ABSTRACT
La Injuria Pulmonar Autoinducida por el Paciente (p-SILI) es una entidad recientemente reconocida. Clásicamente, el daño producido por la ventilación mecánica (VM) se asoció al uso de presión positiva, y para disminuirlo se crearon distintas estrategias conocidas como parámetros de protección pulmonar. Sin embargo, es importante reconocer los potenciales efectos deletéreos de la ventilación espontánea dependientes de la injuria pulmonar previa que sufra el paciente y del esfuerzo que realice. En este artículo se explican los distintos mecanismos que pueden producir p-SILI y las estrategias descritas en la literatura para prevenirla (AU)
Patient self-inflicted lung injury (p-SILI) is a recently recognized disorder. Classically, damage produced by mechanical ventilation (MV) was associated with the use of positive pressure, and different strategies known as lung protection parameters were created to reduce it. Nevertheless, it is important to recognize the potential deleterious effects of the effort made during spontaneous breathing due to previous lung injury suffered by the patient. This article explains the different mechanisms that may produce p-SILI and the prevention strategies described in the literature. (AU)
Subject(s)
Respiration, Artificial/methods , Respiratory Distress Syndrome, Newborn , Intensive Care Units, Pediatric , Tidal Volume , Positive-Pressure Respiration/methods , Lung Injury/physiopathology , Lung Injury/prevention & controlABSTRACT
A patient with melanoma and sporadic positive melanuria developed Parkinson's disease. Treatment with levodopa failed to modify tumoral progress. However, during chemotherapy with dacarbazine, the patient experienced a significant impairment to levodopa response.
Subject(s)
Dacarbazine/adverse effects , Levodopa/therapeutic use , Melanoma/complications , Parkinson Disease/drug therapy , Skin Neoplasms/complications , Adult , Dacarbazine/therapeutic use , Dopamine/blood , Drug Interactions , Humans , Male , Melanins/urine , Melanoma/drug therapy , Parkinson Disease/complications , Skin Neoplasms/drug therapyABSTRACT
To evaluate clinically the slowing of cognitive processing in Parkinson's disease, we used a visual discrimination task consisting of 15 superimposed images of objects. The time needed to identify 12 objects increased by 58% in 70 patients withdrawn from levodopa treatment compared with 20 controls matched for age and education. Perceptual, motor, and psycholinguistic factors, as well as mood, only partially accounted for the slowness of performance. The 15-objects test scores of the parkinsonian patients correlated significantly with both their intellectual impairment and the severity of their parkinsonian disability, but not with the duration of the disease. The scores did not correlate with depression. Levodopa had no effect on the score, although the parkinsonian motor disability score was improved by 54%. The results indicate a cognitive slowing in Parkinson's disease which is probably related to abnormalities of nondopaminergic neuronal systems in the brain.
Subject(s)
Cognition , Levodopa/therapeutic use , Neuropsychological Tests , Parkinson Disease/psychology , Adolescent , Adult , Aged , Cognition/drug effects , Discrimination, Psychological , Humans , Middle Aged , Parkinson Disease/drug therapy , Regression Analysis , Visual PerceptionABSTRACT
Seven patients with Parkinson's disease and severe motor fluctuations were studied with event-related potentials, reaction and movement times and neuropsychological tests while in "off" and "on" phases. While there was a significant decrement in the P300 latency of the event-related potentials and in the duration of movement time in the "on" phase, no significant differences between on and off phases were observed in reaction time and neuropsychological tasks.
Subject(s)
Attention/physiology , Dementia/physiopathology , Electroencephalography , Motor Skills/physiology , Parkinson Disease/physiopathology , Reaction Time/physiology , Aged , Arousal/physiology , Cerebral Cortex/physiopathology , Dementia/psychology , Evoked Potentials, Auditory , Female , Humans , Male , Middle Aged , Neuropsychological Tests , Parkinson Disease/psychology , Psychomotor Performance/physiologyABSTRACT
Vigabatrin (gamma-vinyl GABA; GVG), an irreversible inhibitor of GABA-transaminase, at a daily dose of 2-4 g, and a placebo were each administered orally for 4 months to 14 patients with cerebellar ataxia (9 with Friedreich's ataxia, 5 with olivopontocerebellar atrophy), in a double-blind, placebo-controlled crossover study. For the group as a whole, there was no significant difference between the GVG and placebo periods in any of the parameters of cerebellar symptomatology measured. Individually, one patient showed some improvement after 3 months of treatment with 2 g/day GVG. Tolerance to 4 g/day GVG was poor, whereas 2 g/day was well tolerated. The results suggest that agents which increase central GABA concentrations are not likely to be of benefit to patients with Friedreich's ataxia or olivopontocerebellar atrophy.
Subject(s)
Aminocaproates/therapeutic use , Friedreich Ataxia/drug therapy , Olivopontocerebellar Atrophies/drug therapy , Spinocerebellar Degenerations/drug therapy , Adolescent , Adult , Aminocaproates/adverse effects , Double-Blind Method , Drug Evaluation , Humans , Male , Middle Aged , Neurologic Examination , Random Allocation , VigabatrinABSTRACT
Seventy parkinsonian patients (mean age: 59.6 +/- 1.2 years; duration of disease: 9 +/- 0.6 years) with severe fluctuations of disability under L-Dopa treatment received a single dose of L-Dopa (200 mg + benserazide, a peripheral decarboxylase inhibitor) after 24-72 h interruption of treatment. The delay and duration of action of a single dose of L-Dopa, and the percentage of improvement of the parkinsonian symptoms were 39 +/- 2 and 162 +/- 6 minutes, and 57 +/- 2 p. 100 respectively. Estimation of the difference between the basal parkinsonian score and the score during maximum clinical improvement under levodopa treatment, and the score under levodopa treatment may reflect the severity of dopaminergic and of non dopaminergic lesions in the brain respectively. Modification of the treatment to obtain continuous clinical improvement can be performed according to the delay and duration of action of a single dose of L-Dopa.
