7 research outputs found

    Revisiting the term neuroprotection in chronic and degenerative diseases

    Get PDF
    Thanks to the development of several new researches, the lifetime presented a significant increase, even so, we still have many obstacles to overcome - among them, manage and get responses regarding neurodegenerative diseases. Where we are in the understanding of neuroprotection? Do we really have protective therapies for diseases considered degeneratives such as amyotrophic lateral sclerosis and its variants, Parkinson's disease, Alzheimer's disease and many others? Neuroprotection is defined by many researches as interactions and interventions that can slow down or even inhibit the progression of neuronal degeneration process. We make some considerations on this neuroprotective effect.Department of Neurology, Antonio Pedro University Hospital, Fluminense Federal University , NiteróiNeurology Service, Nova Iguaçu Hospital , PosseBrain Mapping Laboratory and Electroencephalogram, Federal University of Rio de JaneiroBrain Mapping and Functionality Laboratory, Federal University of PiauíSeverino Sombra University Center, School of Medicine , VassourasDepartment of Neurology, Federal University of São Paulo , BrazilDepartment of Neurology, Federal University of São Paulo , BrazilWeb of Scienc

    Fraqueza muscular adquirida na UTI (ICU-AW): efeitos sistêmicos da eletroestimulação neuromuscular

    Get PDF
    Com os avanços tecnológicos alcançados atualmente na terapia intensiva e maior sobrevida dos pacientes, outros desafios têm surgido para os profissionais de saúde. Dentre alguns, destaca-se a fraqueza muscular adquirida na UTI (ICU-AW), caracterizada por paresia esquelética e respiratória dos músculos promovendo aumento nastaxas de mortalidade e comprometimento da qualidade de vida. Sua incidência varia de 30% a 60% e tem na síndrome da resposta inflamatória sistêmica (SIRS) e na disfunção de múltiplos órgãos (DMO) sua principal etiologia. Outros fatores de risco como a hiperglicemia,o uso de bloqueadores neuromusculares e sedativos, a imobilidade e a própria ventilação mecânica estão entre os mais comuns. Entre as medidas de combate à ICU-AW, está o conceito de mobilização precoce, bem como despertar diário e controle estreito da glicemia. Nesse contexto, a eletroestimulação muscular apresenta-se como recurso de grande valia. Sua principal vantagem está no fato de poder ser empreendida independentemente da cooperação do paciente, epor ser capaz de gerar respostas musculares eficientes, bem como resultados satisfatórios na preservação da massa muscular, condicionamento físico e funcionalidade dos que usam essa ferramenta. Desfechos interessantes têm sido observados em diversos perfis de pacientes, como os de doença pulmonar obstrutiva crônica (DPOC)e traumatismo raquimedular (TRM). No paciente crítico, seu uso tem mostrado redução nos tempos de ventilação mecânica (VM), internação na UTI e maior funcionalidade dos pacientes. A relevância dos efeitos sistêmicos e metabólicos provenientes da eletroestimulação neuromuscular (ENM) tem sido a base para os estudos nos pacientes críticos. Portanto, a ICU-AW é uma realidade no cenário da terapia intensiva e sua prevenção tem dado margem à aparição de novas propostas e ferramentas na prevenção dessas complicações

    Amyotrophic Lateral Sclerosis: New Perpectives and Update

    No full text
    Amyotrophic lateral sclerosis (ALS), Charcot’s disease or Lou Gehrig’s disease, is a term used to cover the spetrum of syndromes caracterized by progressive degeneration of motor neurons, a paralytic disorder caused by motor neuron degeneration. Currently, there are approximately 25,000 patients with ALS in the USA, with an average age of onset of 55 years. The incidence and prevalence of ALS are 1-2 and 4-6 per 100,000 each year, respectively, with a lifetime ALS risk of 1/600 to 1/1000. It causes progressive and cumulative physical disabilities, and leads to eventual death due to respiratory muscle failure. ALS is diverse in its presentation, course, and progression. We do not yet fully understand the causes of the disease, nor the mechanisms for its progression; thus, we lack effective means for treating this disease. In this chapter, we will discuss the diagnosis, treatment, and how to cope with impaired function and end of life based on of our experience, guidelines, and clinical trials. Nowadays ALS seems to be a more complex disease than it did two decades – or even one decade – ago, but new insights have been plentiful. Clinical trials should be seen more as experiments on pathogenic mechanisms. A medication or combination of medications that targets more than one pathogenic pathway may slow disease progression in an additive or synergistic fashion

    Botulinum Neurotoxin Type A in Neurology: Update

    No full text
    This paper reviews the current and most neurological (central nervous system, CNS) uses of the botulinum neurotoxin type A. The effect of these toxins at neuromuscular junction lends themselves to neurological diseases of muscle overactivity, particularly abnormalities of muscle control. There are seven serotypes of the toxin, each with a specific activity at the molecular level. Currently, serotypes A (in two preparations) and B are available for clinical purpose, and they have proved to be safe and effective for the treatment of dystonia, spasticity, headache, and other CNS disorders in which muscle hyperactivity gives rise to symptoms. Although initially thought to inhibit acetylcholine release only at the neuromuscular junction, botulinum toxins are now recognized to inhibit acetylcholine release at autonomic cholinergic nerve terminals, as well as peripheral release of neuro-transmitters involved in pain regulation. Its effects are transient and nondestructive, and largely limited to the area in which it is administered. These effects are also graded according to the dose, allowing individualized treatment of patients and disorders. It may also prove to be useful in the control of autonomic dysfunction and sialorrhea. In over 20 years of use in humans, botulinum toxin has accumulated a considerable safety record, and in many cases represents relief for thousands of patients unaided by other therapy

    Neurological complications due to the use of illicit drugs: a mini review

    No full text
    In this paper, it is approached the neurological complications caused by the use of illicit drugs, such as LSD, Crack, Cocaine and Marijuana. These illicit drugs are used recreationally, but they are closely related to signals and symptoms many times unexplained. Many of these reactions involve the neurological system, causing common and known complications, which are present in the use of all the drugs discussed here, like visual illusions, paranoia, psychosis, hallucination, anxiety and euphoria, for instance. However, more uncommon and serious complications need special treatment for quickly actions or patient instructions, such as seizures, strokes, encephalopathies, cognitive deficits, worsening of verbal fluency and attention. In the specific case of the LSD use, the patient may present flashbacks even after the end of the drug effect.SimIn this paper, it is approached the neurological complications caused by the use of illicit drugs, such as LSD, Crack, Cocaine and Marijuana. These illicit drugs are used recreationally, but they are closely related to signals and symptoms many times unexplained. Many of these reactions involve the neurological system, causing common and known complications, which are present in the use of all the drugs discussed here, like visual illusions, paranoia, psychosis, hallucination, anxiety and euphoria, for instance. However, more uncommon and serious complications need special treatment for quickly actions or patient instructions, such as seizures, strokes, encephalopathies, cognitive deficits, worsening of verbal fluency and attention. In the specific case of the LSD use, the patient may present flashbacks even after the end of the drug effect

    Palm to finger ulnar sensory nerve conduction

    No full text
    Ulnar neuropathy at the wrist (UNW) is rare, and always challenging to localize. To increase the sensitivity and specificity of the diagnosis of UNW many authors advocate the stimulation of the ulnar nerve (UN) in the segment of the wrist and palm. The focus of this paper is to present a modified and simplified technique of sensory nerve conduction (SNC) of the UN in the wrist and palm segments and demonstrate the validity of this technique in the study of five cases of type III UNW. The SNC of UN was performed antidromically with fifth finger ring recording electrodes. The UN was stimulated 14 cm proximal to the active electrode (the standard way) and 7 cm proximal to the active electrode. The normal data from amplitude and conduction velocity (CV) ratios between the palm to finger and wrist to finger segments were obtained. Normal amplitude ratio was 1.4 to 0.76. Normal CV ratio was 0.8 to 1.23.We found evidences of abnormal SNAP amplitude ratio or substantial slowing of UN sensory fibers across the wrist in 5 of the 5 patients with electrophysiological-definite type III UNW
    corecore