Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0426980 (motor symptom)
471 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

More therapeutic options have become available for Parkinson's disease (PD) in recent years, leading to significant improvements in motor control both at early and advanced disease stages. More importantly, the need to expand disease management beyond motor symptom control has been recently highlighted and contribution of non-motor features to quality of life is now relevant. Dopamine agonists represent a valid therapeutic option in PD and their effect on non-motor domains like mood or cognition is now acknowledged as a key factor in fully addressing patients' needs. Pramipexole is a well established dopamine agonist that is currently being investigated for its potential disease-modifying effect and action on mood in PD. In this review we will examine factors contributing to treatment decision-making and discuss how a proper balance between motor and non-motor features should be aimed for in approaching PD therapy.
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PMID:Dopamine agonist-based strategies in the treatment of Parkinson's disease. 1938 65

Motor symptoms in Parkinson's disease (PD) are caused by a severe loss of pigmented dopamine-producing nigro-striatal neurons. Symptomatic therapies provide benefit for motor features by restoring dopamine receptor stimulation. Studies have demonstrated that delaying the introduction of dopaminergic medical therapy is associated with a rapid decline in quality of life. Nonmotor symptoms, such as depression, are common in early PD and also affect quality of life. Therefore, dopaminergic therapy should typically be initiated at, or shortly following, diagnosis. Monamine oxidase-B inhibitors provide mild symptomatic benefit, have excellent side effect profiles, and may improve long-term outcomes, making them an important first-line treatment option. Dopamine agonists (DAs) provide moderate symptomatic benefit but are associated with more side effects than levodopa. However, they delay the development of motor complications by delaying the need for levodopa. Levodopa (LD) is the most efficacious medication, but its chronic use is associated with the development of motor complications that can be difficult to resolve. Younger patients are more likely to develop levodopa-induced motor complications and they are therefore often treated with a DA before levodopa is added. For older patients, levodopa provides good motor benefit with a relatively low-risk of motor complications. Using levodopa with a dopa-decarboxylase inhibitor lessens adverse effects, and further adding a catechol-O-methyl transferase inhibitor can improve symptom control.
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PMID:Improving symptom control in early Parkinson's disease. 2118 Jun 28

Pain is a common non-motor symptom of Parkinson's disease (PD) that markedly impacts patients' quality of life. Although pain occurs mostly secondary to motor disability of PD, pain may antedate motor symptoms by years. Numerous studies have shown that PD patients manifest altered sensory and pain thresholds compared with control subjects. Although both levodopa and deep brain stimulation improve motor symptoms, there remains no direct correlation between motor improvement and altered pain sensitivity, suggesting that motor symptoms and pain do not necessarily share pathogenetic mechanisms. Whether nociceptive processing is dysfunctional in the early stages of PD, when motor symptoms are not prominent, remains uncertain. In this review, we highlight the evidence for disrupted nociceptive processing in patients with early-stage PD. Painful symptoms and aberrant pain processing in early PD are associated with both central and peripheral deafferentation. Dopamine depletion in selective striatal regions, and the development of Lewy pathology in specific non-dopaminergic subcortical areas, underlie the clinical features of pain at this early disease stage. An increased awareness of pain as an early feature of PD might provide further insights into a mechanism-based approach to sensory system dysregulation in this disease.
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PMID:Pain in early-stage Parkinson's disease: Implications from clinical features to pathophysiology mechanisms. 2853 82

Autonomic dysfunction is a common non-motor symptom in Parkinson's disease (PD). Dopamine and serotonin are known to play a role in autonomic regulation, and, therefore, PD-related degeneration of serotonergic and dopaminergic neurons in these regions may be associated with autonomic dysfunction. We sought to clarify the association between extrastriatal serotonergic and striatal dopaminergic degeneration and the severity of autonomic symptoms, including gastrointestinal, pupillomotor, thermoregulatory, cardiovascular, and urinary dysfunction. We performed hierarchical multiple regression analyses to determine the relationships between (extra)striatal serotonergic and dopaminergic degeneration and autonomic dysfunction in 310 patients with PD. We used [¹²³I]FP-CIT SPECT binding to presynaptic serotonin (SERT) and dopamine (DAT) transporters as a measure of the integrity of these neurotransmitter systems, and the SCOPA-AUT (Scales for Outcomes in Parkinson's Disease-Autonomic) questionnaire to evaluate the perceived severity of autonomic dysfunction. Motor symptom severity, medication status, and sex were added to the model as covariates. Additional analyses were also performed using five subdomains of the SCOPA-AUT: cardiovascular, gastrointestinal, urinary, thermoregulatory, and pupillomotor symptoms. We found that autonomic symptoms were most significantly related to lower [¹²³I]FP-CIT binding ratios in the right caudate nucleus and were mainly driven by gastrointestinal and cardiovascular dysfunction. These results provide a first look into the modest role of dopaminergic projections towards the caudate nucleus in the pathophysiology of autonomic dysfunction in PD, but the underlying mechanism warrants further investigation.
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PMID:Autonomic failure in Parkinson's disease is associated with striatal dopamine deficiencies. 3216 62

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