Chronic CerebroSpinal Venous Insufficiency (CCSVI) has been described as a hemodynamic disturbance of the CNS venous drainage. The theory being that CCSVI results from obstructing lesions of the extra-cranial veins in the CNS drainage pathway. Venous hypertension, as a result of the impaired venous drainage seen with CCSVI, is postulated to play a role in the pathogenesis of multiple sclerosis (MS). However, subsequent studies have been inconclusive in establishing a relationship between extra-cranial venous abnormalities and manifestations of MS.
Autonomic nervous system dysfunction has been described as a possible explanation for the occurrence of CCSVI by Z. Sternberg. This theory is supported by my clinical experience of autonomic symptoms commonly being present in patients presenting for evaluation of CCSVI. While autonomic symptoms may be variable and diverse in nature, our patients tend to experience fatigue, interrupted sleep, brain fog, thermal intolerance, awakening headache, bowel and bladder dysfunction. Signs of autonomic dysfunction such as low blood pressure (BP), low body temperature and abnormalities in heart rate variability (HRV) are also commonly present.
In my experience, when this constellation of symptoms is present, patients are likely to respond to venous angioplasty. Additionally, the patients showing deviation from normal in systolic and diastolic BP were often corrected in patients after BA. Therefore, normalization of BP and HRV may be used as surrogate markers to assess the utility of therapeutic intervention.
Decentralized venous drainage has been described following spinal cord injury, a common inciting factor for acute autonomic dysfunction. Abnormal cerebral venous drainage may therefore be one of the many manifestations of the autonomic dysfunction rather than a cause as Zamboni has suggested. Another test of autonomic function showing abnormalities in MS patients is HRV. HRV reflects the influence of autonomic system on the function of the heart.
The implications of autonomic dysfunction in the pathology of the cerebral venous system also necessitated a reappraisal of our treatment approach. The physiologic basis of renal denervation served as a theoretical model. Renal denervation therapy, with its transvascular augmentation of periadventitial autonomic fibers, offers an alternate route to modulate the ANS function. Therefore, we have modified Zamboni’s technique of angioplasty to extend beyond dilation of venous obstructing lesion, in an effort to effect autonomic stimulation. This modification involved delivery of mechanical energy to the periadventitial fibers associated with the internal jugular veins, as well as the renal vein. This modified technique can best be described by the term Transvascular Autonomic Modulation (TVAM).
Find out more about TVAM here.
