Increased incidence of jugular valve insufficiency in patients with transient global amnesia

Nedelmann, Max; Eicke, B. Martin; Dieterich, Marianne

doi:10.1007/s00415-005-0894-9

Cited by 60 publications

(47 citation statements)

References 21 publications

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“…7 Several mechanisms have been proposed to explain TGA, such as focal arterial ischemia, migraine, epilepsy, and retrograde cerebral venous congestion, 8,9 due to a venous reflux during Valsalva-like activities before symptom onset. [10][11][12][13][14][15] With regard to the first hypothesis, studies have shown that patients with TGA have fewer risk factors for thromboembolic disease than patients with transient ischemic attacks (TIAs); moreover, in patients with TGA the recurrence rate is much lower (usually a single event) and the prognosis for vascular events and mortality is significantly better than in patients with TIAs. 16,17 These findings suggest that arterial thromboembolic disease is an Copyright • C 2014 by the American Society of Neuroimaging 1 unlikely explanation for TGA.…”

Section: Introductionmentioning

confidence: 99%

No Signs of Intracranial Arterial Vasoconstriction in Transient Global Amnesia

Baracchini

Farina

Ballotta

et al. 2014

Journal of Neuroimaging

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Section: Introductionmentioning

confidence: 99%

No Signs of Intracranial Arterial Vasoconstriction in Transient Global Amnesia

Baracchini

Farina

Ballotta

et al. 2014

Journal of Neuroimaging

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“…The mean duration of the insufficiency jet was the same although patients with a trigger for their global amnesia had longer insufficiency (3.84 sec) than those without triggers (2.55 sec). 85 It remains a matter of debate as to whether the evidence regarding IJV incompetence is circumstantial or definitive in proving the etiology of this syndrome. 86 Occlusion of the jugular bulb catheter after extracorporeal membrane oxygenation resulted in reduced superior sagittal sinus blood flow velocities.…”

Section: Venous Hypertension and Flow Reversals From Nonmultiple Sclementioning

confidence: 99%

Multiple Sclerosis - A Vascular Etiology?

Weir

2010

Can. j. neurol. sci.

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There has been a recent resurgence of interest in the possibility that cerebrospinal venous outflow obstruction, venous hypertension, development of collateral channels and flow reversal might be the primary inciting factor(s) for multiple sclerosis (MS). 1 The evidence should be considered bearing in mind Hill's criteria for causation as outlined by Giovannoni and Cutter: consistency and unbiasedness of findings, strength of association, temporal sequence, biological gradient, specificity, coherence of biological background and previous knowledge, biological plausibility, reasoning by analogy and experimental evidence.2 At the present state of our knowledge, despite monumental efforts, the cause is unknown. Anatomy Of Venous Outflow From The Brain And Spinal CordCapillaries drain into venules (10 -20 µ) that combine, almost at right angles to form larger venules within the grey matter. At a size of 50 -100 µ the venules lead on to the cortical surface at right angles to it. At the surface they combine in a two dimensional network. The craniospinal venous system is valveless and consists of veins and plexuses whose flow is potentially bidirectional. The superior cortical cerebral veins drain rostrally into the superior sagittal sinus. The inferior lateral ABSTRACT: From the earliest pathological studies the perivenular localization of the demyelination in multiple sclerosis (MS) has been observed. It has recently been suggested that obstructions to venous flow or inadequate venous valves in the great veins in the neck, thorax and abdomen can cause damaging backflow into the cerebral and spinal cord circulations. Paolo Zamboni and colleagues have demonstrated abnormal venous circulation in some multiple sclerosis patients using non-invasive sonography and invasive venography. Furthermore, they have obtained apparent clinical improvement or stabilization by endovascular ballooning of points of obstruction in the great veins in some, at least temporarily. If non-invasive observations by others validate their initial observations of a significantly increased prevalence of venous obstructions in MS then trials of angioplasty/stenting would be justified in selected cases in view of the biological plausibility of the concept.RÉSUMÉ: Étiologie vasculaire de la sclérose en plaques. La localisation périveineuse de la démyélinisation a été observée dès les premières études anatomopathologiques sur la sclérose en plaques (SP). L'obstruction du flux veineux ou la présence de valves veineuses inadéquates dans les grandes veines du cou, du thorax et de l'abdomen pourraient causer un reflux dommageable à la circulation cérébrale et la moelle épinière selon une hypothèse récente. Paolo Zamboni et ses collègues ont démontré la présence d'une circulation veineuse anormale chez certains patients atteints de SP au moyen l'échographie non effractive et de la veinographie effractive. De plus ils auraient obtenu une amélioration clinique ou une stabilisation de l'état des patients par dilatation endovasculaire de points d'obstruction d...

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“…The presence of jugular valve incompetence (JVI) has been demonstrated to be strongly associated with transient global amnesia (TGA) [1]. In previous studies, JVI (left-sided, right-sided or bilateral) has been identified in up to 85% of patients with TGA, compared to 45% of the controls [1,2].…”

Section: Introductionmentioning

confidence: 99%

“…In previous studies, JVI (left-sided, right-sided or bilateral) has been identified in up to 85% of patients with TGA, compared to 45% of the controls [1,2]. Whether the presence of JVI might represent a specific, underscored, pathogenetic mechanism needs to be clarified.…”

Section: Introductionmentioning

confidence: 99%

Cerebrovascular Risk Factors and Triggers in Transient Global Amnesia Patients with and without Jugular Valve Incompetence: Results from a Sample of 243 Patients

Agosti

Borroni

Akkawi³

et al. 2010

Eur Neurol

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Background/Aims: Different etiologies for transient global amnesia (TGA) have been proposed, such as venous flow abnormalities, spreading depression and migraine-related mechanisms like focal ischemia. Jugular vein valve incompetence (JVI) is commonly described in TGA patients, but its contributing role in TGA pathogenesis is still unknown. We investigated the possible relationship between JVI and pathogenetic mechanisms in TGA. Methods: 243 TGA patients underwent clinical and neurological assessment. Demographic characteristics, TGA-precipitating factors and vascular comorbidities were carefully recorded. In each patient, JVI was assessed by Doppler ultrasonography. Results: TGA patients were grouped according to the presence (n = 171, 70.4%) or absence (n = 72, 29.6%) of JVI. TGA patients with JVI showed a higher presence of precipitating factors, namely a Valsalva-like maneuver (JVI-positive vs. JVI-negative, 35.8 vs. 17.1%, p = 0.004) and emotional stress (36.6 vs. 21.4%, p = 0.023), but had fewer vascular comorbidities, namely hypertension (37.2 vs. 51.4%, p = 0.047) and carotid arteriosclerosis (20.5 vs. 31.9%, p = 0.050). Conclusions: These findings support the argument for the existence of at least 2 different TGA-associated mechanisms defined by JVI. On the one hand, JVI associated with a Valsalva-like maneuver and emotional stress supported the venous blood congestion hypothesis, and on the other, the JVI-negative group may have another vascular basis, unrelated to venous congestion.

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Increased incidence of jugular valve insufficiency in patients with transient global amnesia

Cited by 60 publications

References 21 publications

No Signs of Intracranial Arterial Vasoconstriction in Transient Global Amnesia

No Signs of Intracranial Arterial Vasoconstriction in Transient Global Amnesia

Multiple Sclerosis - A Vascular Etiology?

Cerebrovascular Risk Factors and Triggers in Transient Global Amnesia Patients with and without Jugular Valve Incompetence: Results from a Sample of 243 Patients

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