Over 100,000 cases of psychiatric disorders reported following COVID vaccination

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A novel adverse effect of the BNT162b2 mRNA vaccine: First episode of acute mania with psychotic features

12/18/21


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8492001/


A vaccine against SARS-CoV2, which is causing the global COVID-19 pandemic, was developed for the first-time using mRNA technology. Although the short- and long-term side-effects of the vaccine were unknown, emergency use authorization (EUA) was granted by the Food and Drug Administration (FDA) in December 2020(Parkash et al., 2021). Adverse effects such as tiredness, headache, muscle pain, chills, fever, and nausea were defined by the Centers for Disease Control and Prevention (CDC); nonetheless, other adverse effects are continuously being reported in individual patients(Edriss et al. 2021). Here, we describe two patients displaying first episode of acute mania with psychotic features one day after the administration of the BNT162b2 mRNA vaccine.


1. Case 1

A 42-year-old male was admitted to the psychiatric emergency department five days after being vaccinated with the first dose of the BNT162b2 mRNA vaccine with complaints of irritability and sleeplessness. Although the patient did not have any symptoms outside of weakness on the day of vaccination, the complaints started one day after receiving the vaccine. The patient had delusions that his family was being followed by the deep state and that they were in danger. This was the patients first psychiatric admission. The medical history of the patient showed absence of any illnesses or regular use of medication. In addition, the patient was vaccinated voluntarily and did not have extreme anxiety about vaccination. At the clinical examination, the patient's cooperation and orientation were intact; however, his speech output, speed as well as psychomotor activity were increased. The patients affect was anxious and the mood was dysphoric. He exhibited a loosening of associations, described persecutory and reference delusions and displayed a lack of insight. The Young Mania Rating Scale (YMRS) score was 45. Physical and neurological examinations were non-significant, blood screening results at admission showed a C-reactive protein (CRP) level of 4.2 mg/dL, the white blood cell (WBC) count was 8.8mg/dL and thyroid, liver and renal functions, as well as creatine kinase (CK), ferritin, D-Dimer and electrolytes were in the normal range. Brain magnetic resonance imaging (MRI) was also unremarkable. The patient was hospitalized for treatment. 5mg/day olanzapine per oral (p.o.) was initiated for psychiatric symptoms. At the 7th day of olanzapine treatment, agitated behavior was improved (YMRS: 15). At the routine psychiatric evaluation 15 days after discharge, the patient declared that he was unable to remember the initiation of psychiatric symptoms.

2. Case 2

A 57-year-old male was admitted to the psychiatric emergency department with complaints of irritability, sleeplessness, talking to himself and suicidal attempt with thoughts of extinction three days after receiving the second dose of the BNT162b2 mRNA vaccine. While firstly the patient only had local myalgia on the arm on the day of vaccination, psychiatric symptoms started at night on the day he was vaccinated. The patient did not have a history of any diseases that required the use of medication, was vaccinated voluntarily and did have any anxiety about vaccination. Clinical evaluation suggested intact cooperation and orientation while speech output, speed as well as psychomotor activity were increased. The patient was anxious, and his mood was dysphoric. Nihilistic delusions with no insight were recorded. The YMRS score was 42. This patient also did not have any history of psychiatric illnesses. Physical and neurological examinations. Brain MRI results were also normal. The patient was hospitalized for treatment. 2 mg/day risperidone p.o. treatment was initiated for the management of psychiatric symptoms. At the 5th day of risperidone treatment, manic symptoms were improved (YMRS: 11) and the patient was discharged with risperidone 2 mg/day p.o.

To the best of our knowledge, this is the first report of adverse neuropsychiatric side-effects of the BNT162b2 mRNA vaccine. One hypothesis is that SARS-CoV-2 can damage the central nervous system via autoimmune mechanisms due to excessive production and release of pro-inflammatory chemokines and cytokines, particularly TNF-α, IL-1 and IL-6. mRNA vaccines contain nucleotides from the genetic code of the virus that encode a viral protein. This protein is a viral antigen that can cause neuropsychiatric symptoms such as autoimmune psychosis (anti- NMDAR, AMPAR, CAPR2 encephalitis) by rapidly increasing a pro-inflammatory response and activated autoimmune mechanism (Pollak et al., 2020; Sen et al. 2021). Another hypothesis suggests that the inflammatory mechanisms caused by COVID-19 can trigger neuropsychiatric symptoms via thiamine deficiency. Therefore, vaccination may also lead to neuropsychiatric symptoms by damaging thiamine metabolism (Branco de Oliveira et al., 2021; de Oliveira et al., 2021).

The current letter has some limitations. Inflammatory markers such as IL-6, TNF alpha and IL-1 were not investigated in the blood and CSF. In addition, because the patients were clinically agitated and restless, consent for LP could not be obtained from their relatives. CSF values could not be measured in the patients.

The BNT162b2 mRNA vaccine, which is very important to end the pandemic, nonetheless may have such rare but severe side effects. Risk groups should therefore be carefully determined.
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Re: Over 100,000 cases of psychiatric disorders reported following COVID vaccination

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The mental health aspect of this pandemic is so under reported it isn't funny at all. As you know CNS is working hard on the matter.
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Re: Over 100,000 cases of psychiatric disorders reported following COVID vaccination

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Acute Psychosis Due to Anti-N-Methyl D-Aspartate Receptor Encephalitis Following COVID-19 Vaccination: A Case Report

11/4/21


https://www.frontiersin.org/articles/10 ... 64197/full


Anti-N-methyl D-aspartate (NMDA) receptor (anti-NMDAR) encephalitis has been reported after SARS-CoV-2 infection, but not after SARS-CoV-2 vaccination. We report the first known case of anti-NMDAR encephalitis after SARS-CoV-2 immunization in a young female presenting with acute psychosis, highlighting a rare potential immunological complication of vaccination against SARS-CoV-2 that is currently being distributed worldwide. The patient presented initially with anxiety and hypochondriacal delusions which progressed to psychosis and catatonia but returned to baseline with aggressive immunomodulatory therapy consisting of intravenous immunoglobulin, high-dose glucocorticoids, and rituximab. This study highlights that the workup of acute psychosis should include establishing a history of recent vaccination followed by a thorough neurological assessment, including for anti-NMDAR antibodies in blood and cerebrospinal fluid.
Introduction

Anti-N-methyl-D-aspartate receptor (anti-NMDAR) encephalitis is an autoimmune mediated condition characterized by complex neuropsychiatric syndromes and the presence of antibodies against the GluN1 receptors in the CSF (1). This disease was first described in 2007 as a paraneoplastic syndrome in women presenting with ovarian teratomas but has since been designated as the second most common immune mediated encephalopathy (2, 3). Anti-NMDAR encephalitis has been associated with viral illnesses such as Japanese encephalitis, HSV-1, Epstein-Barr virus, and most recently COVID-19 infection (Table 1) (5, 9–11). Additionally, anti-NMDAR encephalitis has been associated with vaccinations against H1N1, yellow fever, TdaP-IPV booster, and the Japanese Encephalitis (3, 12–14). In this case report, we present the first instance of anti-NMDAR encephalitis after receiving the Pfizer-BioNTech COVID-19 vaccine.

TABLE 1

https://www.frontiersin.org/files/Artic ... 7-t001.jpg


A female in her 20's presented to the Emergency Department (ED) with a chief complaint of urinary frequency 1 week after receiving her first dose of the Pfizer-BioNTech COVID-19 vaccine (Figure 1). The patient's family stated she had increasingly frequent bouts of anxiety, decreased mentally acuity, insomnia, and a fixation that she suffered from irritable bowels and kidney disease. She displayed waxing and waning hypochondriacal delusions that she had contracted COVID-19 and that “her body was shutting down.” The patient was also noted to have some motor dysfunction and a transient bout of aphasia during this time. There were no complaints of antecedent infection, fever, or headache. Family history and past medical history were non-contributary. The physical examination showed tachycardia and hypertension but otherwise unremarkable. Hematology and metabolic labs and urinalysis were normal.

FIGURE 1

https://www.frontiersin.org/files/Artic ... 7-g001.jpg

Figure 1. Timeline of the evolution of the patient's condition in relation to treatments and findings. CEP, Cephalexin; LEV, Levetiracetam; LOR, Lorazepam; RIX, Rituximab; FAZ, Cefazolin; ENOX, Enoxaparin; MET, Metoprolol; BAC, Bactrim; ZIP, Ziprasidone; OLA, Olanzapine; HAL, Haldol; RIS, Risperadol; Ben, Benztropine.

The patient was discharged from the ED with instructions to follow up with her primary care physician but returned the following day with complaints of increasing anxiety as well as continued somatization of bowel and kidney disease. The patient also endorsed accusatory auditory hallucinations but denied suicidal or homicidal ideation. Repeat blood tests demonstrated mild leukocytosis and slightly increased alanine aminotransferase (ALT) and aspartate aminotransferase (AST). The physical exam was again normal except for elevated blood pressure and tachycardia. SARS-CoV-2 nasopharyngeal polymerase chain reaction (PCR) was negative. Due to the persistent tachycardia and hypertension, she was kept overnight for observation. No cerebrospinal fluid (CSF) analysis was performed during these initial two ED visits.

The following morning the patient removed her clothing and had a bowel movement on the floor. With no discovery of metabolic or toxic causes based on bloodwork and imaging for her acute psychosis, she was transferred to an inpatient psychiatric unit for voluntary admission. Treatment was begun with olanzapine and haloperidol (5 mg, Q4H). Despite these therapies, patient became increasingly psychotic, which was initially managed with lithium, but this was discontinued due to symptoms of catatonia. Risperidone therapy was then trialed (0.5 mg, Q4H), however the patient experienced a grand mal seizure which prompted transfer back to the ED and subsequent admission to the intensive care unit. Detailed question of family members revealed no evidence of upper respiratory, gastrointestinal, or other antecedent illness in the preceding few weeks.

At that time, the patient's memory was intact, and she was responsive to questions but lethargic. She also exhibited symptoms of ongoing catatonia, answered questions in short sentences in a monotonous tone with low phonation. She could ambulate, but slowly and with a one-person assist mainly to aid with initiation of movement. Computerized tomography (CT) and magnetic resonance imaging (MRI) of the brain were normal, as were and hematologic and metabolic laboratory evaluations. Eventually, a lumbar puncture was performed, and patient's CSF analysis showed a mild lymphocyte pleocytosis with 12–14 nucleated cells/mm3. CSF polymerase chain reaction studies for enterovirus, herpes simplex, varicella zoster, and Epstein-Barr virus were negative. Blood serologies for Mycoplasma pneumoniae, and HIV were negative. Studies for Cryptococcus neoformans and Coccidioides immitis were negative.

The constellation of symptoms (spontaneous defecation, catatonia, sudden encephalopathy without metabolic or infectious findings) coupled with the preliminary CSF results and the history of deterioration after SARS-CoV-2 vaccination led to a strong clinical suspicion of an autoimmune-mediated encephalitis driven by the vaccine. While awaiting for the appropriate diagnostic test results, a 5-day course of IVIG (25 g given at 0.5 mg/kg/min initially and increased to 8 mg/kg/min as tolerated) and steroid treatment (methylprednisolone, 40 mg Q8H) were begun, with clinical improvement demonstrated within 24 h. The patient become fully alert and oriented, with increased dexterity and decreased catatonia, although her affect remained flat. Additionally, metoprolol was prescribed to manage the patient's tachycardia and hypertension.

Eventually, CSF anti-NMDA titers of 1:20 returned. Due the high correlation between anti-NMDAR encephalitis and paraneoplastic teratomas, a transvaginal ultrasound, chest x-ray and CT, and MRI of the chest, pelvis, and abdomen were performed, all of which were unremarkable. EEG revealed no abnormalities. When the 5-day IVIG course was completed, her neurological status deteriorated. The patient continued to present with a flat affect and increasingly poor volitional initiation of movement and speech.

Weekly rituximab therapy was initiated (375 mg/m2 initial infusion of 50 mg/h increased to a maximum of 400 mg/h), and methylprednisolone dose was increased. The patient's mental acuity and catatonia continued to wax and wane in severity until the administration of her third dose of Rituximab. Repeat evaluation of CSF revealed resolution of her lymphocytic pleocytosis (4 WBC/mm3, normal ≤) Anti-NMDAR CSF titers had decreased to 1:10. Slow but consistent improvements in her neurological status were observed following her third rituximab dose. Eventually, 45 days in the hospital and 61 days after receiving the SARS-CoV-2 vaccine, she was discharged from the hospital with minor neurological deficits. She remains well 3 months after hospital discharge on anticonvulsant therapy, with no signs of relapse and has returned to work.
Discussion

SARS-CoV-2 vaccines have been critical in reducing COVID-19 morbidity and mortality and facilitated the societal return to normalcy during the COVID-19 pandemic. While numerous psychiatric conditions, including anti-NMDAR encephalitis, have been shown to complicate COVID-19 infections (Table 1), this case report is the first reported incident of anti-NMDAR encephalitis temporally linked to SARS-CoV-2 vaccination (4, 5, 7, 8, 15). Extensive workup showed no evidence that patient's symptoms were due to a paraneoplastic condition, which is more common for this specific neurologic condition. Instead, based on precedent cases of anti-NMDAR encephalitis caused by vaccines against influenza, yellow fever, Japanese encephalitis, and tetanus/diphtheria vaccines, clinicians in this case quickly considered the recent receipt of SARS-CoV-2 vaccine as a possible trigger of anti-NMDAR encephalitis (3, 12–14).

The diagnosis of an auto-immune encephalitis was not considered during the initial presentation to the emergency room because the anxiety, hallucinations, insomnia, psychosis, and were initially considered symptoms of primary psychiatric diseases, further supported by absence of fever or other objective signs of systemic infection or inflammation. Therefore, one of the major teaching points of this case is the need for serious consideration of organic nervous system causes of psychosis, despite the absence of recent or current signs of infection. This requires careful imaging of the brain, performance of a lumbar puncture, and the search for anti-NMDAR in both CSF and peripheral blood. There have been two recent studies on the psychiatric manifestations of anti-NMDAR encephalitis which report that severe agitation, speech disturbance, and catatonia amongst other psychiatric features, may signal the presence of organic pathology, particularly when dealing with a young female presenting at an atypical age for primary psychosis (16). The concomitant presence of seven features-agitation, aggression, hallucinations, delusions, mutism, irritability or mood instability, and depressed mood would not be typical of any single psychiatric diagnosis and point to organic brain pathology (17).

Despite initial delay in establishing the diagnosis, the presentation of seizure, psychiatric symptoms, and history of recent of SARS-CoV-2 vaccination resulted in prompt treatment with IVIG and glucocorticoids even before the diagnosis was established via anti-NMDAR antibody detection. This provided temporary improvement of symptoms, perhaps due to the blockade of harmful anti-NMDAR antibodies driving the disease. However, it was not until rituximab-mediated B-lymphocyte depletion blocking formation of new anti-NMDAR antibodies that the patient's symptoms finally started to show signs of improvement (6). However, given the long 3-week half-life of IgG, the process of clinical improvement was very slow, dependent on gradual clearance of previously formed anti-NMDAR antibodies induced by the vaccine while rituximab prevented formation of new antibodies. We hypothesize that concomitant plasmapheresis alongside rituximab may have hastened the neurological recovery by more rapid removal of harmful anti-NMDAR antibodies.

In summary, we present the first case of anti-NMDAR encephalitis complicating SARS-CoV2 vaccination in a previously healthy young woman. This case provides an important reminder that (i) psychiatric clinical presentations warrant a thorough medical workup, including brain imaging, CSF analysis, anti-NMDAR antibody testing, and a vaccine history; (ii) combined therapies of blocking (IVIG), reducing production of (rituximab), and even removing (plasmapheresis) harmful anti-NMDAR may be the optimal strategy to reverse the neurological and psychiatric symptoms driven by anti-NMDAR antibody production. Fortunately, prompt therapy targeting anti-NMDAR antibodies resulted in achieving and sustaining an excellent clinical outcome. In addition to providing clinicians the opportunity to identify potential vaccine-associated anti-NMDAR encephalitis, particular attention may be needed to patients receiving COVID-19 vaccine who have previously have had anti-NMDAR encephalitis.

References

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Re: Over 100,000 cases of psychiatric disorders reported following COVID vaccination

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Psychosis may be triggered by antibody reaction to brain protein

Written by David McNamee on March 9, 2015


https://www.medicalnewstoday.com/articles/290534


A new study published in the journal Biological Psychiatry investigates the role antibodies may play in cases of psychosis, suggesting that psychosis symptoms such as hallucinations and delusions may be triggered by an antibody response to a protein in the brain.

It is well known that antibodies defend the body against bacteria and viruses, and that in some people antibodies also attack healthy cells, causing autoimmune disorders.

Less well known is the role autoimmune disorders may play in psychosis. However, scientists have been aware of a link between immune abnormalities and psychosis for over 100 years.

Only recently, though, have scientists been able to pinpoint the specific mechanisms in the immune system that appear to influence psychosis symptoms, such as the mechanism identified in the new study.

The authors of the new study found an antibody reaction to the dopamine D2 receptor or the N-methyl-D-aspartate (NMDA) glutamate receptor among a subgroup of children experiencing their first episode of psychosis, but no similar antibody response among healthy children.


Both of these receptors have been implicated in psychosis. In fact, psychiatrists commonly administer drugs that stimulate dopamine D2 receptors or block NMDA receptors.

These drugs have been associated with side effects that resemble psychosis symptoms – such as changes in perception, delusions and disorganized thought processes. The researchers believe that the antibodies described in the study may have a similar effect on the brain to these drug side effects.

“The antibodies we have detected in children having a first episode of acute psychosis suggest there is a distinct subgroup for whom autoimmunity plays a role in their illness,” says Dr. Fabienne Brilot, senior study author and head of the Neuroimmunology Group at The Children’s Hospital at Westmead in Sydney, Australia.

“The data from this study suggests that better interventions are possible, providing hope that major disability can be prevented for the subset of children experiencing acute psychosis with antibodies,” Dr. Brilot adds.

Study adds to growing scientific awareness of antibody reactions to NMDA receptors

Within the last decade, similar research has identified anti-NMDA receptor encephalitis – an inflammation of the brain responsible for acute psychiatric symptoms including psychosis. Though commonly misdiagnosed as schizophrenia or bipolar disorder, the brain inflammation characterized by the disease is caused by an antibody attack on NMDA receptors and is treatable.

Dr. John Krystal, editor of Biological Psychiatry writes that the study fuels growing discussions on the importance of antibodies targeting neural proteins and raises many important questions for scientists working in this field: “Do these antibodies simply function like drugs in the brain or do they ‘attack’ and damage nerve cells in some ways? Also, are these antibodies producing symptoms in everyone or do they function as a probe of an underlying, perhaps genetic, vulnerability for psychosis?”

Dr. Brilot concludes of his team’s findings:

“These findings also contribute significantly to an emerging acceptance in the field of the involvement of autoimmune antibodies in neurological diseases. Combined, these investigations are providing a better understanding of the biology of psychiatric and neurological diseases, as well as pointing to novel treatment approaches for children with these debilitating illnesses.”
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