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

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.

[1]  J. Bogousslavsky,et al.  ‘Les ictus amnésiques’ and Transient Global Amnesia , 2009, European Neurology.

[2]  B. Desgranges,et al.  What does transient global amnesia really mean? Review of the literature and thorough study of 142 cases. , 2006, Brain : a journal of neurology.

[3]  M. Dieterich,et al.  Increased incidence of jugular valve insufficiency in patients with transient global amnesia , 2005, Journal of Neurology.

[4]  T. Etgen,et al.  DWI in transient global amnesia and TIA: proposal for an ischaemic origin of TGA , 2005, Journal of Neurology, Neurosurgery & Psychiatry.

[5]  A. Gass,et al.  Detection of delayed focal MR changes in the lateral hippocampus in transient global amnesia , 2004, Neurology.

[6]  L. Vignolo,et al.  Transient Global Amnesia: A Clinical and Sonographic Study , 2003, European Neurology.

[7]  G. Anzola,et al.  Transient global amnesia and venous flow patterns , 2001, The Lancet.

[8]  L. Pantoni,et al.  Transient global amnesia: a review emphasizing pathogenic aspects , 2000, Acta neurologica Scandinavica.

[9]  A. Gass,et al.  Lack of evidence of acute ischemic tissue change in transient global amnesia on single-shot echo-planar diffusion-weighted MRI. , 1999, Stroke.

[10]  K. Furie,et al.  Diffusion-weighted MRI characterizes the ischemic lesion in transient global amnesia , 1998, Neurology.

[11]  S. Lewis Aetiology of transient global amnesia , 1998, The Lancet.

[12]  M. Reiser,et al.  Diffusion‐weighted MRI in transient global amnesia: Elevated signal intensity in the left mesial temporal lobe in 7 of 10 patients , 1998, Annals of neurology.

[13]  S. Taki,et al.  Changes in cerebral blood flow and vasoreactivity in response to acetazolamide in patients with transient global amnesia , 1997, Journal of neurology, neurosurgery, and psychiatry.

[14]  A. Norbash,et al.  Diffusion-weighted MRI in transient global amnesia precipitated by cerebral angiography. , 1997, Stroke.

[15]  J. Hodges,et al.  Syndromes of transient amnesia: towards a classification. A study of 153 cases. , 1990, Journal of neurology, neurosurgery, and psychiatry.

[16]  M. Riepe,et al.  Transient Global Amnesia. Evidence against vascular ischemic etiology from diffusion weighted imaging. , 2002, Journal of neurology.