Neonatal treatment with fluoxetine alters locomotor activity and the cortical glial/neuron index in rats with cerebral palsy.

Cerebral palsy (CP) is characterized by motor disorders, including deficits in locomotor activity, coordination, and balance. Selective serotonin reuptake inhibitors have been shown to play an important role in brain plasticity. This study investigates the effect of neonatal treatment using fluoxetine on locomotor activity and histomorphometric parameters of the primary somatosensory cortex (S1) in rats submitted to an experimental model of CP. CP was found to reduce bodyweight and locomotion parameters and also to increase the glia/neuron index in the S1. Administration of fluoxetine 10 mg/kg reduced bodyweight, impaired locomotor activity parameters, and increased the number of glial cells and the glia/neuron ratio in the S1 in rats with CP. However, treatment with fluoxetine 5 mg/kg was not found to be associated with adverse effects on locomotor activity and seems to improve histomorphometric parameters by way of minor changes in the S1 in animals with CP. These results thus indicate that experimental CP, in combination with the use of a high dose of fluoxetine (10 mg/kg), impairs locomotor and histomorphometric parameters in the S1, while treatment with a low dose of fluoxetine (5 mg/kg) averts the negative outcomes associated with a high dose of fluoxetine in relation to these parameters but produces no protective effect.

Acute effects of whole-body vibration on spinal excitability level and ankle plantar flexion spasticity in post-stroke individuals: A randomized controlled trial.

INTRODUCTION: This study aimed to evaluate the acute effects (up to 30 min) of whole-body vibration (WBV) on spinal excitability level and ankle plantar flexion spasticity in chronic stroke subjects. METHODS: Twenty-one subjects (age 30-70 years old) with chronic stroke and ankle plantar flexion spasticity were randomly assigned to the vibration group (VG, n = 11) or the control group (CG, n = 10). Subjects in the VG underwent 10 minutes of WBV with a frequency of 35 Hz and amplitude of 2 mm. Subjects in the CG remained on the platform for 10 min without receiving vibratory stimulus. The spinal excitability level was estimated by the Hmax/Mmax ratio extracted from the H-reflex with simple stimulus examination. The value of the second/first wave ratio (H2/H1 ratio) at the peak of the first facilitation was also considered through the recovery curve with double stimulation. Spasticity was estimated by the Modified Ashworth Scale (MAS) and global perception of change. All outcomes were assessed before and at 10, 20, and 30 min after the WBV, except for MAS, which was evaluated only 10 min after WBV. RESULTS: No between-group differences were found in either the spinal excitability level or plantar flexor spasticity at the three evaluated moments after WBV. CONCLUSION: These results suggest that WBV does not reduce spinal excitability level or spasticity of the plantar flexor muscles in chronic stroke patients in the first 30 min after vibratory stimulus.