Events Exposure as a Trigger of the Clinical Manifestations of Parkinson's Disease

Parkinson Disease, Parkinsonism

Stress has been implicated as a trigger of many diseases, throughout different mechanisms. Potentially traumatic/stressful events exposure might be a factor that triggers subclinical disabilities related to PD becoming evident to the patient. In this observational study, the investigators will evaluate with a validated events exposure questionnaire the occurrence and severity of potentially traumatic or stressful events in Parkinson's disease patients and in patients with recent-onset parkinsonism.

Parkinson's disease (PD) is one of the most common neurodegenerative disorders worldwide, affecting approximately 1% of individuals older than 60 years and causing progressive disability. Clinical signs and symptoms of PD include asymmetric bradykinesia, rest tremor, rigidity, postural instability, and gait abnormalities. Stress has been implicated as a trigger of many diseases, throughout different mechanisms. Potentially traumatic/stressful events exposure might be a factor that triggers subclinical disabilities related to PD becoming evident to the patient. Stress or events exposure can be associated with the clinical expression of Parkinson's sisease, acting as the final hit in a predisposed person. The prevalence of exposure to traumatic events (TE) throughout life in different populations has been analyzed in multiple studies, with variable percentages, ranging from 30 -70%. It is well known that stress activates both the sympathetic nervous system and the hypothalamic - pituitary - adrenal (HPA) axis, resulting in increases in the secretion of catecholamines and glucocorticoids (GCs) into the peripheral circulation. Stress also can increase the release of dopamine (DA) and glutamate in the striatum as well as other brain regions. It is likely that these effects of stress have evolved as part of a generalized response to potential danger, facilitating the ability of the organism to respond appropriately to the stressor. More specifically, given the impact of DA and glutamate on striatal function, these changes can be expected to increase the capacity of the CNS to focus, process, and ultimately respond appropriately to emergencies. These effects are likely to be reinforced by the increased availability of GCs. Yet, when the amplitude or duration of these biological changes becomes excessive, the possibility of neuronal cell death develops. The greatest risk factor for PD appears to be age. The tendency for the symptoms of PD to emerge after the age of 55 may be due in part to a failure of compensatory mechanisms that underlie the extended preclinical phase of the disease. However, it is likely that another factor in the late onset of PD is the increased vulnerability of DA neurons to insult. In this regard, it is important to note that dysfunctions in the stress response develop during the aging process. For example, as organism ages, the response of the HPA axis to stress becomes hyperactive and is slower to return to homeostatic conditions after activation, thus exposing cells to higher levels of GCs for a prolonged period. This dysregulation might render cells in the aged brain more susceptible to degeneration in the face of subsequent stress. In this observational study, the investigators will evaluate with a validated events exposure questionnaire the occurrence and severity of potentially traumatic or stressful events in Parkinson's disease patients and in patients with recent-onset parkinsonism.

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