scholarly journals First-Time Psychotic Symptoms in a Patient After COVID-19 Infection—A Case Report

2021 ◽  
Vol 12 ◽  
Author(s):  
Kacper Łoś ◽  
Joanna Kulikowska ◽  
Napoleon Waszkiewicz

A 39-year-old, previously healthy, white male with no personal or family history of mental illness presented with new, first-time psychotic symptoms. The new psychotic symptoms appeared on patient admission to the hospital, occurring during a diagnosis of symptomatic SARS-CoV-2 infection. On the first day of hospitalization for worsening psychotic symptoms and the appearance of aggression toward the staff, the patient was transferred to the psychiatric hospital. After the initial treatment with antipsychotics and benzodiazepines, his mental condition improved. The patient was then transferred for further treatment of his somatic condition in the internal medicine ward, with a recommendation to continue treatment in the psychiatric ward once his somatic condition was stabilized. This is one of the few reported cases of COVID-19-related psychosis in a patient without a personal or family history; moreover, this description contains important data regarding elevated IL-6, which may prove to be a key factor in the induction of new psychotic symptoms. It indicates the important need for careful monitoring of neuropsychiatric symptoms among COVID-19 patients.

2020 ◽  
Vol 13 (8) ◽  
pp. e236940 ◽  
Author(s):  
Colin M Smith ◽  
Jonathan R Komisar ◽  
Ahmad Mourad ◽  
Brian R Kincaid

A 36-year-old previously healthy woman with no personal or family history of mental illness presented with new-onset psychosis after a diagnosis of symptomatic COVID-19. Her psychotic symptoms initially improved with antipsychotics and benzodiazepines and further improved with resolution of COVID-19 symptoms. This is the first case of COVID-19-associated psychosis in a patient with no personal or family history of a severe mood or psychotic disorder presenting with symptomatic COVID-19, highlighting the need for vigilant monitoring of neuropsychiatric symptoms in these individuals.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
A Wahrenberg ◽  
P Magnusson ◽  
R Kuja-Halkola ◽  
H Habel ◽  
K Hambraeus ◽  
...  

Abstract Background Despite recent advances in secondary prevention, recurrent cardiovascular events are common after a myocardial infarction (MI). It has been reported that genetic risk scores may predict the risk of recurrent cardiovascular events. Although patient-derived family history is a composite of both genetic and environmental heritability of atherosclerotic cardiovascular disease (ASCVD), it is an easily accessible information compared to genetically based risk models but the association with recurrent events is unknown. Purpose To evaluate whether a register-verified family history of ASCVD is associated with recurrent cardiovascular events (rASCVD) in patients after a first-time MI. Methods We included patients with a first-time MI during 2005 – 2014, registered in the SWEDEHEART SEPHIA registry and without prior ASCVD. Follow-up was available until Dec 31st, 2018. Data on relatives, diagnoses and prescriptions were extracted from national registers. A family history of ASCVD was defined as a register-verified hospitalisation due to MI, angina with coronary revascularization procedures, stroke or cardiovascular death in any parent. Early history was defined as such an event before the age of 55 years in fathers and 65 years in mothers. The association between family history and a composite outcome including recurrent MI, angina requiring acute revascularization, ischaemic stroke and cardiovascular death during follow-up was studied with Cox proportional hazard regression with time from SEPHIA registry completion as underlying time-scale, adjusted for age with splines, gender and year of SEPHIA registry. Regression models were then further adjusted for hypertension, diabetes, smoking and for a subset of patients, LDL-cholesterol (LDL_C) at time of first event. Results Of 25,615 patients, 2.5% and 32.1% had an early and ever-occurring family history of ASCVD, respectively. Patients with early family history were significantly younger than other patients and were more likely to be current smokers and have a higher LDL-C (Median (IQR) 3.5 (1.1) vs 3.3 (1.1) mmol/L). In total, 3,971 (15.5%) patients experienced the outcome. Early family history of ASCVD was significantly associated with rASCVD (Hazard ratio (HR) 1.52, 95% confidence interval (CI) 1.23–1.87), and the effect was sustained when adjusted for cardiovascular risk factors (HR 1.48, 95% CI 1.20–1.83) and LDL-C (HR 1.35, 95% CI 1.04–1.74). Ever-occurring family history was weakly associated with ASCVD (HR 1.09, 95% CI 1.02 – 1.17) and the association remained unchanged with adjustments for risk factors. Conclusions Early family history of cardiovascular disease is a potent risk factor for recurrent cardiovascular events in a secondary prevention setting, independent of traditional risk factors including LDL-C. This is a novel finding and these patients may potentially benefit from intensified secondary preventive measures after a first-time MI. Funding Acknowledgement Type of funding source: Private grant(s) and/or Sponsorship. Main funding source(s): This work was funded by grants from The Swedish Heart and Lung Association


2006 ◽  
Vol 96 (1-2) ◽  
pp. 127-131 ◽  
Author(s):  
Richard Rende ◽  
Boris Birmaher ◽  
David Axelson ◽  
Michael Strober ◽  
Mary Kay Gill ◽  
...  

Author(s):  
Nikole Benders-Hadi

This chapter on postpartum psychosis notes that the risk of postpartum psychosis in the general population is very rare at less than 1%. In a mother with a known history of schizophrenia, this risk increases to 25%. Psychotic symptoms appearing postpartum may also be evidence of a bipolar disorder. The presence of elevated mood, increased activity levels and energy, poor sleep, and a family history of manic episodes all increase the likelihood that a bipolar disorder is present. Women with a personal or family history of a bipolar disorder are at an elevated risk of developing a mania or depression with psychotic symptoms postpartum. Postpartum psychosis due to any cause is a psychiatric emergency and treatment should be initiated early and aggressively to ensure the safety of mother and infant. Hospitalization and/or separation of the baby and mother may be necessary. The use of medication to treat schizophrenia or bipolar disorder during pregnancy may decrease the risk of a postpartum psychosis. With appropriate postpartum medication and support, the majority of women experiencing postpartum psychosis recover well and the risk of recurrent psychotic symptoms can be greatly reduced.


2005 ◽  
Vol 8 (2) ◽  
pp. 235-239 ◽  
Author(s):  
Dale A. Ellison ◽  
Julissa Corredor-Buchmann ◽  
David M. Parham ◽  
Richard J. Jackson

We report the case of an 11-month-old white male who had a family history of neurofibromatosis, had multiple café-au-lait spots on the trunk and extremities, and was diagnosed with a malignant triton tumor of the rectum. To our knowledge, this is the first report of a malignant triton tumor of the rectum and one of the youngest patients reported with the tumor.


2013 ◽  
Vol 2013 ◽  
pp. 1-5 ◽  
Author(s):  
Fatemeh Ranjbar ◽  
Alireza Ghanepour ◽  
Homayoun Sadeghi-Bazargani ◽  
Mahbob Asadlo ◽  
Amineh Alizadeh

Induced weight gain is a disturbing side effect of Olanzapine that affects the quality of life in psychotic patients. The aim of this study was to assess the efficacy of Ranitidine in attenuating or preventing Olanzapine-induced weight gain. A parallel 2-arm clinical trial was done on 52 patients with schizophrenia, schizoaffective and schizophreniform disorders who received Olanzapine for the first time. All these were first-episode admitted patients. They were randomly allocated to receive either Ranitidine or placebo. The trend of body mass index (BMI) was compared between groups over 16-week course of treatment. Mean weight was 62.3 (SD: 9.6) kg at baseline. Thirty-three subjects (63.5%) had positive family history of obesity. The average BMI increment was 1.1 for Ranitidine group and 2.4 for the placebo group. The multivariate analysis showed this effect to be independent of sex, family history of obesity, and baseline BMI value. The longitudinal modeling after controlling for baseline values failed to show the whole trend slope to be different. Although the slight change in trend’s slope puts forward a hypothesis that combined use of Ranitidine and Olanzapine may attenuate the weight gain long run, this needs to be retested in future larger scale long-term studies. This trial is registered with IRCT.ir201009112181N5.


2002 ◽  
Vol 17 (6) ◽  
pp. 311-320 ◽  
Author(s):  
Almudena Guerra ◽  
Paul Fearon ◽  
Pak Sham ◽  
Peter Jones ◽  
Shon Lewis ◽  
...  

SummaryBackground.Increasing evidence suggests psychosis may be more meaningfully viewed in dimensional terms rather than as discrete categorical states and that specific symptom clusters may be identified. If so, particular risk factors and premorbid factors may predict these symptom clusters.Aims.(i) To explore, using principal component analysis, whether specific factors for psychotic symptoms can be isolated. (ii) To establish the predictors of the different symptom factors using multiple regression techniques.Method.One hundred and eighty-nine inpatients with psychotic illness were recruited and information on family history, premorbid factors and current symptoms obtained from them and their mothers.Results.Seven distinct symptom components were identified. Regression analysis failed to identify any developmental predictors of depression or mania. Delusions/hallucinations were predicted by a family history of schizophrenia and by poor school functioning in spite of normal premorbid IQ (F = 6.5; P < 0.001); negative symptoms by early onset of illness, developmental delay and a family history of psychosis (F = 4.1; P = 0.04). Interestingly disorganisation was predicted by the combination of family history of bipolar disorder and low premorbid IQ (F = 4.9; P = 0.003), and paranoia by obstetric complications (OCs) and poor school functioning (F = 4.2; P = 0.01).Conclusion.Delusions and hallucinations, negative symptoms and paranoia all appeared to have a developmental origin though they were associated with different childhood problems. On the other hand, neither mania nor depression was associated with childhood dysfunction. Our most striking finding was that disorganisation appeared to arise when a familial predisposition to mania was compounded by low premorbid IQ.


2021 ◽  
Vol 7 (1&2) ◽  
pp. 11-13
Author(s):  
Manjulika Debnath ◽  

Background: COVID-19 causes reactive psychiatric symptoms like anxiety, depression, insomnia etc besides significant inflammatory response. A number of COVID-19 patients are found to present with complex neuropsychiatric syndromes, including the first onset of psychosis, that seem to be directly related to brain damage in the context of COVID-19. Most cases of psychotic disorder in COVID-19 patients are being found in individuals with no personal or family history of mental illness. Case Description: A 33-year-old man presented with acute restlessness, agitation, wandering, vandalizing things, suspiciousness, hallucinatory behaviour, decreased sleep for 3 days duration. There was no past history or family history of any psychiatric illness. There was a history of mild grade fever 7 days before the onset of the psychotic symptoms. The patient was uncooperative, irritable, and had hallucinatory behaviour. Rapid Antigen Test (RAT) was positive. The patient responded to injectable antipsychotic haloperidol which was later changed to Tab Olanzepine 5 mg. The patient developed no COVID symptoms and no psychotic symptoms were seen further. Conclusion: There is a possibility of a psychosis break as a COVID-19 clinical presentation, suggesting potential participation of inflammatory and autoimmunologic phenomena triggered as a response to the coronavirus infection.


2021 ◽  
pp. 113-115
Author(s):  
Andrew McKeon

A 67-year-old man visited the neurology clinic for new-onset, generalized, uncontrollable movements. His wife noticed onset of some unusual facial expressions and facial movements. This then evolved to him having some writhing movements of the left upper and left lower extremity. His speech and swallowing also became affected. He noted a tendency to bite his tongue, which was moving uncontrollably. Shortly before his neurology clinic visit, the same writhing movements of right-sided limbs developed. No cognitive or behavioral changes were reported. He had been diagnosed with cutaneous lupus erythematosus 5 years previously after a malar rash of his face developed after sun exposure. The patient had a strong family history of autoimmunity, with 3 sisters having systemic lupus erythematosus. On physical examination, he had marked chorea, hyperkinetic movements that were unpredictable. When he walked in the hallway, he had a narrow-based gait, with some mild upper extremity hyperkinetic movements. Because of the time course and the personal and family history of autoimmunity, autoimmune chorea was suspected. His cerebrospinal fluid demonstrated normal protein concentration, blood cell count, immunoglobulin G index and synthesis rate, and oligoclonal bands. Indirect immunofluorescence assays using HEp-2 substrate were positive for antinuclear antibody and Sjö‎gren syndrome-A antibody (anti-Ro). Autoimmune chorea was diagnosed in the context of a known history of a limited form of systemic lupus erythematosus. The patient received intravenous methylprednisolone infusions. Trimethoprim-sulfamethoxazole, double strength was given for Pneumocystis jirovecii prophylaxis. A rash developed, and the patient was determined to be sulfa allergic. Instead, he received atovaquone as prophylaxis. Three years later, the patient remained in remission from his chorea except for mild occasional hyperkinetic movements of his tongue. In adults, autoimmune chorea is the most common form of chorea after levodopa-induced dyskinesias and Huntington disease. Patients have a subacute onset of symptoms and rapid progression. Patients may have accompanying neuropsychiatric symptoms.


2008 ◽  
Vol 38 (10) ◽  
pp. 1505-1514 ◽  
Author(s):  
S. Soni ◽  
J. Whittington ◽  
A. J. Holland ◽  
T. Webb ◽  
E. N. Maina ◽  
...  

BackgroundPsychotic illness is strongly associated with the maternal uniparental disomy (mUPD) genetic subtype of Prader–Willi syndrome (PWS), but not the deletion subtype (delPWS). This study investigates the clinical features of psychiatric illness associated with PWS. We consider possible genetic and other mechanisms that may be responsible for the development of psychotic illness, predominantly in those with mUPD.MethodThe study sample comprised 119 individuals with genetically confirmed PWS, of whom 46 had a history of psychiatric illness. A detailed clinical and family psychiatric history was obtained from these 46 using the PAS-ADD, OPCRIT, Family History and Life Events Questionnaires.ResultsIndividuals with mUPD had a higher rate of psychiatric illness than those with delPWS (22/34 v. 24/85, p<0.001). The profile of psychiatric illness in both genetic subtypes resembled an atypical affective disorder with or without psychotic symptoms. Those with delPWS were more likely to have developed a non-psychotic depressive illness (p=0.005) and those with mUPD a bipolar disorder with psychotic symptoms (p=0.00005). Individuals with delPWS and psychotic illness had an increased family history of affective disorder. This was confined exclusively to their mothers.ConclusionsPsychiatric illness in PWS is predominately affective with atypical features. The prevalence and possibly the severity of illness are greater in those with mUPD. We present a ‘two-hit’ hypothesis, involving imprinted genes on chromosome 15, for the development of affective psychosis in people with PWS, regardless of genetic subtype.


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