ABSTRACT
Immunoparalysis and apoptosis of T cells are serious problems for the evolution of septic patients. We aimed to relate changes in the number of αß and γδ T cells during hospital stay to the poor evolution of sepsis. In this prospective study, we recruited a total of 92 septic patients from the Emergency and Intensive Care Departments of two Hospitals, according to the latest criteria for the definition and management of sepsis. According to the severity of the septic process, there was a progressive decrease in T cells, being much more intense in γδ T cells. This decrease recovered in surviving patients, but CD3+CD56+ γδ T cells continued to decreased during hospital stay in non-surviving patients. Apoptosis increased in sepsis. Cell death of CD3+CD56+ γδ T cells progressively increased according to the severity of sepsis, especially in non-surviving patients.
Subject(s)
Sepsis , Shock, Septic , Apoptosis , CD3 Complex/immunology , CD56 Antigen/immunology , Hospitals , Humans , Lymphocyte Count , Prospective Studies , Receptors, Antigen, T-Cell, gamma-delta/metabolismABSTRACT
INTRODUCTION: Anosognosia is a frequent symptom in Alzheimer disease (AD). The objective of this article is to describe prevalence of this condition at time of diagnosis and analyse any predisposing factors and their influence on disease progression. METHODS: Observational, prospective, and analytical multi-centre study in an outpatient setting. Patients recently diagnosed with AD (NINCDS-ADRDA criteria) were included. Each patient underwent two cognitive, functional, and neuropsychiatric assessments separated by an interval of 18 months. The Clinical Insight Rating Scale was employed as a measure of anosognosia (CIR, scored 0-8). Progression was defined as an increase in the Clinical Dementia Rating Scale-sum of boxes of more than 2.5 points. The predictor variables were analysed using binary logistic regression. RESULTS: The study included 127 patients, and 94 completed both assessments. Of the total, 31.5% displayed severe anosognosia (CIR 7-8); 39.4%, altered level of consciousness (CIR 3-6); and 29.1%, normal awareness (CIR 0-2). The median baseline CIR in this cohort was 4 (Q1-Q3: 1-7), and at 18 months, 6 (Q1-Q3: 3-8), P<.001. Advanced age (odds ratio (OR) 2.43; CI 95%:1.14-5.19), lower educational level (OR 2.15; CI 95%:1.01-4.58), and more marked neuropsychiatric symptoms (OR 2.66; CI 95%:1.23-5.74) were predictor variables of anosognosia. Baseline CIR was similar in the groups with and without significant clinical progression. CONCLUSIONS: The large majority of patients with AD at the time of diagnosis showed significant anosognosia, and this condition was associated with advanced age, lower educational level, and more marked behavioural symptoms. Our results did not show that anosognosia had an effect on the initial clinical progression of AD after diagnosis.
Subject(s)
Agnosia/epidemiology , Alzheimer Disease/diagnosis , Disease Progression , Aged , Aged, 80 and over , Agnosia/diagnosis , Agnosia/etiology , Female , Humans , Male , Middle Aged , Neuropsychological Tests , Prevalence , Prospective Studies , Psychiatric Status Rating Scales , Surveys and QuestionnairesABSTRACT
A multicystic intraventricular tumour of the right ventricular atrium was incidentally diagnosed on follow-up imaging of a 61-year-old man with a history of prostatic adenocarcinoma. Surgical resection of the lesion was performed after a one-year radio-clinical follow-up due to progressive expansion of the lesion size and a rising prostate specific antigen blood-level. Morphological features with papillary pattern on pathological examination were compatible with malignant adenocarcinoma or choroid plexus carcinoma. The immunoprofile was conclusive for an exceptional choroid plexus metastasis (CPM) of a prostatic adenocarcinoma. To our knowledge, this is the first report of a proven prostatic origin of a CPM.
Subject(s)
Adenocarcinoma , Carcinoma , Choroid Plexus Neoplasms , Prostatic Neoplasms , Adenocarcinoma/pathology , Choroid Plexus , Choroid Plexus Neoplasms/diagnosis , Choroid Plexus Neoplasms/secondary , Choroid Plexus Neoplasms/surgery , Humans , Magnetic Resonance Imaging , Male , Middle Aged , Prostatic Neoplasms/pathologyABSTRACT
INTRODUCTION: Nutritional deficiencies are frequent in Alzheimer disease (AD), even in early stages. Nutritional impairment (NI) may be associated with faster disease progression. The objective of this study was to describe the frequency of NI and the associated risk factors at the time of diagnosis and to analyse its influence on subsequent progression. METHODS: We performed a prospective, multicentre, observational study of patients recently diagnosed with prodromal AD (pAD) or dementia due to AD (ADd). Two clinical assessments were conducted over a period of 18 months. The Mini Nutritional Assessment test (MNA; score range, 0-30; cut-off point for NI, < 24) was used to estimate nutritional status. Progression was defined as an increase of ≥ 3 points on the Clinical Dementia Rating-sum of boxes test. RESULTS: The sample included 50 patients with pAD (mean [standard deviation] age, 76.1 [5.3] years; 68% women), and 127 with ADd (80 [5.9] years; 72.4% women). A total of 141 (79.7%) completed both evaluations. The prevalence of NI was 28.2% (24% for pAD, 29.9% for ADd; P = .43), with the majority (92%) at risk of malnutrition. NI was associated with female sex (odds ratio [OR]: 4.2; 95% confidence interval [CI]: 1.7-10.5; P < .001) and greater behavioural involvement (OR: 5.8; 95% CI: 2.6-12.7; P < .001). A larger proportion of patients with progression was observed among those with NI than among those with normal nutritional status (50% vs 28.7%, P < .05; ADd: 53.6% vs 31.8%, P < .05; pAD: 41.7% vs 22.9%, P = .21). Greater cognitive impairment (OR: 2.1; 95% CI: 1.03-4.4; P < .05) and NI (OR: 2.4; 95% CI: 1.1-5.1; P < .05) were independent risk factors for disease progression. CONCLUSIONS: NI is highly prevalent in patients with AD. Assessing nutritional status at the time of diagnosis may enable identification of patients at greater risk of disease progression.
Subject(s)
Alzheimer Disease , Malnutrition , Female , Humans , Aged , Male , Nutrition Assessment , Alzheimer Disease/epidemiology , Alzheimer Disease/diagnosis , Nutritional Status , Prospective Studies , Malnutrition/epidemiology , Malnutrition/complications , Disease ProgressionABSTRACT
INTRODUCTION: Nutritional deficiencies are frequent in Alzheimer disease (AD), even in early stages. Nutritional impairment (NI) may be associated with faster disease progression. The objective of this study was to describe the frequency of NI and the associated risk factors at the time of diagnosis and to analyse its influence on subsequent progression. METHODS: We performed a prospective, multicentre, observational study of patients recently diagnosed with prodromal AD (pAD) or dementia due to AD (ADd). Two clinical assessments were conducted over a period of 18months. The Mini Nutritional Assessment test (MNA; score range, 0-30; cut-off point for NI, <24) was used to estimate nutritional status. Progression was defined as an increase of ≥3points on the Clinical Dementia Rating-sum of boxes test. RESULTS: The sample included 50 patients with pAD (mean [standard deviation] age, 76.1 [5.3] years; 68% women), and 127 with ADd (80 [5.9] years; 72.4% women). A total of 141 (79.7%) completed both evaluations. The prevalence of NI was 28.2% (24% for pAD, 29.9% for ADd; P=.43), with the majority (92%) at risk of malnutrition. NI was associated with female sex (odds ratio [OR]: 4.2; 95% confidence interval [CI]: 1.7-10.5; P<.001) and greater behavioural involvement (OR: 5.8; 95%CI: 2.6-12.7; P<.001). A larger proportion of patients with progression was observed among those with NI than among those with normal nutritional status (50% vs 28.7%, P<.05; ADd: 53.6% vs 31.8%, P<.05; pAD: 41.7% vs 22.9%, P=.21). Greater cognitive impairment (OR: 2.1; 95%CI: 1.03-4.4; P<.05) and NI (OR: 2.4; 95%CI: 1.1-5.1; P<.05) were independent risk factors for disease progression. CONCLUSIONS: NI is highly prevalent in patients with AD. Assessing nutritional status at the time of diagnosis may enable identification of patients at greater risk of disease progression.
ABSTRACT
INTRODUCTION: Metronidazole is a widely known and used antibiotic. In exceptional cases, an encephalopathy with characteristic lesions on magnetic resonance imaging (MRI), usually located in the cerebellum and splenium of the corpus callosum, may be an adverse effect. The incidence and pathogenesis are unknown. The suspension of the treatment usually resolves the symptoms and normalizes the MRI in a few weeks. Due to the usual good prognosis, the anatomopathological findings are exceptional. We present a clinical case with the radiological findings suggestive of metronidazole-induced encephalopathy and, exceptionally, we provide the anatomopathological findings. CASE REPORT: A 72 years-old woman with severe Crohn's disease who, months after starting treatment with metronidazole, presented a slowly progressing bradypsychia and difficulty walking until she came to coma. In MRI it showed hyperintense images in T2 in the corpus callosum, red and dentate nuclei. He improved by stopping metronidazole but later developed sepsis and died. At autopsy, softening of the red nucleus was observed and, microscopically, cell necrosis and demyelination. CONCLUSION: With the publication of the clinical, radiological and anatomopathological information of our case we intend to promote the knowledge of this infrequent treatable cause of subacute encephalopathy and provide data that help to clarify its pathogenesis.
TITLE: Encefalopatia inducida por metronidazol: descripcion de un caso con hallazgos radiologicos y anatomopatologicos.Introduccion. El metronidazol es un antibiotico ampliamente conocido y utilizado. En casos excepcionales puede producir como efecto adverso un cuadro de encefalopatia con unas lesiones caracteristicas en la resonancia magnetica, localizadas generalmente en el cerebelo y el esplenio del cuerpo calloso. La incidencia y la patogenia se desconocen. La suspension del tratamiento habitualmente resuelve los sintomas y normaliza la resonancia magnetica en pocas semanas. Debido al habitual buen pronostico, los hallazgos anatomopatologicos son excepcionales. Se presenta un caso clinico con los hallazgos radiologicos sugestivos de la encefalopatia inducida por metronidazol y, de forma excepcional, se aportan los hallazgos anatomopatologicos. Caso clinico. Mujer de 72 años, con enfermedad de Crohn grave, que meses mas tarde de iniciar tratamiento con metronidazol presento de forma lentamente progresiva bradipsiquia y dificultad para caminar hasta llegar al coma. En la resonancia magnetica mostraba caracteristicas imagenes hiperintensas en T2 en el cuerpo calloso, y los nucleos rojos y dentados. Mejoro al suspender el metronidazol, pero posteriormente desarrollo una sepsis y fallecio. En la autopsia se observo reblandecimiento del nucleo rojo y, microscopicamente, necrosis celular y desmielinizacion. Conclusion. Con la publicacion de la informacion clinica, radiologica y anatomopatologica de este caso se pretende fomentar el conocimiento de esta infrecuente causa tratable de encefalopatia subaguda y aportar datos que ayuden a aclarar su patogenia.
Subject(s)
Anti-Bacterial Agents/adverse effects , Brain Diseases/chemically induced , Brain Diseases/diagnosis , Metronidazole/adverse effects , Aged , Brain Diseases/diagnostic imaging , Brain Diseases/pathology , Female , Humans , Magnetic Resonance ImagingABSTRACT
We report on a young woman with a left temporal diffuse low-grade glioma treated initially by a subtotal resection. A focal anaplastic area appeared 5years later and was treated by radiosurgery. A long-time stabilization was therefore obtained and lasted even after pregnancy, which is a known factor of faster tumour progression. This report shows that radiosurgery could be an option in the multimodal treatment of a selected group of patients with focal malignant transformation of diffuse low-grade glioma. It could permit long-term stabilization of the tumour without any other adjuvant treatment and without compromising the quality of life.
Subject(s)
Brain Neoplasms/surgery , Carcinoma/surgery , Oligodendroglioma/surgery , Radiosurgery/methods , Adolescent , Anticonvulsants , Female , Humans , Magnetic Resonance Imaging , Pregnancy , Seizures/drug therapy , Seizures/etiology , Survivors , Treatment OutcomeABSTRACT
We report a family with branchial myoclonus, spastic paraparesis, and cerebellar ataxia in which six members were affected in two generations and the inheritance appeared to be autosomal dominant. Age at onset ranged from 40 to 50 years. Rhythmic myoclonus involving the palate, pharynx, larynx, and face was followed by truncal ataxia and spastic paraparesis in most patients. CT and MRI revealed mild atrophy of the cerebral and cerebellar cortex and severe atrophy of the medulla and spinal cord. The pons appeared normal and the olives not hypertrophic. CSF studies revealed severe reduction of the serotonin metabolite 5-hydroxyindoleacetic acid. Treatment with 5-hydroxytryptophan and carbidopa at highest tolerated dose mildly improved ataxia but did not modify the myoclonus. Treatment with anticholinergics, benzodiazepines, phenytoin, valproate, carbamazepine, and baclofen was unsuccessful. The clinical symptoms were progressive, leading to death or severe disability 5 to 10 years after the onset of the disease.
Subject(s)
Cerebellar Ataxia/genetics , Muscle Spasticity/genetics , Myoclonus/genetics , Paraplegia/genetics , Adult , Cerebellar Ataxia/complications , Cerebellar Ataxia/diagnosis , Female , Humans , Male , Middle Aged , Muscle Spasticity/complications , Muscle Spasticity/diagnosis , Myoclonus/complications , Myoclonus/diagnosis , Paraplegia/complications , Paraplegia/diagnosisABSTRACT
AIMS: To describe the neurological complications of cardiac catheterization, together with its risk factors and pathogenic mechanisms. METHOD: Over the past few years there has been a marked increase in the number of interventions involving cardiac catheterizations. For this very reason, we can expect a proportional rise in the number of complications. The incidence of neurological pathologies secondary to heart interventions oscillates between 0.01 and 0.4% of procedures performed. The most frequent clinical pictures are cerebrovascular disease, neuro ophthalmological syndromes and peripheral neuropathies, due to damage done to the median, femoral and lateral femoral cutaneous nerves, and to the lumbar plexus. The most usual mechanisms are cerebral ischemia originated by embolisms and direct compression of the peripheral nerves. Factors increasing the likelihood of complications are old age, the presence of classic vascular risk factors and, probably, the patient s being female. More risk is involved in mitral and aortic valvuloplasties and non elective revascularization procedures. The personal experience of the operator and the overall activity of the department of haemodynamics where the physician works are factors that are very closely linked to the incidence of complications. CONCLUSIONS: Knowledge about neurological illness secondary to cardiac catheterization and its mechanisms of production may allow us to identify higher risk patients, to develop protocols to prevent it and to apply early therapeutic measures.
Subject(s)
Cardiac Catheterization/adverse effects , Nervous System Diseases/etiology , Humans , Nervous System Diseases/diagnosis , Risk FactorsABSTRACT
INTRODUCTION: Ophthalmoparesias is a frequent complication of ophthalmic herpes zoster. It occurs in 31% of all cases. However, the presence of Horner's syndrome during viral reactivation is a rarity which has only been previously described on two occasions, and never associated with cranial nerve involvement. CLINICAL CASE: We describe a patient with the first case of Horner's syndrome secondary to ophthalmic herpes zoster, with simultaneous, homolateral lesions of the third and sixth cranial nerves. Clinical evaluation, the course of the disorder, negative magnetic resonance studies and tests with cocaine and foledrin eye drops confirmed the presence of a post-ganglionar sympathetic lesion, probably situated in the ipsilateral cavernous sinus. CONCLUSIONS: Ophthalmoparesias as a complication of ophthalmic herpes zoster may have various origins. Diffusion of viral particles from the Gasserian ganglion and branches of the trigeminal nerve to adjacent structures, muscles, nerves and vessels, is the mechanism often mentioned. Presence of a simultaneous sympathetic lesion is very rare and of unknown pathology. However, it is probable that the origin of the lesion of the vegetative fibres is the same as that of the sensory or motor fibres, and adjacent inflammatory process caused by the virus extending. We analyze the factors involved in the low incidence of this association.
Subject(s)
Herpes Zoster Ophthalmicus/complications , Horner Syndrome/virology , Abducens Nerve/pathology , Cocaine , Herpes Zoster Ophthalmicus/diagnosis , Humans , Magnetic Resonance Imaging , Male , Methamphetamine/analogs & derivatives , Middle Aged , Oculomotor Nerve/pathology , Ophthalmoplegia/etiology , Ophthalmoplegia/pathology , Orbit/pathology , Sympathomimetics , Vasoconstrictor AgentsABSTRACT
From September 1976 to November 1991 a series of 34 patients with peripheral iatrogenal facial paralysis after removal of cerebellopontine angle tumors or parotid-gland surgery were treated by hypoglossal-facial anastomosis (hypoglossal-facial/hypoglossal-hypoglossal in 38.24% of cases). Patients were divided into two groups: Group A with early anastomosis and Group B with delayed anastomosis. In the first group, 57.14% of the cases presented "excessive reinnervation"; and in the second group, 95.0% of cases presented "good" or "excellent" results. In this paper we analyze and discuss our results and review the literature.