Neuroimaging of nonmotor features of Parkinson's disease.

Ahmanson-Lovelace Brain Mapping Center, University of California, Los Angeles, CA, USA.
Reviews in neurological diseases 02/2008; 5(3):125-33.
Source: PubMed

ABSTRACT Parkinson's disease (PD) is a neurodegenerative disorder characterized by motor symptoms that respond to dopaminergic therapy. However, there is increasing interest in nonmotor PD features such as hyposmia, sleep disorders, dementia, depression, and psychoses. We review neuroimaging studies in nonmotor symptoms of PD and the use of dopaminergic imaging to support screening of nonmotor symptoms for early PD. Neuroimaging data document nonmotor pathophysiologic involvement of systems beyond the nigrostriatal dopaminergic pathway. These neuroimaging studies support a broader view of PD with early involvement in time and wider involvement of monoamine and cortical systems that may provide targets for novel therapies for nonmotor symptoms.

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    ABSTRACT: A dopaminergic deficiency in patients with Parkinson's disease (PD) causes abnormalities of movement, behaviour, learning, and emotions. The main motor features (ie, tremor, rigidity, and akinesia) are associated with a deficiency of dopamine in the posterior putamen and the motor circuit. Hypokinesia and bradykinesia might have a dual anatomo-functional basis: hypokinesia mediated by brainstem mechanisms and bradykinesia by cortical mechanisms. The classic pathophysiological model for PD (ie, hyperactivity in the globus pallidus pars interna and substantia nigra pars reticulata) does not explain rigidity and tremor, which might be caused by changes in primary motor cortex activity. Executive functions (ie, planning and problem solving) are also impaired in early PD, but are usually not clinically noticed. These impairments are associated with dopamine deficiency in the caudate nucleus and with dysfunction of the associative and other non-motor circuits. Apathy, anxiety, and depression are the main psychiatric manifestations in untreated PD, which might be caused by ventral striatum dopaminergic deficit and depletion of serotonin and norepinephrine. In this Review we discuss the motor, cognitive, and psychiatric manifestations associated with the dopaminergic deficiency in the early phase of the parkinsonian state and the different circuits implicated, and we propose distinct mechanisms to explain the wide clinical range of PD symptoms at the time of diagnosis.
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