Neurovaskularna kompresija (konflikt)

Since Dandy first reported vascular compression of the trigeminal nerve, the concept of neurovascular compression syndrome for trigeminal neuralgia and hemifacial spasm (HFS) has been accepted, and neurovascular decompression has been performed for this condition. The further investigations indicate...

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Veröffentlicht in:Acta chirurgica Iugoslavica 2008, Vol.55 (2), p.161-168
Hauptverfasser: Slavik, E.E., Djurovic, B.M., Radulovic, D.V., Jokovic, M.B., Rakic, M.Lj, Rasulic, L.G., Tasic, G.M., Nikolic, I.M.
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container_issue 2
container_start_page 161
container_title Acta chirurgica Iugoslavica
container_volume 55
creator Slavik, E.E.
Djurovic, B.M.
Radulovic, D.V.
Jokovic, M.B.
Rakic, M.Lj
Rasulic, L.G.
Tasic, G.M.
Nikolic, I.M.
description Since Dandy first reported vascular compression of the trigeminal nerve, the concept of neurovascular compression syndrome for trigeminal neuralgia and hemifacial spasm (HFS) has been accepted, and neurovascular decompression has been performed for this condition. The further investigations indicated that some other clinical syndromes such as glossopharyngeal neuralgia, disabling positional vertigo, tinnitus, geniculate neuarlgia, spasmodic torticolis, essential hypertension, cyclic oculomotor spasm with paresis and superior oblique myokymia also may be initiated by vascular compression of the glosopharyngeal, cochleovestibular, intermediate, accessory, oculomotor and trochlear nerves or the ventrolateral medulla oblongata. In this study several hypotheses regarding the development of cranial nerves vascular compression syndromes are presented. It is also emphasized the value of high-resolution magnetic resonance tomographic angiography for visualization of vascular compression. The most frequent clinical syndromes caused by vascular compression of the cranial nerves are discussed regarding the pathogenesis, symptoms and therapy. We present our series of 124 patients with preoperative evidently positive finding of vascular compression to the trigeminal nerve (MRI). Microvascular decompression (MVD)was performed in all of them. Initial postoperative result was excellent in 110/124 (89%) patients, while in 11/124 (9%) patients the pain relief was satisfactory. In the remaining three patients MVD failed. Recurrence of pain after two years reached 19 %. Complications were related to diplopia associated with transient fourth nerve dysfunction in 5 (4%) patients, facial motor dysfunction in 4 (3%) patients, transient facial hypesthesia in 27 (22%) patients and partially hearing loss in 4 (3%) patients. Cerebellar hemorrhagic infarction occurred in 1 ( 0,8 %) patient and cerebrospinal fluid leaks appeared in two (1,6%) cases. There was no lethal outcome. Od prvog Dendijevog saopstenja o vaskularnoj kompresiji trigeminalnog nerva, koncept sindroma neurovaskularne kompresije kod nerualgije trigeminusa i hemifacijalnog spazma je bio prihvacen. Kasnija istrazivanja su ukazala da neki drugi sindromi poput glosofaringealne neuralgije, tinitusa, genukulatne neuralgije, spasticnog tortikolisa, esencijalne hipertenzije i dr. mogu biti uzrokovani vaskularnom kompresijom glosofaringealno, vestibulokohlearnog, akcesornog, okulomotornog ili trohlearnog nerva ili vetnrolateral
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The further investigations indicated that some other clinical syndromes such as glossopharyngeal neuralgia, disabling positional vertigo, tinnitus, geniculate neuarlgia, spasmodic torticolis, essential hypertension, cyclic oculomotor spasm with paresis and superior oblique myokymia also may be initiated by vascular compression of the glosopharyngeal, cochleovestibular, intermediate, accessory, oculomotor and trochlear nerves or the ventrolateral medulla oblongata. In this study several hypotheses regarding the development of cranial nerves vascular compression syndromes are presented. It is also emphasized the value of high-resolution magnetic resonance tomographic angiography for visualization of vascular compression. The most frequent clinical syndromes caused by vascular compression of the cranial nerves are discussed regarding the pathogenesis, symptoms and therapy. We present our series of 124 patients with preoperative evidently positive finding of vascular compression to the trigeminal nerve (MRI). Microvascular decompression (MVD)was performed in all of them. Initial postoperative result was excellent in 110/124 (89%) patients, while in 11/124 (9%) patients the pain relief was satisfactory. In the remaining three patients MVD failed. Recurrence of pain after two years reached 19 %. Complications were related to diplopia associated with transient fourth nerve dysfunction in 5 (4%) patients, facial motor dysfunction in 4 (3%) patients, transient facial hypesthesia in 27 (22%) patients and partially hearing loss in 4 (3%) patients. Cerebellar hemorrhagic infarction occurred in 1 ( 0,8 %) patient and cerebrospinal fluid leaks appeared in two (1,6%) cases. There was no lethal outcome. Od prvog Dendijevog saopstenja o vaskularnoj kompresiji trigeminalnog nerva, koncept sindroma neurovaskularne kompresije kod nerualgije trigeminusa i hemifacijalnog spazma je bio prihvacen. Kasnija istrazivanja su ukazala da neki drugi sindromi poput glosofaringealne neuralgije, tinitusa, genukulatne neuralgije, spasticnog tortikolisa, esencijalne hipertenzije i dr. mogu biti uzrokovani vaskularnom kompresijom glosofaringealno, vestibulokohlearnog, akcesornog, okulomotornog ili trohlearnog nerva ili vetnrolateralne produzene mozdine. Prikazujemo seriju od 124 bolesnika sa preoperativnim evidentnim nalazom vaskularne kompresije trigeminalnog nerva. Mikrovaskularna dekompresija je uradjena kod svih bolesnika. Inicijalno postoperativni nalaz je bio odlican kod 110 od 124 bolesnika. Ponovni bol se javio nakon dve godine kod 19% bolesnika. Komplikacije u vidu diplopije sa tranzijentnom disfunkcijom n. IV javile su se kod 5 bolesnika, facijalna motorna disfunkcija kod 4, tranzientna facijalna hipestezija kod 27 i kod 4 parcijalna slabost sluha. Kod jednog bolesnika vidjena je postoperativno cerebelarna hemoragicna infarkcija. 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The further investigations indicated that some other clinical syndromes such as glossopharyngeal neuralgia, disabling positional vertigo, tinnitus, geniculate neuarlgia, spasmodic torticolis, essential hypertension, cyclic oculomotor spasm with paresis and superior oblique myokymia also may be initiated by vascular compression of the glosopharyngeal, cochleovestibular, intermediate, accessory, oculomotor and trochlear nerves or the ventrolateral medulla oblongata. In this study several hypotheses regarding the development of cranial nerves vascular compression syndromes are presented. It is also emphasized the value of high-resolution magnetic resonance tomographic angiography for visualization of vascular compression. The most frequent clinical syndromes caused by vascular compression of the cranial nerves are discussed regarding the pathogenesis, symptoms and therapy. We present our series of 124 patients with preoperative evidently positive finding of vascular compression to the trigeminal nerve (MRI). Microvascular decompression (MVD)was performed in all of them. Initial postoperative result was excellent in 110/124 (89%) patients, while in 11/124 (9%) patients the pain relief was satisfactory. In the remaining three patients MVD failed. Recurrence of pain after two years reached 19 %. Complications were related to diplopia associated with transient fourth nerve dysfunction in 5 (4%) patients, facial motor dysfunction in 4 (3%) patients, transient facial hypesthesia in 27 (22%) patients and partially hearing loss in 4 (3%) patients. Cerebellar hemorrhagic infarction occurred in 1 ( 0,8 %) patient and cerebrospinal fluid leaks appeared in two (1,6%) cases. There was no lethal outcome. Od prvog Dendijevog saopstenja o vaskularnoj kompresiji trigeminalnog nerva, koncept sindroma neurovaskularne kompresije kod nerualgije trigeminusa i hemifacijalnog spazma je bio prihvacen. Kasnija istrazivanja su ukazala da neki drugi sindromi poput glosofaringealne neuralgije, tinitusa, genukulatne neuralgije, spasticnog tortikolisa, esencijalne hipertenzije i dr. mogu biti uzrokovani vaskularnom kompresijom glosofaringealno, vestibulokohlearnog, akcesornog, okulomotornog ili trohlearnog nerva ili vetnrolateralne produzene mozdine. Prikazujemo seriju od 124 bolesnika sa preoperativnim evidentnim nalazom vaskularne kompresije trigeminalnog nerva. Mikrovaskularna dekompresija je uradjena kod svih bolesnika. Inicijalno postoperativni nalaz je bio odlican kod 110 od 124 bolesnika. Ponovni bol se javio nakon dve godine kod 19% bolesnika. Komplikacije u vidu diplopije sa tranzijentnom disfunkcijom n. IV javile su se kod 5 bolesnika, facijalna motorna disfunkcija kod 4, tranzientna facijalna hipestezija kod 27 i kod 4 parcijalna slabost sluha. Kod jednog bolesnika vidjena je postoperativno cerebelarna hemoragicna infarkcija. 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The further investigations indicated that some other clinical syndromes such as glossopharyngeal neuralgia, disabling positional vertigo, tinnitus, geniculate neuarlgia, spasmodic torticolis, essential hypertension, cyclic oculomotor spasm with paresis and superior oblique myokymia also may be initiated by vascular compression of the glosopharyngeal, cochleovestibular, intermediate, accessory, oculomotor and trochlear nerves or the ventrolateral medulla oblongata. In this study several hypotheses regarding the development of cranial nerves vascular compression syndromes are presented. It is also emphasized the value of high-resolution magnetic resonance tomographic angiography for visualization of vascular compression. The most frequent clinical syndromes caused by vascular compression of the cranial nerves are discussed regarding the pathogenesis, symptoms and therapy. We present our series of 124 patients with preoperative evidently positive finding of vascular compression to the trigeminal nerve (MRI). Microvascular decompression (MVD)was performed in all of them. Initial postoperative result was excellent in 110/124 (89%) patients, while in 11/124 (9%) patients the pain relief was satisfactory. In the remaining three patients MVD failed. Recurrence of pain after two years reached 19 %. Complications were related to diplopia associated with transient fourth nerve dysfunction in 5 (4%) patients, facial motor dysfunction in 4 (3%) patients, transient facial hypesthesia in 27 (22%) patients and partially hearing loss in 4 (3%) patients. Cerebellar hemorrhagic infarction occurred in 1 ( 0,8 %) patient and cerebrospinal fluid leaks appeared in two (1,6%) cases. There was no lethal outcome. Od prvog Dendijevog saopstenja o vaskularnoj kompresiji trigeminalnog nerva, koncept sindroma neurovaskularne kompresije kod nerualgije trigeminusa i hemifacijalnog spazma je bio prihvacen. Kasnija istrazivanja su ukazala da neki drugi sindromi poput glosofaringealne neuralgije, tinitusa, genukulatne neuralgije, spasticnog tortikolisa, esencijalne hipertenzije i dr. mogu biti uzrokovani vaskularnom kompresijom glosofaringealno, vestibulokohlearnog, akcesornog, okulomotornog ili trohlearnog nerva ili vetnrolateralne produzene mozdine. Prikazujemo seriju od 124 bolesnika sa preoperativnim evidentnim nalazom vaskularne kompresije trigeminalnog nerva. Mikrovaskularna dekompresija je uradjena kod svih bolesnika. Inicijalno postoperativni nalaz je bio odlican kod 110 od 124 bolesnika. Ponovni bol se javio nakon dve godine kod 19% bolesnika. Komplikacije u vidu diplopije sa tranzijentnom disfunkcijom n. IV javile su se kod 5 bolesnika, facijalna motorna disfunkcija kod 4, tranzientna facijalna hipestezija kod 27 i kod 4 parcijalna slabost sluha. Kod jednog bolesnika vidjena je postoperativno cerebelarna hemoragicna infarkcija. Nije bilo smrtnog ishoda.</abstract><doi>10.2298/ACI0802161S</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record>
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title Neurovaskularna kompresija (konflikt)
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