Hymenolepis diminuta observations and paper

As described in my previous posts, I have started HDC helminth therapy on June 4th. It has now been over a month. So far I have taken HDC three times – 10 on June 4th, 10 on June 9th, and 20 on June 25th. I have also updated my NA by adding three more on July 6th. It has now been over two weeks since my last HDC dose, helminth therapy wiki suggests dosing every two weeks and adult dosing is in range 30-60 HDC bi-weekly. I am waiting for my next order of 20, the delivery has been slow, and it’s expected to arrive on Friday. After that I plan to increase the dose to 30 as is advised, 20 may be not enough of a therapeutic dose for an adult.

One important observation is that during my period, which happened soon after the third dose of HDC, I did not have to take any pain relievers. I see this as not just a coincidence because last such occurrence happened almost a year ago in July 2018, after I started NA therapy. After that one time unfortunately pain levels during periods went back to usual unbearable and as usual I would take at least two Naproxen gels, sometimes also an ibuprofen. Several times I had to leave work early or work from home. Therefore I was quite surprised that when my period occurred in the end of June the pain began as usual but did not increase to unbearable levels. I went to work as usual, I always keep Naproxen in the drawer in the office and at home, but the pain never rose to the level where I would need a pain killer. I would say that just for this benefit HDC is already worth continuing as not being crippled by pain made me feel more free. Even though it’s not my fault, I often feel guilty leaving home early or asking to work from home every month. I am also not pleased with having to take Naproxen as for me it causes acid reflux and it makes me think that I am undoing the benefits of my efforts to heal the gut.

Another observation was recently increased heat tolerance.  In beginning of July temperatures rose to over 30 degrees Celsius and there is no central AC where I live. In order to cool down the house, I usually have to install two window air conditioner units. These units were taken down for the winter, so there were several days of temperatures around 30 degrees inside. I noticed that my sleep was not as disrupted as it previously would during heat. Also in general I was not as incapacitated by the temperature, I did feel lethargic, but did not have as severe indecisiveness nor mood swings exacerbation that often occur for me during summer heat.

The new lab test results are also encouraging. Free T4 and T3 stayed at the same levels, within normal range. TSH went down to 2.0, which is below the previous value of 2.58. This is a positive result, since some research indicates that the optimal cut- off value of TSH is 2.5 MIU/L. Anti-TPO antibodies have also decreased.

TSH cut off point based on depression in hypothyroid patients

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On a side note, I found that someone wrote their undergrad honors thesis on Hymenolepis diminuta. “Impacts of Hymenolepis diminuta (benign helminth worm) colonization on chronic pain and the central nervous system in Sprague Dawley rats“. If I would go back in time, I would prefer to also study neuropsychology. Unfortunately in my undergrad I was calculating bond and option prices. Glad to hear whenever someone is doing research on treatments for autoimmune disorders, specifically the connection between neuropsychiatric problems and inflammation. “The results from this project partially support the tenets of the hygiene hypothesis. Though behavioral results following CCI surgeries were inconclusive, molecular investigation of cytokine levels in the hippocampus showed promotion of an anti-inflammatory cytokine milieu due to the upregulation of IL-10 and downregulation of its receptor. These promising results guide future research toward investigation of cytokine levels in other brain regions, such as the amygdala.

Impacts of Hymenolepis diminuta (benign helminth worm) colonization on chronic pain and the central nervous system in Sprague Dawley rats

CAMH ER Waiting Room

The room is in the building at College and Spadina. The room doesn’t have any windows,  but it does have a clock, so you can know what time of day it is. What you can’t know is when you will be let out (but to be fair, involuntarily hospitalization can be a maximum of 72 hours). There are armchairs along the perimeter of the area and in the middle. There are about six of us at the moment. Some will be released soon and new ones will arrive. None of us want to be waiting here, twisting on the pale green chairs. Also most don’t agree that they should be here. A young black woman is banging on the locked door of the staff room, a nurse comes out. The woman is nearly dressed with a designer purse and fur boots. She starts pacing back and forth. “If I knew what this place is like, – she yells at the nurse, – I would have never come here. Look at me, I don’t need to be here. I don’t cut myself and shit.” The nurse talks to her calmly, she tells her what she tells everyone – you have to wait to speak with the psychiatrist. The woman continues to yell that she is not like the rest of us. She complained to her family doctor about stress at work and the doctor referred her to this address,  told her that she could get a note for stress leave. She just wants a note,  she assures that she doesn’t cut herself.

As of that is what we all do. If only it was that simple – you either cut yourself and are insane, or you don’t,  and are not. I’ve never cut myself and yet I voluntarily checked myself into the CAMH ER. I also didn’t think that I needed to be in there, but there was no other way. I wanted to be set free from my inflamed brain, from the malfunctioning neuronal synapses. I wanted to be free to get lost in writings of other people’s ideas, to play Bach’s Gavotte, to be attracted and be attractive. I wanted to be released from the dark well inside my own mind. I wanted to suppress the hell, to get the intravenous immunoglobulin treatment. But how to convince them, how to make them understand that is what I needed?

After sometime the black woman was released. I was still waiting. There was renewed yelling,  coming from a different patient. Similar to the woman who just left,  she was yelling at the nurse that she didn’t need to be here. She was also getting extremely agitated,  I think if she had something to throw,  she would. The whole room now was aware that she was old enough to have ten children and that she didn’t want this visit on her record. Her sister couldn’t take care of her own kids and who would then be doing it if not her? But with a CAMH visit on the papers, maybe she wouldn’t be allowed to take the children in. The nurse tried to explain that visiting CAMH was not same as police record, but the woman already went into rage, reasoning does not work at that point.

So why do we all scream in fear – I shouldn’t be here, I am not like the rest of them? We must have evolved to have this fear of being declared insane. Insane means being banned from the tribe, starving alone in the savannah. It’s hard to let go of that basic fear of being abandoned by our tribe. Even in the isolated room at CAMH, where only the doctors and about five other strangers could hear you, we still don’t want to admit that something could be wrong. We could admit cancer, meningitis, infertility, but not that we are not mentally well. Most diseases are just affecting our body, but it is our mind that makes us who we are. And if there is something wrong with that, then what are we? Of course this is not what I think, this is an assumption of what goes on through people’s minds in this state of fear. There is no separation from mind and body, both are a combination of cells, proteins, amino acids. Signalling to each other, reproducing. And any part of the whole mechanism can malfunction.

I would say – learn to accept. You didn’t choose this body, you just sort of woke up in it. I would have chosen another model, if I could, but no choices were given. Well here I am, at CAMH ER, because some signals are malfunctioning, and it’s not my fault. This is the situation though, and I have to accept.

Autoimmune Encephalitis and Genes

I was involuntarily hospitalized for the first time in the psych ward in October 2015, in June 2016 I was diagnosed with Hashimoto’s thyroiditis, and then in April 2017 I was diagnosed with autoimmune encephalitis (specifically Hashimoto’s encephalitis). I was diagnosed also with coeliac disease, which is a permanent autoimmune disorder. That is a lot of diagnoses, all autoimmune related, and they all came in a short period of time (it’s not surprising though, because often people with an autoimmune disease tend to have more than one – this fact points to the genetic cause of a faulty immune system).

Since then I have done a lot of research on my condition, but in 2015/2016 I was probably still in denial. I remember being certain that my depression was due to only external circumstances such as my job, not having kids, small apartment, etc. I kept thinking  – I know it’s the bachelor apartment that is making me feel claustrophobic and trapped, I have never lived in such a small space, this is not how people should live, this is causing my depressive state. I was living in a small bachelor apartment together with my boyfriend and it was not enough space for two people, you start to irritate each other, and that could have been contributing to stress. But I also know that I was not accepting that something was also biologically wrong with me, that I needed to investigate medical causes. At that point I was already seeing a correlation between eating wheat and brain fog, but then I would go again to buy a chicken wrap and when my thoughts would become less clear, I still kept repeating – it cannot be the wrap, this seems very unlikely, it must be something else – probably I am allergic to mold in the apartment. It’s also very difficult to analyze the situation when your brain is getting worse daily and you don’t realize it.

The correlation between eating wheat and brain fog, based on my observations, was very strong though, and I did finally start eating gluten-free. Then I received my test results for antibodies associated with coeliac disease and the values were right at the threshold. To me this was a clear indication of disease, since even though I had been not eating gluten for a while, the antibodies were still present and the value was right at the point of making a positive diagnosis.

What also helped me understand and accept why I was hit with a number of autoimmune disorders. Several years ago I sent my saliva to 23andme and got back results telling me that I was mostly Eastern European (obvious to me) and Balkan (was a surprise). Also that I had increased risk of developing age-related macular degeneration. I thought this was irrelevant to my symptoms and I did not open 23andme again for a while. I logged in a few months ago and the website had been updated, there was a new result – Celiac Disease.

23andme_1

From 23andme – the variant tested is a change from a C to a T in the DNA sequence of the HLA-DQA1 gene. The rs2187668 marker is a tag SNP for the HLA-DQ2.5 haplotype.

From Wiki: DQ2.5 and the linked DR3 are associated with probably the greatest frequency of autoimmune occurrence relative to any other haplotypes. The haplotype is positively associated with coeliac disease, dermatitis herpetiformis, juvenile diabetes, Lambert-Eaton myasthenic syndrome (LEMS), Sjögren’s syndrome, and autoimmune hepatitis (although significant proportion of the risk is secondary to coeliac disease). DR3 and/or DQ2.5 are linked to the following diseases: Moreen’s ulceration, “bout onset” multiple sclerosis, Grave’s disease and systemic lupus erythematosus.

I can’t say that I felt great when I read this, but I was able to say to myself – “now I understand”. I was not unlucky to have an onset of autoimmune encephalitis, a very rare disease, I am unlucky to carry this genetic mutation, but given this mutation, coeliac disease and encephalitis are not so unlikely. How to use this information? I printed out my test results and handed them to my family doctor and my neuropsychiatrist. There is a difference between a one in a lifetime occurrence of brain inflammation after some virus and being genetically predisposed to multiple autoimmune diseases. Unfortunately it is the second case for me and I want to make sure that doctors are aware of this.

Another genetic mutation listed in my 23andme results is Gene: CFH. The variant tested is a change from a T to a C in the DNA sequence of the CFH gene. It results in a version of the complement factor H protein that may not be able to regulate the immune system as well. I have read about this mutation and did not find that much information, but it does mention that it also affects immune system regulation. Perhaps it is the combination of the two mutations – in the HLA and CFH genes that for me lead to development of several autoimmune diseases. Research and time will tell us more.

List of medications and supplements for depression and obsessive thoughts

Here I will list different medications, supplements, and  procedures that are used to treat depression, anxiety, and obsessive/suicidal thoughts. I am not suggesting that you go out and buy a bunch of antidepressants and try them one by one, I just want you to be aware of what exists out there so that you can discuss this with your doctor. Some things, such as a daylight lamp, or omega 3s, don’t require prescription. Since I have been dealing with autoimmune encephalitis for more than three years already,  I have tried most of these treatments in attempts to reduce my depressive symptoms, psychosis, and intrusive thoughts.

Many people do get better with antidepressants. I have to note though, that in my case, the most useful treatment was high-dose intravenous steroids (IV Solu-Medrol) for five days. I did have severe psychotic depression with suicidal tendencies, my neurologist and psychiatrist propose that this was due to autoimmune encephalitis (Hashimoto’s encephalitis) – brain inflammation. Many people have milder depression and do well after antidepressant treatment. My state has improved but it is not without moments of intrusive thoughts and for this reason I continue trying different methods.

Medication

Antidepressants

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How does your psychiatrist determine which antidepressant to try? It seems that in general this is not based on any specific medical tests, but is based on the discussion with you about your symptoms. I did get a genetic test done on my saliva. This was part of CAMH Impact Study in Toronto, the provided report is called GeneSight Psychotropic Test. The company states that their test “analyzes how your genes affect your response to psychotropic medications commonly prescribed to treat depression, anxiety, bipolar disorder, posttraumatic stress disorder (PTSD), obsessive compulsive disorder, schizophrenia and other behavioral health conditions. There are dozens of medications used to treat depression and other mental illnesses and selecting the right antidepressant medication or other medication can be a challenging and frustrating process. GeneSight Psychotropic’s genetic testing enables your clinician to identify and avoid depression, anxiety and/or other medications that are unlikely to work or may cause side effects.” This test was provided to me for free by CAMH in Toronto.

GeneSight Psychotropic Test link

New antidepressants: 

There are three new antidepressants that have become recently available in US and Canada – vortioxetine, levomilnacipran extended-release (ER), and vilazodone. Vortioxetine – may enhance serotogenic activity via reuptake inhibition of serotonin receptors. Levomilnacipran is a a serotonin norepinephrine reuptake inhibitor. Vilazodone is a serotonin reuptake inhibitor and partial serotonergic 5-HT1A receptor agonist.

The role of new antidepressants in clinical practice in Canada: a brief review of vortioxetine, levomilnacipran ER, and vilazodone

Antipsychotics

Sometimes antipsychotics are added to antidepressants during treatment. Usually antipsychotics are used to treat schizophrenia, why are they given to depressed patients? I think the reason is that many patients don’t achieve remission with antidepressants, so other medications/methods must be tried. In the large National Institute of Mental Health Sequenced Treatment Alternatives to Relieve Depression (STAR*D) trial, only about 30% of patients achieved remission (virtual absence of depressive symptoms) after up to 12 weeks of first-line treatment with citalopram. Evidence of the usefulness of atypical antipsychotics in treating MDD goes back more than 7 years (statement from 2009). A controlled trial found that the combination of olanzapine and fluoxetine was more helpful in treating patients with MDD (without psychosis) than fluoxetine or olanzapine alone.2 The group that received combination therapy did significantly better than the others. In November 2007, the FDA approved aripiprazole as the first atypical antipsychotic to treat MDD. It is specifically for adjunctive treatment, along with an antidepressant, for the treatment of refractory MDD.

Atypical Antipsychotics for Treating Major Depression

Aripiprazole (Abilify) – was approved by FDA for major depressive disorder in 2007, for patients who had inadequate response to antidepressants. Aripiprazole is a partial agonist at dopamine D(2) and D(3) and serotonin 5-HT1A receptors, and is an antagonist at 5-HT(2A) receptors.

Ripseridone – risperidone has actions at several 5-HT (serotonin) receptor subtypes. A study showed that depression symptoms improved modestly but significantly more in the risperidone group compared with the placebo group, as measured by clinician-rated symptom response and patient-rated self-assessment. The 17-item Hamilton Rating Scale for Depression score improved more in the risperidone group versus the placebo group.

Quetiapine (Seroquel) – quetiapine is a dopamine, serotonin, and adrenergic antagonist, and a potent antihistamine with some anticholinergic properties. Quetiapine binds strongly to serotonin receptors; the drug acts as partial agonist at 5-HT1A receptors. One study involved more than 700 people who had suffered from depression for at least one month but less than one year. Patients were randomly assigned to take one of three doses of Seroquel or a placebo once a day for six weeks. Those taking Seroquel showed greater improvement in depression symptoms than those on placebo.

Supplements

St. John’s Wort  – hypericum perforatum, it is a flowering plant. Sold in health stores/drug stores/online. A 2008 review of 29 international studies suggested that St. John’s wort may be better than a placebo and as effective as different standard prescription antidepressants for major depression of mild to moderate severity. A 2015 meta-analysis review concluded that it has superior efficacy to placebo in treating depression, is as effective as standard antidepressant pharmaceuticals for treating depression, and has fewer adverse effects than other antidepressants.[23] The authors concluded that it is difficult to assign a place for St. John’s wort in the treatment of depression owing to limitations in the available evidence base, including large variations in efficacy seen in trials performed in German-speaking relative to other countries. In Germany, St. John’s wort may be prescribed for mild to moderate depression, especially in children and adolescents.

Omega – 3 – omega-3 fatty acids are found in oily fish such as salmon. You can also purchase fish oil supplements in health stores/online. In general eating oily fish is considered to be a healthy choice. There is some evidence that omega-3s might help with depression, but this evidence is not very strong. From Cochrane review: “At present, we do not have enough high quality evidence to determine the effects of n-3PUFAs as a treatment for MDD. We found a small-to-modest positive effect of n-3PUFAs compared to placebo, but the size of this effect is unlikely to be meaningful to people with depression, and we considered the evidence to be of low or very low quality, with many differences between studies.

SAMe – S-adenosyl-L-methionine (SAMe) is a compound found naturally in the body. SAMe helps produce and regulate hormones and maintain cell membranes. A synthetic version of SAMe is available as a dietary supplement in the U.S. In Europe, SAMe is a prescription drug.  From Cochrane review: “We included eight studies involving 934 people in this review. There was no strong evidence of a difference in effectiveness between SAMe and imipramine or escitalopram when used alone. It was superior to placebo when used in combination with selective serotonin reuptake inhibitor antidepressants, but this evidence was of low quality. There was no significant difference in terms of effectiveness between SAMe and placebo alone, but again this evidence was of very low quality.

Folic acid – also known as vitamin B9. Foods that are naturally high in folate include leafy vegetables (such as spinach, broccoli, and lettuce), okra, asparagus, fruits (such as bananas, melons, and lemons) beans, yeast, mushrooms, meat (such as beef liver and kidney), orange juice, and tomato juice.

“The evidence for a link between depression and folate levels comes from various sources. Along with vitamins B6 and B12, folate helps break down the amino acid homocysteine. High blood levels of homocysteine are associated with Alzheimer’s disease and depression, although a cause-and-effect relationship hasn’t been proven. The breakdown of homocysteine generates SAMe, a major constituent of brain cells and, some think, a possible treatment for depression. Low levels of SAMe might explain any connection between folate and depression.”

Folate for depression

Probiotics – there is one combination of two bacterial strains that has shown some promise in treating mental health issues. Bifdobacterium longum R0175 and L. helveticus R0052 have been found to reduce symptoms of stress and anxiety. In Canada there are two brands with these strains – CalmBiotic and Jamieson Probiotic Sticks.

Clinical Guide to Probiotic Products Available in Canada

Other things to consider

  • Getting tested for hypo/hyperthyroidism – potential need for thyroid hormones

Treating an underactive thyroid gland may improve mood

  • Getting tested for anemia

Sometimes the first symptoms of iron deficiency are neurologic

  • Getting tested for coeliac disease – possible benefit from excluding gluten from diet

The Link between Celiac Disease and Depression

  • Autoimmune disease testing – includes coeliac disease, hashimoto’s thyroiditis, autoimmune encephalitis, lupus, type 1 diabetes, etc.

Infection, autoimmune disease linked to depression

  • Don’t forget to exercise and eat healthy! I really mean it, you just really need to do it, there is no other way…

Depression and anxiety: Exercise eases symptoms

Mediterranean diet tied to lower risk of depression

Following the MIND diet for autoimmune encephalitis and depression

So there has been the MIND diet going around. Some research indicates that it can reduce the risk of developing Alzheimer’s/dementia. The MIND diet is very similar to the Mediterranean diet. As most people know, that means eating a lot of oily fish, whole grains, vegetables, nuts, and beans/legumes. The MIND diet is a bit more specific – it recommends green leafy vegetables every day, berries (especially blueberries), whole grains three! times a day, nuts every day. You can see the list below:

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Dietitians provide some information on how this diet might work: “A diet that supports vascular health is certainly protective against vascular dementia, but certain foods and food components have been directly linked to improved neurological function or reduced AD biomarkers in the brain.1,8 “MIND diet foods reflect nutrients shown to slow cognitive decline, lower risk of AD, decrease amyloid in the brain or neuron loss in animal studies, or decrease oxidative stress and inflammation”.

Food for Thought: The MIND Diet — Fighting Dementia With Food

Well since my brain seems to be screwed up, anything that might fight inflammation while improving neurological function sounds good to me! It’s also a lot less restrictive than the AIP diet or ketogenic diet. Definitely much easier than intermittent fasting. I see myself being able to follow this diet long-term. I want to eat my grains, I also haven’t found much evidence that excluding grains helps with depression or inflammation. I like to eat my quail eggs and goat yougurt, so I don’t want to be excluding eggs or dairy (AIP excludes these foods). I don’t think the strict AIP diet should be followed for a long time, neither the ketogenic diet. I am not even sure whether keto diet can help with inflammation and depression, it includes tons of saturated fat. The MIND diet researchers actually recommend limiting saturated fat.

So how do you follow the MIND diet list in practice? Green leafy vegetables every day, berries, olive oil, nuts… how do you fit all of that into one day? And what if you don’t like looking or don’t have time? What if you are not one of those people who post on their vlog about avocado toast? I came up with some quick recipes, here I will post my breakfast idea. The breakfast consists of onions (vegetable √ ), kale (green leafy vegetable √ ), cooked with olive oil √, yougurt with blueberries (berries √), also you can add some toast (I don’t eat gluten, but I make gluten-free sourdough buns  – whole grain flour √), or you can easily make a lot of brown rice pudding – also whole grain √.

I want to make this simple. This is for actual practical eating, now a decorative meal. I prepare several items in the evening so that in the morning I can cook my breakfast in several minutes. I start work at 9 am and I try to wake up as late as possible, I don’t want to be cooking for even fifteen minutes in the morning.

Ingredients to buy:

  • Buy some frozen chopped onions, chopped kale, olive oil, eggs. Yougurt, frozen blueberries, nuts/seeds. Bread/sourdough bread. I don’t consume cow milk, so I buy goat/sheep yougurt, I also make soy yougurt. I also eat gluten-free, so I make sourdough buns at home. I make a lot of buns and a liter yougurt at once, so I don’t have to do this every day.
  • Why frozen vegetables? Because they are chopped and I don’t like chopping. Also they don’t go rotting in my fridge if I forget about them. Also you don’t need to wash frozen vegetables. So many benefits!

Evening preparation:

  • Get a frying pan. I hope you have one in your house. You do need at least one frying pan for this MIND diet project. If you don’t have one – go to the Dollar Store and get one please. Place the pan on your your counter. 20 seconds
  • Take out frozen kale and frozen onions out of the freezer. 10 seconds20181101_213108           20181101_213148 
  • Place some kale and onions into the frying pan. Add salt, pepper, and olive oil. 30 seconds

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  • Place the pan in the fridge. The vegetables will defrost overnight. 10 seconds

Morning cooking:

  • Take out some eggs from the fridge, take out the pan

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  • Turn on the burner, place frying pan on the burner, leave it on medium-high for about five minutes. And don’t just stand there those five minutes, go brush your teeth, or something!
  • After five minutes crack the eggs onto the pan, mix everything together with a spatula
  • Fry for another three- four minutes
  • Place in a container and take to work, if you work in an office using a computer – you can easily enjoy eating while pretending to work
  • Take a jar of yougurt with you, add frozen blueberries – another item checked off from the MIND list

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  • Don’t forget toast/sourdough bread – because they say whole grains three times a day. Can be gluten-free. Eating toast should be easy, not like eating a bunch of kale. Toast is good!

So there, in one breakfast – kale – green leafy vegetable √ , onion – a vegetable , good enough! √, olive oil √, toast/sourdough – whole grains √

What else did they say… nuts? just add them to yougurt √ add blueberries √ don’t add oily fish to your yougurt… Χ

Wine? Well I think you can have that any time 😉

Cases of depression treatment with immunotherapy

I am such a case and I want to present other cases found in literature where depression/psychosis was ameliorated with immunotherapy treatment. Dr. Joseph Dalmau is one researcher who has written extensively about psychosis resulting from autoimmune encephalitis and I am very thankful to him for his work. The paper below is a good overview of 100 anti-NMDA receptor encephalitis cases. It’s interesting to note that 91 out of 100 patients were female. This is consistent with the general finding that that autoimmune diseases affect more woman than men. Also not all patients suffered seizures, it was 76 out of 100, therefore seizures are not a necessary symptom of anti-NMDAR encephalitis. I personally was diagnosed not with anti-NMDAR encephalitis, but with Hashimoto’s encephalitis. I had about two seizure-like episodes, but it’s hard to say if they were actual seizures. Given the patient stories from the Hashimoto’s encephalitis Facebook support group, I would say definitely not everyone experiences seizures with autoimmune encephalitis. My neurologist and psychiatrist stated that encephalitis can present itself as ongoing mild chronic inflammation. This can result in severe depression, black and white thinking, experiences of extreme fear, but present no severe physical symptoms. Anti-NMDAR encephalitis is usually not mild, but severe inflammation of the brain. The authors of the paper state that 25 out of the 100 patients were left with severe deficits or died even after receiving treatment.

Of 100 patients with anti-NMDA-receptor encephalitis, a disorder that associates with antibodies against the NR1 subunit of the receptor, many were initially seen by psychiatrists or admitted to psychiatric centres but subsequently developed seizures, decline of consciousness, and complex symptoms requiring multidisciplinary care. While poorly responsive or in a catatonic-like state, 93 patients developed hypoventilation, autonomic imbalance, or abnormal movements, all overlapping in 52 patients. 59% of patients had a tumour, most commonly ovarian teratoma. Despite the severity of the disorder, 75 patients recovered and 25 had severe deficits or died.

Anti-NMDA-receptor encephalitis: case series and analysis of the effects of antibodies

Below is another good case study of a patient who had ongoing depression for many years. The person was not able to work due to his psychiatric state, and his condition did not improve with psychotherapy or psychiatric medications. “At age 29, the patient found himself easily fatigued despite excessive sleep. His energy was persistently low. His capacity to be productive at work was drastically reduced. He was psychiatrically hospitalized for a major depressive episode and was treated aggressively with a combination of psychotherapy and pharmacotherapy…  By age 35, the patient could not sustain work because of persistent mood symptoms and cognitive dysfunction.” Unfortunately the patient got to a neurologist at the age of 39, after clearly suffering for many years, but better late than never. It was found that neurological testing returned some abnormal results, presence of brain inflammation was then confirmed and it was decided to treat the patient with intravenous immunoglobulin (IVIG) therapy. This treatment was quite successful in reducing the patient’s depressive symptoms.

Ten months after initiation of IVIG, a repeat SPECT scan showed complete normalization of frontal hypoperfusion. Of note, the psychotropic regimen remained essentially constant over this 10-month period. At the time of a neuropsychiatric reevaluation 13 months after starting IVIG, the patient reported significant improvement in his mood and much better control of his anxiety. His wife reported a positive personality change in her husband. He was much more active in general and more appropriately engaged with his family. He was more interested in socializing, and he became an active participant in raising his child.  In fact, he was excited to report that he and his wife were expecting a second child.

Brain Biopsy Findings Link Major Depressive Disorder to Neuroinflammation, Oxidative Stress, and Neurovascular Dysfunction

Here is another brief description of a 74 -year-old woman presenting with severe depressive symptoms, not responding to antidepressants, and then being successfully treated with prednisolone: “We report on a 74-year-old female patient with a severe depressive episode who showed no treatment response to citalopram 40 mg/day and venlafaxine 150 mg/day. Diagnostic examination revealed an abnormal EEG, elevated thyroid peroxidase antibodies (TPO-Ab), and older postinflammatory changes in thyroidal sonography. We diagnosed a depression in HE and began treatment with prednisolone 70 mg/day with stepwise dose reduction, continuing treatment with venlafaxine 150 mg/day. Within 4 weeks of treatment, the severe depressive episode disappeared as well as abnormal EEG. In addition, serum values of TPO-Ab decreased.

Depression in Hashimoto’s encephalopathy. Successful treatment of a severe depressive episode with a glucocorticoid as an add-on therapy

The following article describes the case of a 50-year-old patient who presented with depressive symptoms and cognitive impairment and was then diagnosed with Hashimoto’s encephalitis, after not responding to regular antidepressant medication.

“In 2011, after experiencing a noticeable loss of energy and feelings of exhaustion, the patient presented for evaluation of classic depressive symptoms, including melancholic mood, impaired concentration, and psychomotor retardation.

The patient had no prior medical history of psychiatric disorders, and had no family history of psychiatric, neurological, or autoimmune disorders. Physicians diagnosed the patient with major depression, and prescribed 112.5 mg venlafaxine and 25 mg agomelatine in conjunction with cognitive behavioral therapy (CBT).

After 2 years of CBT, the patient showed little to no improvement, with persistent memory loss, depressed mood, and reduced energy level.

This case sounds very similar to mine, as I did not have very pronounced physical symptoms such as multiple seizures. I complained to the doctors about constant fatigue and abdominal pain, and then I had to be involuntarily hospitalized due to severe depression and suicidal thoughts. I did not improve after treatment with mirtazapine, bupropion, risperidone, olanzapine, duloxetine, etc. I have also attended CBT sessions for more than half a year. This patient, like me, was finally diagnosed with Hashimoto’s encephalitis, and treated with immunosuppressant medication, after which the patient improved.

The patient was treated with high-dose methylprednisolone (1000 mg intravenously administered over 3 days; 500 mg over 2 days), which was well-tolerated. Methylprednisolone was then transitioned to oral dosing initiated at 40 mg and then tapered until discontinuation by halving the dose every fifth day. Venlafaxine, agomelatine, and T4 treatment continued unchanged.

The patient reported reduced cognitive impairment and improved alertness after steroid treatment, confirmed by neuropsychological testing. Basal alertness and processing speed were both improved, but remained below average. After 5 weeks, the patient’s mood and energy levels normalized and cognitive impairment had disappeared.”

An Uncommon Presentation of Hashimoto’s Encelophathy

Depression is an awful experience, it literally makes you not want to be alive. I’ve been there. Researchers are starting to have a better understanding of causes of depression and therefore there is hope. If you are suffering from depression resistant to standard antidepressant treatments, consider getting investigated for autoimmune disease/inflammation. I am very thankful to all the researchers who put this information out there and we are able to access it online for free. Learning about the link between depression and inflammation has definitely been helping me climb out from a very dark place.

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