Arch Neurol Chicago
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Arch Neurol Chicago · Jun 2007
Risk factors for the development of pedal edema in patients using pramipexole.
To determine risk factors for pedal edema among patients with Parkinson disease (PD) using pramipexole hydrochloride therapy. ⋯ Pedal edema is a relatively common outcome in patients with PD receiving pramipexole. History of coronary artery disease increases the risk for developing edema.
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When human beings venture back to the moon and then on to Mars in the coming decade or so, we will be riding on the accumulated data and experience from approximately 50 years of manned space exploration. Virtually every organ system functions differently in the absence of gravity, and some of these changes are maladaptive. ⋯ Astronauts traveling to Mars will live in the absence of gravity for more than 1 year en route and will have to transition between weightlessness and planetary gravitational forces at the beginning, middle, and end of the mission. We discuss some of what is known about the effects of spaceflight on nervous system function, with emphasis on the neuromuscular and vestibular systems because success of a Mars mission will depend on their proper functioning.
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Arch Neurol Chicago · Apr 2007
Clinical TrialNeurological, cardiological, and oculomotor progression in 104 patients with Friedreich ataxia during long-term follow-up.
Friedreich ataxia (FA) is the most frequent autosomal recessive cerebellar ataxia. Although the phenotype is well known, disease progression has not been evaluated in a prospective manner. ⋯ The neurological condition of FA patients deteriorated slowly over time, even with idebenone treatment. Although cardiac hypertrophy decreased under treatment, cardiac function did not improve. The ICARS scale is not appropriate to evaluate the progression of FA in patients with long disease durations. Additional quantitative measures may improve the reliability of this scale.
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Arch Neurol Chicago · Apr 2007
Association of increased cortical soluble abeta42 levels with diffuse plaques after severe brain injury in humans.
Traumatic brain injury (TBI) is an environmental risk factor for developing Alzheimer disease. This may be due, in part, to changes associated with beta-amyloid (Abeta) plaque formation, which can occur within hours after injury, regardless of the patient's age. In addition to being precursors of toxic fibrils that deposit into plaques, soluble (nonfibrillar) Abeta peptides are posited to disrupt synaptic function and are associated with cognitive decline in Alzheimer disease. Changes in soluble Abeta levels and their relationship to Abeta plaque formation following TBI are unknown. ⋯ Selective increases in soluble Abeta(1-42) after TBI may predispose individuals with a brain injury to Alzheimer disease pathology. This may be influenced by the APOE genotype, and it may confer increased risk for developing Alzheimer disease later in life.
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Arch Neurol Chicago · Mar 2007
Comparative StudyIncidence of dementia in mild cognitive impairment in the cardiovascular health study cognition study.
To examine the incidence of dementia in subjects with mild cognitive impairment (MCI) in the Cardiovascular Health Study Cognition Study. ⋯ Subjects with MCI are at high risk for dementia. The probable MCI diagnosis identified individuals in the earliest stages of dementia, usually AD, whereas the possible MCI diagnosis identified a more heterogeneous group. However, this latter group had only a slightly lower rate of conversion to dementia than the group with probable MCI, suggesting that even with comorbid conditions, there is a high likelihood of the presence of a progressive dementing disorder.