Translate
Ronny Allan
One of the curious things about Neuroendocrine Cancer (NETs elsewhere in the text) is that it can very often exhibit one or more vague symptoms collectively known as a ‘syndrome’. Syndrome is an apt word to describe these complications as the most general meaning in medical terms is a group of symptoms that together are characteristic of a specific disorder or disease”. Having a syndrome can often be the difference between having a ‘functional’ condition or a non-functional’ condition – see more below.
This frequently makes Neuroendocrine Cancer very difficult to diagnose quickly. It’s a very devious disease.
It’s NOT all about Carcinoid Syndrome!
Most people think of Carcinoid Syndrome when they discuss NETs. Anyone suggesting that all NET patients get carcinoid syndrome or that all symptoms of NETs are caused by carcinoid syndrome, is WAY off the mark. Firstly, not everyone will have a ‘syndrome’ in addition to their tumours – the percentage is actually well below 50%. Secondly, there are in actual fact, several associated syndromes depending on the anatomical location and type of NET. As an example of one syndrome, statistics vary from source to source but it is estimated that around a 30-45% of all ‘midgut’ patients will present with metastatic disease and around a third of those (∼10-15% of all midgut) will exhibit Carcinoid Syndrome indicating their tumours are ‘functional’ (secreting excess hormones, particularly serotonin). It follows that Carcinoid Syndrome itself is not that common and it could be the same with other types of NET (even though it can appear more prevalent on forums).
There’s a highly prevalent issue in NET patient forums where many assume they have so called “carcinoid syndrome” or have been told “carcinoid syndrome” by their doctor. I always raise an eyebrow when I look at the NET type or primary location of some of these claims. Take Pancreatic NETs as example, they were never historically called “carcinoid tumours” and they do not typically cause carcinoid syndrome. It’s not impossible to have a predominately serotonin producing tumour in the pancreas but it is highly unusual. When a patient presents with vague symptoms and has a pancreatic NET, the easy option is to declare “carcinoid syndrome” rather than check for the known pancreatic NET hormones or other illnesses. It also happens with other types of NET. Of course part of the issue is the ‘carcinoid’ nomenclature which seems to linger like a bad smell.
Functional / Non-Functional
These tumours and associated syndromes are treatable for most but the difficult part can be arriving at a diagnosis. Moreover, without a syndrome, some of these tumours can be silently growing and as they grow slowly, the ‘silence’ can go on for some years. Even with a syndrome, the root cause can remain disguised as the symptoms are similar to many day-to-day illnesses, again the reason for the title of this blog. Curiously, the lack of a syndrome can sometimes lead to an even later presentation and the consequences that arise (i.e. no signs to aid a diagnosis). In fact a large proportion of Pancreatic NETs are non-functional at diagnosis.
There can be the odd exception but in general terms, NETs are either functional (with a syndrome) or non-functional (no syndrome). It’s also possible that patients can move from one state to another.
Non-functioning tumours—no specific clinical syndrome is observed or excess hormone secretion isn’t sufficient enough to cause symptoms.
Functioning tumors—the tumours’ secretions lead to clinical symptoms due to elevated levels of the associated hormone(s), some more distinct than others.
It’s useful to know about the range of tumor markers and hormone markers – read more here
Syndrome and Tumors – ‘Chicken or Egg’ ?
I’m always confused when someone says they have been diagnosed with a Syndrome rather than a NET type. You normally need a tumor to produce the symptoms of a syndrome. The exception to this rule might be hereditary syndromes e.g. MEN. MEN syndromes are genetic conditions. This means that the cancer risk and other features of MEN can be passed from generation to generation in a family. A mutation (alteration) in the various MEN genes gives a person an increased risk of developing endocrine/neuroendocrine tumors and other symptoms of MEN. It’s also possible that the tumors will be discovered first. It’s complex! MEN is just one of the NET related hereditary syndromes, there are others, read more here.
Major NET Syndromes
(information mainly taken from the ISI Book on NETs with a cross-reference from ENETS and UKINETS Guidelines)
The ISI Book on Neuroendocrine Tumors (Woltering et al) confirms there are a number of syndromes associated directly and indirectly with NETs and are described as individual syndromes according to their secretory hormones and peptides. The reference publication expands on this list to aid diagnoses by including common presentations, associated tumour types and locations and the offending secreting hormones. You can see why Neuroendocrine Cancer is a diagnostic challenge!
Carcinoid Syndrome
A syndrome connected with (mainly) serotonin secreting tumours in certain locations, mainly metastatic instances of NETs in the small intestine, lung, stomach, appendix, rectum. The key symptoms include diarrhoea, flushing of the skin (particularly the face), stomach cramping, heart problems such as palpitations, fatigue, wheezing. The syndrome is actually caused by the release of a number of hormones, in particular Serotonin, Bradykinin, Tachykinin (Substance P), Histamine, and Prostaglandins. It’s a real witch’s brew!
Carcinoid syndrome occurs when biologically active amines and peptides enter the systemic circulation escaping the first-pass metabolism of the liver. Normally, these bioactive products are inactivated by the liver. However, in cases of neuroendocrine tumors with liver metastasis, either these bioactive products are directly released into the systemic circulation, or they escape inactivation due to deranged liver function.
Less commonly, carcinoid syndrome can occur without liver metastasis in conditions like a primary gut tumor with extensive retroperitoneal nodal metastases, a bronchial or ovarian NET, where it’s possible for bioactive amines to be released directly into the systemic circulation.
It is reported that neuroendocrine tumors release about 40 different types of biologically active amines and peptides. The most common related to carcinoid syndrome are serotonin, histamine, tachykinins, kallikrein, and prostaglandins (read more about NET-related hormones here) The majority of midgut symptoms are said to be due to serotonin which is a product of tryptophan metabolism.
Usually, only 1% of dietary tryptophan is converted into serotonin. However, in a patient with carcinoid syndrome, up to 70% of tryptophan can be converted into serotonin. Serotonin undergoes oxidative reaction and leads to the formation of 5-hydroxy indoleacetic acid (5-HIAA) by aldehyde dehydrogenase, which subsequently is eliminated into the urine.
Serotonin causes increased motility and secretion of gastrointestinal tract resulting in diarrhea. As most of the body’s tryptophan is diverted to serotonin formation pathway by neuroendocrine tumors, it can sometimes lead to a deficiency of tryptophan which is needed for synthesis of niacin. Subsequently, in extreme cases, deficiency of niacin occurs causing Pellagra which manifests as dermatitis, dementia, and diarrhea. Prostaglandins also mediate increased intestinal motility and fluid secretion in GI tract causing diarrhea.
Neuroendocrine tumors of foregut and lungs do not contain the enzyme aromatic L-amino acid decarboxylase which converts 5-hydroxytryptophan to serotonin. Thus, lungs and foregut neuroendocrine tumors do not normally produce serotonin. Hindgut neuroendocrine tumors usually do not normally produce any bioactive hormone.
Histamine is released mostly by pulmonary neuroendocrine tumors which can cause atypical flushing and pruritus. Flushing is also secondary to the vasodilatory effect of tachykinins (substance p, neurokinin A, neuropeptide k).
Pancreatic NET syndromes
Most pancreatic NETs are non-functional but may have been growing for some time presenting some symptoms including but not limited to: diarrhea, indigestion, a lump in the abdomen, pain in the abdomen or back, yellowing of the skin and whites of the eyes.
But there are several distinct clinical syndromes related to pancreatic NETs and these are normally related to highly elevated predominant hormone secretions. There’s also a very rare instance of pancreatic based tumours producing carcinoid syndrome effects – according to ENETs less than 1% of all tumours associated with carcinoid syndrome. It’s clear from what I see in patient groups that many pancreatic NET patients believe they have carcinoid syndrome (perhaps told this by a doctor) when in fact they are experiencing symptoms of other syndromes specifically related to the pancreas area, comorbidities (other illness unrelated to NETs) or side effects of tumour growth or therapy.The main pancreatic NET Syndromes and their signs and symptoms are:
Whipple’s Triad – Whipple’s Triad is the classic description of insulinoma which includes symptoms of hypoglycemia with a low blood glucose concentration relieved by the ingestion of glucose. These tumours can be located anywhere within the pancreas in the cells that make insulin. Insulin is a hormone that controls the amount of glucose (sugar) in the blood. It moves glucose into the cells, where it can be used by the body for energy. Insulinomas are usually slow-growing tumors that rarely spread. Some of these tumours will be associated with MEN1 syndrome.
Symptoms – too much insulin may cause:
- Low blood sugar. This can cause blurred vision, headache, and feeling lightheaded, tired, weak, shaky, nervous, irritable, sweaty, confused, or hungry.
- Fast heartbeat.
Zollinger-Ellinson Syndrome. A tumour that forms in cells that make gastrin and can be known as a Gastrinoma. Gastrin is a hormone that causes the stomach to release an acid that helps digest food. Both gastrin and stomach acid are increased by gastrinomas. This is a condition in which one or more tumours form in the pancreas, the upper part of the duodenum or the stomach (these organs are very close and tightly packed together). These tumours secrete large amounts of the hormone gastrin, which causes your stomach to produce too much acid. The excess acid can lead to peptic ulcers, in addition to diarrhea and other symptoms. Associated with Gastrinoma (pNET) and Gastric NETs. Some of these tumours may be associated with MEN1 syndrome.
Symptoms – too much gastrin may cause:
Too much gastrin causes a condition known as Zollinger-Ellison syndrome, in which the stomach makes too much acid. In addition to Gastroesophageal reflux, this leads to stomach ulcers, which can cause pain, nausea, and loss of appetite. These ulcers can be recurring. If the ulcers are prone to bleeding, it has the potential to lead to anemia (too few red blood cells), which can cause symptoms like feeling tired and being short of breath. Diarrhea if often a gastrinoma symptom.
Verner-Morrison Syndrome. Vasoactive Intestinal Peptide (VIP) is secreted thus the pNET term – VIPoma – Sometimes the syndrome is referred as WDHA – Watery Diarrhea, Hypokalemia (potassium deficiency), and Achlorhydria (absence of hydrochloric acid in gastric secretions). Sometimes known as Pancreatic Cholera. Some of these tumours may be associated with MEN1 syndrome.
Symptoms – too much vasoactive intestinal peptide (VIP) may cause:
- Very large amounts of watery diarrhea.
- Dehydration. This can cause feeling thirsty, making less urine, dry skin and mouth, headaches, dizziness, or feeling tired.
- Low potassium level in the blood. This can cause muscle weakness, aching, or cramps, numbness and tingling, frequent urination, fast heartbeat, and feeling confused or thirsty.
- Cramps or pain in the abdomen.
- Facial flushing.
- Weight loss for no known reason.
Glucagonoma. A tumour that forms in cells that make make glucagon. Glucagon is a hormone that increases the amount of glucose in the blood. It causes the liver to break down glycogen. Too much glucagon causes hyperglycemia (high blood sugar) rendering most patients diabetic. A glucagonoma usually forms in the tail of the pancreas. Some of these tumours may be associated with MEN1 syndrome. Sometimes known as the 4D syndrome – Dermatological, Diabetes, DVT, Depression. The dermatological side effect has been described as necrolytic migraotry erythema.
Symptoms – too much glucagon may cause:
- Skin rash on the face, stomach, or legs.
- High blood sugar. This can cause headaches, frequent urination, dry skin and mouth, or feeling hungry, thirsty, tired, or weak.
- Blood clots. Blood clots in the lung can cause shortness of breath, cough, or pain in the chest. Blood clots in the arm or leg can cause pain, swelling, warmth, or redness of the arm or leg.
- Diarrhea.
- Weight loss for no known reason.
- Sore tongue or sores at the corners of the mouth.
Somatostatinoma is a very rare type of NET, with an incidence of one in 40 million persons. These tumours produce excess somatostatin arise from the delta cells in the pancreas, although these cells can also be present in duodenal/jejunum tissue where around 44% of these tumours occur. Somatostatin is a naturally occurring peptide that inhibits the function of almost all gut hormones (author’s note – this fact should give you an appreciation of how somatostatin analogues tackle associated syndromes whilst giving you certain side effects as a result!)
Somatostatinoma – too much somatostatin may cause:
- High blood sugar. This can cause headaches, frequent urination, dry skin and mouth, or feeling hungry, thirsty, tired, or weak.
- Diarrhea.
- Steatorrhea (very foul-smelling stool that floats).
- Gallstones.
- Yellowing of the skin and whites of the eyes.
- Weight loss for no known reason.
Pancreatic Polypeptide (PP) – PPoma. A complicated one and not too much information (even in the ISI book or ENETS Guidelines). However, it’s the third most common type of islet cell tumour (i.e. pNET). The function of pancreatic polypeptide is not completely understood. Patients present with weight loss, jaundice, and abdominal pain. The diagnosis is confirmed by pancreatic polypeptide levels > 300 pg/ml. Some of these tumours may be associated with MEN1 syndrome.
PPoma – too much pancreatic polypeptide may cause:
- Belly pain.
- An enlarged liver.
Other NET or NET related syndromes
Hedinger Syndrome – the technical name for Carcinoid Heart Disease and an ideal replacement term now that Carcinoid is being phased out. Not a hormonal syndrome per se, but it can often be a manifestation of severe cases of so called carcinoid syndrome. Normally related to really high levels of 5HIAA.
Cushing’s – also known as hypercortisolism. A collection of symptoms caused by very high levels of a hormone called cortisol in the body. In Cushing’s disease, oversecretion of pituitary ACTH induces bilateral adrenal hyperplasia. This results in excess production of cortisol, adrenal androgens, and 11-deoxycorticosterone. Cushing’s disease, a subset of Cushing’s syndrome, is due to a pituitary corticotroph adenoma and results in a partial resistance to the suppression of ACTH by cortisol so that secretion is unrestrained. In contrast, causes of Cushing’s syndrome may include the following:
• Adrenal adenoma or carcinoma arise spontaneously. ACTH levels are undetectable.
• Non-pituitary (ectopic) tumours produce ACTH. They most frequently originate in the thorax and are highly aggressive small cell carcinomas of the lung or slow- growing bronchial or thymic carcinoid tumours. Some produce corticotropin- releasing hormone (CRH) instead, which stimulates pituitary ACTH secretion and can therefore mimic a pituitary tumour.
• Other causes include NETs of the gastric, pancreatic, and intestinal organs; Pheochromocytomas, and MCT.
The hallmark of Cushing’s syndrome is that ACTH levels are partially resistant to suppression with dexamethasone, even at very high doses. Some MEN patients with pituitary tumours may have Cushing’s Syndrome. AdrenoCorticoTropic Hormone (ACTH) releasing tumours are sometimes known as ACTHoma.
Hereditary/Inherited familial syndromes
Some sites describe these as types of NET but that is totally wrong – they are recognised syndromes that increase the risk of deveoping Neuroendcrine Tumours. Neuroendocrine / Endocrine tumors can be seen in several inherited familial syndromes, including but not limited to:
- Multiple Endocrine Neoplasia type 1 (MEN1)
- Multiple Endocrine Neoplasia type 2 (MEN2)
- Multiple Endocrine Neoplasia type 4 (MEN4)
- SDHx mutations – Hereditary Pheochromocytoma/Paraganglioma Syndromes.
- Von Hippel-Lindau (VHL) Disease (see below)
- Neurofibromatosis Type 1 (also known as Recklinghausen’s Disease) – associated with Duodenal/Pancreatic NETs and Pheo/Para.
- Tuberous Sclerosis – loose association restricted to case studies of many sites including pancreas, parathyroid and pituitary.
- Carney Complex – associated with adrenal and pituitary glands.
see more here Genetics and Neuroendocrine Tumors
MEN1 – Mainly involved the 3 Ps, Pituitary, Pancreas and Parathyroid. The pituitary tumours are primarily Prolactinomas, the pancreatic tumours are mainly PPomas, Gastrinomas and Insulinoma. Many also have association with Zollinger-Ellinson syndrome (ZES). Sometimes known as Wermer Syndrome. Associated with the MEN1 gene.
MEN2A – associated with the RET gene, can result in Medullary Thyroid Carcinoma, Pheochromocytoma, and overactive parathyroid glands characterised by a high calcium level.
MEN2B. An inherited disorder characterised by the certain development of Medullary Thyroid Carcinoma, plus the possible development of pheochromocytomas and characteristic tumours (mucosal neuromas) of the lips, tongue and bowels. Parathyroid disease is extremely rare in MEN2B. Also connected with the RET gene.
MEN4. A relatively new MEN variant and related to the CDKN1B gene. Similar to MEN1 but normally only 2 of the 3 Ps, parathyroid and pituitary; and potentially other places.
SDHx mutations/Hereditary pheochromocytoma/paraganglioma syndromes
- Succinate dehydrogenase (SDH) is an enzyme which is important for the metabolic function of mitochondria. Patients with mutations of these genes have increased risk of pheochromocytomas, paragangliomas, stomach tumors and kidney tumors.
- SDHx mutations (SDHA, SDHB, SDHC, and SDHD) can present as Pheochromocytomas/Paragangliomas and other non-NET conditions. If this interests you see site http://www.SDHcancer.org
Von Hippel-Lindau (VHL) – not an exclusively NET syndrome. VHL is a rare disorder caused by a faulty gene. It is named after the two doctors who first described the disease, and affects about one in 35,000 people. Tumours develop in one or more parts of the body. Many of these tumours involve the abnormal growth of blood vessels in parts of the body which are particularly rich in blood vessels. Areas most frequently affected are the eyes, the back of the brain (cerebellum), the spinal cord, the kidneys, the adrenal glands and the pancreas. People are affected differently, even within the same family. The only VHL tumour which tends to run in families affects the adrenal glands (Pheochromocytoma). Different VHL features tend to develop at different ages. The eye angiomas often develop in childhood. Others, including tumours found in the cerebellum, spinal cord or adrenal glands (Haemangioblastomas and Pheochromocytomas) can develop from late childhood onwards. The kidney tumours are usually the last things that develop, from the mid-twenties onwards. Most VHL related tumours are benign.
Summary
As for my own experience of syndromes, I did once show symptoms of the most common NET syndrome (currently known as Carcinoid syndrome) where the key symptoms include diarrhoea, flushing of the skin (particularly the face), stomach cramping, heart problems such as palpitations, and wheezing. You can see why those symptoms are frequently and easily confused with other conditions. If you have a similar diagnosis, you may benefit from looking at something known as The 5 E’s which is a useful list of things to be wary of.
I did have issues for a year or two in 2010 leading up to diagnosis and until my treatment was underway. I was experiencing flushing and infrequent bouts of diarrhea but I totally ignored it (hear me talk about this). However, it ended up being instrumental in my diagnosis albeit some good luck was involved in getting to that point. My twist of fate which involved a low hemoglobin score led me to a scan and ‘bingo’. I had a ‘gastrointestinal blip’ some 18 months previously but that proved colonoscopy negative. Despite my distant and metastatic tumour disposition and seemingly late diagnosis, I’m current non-syndromic due to “early” intervention and good treatment. However, my ongoing treatment continues to play its part.
For many, vague and routine symptoms generated by a syndrome contribute to the fact that NETs are frequently misdiagnosed with some people suffering from the side effects for many years before a correct diagnosis is made.
There are many other less known syndromes that appear to be directly or indirectly connected with NETs and I may update this post if I discover they are more prevalent than I think. Please let me know if you’ve been told you have a NET related syndrome not listed.
Related reading:
- Horrible Hormones – click here
- Tumour and Hormone Markers – click here
- A Witch’s Brew – click here
#NeuroendocrineCancer would love you to ignore this post. Don't let it win so please RT. https://t.co/sMbDDexdr3 via @RonnyAllan1
— Ronny Allan (@RonnyAllan1) March 3, 2016
Top 10 Posts & Pages in the last 48 hours (auto updates) (Click the titles to read them)
Thanks for reading.
I’m also active on Facebook. Like my page for even more news. Help me build up my new site here – click here and ‘Like’
Sign up for my newsletters – Click Here
My Diagnosis and Treatment History
Check out my online presentations
Check out my WEGO Health Awards
Like my new awareness page – click here or on the photo. (Like rather than follow please!)
Check out my Glossary of Terms – click here
Always good to read and be reminded. Thank you.
Thank you for this article. I have been duagnosed with carsinoid tumours in my liver. Back in 96/7 I had a blockage in my bile duct which turned out to be a carsinoid tumour which was removed through a Whipple’s procedure. In 2012 I had an appendectomy the, surgen saw lesions on my liver. A biopsy was taken a few months later show them to bd carsinoid tumours. There are at least 5 lesions which two or three are carsinoid tumours. I’ve had no symptoms other than pain. the doctors have said they wouldn’t have found out if I didn’t have the biopsy. My blood tests are all over the place sometimes up sometimes down. Next month I have another scan to see how they are changing. I’ve had scans every 6 to 12 months over the last few years. After all these scans they found in my case an MRI gives them the best result to see how the tumours are .If there is, any Change then they will do a PET scan again. My situation has been difficult for them because it’s not your avaverage case.
good luck going forward Geoff
Thanks for your posts Ronny. I learn something new every time I read them. I was diagnosed with a neuroendocrine tumour last September 2017. I had been having explosive diarrhoea for a few years and bowel cramps which I thought was due to IBS. I work as an endoscopy nurse and had previously refused a colonoscopy having seen many a patient suffer a lot of pain during this procedure. But to cut a long story short I agreed to have one at a different trust to where I work. A number of polyps were removed during the colonoscopy, but the one containing the NET was in a caecal polyp, which was later found to have originated in the terminal illium 4.7cm. With liver, mediastinum, humerus and pelvic metastases. I was informed by the local NET team that the only treatment available was Somatostatin which I commenced on last November. I have been amazed at how quickly it stopped diarrhoea and hot flushes. It also stopped me having to get up for a pee several times a night. It improved my skin, I used to get frequent boils which I don’t now seem to get. These symptoms I never imagined could be anything to do with NET’S. But it’s too much of a coincidence for them not to be associated. I had also become intolerant to alcohol in the last couple of years before diagnoses. One or two sips of alcohol or a few spoons of sherry trifle and whoosh a big flush and bad headache – which is still a problem I discovered last night after couple of sips of shandy. Anyway, I asked to be referred to the Royal Free Hospital in London for a 2nd opinion. I’m pleased I did, as they have said my tumour is resectable, and other treatments are available. I am awaiting gallium PET scan and echocardiogram and, fingers crossed, I could be having surgery very soon, plus other treatments to extend my life from a previous prognosis of 5 years to possibly 20+ years. I would definitely recommend anyone diagnosed with NET’S to seek a 2nd opinion, and the Royal Free Hospital NET team are the best in the world. I thank God that I have the wherewithall to research my condition and to find out where I am going to receive the best care and treatment.
https://polldaddy.com/js/rating/rating.js
Glad to hear you’re getting sorted. One surgeon’s ‘unresectable’ is another’s ‘resectable’. Seen that so many times. Good luck with rest of treatment!
Thanks for sharing this information. I will subscribe so I can keep reading!
https://polldaddy.com/js/rating/rating.js
Just for the record, no other reason except for someone else’s benefit, my only symptom, and that was just around the time of my diagnosis, was profuse sweating on the outer edges of my scalp. At an interview with a doctor, after my diagnosis, before meeting my surgeon, it was put down to hot flashes. I wanted to reply with what I was thinking but kept quiet. I certainly would have known by then what a hot flash felt like!!
Thankyou for this. the diagram is very interesting. I had late-diagnosed Cushings; the uncontrollable weight went on in the early ’80s. When I started having problems with my balance/vision in ’98 my Dr sent me for head MRI. Even this was misiagnosed by an ‘expert’ as Multiple Sclerosis and he took me into hospital to put me on a week of IV cortisol! I was saved by his Registrar who carefully read all my notes which showed abnormally high levels of cortisol, sent me for another MRI and correctly diagnosed a pituitary adenoma. This was removed in ’99 and after a year my weight went back to 9stone (from @ 13stone). Life got back to normal. Until 2011 when I suddenly had bouts of excruciating mid-gut pain about an hour after eating. To cut a long story short a midgut tumour was removed in Nov. 2011 along with a 60% liver resection due to metastisis.
I never had any NET symptoms/syndrome until after the operations and new metastisis showed-up in a 2013 scan. That’s when I was put on 90mg monthly Lanreotide injections.
But My symptoms are still not stable and I suffer with a mimick of IBS. My diet has been pruned as much as it can be. One day I’m ok, the next i have diaorrhea. It is a very isolating disease in that it’s so unpredictable. Gone are the days of eating out with friends/family.
I’ve adjusted, but it’s a very lonely life….
I really enjoy your blogs as they ‘understand’ – because, of course, you yourself are a sufferer.
Grateful thanks,
Dee Vickery
I’ve read a bit about pituitary and Cushing’s…… complex. I know a blogger with issues in both of those areas (or at least potential issues). There is a link to her blog here https://ronnyallan.com/2016/06/15/neuroendocrine-cancer-it-can-be-smoke-and-mirrors/
Would you mind emailing me a copy of the chart as well. I wish many physicians had a copy of this chart. Thank you – for this and all that you do.
Will do Karen
Im having my brain scans this morning and after yesterday’s results Dave and I have a guy feeling how these scans will turn out.. We have driven 240 miles and not one word!
good luck with the results. Better to have them looked at carefully rather than rushed 🙂
I wanted to copy the chart at the top, the one in different shades of blue, as I had many of those things before I was diagnosed. I still have many But it won’t copy. Any suggestions?
I emailed it to you, let me know if you get it!
Well Done! The same E’s do not apply to everyone. We each must find out what the culprits are in our syndrome. This disease is so frustrating!