POTS Page 12

  Support During Recovery: Those who join the DNRS program gain access to a forum with others who are recovering from limbic system impairments. This is a very supportive environment, and one in which there is much support - both from coaches and other ‘brain retrainers’. It is recommended to book a one to one Skype coaching session following completion of the DVD program so as to ensure a correct understanding of the program before beginning properly. This can be done via the DNRS website.

  Oh, I’ll just meditate - that will calm my limbic system down: Meditation may help to a degree, and in some cases may lead to recovery, but I do not think that, in general, it is powerful enough to certainly change limbic system function to the degree required. Furthermore, meditation does not change the limbic system in a targeted way. Rather, it creates ‘psychological distance’ between the person meditating and what is going on in the limbic system. Under normal circumstances, this can create calm but for someone with limbic system trauma it can make things worse as it is very difficult to gain ‘psychological distance’ from a brain in such distress. Indeed, meditation for those with limbic system trauma can actually increase distress as it is hard not to be ‘sucked in’ to the traumatic state the brain is in. The DNRS, on the other hand, is an intervention to change the limbic system itself, on its own terms and in deliberately positive directions, and is therefore more focussed on what is needed to rehabilitate the limbic system. After this rehabilitation has been completed, however, a more acceptance-based approach, as found in mindfulness, could be adopted.

  Residual Anxieties / Release of Adrenalin After Recovery: Once the recovery process is complete, it is not uncommon - as with recovery from any health condition - to experience ‘residual anxieties’, i.e.: ‘will my condition come back?’ Fully recovered patients may feel ‘remnants’ of fear upon standing up, for example. Sometimes, these residual anxieties are amusing: a person may hear someone else talk about ‘flower pots’ and feel a twinge of anxiety (this frequently happens to the author of this book!). It is wise to see the humour in such anxieties and the best possible cure for them is consistently to engage in other activities, activities which take up your whole attention. Timetable your day to fill it with interesting activities of all sorts. Move away from non-anxious behaviour to normal behaviour and let the days pass. Do not preoccupy yourself with thoughts about health. Over time, your brain will forget these residual anxieties, as long as you keep it occupied for long enough with other things. I also note here that if the recovered person ever does start to feel adrenalin going off inappropriately and consistently, they should return for a few days to the DNRS exercises. A steady release of adrenalin over a few days will not damage the NET protein, but it is best - in the unlikely event this does happen - to cut it off in its tracks. As regards ‘appropriate’ adrenalin release in response to stressful situations, this should not be a cause for concern. Indeed, adrenalin is meant to help you cope with difficult situations! When it is not released as a result of an impairment, then adrenalin is your friend: use it to deal with the situation in front of you and get stuck in! Don’t fall into the trap of thinking that adrenalin is in and of itself bad and don’t fear its ‘appropriate’ release.

  Cognitive Impairment: All POTS patients suffer from cognitive impairment - some to a considerable degree - and may find the DNRS exercises daunting as a result. The practice may feel ‘murky’ and ‘cloudy’ initially. This should not discourage the brain rewirer from continuing in her practice, however. Even a ‘murky’ DNRS practice is making the changes needed and, over time, this murkiness will recede as the limbic system starts to come out of a crisis state. Other changes such as giving up caffeine, sugar and perhaps limiting the use of technology, can all help with cognitive impairment.

  Endnotes

  [1] See mins. 22.00 ff. of Prof. Raj's talk 'Connecting the dots between EDS and POTS', accessible at: www.YouTube.com/watch?v=srUJRRihvsE

  [2] In writing the sections of this book concerning pre-existing research on POTS, I have found the following two resources especially helpful. First of all, Prof. Raj's 2013 overview of POTS published in the journal, Circulation (accessible here: http://circ.ahajournals.org/content/127/23/2336.long) and, second, the thorough collection of articles in the third edition of The Primer on the Autonomic Nervous System, edited by Robertson, Biaggioni, Burnstock, Low and Paton. I also note here that, throughout this book, I do not always reference page numbers, but the paper or chapter number,of the article or paper in question. This only pertains to electronic resources I made use of when the print page number was not available. For other works, for example, Annie Hopper's Wired for Healing, I include page numbers.

  [3] Raj, 2013.

  [4] Raj, 2013.

  [5] From The Primer on the Autonomic Nervous System (eds. Robertson, Biaggioni, Burnstock, Low and Paton), 2011, chapter 39. [Henceforth: ANS Primer, 2011].

  [6] ANS Primer (2011), Chapter 106.

  [7] Indeed, Low and Sandroni (ANS Primer, chapter 106) note that around 50% of patients have an antecedent viral illness.

  [8] Levine (2012), 3496.

  [9] Ibid.

  [10] Levine (2011), 76.

  [11] Levine (2010), 2864.

  [12] Levine (2011), 74-75.

  [13] See Levine (2010), 2866: "Left ventricular mass and end-diastolic volume increased by 12% and 8% after training, resulting in significant cardiac remodeling. The heart became much larger and probably more distensible after exercise training. Blood and plasma volumes also increased markedly after training. Ten (53%) of 19 patients no longer met criteria for POTS after completion of the 3-month exercise training program and thus were cured."

  [14] See the graphs in Levine, 2010, 2011, 2012.

  [15] Levine (2010), 75.

  [16] Levine 2012, 3503.

  [17] Raj, 2013.

  [18] Goldstein, ANS Primer, Chapter 6: 'NE (norepinehprine) is inactivated mainly by uptake into cells, with subsequent intracellular metabolism or storage. Reuptake into nerve terminals…via the cell membrane NET is the predominant means of terminating the actions of released NE'.18

  [19] See bibliography at the end of this chapter.

  [20] For more details of healthy NET function and NET deficiency in POTS, see mins. 49.00-55.00 of this excellent Youtube lecture by Prof. Carrie Burdzinski: 'Postural Orthostatic Tachycardia Syndrome (POTS), Dysautonomia and the Autonomic Nervous System' (www.youtube.com/watch?v=faScrmgKcWg).

  [21] Raj, 2013.

  [22] See: www.mc.vanderbilt.edu/root/vumc.php?site=adc&doc=43572

  [23] Hopper (2014), 13-14.

  [24] 2014, 18-19.

  [25] ANS Primer, chapter 55, 2015.

  [26] 2014, 22.

  [27] ANS Primer, chapter 107.

  [28] 74.

  [29] ANS Primer, chapter 107.

  [30] ANS Primer, chapter 23.

  [31] ANS Primer, chapter 23.

  [32] ANS Primer, chapter 23.

  [33] Raj, 2013.

  [34] The Biology of Belief, 2008, 106.

  [35] Raj, 2013.

  [36] Raj, 2013.

  [37] ANS Primer, chapter 106.

  [38] For both studies, see the Raj lecture ('Connecting the Dots Between EDS and POTS') on YouTube (www.YouTube.com/watch?v=srUJRRihvsE), at 39.40 and ff.

  [39] ANS Primer, chapter 111.

  [40] A specific and severe form of MCS which is well-known is 'Gulf War Syndrome' which affected soldiers in that conflict following chemical exposure.

  [41] As reported in the Daily Mail. See: www.dailymail.co.uk/health/article-2659736/Third-ME-cases-wrongly-diagnosed-Experts-says-thousands-thought-chronic-fatigue-actually-similar-condition-treated.html

  [42] This list is paraphrased from the work of Okamoto, Raj and Biaggioni in the ANS Primer, Chapter 110.

  [43] For Myhill's paper, see: www.ncbi.nlm.nih.gov/pmc/articles/PMC2680051/

  [44] The Biology of Belief (2008), 119.

  [45] ANS Primer, chapter 110.

  [46] See: www.
webmd.com/fibromyalgia/news/20131105/brain-scans-show-fibromyalgia-patients-process-pain-differently

  [47] The following summary of Annie Hopper's story is adapted from the first chapter of her book, Wired for Healing.

  [48] 2014, 5.

  [49] 2014, 9.

  [50] 2014, 9.

  [51] I include here, for those interested, more information about the neuroplasticity studies into rewiring the brains of those with OCD. Brain scans have shown that OCD develops as a result of the overactivation of the part of the brain known as the 'caudate nucleus', which is responsible for many functions, but one of which includes the simple ability shift one's attention one from thing to the next. In the person with OCD, it has been shown that the caudate nucleus gets 'stuck', unable to disengage from the worrying thoughts and compulsions. Dr. Jeffrey Schwartz of the University of Pittsburgh designed a mindfulness-based cognitive behavioural programme to treat OCD which entailed the patients gaining 'psychological distance' from their OCD, seeing it not as part of them but as the result of 'confused' overactivation of the caudate nucleus, and deliberately attempting to form new healthy behaviours whenever an OCD thought occurred so as to 'act back' on the brain and change its structure. And this is precisely what happened. After just eight weeks of practice, the activity of the caudate nucleus had quietened down. Their 'attention processing' part of the brain was acting closer and closer to normal. They had, therefore, successfully changed the physical structure of their brains, through discipline, commitment and knowing what to do.

  [52] The use of neuroplasticity in recovering from the neurological effects of stroke also deserve further mention. For, in the case of recovering from stroke, it is not just a case of replacing one dominant set of neuronal pathways with another, for the affected movement patterns in the case of the stroke patient have actually been destroyed. The patient needs, therefore, to create new neurological movement patterns 'from the ground up'. Edward Taub of the University of Alabama at Birmingham designed an intensive rehabilitation programme called "C.I." or (Constraint Induced Movement Therapy). Patients, through repetitive exercises for up to eight hours a day initially, learn how to move the affected parts again, by 'acting back' on their own brains so as to change brain structure positively, creating new neuronal connections related to movement. Truly the brain is a neuroplastic organ.

  [53] 2014, 82.

  [54] 2014, xi.

  [55] This data was presented by Annie Hopper at the American Academy of Environmental Medicine Conference in October 2013. A YouTube video of that talk can be found here: www.YouTube.com/watch?v=0_-nM2dHXMk (or look up 'Hopper AAEM presentation').

  [56] For the scale, see: www.institutferran.org/documentos/SQM/interpreting_QEESI.pdf

  [57] Available here: www.YouTube.com/watch?v=KLjgBLwH3Wc

  [58] See: http://terrywahls.com/research-update-full-edition/

  [59] 2014, xx.