الفهرس 
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Abstract
Parkinson’s disease (PD), the second most common neurodegenerative disorder following Alzheimer’s disease, is characterized by the progressive loss of dopaminergic neurons in the substantia nigra. Patients present with resting tremor, muscle rigidity, postural instability and bradykinesia.
Recent studies have shown that inflammatory responses are observed in the nigrostriatal regions of dopaminergic degeneration and some protective benefits against oxidative stress and inflammatory progression occur. Among the inflammatory mediators, UA, which exerts antioxidant stress on neurons, has received substantial attention over the past few years.
Vascular Parkinsonism (VP), resulting from cerebrovascular disease, is a rare disorder showing a variety of clinical and pathological presentations distinct from sporadic Parkinson’s disease (PD),predominantly involving lower limbs; postural instability; shuffling gait; falls; dementia; and corticospinal findings.
Neuropathology shows multiple subcortical ischemic lesions owing to small vessel disease in striatum, globus pallidus, and white matter and, less often, substantia nigra, involving cortico-striato-pallidal (nigral), thalamofrontal and other loops, without evidence of Lewy bodies.
However, direct effects of UA on vascular physiology have also been explored. Elevated UA levels are associated with increased arterial stiffness, endothelial dysfunction and blunted vasodilatory response. Although UA is typically an anti-oxidant some authors have suggested that it can take on pro-oxidant properties under certain conditions.
Oxidative damage is known to take part in cerebral ischemia and increase infarct size, which proposed to be incriminated in Vascular Parkinsonism.
Recent studies indicate that Mn-Superoxide dismutase protects against vascular mitochondrial DNA damage and development of atherosclerosis. In contrast, although whether Mn plays an important role in PD is still unclear, previous findings suggest that chronic occupational exposure to Mn is associated with PD.
When non-human primates exposure to Mn, dopamine levels are decreased in the Globus pallidus, striatum, midbrain and the caudate. Excessive accumulation of Manganese has also induced the phenomenon also seen in PD, such as oxidative stress, impairment of glutamate transporters and excitatory neurotoxicity.
The evaluations and neurological examinations of both inpatients and outpatients were performed and completed. All patients with PD in this study fulfilled the criteria of the UK PD Society Brain Bank. The exclusion criteria were met and all patients with Vascular Parkinsonism in this study fulfilled the criteria presented in Benamer and Zijlmans’ reports. All subjects completed the following battery of standard assessment measures: a standard demography form, The UPDRS (III) ‘motor’ scale was used to evaluate motor dysfunctions and disease severity.
There was a highly significant difference between PD and VP cases as regard uric acid and manganese. Higher mean uric acid among VP cases and higher manganese among PD cases.
Using ROC curve, it was shown that uric acid could discriminate PD from VP cases at a level of ≤5.35 with 75% and 95% sensitivity and specificity respectively
Using ROC curve, it was shown that Manganese could discriminate PD from VP cases at a level of ≥2.15 with 90% and 75% sensitivity and specificity respectively
Also there was no significant Correlation between personal data, medical data (disease duration by years, The UPDRS (III) ‘motor’ scale, dopa dosage by mg and uric acid among PD cases.
There was no significant Correlation between personal data, medical data and manganese among PD cases. There was no significant Correlation between males and females according to uric acid and manganese level among PD cases. There was no significant Correlation between medical data and uric acid among VP cases. However, a significant negative correlation was found between age and uric acid.