Academic literature on the topic 'Neuropsychiatric fluctuations'
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Journal articles on the topic "Neuropsychiatric fluctuations":
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Magalhães, Andreia D., Deborah Amstutz, Katrin Petermann, Ines Debove, Mário Sousa, Marie E. Maradan-Gachet, Martin Lenard Lachenmayer, et al. "Subthalamic stimulation has acute psychotropic effects and improves neuropsychiatric fluctuations in Parkinson’s disease." BMJ Neurology Open 6, no. 1 (January 2024): e000524. http://dx.doi.org/10.1136/bmjno-2023-000524.
Abstract:
BackgroundSubthalamic nucleus deep brain stimulation (STN-DBS) is a well-established treatment for motor complications in Parkinson’s disease (PD). However, its effects on neuropsychiatric symptoms remain disputed. The aim of this study was to evaluate the effects of STN-DBS on neuropsychiatric symptoms in PD.MethodsWe retrospectively assessed 26 patients with PD who underwent a preoperative levodopa challenge and postoperative levodopa and stimulation challenges 1 year after STN-DBS. Based on the Neuropsychiatric Fluctuations Scale, Neuropsychiatric State Scores and Neuropsychiatric Fluctuation Indices (NFIs) were calculated. Mixed-effects models with random effects for intercept were used to examine the association of Neuropsychiatric State Score and NFI with the different assessment conditions.ResultsIn acute challenge conditions, there was an estimated increase of 15.9 points in the Neuropsychiatric State Score in stimulation ON conditions (95% CI 11.4 to 20.6, p<0.001) and 7.6 points in medication ON conditions (95% CI 3.3 to 11.9, p<0.001). Neuropsychiatric fluctuations induced by levodopa, quantified with NFI, decreased by 35.54% (95% CI 49.3 to 21.8, p<0.001) 1 year after STN-DBS.ConclusionsBilateral STN-DBS at therapeutic parameters has acute psychotropic effects similar to levodopa and can modulate and decrease levodopa-induced neuropsychiatric fluctuations.
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Fox, Susan H., Naomi Visanji, Gaby Reyes, Philippe Huot, Jordi Gomez-Ramirez, Tom Johnston, and Jonathan M. Brotchie. "Neuropsychiatric Behaviors in the MPTP Marmoset Model of Parkinson’s Disease." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 37, no. 1 (January 2010): 86–95. http://dx.doi.org/10.1017/s0317167100009707.
Abstract:
Objectives:Neuropsychiatric symptoms are increasingly recognised as a significant problem in patients with Parkinson's disease (PD). These symptoms may be due to ‘sensitisation’ following repeated levodopa treatment or a direct effect of dopamine on the disease state. The levodopa-treated MPTP-lesioned marmoset was used as a model of neuropsychiatric symptoms in PD patients. Here we compare the time course of levodopa-induced motor fluctuations and neuropsychiatric-like behaviors to determine the relationship between duration of treatment and onset of symptoms.Methods:Marmosets were administered 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (2.0 mg/kg s.c.) for five days, resulting in stable parkinsonism. Levodopa (15 mg/kg and benserazide, 3.75 mg/kg) p.o. b.i.d. was administered for 30 days. Animals were evaluated for parkinsonian disability, dyskinesia and on-time (motor fluctuations) and neuropsychiatric-like behaviors on Day 0 (prior to levodopa) and on Days 1, 7, 13, 27 and 30 of treatment using post hoc DVD analysis by a trained rater, blind to the treatment day.Results:The neuropsychiatric-like behavior rating scale demonstrated high interrater reliability between three trained raters of differing professional backgrounds. As anticipated, animals exhibited a progressive increase in levodopa-induced motor fluctuations, dyskinesia and wearing-off, that correlated with the duration of levodopa therapy. In contrast, levodopa-induced neuropsychiatric-like behaviors were present on Day 1 of levodopa treatment and their severity did not correlate with duration of treatment.Conclusions:The data suggest that neuropsychiatric disorders in PD are more likely an interaction between levodopa and the disease state than a consequence of sensitisation to repeated dopaminergic therapy.
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Abbes, Marie, Eugénie Lhommée, Stéphane Thobois, Hélène Klinger, Emmanuelle Schmitt, Amélie Bichon, Anna Castrioto, et al. "Subthalamic stimulation and neuropsychiatric symptoms in Parkinson’s disease: results from a long-term follow-up cohort study." Journal of Neurology, Neurosurgery & Psychiatry 89, no. 8 (February 7, 2018): 836–43. http://dx.doi.org/10.1136/jnnp-2017-316373.
Abstract:
BackgroundReports on behavioural outcomes after subthalamic nucleus deep brain stimulation in Parkinson’s disease are controversial and limited to short-term data. Long-term observation in a large cohort allows a better counselling and management.MethodsTo determine whether a long-term treatment with subthalamic stimulation induces or reduces impulse control behaviours, neuropsychiatric fluctuations and apathy, 69 patients treated with subthalamic stimulation are prospectively and retrospectively assessed using Ardouin Scale of Behavior in Parkinson’s Disease before and after 3–10 years of stimulation.ResultsAt a mean follow-up of 6 years, all impulse control disorders and dopaminergic addiction were significantly decreased, apart from eating behaviour and hypersexuality. Neuropsychiatric fluctuations also significantly improved (ON euphoria: 38% of the patients before surgery and 1% after surgery, P<0.01; OFF dysphoria: 39% of the patients before surgery and 10% after surgery, P<0.01). However, apathy increased (25% of the patients after surgery and 3% before, P<0.01). With the retrospective analysis, several transient episodes of depression, apathy, anxiety and impulse control disorders occurred.ConclusionsBilateral subthalamic nucleus stimulation was overall very effective in improving impulse control disorders and neuropsychiatric fluctuations in parkinsonian patients in the long term despite a counteracting frequent apathy. Transient episodes of impulse control disorders still occurred within the follow-up. These findings recommend a close follow-up in parkinsonian patients presenting with neuropsychiatric symptoms before deep brain stimulation surgery.Clinical trial registrationNCT01705418;Post-results.
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Schmitt, Emmanuelle, Paul Krack, Anna Castrioto, Helene Klinger, Amelie Bichon, Eugénie Lhommée, Pierre Pelissier, et al. "The Neuropsychiatric Fluctuations Scale for Parkinson's Disease: A Pilot Study." Movement Disorders Clinical Practice 5, no. 3 (March 23, 2018): 265–72. http://dx.doi.org/10.1002/mdc3.12607.
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Matar, Elie, Simon R. White, John-Paul Taylor, Alan Thomas, Ian G. McKeith, Joseph P. M. Kane, Ajenthan Surendranathan, Glenda M. Halliday, Simon J. G. Lewis, and John T. O'Brien. "Progression of Clinical Features in Lewy Body Dementia Can Be Detected Over 6 Months." Neurology 97, no. 10 (August 17, 2021): e1031-e1040. http://dx.doi.org/10.1212/wnl.0000000000012450.
Abstract:
ObjectiveThis study aimed to quantify the trajectory and magnitude of change of the key clinical features and corresponding symptom domains of dementia with Lewy bodies (DLB) and Parkinson disease dementia (PDD), including global cognition, parkinsonism, recurrent visual hallucinations, cognitive fluctuations, and sleep disturbance.MethodsOne hundred sixteen patients with Lewy body dementia (DLB = 72, PDD = 44) underwent assessment at baseline and 3 and 6 months as part of a prospective multicenter randomized controlled trial. Linear mixed models were constructed for core outcome measures using the Mini-Mental State Examination (MMSE), motor section of the Unified Parkinson's Disease Rating Scale (UPDRS-III), Dementia Cognitive Fluctuations Scale (DCFS), and Neuropsychiatric Inventory (NPI).ResultsWithin the time frame of our study (6 months), we were able to identify a significant cognitive decline of 1.3 points on the MMSE (p = 0.002) and significant worsening of motor parkinsonism with an increase in UPDRS-III score of 3.2 points (p = 0.018). Fluctuation severity also increased using the DCFS with a 6-month change in score of 1.3 points (p = 0.001). Uniquely, a signal for increased severity of sleep symptoms of 1.2 points (NPI-sleep) was also detectable (p = 0.04). Significant changes in neuropsychiatric symptoms were not detected. There was no difference in rates of change of scores between DLB and PDD.DiscussionClinically significant rates of change in core clinical features can be detected and quantified in Lewy body dementia over a relatively short period (6 months) using common clinical instruments and thus may be useful as clinical endpoints for therapeutic trials of disease-modifying and symptomatic agents.
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Zimmer, Eduardo R., Maxime J. Parent, Antoine Leuzy, Antonio Aliaga, Arturo Aliaga, Luc Moquin, Esther S. Schirrmacher, et al. "Imaging in Vivo Glutamate Fluctuations with [11C]ABP688: A GLT-1 Challenge with Ceftriaxone." Journal of Cerebral Blood Flow & Metabolism 35, no. 7 (March 25, 2015): 1169–74. http://dx.doi.org/10.1038/jcbfm.2015.35.
Abstract:
Molecular imaging offers unprecedented opportunities for investigating dynamic changes underlying neuropsychiatric conditions. Here, we evaluated whether [11C]ABP688, a positron emission tomography (PET) ligand that binds to the allosteric site of the metabotropic glutamate receptor type 5 (mGluR5), is sensitive to glutamate fluctuations after a pharmacological challenge. For this, we used ceftriaxone (CEF) administration in rats, an activator of the GLT-1 transporter (EAAT2), which is known to decrease extracellular levels of glutamate. MicroPET [11C]ABP688 dynamic acquisitions were conducted in rats after a venous injection of either saline (baseline) or CEF 200 mg/kg (challenge). Binding potentials (BPND) were obtained using the simplified reference tissue method. Between-condition statistical parametric maps indicating brain regions showing the highest CEF effects guided placement of microdialysis probes for subsequent assessment of extracellular levels of glutamate. The CEF administration increased [11C]ABP688 BPND in the thalamic ventral anterior (VA) nucleus bilaterally. Subsequent microdialysis assessment revealed declines in extracellular glutamate concentrations in the VA. The present results support the concept that availability of mGluR5 allosteric binding sites is sensitive to extracellular concentrations of glutamate. This interesting property of mGluR5 allosteric binding sites has potential applications for assessing the role of glutamate in the pathogenesis of neuropsychiatric conditions.
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Donaghy, Paul C., John-Paul Taylor, John T. O'Brien, Nicola Barnett, Kirsty Olsen, Sean J. Colloby, Jim Lloyd, George Petrides, Ian G. McKeith, and Alan J. Thomas. "Neuropsychiatric symptoms and cognitive profile in mild cognitive impairment with Lewy bodies." Psychological Medicine 48, no. 14 (January 24, 2018): 2384–90. http://dx.doi.org/10.1017/s0033291717003956.
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AbstractBackgroundThe accurate clinical characterisation of mild cognitive impairment (MCI) is becoming increasingly important. The aim of this study was to compare the neuropsychiatric symptoms and cognitive profile of MCI with Lewy bodies (MCI-LB) with Alzheimer's disease MCI (MCI-AD).MethodsParticipants were ⩾60 years old with MCI. Each had a thorough clinical and neuropsychological assessment and 2β-carbomethoxy-3β-(4-iodophenyl)-N-(3-fluoropropyl)-nortropane single photon emission computed tomography FP-CIT SPECT). MCI-LB was diagnosed if two or more diagnostic features of dementia with Lewy bodies were present (visual hallucinations, cognitive fluctuations, motor parkinsonism, rapid eye movement sleep behaviour disorder or positive FP-CIT SPECT). A Lewy body Neuropsychiatric Supportive Symptom Count (LBNSSC) was calculated based on the presence or absence of the supportive neuropsychiatric symptoms defined by the 2017 DLB diagnostic criteria: non-visual hallucinations, delusions, anxiety, depression and apathy.ResultsMCI-LB (n = 41) had a higher LBNSSC than MCI-AD (n = 24; 1.8 ± 1.1 v. 0.7 ± 0.9, p = 0.001). 67% of MCI-LB had two or more of those symptoms, compared with 16% of MCI-AD (Likelihood ratio = 4.2, p < 0.001). MCI-LB subjects scored lower on tests of attention, visuospatial function and verbal fluency. However, cognitive test scores alone did not accurately differentiate MCI-LB from MCI-AD.ConclusionsMCI-LB is associated with neuropsychiatric symptoms and a cognitive profile similar to established DLB. This supports the concept of identifying MCI-LB based on the presence of core diagnostic features of DLB and abnormal FP-CIT SPECT imaging. The presence of supportive neuropsychiatric clinical features identified in the 2017 DLB diagnostic criteria was helpful in differentiating between MCI-LB and MCI-AD.
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Krouse, Adam, Huihua Li, Joseph A. Krenzer, and William Nicholas Rose. "Plasmapheresis, Rituximab, and Ceftriaxone Provided Lasting Improvement for a 27-Year-Old Adult Male with Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections (PANDAS)." Case Reports in Psychiatry 2021 (November 2, 2021): 1–4. http://dx.doi.org/10.1155/2021/8697902.
Abstract:
Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS) is a specific autoimmune response to group-A streptococcal (GAS) infections in children and adolescents with a sudden onset of neuropsychiatric disorders including obsessive-compulsive disorder (OCD) or tic-like symptoms. We present a case report of a 27-year-old male patient who had lasting improvement with plasmapheresis, rituximab, and ceftriaxone. Our patient first developed sudden psychosis and confusion after GAS infections at age 17. He had elevated anti-streptolysin O (ASO) titers, negative urine drug screen, no ETOH in blood, normal CBC, normal TSH, normal salicylate, normal acetaminophen, and a normal head CT. The tentative diagnosis of PANDAS was made, and the patient was thereafter treated with antipsychotics, antibiotics, tonsillectomy, and IVIG which resulted in remissions and relapses of his neuropsychiatric symptoms. Once he reached age 27, he received a trial of therapeutic plasma exchange (TPE), rituximab, and ceftriaxone. This eventually resulted in sustained benefit and minimal fluctuations of his clinical symptoms. Our report is noteworthy in three ways.One, he is a 27-year-old adult with PANDAS.Two, he improved after TPE, rituximab, and ceftriaxone. Our literature search yielded minimal data on the use of plasmapheresis for nonteenage adults with PANDAS. Three, he had unusual symptoms of PANDAS, as the typical OCD and/or tic-like symptoms were not observed.
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Infante, Roberto, Emmanuelle Schmitt, Sara Meoni, Valerie Fraix, Amelie Bichon, Andrea Kistner, Pierre Pelissier, Bettina Debu, and Elena Moro. "Effects of subthalamic deep brain stimulation on neuropsychiatric fluctuations in patients with Parkinson's disease (psychostim study)." Journal of the Neurological Sciences 429 (October 2021): 117639. http://dx.doi.org/10.1016/j.jns.2021.117639.
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Oliveira, S. G., S. M. Pereira, and J. Mendes. "Dementia in Parkinson's disease: Case report." European Psychiatry 26, S2 (March 2011): 846. http://dx.doi.org/10.1016/s0924-9338(11)72551-2.
Abstract:
IntroductionParkinson's disease (PD) dementia is a rapidly growing global health problem. Dementia in PD is often accompanied with neuropsychiatric manifestations, such as depression, insomnia, visual hallucinations and psychomotor agitation, which need psychiatric attention.ObjectivesThe authors’ aim is to report a case of a 76-year-old female suffering from PD who was admitted to the psychiatric yard exhibiting neuropsychiatric symptoms. A literature's review about PD dementia was also made.Case reportPatient had one psychiatric hospitalization at age 41, due to depressive symptoms. PD diagnose was made at age 65 and initially responded well to levodopa. Over the subsequent years, motor fluctuations and dyskinesias as well as autonomic, cognitive and psychological symptoms gradually developed. At 75 years, patient's family stated that she had been more forgetful, impulsive, showing signs of anxiety and dysphoria. She was hospitalized exhibiting psychomotor agitation, disorientation, insomnia and mainly nocturnal visual hallucinations with persons. Diagnostic testing included: cranial tomography which showed mild generalized atrophy but no other structural cause of her symptoms; laboratory tests with B12, folic acid, thyroid function; syphilis detection test and examinations of serum and urine were normal. The MMSE scored 19. Attention deficits and constructional apraxia were present in clock drawing test. Treatment was initiated with memantine and a low dose of quetiapine. She was discharged after 20 days with improvement of neuropsychiatric symptoms.ConclusionsEarly diagnosis and treatment of dementia in PD may prevent psychiatric hospitalization and avoid patient's and family's distress.
Dissertations / Theses on the topic "Neuropsychiatric fluctuations":
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Schmitt, Emmanuelle. "Qualification et quantification des fluctuations neuropsychiatriques dans la maladie de Parkinson : Validation d'un auto-questionnaire grenoblois." Electronic Thesis or Diss., Université Grenoble Alpes, 2023. http://www.theses.fr/2023GRALS060.
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La maladie de Parkinson (MP) est la deuxième maladie neurodégénérative la plus fréquente. Elle est décrite depuis plusieurs années comme une maladie neuropsychiatrique, du fait de son expression clinique, mêlant des symptômes moteurs et non-moteurs, notamment psychiques et émotionnels. Au décours de l’évolution de la MP, apparaissent des fluctuations non-motrices qui sont connues pour leur impact négatif majeur sur l'autonomie et la qualité de vie des patients. Parmi elles, les fluctuations neuropsychiatriques (FNpsy) sont probablement les plus invalidantes. Elles se caractérisent par l’alternance de phases dites OFF « hypo-dopaminergiques », caractérisées par l'anxiété, la fatigue, le manque de motivation, la tristesse et la lenteur de la pensée et se manifestent lors de périodes de moindre efficacité du traitement antiparkinsonien (phase OFF) ; et de phases dites ON « hyper-dopaminergiques », synonymes d’un sentiment général de bien-être, une humeur élevée (voire hypomaniaque) et une hyperactivité ; apparaissant lors de périodes d’efficacité du traitement antiparkinsonien ( phase ON). La présence et la gravité des FNpsy peuvent varier d'un patient à l'autre. L'identification et la prise en charge de ces FNpsy jouent un rôle essentiel dans la prise en charge globale et personnalisée de la MP. Dans cette optique, notre groupe a développé, il y a quelques années une échelle de fluctuations neuropsychiatriques (l’EFN). Cette échelle a l’objectif de définir et peser l’impact des FNpsy en termes réels.L’objectif principal de ce travail de thèse est d’étudier les caractéristiques psychométriques de l’EFN (Etudes EFN Pré-Valid et EFN-Valid), et secondairement, d’utiliser l’EFN pour étudier les propriétés cliniques des patients parkinsoniens fluctuants. Nous avons également analysé l’impact du traitement par stimulation cérébrale profonde sur les FNpsy mesurées avec l’EFN (Étude PSYCHOStim)Parkinson's disease (PD) is the second most common neurodegenerative disorder. For many years, it has been described as a neuropsychiatric disease, due to its clinical expression which combines motor and non-motor symptoms, particularly psychological and emotional. During the course of PD, non-motor fluctuations appear and have a major negative impact on patients' autonomy and quality of life. Of these, neuropsychiatric fluctuations (NPsyF) are probably the most disabling. NPsyF are characterized by the alternation of the so-called OFF "hypo-dopaminergic" phase, characterized by anxiety, fatigue, lack of motivation, sadness and slowness of thought, and appearing during periods of reduced efficacy of antiparkinsonian treatment (OFF phase) ; and so-called ON "hyper-dopaminergic" phase, characterized by a general feeling of well-being, elevated mood (even hypomania), and hyperactivity; appearing during periods of antiparkinsonian treatment efficacy (ON phase). The presence and severity of NPsyF can vary from patient to patient. The identification and management of NPsyF play an essential role in the global and personalized management of PD. With this in mind, our group developed a neuropsychiatrics fluctuations scale (the NFS) a few years ago. This scale aims at defining and quantifying the impact of MPsyF on real time.The main aim of this thesis work is to study the psychometric characteristics of the NFS (NFS Pre-Valid and NFS-Valid studies), and secondarily, to use the NFS to study the clinical properties of fluctuating parkinsonian patients. We also analyzed the impact of deep brain stimulation treatment on NPsyF measured with NFS (PSYCHOStim Study)
Book chapters on the topic "Neuropsychiatric fluctuations":
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Zhou, Yuan, Kun Wang, Yong Liu, Ming Song, Sonya W. Song, and Tianzi Jiang. "Spontaneous Low-Frequency Fluctuation Observed with Functional Magnetic Resonance Imaging as a Potential Biomarker in Neuropsychiatric Disorders." In Advances in Cognitive Neurodynamics (II), 47–57. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-9695-1_7.
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Ramirez-Zamora, Adolfo. "Acute Neuropsychiatric Symptoms and Impulse Control Disorders After Subthalamic Nucleus Deep Brain Stimulation." In Deep Brain Stimulation, edited by Laura S. Surillo Dahdah, Padraig O’Suilleabhain, Hrishikesh Dadhich, Mazen Elkurd, Shilpa Chitnis, and Richard B. Dewey, 149–54. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780190647209.003.0031.
Abstract:
Neuropsychiatric symptoms, including impulse control disorders and mood changes, are common nonmotor features across all Parkinson disease (PD) stages. Subthalamic nucleus (STN) deep brain stimulation (DBS) is a safe and well-established treatment for the management of refractory motor fluctuations in PD; however, it has been associated with worsening neuropsychiatric symptoms in the short and long term. Recognizing the occurrence of stimulation-induced behavioral symptoms is critical to implement effective and timely treatment. Most reports indicate that stimulation of the ventral and medial region within the STN and surrounding structures, including the substantia nigra, might account for the occurrence of acute impulsive behaviors and hypomania, requiring adopting different programming strategies aimed at limiting behavioral side effects while reducing parkinsonism. Stimulation of the most dorsal and lateral contacts can mitigate behavioral side effects after STN DBS, but specific treatment needs to be applied based on the patient’s individual neuropsychiatric and motor presentations and specific imaging-based brain localization of DBS lead contacts.
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Huang, Xiaohong, Xiaohua Li, and Heng-Wei Cheng. "Gestational Tryptophan Fluctuation Underlying Ontogenetic Origin of Neuropsychiatric Disorders." In Personality Traits - The Role in Psychopathology [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.106421.
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Neuropsychiatry underlies personality development and social functioning. Borderline personality disorder exhibits high trait aggression and is associated with tryptophan hydroxylase polymorphisms. The acute tryptophan depletion reduces plasma and cerebrospinal fluid tryptophan availability and brain serotonin concentrations, leading to alterations in personality and trait-related behaviors. Tryptophan is essential for fatal neurodevelopment and immunomodulation in pregnancy. Gestational tryptophan fluctuation induced by maternal metabolic disorders or drug administrations may account for the maternal-fetal transmission determining neurogenesis and microbial development, consequentially shaping the long-standing patterns of thinking and behavior. However, it is not possible to assess the gestational tryptophan exposure effects on fetal brain and gastrointestinal system in humans for ethical reasons. The maternal–fetal microbe transmission in rodents during gestation, vaginal delivery, and breastfeeding is inevitable. Chicken embryo may be an alternative and evidence from the chicken embryo model reveals that gestational tryptophan fluctuation, i.e., exposed to excessive tryptophan or its metabolite, serotonin, attenuates aggressiveness and affects peer sociometric status. This chapter discusses the gestational tryptophan fluctuation as a risk factor of personality disorders in offspring and the prevention of personality disorders by dietary tryptophan control and medication therapy management during pregnancy.
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Manschreck, Christopher, Yesne Alici, and William Breitbart. "Delirium in the Terminally Ill." In Handbook of Psychiatry in Palliative Medicine 3rd edition, edited by Harvey Max Chochinov and William Breitbart, 77—C6.P129. 3rd ed. Oxford University Press, 2022. http://dx.doi.org/10.1093/med/9780197583838.003.0006.
Abstract:
Abstract Delirium is one of the most common neuropsychiatric complications in the management of terminally ill patients. Delirium is characterized by an abrupt onset and fluctuating disturbance in arousal, attention, cognition, and perception. Delirium is a serious neuropsychiatric condition that is associated with increased morbidity and mortality, causing distress in patients, family members, and staff. Delirium signals a medical emergency. Emerging from significant physiologic disturbance, usually involving multiple medical etiologies, delirium requires prevention, early identification, and vigorous treatment. Unfortunately, delirium is often underrecognized, misdiagnosed, inappropriately treated, or untreated in the medical setting. Palliative care specialists and others who care for terminally ill patients must be able to diagnose delirium accurately, undertake appropriate assessment of etiologies, and understand the benefits and risks of pharmacologic and nonpharmacologic interventions currently available. This chapter presents a comprehensive overview of the epidemiology, pathophysiology, clinical features, assessment, and management of delirium in the terminally ill.
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Davis, Daniel, Sarah Richardson, and Esteban Sepulveda. "Delirium." In Oxford Textbook of Neurologic and Neuropsychiatric Epidemiology, edited by Carol Brayne, Valery L. Feigin, Lenore J. Launer, and Giancarlo Logroscino, 259–66. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198749493.003.0026.
Abstract:
Delirium is a common and severe neuropsychiatric syndrome of brain dysfunction characterized by acute and fluctuating inattention and other cognitive and perceptual deficits precipitated by acute illness. Despite being first described by Hippocrates more than two thousand years ago, there exists considerable uncertainty regarding the diagnosis of delirium due to our limited understanding of fundamental concepts, including its definition and pathophysiology. The ensuing lack of standardization results in delirium being frequently undiagnosed and significant misclassification bias in existing research. This chapter discusses the descriptive epidemiology of delirium, including methodological issues around case ascertainment in different population and clinical settings. There remains a lack of epidemiological research in the field, but we indicate the potential for observational longitudinal studies to address key questions on the population impact of delirium alongside fundamental questions of major importance to patients and their families regarding outcomes after delirium.
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Trzepacz, Paula, and Roos van der Mast. "The neuropathophysiology of delirium." In Delirium in Old Age, 51–90. Oxford University PressNew York, NY, 2002. http://dx.doi.org/10.1093/oso/9780192632753.003.0004.
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Abstract Introduction Multiple higher cortical functions and neural circuits are affected in delirium, hence Lipowski’s description of the disorder as ‘acute brain failure’. With its characteristic abrupt onset and fluctuating symptom severity, delirium is a severe neuropsychiatric disorder. It is usually associated with generalized EEG slowing, consistent with widespread cortical dysfunction causing a range of symptoms arising from different functional brain regions. Additionally, evoked potential abnormalities suggest involvement of subcortical areas including the brainstem and thalamus (Trzepacz 1994). Lack of primary motor and sensory signs (unless related to specific aetiologies, like asterixis) suggests that association cortices (secondary and tertiary), limbic structures and ascending neurotransmitter systems are principally affected in delirium. Neuroimaging and lesion reports suggest that prefrontal cortex, anterior thalamus, non-dominant parietal and fusiform cortex are also involved (Trzepacz 1999).
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Alici, Yesne, and William S. Breitbart. "Delirium." In Psycho-Oncology, edited by William S. Breitbart, 345–54. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780190097653.003.0045.
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Delirium is one of the most common and often serious neuropsychiatric complications in the management of cancer patients that is characterized by abrupt-onset, fluctuating disturbance in awareness, attention, cognition, and perception. Delirium is associated with increased morbidity and mortality, causing distress in patients, family members, and staff. Delirium is a medical emergency, a sign of significant physiologic disturbance, usually involving multiple medical etiologies, that needs to be prevented, identified, and treated vigorously. Unfortunately, delirium is often underrecognized or misdiagnosed and inappropriately treated or untreated in the medical setting. Psycho-oncologists who care for patients with cancer must be able to diagnose delirium accurately, undertake appropriate assessment of etiologies, and understand the benefits and risks of pharmacologic and nonpharmacologic interventions currently available. This chapter presents a comprehensive overview of the epidemiology, pathophysiology, clinical features, assessment, and management of delirium in cancer patients.
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Alici, Yesne, Soenke Boettger, and William S. Breitbart. "Delirium and Cognitive Impairment." In Psycho-Oncology in Palliative and End of Life Care, 94—C5.P124. Oxford University PressNew York, 2022. http://dx.doi.org/10.1093/med/9780197615935.003.0005.
Abstract:
Abstract Cognitive syndromes are prevalent in palliative care settings. Delirium is the most common and often serious neuropsychiatric disorder found in palliative care settings. Delirium is characterized by abrupt onset, fluctuating disturbance in awareness, attention, cognition, and perception. Delirium is associated with increased morbidity and mortality, causing distress in patients, family members, and staff. Delirium is often underrecognized or misdiagnosed and inappropriately treated or untreated. Clinicians who care for patients with advanced cancer and at the end-of-life must be able to diagnose delirium accurately, undertake appropriate assessment of etiologies, and understand the benefits and risks of pharmacologic and nonpharmacologic interventions currently available. Dementia and other neurocognitive disorders can also be encountered in palliative care settings, have multifactorial etiologies ranging from cancer-treatments to brain metastases, and include neurodegenerative illnesses comorbidly, especially in the oldest old patient population. This chapter presents an overview of the assessment and management of delirium in cancer patients in palliative care settings. Other cognitive syndromes will be briefly described with a focus on the assessment and differential diagnosis. Professional issues, including communication challenges, ethical dilemmas, legal requirements, and service development agendas will be considered.
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Jyonouchi, Harumi, and Lee Geng. "Associations between Monocyte Cytokine Profiles and Co-Morbid Conditions in Autism Spectrum Disorders." In Autism Spectrum Disorder - Profile, Heterogeneity, Neurobiology and Intervention. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.95548.
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Autism spectrum disorder (ASD) is a behaviorally defined syndrome with frequent co-morbidities. Evidence indicate a role of innate immunity in ASD pathogenesis. This study addressed whether innate immune abnormalities are associated with ASD co-morbid conditions and/or other clinical co-variables when assessed as changes in monocyte cytokine profiles. This study included 109 ASD (median 11.5 year) and 26 non-ASD subjects (median 11.4 year). Monocyte cytokine profiles were evaluated in association with age/ethnicity, ASD severity, medications, and co-morbidities present in >15% of ASD subjects [gastrointestinal (GI) symptoms, epilepsy, allergic rhinitis, specific antibody deficiency (SAD), and fluctuating behavioral symptoms resembling pediatric acute-onset neuropsychiatric syndrome (PANS)]. ASD severity did not affect frequency of co-morbid conditions. GI symptoms, epilepsy, SAD, and PANS like symptoms revealed associations with changes in production of tumor necrosis factor-α (TNF-α)/soluble TNF-receptor II (sTNFRII), interleukin-1ß (IL-1ß)/IL-6/IL-10, and IL-6, respectively, mostly independent of other co-variables. ASD severity was associated with changes in multiple cytokines but frequently affected by other clinical co-variables. Our findings revealed associations between specific monocyte cytokine profiles and certain co-morbid conditions in ASD subjects, independent of other clinical co-variables. Our findings will aid in assessing treatment options for ASD co-morbidities and their effects on ASD behavioral symptoms.
Reports on the topic "Neuropsychiatric fluctuations":
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Wang, Xiaoyu. Pediatric TuiNa for Tourette syndrome in children: A systematic review and meta-analysis of randomized controlled trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2023. http://dx.doi.org/10.37766/inplasy2023.4.0077.
Abstract:
Review question / Objective: Efficacy and Safety of Pediatric TuiNa for Tourette Syndrome: A Systematic Review and Meta-Analysis of randomized controlled trials. Condition being studied: Tourette syndrome (TS) is a common psychological, behavioural and neuropsychiatric disorder characterized by chronic, fluctuating, multiple muscle convulsions, or accompanied by involuntary laryngeal abnormalities and indecent language. It mainly appears in childhood. At present, Tourette syndrome generally has a long course of the disease and is difficult to cure, which seriously affects the children's learning and physical and mental health, and also causes panic and anxiety to many parents. The incidence of Tourette syndrome was increasing year by year. Clinical studies found that only relying on Western medicine for treatment was easy to have recurrent symptoms and serious adverse reactions. Traditional Chinese medicine has great advantages in the treatment of Tourette syndrome, especially in children's massage, because it has no side effects and is more likely to be favoured by parents. To provide a better basis and guidance for clinical treatment by Meta-analysis of the literature on tuina treatment of Tourette syndrome in children.