BackgroundCotard’s Syndrome (CS) is a rare clinical entity where patients can report nihilistic, delusional beliefs that they are already dead. Curiously, while weight loss, dehydration, and metabolic derangements have been described as discussed above, a review of the literature revealed neither a single case of a severely underweight patient nor a serious metabolic complication such as Diabetic Ketoacidosis. Further, a search on PubMed revealed no articles discussing the co-occurrence of Cotard’s Delusion and eating disorders or comorbid metabolic illnesses such as diabetes mellitus. In order to better examine the association between Cotard’s Delusion and comorbid eating disorders and metabolic illness, we will present and discuss a case where Cotard’s delusion led to a severe metabolic outcome of DKA and a BMI of 15.Case presentationMr. B is a 19 year old transgender man admitted to the hospital due to diabetic ketoacidosis secondary to Type 1 Diabetes Mellitus. Mr. B had a history of Obsessive–Compulsive Disorder, Major Depressive Disorder, and Post-Traumatic Stress Disorder. The primary pediatric team discovered that Mr. B had not been using his insulin appropriately and was severely underweight, and they believed this could be due to his underlying mental illness. The psychiatric consultation/liaison service found that Mr. B was suffering from Cotard’s delusion leading him to be noncompliant with his insulin due to a belief that he was already dead. Cotard’s delusion had in this case led to a severe metabolic outcome of DKA and a BMI of 15.ConclusionsThis case provides clinical insight into the interactions of eating disorders and Cotard’s delusion as well as the potential medical complications when Cotard’s delusion is co-morbid with medical conditions such as Diabetes Mellitus. We recommend that clinicians routinely screen patients for Cotard’s delusion and assess whether the presence of which could exacerbate any underlying medical illness. This includes clinicians taking special care in assessing patient’s caloric and fluid intake as well as their adherence to medications both psychiatric and medical. Further research could be conducted to explore the potential overlap of Cotard’s delusion and eating disorder phenomenology.

BackgroundRare cases of COVID-19 infection- and vaccine-triggered autoimmune diseases have been separately reported in the literature. In this paper, we report the first and unique case of new onset acute psychosis as a manifestation of lupus cerebritis following concomitant COVID-19 infection and vaccination in a previously healthy 26-year-old Tunisian female.Case presentationA 26-years old female with a family history of a mother diagnosed with schizophrenia, and no personal medical or psychiatric history, was diagnosed with mild COVID-19 infection four days after receiving the second dose of Pfizer-BioNTech COVID-19 vaccine. One month after receiving the vaccine, she presented to the psychiatric emergency department with acute psychomotor agitation, incoherent speech and total insomnia evolving for five days. She was firstly diagnosed with a brief psychotic disorder according to the DSM-5, and was prescribed risperidone (2 mg/day). On the seventh day of admission, she reported the onset of severe asthenia with dysphagia. Physical examination found fever, tachycardia, and multiple mouth ulcers. Neurological evaluation revealed a dysarthria with left hemiparesis. On laboratory tests, she had severe acute kidney failure, proteinuria, high CRP values, and pancytopenia. Immune tests identified the presence of antinuclear antibodies. Brain magnetic resonance imaging (MRI) revealed hyperintense signals in the left fronto-parietal lobes and the cerebellum. The patient was diagnosed with systemic lupus erythematosus (SLE) and put on anti-SLE drugs and antipsychotics, with a favorable evolution.ConclusionsThe chronological relationship between COVID-19 infection, vaccination and the first lupus cerebritis manifestations is highly suggestive, albeit with no certainty, of the potential causal link. We suggest that precautionary measures should be taken to decrease the risk of SLE onset or exacerbation after COVID-19 vaccination, including a systematic COVID-19 testing before vaccination in individuals with specific predisposition.

This report highlights a rare single-gene cause of early-onset, treatment-resistant schizophrenia, and its unique responsiveness to clozapine therapy. This case describes a pediatric female who was diagnosed with early-onset schizophrenia and catatonia in her early adolescence, and was later found to have DLG4-related synaptopathy, also known as SHINE syndrome. SHINE syndrome is a rare neurodevelopmental disorder caused by dysfunction of the postsynaptic density protein-95 (PSD-95), encoded by the DLG4 gene. After failing three antipsychotic drug treatments, the patient was started on clozapine, which resulted in significant improvements in positive and negative symptoms. This case illustrates the impact of clozapine in treatment-resistant early-onset psychosis and exemplifies practical implications for genetic testing in early-onset schizophrenia.

BackgroundMethamphetamine is an addictive drug with various effects on the neurotransmitters in the central nervous system. Methamphetamine-induced encephalopathy in the absence of hyperammonemia presents a unique challenge in a clinical setting. Previously published cases of methamphetamine-induced encephalopathy suggested that methamphetamine-induced hepatotoxicity and subsequent hyperammonemia may be the cause of encephalopathy. However, the literature is limited on methamphetamine-induced encephalopathy without hyperammonemia.CaseThis case presents a disoriented patient with methamphetamine use disorder in acute toxicity, unable to ambulate independently, and poorly responsive to verbal stimuli. The patient was found to have normal ammonia levels.DiscussionThis patient’s presentation and laboratory findings, namely normal ammonia levels, suggest a different pathophysiological pathway for methamphetamine-induced encephalopathy. One potential pathway is through the direct action of methamphetamine on the central nervous system through acute disruption of neurotransmitter signaling and disruption of the blood-brain barrier.ConclusionFurther research should be conducted into the prevalence and pathophysiology of methamphetamine-induced encephalopathy in the absence of hyperammonemia.Key PointsMethamphetamine-induced encephalopathy (MIE) in the absence of hyperammonemia presents a unique challenge in a clinical setting.Previously published cases of MIE suggest that methamphetamine-induced hepatotoxicity and subsequent hyperammonemia may be the cause of encephalopathy.Further research should be conducted into the prevalence and pathophysiology of MIE in the absence of hyperammonemia.

Autoimmune diseases (AID) cause inflammatory changes in the peripheral blood, which might be a predisposing factor for the development of comorbid bipolar disorder (BD). The levels of peripheral inflammatory indicators and cytokines may also serve as potential biomarkers for predicting BD susceptibility and the efficacy of antipsychotics in patients with AID. Herein, we present the case of a 43-year-old female who has suffered from AID for over 16 years and was recently diagnosed with “bipolar and related disorder due to another medical condition”.