RESUMEN
OBJECTIVES: The aim of this study was to determine the prevalence of Motoric Cognitive Risk (MCR) syndrome, describe associated risk factors and to determine the risk of progression to cognitive impairment after three years of follow-up, in a sample of Mexican older adults. DESIGN: A prospective panel study of health and aging in Mexico. SETTING AND PARTICIPANTS: Baseline and follow-up information was obtained from the Mexican Health and Aging Study's 2012 and 2015 waves. A total of 726 subjects aged 60 years or older with normal cognition at baseline were classified into 4 groups: 1) with MCR, 2) with memory complaint only, 3) with slow gait speed only and, 4) without MCR. Cox regression analysis controlling for confounder factors was performed to determine the risk of progression to cognitive impairment in the MCR group. MEASURES: Data such as gait speed, functional status and cognitive performance (standardized by age and sex in Mexican population) was collected. RESULTS: MCR prevalence was 14.3%. When compared with non-MCR subjects, the presence of MCR was associated with older age (p<0.01), lower educational status (p=0.05), having two or more comorbidities (p<0.05) and diabetes mellitus diagnosis (p<0.05). At follow-up and after adjusting for confounders, MCR was associated with a 2.4-fold increased risk (95% CI: 1.28-4.26, p=.000) of cognitive impairment. CONCLUSIONS: MCR syndrome increases the risk of cognitive impairment in Mexican older adults. Simple measurements such as gait evaluation in subjects with memory complaints could allow early identification of those at risk of developing cognitive impairment.
Asunto(s)
Disfunción Cognitiva/diagnóstico , Conductas Relacionadas con la Salud/fisiología , Pruebas Neuropsicológicas/normas , Anciano , Envejecimiento , Disfunción Cognitiva/complicaciones , Progresión de la Enfermedad , Femenino , Estudios de Seguimiento , Marcha , Historia del Siglo XXI , Humanos , Masculino , México , Persona de Mediana Edad , Prevalencia , Estudios Prospectivos , Factores de Riesgo , SíndromeRESUMEN
AIMS: To describe the pathophysiology, diagnosis and clinical manifestations of the neurological complications that critically ill patients often develop in intensive care units, and to discuss their treatment and prognosis, in the light of the most significant contemporary literature. DEVELOPMENT: The most frequent complication suffered by critically ill patients is sepsis, with encephalopathy as the main manifestation, and this has a direct effect on their prognosis. Polyneuropathy of the critically ill patient is linked to sepsis, as the main precipitating factor, as well as to the presence of high levels of glucose, which plays an important role in deciding whether mechanical ventilation can be withdrawn or not. Myopathy of the critically ill patient is related to the use of fluorinated steroids and neuromuscular blockers, which are frequently administered to these patients. All these entities represent a significant diagnostic challenge for the physician and are accompanied by important sequelae that continue after the patient's discharge from hospital, as well as myopathies and neuropathies associated to the use of drugs that are commonly administered to critically ill patients. It is therefore necessary to be familiar with the pathophysiology of the damage and with the associated factors, if a suitable diagnostic approach is to be employed. CONCLUSIONS: The incidence of these pathologies and their complications makes them important conditions that require a swift, accurate diagnosis so that treatment can be established early on and a prognosis can also be determined.
Asunto(s)
Enfermedad Crítica , Enfermedades Neuromusculares , Antagonistas Adrenérgicos/efectos adversos , Antagonistas Adrenérgicos/uso terapéutico , Aminoglicósidos/efectos adversos , Aminoglicósidos/uso terapéutico , Amiodarona/efectos adversos , Amiodarona/uso terapéutico , Anestésicos Intravenosos/efectos adversos , Anestésicos Intravenosos/uso terapéutico , Antiarrítmicos/efectos adversos , Antiarrítmicos/uso terapéutico , Antiinfecciosos/efectos adversos , Antiinfecciosos/uso terapéutico , Antiulcerosos/efectos adversos , Antiulcerosos/uso terapéutico , Anticonvulsivantes/efectos adversos , Anticonvulsivantes/uso terapéutico , Ciclosporina/efectos adversos , Ciclosporina/uso terapéutico , Diagnóstico Diferencial , Humanos , Inmunosupresores/efectos adversos , Inmunosupresores/uso terapéutico , Unidades de Cuidados Intensivos , Labetalol/efectos adversos , Labetalol/uso terapéutico , Metronidazol/efectos adversos , Metronidazol/uso terapéutico , Enfermedades Neuromusculares/tratamiento farmacológico , Enfermedades Neuromusculares/etiología , Enfermedades Neuromusculares/patología , Enfermedades Neuromusculares/fisiopatología , Omeprazol/efectos adversos , Omeprazol/uso terapéutico , Fenitoína/efectos adversos , Fenitoína/uso terapéutico , Polineuropatías/etiología , Polineuropatías/metabolismo , Pronóstico , Propofol/efectos adversos , Propofol/uso terapéutico , Sepsis/complicaciones , Sepsis/metabolismo , Tacrolimus/efectos adversos , Tacrolimus/uso terapéuticoRESUMEN
OBJECTIVES: The purpose of this study is to review the different studies published in the literature concerning the different physiological mechanisms involved in the genesis of painful neuropathy, as well as the diagnostic options and the different pharmacological treatments currently available. DEVELOPMENT: Distinct pathologies usually condition painful neuropathy, one of the main ones being diabetes mellitus. The triggering phenomenon is often some kind of damage to the tissues that contain nervous pain receptors, which later gives rise to a release of proinflammatory molecules, and triggers a cascade of phenomena that result in disorders in the central and peripheral nervous system (peripheral and central sensitisation). These disorders usually produce clinical manifestations, such as allodynia, paresthesias, among others, and these are sometimes the sole manifestation of painful neuropathy. Diagnosis of this syndrome is at times complicated due to the involvement of thin fibres, which cannot be identified by the conventional methods used in neurophysiological studies. There is also a broad range of pharmaceuticals used in the treatment of painful neuropathy that range from tricyclic antidepressants, non-steroidal anti-inflammatory drugs, opioid analgesics, antiarrhythmics and even agents for topical use. CONCLUSIONS: Diagnosis of thin fibre neuropathy is usually performed by carrying out a Quantitative Sudomotor Axon Reflex Test, quantitative sensory tests and a skin biopsy. As regards the pharmacological treatment, the new generation of anticonvulsive drugs like gabapentin seems to have advantages over the traditional pharmaceuticals, although their widespread use is still largely restricted by their cost.
Asunto(s)
Manejo del Dolor , Dolor/fisiopatología , Enfermedades del Sistema Nervioso Periférico/fisiopatología , Enfermedades del Sistema Nervioso Periférico/terapia , Humanos , Dolor/etiología , Enfermedades del Sistema Nervioso Periférico/complicacionesRESUMEN
INTRODUCTION: The frequency with which the central nervous system (CNS) is affected by systemic lupus erythematosus (SLE) varies, according to different series, between 13 and 59%, whereas the brain stem is affected in 5%. CASE REPORTS: Case 1: a 33 year old male who was submitted to a Nissen funduplicature as a treatment of (hypo)incoercible hiccups. The singultus persisted and some time after a paraplegia appeared. Magnetic resonance (MRI) showed images in the medulla oblongata, and in the cervical and thoracic spine. A biopsy was also performed to examine the cervical lesions and vasculitis was diagnosed. The patient began treatment with prednisone (1 mg/kg) and two months after symptoms had begun to improve he presented an episode of bilateral optic neuritis. Until this last event, the immunological studies had been positive. Case 2: female aged 19 who had had SLE for eight months. The illness began suddenly with bilateral paralysis of the sixth cranial nerve, vertical and horizontal nystagmus, dysdiadochokinesia, truncal ataxia, 4/5 muscular strength in the upper limbs and 3/5 in the lower limbs, and left flexor plantar response, but indifferent on the right hand side. MR showed T2 hyperintensities in the pons, medulla oblongata and the junction of medulla and upper spinal cord. Case 3: female aged 31 with sudden onset of the illness, characterised by diplopy and presence of internuclear ophthalmoplegia. Brain MR showed images of T1 hypointense and T2 hyperintense in the pontobulbar region. CONCLUSION: A brain stem disorder in patients suffering from SLE is one of the rarest manifestations of this pathological condition of the CNS and is probably caused by vasculitis