Are dysautonomic and sensory symptoms present in early Parkinson’s disease?
O.-B. Tysnes
Department of Neurology, Haukeland University Hospital, Bergen, Norway
Institute for Clinical Medicine, University of Bergen, Bergen, Norway
Search for more papers by this authorB. Müller
Department of Neurology, Haukeland University Hospital, Bergen, Norway
Institute for Clinical Medicine, University of Bergen, Bergen, Norway
Search for more papers by this authorJ. P. Larsen
Institute for Clinical Medicine, University of Bergen, Bergen, Norway
Department of Neurology, Stavanger University Hospital, Stavanger, Norway
The Norwegian Centre for Movement Disorders, Stavanger, Norway
Search for more papers by this authorO.-B. Tysnes
Department of Neurology, Haukeland University Hospital, Bergen, Norway
Institute for Clinical Medicine, University of Bergen, Bergen, Norway
Search for more papers by this authorB. Müller
Department of Neurology, Haukeland University Hospital, Bergen, Norway
Institute for Clinical Medicine, University of Bergen, Bergen, Norway
Search for more papers by this authorJ. P. Larsen
Institute for Clinical Medicine, University of Bergen, Bergen, Norway
Department of Neurology, Stavanger University Hospital, Stavanger, Norway
The Norwegian Centre for Movement Disorders, Stavanger, Norway
Search for more papers by this authorConflicts of interest: O-BT has received fees from GlaxoSmithKline, Lundbeck, Orion Pharma, Pfizer and Boehringer. The remaining authors have declared no conflicts.
Abstract
Tysnes O-B, Müller B, Larsen JP. Are dysautonomic and sensory symptoms present in early Parkinson’s disease? Acta Neurol Scand: 2010: 122 (Suppl. 190): 72–77. © 2010 John Wiley & Sons A/S.
Parkinson’s disease (PD) occurs with an annual incidence of 13/100.000, is slightly more frequent in men and is characterized by the motor symptoms tremor, rigidity, bradykinesia and postural instability. In addition, non-motor symptoms have been increasingly connected to the disease although already described in James Parkinson’s ‘Essay on the shaking palsy’ from 1817. The motor symptoms in PD are related to the degeneration of dopaminergic cells in the substantia nigra (SN). These symptoms respond well to dopaminergic substitution. It is much more unclear whether non-motor symptoms like dysautonomia, insomnia, day-time sleepiness, fatigue, pain and neuropsychiatric symptoms respond to levodopa. Autonomic symptoms include dizziness because of orthostatic hypotension, constipation, nausea, voiding symptoms and increased sweating. Such symptoms as well as sensory symptoms like hyposmia and pain are very frequently reported in PD and seem to occur early in the disease process. Braak proposed a sequential model of neuropathology in PD starting with affection of the olfactory bulb and the autonomic innervation of the heart and gut. Affection of SN is seen from Braak stage 3, and limbic and cortical structures are affected in the later stages of the disease. Currently, the evidence for sensory and autonomic involvement in PD is reviewed with special focus on the early phase of the disease.
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