Clams and coffee for a good morning

I like B vitamins and caffeine, that is a good combinations. And a bit of carbs. Coffee, clams, and oatmeal bar with dates makes a good breakfast. I don’t know the mechanism, but I am finding that coffee helps me to be more present in the moment with fewer anxious thoughts about the future. Going back to coffee was not a random idea, there are several studies in regards to the use of caffeine for treatment resistant OCD. By the way, OCD is not just about washing your hands multiple times or checking five times that you locked the door. The worst aspect of if it is how your mind is affected by unwanted and intrusive thoughts. There are infinite types of OCD, it can impact on any thought, on any subject, on any person, on any fear, and frequently fixates on what’s important in a person’s life. For example, if religion is important to someone, OCD fixates on unwanted intrusive thoughts around religion, perhaps making the sufferer believe their actions/thoughts will offend their god. Another example is if someone begins a new relationship, OCD can make a person question that relationship, their feelings, their sexuality resulting in almost constant rumination, perhaps with the sufferer worrying that they may be misleading their partner.

Obsessive thoughts are what happens when you just want to go for a walk in the forest. It’s a warm day, finally summer, you are surrounded by colourful moss on intriguing rocks. You want to wander around observing the details of nature, but your mind is fixated on the thought that there is no point. There is no god, therefore our lives are meaningless, and there is no point of this wandering. Or the thought is – I don’t have a child, so I need to work on getting a family. And then you feel that because you haven’t achieved this goal, you will be punished for wandering around the forest. You should be punished for any enjoyment as those are not focused on the goal. You need to solve the problem at hand, you need to act now, you need to think through the plan. And it goes on.

B vitamins are essential for creating dopamine, epinephrine, serotonin, and myelin. They also help the mind focus, help hemoglobin hold oxygen and lower cholesterol. Vitamin B is essential to good health. It is also used for energy production in the human cells. B vitamins help convert food often consumed as carbohydrates into fuel. They also help the nervous system function properly. B vitamins are water-soluble, which means that they are easily dissolvable in water and easily excreted out of the body via urine output. As a result of this type of vitamin that can be dissolved in water, individuals cannot overdose on them because all excess will simply be excreted.

Solubility – Solubility is defined as the maximum quantity of a substance that may be dissolved in another. How a solute dissolves depends on the types of chemical bonds in the solute and solvent. For example, when ethanol dissolves in water, it maintains its molecular identity as ethanol, but new hydrogen bonds form between ethanol and water molecules. For this reason, mixing ethanol and water produces a solution with a smaller volume than you would get from adding together the starting volumes of ethanol and water.

When sodium chloride (NaCl) or other ionic compound dissolves in water, the compound dissociates into its ions. The ions become solvated or surrounded by a layer of water molecules.

Thiamin is vitamin B1, it is essential in carbohydrate metabolism and neural function. It is water soluble and is absorbed through both active transport and passive diffusion. Not being endogenously synthesized, the only available source of thiamine is dietary (beef, poultry, cereals, nuts, and beans). In the human body, thiamine-rich tissues are skeletal muscles, heart, liver, kidney, and brain. Thiamine serves as a cofactor for a series of enzymes in different metabolic pathways and is required for the production of ATP, ribose, NAD, and DNA. Thiamin plays a key role in the maintenance of brain function. Thiamin diphosphate is cofactor for several enzymes involved in glucose metabolism whereas thiamin triphosphate has distinct properties at the neuronal membrane.

Thiamin metabolism in the brain is compartmented between neurons and neighbouring glial cells. Thiamin deficiency is commonly encountered in severe malnutrition associated with chronic alcoholism, HIV-AIDS and gastrointestinal disease where it frequently results in Wernicke’s encephalopathy (the Wernicke-Korsakoff syndrome).

In developed countries, the predominant use of industrial food processing often depletes thiamine content along with other vitamins and nutrients. An increased consumption of processed food in the form of simple carbohydrates, not supplemented with adequate levels of thiamine, has been named “high calorie malnutrition”. As thiamine is a key factor in the metabolism of glucose, an increased carbohydrate intake will proportionally increase thiamine’s dietary demand. Heavy consumption of tannin-containing or food rich in caffeine, theobromine, and theophylline (such as those present in coffee, chocolate, and tea, respectively) can inactivate thiamine, thereby compromising the thiamine status. Other risk factors that increase the likelihood of insufficient thiamine intake include aging, economic status, eating disorders, medical conditions affecting the gastrointestinal tract, subjects receiving parental nutrition, bariatric surgery, diabetes, and alcohol abuse.

Thiamine deficiency might cause brain tissue injury by inhibiting brain energy utilization given the critical role of thiamine-dependent enzymes associated within glucose utilization. This is supported by the significant rate of thiamine uptake by the blood–brain barrier emphasizing the high brain demand for thiamine and the need for its supply to sustain adequate brain functions.

Throughout the digestive tract, dietary proteins get hydrolyzed, releasing thiamine. In the intestinal lumen, alkaline phosphatases catalyze the hydrolysis of thiamine-phosphorylated derivatives into free thiamine.

There are cases of psychosis resulting from thiamine deficiency.

Case 1 – a 63-year-old woman with thiamine deficiency who showed auditory hallucinations, a delusion of persecution, catatonic stupor, and catalepsy but no neurological symptoms including oculomotor or gait disturbance. Her thiamine concentration was 19 ng/mL, only slightly less than the reference range of 20-50 ng/mL. Her psychosis was unresponsive to antipsychotics or electroconvulsive therapy, but was ameliorated by repetitive intravenous thiamine administrations at 100-200 mg per day. However, one month after completing intravenous treatment, her psychosis recurred, even though she was given 150 mg of thiamine per day orally and her blood concentration of thiamine was maintained at far higher than the reference range. Again, intravenous thiamine administration was necessary to ameliorate her symptoms. The present patient indicates that the possibility of thiamine deficiency should be considered in cases of psychosis without neurological disturbance and high-intensity T2 MRI lesions. Also, this case suggests that a high blood thiamine concentration does not necessarily correspond to sufficient thiamine levels in the brain. Based on this, we must reconsider the importance of a high dose of thiamine administration as a therapy for thiamine deficiency.

Case 2 – Mr A, a 40-year-old man, was transferred to our drug and alcohol dependency clinic after admission to the emergency department of a general hospital. He had a 25-year history of regular alcohol consumption (2 bottles of wine and 3–4 bottles of beer per day recently). Notably, he gradually increased his alcohol intake. His family stated that for the last 2 years he started his mornings with his usual “eye opener,” and he had not been eating enough or regularly. They also described periods of alcohol withdrawal, which resulted in delirium tremens symptoms such as confusion and auditory and visual hallucinations. He presented to the emergency room with forgetfulness, difficulty walking, falling down, urinary incontinence, losing his belongings, and not being able to recognize where he was or the current date. His family also reported that he had been telling incongruent stories that never seemed to have happened.

Mr A was diagnosed with Wernicke-Korsakoff syndrome according to DSM-IV diagnostic criteria, and diazepam detoxification, rehydration, and thiamine repletion therapy were started. He had no signs of alcohol withdrawal in the clinical follow-up. He was administered intravenous (IV) 2,000 cm3 of 5% dextrose and 1,000 mg thiamine hydrochloride. This regimen was administered until the fifth day of treatment since gait ataxia and restriction of eye movements were no longer prominently present. On the sixth day of treatment, the IV thiamine was replaced with 100 mg oral thiamine. Within the third week of the treatment regimen, his gait and postural ataxia improved and his orientation to time, place, and person was intact. By the fourth week of treatment, he was able to find his way around the city and back home when he was on home leave for 2 days. However, it was observed that it took him longer to remember his past experiences when questioned. He was discharged 41 days after his hospitalization. He had no significant mental symptoms apart from a minimally longer reaction time and minimal impairments in current memory, although he still had difficulty in tandem walk and a minimal nystagmus in his neurologic examination at discharge.

Neuropathology of Wernicke-Korsakoff syndrome is characterized by gliosis and microhemorrhages specifically in the periaqueductal and paraventricular gray matter, atrophy in the mammillary bodies and thalamus, and volume deficits in the hippocampus, cerebellar hemispheres, pons, and anterior superior vermis; however, anterior thalamus, mammillary bodies, and the mammillo-thalamic tract are reported to be related with later memory impairment and Korsakoff syndrome.

Active transport – the movement of molecules across a membrane from a region of their lower concentration to a region of their higher concentration—against the concentration gradient or other obstructing factor.

Passive diffusion – is a movement of ions and other atomic or molecular substances across cell membranes without need of energy input. Unlike active transport, it does not require an input of cellular energy because it is instead driven by the tendency of the system to grow in entropy.

Hyrdolysis – any chemical reaction in which a molecule of water ruptures one or more chemical bonds.

Alkaline phosphatase – an enzyme that liberates phosphate under alkaline conditions and is made in liver, bone, and other tissues.

Gliosis – is a nonspecific reactive change of glial cells in response to damage to the central nervous system (CNS). The glial cells surround neurons and provide support for and insulation between them. Glial cells are the most abundant cell types in the central nervous system. The four main functions of glial cells are: to surround neurons and hold them in place, to supply nutrients and oxygen to neurons, to insulate one neuron from another, and to destroy and remove the carcasses of dead neurons (clean up).

Microhemorrhages – cerebral microhemorrhages, best visualized by MRI, result from rupture of small blood vessels in basal ganglia or subcortical white matter.

Mammillary bodies – the mammillary bodies are part of the diencephalon, which is a collection of structures found between the brainstem and cerebrum. The mammillary bodies are best known for their role in memory, although in the last couple of decades the mammillary bodies have started to be recognized as being involved in other functions like maintaining a sense of direction.

Auditory Hallucinations Simulation

I hope technology will help us to simulate others’ experiences. This is especially needed in psychiatry. I often found myself lacking appropriate words to describe what I felt. My previous psychiatrist misdiagnosed me with schizophrenia. There is currently no lab test to verify whether someone does have schizophrenia, my diagnosis was based on a verbal consultation. I don’t know what people with schizophrenia experience so I can’t know whether my experiences were actually similar or not. Did we all feel this extreme fear in the same way or was ‘fear’ just a common word that we used but our experiences were actually different? I’m sure many people out there, like me, dream of a machine that would allow us to project our feelings onto someone else. We don’t have such an invention at the moment, but the first step is through the use of audio and video. I discovered an interesting representation of auditory hallucinations on YouTube, link below. I know that it doesn’t convey the emotions that a person could be experiencing along with the hallucinations, but it is a start in explaining how schizophrenia/psychosis can affect a person.

Auditory hallucinations – representation

It’s better to listen to this audio in headphones in order to get a better simulation of the surrounding sound. Put on your headphones and try to go through the whole length of the audio. It’s quite unpleasant. It’s nice to know that any second you can pause the video. With real psychosis unfortunately you don’t know when it’s going to end. Psychosis also is usually not just hearing voices that aren’t there, it’s thoughts and emotions – panic, fear, distrust. How can someone know that they are having a psychotic episode versus rational thoughts that are unpleasant? The line is not clear. Recently I had an episode at work during which I kind of heard my boyfriend’s voice inside my head saying that what I did was a ‘low level job’, ‘it was pointless’, that he wouldn’t do such a job, that I was wasting my life. Was that a psychotic episode caused by my immune system acting up or does everyone experience such moments? I would say it was closer to psychosis as it was similar to the audio representation – the voice was not part of my thoughts, it was inside my head, but I could not control it. This seems similar to what people with schizophrenia describe about auditory hallucinations, but then many people without schizophrenia also complain about inside negative ‘voices’. Perhaps by ‘inside voice’ in general people really mean thoughts, and these are more under their control, unlike the hallucinations.

Below is another video of schizophrenia simulation. As one comment states, “This is KINDA accurate but you can’t really recreate the feeling of panic and doubt and paranoia. During an episode you’re possessed by so many emotions that a video just can’t convey.”

Schizophrenia Simulation

What I experienced in the most acute stages of encephalitis also could not be portrayed well with just audio or video. What I experienced was primal fear. Imagine maybe being in an airplane, a long trans-Atlantic flight. You are going 900 kilometers per hour, ten thousand meters above the ocean. Suddenly there is severe turbulence. You’ve experienced turbulence before, but not of this magnitude. You hope it will cease soon, because the pilots know what they are doing, right? But it doesn’t, there is another fall through the air, you can feel it. Perhaps before the turbulence started you were reading a book, do you think you will be able to continue? Or you were talking to the person you are flying with about housing prices, will you be able to hold the conversation, or will you be overwhelmed with the primal fear? The fear that we experience when we are suddenly reminded of our mortality with an added rush of adrenaline. And not just our mortality, but also the mortality of people who for us make our world. That’s what acute encephalitis episodes were like for me. It was like constantly being in that passenger plane above the ocean in severe turbulence. And if that goes on for long enough, when the fear is constantly present, you may then actually start to wish for the situation to resolve in any way, as long as it resolves quickly. I mean that you may wish for the plane to just fall quickly, you no longer believe in safe arrival, but you just want to already escape the fear and the anticipation of pain.

Autoimmune Encephalitis vs. Schizophrenia

I don’t have schizophrenia so I can’t say that I experienced it, but I was misdiagnosed with it, therefore it’s possible that some of my experiences are similar to those of people with schizophrenia. Unfortunately autoimmune encephalitis is often  misdiagnosed as a psychiatric disorder. I spent a lot of time in the Understanding Hashimoto’s Encephalopathy Facebook group and after talking to the women there, the commont story that emerged was that most of them were initially referred to a psychiatrist and treated with antipsychotics/antidepressants/benzodiazepines. I say women because the group members are mostly female, probably over 90%. Autoimmune diseases affect women more often than men and this seems to hold true for autoimmune encephalitis. Schizophrenia on the other hand is more common among males.

I am not a schizophrenia expert, but since my psychiatrist assumed that I had it and I was treated for it, from experience I can say that schizophrenia is usually treated with antipsychotics such as risperidone and olanzapine. Psychotherapy can also be recommended but in addition to the antipsychotics, it would not be enough on its own usually. Autoimmune encephalitis does not improve with antipsychotics. AE is inflammation of the brain that is caused by the immune system and it required immune suppression such as IV steroids, IVIG or plasmapheresis. Many patients have to stay on oral immune suppressants such as prednisone or Cellcept. Some get regular Rituxan infusions. Some patients do take antidepressants or antipsychotics in addition to the immunosuppressant treatment, but the first step should really be suppressing the immune system.

Autoimmune encephalitis often does cause psychiatric symptoms such as intense fear, panic, paranoia, delusional thoughts and depression. All these symptoms could be present in patients with schizophrenia. Schizophrenia is also much more common than autoimmune encephalitis, it affects about 1% of population. Since psychosis due to autoimmune reaction is quite rare, it’s reasonable for a psychiatrist to assume schizophrenia, schizoaffective disorder, or psychotic depression. I do think though that if the psychosis is present along with physical symptoms, a blood test for autoimmune conditions should be performed as well. I don’t think schizophrenia is associated with facial swelling, lightheadedness, brain fog, extreme fatigue, etc. Autoimmune encephalitis on the other hand does cause all these physical symptoms and more severe ones as well such as seizures and going into a coma. Also I think that if a patient has tried different antipsychotics for several months and has not responded to them, it’s probably time to consider that there might be a different cause and perform further testing. My psychiatrist for some reason did not consider this. I was not aware of existence of autoimmune diseases, it was my mom who suggested specific blood tests.

BBC – Some psychosis cases an immune disorder

Further on, once I started reading more about causes of panic, anxiety, and mood swings, I bought a glucometer and decided to check my blood glucose. My fasting blood sugar was checked previously at the hospital and it was fine, but after performing my own measures, I noticed a problem. After specific meals that contained high glycemic index foods, my blood sugar could stay at higher than 11 mmol/L two hours after eating. Diabetes UK states that blood glucose over 8 mmol / L two hours after a meal is of concern. Later on I spoke about these results to a doctor and she said I may have hyperglycemia. I also noticed feeling psychologically worse when my blood sugar was high. My point here is that if you are not responding to antipsychotics, there are further things to investigate. There is autoimmune testing – high levels of thyroid antibodies could indicate Hashimoto’s encephalitis, there are also other types of autoimmune encephalitis with different antibodies (NMDA receptor encephalitis, for example). TSH, free T3, and free T4 is a standard test to check the thyroid function, hypo/hyper thyroidism can also cause psychosis. Diabetes/hyperglycemia can affect your mood. Usually fating blood sugar is checked, but I would also verify blood glucose levels two hours after a meal with high glycemic carboydrates.

Diabetes UK – Diabetes and Hyperglycemia

 

Autoimmune Encephalitis and Diet

This post will be mostly based on anecdotal evidence , but I believe this information is still useful and there is not much harm in the suggested diets. In the worst case, the diet won’t help with autoimmune symptoms,  and you’ll just end up eating more vegetables. I don’t think that’s a terrible outcome.

The most popular diet for autoimmune diseases is the Autoimmune Protocol Diet (AIP). Most popular doesn’t mean it has the most evidence to back it up, but for whatever reason, it got around the internet. The AIP diet excludes many foods that are considered to be inflammatory and claims to reduce levels of thyroid antibodies. I cannot claim that his mechanism is true as there are almost no scientific papers on this, only anecdotal evidence. On the other hand, this diet is not unhealthy, so I doubt someone would be worse off by trying it. Usually bloggers/naturopaths recommending the diet suggest to try it for at least thirty days. Food groups that are excluded are gluten, all grains, pseudo-grains, dairy, legumes, beans, nuts, seeds, nightshades, eggs, vegetable oils, processed foods, and sugar. I might be forgetting something because there are so many items that get excluded, but if you are interested, you can read about the diet below.

Autoimmune Protocol Diet

What evidence is there? Well when I googled “AIP diet evidence”, I found one paper. You can try the same Google search. This particular study found that following the AIP diet, 6 weeks elimination phase and 5 weeks maintenance phase, improved endoscopic inflammation in patients with IBD (irritable bowel disease). Only 18 patients were enrolled in the study, so that is a very small sample size. Also such a study does not tell us whether it was necessary for all these food groups to be eliminated, maybe the results would be the same if only gluten and processed foods were eliminated. So it is some evidence that the diet helps but it is only one study and it doesn’t tell us about the mechanism of action of this dietary intervention.

Efficacy of the Autoimmune Protocol Diet for Inflammatory Bowel Disease

Personally I did follow the AIP diet for about a year. When I found out in June 2016 that I had high levels of thyroid antibodies, I finally started to have some hope that maybe I have an autoimmune disease that can be treated instead of treatment resistant schizophrenia and psychotic depression. My mom googled a lot at that time, I didn’t have the energy or motivation to do it, and she convinced me to start trying dietary changes. I started by excluding gluten and dairy and later on went on the AIP diet and stayed on it until December 2017. In June 2016 my Anti-Tg antibodies were over 1000, Anti-TPO was 40 something. Comparing to spring/summer 2016, I did improve by fall 2017, and my Anti-Tg antibodies reduced to about 500. Anti-TPO stayed the same. Was this improvement directly related to the AIP diet and was it necessary for me to eliminate all the food groups? I don’t know the answer to that question. I did go to a gastroenterologist who diagnosed me with chronic gastrointestinal inflammation and advised me to go on a low FODMAP diet. AIP diet overlaps with low FODMAP diet, therefore it could be that it was the elimination of high FODMAP foods that helped me.

The low FODMAP diet is based on the idea that certain foods contain compounds that contribute to gastrointestinal disorders such as IBS. FODMAPS are short chain carbohydrates and sugar alcohols, such as fructose, fructans, galacto-oligosaccharides, lactose, and polyols. Research indicates that some people might not be able to digest these compounds well and this could lead to inflammation in the intestines and gas produced by bacteria as they break down undigested carbohydrates.

Below is a list of high and low FODMAP foods (for those that are FODMAP intolerant it is advised to avoid high FODMAP foods, this can be discussed with a gastrointerologist).

High and Low FODMAP Foods

Could a bad diet cause brain inflammation and psychotic depression? Could a change in diet reduce symptoms if there is inflammation? I don’t think at this point we have a concrete answer, there have been studies though which indicate that a specific diet could improve your mood and physical health. Autoimmune encephalitis is quite rare and I haven’t seen studies on AE patients and diet changes, but I still encourage you to consider whether you are eating healthy and to consider making changes. In general, from what I’ve read, many doctors consider the Mediterranean Diet. This diet includes whole grains, a lot of vegetables,  yogurt , nuts and seeds, and more fish instead of meat (increasing Omega 3 content). There has been a study with positive results, indicating that Mediterranean diet can help patients with depression.

Mediterranean Diet Depression Article

So which diet is best, should you try a specific diet, which one? There is no medical test for this at the moment, only trial and error. As I mentioned, I was on the Autoimmune Protocol Diet for about a year and I did see an improvement in symptoms and reduction in Anti-Tg antibodies . My gastroenterologist also advised me to stick to a low FODMAP diet due to my abdominal issues and I have been following this advice. After I received the IV steroids treatment in December 2017, I relaxed my AIP dietary restrictions and tested several items. I stick to eating gluten-free free and cow dairy free, also I felt that I had skin/abdominal issues become aggravated by potatoes, peanuts, and hot peppers. I avoid processed foods and vegetable oils.

It sounds restrictive but I found this diet to be working for me and I feel that I have enough variety. I eat a lot of goat/sheep/buffalo plain yogurt with nuts and seeds, tea with goat milk, quail eggs, poultry , seafood. In terms of vegetables – zucchini, carrots, squash, plantains, sweet potatoes, kale, spinach, bell peppers, etc. Grains – black rice,  quinoa, buckwheat, oatmeal. For bread I eat sourdough version and sometimes I make cassava flour tortillas. I don’t eat beans and legumes much because they are high FODMAP, sometimes I add canned chickpeas or sprouted mung beans. For cooking I use olive, avocado , and coconut oils.

My story at Autoimmune Encephalitis Alliance Org.

Hi everyone, I am very happy that my story got posted in AE Alliance blog. I hope it will help some readers to receive a proper diagnosis. I cannot say that I recovered 100%, but there is improvement after IV steroids, and at least now I know the specific diagnosis. I’m sure that for many being told by doctors multiple diagnoses is a horrible experience. Going from one doctor to next, being told it’s schizophrenia, major depression, schizoaffective disorder… More doctors need to be aware of HE!

Hashimoto’s Encephalitis – Diagnosis and Treatment

Hashimoto’s Encephalitis (HE) is a diagnosis that is made through exclusions of other causes. There is no one specific test to diagnose HE, but usually the tests that are performed are thyroid antibodies (Anti-Tg and Anti-TPO) blood test, MRI, EEG, and spinal tap. HE is a quite rare disease, therefore it is definitely not something that would be tested for right away. Many healthy people have elevated thyroid antibodies, these antibodies can also be an indicator of Hashimoto’s thyroiditis, which is not the same as Hashimoto’s Encephalitis. After I continued to not respond well to anti-depressants and anti-psychotics, I consulted with an endocrinologist to discuss whether I had any thyroid issues. My thyroid hormone levels were normal but elevated Anti-Tg and Anti-TPO antibody levels were discovered. At that point the endocrinologist diagnosed me with Hashimoto’s thyroiditis and stated that the thyroid antibodies were not something to worry about at the current moment as they were just an indicator that I might develop thyroid disease twenty years from now on. There is still no exact proof that it is these thyroid antibodies that caused my symptoms, but my condition did improve after intra-venous treatment with Solu-Medrol (anti-inflammatory glucocorticoid), and my antibody levels decreased as well. I will not claim causation, but there is correlation here, and my neurologist agrees that I have improved since the steroids treatment.

I am not sure whether the numbers are meaningful, it had been stated that specific values are not correlated with the severity of HE symptoms, but initially in June 2016 my Anti-Tg levels were over 1,000 and my Anti-TPO levels were above 40. This was during the period of time when I lost my job and was on Latuda and Sertraline. I was finding it physically difficult to wake-up, to move, and to talk. My speech was becoming slower and everything was also followed by intense emotional pain. It was sort of a state of grief without cause. As I mentioned in my previous posts, I did go on AIP (autoimmune protocol diet) diet after discovering that I potentially had autoimmune disease, and my symptoms did improve. I was able to go back to full-time work in November 2016 and after awhile tests showed that my Anti-Tg levels decreased to around 500, Anti-TPO levels stayed about the same. Again, this is anecdotal evidence, and I cannot claim that it is specifically the AIP diet that helped me. A gastrointerologist did advise me to try a low-FODMAP diet and AIP overlaps with low-FODMAP. Also I did have a ‘maybe’ result for celiac testing and I went gluten-free. I also stopped taking anti-psychotics and a new diagnosis of Hashimoto’s thyroiditis (at that time), instead of schizophrenia (diagnosis that I received previously), provided me with psychological benefits. Therefore it is not possible to untangle all the changes that I made during the summer and we don’t know which factor improved my condition. Some conditions improve and relapse in cycles as well, therefore changes in symptoms could be not due to the actions of the individual.

Autoimmune Encephalitis Story (part 3)

Part 1:

Autoimmune Encephalitis Story (part 1)

Part 2:

Autoimmune Encephalitis Story (part 2)

In June 2016 I actually started to have some hope. No, I didn’t throw away my charcoal grills, but at least now there was something to research, testing to be done. Previously my psychiatrist told me that I had a choice between psychosis and antipsychotics and I don’t think that should ever be said to a patient. If the antipsychotics are not working and the psychosis is emotionally unbearable, what message are you sending your patient? Well you are giving them another reason to commit suicide – why live if the only choices you have are being non-functional and psychotic or being on olanzapine. Anytipsychotics do help some people and therefore they are a good choice for them but for me they were not working at all, so the right thing to say would be that more investigations would be done. As you see from the story, it was not the psychiatrist who ended up investigating, but my mom. So I got lucky, but it should not be this way. Access to proper treatment should not be based on luck and having someone googling your symptoms for you, this is the doctor’s job.

So in June 2016 I went off Trazadone, Latuda, Mirtazapine, Lorazepam. I only continued with Sertraline until October 2016. I started taking Cytomel (man-made version of thyroid hormone T3) and I got tested for celiac disease. The results were a ‘maybe’, inconclusive, but  I still decided to try going gluten free and dairy free as some people with autoimmune disease do report improvement after eliminating those foods. Yes, some will say it is only anecdotal evidence, but when the way you feel on a daily basis makes you purchase hibachi grills, anecdotal evidence is good enough. Especially when the doctors have no suggestions or solutions for you. I was told that Hashimoto’s thyroiditis was not something to be too concerned about because it could affect the thyroid in the long run but at the moment my thyroid hormone levels were normal. I was told that I had nothing to worry about for the next twenty years. But then why were there old women, whom no one else notices, asking me to help them die? Why was I afraid of passing by Starbucks because hearing music from the speaker caused a feeling of grief? At that point I have not yet heard about autoimmune encephalitis, which is brain inflammation, so I had no answers to these questions.

I was now off the antipsychotics and at first I eliminated just dairy and gluten. It was quite difficult for me and I made a mistake of substituting everything with gluten-free labeled products, which actually contain a lot of refined carbs. Still, this change in diet, or coming off the neuroleptics, or feeling some hope after reading overly positive reviews on AIP diet promoters’ blogs, but I started to feel a sort of feeling of waking up.