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Injuries may cause unilateral deterioration of brain areas related to postural control resulting in lateralized motor disability with abnormal asymmetry in weight-bearing distribution. Although overloading toward the nonaffected limb has been described as the preferred posture among individuals with hemiparesis, characterization of the weight-bearing asymmetry is poorly and indirectly described. Therefore, this study aimed to describe weight-bearing distribution during upright stance, establishing criteria to consider asymmetry in hemiparesis when analyzed within the limits defined by controls matched by age and gender. Forty subjects with (n = 20) or without hemiparesis (n = 20) were included in procedures to record weight-bearing values between hemibodies, and these values were used to calculate a symmetry ratio. Control presented 95% confidence interval (CI) of the mean for symmetry ratio ranging from 0.888 to 1.072, defining limits to symmetry. Four subjects with hemiparesis (20%) had symmetry ratios inside limits defined by controls (i.e., weight-bearing symmetrically distributed), and 11 (55%) subjects without hemiparesis showed symmetry ratios outside the limits, suggesting asymmetrical weight-bearing distribution. It was concluded that asymmetry, when present in a control group, was more frequently overloading nonpredominantly used hemibody (nondominant side), differing from a hemiparesis group commonly forced to assume the nonaffected side as the predominantly used hemibody and where the overload was observed.

Classically, Parkinson's disease (PD) is considered to be a motor system affliction and its diagnosis is based on the presence of a set of cardinal motor signs (e.g. rigidity, bradykinesia, rest tremor and postural reflex disturbance). However, there is considerable evidence showing that non-motor alterations (e.g. anxiety, depression, sleep, gastrointestinal and cognitive functions) precede the classical motor symptoms seen in PD. The management of these nonmotor symptoms remains a challenge. A pattern of regional neurodegeneration that varies considerably depending upon the neuronal population affected may explain the different symptoms. In fact, differential mechanisms of neuronal vulnerability within the substantia nigra pars compacta (SNpc) suggests that factors other than location contribute to the susceptibility of these neurons. In this review we discuss how these factors interact to ultimately target the SNpc. Remarkably, this region consists of approximately 95% of the tyrosine hydroxylase (TH)-immunoreactive neurons in both human and rat brains, and consequently this implicates elevated levels of dopamine metabolites, free radicals and other hazard species in these neurons. An understanding of how these factors promote neuronal death may be useful for the development of novel neuroprotective and/or neurorestorative strategies for PD.