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.“
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.“
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.
Notes of a Neuropsychiatry Amateur 