Similar to the initial description by James Parkinson, the self-report of PD onset by Wilhelm von Humboldt or Michael J. Fox also initially mentions motor symptoms as a guiding clinical feature. But both of them also report apathy, anhedonia-like depressive symptoms, which occur initially and later in the course of PD (7,8). These unspecific

Oxidative Stress and Neurodegenerative Disorders Edited by G. Ali Qureshi and S. Hassan Parvez

© 2007 Elsevier B.V. All rights reserved.

fatigue-like symptoms, disturbances of sleep, emotional and personal behavior, reduced tolerance to stress, deficits of motivation and impulse, lack of concentration, restlessness and anxiety clinically often appear prior to the often intermittent manifestation of motor symptoms. These psychopathological signs of psychomotor retardation are often clinically diagnosed as depression of the elderly or as early signs of mild cognitive impairment or dementia in clinical practice (9). This view is confirmed by a trial, which uses a case-control design and investigates an association between preceding anxiety, depression and later diagnosis of PD. In the case of depression, the significance of the association was lost when depressive disorders first recognized within the 5 years preceding the onset of PD were excluded. However, this trial also reports significant relations between anxiety disorders and PD up to 20 years before the onset of PD and that anxiety preceded depression in 72% of the PD patients, who had both conditions. These results are consistent with earlier studies and support the view that anxiety and depressive episodes are early non-motor manifestations of the underlying disease process (9,10). This view is supported by the still hypothetical revolutionary, only partially confirmed approach of a pathological process description with a somewhat stereotypic topographic expansion pattern of lesions in PD, which may even start outside the brain. These current neuropathological results also indicate that neurodegeneration not only takes place in nigral dopaminergic neurons, but also appears in non-dopaminergic neurotransmitter systems and in extranigral structures in these early and late advanced stages. One may even postulate that extranigral neurodegeneration may also play an essential role in the pathophysiology of PD, since it causes cognitive and behavioral disturbances, which precede the alteration of motor function. Thus, these predominant psychopathological symptoms clinically reflect the still hypothetical neuropathologic route of neurodegeneration in PD patients to a certain extent (11-13). In PD, this may be associated with a compensatory downregulation of 5-HT and an associated development of mild depression, since 5-HT regulates dopamine turnover in the brain, i.e. the frontal lobe or the brainstem. Research on relationships between neurotransmission, motor features of PD, frequency and severity of depression or anxiety in predominant previously untreated PD patients in the early stage of PD is rare. Then mostly occurrence of motor symptoms leads to the diagnosis of PD. At this stage, nigrostriatal cell loss is about 50% and striatal dopamine content is reduced to approximately 80% (1).

Anxiety and Depression 101

Anxiety and Depression 101

Everything you ever wanted to know about. We have been discussing depression and anxiety and how different information that is out on the market only seems to target one particular cure for these two common conditions that seem to walk hand in hand.

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