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1.
Neurorehabil Neural Repair ; 27(4): 296-305, 2013 May.
Article in English | MEDLINE | ID: mdl-23213077

ABSTRACT

BACKGROUND: Repetitive facilitative exercise (RFE), a combination of high repetition rate and neurofacilitation, is a recently developed approach to the rehabilitation of stroke-related limb impairment. Preliminary investigations have been encouraging, but a randomized controlled evaluation has yet to be performed. OBJECTIVES: To compare the efficacy of RFE with that of conventional rehabilitation in adults with subacute stroke. METHODS: A total of 52 adults with stroke-related upper-limb impairment (Brunnstrom stage ≥III) of 3 to 13 weeks' duration participated in this randomized, controlled, observer-blinded trial. Participants were randomized into 2 groups and received treatment on a 4-week, 40 min/d, 5 d/wk schedule. Those assigned to RFE received 100 standardized movements of at least 5 joints of their affected upper extremity, whereas those in the control group participated in a conventional upper-extremity rehabilitation program. Primary and secondary outcomes (improvement in group action research arm test [ARAT] and Fugl-Meyer Arm [FMA] scores, respectively) were assessed at the end of training. RESULTS: In all, 49 participants (26 receiving RFE) completed the trial. ARAT and FMA scores at baseline were 19 ± 21 and 39 ± 21 (mean ± standard deviation). Evaluation at the trial's completion revealed significantly larger improvements in the RFE group than in the control group in both ARAT (F = 7.52; P = .009) and FMA (F = 5.98; P = .019) scores. CONCLUSIONS: These findings suggest that RFE may be more effective than conventional rehabilitation in lessening impairment and improving upper-limb motor function during the subacute phase of stroke.


Subject(s)
Exercise Therapy/methods , Paresis/rehabilitation , Stroke Rehabilitation , Upper Extremity/physiopathology , Aged , Female , Humans , Male , Middle Aged , Paresis/etiology , Recovery of Function , Severity of Illness Index , Single-Blind Method , Stroke/complications , Time Factors , Treatment Outcome
2.
Urology ; 72(3): 701-5, 2008 Sep.
Article in English | MEDLINE | ID: mdl-18336880

ABSTRACT

OBJECTIVES: To investigate the effects of menthol, an activator of the temperature-sensitive transient receptor potential family member TRPM8, on detrusor smooth-muscle contraction and the micturition reflex in rats. METHODS: We evaluated the effect of intravesical infusion of 1 or 3 mM menthol by cystometry in conscious female Sprague-Dawley rats. Some of the animals were pretreated with 125 mg/kg capsaicin subcutaneously 4 days earlier. The parameters measured were voided volume (VV), residual volume (RV), volume threshold for inducing micturition (VT), voiding efficiency (VE), micturition pressure (MP), and pressure threshold for inducing micturition (PT). Strips of detrusor muscle were mounted in organ baths to study the effect of menthol on the contractile response to 0.01 mM carbachol. RESULTS: Intravesical infusion of 3 mM menthol reduced VV by 20%, VT by 19%, and PT by 31%. RV, VE, and MP were unaltered. Capsaicin pretreatment had no effect on baseline cystometric parameters, and 3 mM menthol caused similar reductions in VV (24%), VT (22%), and PT (30%), while having no effect on RV, VE, and MP. Menthol at 0.1, 0.3, and 1 mM inhibited carbachol-induced contractions by 10.7%, 36.7%, and 97.3%, respectively. CONCLUSIONS: Our results demonstrated that intravesical infusion of menthol facilitated the micturition reflex, and capsaicin pretreatment had no effect on this response. Menthol inhibited carbachol-induced contraction of the detrusor smooth muscle. This suggests that intravesically infused menthol cannot relax detrusor muscle, and acts on capsaicin-resistant afferents (probably through TRPM8 in urothelium or sensory nerve endings) to facilitate the micturition reflex.


Subject(s)
Menthol/pharmacology , Muscle, Smooth/drug effects , Urinary Bladder, Overactive/drug therapy , Urination/drug effects , Animals , Antipruritics/pharmacology , Capsaicin/pharmacology , Carbachol/pharmacology , Female , Menthol/chemistry , Muscle Contraction/drug effects , Muscle, Smooth/metabolism , Rats , Rats, Sprague-Dawley , TRPM Cation Channels/metabolism , Temperature , Urinary Bladder/drug effects
3.
Int J Neurosci ; 117(3): 315-26, 2007 Mar.
Article in English | MEDLINE | ID: mdl-17365117

ABSTRACT

Glial cell line-derived neurotrophic factor (GDNF) is a potent neurotrophic factor involved in the survival and proliferation of neurons. However, there have been few reports examining the relationship between GDNF and functional recovery after cerebral infarction. The authors investigated the change in the expression of GDNF proteins during functional recovery in rats following photochemically induced cerebral infarctions. Functional recovery for the first 14 days after the infarction was evaluated using a beam-walking test. The number of GDNF-like immunoreactive cells around the infarction were counted at various times (24 h, 72 h, 7 days, and 14 days) post-infarction. Immunohistochemical analysis of brain sections showed that the expression of GDNF-like immunoreactive cells was significantly increased in the temporal cortex until 7 days on the side ipsilateral to the infarction, and had decreased by 14 days. Likewise, the functional recovery of paralysis was substantial until 7 days post-infarction, after which the improvement was mild. Therefore, the expression of GDNF protein might have some relationship with the functional recovery of paralysis. There are great hopes that GDNF could be used as a therapeutic agent for cerebral infarction.


Subject(s)
Cerebral Infarction/metabolism , Cerebral Infarction/physiopathology , Glial Cell Line-Derived Neurotrophic Factor/metabolism , Recovery of Function/physiology , Analysis of Variance , Animals , Cell Count , Cerebral Infarction/chemically induced , Gene Expression Regulation/physiology , Immunohistochemistry/methods , Photochemistry/methods , Psychomotor Performance/physiology , Rats , Rats, Wistar , Rose Bengal , Time Factors
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