Transient Global Amnesia: Cerebral Venous Outflow Impairment—Insight from the Abnormal Flow Patterns of the Internal Jugular Vein (original) (raw)
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Obstruction of Venous Drainage Linked to Transient Global Amnesia
PloS one, 2015
Abnormal extracranial venous drainage modality has been considered an etiology of transient global amnesia (TGA). Evidence suggests that the transmission of the intrathoracic/intraabdominal pressure during a Valsalva maneuver (VM) is mainly through the vertebral venous system, and patency of internal jugular vein (IJV) is essential for venous drainage and pressure releasing. We hypothesize that obstruction of IJV venous drainage is a contributing factor in TGA pathogenesis. A magnetic resonance (MR) imaging protocol was used in 45 TGA patients and 45 age- and sex-matched controls to assess the morphologies of IJV, brachiocephalic vein (BCV) and asymmetry of transverse sinus (TS). The IJV was divided into the upper- and middle-IJV segments. Compared to the controls, TGA patients had significantly higher rates of moderate and severe compression/stenosis at the bilateral upper-IJV segment (left: 37.8% vs. 17.8%, P = 0.0393; right: 57.8% vs.15.6%, P<0.0012), in left BCV (60% vs. 8.9%...
Internal Jugular Vein Valve Incompetence Is Highly Prevalent in Transient Global Amnesia
Stroke, 2009
Background and Purpose— Transient global amnesia (TGA) is the inability to retain new information and to recall past events during a period of minutes or hours. Its etiology is unclear, and flow disturbances in the mesial temporal lobes secondary to venous congestion have been proposed as a potential cause. Ultrasonographic evaluation of the internal jugular vein (IJV) has demonstrated valvular insufficiency in TGA. The prevalence of valvular insufficiency in the IJV in patients with TGA was assessed. Subjects without TGA of similar sex, age, and vascular risk factor profiles served as controls. Methods— A group of 142 patients with a clinical diagnosis of TGA within 7 days of the clinical event and 40 controls were prospectively evaluated. Venous Doppler examination of both IJVs was performed at baseline and after a manometer-controlled Valsalva maneuver. Valvular insufficiency was diagnosed when there was reflux for >0.8 seconds during the Valsalva maneuver. Results— Valve insu...
Journal of the Neurological Sciences, 2017
Background: The etiology of transient global amnesia (TGA) remains unclear. We studied the pathophysiology of TGA in 165 Japanese patients. Subjects and Methods: TGA was diagnosed in hospitalized patients from 2004 to 2015. We analyzed clinical characteristics, magnetic resonance imaging findings, and maximum intimamedia thickness of the common carotid artery, and the reflux of internal jugular venous (IJV) flow by ultrasonography, and statistically compared patients with TGA with age-matched and sex-matched patients who have had a transient ischemic attack (TIA), small-vessel occlusion (SVO), and normal controls (each group, N = 165). Results: Patients with TGA showed lower prevalence of vascular risk factors than patients with TIA and SVO did. Eleven patients (6.7%) had 2 episodes of TAG, but specific clinical variables could not be recognized in these patients. The maximum intima-media thickness was significantly thinner in TGA (1.1 ± .7 mm) than in SVO (1.6 ± .9 mm; P = .001). The percentages of cases whose IJV flow reflux was increased by Valsalva maneuver showed no difference (P = .573) between TGA (26.0 %) and SVO (29.4%). MR diffusion-weighted imaging yielded small hyperintense signals in the hippocampus in 64 of 90 (71.1%) patients between 24 and 72 hours. Potential precipitating specific factors or events before the attacks could be recognized in 40 cases (24.2%) of 165 patients. Conclusion: Arterial ischemia and IJV flow reflux might not contribute to TGA pathophysiology. The vulnerability of the hippocampus to physical or emotional stress might be suspected as an underlying mechanism in some patients with TGA.
Transient global amnesia may be caused by cerebral vein thrombosis
Medical Hypotheses, 2005
Transient global amnesia (TGA) is a disorder of unknown aetiology, characterized by sudden loss of anterograde memory, in the absence other neurological signs or symptoms, followed by complete recovery in less than 24 h. Precipitating actions such as strenuous physical activity or valsalva-like manoeuvres are frequently reported. Since first described in 1958, by Fisher and Adams, the possible pathophysiology has undergone much speculation. Nonconvulsive epileptic seizures, migraine, paradoxical embolism thorough a patent foramen ovale, and transient ischemic attacks have been proposed as potential mechanisms. One of the latest hypotheses is that venous congestion causes either ischemia or induces spreading depression in the medial temporal lobes. It has been demonstrated that retrograde flow in the internal jugular veins occurs more frequently during valsalva manoeuvres in TGA patients than in controls, supporting a dysfunctional venous circulation as part of the pathogenesis. However, earlier hypotheses typically fail to explain the relatively low recurrence rate of TGA, lack of comorbidity and the relation to precipitating events. If cerebral venous hypertension was the solely cause of TGA it would presumably be much more common with very high recurrence rates among those predisposed of the condition. Structural changes observed in MRI and SPECT studies along with reports of mild cognitive impairment lasting much longer than the amnestic episodes, indicate that TGA is less transient and perhaps somewhat less benign than earlier believed. Many cases of TGA seem to be associated with factors of increased risk of cerebral venous thrombosis, such as polycythemia, antiphospholipid antibodies, venous hypertension, female sex and more. We suggest that most cases of TGA may be due to small thrombi in the deep cerebral venous system. Small venous thrombi may difficult to visualize even when using modern imaging technology. Further studies of TGA patients with for example blood analysis of D-dimer together with MR venography or CT venography could be done to evaluate this new hypothesis.