Sigmoid Sinus Diverticulum, Dehiscence, and Venous Sinus Stenosis: Potential Causes of Pulsatile Tinnitus in Patients with Idiopathic Intracranial Hypertension?
Pulsatile tinnitus is experienced by most patients with idiopathic intracranial hypertension. The pathophysiology remains uncertain; however, transverse sinus stenosis and sigmoid sinus diverticulum/dehiscence have been proposed as potential etiologies. We aimed to determine whether the prevalence o...
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Published in | American journal of neuroradiology : AJNR Vol. 38; no. 9; pp. 1783 - 1788 |
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01.09.2017
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Abstract | Pulsatile tinnitus is experienced by most patients with idiopathic intracranial hypertension. The pathophysiology remains uncertain; however, transverse sinus stenosis and sigmoid sinus diverticulum/dehiscence have been proposed as potential etiologies. We aimed to determine whether the prevalence of transverse sinus stenosis and sigmoid sinus diverticulum/dehiscence was increased in patients with idiopathic intracranial hypertension and pulsatile tinnitus relative to those without pulsatile tinnitus and a control group.
CT vascular studies of patients with idiopathic intracranial hypertension with pulsatile tinnitus (
= 42), without pulsatile tinnitus (
= 37), and controls (
= 75) were independently reviewed for the presence of severe transverse sinus stenosis and sigmoid sinus diverticulum/dehiscence according to published criteria. The prevalence of transverse sinus stenosis and sigmoid sinus diverticulum/dehiscence in patients with idiopathic intracranial hypertension with pulsatile tinnitus was compared with that in the nonpulsatile tinnitus idiopathic intracranial hypertension group and the control group. Further comparisons included differing degrees of transverse sinus stenosis (50% and 75%), laterality of transverse sinus stenosis/sigmoid sinus diverticulum/dehiscence, and ipsilateral transverse sinus stenosis combined with sigmoid sinus diverticulum/dehiscence.
Severe bilateral transverse sinus stenoses were more frequent in patients with idiopathic intracranial hypertension than in controls (
< .001), but there was no significant association between transverse sinus stenosis and pulsatile tinnitus within the idiopathic intracranial hypertension group. Sigmoid sinus dehiscence (right- or left-sided) was also more common in patients with idiopathic intracranial hypertension compared with controls (
= .01), but there was no significant association with pulsatile tinnitus within the idiopathic intracranial hypertension group.
While our data corroborate previous studies demonstrating increased prevalence of sigmoid sinus diverticulum/dehiscence and transverse sinus stenosis in idiopathic intracranial hypertension, we did not establish an increased prevalence in patients with idiopathic intracranial hypertension with pulsatile tinnitus compared with those without. It is therefore unlikely that these entities represent a direct structural correlate of pulsatile tinnitus in patients with idiopathic intracranial hypertension. |
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AbstractList | BACKGROUND AND PURPOSEPulsatile tinnitus is experienced by most patients with idiopathic intracranial hypertension. The pathophysiology remains uncertain; however, transverse sinus stenosis and sigmoid sinus diverticulum/dehiscence have been proposed as potential etiologies. We aimed to determine whether the prevalence of transverse sinus stenosis and sigmoid sinus diverticulum/dehiscence was increased in patients with idiopathic intracranial hypertension and pulsatile tinnitus relative to those without pulsatile tinnitus and a control group. MATERIALS AND METHODSCT vascular studies of patients with idiopathic intracranial hypertension with pulsatile tinnitus (n = 42), without pulsatile tinnitus (n = 37), and controls (n = 75) were independently reviewed for the presence of severe transverse sinus stenosis and sigmoid sinus diverticulum/dehiscence according to published criteria. The prevalence of transverse sinus stenosis and sigmoid sinus diverticulum/dehiscence in patients with idiopathic intracranial hypertension with pulsatile tinnitus was compared with that in the nonpulsatile tinnitus idiopathic intracranial hypertension group and the control group. Further comparisons included differing degrees of transverse sinus stenosis (50% and 75%), laterality of transverse sinus stenosis/sigmoid sinus diverticulum/dehiscence, and ipsilateral transverse sinus stenosis combined with sigmoid sinus diverticulum/dehiscence. RESULTSSevere bilateral transverse sinus stenoses were more frequent in patients with idiopathic intracranial hypertension than in controls (P < .001), but there was no significant association between transverse sinus stenosis and pulsatile tinnitus within the idiopathic intracranial hypertension group. Sigmoid sinus dehiscence (right- or left-sided) was also more common in patients with idiopathic intracranial hypertension compared with controls (P = .01), but there was no significant association with pulsatile tinnitus within the idiopathic intracranial hypertension group. CONCLUSIONSWhile our data corroborate previous studies demonstrating increased prevalence of sigmoid sinus diverticulum/dehiscence and transverse sinus stenosis in idiopathic intracranial hypertension, we did not establish an increased prevalence in patients with idiopathic intracranial hypertension with pulsatile tinnitus compared with those without. It is therefore unlikely that these entities represent a direct structural correlate of pulsatile tinnitus in patients with idiopathic intracranial hypertension. BACKGROUND AND PURPOSE:Pulsatile tinnitus is experienced by most patients with idiopathic intracranial hypertension. The pathophysiology remains uncertain; however, transverse sinus stenosis and sigmoid sinus diverticulum/dehiscence have been proposed as potential etiologies. We aimed to determine whether the prevalence of transverse sinus stenosis and sigmoid sinus diverticulum/dehiscence was increased in patients with idiopathic intracranial hypertension and pulsatile tinnitus relative to those without pulsatile tinnitus and a control group.MATERIALS AND METHODS:CT vascular studies of patients with idiopathic intracranial hypertension with pulsatile tinnitus (n = 42), without pulsatile tinnitus (n = 37), and controls (n = 75) were independently reviewed for the presence of severe transverse sinus stenosis and sigmoid sinus diverticulum/dehiscence according to published criteria. The prevalence of transverse sinus stenosis and sigmoid sinus diverticulum/dehiscence in patients with idiopathic intracranial hypertension with pulsatile tinnitus was compared with that in the nonpulsatile tinnitus idiopathic intracranial hypertension group and the control group. Further comparisons included differing degrees of transverse sinus stenosis (50% and 75%), laterality of transverse sinus stenosis/sigmoid sinus diverticulum/dehiscence, and ipsilateral transverse sinus stenosis combined with sigmoid sinus diverticulum/dehiscence.RESULTS:Severe bilateral transverse sinus stenoses were more frequent in patients with idiopathic intracranial hypertension than in controls (P < .001), but there was no significant association between transverse sinus stenosis and pulsatile tinnitus within the idiopathic intracranial hypertension group. Sigmoid sinus dehiscence (right- or left-sided) was also more common in patients with idiopathic intracranial hypertension compared with controls (P = .01), but there was no significant association with pulsatile tinnitus within the idiopathic intracranial hypertension group.CONCLUSIONS:While our data corroborate previous studies demonstrating increased prevalence of sigmoid sinus diverticulum/dehiscence and transverse sinus stenosis in idiopathic intracranial hypertension, we did not establish an increased prevalence in patients with idiopathic intracranial hypertension with pulsatile tinnitus compared with those without. It is therefore unlikely that these entities represent a direct structural correlate of pulsatile tinnitus in patients with idiopathic intracranial hypertension. Pulsatile tinnitus is experienced by most patients with idiopathic intracranial hypertension. The pathophysiology remains uncertain; however, transverse sinus stenosis and sigmoid sinus diverticulum/dehiscence have been proposed as potential etiologies. We aimed to determine whether the prevalence of transverse sinus stenosis and sigmoid sinus diverticulum/dehiscence was increased in patients with idiopathic intracranial hypertension and pulsatile tinnitus relative to those without pulsatile tinnitus and a control group. CT vascular studies of patients with idiopathic intracranial hypertension with pulsatile tinnitus ( = 42), without pulsatile tinnitus ( = 37), and controls ( = 75) were independently reviewed for the presence of severe transverse sinus stenosis and sigmoid sinus diverticulum/dehiscence according to published criteria. The prevalence of transverse sinus stenosis and sigmoid sinus diverticulum/dehiscence in patients with idiopathic intracranial hypertension with pulsatile tinnitus was compared with that in the nonpulsatile tinnitus idiopathic intracranial hypertension group and the control group. Further comparisons included differing degrees of transverse sinus stenosis (50% and 75%), laterality of transverse sinus stenosis/sigmoid sinus diverticulum/dehiscence, and ipsilateral transverse sinus stenosis combined with sigmoid sinus diverticulum/dehiscence. Severe bilateral transverse sinus stenoses were more frequent in patients with idiopathic intracranial hypertension than in controls ( < .001), but there was no significant association between transverse sinus stenosis and pulsatile tinnitus within the idiopathic intracranial hypertension group. Sigmoid sinus dehiscence (right- or left-sided) was also more common in patients with idiopathic intracranial hypertension compared with controls ( = .01), but there was no significant association with pulsatile tinnitus within the idiopathic intracranial hypertension group. While our data corroborate previous studies demonstrating increased prevalence of sigmoid sinus diverticulum/dehiscence and transverse sinus stenosis in idiopathic intracranial hypertension, we did not establish an increased prevalence in patients with idiopathic intracranial hypertension with pulsatile tinnitus compared with those without. It is therefore unlikely that these entities represent a direct structural correlate of pulsatile tinnitus in patients with idiopathic intracranial hypertension. |
Author | Lansley, J A Riordan-Eva, P Connor, S E J Tucker, W Eriksen, M R |
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References_xml | – volume: 8 start-page: 54 year: 2002 ident: 2018022808151805000_38.9.1783.17 article-title: A new therapeutic procedure for treatment of objective venous pulsatile tinnitus publication-title: Int Tinnitus J contributor: fullname: Sanchez – ident: 2018022808151805000_38.9.1783.27 doi: 10.1136/jnnp.2006.111765 – ident: 2018022808151805000_38.9.1783.15 doi: 10.1007/s00234-015-1517-5 – ident: 2018022808151805000_38.9.1783.19 doi: 10.1097/01.mao.0000247814.85829.f6 – ident: 2018022808151805000_38.9.1783.34 doi: 10.1007/s00276-012-0992-1 – ident: 2018022808151805000_38.9.1783.3 doi: 10.1016/S1474-4422(15)00298-7 – ident: 2018022808151805000_38.9.1783.1 doi: 10.1097/MAO.0b013e3182a4756c – volume: 19 start-page: 472 year: 1998 ident: 2018022808151805000_38.9.1783.4 article-title: Pulsatile tinnitus: a 15-year experience publication-title: Am J Otol contributor: fullname: Sismanis – ident: 2018022808151805000_38.9.1783.21 doi: 10.1212/01.WNL.0000066683.34093.E2 – ident: 2018022808151805000_38.9.1783.31 doi: 10.1007/BF01628311 – ident: 2018022808151805000_38.9.1783.11 doi: 10.1080/00016480701840106 – ident: 2018022808151805000_38.9.1783.33 doi: 10.1001/archotol.126.2.137 – ident: 2018022808151805000_38.9.1783.13 doi: 10.1177/0284185114559762 – ident: 2018022808151805000_38.9.1783.14 doi: 10.1097/MAO.0b013e31829ab6d7 – ident: 2018022808151805000_38.9.1783.24 doi: 10.1136/jnnp.2003.021006 – ident: 2018022808151805000_38.9.1783.2 doi: 10.1155/2012/814696 – ident: 2018022808151805000_38.9.1783.8 doi: 10.3174/ajnr.A2575 – ident: 2018022808151805000_38.9.1783.7 doi: 10.1212/01.wnl.0000299894.30700.d2 – volume: 265 start-page: 123 year: 2008 ident: 2018022808151805000_38.9.1783.30 article-title: Subjective pulsatile tinnitus associated with extensive pneumatization of temporal bone publication-title: Eur Arch Otorhinolaryngol doi: 10.1007/s00405-007-0400-3 contributor: fullname: Topal – ident: 2018022808151805000_38.9.1783.10 doi: 10.1007/s00405-009-0973-0 – volume: 17 start-page: 2 year: 2012 ident: 2018022808151805000_38.9.1783.23 article-title: Brain pulsatility and pulsatile tinnitus: clinical types publication-title: Int Tinnitus J contributor: fullname: Shulman – volume: 97 start-page: 1 issue: 8 pt 2 year: 1987 ident: 2018022808151805000_38.9.1783.28 article-title: Otologic manifestations of benign intracranial hypertension syndrome: diagnosis and management publication-title: Laryngoscope doi: 10.1288/00005537-198708001-00001 contributor: fullname: Sismanis – ident: 2018022808151805000_38.9.1783.18 doi: 10.1097/MAO.0b013e31822a1c7d – volume: 32 start-page: 238 year: 2012 ident: 2018022808151805000_38.9.1783.22 article-title: Bilateral transverse sinus stenosis in patients with tinnitus publication-title: Acta Otorhinolaryngol Ital contributor: fullname: Chiarella – ident: 2018022808151805000_38.9.1783.25 doi: 10.1054/jocn.2001.0986 – ident: 2018022808151805000_38.9.1783.32 doi: 10.3238/arztebl.2013.0451 – ident: 2018022808151805000_38.9.1783.12 doi: 10.1177/0194599813520291 – ident: 2018022808151805000_38.9.1783.9 doi: 10.1097/MOO.0b013e3283493fd8 – ident: 2018022808151805000_38.9.1783.29 doi: 10.1258/ar.2012.110705 – ident: 2018022808151805000_38.9.1783.20 doi: 10.1001/archneur.59.9.1492 – volume: 1 start-page: 127 year: 1995 ident: 2018022808151805000_38.9.1783.6 article-title: Objective pulse-synchronous “essential” tinnitus due to narrowing of the transverse dural venous sinus publication-title: Int Tinnitus J contributor: fullname: Russell – ident: 2018022808151805000_38.9.1783.5 doi: 10.1097/MAO.0b013e3182990d52 – ident: 2018022808151805000_38.9.1783.26 doi: 10.1016/S0140-6736(02)07440-8 – ident: 2018022808151805000_38.9.1783.16 doi: 10.1007/s00330-015-3827-8 |
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Snippet | Pulsatile tinnitus is experienced by most patients with idiopathic intracranial hypertension. The pathophysiology remains uncertain; however, transverse sinus... BACKGROUND AND PURPOSE:Pulsatile tinnitus is experienced by most patients with idiopathic intracranial hypertension. The pathophysiology remains uncertain;... BACKGROUND AND PURPOSEPulsatile tinnitus is experienced by most patients with idiopathic intracranial hypertension. The pathophysiology remains uncertain;... |
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SubjectTerms | Aged Constriction, Pathologic - complications Constriction, Pathologic - epidemiology Control methods Cranial Sinuses - pathology Dehiscence Diverticulum Etiology Female Head & Neck Humans Hypertension Male Middle Aged Patients Pseudotumor Cerebri - complications Pseudotumor Cerebri - pathology Sinus Sinuses Stenosis Tinnitus Tinnitus - etiology |
Title | Sigmoid Sinus Diverticulum, Dehiscence, and Venous Sinus Stenosis: Potential Causes of Pulsatile Tinnitus in Patients with Idiopathic Intracranial Hypertension? |
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