RESUMEN
Neuropsychiatric symptoms are prevalent in neurologic practice, but their complexity makes them challenging to manage. Many cognitive, affective, behavioral, and perceptual symptoms span multiple neurologic diagnoses-and there is prominent variability in neuropsychiatric symptom burden for a given condition. There is also a relative lack of robust controlled clinical trial evidence and expert consensus recommendations for a range of neuropsychiatric symptom presentations. Thus, the categorical approach (e.g., a discrete diagnosis equals a specific set of medication interventions) used in many other medical conditions can sometimes have limited utility in commonly encountered neuropsychiatric clinical scenarios. In this review, we explore medication management for a range of neuropsychiatric symptoms using a dimensional transdiagnostic approach applied to the neurological patient. This approach allows the clinician to think beyond the boundaries of a discrete diagnosis and treat specific symptom domains (e.g., apathy, impulsivity). Pharmacologic considerations, including mechanisms of action and their application to various neurotransmitter systems and brain networks, are discussed, as well as general recommendations to optimize medication adherence and rapport with the patient. The dimensional, transdiagnostic approach to pharmacological management of patients with neurological conditions will help the clinician treat neuropsychiatric symptoms safely, effectively, and confidently.
Asunto(s)
Administración del Tratamiento Farmacológico , Trastornos Mentales , Humanos , Trastornos Mentales/diagnóstico , Trastornos Mentales/tratamiento farmacológicoRESUMEN
Functional neurological disorders (FND) are complex and prevalent neuropsychiatric conditions. Importantly, some patients with FND develop acute onset symptoms requiring emergency department (ED) evaluations. Historically, FND was a "rule-out" diagnosis, making assessment and management in the ED difficult. While the rapid triage of potential neurological emergencies remains the initial task, advancements have altered the approach to FND. FND is now a "rule-in" diagnosis based on validated neurological examination signs and semiological features. In this perspective article, we review signs and semiological features that can help guide the initial assessment of FND in the acute setting. Thereafter, we outline potential approaches to introduce a suspected diagnosis of FND to patients in the ED, while emphasizing the need for a comprehensive neurological evaluation. Physical and occupational therapy may be useful adjunct assessments in some individuals. Notably, clinicians in the ED setting are important members of the interdisciplinary approach to FND.
Asunto(s)
Trastornos de Conversión , Servicio de Urgencia en Hospital , Enfermedades del Sistema Nervioso/diagnóstico , Trastornos Psicofisiológicos , Trastornos de Conversión/diagnóstico , Trastornos de Conversión/psicología , Trastornos de Conversión/terapia , Humanos , Trastornos Psicofisiológicos/diagnóstico , Trastornos Psicofisiológicos/psicología , Trastornos Psicofisiológicos/terapiaRESUMEN
Our primary goal was to evaluate the behavioral and histological outcome of fluid percussion injury (FPI) and cortical contusion injury (CCI) to the sensorimotor cortex (SMC). The SMC has been used to evaluate neuroplasticity following CCI, but has not been extensively examined with FPI. In both the CCI and FPI models, a mechanical force of 4mm in diameter was applied over the SMC, allowing for a direct comparison to measure the relative rates of histology and recovery of function in these models. Gross behavioral deficits were found on the sensory task (tactile adhesive removal task) and multiple motor assessments (forelimb asymmetry task, forelimb placing task, and rotorod). These sensorimotor deficits occurred in the absence of cognitive deficits in the water maze. The CCI model creates focal damage with a localized injury wheras the FPI model creates a more diffuse injury causing widespread damage. Both behavioral and histological deficits ensued following both models of injury to the SMC. The neuroplastic changes and ease at which damage to this area can be measured behaviorally make this an excellent location to assess traumatic brain injury (TBI) treatments. No injury model can completely mimic the full spectrum of human TBI and any potential treatments should be validated across both focal and diffuse injury models. Both of these injury models to the SMC produce severe and enduring behavioral deficits, which are ideal for evaluating treatment options.