Perfil de dispensação da toxina botulínica para tratamento da espasticidade: dados nacionais brasileiros / Dispensing profile of botulinum toxin for treating spasticity: Brazilian national data

Os fisiatras especializados no tratamento de espasticidade foram reunidos para um painel de discussão a respeito do uso de toxina botulínica (TB) na rede pública de diferentes estados do Brasil. Os dados analisados durante a discussão do Datasus demonstram um baixo perfil de demanda desse produto dispensado pelo Sistema Único de Saúde (SUS), com uma heterogeneidade na distribuição da TB nos estados brasileiros. Esse quadro parece se configurar principalmente por falta de uma política pública devidamente planejada, como a falta de unificação e normatização dos centros de distribuição, pela falta ou inadequação da remuneração do procedimento de aplicação da TB aos centros de tratamento, de modo padronizado pela tabela SUS e escassez de médicos capacitados para realizá-lo junto à falta de centros de reabilitação multidisciplinar habilitados. O uso de toxina botulínica com finalidade terapêutica no Brasil teve início nos anos 90, para tratamento de distonia e de espasticidade. Atualmente, é empregada em diferentes condições clínicas, porém, apesar da crescente demanda e indicações ao longo dos anos, há poucos relatos ou publicações sobre seu uso e benefício para pacientes atendidos pela Sistema Único de Saúde (SUS). Para abordar esse tema, em maio de 2015, na cidade de São Paulo, fisiatras de diferentes estados do Brasil se encontraram e discutiram a relevância da toxina botulínica no tratamento de espasticidade

The physiatrists specialized in treating spasticity were brought together for a panel discussion about the use of botulinum toxin (BT) in the public system in different states of Brazil. The data analyzed during the discussion of Datasus demonstrate a low-demand profile of the product dispensed by the Unified Health System (SUS), with heterogeneity in the distribution of TB in the Brazilian states. This scenario seems to be set up mainly for lack of a properly planned public policy, such as lack of unification and standardization of distribution centers, the lack or inadequacy of TB compensation proceeding to treatment centers, in a standardized manner by SUS and shortage of trained doctors to do it together with the lack of qualified multidisciplinary rehabilitation centers. The use of botulinum toxin for therapeutic purposes in Brazil began in the 90s, to treat dystonia and spasticity. It is currently employed in different clinical conditions; however, despite growing demand and indications over the years, there are few reports or publications on its use and benefit to patients served by the Unified Health System (SUS). To address this issue, in May 2015, in São Paulo, physiatrists from different states of Brazil met and discussed the relevance of botulinum toxin in treating spasticity

Physical rehabilitation to treat neuropathic pain / Reabilitação física no tratamento de dor neuropática

ABSTRACT BACKGROUND AND OBJECTIVES: Neuropathic pain is disabling, decreases quality of life, impairs professional performance, and limits social participation of patients living with excruciating pain. In this context, it is easy to see physical rehabilitation as facilitator of autonomy and mobility. However, therapeutic action goes beyond these actions. With technological advances, new approaches are proposed and it now it is possible to measure the performance of physical methods for pain modulation. CONTENTS: The innovative potential of physical rehabilitation to treat neuropathic pain is discussed. Reflections are made on therapeutic options such as: electrothermotherapy, manual therapy, physical exercise, transcranial stimulation with constant current, repetitive transcranial magnetic stimulation, visual mental exercises and mirror therapy, among others. Therapeutic modalities shall be addressed according to some neuropathic pain conditions, so the authors propose a parallel between specific pathologic mechanism of some neuropathic pain conditions and the neurophysiologic mechanism of the proposed therapeutic modality. CONCLUSION: In spite of different pathological mechanisms and different ways of physical and mental approach with patients, the importance of active participation of patients during the rehabilitation process has to be stressed.

RESUMO JUSTIFICATIVA E OBJETIVOS: Dores neuropáticas são incapacitantes, reduzem a qualidade de vida, prejudicam a atuação profissional, limitam a participação social dos pacientes que convivem com dores lancinantes. Neste contexto visualiza-se rapidamente a reabilitação física como facilitador de autonomia e mobilidade. Contudo, a ação terapêutica estende-se além destas. Com avanços tecnológicos, novas abordagens são propostas e tornou-se possível mensurar a atuação de métodos físicos na modulação da dor. CONTEÚDO: Discute-se o potencial inovador da reabilitação física no tratamento das dores neuropáticas. Reflexões sobre opções terapêuticas como, por exemplo: eletrotermoterapia, terapia manual, exercício físico, estimulação transcraniana com corrente constante, estimulação magnética transcraniana repetitiva, exercícios mentais visuais, terapia do espelho entre outros. As modalidades terapêuticas serão abordadas de acordo com algumas condições de dor neuropática, desta forma os autores propõem um paralelo entre o mecanismo patológico específico de algumas condições de dor neuropática e o mecanismo neurofisiológico da modalidade terapêutica proposta. CONCLUSÃO: Embora mecanismos patológicos diferentes e várias vias de abordagem física e mental com os pacientes, destaca-se a importância da participação ativa do paciente durante o processo de reabilitação.

Atorvastatin prevents hippocampal cell death due to quinolinic acid-induced seizures in mice by increasing Akt phosphorylation and glutamate uptake.

Statins are cholesterol-lowering agents due to the inhibition of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase. Recent studies have shown statins possess pleiotropic effects, which appear to be independent from its cholesterol-lowering action. In this study, we investigated whether atorvastatin would have protective effects against hippocampal cell death promoted by quinolinic acid (QA)-induced seizures in mice. Mice were pretreated with Atorvastatin (1 or 10 mg/kg) or vehicle (saline, 0.9%), orally, once a day for 7 days before the intracerebroventricular (i.c.v.) QA infusion (36.8 nmol/site). Atorvastatin treatment with 1 mg/kg/day did not significantly prevent QA-induced seizures (13.34%). However, administration of atorvastatin 10 mg/kg/day prevented the clonic and/or tonic seizures induced by QA in 29.41% of the mice. Additionally, administration of atorvastatin 10 mg/kg/day significantly prevented QA-induced cell death in the hippocampus. Atorvastatin treatment promoted an increased Akt phosphorylation, which was sustained after QA infusion in both convulsed and non-convulsed mice. Moreover, atorvastatin pretreatment prevented the reduction in glutamate uptake into hippocampal slices induced by QA i.c.v. infusion. These results show that atorvastatin attenuated QA-induced hippocampal cellular death involving the Akt pathway and glutamate transport modulation. Therefore, atorvastatin treatment might be a useful strategy in the prevention of brain injury caused by the exacerbation of glutamatergic toxicity in neurological diseases such as epilepsy.

Involvement of cellular prion protein in the nociceptive response in mice.

The role of the cellular prion protein (PrP(c)) in neuronal functioning includes neuronal excitability, cellular adhesion, neurite outgrowth and maintenance. Here we investigated the putative involvement of the PrP(c) function on the nociceptive response using PrP(c) null (Prnp(0/0)) and wild-type (Prnp(+/+)) mice submitted to thermal and chemical models of nociception. PrP(c) null mice were more resistant than wild-type mice to thermal nociception of the tail-flick test. However, no significant difference was found on the hot plate test. In the acetic acid-induced visceral nociception, PrP(c) null mice showed an enhanced response when compared to wild-type mice. However, there was no difference between Prnp(0/0) and wild-type mice on glutamate- and formalin-induced licking behaviour and Freund's Complete Adjuvant (FCA)-induced mechanical allodynia. PrP(c) null mice developed significantly lower paw edema than wild-type mice. In addition, the visceral conditioning stimuli produced by a previous injection of acetic acid (20 days before testing) significantly reduced early and late phases of formalin-induced nociception in wild-type mice. In contrast, the same pre-treatment did not alter the formalin response in PrP(c) null mice. These results indicate a role of PrP(c) in the nociceptive transmission, including the thermal tail-flick test and visceral inflammatory nociception (acetic acid-induced abdominal constriction). Our findings show that PrP(c) is involved with a response mediated by inflammation (paw edema) and by visceral conditioning stimuli.

Normal brain mitochondrial respiration in adult mice lacking cellular prion protein.

Cellular prion protein (PrP(c)) gene (Prnp) null mice (Prnp0/0) show higher sensitivity to seizures, enhanced brain oxidative stress, and their neurons exhibit higher excitability "in vitro". Mitochondrial respiration is a useful parameter for the determination of cellular metabolic rate and it is a major source of reactive oxygen species (ROS). In the present study, we investigated the mitochondrial function of different brain areas of Prnp0/0 adult mice and then compared this to normal control animals. Baseline mitochondrial respiration (stages 3 and 4), respiratory control ratio (RCR) and membrane potential were evaluated in the neocortex, entorhinal cortex, hippocampus, and cerebellum. No differences in these parameters were detected between Prnp0/0 and wild-type mice. Thus, we concluded that baseline mitochondrial respiration might not be directly related with the higher oxidative stress previously observed in brains from Prnp0/0 mice.

Resultados do atendimento concentrado da espasticidade com toxina botulítica tipo A em pacientes hemiplégicos / Outcome of spasticity concetrated attendance program with botulinum toxin type A in patients with hemiplegia

Neste artigo apresentamos os resultados do tratamento de vinte e cinco pacientes com hemiplegia espástica com toxina botulítica tipo A e fenol aquoso 6 por cento.Os procedimentos de neurólise química foram realizados entre os dias 28 e 30 de agosto de 2002. Os pacientes apresentavam idades entre 41 e 73 anos (56 mais ou menos 8,65) sendo 13 homens e 12 mulheres.Os pacientes foram acompanhados durante três meses apresentando melhora clínica e funcional após o tratamento de reabilitaçäo