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About ramakentesh

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  1. Fatigue is the most common reported symptom in POTS according to the recent Canadian Consensus Statement. Million dollar question is how to treat it. B12 is a good suggestion. Mestinon helps some mildly as does volume expansion. Ive done ok with midodrine and on very bad days pseudoephedrine. A supplement called NAC can also be helpful. Some friends are prescribed modafinil or stronger but these may augment tachycardia
  2. All POTS by definition is a hyperadrenergic state. The concept of hyper pots being a separate entity with unique etiologies is challenged by the fact that as many 'hyperadrenergic POTS' patients as neuropathic POTS patients have patchy small fiber neuropathy. I have neuropathic pots with hyperadrenergic features such as orthostatic hypertension (which paradoxically improves when i take midodrine). Hyperadrenergic POTS - according to Vanderbilt - is a description of clinical features and not a diagnosis
  3. Pots seems to involve - in some cases - excessive venodilation with compensatory tachycardia although NET deficiency can also cause excessive tachycardia and blunted sympathetic vasoconstriction Histamine is another option but its effrcts are mainly at the microvascular level.
  4. Old school antihistamines do have affinity for mainly muscarinic receptors where they might decrease the effects of acetylcholinesterase inhibition to a degree. Clonidine acts mainly on alpha 2a receptors in the brain to suppress sympathetic outflow. Unless Latuda is an alpha 2 antagonist i doubt it would interact with clonidine. Does clonidine help your situation in a setting where licorice also does?
  5. My pots has followed a relapsing remitting course since it started in 2003.
  6. All POTS by definition is a hyperadrenergic state.
  7. Butchers broom Is a pretty mild pressor but it does have a mild diuretic effect. It also forces the release of norepinephrine via tyramine content which may benefit some but not others
  8. Interestingly my BP is all over the place when symptomatic and unmedicated - usually on the higher side. Midodrine and phenylephrine actually lower my heart rate and orthostatic BP presumably by stabilising things.
  9. I found that modafinil stimulated beta receptors (enhanced tachycardia) without any improvement to energy levels or vasoconstriction. Ritalin and Concerta are far better tolerated and helpful medications in my opinion.
  10. Im not convinced that excessive norepinephrine or impaired norepinephrine reuptake causes POTS or that it can be caused chronically from taking an SNRI that is then stopped. The short answer to your question is that its unknown what causes POTS although there seem to be some interesting associations - small fiber neuropathy in some, impaired NET and NE clearance in some, but nearly always reduced venous return to the heart and reduced stroke volume which would not suggest a state of increased NE mediated venoconstriction.
  11. This symptom seems related to the ineffectual attempts the body makes to adjust for reduced cerebral perfusion. the body attempts to rely on beta receptor activation and ramps up sympatgetic activity to compensate for impaired sympathetic vasoconstriction. it is also possible that there are central abnormalities in norepinephrine and dopamine regulation in some patients. Serotonin could be at play but I suspect fatigue is centrally mediated from reduced norepinephrine or dopamine release the former which is centrally calming and is intimately involved in governing levels if glut
  12. The most likely reason you are experiencing these symptoms is because you have reduced blood flow to your brain meaning there is limited glucose and oxygen metabolism in your brain. In fact there are studies by Dr Medow and Stewart that suggest that POTs patients dont experience cerebral vasodilation in response to cognitive challenges.
  13. U guys have ppts or ncs being prescribed northera?
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