Response to Letter by Caplan
We appreciate Dr Caplan’s comments regarding our study.1,2 We provided evidence of a high prevalence of jugular vein incompetence in subjects with recent transient global amnesia (TGA). There are still several areas of uncertainty and no generalized consensus regarding the pathogenesis of TGA.3 We stated that our findings appear to support the hypothesis of venous congestion in areas of the brain associated with memory function as a potential explanation for episodes of benign TGA. The investigation was not designed to assess the status of the arterial circulation.
Dr Caplan suggests a key role of vasoconstriction in this setting and wonders about a potential association between venous congestion and vasoconstriction. It is not clear what are the mechanisms, if any, by which transient venous congestion can cause hours or days later prolonged vasoconstriction. Transient reduction in vessel caliber may not be a universal phenomenon in TGA. Drs Savitz and Caplan reported TGA associated with sildenafil use, a drug known to cause vasodilatation.4 Furthermore, most modern diagnostic techniques have not been able to consistently demonstrate vasoconstriction in patients with TGA.
Undoubtedly, further studies using dynamic evaluation of blood flow (ie, transcranial Doppler, positron-emission tomography) will help test Dr Caplan’s interesting hypothesis.
Caplan LR. Transient global amnesia and jugular vein incompetence. Stroke. 2010; 41: e568.
Cejas C, Fernandez Cisneros L, Lagos R, Zuk C, Ameriso SF. Internal jugular vein valve incompetence is highly prevalent in transient global amnesia. Stroke. 2010; 41: 67–71.
Owen D, Paranandi B, Sivakumar R, Seevaratnam M. Classical diseases revisited: transient global amnesia. Postgrad Med J. 2007; 83: 236–239.
Savitz SA, Caplan LR. Transient global amnesia after sildenafil (Viagra) use. Neurology. 2002; 59: 778.