Effects of a full-body electrostimulation garment application in a cohort of subjects with cerebral palsy, multiple sclerosis, and stroke on upper motor neuron syndrome symptoms.

OBJECTIVES: Dysfunction of the central nervous system may inflict spastic movement disorder (SMD). Electrical stimuli were identified as promising therapeutic option. Electrical stimulation provided by a 58-electrode full body garment was investigated based on data from regular trial fittings. METHODS: Data from 72 testees were investigated. Age averages 36.6 (19.8) ys with 44 females. The cohort spans infantile cerebral paresis (CP) (n=29), multiple sclerosis (MS) (n=23) and stroke (n=20). Data were stratified by etiology and an entry BBS Score<45. RESULTS: Effect sizes (Cohen`s d) related BBS, TUG, FGA, 10mWT, WMFT, EQ5D5L and Pain. Significance levels are indicated by *: p<0.05, **: p<0.01, ***: p<0.001, (t): p<0.1: CP: 1.64***, 0.29*, 1.59***, 0.76(t), 1.00***, 0.5*, 1.28***; MS: 1.83***, 0.83***, 1.28**, 1.07***, 0.93*, 1,11**, 0.78*; Stroke: 1.28**, 0.78**, 0.89, 0.92**, 0.71, 1.26*, 0.78*. CONCLUSIONS: Multi-site transcutaneous electrical stimulation may increase ambulation related skills in subjects with SMD stemming from CP, MS and stroke. The results indicate effects on static and dynamic balance, fall risk, mobility, upper extremity improvement and an overall increase in health utility and a reduction in spasticity related pain. Effects are immediate as well as sustained. These results may inspire individual trial fittings and inform further controlled trials.

High and complementary expression patterns of alcohol and aldehyde dehydrogenases in the gastrointestinal tract: implications for Parkinson's disease.

Parkinson's disease (PD) is a heterogeneous movement disorder characterized by progressive degeneration of dopamine neurons in substantia nigra. We have previously presented genetic evidence for the possible involvement of alcohol and aldehyde dehydrogenases (ADH; ALDH) by identifying genetic variants in ADH1C and ADH4 that associate with PD. The absence of the corresponding mRNA species in the brain led us to the hypothesis that one cause of PD could be defects in the defense systems against toxic aldehydes in the gastrointestinal tract. We investigated cellular expression of Adh1, Adh3, Adh4 and Aldh1 mRNA along the rodent GI tract. Using oligonucleotide in situ hybridization probes, we were able to resolve the specific distribution patterns of closely related members of the ADH family. In both mice and rats, Adh4 is transcribed in the epithelium of tongue, esophagus and stomach, whereas Adh1 was active from stomach to rectum in mice, and in duodenum, colon and rectum in rats. Adh1 and Adh4 mRNAs were present in the mouse gastric mucosa in nonoverlapping patterns, with Adh1 in the gastric glands and Adh4 in the gastric pits. Aldh1 was found in epithelial cells from tongue to jejunum in rats and from esophagus to colon in mice. Adh3 hybridization revealed low mRNA levels in all tissues investigated. The distribution and known physiological functions of the investigated ADHs and Aldh1 are compatible with a role in a defense system, protecting against alcohols, aldehydes and formaldehydes as well as being involved in retinoid metabolism.