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Everything posted by ramakentesh

  1. Lately my brain fog has been so bad amd combined with the pandemic ive developed kind of ocd symptoms and was contemplating a low dose SSRI just to calm down my stress levels and compulsions.
  2. Old post but new symptom in new flare and im getting exactly this: Three days during adrenalin surges as soon as id fall asleep id instantly fall into this hypnagogic state where an image or word would flash into my mind's eye amd jolt me awake. So utterly bizarre i was convinced i was having a seizure until a pots friend said they also experienced this.
  3. 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
  4. 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
  5. 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.
  6. 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?
  7. My pots has followed a relapsing remitting course since it started in 2003.
  8. All POTS by definition is a hyperadrenergic state.
  9. 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
  10. 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.
  11. 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.
  12. In some studies hyperadrenergic presentations and low flow states correlated with the lowest blood volume - meaning that in most cases low blood volume is a feature of more hyperadrenergic presentations. In my case Florinef lowered my standing BP and HR. One thing to remember in POTS specifically is that 'blood pressure' measurements only measure arterial pressure. Usually when arterial pressure is elevated, so is elastic recoil in veins. True hypertension is associated with hyperdynamic circulations, increased cerebral blood perfusion, increased cardiac output and stroke volume, increase
  13. 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.
  14. There are actually nearly no longitudinal studies in POTS, there is currently no agreed delineation or phenotypes within POTs, and most of the suggested underlying causes are equivocal and have not been replicated in multiple studies.d When a doctor tells you that patients get better within a specific time frame he or she is basing this either on their own clinical experience (anecdata) or from review documents that have little supporting evidence. The truth is this is probably unknown. When a doctor or a patient diagnoses a patient with 'hyper' POTS all they are doing is describing
  15. Blood pressure measurements are almost meaningless in POTS because they are arterial measurements - they do not tell you anything about what your veins are doing - is there pooling? Is there inadequate venous return? Increased microvascular filtration? Try looking at pulse pressure when symptomatic. That may tell you more. Narrowing stroke volume is a good measure of reducing stroke volume from inadequate venous return.
  16. I hear this reported for Midodrine quite a bit. I take only when needed rather than constantly to avoid tolerance to it. Secondly I cycle my medications so that my body doesn't get used to them. Another virtually identical medication is Phenylephrine which is in Sudafed PE and is also an alpha 1 agonist although it is hampered by poor oral bioavailability. When I am symptomatic I usually take either phenylephrine or midodrine and then the opposite the next day. And then on really bad days I take Pseudoephedrine. Seems to stop the body getting used to the medications. Doctor appr
  17. I think biofeedback is as likely to be more than a placebo at about the same level in POTS as it would be in essential hypertension or MS.
  18. Provigil/modafinil helped a little with this but for me pseudoephedrine is superior and it actually lowers my heart rate. I dont actually agree with vandy on this - i tend to believe there is impaired central norepinephrine activity (which by reciprocal association) causes peripheral norepinephrine overactivity. Pots patients generally seem to show evidence of increased norepinephrine with symptoms of hypotension.
  19. There is lots of work evaluating yhe roke and functional impact of autoimmunity in POTS. There is a study attempting to demonstrate that small fiber neuropathy translates to wider vasomotor nerve involvement. There is a trial on droxydopa in pots. There is also people looking at brain changes in OI.
  20. 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
  21. Dr Julian Stewart described a subset of POTS designated low flow that had resting vasoconstriction. However most pots patients have decreased venous return and although some do have (at least according to older studies) cerebral vasospasm. Initially i had a 'hyper' presentation but over time it morphed into a more neuropathic presentation especially once i corrected the low blood volume.
  22. Can certainly happen (fluctuating symptoms are fairly common) - has yoir doctor talked about Midodrine or Droxydopa in your case?
  23. My symptoms cone and go in a seasonal cycle
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