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Part II presents the definition of orthorexia nervosa and a proposal of its new definition (‘Salussitomania’) due to the inaccurate etymology of the term Orthorexia Nervosa. It includes diagnostic criteria sets for orthorexia nervosa (proposed by Setnick, 2013; Moroze et al., 2015; Barthels et al., 2015; Dunn and Bratman, 2016) to depict key features of orthorexia nervosa, global study distribution on orthorexia nervosa as well as the divergence and overlap of orthorexia nervosa and other mental disorders, namely anorexia nervosa, obsessive-compulsive disorder and avoidant/restrictive food intake disorder, to enable a differential diagnosis. A summation of the highlights is included at the end of this chapter. The commentaries of the invited international experts (Dr Caterina Novara, University of Padova, Italy and Dr Hana Zickgraf, Rogers Behavioral Health, USA) provide valuable insights on orthorexia nervosa.
Edited by
Allan Young, Institute of Psychiatry, King's College London,Marsal Sanches, Baylor College of Medicine, Texas,Jair C. Soares, McGovern Medical School, The University of Texas,Mario Juruena, King's College London
Mood disorders are more common in persons with medical illness than in the general population, and add to suffering, morbidity, and mortality. As to diagnosis, emotional states seen in the context of illness range from denial to bland indifference to “normal” sadness, to pathological anxiety and depressive or manic syndromes. Within this range fall both primary mood disorders and mood disorders secondary to the primary illness and its treatment.Treatment is complicated by difficulties with patient engagement and retention, limited clinical trial data, illness-related sensitivity to medications and alterations in drug metabolism, drug side effects, and drug interactions. Limited data are available about potentially valuable treatments such as exercise, transcranial magnetic stimulation, ketamine and psychedelics. Collaborative care models for depression treatment in medical settings are effective but demanding to implement and sustain. Special considerations apply to treatment of patients near the end of life and those requesting hastened death. Psychiatric treatment of the medically ill patient can evoke strong feelings in the treatment provider.
We investigated how well a visual associative learning task discriminates Alzheimer’s disease (AD) dementia from other types of dementia and how it relates to AD pathology.
Methods:
3,599 patients (63.9 ± 8.9 years old, 41% female) from the Amsterdam Dementia Cohort completed two sets of the Visual Association Test (VAT) in a single test session and underwent magnetic resonance imaging. We performed receiver operating curve analysis to investigate the VAT’s discriminatory ability between AD dementia and other diagnoses and compared it to that of other episodic memory tests. We tested associations between VAT performance and medial temporal lobe atrophy (MTA), and amyloid status (n = 2,769, 77%).
Results:
Patients with AD dementia performed worse on the VAT than all other patients. The VAT discriminated well between AD and other types of dementia (area under the curve range 0.70–0.86), better than other episodic memory tests. Six-hundred forty patients (17.8%) learned all associations on VAT-A, but not on VAT-B, and they were more likely to have higher MTA scores (odds ratios range 1.63 (MTA 0.5) through 5.13 for MTA ≥ 3, all p < .001) and to be amyloid positive (odds ratio = 3.38, 95%CI = [2.71, 4.22], p < .001) than patients who learned all associations on both sets.
Conclusions:
Performance on the VAT, especially on a second set administered immediately after the first, discriminates AD from other types of dementia and is associated with MTA and amyloid positivity. The VAT might be a useful, simple tool to assess early episodic memory deficits in the presence of AD pathology.
Effective assessment is crucial in treating patients with comorbid OCD and EDs. It is important for providers to create comprehensive treatment plans by combining current empirical evidence, their own clinical judgment, and the patient’s willingness to participate in interventions. The success of this process largely depends on the thoroughness of the initial assessment and ongoing follow-up. There is no established treatment manual or approach for addressing both disorders, so a comprehensive approach that combines current empirical evidence, clinical judgment, and the patient’s willingness to participate in interventions is needed. Medical stability is of utmost importance when treating individuals with EDs. Identifying the chief complaint can be difficult due to the overlap of symptoms, and understanding the timeline of symptoms and data from assessment measures is useful, but understanding the specific rituals, rules, and avoided stimuli is the true key to identifying which disorder should be targeted more.
The clinical diagnostic process invokes unvalidated general-causation theory (shaking) as an explanation for clinical findings in infants. These medical findings (subdural haemorrhage, retinal haemorrhage, and encephalopathy) are non-specific and develop in natural diseases and accidents. Yet child protection teams associate these findings with abuse. Such ‘diagnosis’ of abuse, triggers social service and law enforcement intervention. Outside the clinical system, which errs on the side of child safety, the SBS/AHT general-causation theories have been challenged. Biomechanical, neuropathological, and forensic pathology research disputes the validity of the shaking theory. Medical ethicists and epidemiologists question the clinical reliance upon data and studies limited by circular reasoning and case selection bias. While ‘child abuse’ may be a ‘valid diagnosis’ for triggering social service intervention, it is not a scientifically sound diagnosis. Lacking foundational validity and support in the relevant scientific fields, SBS/AHT lacks reliability and general acceptance. Expert opinion of SBS/AHT general causation theory is inadmissible under a Daubert or Frye analysis.
Despite being a relatively new concept, psychiatric comorbidity, i.e. the co-occurrence of two or more mental disorders, has become widespread in clinical practice and psychiatric research. In this article, we trace the origin of the concept of psychiatric comorbidity, discuss the conceptual literature and point to basic problems concerning inadequate definition of the concept, differential diagnostic issues, and reification of mental disorders. We illustrate how these problems may have consequences for diagnostic assessment in current clinical practice and psychiatric research. To address some of the problems related to psychiatric comorbidity, we discuss potential principles for assessing psychiatric comorbidity. Inspired by Feinstein's original concept of comorbidity in general medicine and his differential diagnostic principles, we emphasize the importance of independence of mental disorders when assessing psychiatric comorbidity. We suggest that knowledge of trait v. state conditions and of the multitudinous clinical manifestations beyond what is captured in the diagnostic manuals may be helpful for assessing the independence of mental disorders and thus psychiatric comorbidity. We further argue that a more hierarchical diagnostic system and explicit exclusionary rules could improve clinical practice and research by reducing informational complexity and combating unwarranted psychiatric comorbidity.
Recent systematic reviews and meta-analyses conclude that similar social cognitive impairments are found in autism spectrum disorder (ASD) and schizophrenia spectrum disorder (SSD). While methodological issues have been mentioned as a limitation, no study has yet explored the magnitude of methodological heterogeneity across these studies and its potential impact for their conclusion. The purpose of this study was to systematically review studies comparing social cognitive impairments in ASD and SSD with a focus on methodology. Following the PRISMA guidelines, we searched all publications on PubMed, PsycINFO, and Embase. Of the 765 studies identified in our data base searches, 21 cross-sectional studies were included in the review. We found significant methodological heterogeneity across the studies. In the 21 studies, a total of 37 different measures of social cognition were used, 25 of which were only used in 1 study. Across studies, the same measure was often said to be assessing different constructs of social cognition – a confusion that seems to reflect the ambiguous definitions of what these measures test in the studies that introduced them. Moreover, inadequate differential diagnostic assessment of ASD samples was found in 81% of the studies, and sample characteristics were markedly varied. The ASD and SSD groups were also often unmatched in terms of medication usage and substance use disorder history. Future studies must address these methodological issues before a definite conclusion can be drawn about the potential similarity of social cognitive impairments in ASD and SSD.
You are seeing a patient referred by her primary care provider for consultation at your tertiary center’s high-risk obstetrics unit. She is a 37-year-old primigravida currently at 13+2 weeks’ gestation with an incidental 7-cm complex right adnexal mass detected last week on routine first-trimester sonography performed at an external center. Although the ultrasound report is not yet available to you, the consultation note confirms a singleton intrauterine pregnancy with normal fetal morphology and low risk of aneuploidy using sonographic markers. Routine serum prenatal investigations are only significant for iron-deficiency anemia.
A 34-year-old G3P2 at 20 weeks’ gestation presents to the A&E (E.R.) department of your tertiary care center with a three-hour history of nausea and vomiting associated with recurrent right upper quadrant pain, no longer alleviated by analgesics.
A healthy 27-year-old G1P0 at 10+3 weeks’ gestation, confirmed by sonography two days ago, presents for prenatal care. She arrived last month from overseas and currently lives with her sister and nephew, who has been home from daycare with German measles.
During your call duty, a 37-year-old obese G2P1 patient presents to your hospital center’s obstetric emergency assessment unit at 33+3 weeks’ gestation with pain and bruising in the lower aspect of the mid-abdomen. She holds her lower abdomen for support in between bouts of a residual dry cough after completion of antibiotic treatment for community-acquired pneumonia. Pregnancy has otherwise been unremarkable, and she has been compliant with prenatal care. She does not have vaginal bleeding or fluid loss. Two years ago, she had a Cesarean section for term breech presentation.
During your call duty, a healthy 40-year-old primigravida with a spontaneous dichorionic pregnancy presents, accompanied by her husband, to the obstetric emergency assessment unit of your hospital center at 33+1 weeks’ gestation with new-onset abdominal pain and vomiting after a two-day history of nausea and general malaise. She has no obstetric complaints, and fetal viabilities are ascertained upon presentation. Her face appears yellow tinged relative to her last clinical visit one week ago. You recall that routine prenatal laboratory investigations, aneuploidy screening, morphology surveys of the male fetuses, and serial sonograms have all been unremarkable.
During your obstetric call duty in a tertiary hospital center, you receive a telephone call from a colleague at an external center for an incidental isolated platelet count of 69 × 109/L in a 22-year-old primigravida with a singleton pregnancy at 24+3 weeks’ gestation by early dating sonography. The full/complete blood count (FBC/CBC) was performed to follow up on iron-deficiency anemia. Fetal activity is normal.
Frontotemporal dementia(FTD) is the prevalent type of primary progressive dementia. Psychiatric symptoms can be seen in FTD. So it can imitate psychiatric disorders and be misdiagnosed. However, few studies have investigated the underlying cause of misdiagnosis.
Objectives
The primary aim of this study was to identify the prior psychiatric diagnoses of patients before receiving a definitive diagnosis of FTD and the main reasons to cause diagnostic delay.
Methods
We screened through the records of patients who were admitted to our psychiatry outpatient or inpatient clinic from January 1st, 2018 to June 30th, 2021. The patients with FTD were included in our study.
Results
Our sample consisted of 13 patients with FTD(mean age= 54.77 ± 12.22, 7 females). Psychiatric misdiagnoses were depression(n=6), psychosis(n=5), bipolar affective disorder (n=5), conversion disorder(n=4), and malingering(n=1). As we looked at the first symptoms of the patients, it was revealed that 9 of 12 patients presented with depressive symptoms or at least experienced a short depressive period at the beginning of their behavioral changes. Interestingly, 8 of 12 patients had given a history of stressful life events just before their complaints emerged, which was thought the main misdirector for physicians. The average delays in diagnosis were 14.58(±16.93) months in the psychiatry clinic, 5.66(±11.02) months in the neurology clinic in our hospital.
Conclusions
Our study suggests that the depressive episode preceding behavioral changes may be the prodromal stage for fully developed FTD. Moreover, the depressive episode and the history of stressful life events appear to mislead clinicians in diagnosing FTD.
Autoimmune encephalitis are inflammatory diseases of the CNS mediated by antibodies that attack neurotransmitter receptors or proteins on the surface of neurons, usually in the limbic system. The clinic is different according to the antineuronal Ac involved.
Objectives
To make a correct differential diagnosis between autoimmune encephalitis and primary psychiatric pathologies that may be similar in symptoms through a complete study of the patient including anamnesis, physical examination, imaging tests, cerebrospinal fluid and serum studies.
Methods
Description of a clinical case. A 31-year-old female patient, with no previous history of interest, was brought to the emergency department for a suspected seizure. The previous days she had presented emotional lability, difficulty in concentration and reading, blurred vision, confusion and hemicranial headache. Two days later she returned to the emergency room for insomnia, dysarthria, difficulty in reading, comprehension, naming, and excessive rumination of her problems. Incoherent and repetitive language. The Emergency service requested to rule out a conversive disorder.
Results
Neuropsychiatric manifestations (anxiety, depression, behavioral disturbances, insomnia, memory deficits, psychomotor agitation, mania, auditory and visual hallucinations, delusions) are the first symptom in 70% of autoimmune encephalitis due to anti-NMDA antibodies and usually respond poorly to psychiatric treatment, making the treatment of the primary cause necessary for the remission of these symptoms.
Conclusions
Given their increasing recognition and prevalence, autoimmune causes should always be taken into account in behavioral changes, cognitive or consciousness impairment of subacute installation, especially in young patients and once infectious, metabolic and vascular causes have been ruled out with an appropriate complementary study.
Frontotemporal dementia (FTD) is common in presenile population. The overlapping symptoms with other psychiatric disorders can lead to wrong/late diagnosis which cause delays/difficulties regarding case-management. Especially, long-standing and/or late-onset depression can descriptively envelop bvFTD (behavioral-variant) and leads to unnecessary treatments and increased distress. It’s important to implement a descriptive diagnostic algorithm which will help clinicians to distinguish the phenomenology of these disorders.
Objectives
This presentation aims to call attention of the clinicians/researchers to an elaborated effort concerning differential diagnosis of two common disorders with overlapping features through a case-study of a 59-year-old male patient.
Methods
One case from an inpatient unit of a psychiatric clinic in Lower Saxony, Germany will be reported.
Results
Case: The patient was referred to our acute-psychiatric-ward from the day-clinic-unit because of treatment-resistant, severe and long-lasting depressive symptoms. He was depressed, desperate, hopeless, listless and had suicidal thoughts. During the first days of treatment, symptoms like apathy, bad hygiene, weird eating-behavior, urinary incontinence, lack of empathy, language disorders and other behavioral symptoms were evident. Brain-MRI yielded frontotemporal lobar atrophy. Trail-Making-Test and Frontal-Assessment-Battery showed pronounced impairment of executive functions. Mini mental state examination and DemTect yielded light to moderate memory dysfunction. Diagnostic Criteria for Probable bvFTD (International-Consensus-Criteria) were fulfilled.
Conclusions
The diagnosis of bvFTD enabled a rapid assignment of a legal representative and relieved the long-lasting discomfort of the patient and his family that was caused by multiple unsuccessful treatment trials against depression. The differential diagnostic frame between bvFTD and depression will be discussed in view of the current literature.
Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized with ritualized behavior, difficulties in communication/ social interaction, restricted interests, and sensitivity to external stimuli. The ASD has gained attention in recent years, however it’s still difficult in geropsychiatric setting to identify high-functioning ASD, especially when patients’ coping mechanisms are successful. Not to determine high-functioning ASD structure in older age can lead to wrong diagnosis and inappropriate treatment trials.
Objectives
The aim of this presentation is to emphasize the importance of the evaluation of ASD-structure in old-age-psychiatry through the case study of a 65-years-old man.
Methods
One case report from the inpatient unit of a psychiatric clinic in Lower Saxony, Germany will be presented.
Results
Case: The patient was referred to our acute-psychiatric-ward due to delusional thoughts, depressive symptoms and lorazepam dependency. Delusional disorder was diagnosed in the outpatient-setting since he had interpreted some external stimuli in an eccentric way. During the therapeutic process, some features of high-functioning ASD such as social difficulties, dislike of change and repetitive/restrictive habits were prominent. Developmental history of the patient and the Autism-Spectrum-Quotient-50 also supported the clinical diagnosis of the ASD. Delusional disorder was excluded, and the therapy organized according to the structure characteristics of the high-functioning ASD which yielded to significant amelioration of depressive symptoms and increased perceived life quality of the patient.
Conclusions
Although coping mechanisms of the patients can be successful, identifying high-functioning ASD-structure even in an old-age can be quite helpful in diagnostic/therapeutic processes. An elaborate discussion of the subject through contemporary literature will be presented.
Bipolar disorder (BD) is considered a risk factor for developing Parkinson’s Disease (PD) because of an altered dopamine activity in both entities. Comorbidity may delay diagnosis and difficult therapeutic management.
Objectives
To describe the case of a patient with both BD and PD and to determine the appropriate diagnostic and therapeutic approach for patients presenting both entities.
Methods
We present the case of a 58-year-old woman attended in our neurology unit due to the initial presence of visual hallucinations as a core symptom.
Results
Psychotic symptoms as hallucinations and off-times, frequently observed in PD, may be misdiagnosed with a worsening of depressive polarity of BD. Thus, overlap between symptoms may lead to a challenging differential diagnosis. Moreover, there is no consensus about the therapeutic management of the comorbidity, due to the bidirectional worsening of symptoms when treatment is adjusted. In our case, a diagnosis of dopaminergic psychosis was made so antipsychotic treatment with quetiapine 50 mg/d was initiated. A worsening of symptoms was observed, presenting the patient a stuporous status, mutism and generalized rigidity. Neuroimaging and lumbar puncture were performed showing no alterations; electroencephalogram showed diffuse slowing. Final diagnosis was an off-episode of PD and a multifactorial encephalopathy resulting in visual hallucinations.
Conclusions
Coexistence of PD and BD may lead to a diagnostic and therapeutic delay and therefore a worse prognosis. Although these diseases are well-known, it is still challenging to manage patients presenting both entities. Further research is needed to clarify the proper diagnostic and therapeutic approach for these patients.
Autism spectrum disorders (ASD) is one of the most urgent problems of psychiatry because of their high prevalence, diagnostic difficulties as well as insufficient knowledge of the pathogenetic mechanisms.
Objectives
To determine the number of inflammation markers in patients with various forms of ASD in links with features of a clinical condition for creating diagnostic criteria for differential diagnosis and improve reliability.
Methods
The clinical examination of patients (135 children with various ASD forms) was carried out by using psychometric scales (CARS, BFCRS, CGI-S). The activity of inflammation markers (LE and α1-PI) and the level of autoantibodies to S-100b and MBP were measured in plasma. Complex evaluation of immune system activation was also conducted, taking into consideration interactions of innate and adaptive immunity.
Results
Non-psychotic ASD forms (Asperger’s syndrome and Kanner’s syndrome) were not accompanied by a change of the immunological indices in comparison with control. In psychotic ASD forms, a significant increase of the studied indices was revealed (р<0.05). Correlation between the complex evaluation of the immune system activation and the stage of the disease (r=0.49, р<0.05) was demonstrated. Also the significant correlations between the severity of autistic disorders according to CARS (r=0.48, p<0.05), catatonic disorders by BFCRS (r=0.42, p<0.05), and the assessment by CGI (r= 0.61, p<0.05) were observed.
Conclusions
The immune markers as well as their complex evaluation may be used as additional diagnostic criteria in the clinical examination for differential ASD diagnostics and assessment of the quality of remission, and also monitoring of the patient condition.