ABSTRACT
ABSTRACT Autoimmune encephalitis (AIE) is one of the most common causes of noninfectious encephalitis. It can be triggered by tumors, infections, or it may be cryptogenic. The neurological manifestations can be either acute or subacute and usually develop within six weeks. There are a variety of clinical manifestations including behavioral and psychiatric symptoms, autonomic disturbances, movement disorders, and seizures. We reviewed common forms of AIE and discuss their diagnostic approach and treatment.
RESUMO As encefalites autoimunes (EAI) são a principal causa de encefalite não-infecciosa. As manifestações neurológicas são variadas, incluindo alterações comportamentais ou psiquiátricas, disautonomia, transtornos do movimento e epilepsia. Habitualmente a instalação dos sintomas ocorre em até 6 semanas, de forma aguda ou subaguda. As EAI podem ser desencadeadas por tumores, quadros infecciosos virais ou ainda apresentar etiologia criptogênica. Este artigo revisa as principais EAI, estratégias de diagnóstico e tratamento.
Subject(s)
Humans , Male , Female , Encephalitis/diagnosis , Encephalitis/therapy , Hashimoto Disease/diagnosis , Hashimoto Disease/therapy , Diagnosis, Differential , Encephalitis/etiology , Encephalitis/physiopathology , Hashimoto Disease/etiology , Hashimoto Disease/physiopathology , Anti-N-Methyl-D-Aspartate Receptor Encephalitis/complications , ImmunotherapyABSTRACT
Resumen La encefalopatía de Hashimoto es una enfermedad rara. Se reporta una prevalencia de 2,1 por cada 100 000 habitantes. Entre las manifestaciones clínicas se describen confusión, disminución del estado de consciencia, déficit cognitivo, convulsiones, mioclonus, ataxia y/o déficits neurológicos focales. Debido a la amplia variedad de signos y síntomas, la sospecha clínica diagnóstica es fundamental. El diagnóstico se basa en tres pilares: la presencia de manifestaciones clínicas neurológicas, con la exclusión de otras causas de encefalopatía; presencia de anticuerpos antitiroideos aumentados; una mejoría clínica notable luego de la administración de inmunomoduladores. El tratamiento de la encefalopatía de Hashimoto tiene dos objetivos: controlar el proceso autoinmune y controlar las complicaciones de la enfermedad. Aunque en la mayoría de los casos la recuperación es completa con el tratamiento, el riesgo de recaídas puede oscilar entre 12,5 a 40% en seguimientos a dos años.
Abstract Hashimoto's encephalopathy is a rare disease, with a reported prevalence of 2.1 per 100 000. Clinical manifestations include confusion, decreased state of consciousness, cognitive deficit, seizures, myoclonus, ataxia, and focal neurological deficits. Due to the wide variety of signs and symptoms, clinical diagnostic suspicion is essential. Diagnosis is based on three pillars: the presence of neurological clinical manifestations after ruling out other causes of encephalopathy. 2) Presence of increased antithyroid antibodies. 3) Significant clinical improvement after the administration of immunomodulation. The treatment of Hashimoto's encephalopathy pursues two objectives: to control the autoimmune process and to control the complications of the disease. Although in most cases recovery is complete with treatment, the risk of relapse can range from 12.5 to 40% in follow-ups to 2 years.
Subject(s)
Humans , Autoantibodies/immunology , Encephalitis/therapy , Hashimoto Disease/therapy , Immunologic Factors/therapeutic use , Recurrence , Treatment Outcome , Encephalitis/diagnosis , Encephalitis/physiopathology , Hashimoto Disease/diagnosis , Hashimoto Disease/physiopathologyABSTRACT
Parkinson’s disease (PD) is the second most common neurodegenerative disease affecting approximately 1.6% of the population over 60 years old. The cardinal motor symptoms are the result of progressive degeneration of substantia nigra pars compacta dopaminergic neurons which are involved in the fine motor control. Currently, there is no cure for this pathology and the cause of the neurodegeneration remains unknown. Several studies suggest the involvement of neuroinflammation in the pathophysiology of PD as well as a protective effect of anti-inflammatory drugs both in animal models and epidemiological studies, although there are controversial reports. In this review, we address evidences of involvement of inflammatory process and possible therapeutic usefulness of anti-inflammatory drugs in PD.
A doença de Parkinson (DP) é a segunda doença neurodegenerativa mais comum afetando aproximadamente 1,6% da população acima de 60 anos de idade. Os sinais motores cardinais são o resultado da degeneração progressiva de neurônios dopaminérgicos da substantia nigra pars compacta (SNpc), a qual está intimamente envolvida com o controle motor. Atualmente, não há cura para esta patologia e a causa da neurodegeneração permanece desconhecida. Contudo, muitos estudos sugerem o envolvimento da neuroinflamação na patofisiologia da DP bem como um efeito protetor de drogas antiinflamatórias tanto em modelos animais quanto em estudos epidemiológicos, embora haja relatos controversos. Nesta revisão, foram abordadas evidências de envolvimento do processo inflamatório e uma possível utilidade terapêutica de drogas antiinflamatórias na DP.
Subject(s)
Animals , Humans , Anti-Inflammatory Agents, Non-Steroidal/therapeutic use , Encephalitis/drug therapy , Encephalitis/physiopathology , Parkinson Disease/drug therapy , Parkinson Disease/physiopathology , Anti-Inflammatory Agents, Non-Steroidal/pharmacology , Cytokines , Nerve Degeneration/drug therapy , Nerve Degeneration/physiopathology , Parkinson Disease/etiology , Pars Compacta/physiopathology , Reproducibility of Results , Risk Factors , Treatment OutcomeABSTRACT
Sepsis and the multiorgan dysfunction syndrome are among the most common reasons for admission to an intensive care unit, and are a leading cause of death. During sepsis, the central nervous system (CNS) is one of the first organs affected, and this is clinically manifested as sepsis-associated encephalopathy (SAE). It is postulated that the common final pathway that leads to SAE symptoms is the deregulation of neurotransmitters, mainly acetylcholine. Thus, it is supposed that inflammation can affect neurotransmitters, which is associated with SAE development. In this review, we will cover the current evidence (or lack thereof) for the mechanisms by which systemic inflammation interferes with the metabolism of major CNS neurotransmitters, trying to explain how systemic inflammation drives the brain crazy.
Subject(s)
Humans , Brain/physiopathology , Encephalitis/physiopathology , Sepsis-Associated Encephalopathy/physiopathology , Sepsis/physiopathology , Amines/metabolism , Brain/metabolism , Central Nervous System/metabolism , Central Nervous System/physiopathology , Cytokines/metabolism , Encephalitis/metabolism , Sepsis-Associated Encephalopathy/metabolism , Sepsis/metabolism , gamma-Aminobutyric Acid/metabolismSubject(s)
Humans , Amebiasis/physiopathology , Skin Diseases, Parasitic/etiology , Encephalitis/physiopathology , Granuloma/physiopathology , Lobosea/pathogenicity , Amebiasis/diagnosis , Amebiasis/cerebrospinal fluid , Amoeba/pathogenicity , Latin America , Nose/pathology , Polymerase Chain ReactionABSTRACT
El seguimiento del embarazo, la atención del parto y la reanimación del recién nacido, exigen la detección oportuna y el tratamiento adecuado del sufrimiento cerebral debido a la asfixia. Una vez que la lesión cerebral se establece, todos los esfuerzos estarán encaminados a disminuir sus consecuencias. La coordinación entre el obstetra y el pediatra, fundada en la confianza mutua, el profesionalismo y la experiencia de ambos favorece la toma de decisiones pertinentes, para otorgar al niño la posibilidad de preservar, en lo posible su evolución motora e intelectual
Subject(s)
Asphyxia Neonatorum/diagnosis , Hypoxia, Brain/pathology , Hypoxia, Brain/therapy , Encephalitis/physiopathologyABSTRACT
Se hace una revisión de diferentes tratamientos experimentales en cultivo de células y en ratones con rabdovirus rábico fijo que no ha tenido aplicación práctica. Se plantean tratamientos opcionales no utilizados previamente para la encefalitis rábica humana, basados en hipótesis congruentes. Se señala el empleo del agente quimioterápico 5 fluorouracilo (5-FU). Se sugiere la anestesia por éter, dado que este compuesto a baja concentración inhibe el crecimiento viral. Otra opción sería la radioterapia como la empleada para tumores cerebrales. También se ha sugerido la craniectomía descomprensiva bilateral complementaria y el empleo de inhibidores no-nucleósidos de transcriptasas virales.