الفهرس 
Patology and pathophysiology of parkinson’s diseasOnly 14 pages are availabe for public view
 |  | from | 16 |  |  |
| | | from | 16 | | |
Abstract
PD is one of the most common neurologic disorders, affecting approximately 1% of individuals older than 60 years and causing progressive disability that can be slowed, but not halted, by treatment so it is amajor clinical proplem .The 2 major neuropathologic findings in Parkinson disease are loss of pigmented dopaminergic neurons of the substantia nigra pars compacta and the presence of Lewy bodies and Lewy neuritis
Onset of motor signs in Parkinson disease is typically asymmetric, with the most common initial finding being an asymmetric resting tremor in an upper extremity. Over time, patients notice symptoms related to progressive bradykinesia, rigidity, and gait difficulty. The first affected arm may not swing fully when walking, and the foot on the same side may scrape the floor. Over time, axial posture becomes progressively flexed and strides become shorter.
Some nonmotor symptoms commonly precede motor signs in Parkinson disease. Most Parkinson disease patients have a substantial reduction in olfactory function (smell) by the time motor signs emerge. However, either this is not noticed by the patients or patients may not realize that it is part of the disease. Another common premotor symptom is (REM) behavior disorder (RBD). In this condition, individuals exhibit movements during REM sleep that are often described as hitting or kicking motions. There are also a number of midlife risk factors for the later development of Parkinson disease. These include constipation and excessive daytime sleepiness, although they are far from specific for Parkinson disease.
Parkinson disease is a clinical diagnosis. No laboratory biomarkers exist for the condition, and findings on routine magnetic resonance imaging (MRI) and computed tomography (CT) scan are unremarkable. Positron emission tomography (PET) and single-photon emission CT (SPECT) may show findings consistent with Parkinson disease, and olfactory testing may provide evidence pointing toward Parkinson disease, but these studies are not routinely needed.
Patients with Parkinson disease must have regular follow-up care to ensure adequate treatment of motor and behavioral abnormalities. Once patients are stable on a medication regimen, provide follow-up care at least every 3-6 months, and periodically adjust medication dosages as necessary. Patients also need to be monitored for adverse events, including somnolence, sudden-onset sleep, impulse control disorders, and psychosis. In addition, patients should be evaluated and treated for emergence of clinically relevant nonmotor symptoms, including dementia, psychosis, sleep disorders, and mood disorders.
Early detection of PD is very important to start early management and neuroprotection, but till now there is no valid PD marker is available despite the critical need for improved diagnostic accuracy, earlier diagnosis, monitoring of disease progression, and responses to therapeutic interventions.
To early detection of PD and neuroprotection we should understand the Braak staging and understanding the pathogenesis of PD which help us to be targeting for neuroprotection.
Pathogenesis of PD include several mechanisms such as oxidative stress, mitochondrial dysfunction, protein aggregation and misfolding, inflammation, excitotoxicity, apoptosis and other cell death pathways, and loss of trophic support.
The target of management of PD is to control of signs and symptoms for as long as possible while decrease adverse effects. Studies demonstrate that a patient’s quality of life deteriorates quickly if treatment is not instituted at or shortly after diagnosis
There is no cure for PD, since currently available treatment can neither arrest nor reverse the progression of the disease. However, the symptoms can be managed with several different drugs. The drugs used to treat PD either boost the levels of DA in the brain or mimic the effects of DA.
Medications commonly used for symptomatic benefit of motor symptoms in early Parkinson disease include levodopa, monoamine oxidase (MAO)-B inhibitors, and dopamine agonists.
The barriers to establishing a neuroprotective therapy come from the complexity of the disease process as well as the limits of the clinical tools available to monitor the progression of the disease and to observe the effects of an intervention. Recent studies seeking a neuroprotective effect illustrate the importance of both of these factors.