. 2011

Biomedicinska istraž.

View full text Add to dashboard Cite

Uvod. Kompresija nerava od strane krvnih sudova u pontocerebelarnom uglu može uzrokovati funkcionalne promjene ovih nerava. Radikularni, cisternalni dio vestibulokohlearnog nerva (n.VIII) ishranjuju grančice a. cerebelli anterior inferior (AICA).Metode. Istraživanja su vršena na 40 mozgova odraslih lica, oba pola, dobi od 21 do 78 godina. Po završetku fiksiranja vršeno je fino preparisanje struktura pontocerebelarnog ugla, a zatim evidentiranje varijacija i odnosa krvnih sudova i nerava.Rezultati. AICA je u 17% desno i 6% lijevo bila dvostruka. Hipoplastična AICA je češće viđena na lijevoj strani (30 %). Odnos sa n. abducens-om (n.VI) je ostvarivala češće sa lijeve strane, a sa n. facialis-om (n.VII) i n.VIII češće desno. AICA je u 22% desno i u 30% lijevo pravila omču oko n.VIII. Kada je riječ o odnosu bočnih grana AICA i n.VIII, najčešće su druga desna (45 % slučajeva) i druga lijeva (35 % slučajeva) grana imale blizak odnos sa pomenutim nervom Zaključak. Iako postoji čest nalaz bliskog odnosa n.VIII i krvnih sudova, vrlo su oprečni stavovi o postojanju vaskularnog kompresivnog sindroma, dok jedni autori smatraju da je to normalan anatomski nalaz, drugi potvrđuju svojim radovima postojanje istog. Ključne riječi: vestibulokohlearni živac, krvni sudovi, pontocerebelarni ugao UvodKompresija kranijalnih nerava krvnim sudovima u pontocerebelarnom uglu može da uzrokuje funkcionalne promjene ovih nerava. Mikrovaskularna dekompresija je metoda izbora u medikamentozno rezistentnim slučajevima ovog sindroma. Hirurzi su u toku dugogodišnjeg rada prikazali nalaze bliskog kontakta krvnih sudova i kranijalnih nerava u praktično skoro svim slučajevima trigeminalne neuralgije ili hemifacijalnog spazma. Postoje naznake da kompresija n. vestibulocochlearis-a (n. VIII) od strane vaskularnih petlji a. cerebelli anterior inferior (AICA) može biti uzrok nastanka simptoma tipa gubitka sluha, tinitusa i vestibularnih simptoma, ali je

show abstract

“…The length of the CNS segment of the trigeminal nerve is longer than that of the facial nerve [39][40][41][42]71) . Assuming that the CNS segment of cranial nerves is more vulnerable to microtrauma than the PNS segment, more people would be expected to have trigeminal neuralgia 36) than hemifacial spasm 3,14) . This study was inconsistent with Jannetta's 14) .…”

Section: Pathophysiologymentioning

confidence: 99%

“…Assuming that the CNS segment of cranial nerves is more vulnerable to microtrauma than the PNS segment, more people would be expected to have trigeminal neuralgia 36) than hemifacial spasm 3,14) . This study was inconsistent with Jannetta's 14) . Consequently, the authors hypothesized that the site for a vascular compression to become symptomatic should be at the CNS segment and not only at the REZ.…”

Section: Pathophysiologymentioning

confidence: 99%

Hemifacial Spasm: A Neurosurgical Perspective

Kong

Park

2007

J Korean Neurosurg Soc

View full text Add to dashboard Cite

Hemifacial spasm (HFS) is characterized by tonic clonic contractions of the muscles innervated by the ipsilateral facial nerve. Compression of the facial nerve by an ectatic vessel is widely recognized as the most common underlying etiology. HFS needs to be differentiated from other causes of facial spasms, such as facial tic, ocular myokymia, and blepharospasm. To understand the overall craniofacial abnormalities and to perform the optimal surgical procedures for HFS, we are to review the prevalence, pathophysiology, differential diagnosis, details of each treatment modality, usefulness of brainstem auditory evoked potentials monitoring, debates on the facial EMG, clinical course, and complications from the literature published from 1995 to the present time.

show abstract

Is the Root Entry/Exit Zone Important in Microvascular Compression Syndromes?

Abstract: The evidence we present supports the hypothesis that vascular compression syndromes arise from vascular contact along the CNS segment of the cranial nerves.

Cited by 135 publications

References 30 publications

Vestibular paroxysmia: Diagnostic criteria

Vestibular paroxysmia: Diagnostic criteria

Morfološka i topografska analiza krvnih sudova cisternalnog segmenta vestibulokohlearnog nerva

Hemifacial Spasm: A Neurosurgical Perspective

Contact Info

Product

Resources

About