There is significant evidence that the pathogenesis of several neurodegenerative diseases, including Parkinson's disease, Alzheimer's disease, Friedreich's ataxia and amyotrophic lateral sclerosis, may involve the generation of reactive oxygen species and mitochondrial dysfunction. Here, we review the evidence for a disturbance of glutathione homeostasis that may either lead to or result from oxidative stress in neurodegenerative disorders. Glutathione is an important intracellular antioxidant that protects against a variety of different antioxidant species. An important role for glutathione was proposed for the pathogenesis of Parkinson's disease, because a decrease in total glutathione concentrations in the substantia nigra has been observed in preclinical stages, at a time at which other biochemical changes are not yet detectable. Because glutathione does not cross the blood–brain barrier other treatment options to increase brain concentrations of glutathione including glutathione analogs, mimetics or precursors are discussed.

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Background— Carotid angioplasty and stenting (CAS) is increasingly being used for treatment of symptomatic and asymptomatic carotid artery disease (CAD). To evaluate the efficacy of cerebral protection devices in preventing thromboembolic complications during CAS, we conducted a systematic review of studies reporting on the incidence of minor stroke, major stroke, or death within 30 days after CAS. Summary of Review— We searched for studies published between January 1990 and June 2002 by means of a PubMed search and a cumulative review of reference lists of all relevant publications. In 2357 patients a total of 2537 CAS procedures had been performed without protection devices, and in 839 patients 896 CAS procedures had been performed with protection devices. Both groups were similar with respect to age, sex distribution, cerebrovascular risk factors, and indications for CAS. In many studies the periprocedural complication rates had not been presented separately for patients with symptomatic and asymptomatic CAD. The combined stroke and death rate within 30 days in both symptomatic and asymptomatic patients was 1.8% in patients treated with cerebral protection devices compared with 5.5% in patients treated without cerebral protection devices (χ 2 =19.7, P <0.001). This effect was mainly due to a decrease in the occurrence of minor strokes (3.7% without cerebral protection versus 0.5% with cerebral protection; χ 2 =22.4, P <0.001) and major strokes (1.1% without cerebral protection versus 0.3% with cerebral protection; χ 2 =4.3, P <0.05), whereas death rates were almost identical (≈0.8%; χ 2 =0.3, P =0.6). Conclusions— On the basis of this early analysis of single-center studies, the use of cerebral protection devices appears to reduce thromboembolic complications during CAS. These technical aspects should be taken into account before the initiation of further randomized trials comparing CAS with carotid endarterectomy.

A separate pathway seems to be present in humans for sensing the orientation of gravity apart from the one for orientation perception of the visual world. This second graviceptive system decisively contributes to humans' control of upright body posture. Contraversive pushing occurring after stroke lesions may represent the behavioral correlate of a disturbed neural representation of this system.