RESUMEN
AIM: To: (1) provide greater insight into the psychological and social impact of a range of demyelinating disorders, (2) explore differences between disorders, and (3) provide direction for future research. METHOD: Studies were identified by searching online databases. Studies that explored the psychological, emotional, or social impact of a range of demyelinating disorders in childhood, including acute disseminated encephalomyelitis (ADEM), optic neuritis, transverse myelitis, and multiple sclerosis, were included and screened independently by three authors. Data on the design, sample characteristics, psychosocial measures, key findings, and methodological strengths and limitations were extracted. Twenty-five studies were included in the narrative synthesis. RESULTS: Demyelinating disorders are associated with lower quality of life, affecting young people's emotional, social, school, and behavioural functioning. There is a high prevalence of psychiatric disorders and fatigue, particularly in multiple sclerosis. Subtle differences exist in the psychological presentation between different demyelinating disorders, with clear gaps in the research for the long-term psychosocial impact of monophasic conditions. INTERPRETATION: The difference between the impact of monophasic and relapsing demyelinating disorders on psychosocial functioning is unclear. Future research should aim to identify the psychosocial impact across disorders and over time, ensure that services are capturing those patients who may benefit from tailored interventions. WHAT THIS PAPER ADDS: Prevalence of psychiatric diagnoses in paediatric demyelinating disorders is higher than controls. Depression and emotional concerns are elevated in paediatric demyelinating disorders. Demyelinating disorders impact children's quality of life across school, social, and physical functioning.
Asunto(s)
Síntomas Conductuales , Enfermedades Autoinmunes Desmielinizantes SNC , Fatiga , Trastornos Mentales , Funcionamiento Psicosocial , Calidad de Vida , Síntomas Conductuales/etiología , Síntomas Conductuales/fisiopatología , Síntomas Conductuales/psicología , Niño , Enfermedades Autoinmunes Desmielinizantes SNC/complicaciones , Enfermedades Autoinmunes Desmielinizantes SNC/fisiopatología , Enfermedades Autoinmunes Desmielinizantes SNC/psicología , Fatiga/etiología , Fatiga/fisiopatología , Fatiga/psicología , Humanos , Trastornos Mentales/etiología , Trastornos Mentales/fisiopatología , Trastornos Mentales/psicología , Calidad de Vida/psicologíaRESUMEN
INTRODUCTION: The profile of psychiatric disorders associated with multiple sclerosis (MS) may differ in children. We aimed to assess the risk of psychiatric disorders in children with MS and other demyelinating diseases, and vice versa. PATIENTS AND METHODS: We analyzed linked English Hospital Episode Statistics, and mortality data, 1999-2011. Cohorts were constructed of children admitted with MS and other central nervous system (CNS) demyelinating diseases. We searched for any subsequent episode of care with psychiatric disorders in these cohorts and compared to a reference cohort. RESULTS: Children with CNS demyelinating diseases had an increased rate of psychotic disorders (rate ratio (RR) = 5.77 (95% confidence interval (CI) = 2.48-11.41)); anxiety, stress-related, and somatoform disorders (RR = 2.38 (1.39-3.81)); intellectual disability (RR = 6.56 (3.66-10.84)); and other behavioral disorders (RR = 8.99 (5.13-14.62)). In analysis of the pediatric MS cohort as the exposure, there were elevated rates of psychotic disorders (RR = 10.76 (2.93-27.63)), mood disorders (RR = 2.57 (1.03-5.31)), and intellectual disability (RR = 6.08 (1.25-17.80)). In reverse analyses, there were elevated rates of a recorded hospital episode with CNS demyelinating disease after a previous recorded episode with anxiety, stress-related, and somatoform disorders; attention-deficit hyperactivity disorder (ADHD); autism; intellectual disability; and other behavioral disorders. CONCLUSION: This analysis of a national diagnostic database provides strong evidence for an association between pediatric CNS demyelinating diseases and psychiatric disorders, and highlights a need for early involvement of mental health professionals.
Asunto(s)
Enfermedades Autoinmunes Desmielinizantes SNC/complicaciones , Enfermedades Autoinmunes Desmielinizantes SNC/psicología , Trastornos Mentales/epidemiología , Adolescente , Niño , Preescolar , Estudios de Cohortes , Femenino , Humanos , Lactante , Recién Nacido , Masculino , Estudios RetrospectivosRESUMEN
OBJECTIVES: Multiple sclerosis is a degenerative disease of the CNS with a pathology consistent with immunological mediation. Although its cause is unknown, multiple factors are thought to influence both the onset and exacerbation of the disease, including both genetic background as well as environmental factors. METHODS: We are interested in the effect of psychological stress on the onset and exacerbation of Theiler's virus-induced demyelinating disease (TVID), a murine model of MS in which viral persistence facilitates demyelination. In the current study, we determined whether chronic restraint stress (RS)-induced immunosuppression could result in the establishment of a persistent CNS infection in the normally TVID-resistant C57BL/6 mouse strain, resulting in demyelination. RESULTS: Our data indicated that RS repeated over the course of 7 days was not sufficient to cause decreases in virus-specific adaptive immunity, and did not significantly alter CNS viral levels. Furthermore, chronic repeated RS lasting until 4 weeks after infection altered neither the development of virus-specific IgG nor motor function determined by Rotarod analysis. In addition, histological analysis of the CNS of stressed mice indicated no inflammation or demyelination on day 193 after infection. CONCLUSION: These results suggest that stress alone is not sufficient to overcome genetic resistance to TVID in the C57BL/6 mouse strain.
Asunto(s)
Infecciones por Cardiovirus/inmunología , Enfermedades Autoinmunes Desmielinizantes SNC/inmunología , Susceptibilidad a Enfermedades/inmunología , Tolerancia Inmunológica/inmunología , Estrés Psicológico/inmunología , Theilovirus/inmunología , Inmunidad Adaptativa/inmunología , Animales , Infecciones por Cardiovirus/psicología , Sistema Nervioso Central/inmunología , Sistema Nervioso Central/patología , Sistema Nervioso Central/virología , Enfermedades Autoinmunes Desmielinizantes SNC/fisiopatología , Enfermedades Autoinmunes Desmielinizantes SNC/psicología , Modelos Animales de Enfermedad , Susceptibilidad a Enfermedades/psicología , Femenino , Predisposición Genética a la Enfermedad/genética , Tolerancia Inmunológica/genética , Ratones , Ratones Endogámicos C57BL , Trastornos del Movimiento/inmunología , Trastornos del Movimiento/fisiopatología , Fibras Nerviosas Mielínicas/inmunología , Fibras Nerviosas Mielínicas/patología , Fibras Nerviosas Mielínicas/virología , Neuronas/inmunología , Neuronas/patología , Neuronas/virología , Restricción Física/efectos adversos , Restricción Física/psicología , Carga Viral/inmunologíaRESUMEN
Causes and pathogenesis of psychiatric disorders is poorly understood. Infections by viruses or other agents may disturb neurotransmitters and elicit behavioral abnormalities, and induce long lasting immune reactions, referred to as mild encephalitis (ME). New findings (pathology, biochemistry, imaging) in schizophrenia and bipolar psychoses are compatible with ME hypothesis. In Chorea Sydenham and PANDAS syndrome autoimmune ME seems to explain anxiety-compulsive-hyperactivity symptoms. Add-on-therapy with Cox-II-blockers or valacyclovir improved acute schizophrenia, CSF filtration some cases of therapy resistant psychoses.
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Aciclovir/análogos & derivados , Enfermedades Autoinmunes Desmielinizantes SNC/diagnóstico , Encefalitis Viral/diagnóstico , Trastornos Mentales/virología , Valina/análogos & derivados , Aciclovir/administración & dosificación , Antivirales/administración & dosificación , Encéfalo/efectos de los fármacos , Inhibidores de la Ciclooxigenasa/administración & dosificación , Enfermedades Autoinmunes Desmielinizantes SNC/tratamiento farmacológico , Enfermedades Autoinmunes Desmielinizantes SNC/psicología , Encefalitis Viral/tratamiento farmacológico , Encefalitis Viral/psicología , Humanos , Trastornos Mentales/diagnóstico , Trastornos Mentales/tratamiento farmacológico , Resultado del Tratamiento , Valaciclovir , Valina/administración & dosificaciónRESUMEN
Chronic restraint stress, administered during early infection with Theiler's virus, was found to exacerbate the acute central nervous system (CNS) viral infection and the subsequent demyelinating phase of disease (an animal model of Multiple Sclerosis (MS)) in SJL male and female mice. During early infection, stressed mice displayed decreased body weights and spontaneous activity; while increased behavioral signs of illness and plasma corticosterone (CORT) levels. During the subsequent chronic demyelinating phase of disease, previously stressed mice had greater behavioral signs of the chronic phase, worsened rotarod performance, and increased inflammatory lesions of the spinal cord. In addition, mice developed autoantibodies to myelin basic protein (MBP), proteolipid protein peptide (PLP139-151), and myelin oligodendrocyte glycoprotein peptide (MOG33-55).
Asunto(s)
Enfermedades Autoinmunes Desmielinizantes SNC/psicología , Susceptibilidad a Enfermedades/inmunología , Tolerancia Inmunológica/inmunología , Esclerosis Múltiple/psicología , Estrés Psicológico/inmunología , Theilovirus/inmunología , Animales , Autoanticuerpos/inmunología , Conducta Animal/fisiología , Peso Corporal/inmunología , Enfermedad Crónica , Corticosterona/sangre , Enfermedades Autoinmunes Desmielinizantes SNC/inmunología , Enfermedades Autoinmunes Desmielinizantes SNC/virología , Modelos Animales de Enfermedad , Ingestión de Alimentos/inmunología , Ingestión de Alimentos/psicología , Femenino , Masculino , Ratones , Actividad Motora/inmunología , Esclerosis Múltiple/inmunología , Esclerosis Múltiple/virología , Proteínas de la Mielina/inmunología , Mielitis/inmunología , Mielitis/psicología , Mielitis/virología , Restricción Física , Estrés Psicológico/complicaciones , Estrés Psicológico/fisiopatologíaRESUMEN
Infectious diseases can cause an array of symptoms, including psychiatric symptoms. Psychiatrists serving the medically ill need to be aware not only of classic infectious diseases (e.g., neurosyphilis and HIV), but also of less commonly discussed infectious diseases (e.g., NCC, PANDAS, and Lyme disease). These examples represent an internationally endemic disease (e.g., NCC), a probable immunogenetic disease (e.g., PANDAS), and a frequently overdiagnosed and overtreated disease (Lyme disease).
Asunto(s)
Enfermedades Autoinmunes Desmielinizantes SNC/psicología , Neuroborreliosis de Lyme/psicología , Trastornos Neurocognitivos/psicología , Neurocisticercosis/psicología , Infecciones Estreptocócicas/psicología , Adulto , Encéfalo/patología , Niño , Enfermedades Autoinmunes Desmielinizantes SNC/diagnóstico , Diagnóstico por Imagen , Humanos , Neuroborreliosis de Lyme/diagnóstico , Trastornos Neurocognitivos/diagnóstico , Neurocisticercosis/diagnóstico , Trastorno Obsesivo Compulsivo/diagnóstico , Trastorno Obsesivo Compulsivo/psicología , Infecciones Estreptocócicas/diagnósticoRESUMEN
Adenovirus-mediated gene transfer of interferon gamma (AdIFN) elicits rejection of intracerebral Lewis lung carcinoma. In this system, gene transfer into brain parenchymal cells is both necessary and sufficient to generate the antitumor response. Despite persistent parenchymal inflammation and demyelination, wild-type mice injected intracerebrally with either AdIFN or beta-galactosidase adenovirus (AdBGAL) perform as well as non-injected animals in behavioral, memory, and motor tests. Both AdIFN and AdBGAL elicit demyelination whose incidence rises sharply when the lowest effective dose of AdIFN is exceeded. Therefore, transfer of interferon gamma into brain parenchyma does not seem to elicit detectable cognitive, behavioral or motor deficits. Furthermore, gene transfer into the brain, by adenoviral vectors currently in clinical trials, is associated with a narrow therapeutic window where the incidence of demyelination rises sharply soon after the effective dose is achieved. Gene Therapy (2000) 7, 2094-2098.