Journal of the neurological sciences
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The use of induced hypothermia in the treatment of traumatic spinal cord injury (SCI) has been studied extensively between the 1960s and 1970s. Although the treatment showed some promise, it became less popular by the 1980s, mainly because of its adverse effects. However, a revival of hypothermia in the treatment of traumatic brain injury (TBI) in the last decade has encouraged neuroscientists to conduct experiments to reevaluate the potential benefits of hypothermia in traumatic SCI. ⋯ At present, induced hypothermia has yet to be recognized or approved as a potential treatment having therapeutic value for traumatic SCI in humans. The continued search for a possible synergistic effect of induced hypothermia and pharmacological therapy may yield some promise. It has also been deduced from these laboratory studies that hyperthermia is deleterious and rigorous measures to prevent hyperthermia should be taken to minimize the propagation of secondary neuronal damage after traumatic SCI.
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To compare amyotrophic lateral sclerosis (ALS) patients and their caregivers on measures of quality of life (QOL), depression, and their attitudes toward treatment options. ⋯ Factors contributing to quality of life, depression, and attitudes toward treatment options need to be periodically explored with patients and caregivers throughout the course of the illness. Health care professionals should recognize that the needs and goals of the two groups might differ. For both patients and caregivers, health care professionals should provide education and opportunities for discussion centered on the issues followed by referrals and interventions appropriate to the situation.
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Gastrointestinal (GI) haemorrhage is an important and sometimes serious complication in critically ill neurological patients who suffered from stroke and head injury and those in intensive care. There is no study evaluating frequency, severity and risk factors of GI haemorrhage in patients with primary intracerebral haemorrhage (ICH). ⋯ GI haemorrhage is more likely present in patients with larger haematoma having septicemia. Our study highlights the importance of septicemia, which is an important and modifiable risk factor for GI bleeding in ICH patients.
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Comparative Study
Protection of dopaminergic neurons with a novel astrocyte modulating agent (R)-(-)-2-propyloctanoic acid (ONO-2506) in an MPTP-mouse model of Parkinson's disease.
We examined the neuroprotective effects of a novel astrocyte-modulating agent, (R)-(-)-2-propyloctanoic acid (ONO-2506), in a mouse model of Parkinson's disease. Male C57BL/6 mice received four intraperitoneal injections of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) (10 mg/kg) at 1-h intervals. Dopamine content in the striatum, measured with HPLC 3 days after MPTP injection, was reduced to 23% of control. ⋯ The MPTP injection led to reactive astrocytosis in the striatum after 7 days, but ONO-2506 induced earlier, moderate astrocytic activation after 3-7 days. These findings show that ONO-2506 protects dopaminergic neurons against MPTP neurotoxicity probably through facilitating astrocytic support for neuronal recovery from injury. Pharmacological modulation of astrocytes may offer a novel therapeutic strategy for Parkinson's disease.
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Comparative Study
Short-term effect of cigarette smoking on CO(2)-induced vasomotor reactivity in man: a study with near-infrared spectroscopy and tanscranial Doppler sonography.
Cigarette smoking is a major risk factor for stroke, and quitting reduces the stroke risk within a few years. The aim of our study was to clarify whether CO(2)-induced vasomotor reactivity (VMR) is impaired in smokers after smoking a cigarette as a possible factor of an increased stroke risk. We compared VMR of 23 healthy smokers assessed at baseline, immediately, and 30 min after smoking a cigarette (1.2 mg nicotine) with values from nonsmoking, age-matched controls (n=24), obtained at identical time intervals. ⋯ Increased baseline CBFV in smokers after smoking might be due to arteriolar dilation, increased MAP, and possibly constriction of basal cerebral arteries. Impaired VMR for about 30 min after smoking reflects endothelial dysfunction. This might contribute to the enhanced stroke risk in smokers.